From owner-cardiovascular@net.bio.net Mon Mar 01 22:00:00 1999 Path: biosci!newshost.lanl.gov!awabi.library.ucla.edu!128.230.129.106!news.maxwell.syr.edu!newspeer.monmouth.com!rain.fr!wanadoo.fr!not-for-mail From: "philippe" Newsgroups: bionet.biology.cardiovascular Subject: telex congrès Date: Tue, 2 Mar 1999 12:13:52 +0100 Organization: Wanadoo - (Client of French Internet Provider) Lines: 7 Message-ID: <7bghd9$bnc$2@platane.wanadoo.fr> NNTP-Posting-Host: tntbjn22-77.abo.wanadoo.fr X-Newsreader: Microsoft Outlook Express 4.72.3155.0 X-MimeOLE: Produced By Microsoft MimeOLE V4.72.3155.0 Bonjour, vous étes médecin et voulez recevoir nos prochain telex congrès cardiologie par courriel , écrivez-nous... Merci de nous spécifier votre pays d exercice. From owner-cardiovascular@net.bio.net Mon Mar 01 22:00:00 1999 Path: biosci!news.stanford.edu!newsfeed.berkeley.edu!sunqbc.risq.qc.ca!newsflash.concordia.ca!pitt.edu!not-for-mail From: pxpst2@unixs.cis.pitt.edu (Peter) Newsgroups: bionet.biology.cardiovascular,sci.med.cardiology,alt.support.angioplasty Subject: Re: How much aspirin? Date: Tue, 02 Mar 1999 10:56:58 -0500 Organization: University Of Pittsburgh Lines: 42 Message-ID: References: <36d3eec1.155528720@news.primenet.com> <7b6ebp$c9d$1@news1.cableinet.co.uk> NNTP-Posting-Host: pelli.pathology.pitt.edu Mail-Copies-To: pxpst2@unixs.cis.pitt.edu X-Newsreader: MT-NewsWatcher 2.4.4 In article <7b6ebp$c9d$1@news1.cableinet.co.uk>, "[.chris]" wrote: > > As a result of that duscussion, I asked my Cardioman why I was (at that > time) the only person on 1 x 75mg on alternate days. He explained the > current research re. less is better and in cunjunction with the incidence of > stomache complaints (indigestion, cramps etc) and nosebleeds, the > recommended dose is adjusted and individual to the patient. I am not a doctor but I am a researcher. But I feel that an explination of the mode by which asprin works may shed light on the docters reasoning. Aspirin,Ibupropen, and Naproxin all act to block the action of an enzyme called cyclooxygenase(COX). The reason that aspirin is the prefered drug is due to the fact that it IRREVERSABLY binds to this enzyme and blocks its action. The main action of this enzyme(COX) is to create certain "signal molecules" that tell your body that inflamation is needed. Inflamation is a response by your body to deal with just about all kinds "insults". The signal molecules are called prostoglandins. The Other two drugs Ibupr. and naprox. are reversable inhibitors of cylooxygenase. Due to the fact that asprin is irreversable, The blocked enzyme must be cleared from the body and new enzyme must be made. With the reversable one, the inhibitor will disassociate from the COX and the COX will be able to work. If my memory serves me correctly, Aspirin will clear in about 24 hrs while the other two will clear in about 8 hrs. BTW, extended use of COX inhibitors is believed to reduced prostate cancer rates and probaly aterosclerosis. If you are interested in learning more you should check out the National Lybrary of Medicine at NIH. These and other topics can be explored online. Think of it as your tax dollars working for you. http://www.nlm.nih.gov/medlineplus/ -- Peter " Don't you eat that yellow snow Watch out where the huskies go" FZ From owner-cardiovascular@net.bio.net Tue Mar 02 22:00:00 1999 Path: biosci!ODONT3.U-STRASBG.FR!gaosaofaa12 From: gaosaofaa12@ODONT3.U-STRASBG.FR (gr8ofres) Newsgroups: bionet.biology.cardiovascular Subject: 16 Great Offers! 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For removal from list - call 800-242-0363 x1292 From owner-cardiovascular@net.bio.net Tue Mar 02 22:00:00 1999 Path: biosci!AOL.COM!SPhil79466 From: SPhil79466@AOL.COM Newsgroups: bionet.biology.cardiovascular Subject: Explosive New Marketing Strategy 800 607-6006 Ex 2492 Date: 2 Mar 1999 23:51:06 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 34 Sender: daemon@net.bio.net Distribution: world Message-ID: <1c8625cf.36dce520@aol.com> NNTP-Posting-Host: net.bio.net This is a 1 time mailing Fire the Boss and break the Alarm Clock! I did! after eleven years, I left a $140,000 a year income for this opportunity I can truly say it was one of the best decisions of my life!!! Never commute again! make $2000-$5000 per week from home with a turn key marketing system! To find out how our system works call the 800#. You can start out in your spare time, work part time or work up to full time if you want to! It's your business! Call 1-800 607-6006 ex 2492# then press 1 no selling! stay home with the family! Proven track record of success! 1 800-607-6006 ex 2492# call now! Profit From The Internet Growth-Explosion 800 607-6006 Ex 2492 Thank You From owner-cardiovascular@net.bio.net Tue Mar 02 22:00:00 1999 Path: biosci!newshost.lanl.gov!awabi.library.ucla.edu!208.134.241.18!newsfeed.cwix.com!158.43.192.17!rill.news.pipex.net!pipex!peer.news.th.u-net.net!u-net!newsr2.u-net.net.POSTED!not-for-mail From: "galyles" Newsgroups: bionet.biology.cardiovascular,sci.med.cardiology,alt.support.angioplasty References: <36d3eec1.155528720@news.primenet.com> <7b6ebp$c9d$1@news1.cableinet.co.uk> Subject: Re: How much aspirin? Lines: 113 X-Newsreader: Microsoft Outlook Express 4.72.3110.1 X-MimeOLE: Produced By Microsoft MimeOLE V4.72.3110.3 Message-ID: <6Y%C2.1971$U3.2484@newsr2.u-net.net> Date: Wed, 3 Mar 1999 01:06:04 -0000 NNTP-Posting-Host: 195.102.196.77 X-Complaints-To: news@u-net.net X-Trace: newsr2.u-net.net 920423298 195.102.196.77 (Wed, 03 Mar 1999 01:08:18 BST) NNTP-Posting-Date: Wed, 03 Mar 1999 01:08:18 BST Organization: (Posted via) U-NET Internet Ltd. Peter wrote in message ... >In article <7b6ebp$c9d$1@news1.cableinet.co.uk>, "[.chris]" > wrote: > >> >> As a result of that duscussion, I asked my Cardioman why I was (at that >> time) the only person on 1 x 75mg on alternate days. He explained the >> current research re. less is better and in cunjunction with the incidence of >> stomache complaints (indigestion, cramps etc) and nosebleeds, the >> recommended dose is adjusted and individual to the patient. > >I am not a doctor but I am a researcher. But I feel that an explination >of the mode by which asprin works may shed light on the docters reasoning. >Aspirin,Ibupropen, and Naproxin all act to block the action of an enzyme >called cyclooxygenase(COX). The reason that aspirin is the prefered drug >is due to the fact that it IRREVERSABLY binds to this enzyme and blocks >its action. The main action of this enzyme(COX) is to create certain >"signal molecules" that tell your body that inflamation is needed. >Inflamation is a response by your body to deal with just about all kinds >"insults". The signal molecules are called prostoglandins. It is true that aspirin is an irreversible inhibitor of the cyclooxygenase enzyme. However, the antithrombotic action of low dose aspirin requires a little more explanation. The cyclooxygenase enzyme is the first biochemical step in a process which converts a fatty acid called arachidonic acid into a mixture of different prostaglandin-type molecules. However, the composition of this mixture produced by additional biochemical steps depends upon the cell types one is considering as their source. Some of these prostaglandins are important as contributory mediators of "inflammation" and the irreversible blockade by aspirin of their production in cells (such as those of the immune system) responsible for starting up the inflammatory response is important for the well-known anti-inflammatory (and probably also the anti-fever and pain killing) actions of aspirin. However, in specific reference to the antithrombotic effect of aspirin, one needs to consider the prostaglandin-like molecules that are generated specifically in the blood and in the blood vessels. Here, there are two types of cells which are of relevance to the discussion - the circulating blood platelet cells, and the endothelial cells which constitute the innermost lining of the blood vessel. In platelets, the prostaglandin-like molecule which is produced through the cycloooxygenase pathway is called thromboxane A2, and the properties of this chemical released from platelets passing through the blood vessels is that it promotes the sticking of the platelets to the blood vessel wall around which blood clotting may occur (i.e. it promotes thrombosis), and thromboxane also can constrict (narrow) blood vessels by contracting the muscle cells in the vessel wall, which can also increase the chances of a clot blocking the vessel. On the other hand, the prostaglandin-like molecule produced via cyclooxygenase by the endothelial cells is called prostacyclin (or sometimes prostaglandin I2) and this is good because this agent inhibits platelet aggregration and causes relaxation of the muscle cells i.e. it opposes the actions of thromboxane. In healthy blood vessels, it is generally considered that the two systems (platelets vs.endothelial cells) are operating to produce thromboxane and prostacyclin in a balanced fashion such that the thrombotic effect of thromboxane is not allowed to occur. However, in thrombosis causing heart attacks or strokes it is possible that the thromboxane action of the platelets in some way may become overriding - perhaps due to localized damage in some blood vessel endothelial cells such that they are unable to generate sufficient prostacyclin to prevent platelets sticking and clot formation on the vessel lining. This is where "low-dose" aspirin is believed to come to the rescue and prevent this happening for the following reasons. Firstly, aspirin will inhibit irreversibly the cyclooxygenase in both the platelets and the endothelial cells and so, theoretically, might be expected to block the production of both thromboxane (the bad guy!) and also prostacyclin (the good guy!). Once the cycloooxygenase enzyme has been inhibited, it is totally non-functional and new enzyme has to be synthesized in the cells in order for them to recover their ability to produce thromboxane or prostacyclin. And.... herein lies a difference between the two types of cells. Platelets within the circulation have no protein synthetic machinery to make fresh cyclooxygenase enzyme, whereas endothelial cells do! Consequently, platelet cyclooxygenase (and therefore thromboxane production) effectively remains permanently inhibited as long as aspirin is present (completely new platelet cells are formed and released from the bone marrow slowly, and containing new enzyme, but this is a relatively slow process!). On the other hand, although the cycloooxygenase in the endothelial cells (making prostacyclin) is substantially inhibited by the low-dose aspirin, it is because the endothelial cells can synthesize proteins that new copies of the enzyme are being made at a relatively faster rate in these cells in the blood vessel wall, to partially offset the inhibitory effect of aspirin. The low-dose of aspirin is probably important because it is unable to inhibit all of the new enzyme at the rate it is being produced in the endothelial cells, so this favours a resetting of the balance for some prostacyclin production still to occur from the endothelial cells, while at the same time the aspirin has caused a considerably reduced (and possibly absent) production of thromboxane from the platelets. Incidentally, the side effects of aspirin e.g. gastric bleeding in some patients are also ascribed to a block of cyclooxygenase. Here the natural production of prostaglandins and prostacyclin by this enzyme present in cells within the stomach lining is believed to be beneficial for preserving the "intactness" of that lining. Hence, the ability of aspirin to prevent these "beneficial" prostaglandin-like compounds to be produced in the stomach may promote some breakdown of this lining leading to bleeding in susceptible individuals. Again, "lower-dose" aspirin may reduce the chances of this occurring compared with the usual "higher doses" of aspirin required for its anti-inflammmatory effects, for which gastric bleeding is a side effect of significant incidence. Research is still ongoing into these mechanisms. Recent evidence is beginning to emerge that there are different forms of the cyclooxygenase enzyme present in different cell types, but I won't complicate the story at this stage because the possible significance of this is still at the early stages of investigation . However, our understanding of the actions of aspirin in terms of its antithrombotic effect may be further refined or even new mechanisms proposed in due course. Geoff From owner-cardiovascular@net.bio.net Thu Mar 04 22:00:00 1999 Path: biosci!HOTMAIL.COM!qmesquita From: qmesquita@HOTMAIL.COM ("Quintiliano H. de Mesquita") Newsgroups: bionet.biology.cardiovascular Subject: Myogenic Theory Explains! Date: 5 Mar 1999 03:30:02 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 395 Sender: daemon@net.bio.net Distribution: world Message-ID: <36DFBCAC.A8A8FF3B@hotmail.com> NNTP-Posting-Host: net.bio.net Myogenic Theory Explains! “The Thrombogenic Theory of Myocardial Infarction Tumbled Down and the Ortodoxy Didn’t Have Noticed” The ortodox cardiology stay repressed in their therapeutic behaviour in front of coronary- myocardiopathy, since when the thrombogenic theory (TT) started to tumble down after 25 years of clinical research (1944-69), with the recognition about the failure of coumarin and heparin anticoagulants to stop the unstable angina (UA) and in prevention of myocardial infarction (MI). During 10 years (1944-54) we have participated in clinical studies about anticoagulants, recording its failure to stop the UA and in the MI prevention, what led us to reject such therapeutic agents. In 1969, with the general admission of the anticoagulants failure, happened the introduction of the coronary bypass surgery practiced directly in man, without the previous assessment in experimentation animals. Consequently, heart surgeons and cardiologists with no other visible way to manage chronic coronary-myocardiopathy and acute coronary syndromes, have assumed together the compulsive intervencionism practiced during the last 3 decades: myocardial reperfusion through angioplasty and/or coronary bypass surgery. At the same time they indicate coronary dilators, antiaggregate of platelets and beta blockers. Beta blockers, in our point of view, represents a contradictory behaviour by the cardiologists in front of the contractile deficient condition of the dependent coronary myocardial segment, frequently developing generalized hypotonia. The only actual concern by the ortodox cardiologist is to provide the myocardial reperfusion in any case, independently of sex or age, without any future guarantee regarding the success of the reperfusion act, generally submitted to the repetition practice due to its frequent failure. In 1972, we developed the myogenic theory (MT) stating the acute myocardial infarction (AMI) as the cause and not consequence of coronary thrombus. The myogenic theory met important support in pathological anatomy findings since 1950 decade where the authors preconized the coronary thrombus as consequence of acute myocardial infarction and not its cause. According the myogenic theory concepts the AMI is developed by functional degradation state of the regional myocardial coronary-dependent characterized by a pathophysiology essencially myogenic, in the 3 stages of coronary-myocardiopathy: - The stable angina with or w/out previous myocardial infarction, developed by exertion or emotion and producing regional ventricular ischemia (RVI), coronary-dependent, in which the negative inotropic action develops the regional myocardial insufficiency (RMI), reciprocal, ceasing with the stop of the provoking cause. - The unstable angina (UA) as a spontaneous, reversible and recurrent syndrome resulted from an abrupt, and unexpected RMI followed by RVI of long duration and resistant to all available therapeutic agents. - The UA is perpetuated in the last crises of angina with its transformation in infarctioning clinical picture (ICP) represented by RMI + RVI -> myocardial infarction -> myocardial necrosis -> coronary thrombosis not obligatory; electrocardiographically recognized as myocardial infarction with Q wave and w/out Q wave. In front of this pathophysiological mechanism the cardiotonic appeared as a new therapeutic concept and since 27 years ago proves to be capable to preserve the myocardial and symptomatic stability in the stable angina pectoris with or w/out previous infarction, to stop the UA and to provide the transformation of ICP in avoided myocardial infartion, ICP- interrupted myocardial infarction or characterized as ICP-infarcted according the behaviour of enzymatic peaks. In 1981 the thrombogenic theory suffered the final tumble down when the thrombolytics which were reintroduced in the UA and AMI showed that they are uneffectives regarding the clinical events in the UA and passed to be indicated only in the treatment of AMI. During the last 2 decades has been clearly demonstrated in vast literature that, thrombolytics and angioplasty release the coronary arteries related with the MI, while is recorded the coronary/dependent ventricular dysfunction process. Gregorini, L et al, in a recent article (Circulation, 1999; 99:482-90), besides to confirm such aspects of left ventricular dysfunction after thrombolysis and coronary angioplasty, stressed the role of alpha-adrenergic blockers in reducing the coronary vasoconstriction and improving the left ventricular dysfunction post-ischemic. In the myogenic theory point of view, the left ventricular dysfunction recorded in this way is preconized as a primary process. Also, the paper from Tamura, K et al (Am Heart J, 1996; 131:731-5) reported about successive echocardiographical and electrocardiographical recordings in UA showing myocardial aspects of RMI + RVI which concepts are inside of the MT; If they had applied the cardiotonic during their study, they certainly had the record of immediate clinical and physiological stop of UA. We need to emphasize the paper from Murakami, T et al (Am J Cardiol, 1998; 82 :839-44) about its new methodology represented by aspiration thrombectomy after thrombolysis showing that intracoronary thrombus is absent in a substantial number of patients with acute myocardial infarction. We have the impression that the TT once more have lost its support about the coronary thrombosis in the AMI when these authors came to strenghten our concept of primary myocardial infarction and secondary coronary thrombosis. Their findings after thrombolysis indicate: Recent thrombus (49%), Without thrombus (30%), Atheroma (14%), Organized thrombus (2%) and Not defined thrombus (5%). No doubts that all ways go to the complete demonstration that cases normally submitted to angiographic and ventriculographic studies arrive with the recognition of conflictant aspects with the TT and compatible aspects with the MT. Therefore, we will pass in review such aspects that must be considered as the pathological reality of coronary-myocardiopathy which the Myogenic Theory Explains: - Roberts, WC (Circulation, 1972;49:1) showed that in cases of AMI with early sudden death that coronary thrombosis ocurred in approximately 10% of cases with subendocardial infarction of left ventricle and in around 50% of cases with transmural necrosis. MT explains: the recent findings by Murakami et al during the acute myocardial infarction, confirmed and reinforced old pathological studies realized in the 1950 decade which were stressed by Roberts in 1972. - Spain, DM and Bradess, VA (Am J Med Sci, 1960; 240:701) showed total coronary obstruction of atherosclerotic nature representing around of 75% of cases of AMI and only 25% of cases with coronary thrombosis in autopsy, recorded during 25 years. MT explains: in these cases the total coronary atherosclerotic obstruction was old and the AMI was resulting from severe regional myocardiopathy coronary-dependent with MRI + RVI and secondary coronary thrombosis not obligatory. - Spain, DM and Bradess, VA (Circulation, 1960; 22: 816) recorded the increase of incidence of coronary thrombosis related with the increase of lifetime after AMI: < 1 hour = 16%, 1-14 hours = 37% and > 24 hours = 53%. MT explains: these numbers represent a clear demonstration that AMI is primary and the coronary thrombosis secondary, not obligatory and with slow formation. - Erhardt, LR et al (Lancet, 1973; 1:387; Am Heart J, 1976; 91:592) demonstrated the coronary thrombosis incorporating fibrinogen marked by I-125 and I-131, radioactive agents administered after 10-15 hours from the start of the clinical manifestations of AMI, fact that suggests coronary thrombosis as consequence of primary myocardial necrosis; and the record of the exclusion of I-125 in the thrombus of 1 case, when the radioactive agent was administered 47 hours after the start of clinical manifestations of AMI. MT explains: the radioactive agents I-125 and I-131 incorporated to the fibrinogen in the thrombus in progressive organization, not happened in the referred 1 case because the thrombus was already formed. - Hellstrom, HR (Circulation, 1970; 42 (Suppl III) : 165) demonstrated in a experimental manner, that AMI produced by surgical ligature of coronary artery without endothelial lesion was responsible by the vascular stasis and the consequent coronary thrombosis, recorded in the coronary artery after released. MT explains: significant coronary thrombosis formed as consequence of vascular stasis in the artery blocked by the AMI; such process is similar to the cerebral and cardiac infarctions coincident with the use of anticonceptives. - AMI coincident with rupture of atheromatous plaque and coronary thrombosis from coronary artery related with the infarcted region. MT explains: the coronary thrombosis watched in this way have been conveniently interpreted by the ortodoxy as primary. However, the coronary thrombosis can come late, subsequently to the AMI, whose rupture of the plaque should be provoked by the invasion of white blood cells identified as inflamatories and by its derived products providing the formation of coronary thrombosis. - Coronary arteries angiographically normal related with the infarction area without coronary thrombosis. MT explains: these arteries are widely compromised by the atherosclerotic process, exclusive of wall, apparently canalized but inelastic, what modifies the circulation from continuous to intermitent type which will endanger the dependent myocardium, taking it to the AMI according the MT model. - Case of UA interrupted by the cardiotonic, showing normal coronary arteries with slow flow and defined asynergy of the myocardial region coronary dependent and with systolic residual volume increased > (+/++); which, in the period of 2 years (still using cardiotonic), evolved to the total obstruction of the left descendent anterior artery and ventriculogram identical with systolic residual volume > (++), but without worsening the clinical situation. MT explains: the use of cardiotonic + coronary dilator guaranteed the preservation of myocardial and symptomatic stability, in spite of the evolution of the coronary arterial process to the total obstruction without evolving to the MI. - Bulkley, BH and Hutchins, GM (Circulation, 1977;56:906) published cases of AMI situated in revascularized region by pervious coronary artery bypass, interpreted as paradoxal infarction. MT explains: in these cases the myocardial ischemic effects exist and the ventriculographic aspects are useful to demonstrate that AMI is primary, even without coronary thrombosis which we consider not obligatory. - Old atherosclerotic plaque totally obstructing the coronary artery related with the infarcted region. MT explains: cases of this type are useful to demontrate that the compromised coronary-dependent myocardium is taked to the RMI + RVI and to the AMI by evolutive and degradated coronary-myocardiopathy process. - AMI developed during the habitual or unusual practice of physical activities during or immediate after the ergometric test, sex, sport or during the digestive period plus physical efforts (even light), frequently happens in front of coronaries with not significant, severe or even total obstructions by old plaques, simultaneous or not with coronary thrombosis. MT explains: in that cases the dependent coronary myocardial region compromised in its structure can arrive to the AMI through an abrupt exhaustion of the myocardial region – RMI + RVI – followed by coronary thrombosis. - The occurrence of AMI within 2-21 days after the abrupt interruption of beta blockers, in continued use. MT explains: due to its negative inotropic effect beta blockers develop generalized hypotonia which eliminate the intersegmentary confrontation of the coronary/dependent myocardium, with the effect of temporization but without to avoid the AMI neither other complications like cardiac insufficiency and sudden death. Its abrupt interruption is followed by the reestablishment of the intersegmentar confrontation owing to the unprepared coronary/dependent myocardial region which takes to the UA with manifestations of RMI + RVI, occurrence of AMI, cardiac insufficiency, severe arrhythmias and sudden death. - Occurrence of AMI after the interruption of cardiotonic in continued use for the preservation of the myocardial and symptomatic stability in chronic coronary-myocardiopathy with or without previous myocardial infarction. MT explains: the cardiotonic absence provides the myocardial intersegmentar confrontation which may lead to the UA and consequently to the AMI, according the model preconized by the MT. - Case of UA interrupted by the cardiotonic, showing the 3 coronaries - left descendent anterior, right and circunflex – completely obstructed, but with a rich net of collateral coronary, and left ventricular dysfunction but without recordings of anterior infarction. MT explains: This case came to confirm more one time the immediate results of interruption of UA in 100% of the cases and without mortality, with the use of the new therapeutical concepts of the MT. Treatment of attack followed by the permanently upkeeping with the cardiotonic + coronary dilator which develops the return to the myocardial stability preserved in this way and as prevention of myocardial infarction. - Case of angina, permanent and with great suffering with repeated crises of UA, resistant to all types of medication, lasting 9 months; happening 10 years after the myocardial infarction with total obstruction of the 3 epicardial coronaries – DAE, D and CFx – ventriculogram with large increase of the cardiac area and characteristics of hibernating Heart. He was attended in our coronary care unit during the UA crisis when was submitted to the cardiotonic, recording immediate and complete relief. From this moment on this patient remained under treatment with cardiotonic in a myocardial and symptomatic stability during 13 years of comfortable survival, passing away at 73 years old, due to a cerebral stroke. MT explains: this case was interpreted as permanent deficient myocardial condition mixed with symptomatic instability represented by crises of RMI + RVI finally interrupted by the cardiotonic and therefore upkeeped for long survival. - Cases of chronic stable angina with the symptomatic and myocardial stability preserved by decades, with or w/out previous myocardial infarction showing evolutive coronary atherosclerotic processes to the total obstruction of 2-3 coronaries w/out occurrence of AMI. MT explains: maintained by the cardiotonic + coronary dilator therapeutic since 1991 with the addition of ACE inhibitor, his future has been calm and guaranteed, complementing in this way the effects provided by the coronary collateral circulation. - Cases of UA interrupted by the cardiotonic, maintained by decades, of patients with significant obstructions of 2-3 coronaries have had evolution to total obstruction with rich net of collateral coronary, without recordings of myocardial infarction, during the long survival. MT explains: Interruption of UA by cardiotonic as attack and maintenance treatment have guaranteed the preservation of myocardial and symptomatic stability as well in the prevention of myocardial infarction. - Cases generally admitted in coronary care units as with AMI were treated by cardiotonic in our unit, showing clinical and enzymatic transformations which led us to classify them as clinical infarctioning pictures, determined by the behaviour of enzymatic peaks. MT explains: the cardiotonic in AMI was considered as a myocardial protector (Mesquita, 1973; Pizzarello et al, 1975 and Morrison et al, 1976.1980). Through the enzymatic peaks the cases observed by us were distinguished in tyhe following way: ? Myocardial infarction avoided: 20% of cases with normal enzymatic peaks or < 2x the normal. ? Infarctioning clinical picture- interrupted: 47% of cases with enzymatic peaks < 3x the normal. ? Infarctioning clinical picture- infarcted: 33% of cases with enzymatic peaks > 3x the normal. - The method of Murakami et al using intracoronary thrombectomy aspiration and their findings showing absence of coronary thrombus during acute myocardial infarction and the use of transesophageal echocardiogram for the same purpose. MT explains: the aspiration thrombectomy with thrombolysis and the echocardiography can serve as support to the myogenic theory and keep away forever the TT in vivo, offering to the pathologists the prove that coronary thrombus is secondary. Serve also as a response to the paper of Chandler et al (AM J Cardiol, 1974; 34:823) about coronary thrombosis and AMI simultaneous, indicating what is primary and secondary. In Murakami method the thombolysis release the artery related with the myocardial infarction while the aspiration thombectomy cleans the artery, stressing the left ventricular dysfunction which can be corrected by the cardiotonic or by using the alpha-adrenergic blocker as Gregorini et al. - Important findings in the acute UA about the incidence of intracoronary thrombus (52-85%) few hours after the start of symptoms until 2 weeks, while its incidence in the chronic phase has been always low (0-12%). MT explains: the echocardiography during the UA clearly shows the myogenic mechanism recording the RMI which develops the RVI characterized by ECG, coincident with platelet aggregates and inflammatory blood cells which invade the involved region, becoming to the normal with the stop of crises. - Ambrose et al (Am J Cardiol, 1988;61:244-7) considered the myocardial infarction without Q wave as an intermediary stage from UA to the myocardial infarction with Q wave. They recorded total coronary obstruction in 26% of cases w/out Q wave and in 90% of cases with Q wave. MT explains: the myocardial infarction w/out Q wave as intermediate stage to the myocardial infarction with Q wave must be seen as favourable to the MT, and its mechanism is considered by us as the preconized for the UA of long duration and in smaller level than the reached by the AMI. So, in this case the myocardial lesion is less stressed in subendocardial or subepicardial layers, and with low incidence of coronary thrombosis. - DeWood, MA et al (NEJM, 1986; 315:417-23) recorded total coronary obstruction in 32% of AMI cases without Q wave and in a more detailed study showed an incidence for total coronary obstruction significantly and progressively increased in relation with the execution time of angiographic examination: 26% in 24 hours, 37% from 24-72 hours and 42% from 72 hours to 7 days. They also have recorded that the incidence of subtotal coronary obstruction (> 90%), in myocardial infarction without Q wave, showed evident reduction in gradual manner: 34% in 24 hours, 26% from 24-72 hours and 18% from 72 hours to 7 days. MT explains: These crescent indicators show that the formation of coronary thrombus is secondary to the AMI depending directly of the evolution time of the infarctioning process to become infarcted process; Evidently, the gradual reduction of indicators referring to subtotal obstruction was observed contrary and parallel to the thrombotic transformations recorded secondarily to the infarction. - Thrombolytics in UA improve the arterial events but show inefficiency about the clinical events and regarding to stop the pathophysiological process, what led investigators to recommend its use only in AMI. (Rentrop, P et al, 1981, Williams, DO et al, 1990, Leinbach, RC, 1972, Freeman, MR et al, 1992, TIMI IIIA Investigators, 1993 and Chen, L et al, 1997) MT explains: These results came to confirm the failure of anticoagulants (1969) and completed the tumble down of the TT what the ortodox cardiology make believe that do not happens. - Roberts, WC (Am J Cardiology, 1984; 97:1410) wrote: "When I have an acute myocardial infarction take me to the hospital that has a cardiac catheterization laboratory and open cardiac surgical facilities". MT explains: in case of chronic coronary-myocardiopathy the preservation of myocardial and symptomatic stability and prevention of myocardial infarction have been guaranteed by the association of cardiotonic + coronary dilator + ACE inhibitor, permanently. So, my advice to all them which think like the grand teacher of pathological anatomy represented by William C. Roberts, to defend their heart with calm using the therapeutical efficacy by cardiotonics which complement the providential action of the collateral coronary circulation. Quintiliano H. de Mesquita, M.D. For more information please visit my homepage at http://www.infarctcombat.org/qhm/homepage.html From owner-cardiovascular@net.bio.net Thu Mar 04 22:00:00 1999 Path: biosci!news.stanford.edu!newsfeed.berkeley.edu!usenet.INS.CWRU.Edu!not-for-mail From: JustaPhD Newsgroups: bionet.biology.cardiovascular,sci.med.cardiology,alt.support.angioplasty Subject: Re: How much aspirin? Date: Fri, 05 Mar 1999 10:58:54 -0500 Organization: Case Western Reserve University, Cleveland OH (USA) Lines: 103 Message-ID: <36DFFF3E.632B29E0@juno.com> References: <36d3eec1.155528720@news.primenet.com> <7b6ebp$c9d$1@news1.cableinet.co.uk> NNTP-Posting-Host: meds18972.meds.cwru.edu Mime-Version: 1.0 Content-Type: text/plain; charset=us-ascii Content-Transfer-Encoding: 7bit X-Mailer: Mozilla 4.5 [en] (Win98; I) X-Accept-Language: en Peter wrote: > > In article <7b6ebp$c9d$1@news1.cableinet.co.uk>, "[.chris]" > wrote: > > > > > As a result of that duscussion, I asked my Cardioman why I was (at that > > time) the only person on 1 x 75mg on alternate days. He explained the > > current research re. less is better and in cunjunction with the incidence of > > stomache complaints (indigestion, cramps etc) and nosebleeds, the > > recommended dose is adjusted and individual to the patient. The reason that a single aspirin daily is recommended is that the biggest successful clinical trial used that dose. Smaller studies have shown that lower doses on alternate days can be equally effective - and of course there are reduced GASTRIC side effects. THERE IS NO WAY TO REDUCE BLEEDING SIDE EFFECTS - since the impaired platelet function which leads to those side effects is exactly the effect that reduces the reinfarc rate! One study showed that most of the antiplatelet effect of aspirin occurs in the entero-hepatic circulation ( the blood coming out of the digestive system, carrying nutrients and drugs that have just been absorbed)- even when no detectable aspirin can be found in the systemic circulation (i.e. bloodstream). In theory, a single chilliness aspirin on alternate days SHOULD be effective. But no large scale studies have proven that to be the case ... so docs go with what's been published. If docs weren't too lazy to do the appropriate test, we could all be titrated for the minimal effective dose just by doing a bleeding time - when bleeding time increases from around a minute or so to three minutes or so, the aspirin is doing its job on the platelets. If you suffer from severe GI side effects to aspirin you might just ask your cardiologist to do this. > > I am not a doctor but I am a researcher. Me too - in fact I did some of the early work on aspirin-platelet effects. ' > But I feel that an explination > of the mode by which asprin works may shed light on the docters reasoning. > Aspirin,Ibupropen, and Naproxin all act to block the action of an enzyme > called cyclooxygenase(COX). The reason that aspirin is the prefered drug > is due to the fact that it IRREVERSABLY binds to this enzyme and blocks > its action. The main action of this enzyme(COX) is to create certain > "signal molecules" that tell your body that inflamation is needed. > Inflamation is a response by your body to deal with just about all kinds > "insults". The signal molecules are called prostoglandins. The relevant signal molecule for the anti-thrombotic effect of aspirin is Thromboxane. It is made by platelets and significantly elevates their 'stickyness" - their ability to bind to broken blood vessels and aggregate with each other to form the primary blow-out patch. Unfortunately they also bind to atherosclerotic plaques through similar mechanisms. When you block thromboxane synthesis with aspirin, you diminish their ability to stick - but not to the point that you get serious bleeding disorders (usually). The Other two > drugs Ibupr. and naprox. are reversable inhibitors of cylooxygenase. Ibu yes - other drugs like naprosyn, indomethacin, etc have various degrees of "reversibility". But for the sake of this discussion there are only two drugs that matter - aspirin which is an anti-platelet drug, and ibuprofen which is too - but only for a few hours. Due > to the fact that asprin is irreversable, The blocked enzyme must be > cleared from the body and new enzyme must be made. With the reversable > one, the inhibitor will disassociate from the COX and the COX will be able > to work. If my memory serves me correctly, Aspirin will clear in about 24 > hrs while the other two will clear in about 8 hrs. It aint the enzyme that has to be cleared,or more importantly, regenerated - its the platelets. Unlike most other cells in the body, platelets cannot make significant new cyclooxygenase (what they have is made before they splinter off from their progenitor cells, the megakaryocytes). So, when you take even a single children's aspirin, most of the platelet cyclooxygenase is irreversibly inactivated. It takes on average about a week to renew your platelets so their aggregability goes from zero shortly after taking he aspirin back to normal in about a week - for a day or two it's low enough that likelihood of a thrombotic event is reduced significantly. The other cells in the body that have cyco-oxygenase can resynthesize all they need in anywhere from a few minutes to a few hours. With ibuprofen - the drug is totally cleared (well >99.9%) in about 6 hours and when the ibu is gone so is the platelet effect - take note menstruating women who have a headache. YOu wont lose as much blood if you take ibu rather than aspirin or alleve. > BTW, extended use of COX inhibitors is believed to reduced prostate > cancer rates and probaly aterosclerosis. Yeah - but then they increase the chance of stroke. > If you are interested in > learning more you should check out the National Lybrary of Medicine at > NIH. These and other topics can be explored online. Think of it as your > tax dollars working for you. > > http://www.nlm.nih.gov/medlineplus/ > > -- > Peter > > " Don't you eat that yellow snow > Watch out where the huskies go" > FZ From owner-cardiovascular@net.bio.net Thu Mar 04 22:00:00 1999 Path: biosci!agate!newsfeed.berkeley.edu!howland.erols.net!portc02.blue.aol.com!pitt.edu!not-for-mail From: pxpst2@unixs.cis.pitt.edu (Peter) Newsgroups: bionet.biology.cardiovascular,sci.med.cardiology,alt.support.angioplasty Subject: Re: How much aspirin? Date: Fri, 05 Mar 1999 13:01:42 -0500 Organization: University Of Pittsburgh Lines: 23 Message-ID: References: <36d3eec1.155528720@news.primenet.com> <7b6ebp$c9d$1@news1.cableinet.co.uk> <36DFFF3E.632B29E0@juno.com> NNTP-Posting-Host: pelli.pathology.pitt.edu Mail-Copies-To: pxpst2@unixs.cis.pitt.edu X-Newsreader: MT-NewsWatcher 2.4.4 In article <36DFFF3E.632B29E0@juno.com>, JustaPhD wrote: > It aint the enzyme that has to be cleared,or more importantly, regenerated - its > the platelets. Unlike most other cells in the body, platelets cannot make > significant new cyclooxygenase (what they have is made before they splinter off > from their progenitor cells, the megakaryocytes). I know this but I always thought that when the platlet is formed it has mRNA stores that it will use to transcribe new protein for 60 or so days of life of the platlet. BTW, I appreciate your discusion and thank all who have replied. -- Peter " Don't you eat that yellow snow Watch out where the huskies go" FZ From owner-cardiovascular@net.bio.net Thu Mar 04 22:00:00 1999 Path: biosci!MAIL.USA.COM!amail5 From: amail5@MAIL.USA.COM Newsgroups: bionet.biology.cardiovascular Subject: Revolutionary Plastic Surgery! Read This! 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Order a valid International Driver's License that can never be suspended or revoked. Confidentiality assured. CALL NOW!!! 1-937-586-9313 From owner-cardiovascular@net.bio.net Tue Mar 09 22:00:00 1999 Path: biosci!HOTMAIL.COM!qmesquita From: qmesquita@HOTMAIL.COM ("Quintiliano H. de Mesquita") Newsgroups: bionet.biology.cardiovascular Subject: Myogenic Theory Explains! Date: 9 Mar 1999 23:06:39 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 395 Sender: daemon@net.bio.net Distribution: world Message-ID: <36DFBEA2.B2FDC57F@hotmail.com> NNTP-Posting-Host: net.bio.net Myogenic Theory Explains! “The Thrombogenic Theory of Myocardial Infarction Tumbled Down and the Ortodoxy Didn’t Have Noticed” The ortodox cardiology stay repressed in their therapeutic behaviour in front of coronary- myocardiopathy, since when the thrombogenic theory (TT) started to tumble down after 25 years of clinical research (1944-69), with the recognition about the failure of coumarin and heparin anticoagulants to stop the unstable angina (UA) and in prevention of myocardial infarction (MI). During 10 years (1944-54) we have participated in clinical studies about anticoagulants, recording its failure to stop the UA and in the MI prevention, what led us to reject such therapeutic agents. In 1969, with the general admission of the anticoagulants failure, happened the introduction of the coronary bypass surgery practiced directly in man, without the previous assessment in experimentation animals. Consequently, heart surgeons and cardiologists with no other visible way to manage chronic coronary-myocardiopathy and acute coronary syndromes, have assumed together the compulsive intervencionism practiced during the last 3 decades: myocardial reperfusion through angioplasty and/or coronary bypass surgery. At the same time they indicate coronary dilators, antiaggregate of platelets and beta blockers. Beta blockers, in our point of view, represents a contradictory behaviour by the cardiologists in front of the contractile deficient condition of the dependent coronary myocardial segment, frequently developing generalized hypotonia. The only actual concern by the ortodox cardiologist is to provide the myocardial reperfusion in any case, independently of sex or age, without any future guarantee regarding the success of the reperfusion act, generally submitted to the repetition practice due to its frequent failure. In 1972, we developed the myogenic theory (MT) stating the acute myocardial infarction (AMI) as the cause and not consequence of coronary thrombus. The myogenic theory met important support in pathological anatomy findings since 1950 decade where the authors preconized the coronary thrombus as consequence of acute myocardial infarction and not its cause. According the myogenic theory concepts the AMI is developed by functional degradation state of the regional myocardial coronary-dependent characterized by a pathophysiology essencially myogenic, in the 3 stages of coronary-myocardiopathy: - The stable angina with or w/out previous myocardial infarction, developed by exertion or emotion and producing regional ventricular ischemia (RVI), coronary-dependent, in which the negative inotropic action develops the regional myocardial insufficiency (RMI), reciprocal, ceasing with the stop of the provoking cause. - The unstable angina (UA) as a spontaneous, reversible and recurrent syndrome resulted from an abrupt, and unexpected RMI followed by RVI of long duration and resistant to all available therapeutic agents. - The UA is perpetuated in the last crises of angina with its transformation in infarctioning clinical picture (ICP) represented by RMI + RVI -> myocardial infarction -> myocardial necrosis -> coronary thrombosis not obligatory; electrocardiographically recognized as myocardial infarction with Q wave and w/out Q wave. In front of this pathophysiological mechanism the cardiotonic appeared as a new therapeutic concept and since 27 years ago proves to be capable to preserve the myocardial and symptomatic stability in the stable angina pectoris with or w/out previous infarction, to stop the UA and to provide the transformation of ICP in avoided myocardial infartion, ICP- interrupted myocardial infarction or characterized as ICP-infarcted according the behaviour of enzymatic peaks. In 1981 the thrombogenic theory suffered the final tumble down when the thrombolytics which were reintroduced in the UA and AMI showed that they are uneffectives regarding the clinical events in the UA and passed to be indicated only in the treatment of AMI. During the last 2 decades has been clearly demonstrated in vast literature that, thrombolytics and angioplasty release the coronary arteries related with the MI, while is recorded the coronary/dependent ventricular dysfunction process. Gregorini, L et al, in a recent article (Circulation, 1999; 99:482-90), besides to confirm such aspects of left ventricular dysfunction after thrombolysis and coronary angioplasty, stressed the role of alpha-adrenergic blockers in reducing the coronary vasoconstriction and improving the left ventricular dysfunction post-ischemic. In the myogenic theory point of view, the left ventricular dysfunction recorded in this way is preconized as a primary process. Also, the paper from Tamura, K et al (Am Heart J, 1996; 131:731-5) reported about successive echocardiographical and electrocardiographical recordings in UA showing myocardial aspects of RMI + RVI which concepts are inside of the MT; If they had applied the cardiotonic during their study, they certainly had the record of immediate clinical and physiological stop of UA. We need to emphasize the paper from Murakami, T et al (Am J Cardiol, 1998; 82 :839-44) about its new methodology represented by aspiration thrombectomy after thrombolysis showing that intracoronary thrombus is absent in a substantial number of patients with acute myocardial infarction. We have the impression that the TT once more have lost its support about the coronary thrombosis in the AMI when these authors came to strenghten our concept of primary myocardial infarction and secondary coronary thrombosis. Their findings after thrombolysis indicate: Recent thrombus (49%), Without thrombus (30%), Atheroma (14%), Organized thrombus (2%) and Not defined thrombus (5%). No doubts that all ways go to the complete demonstration that cases normally submitted to angiographic and ventriculographic studies arrive with the recognition of conflictant aspects with the TT and compatible aspects with the MT. Therefore, we will pass in review such aspects that must be considered as the pathological reality of coronary-myocardiopathy which the Myogenic Theory Explains: - Roberts, WC (Circulation, 1972;49:1) showed that in cases of AMI with early sudden death that coronary thrombosis ocurred in approximately 10% of cases with subendocardial infarction of left ventricle and in around 50% of cases with transmural necrosis. MT explains: the recent findings by Murakami et al during the acute myocardial infarction, confirmed and reinforced old pathological studies realized in the 1950 decade which were stressed by Roberts in 1972. - Spain, DM and Bradess, VA (Am J Med Sci, 1960; 240:701) showed total coronary obstruction of atherosclerotic nature representing around of 75% of cases of AMI and only 25% of cases with coronary thrombosis in autopsy, recorded during 25 years. MT explains: in these cases the total coronary atherosclerotic obstruction was old and the AMI was resulting from severe regional myocardiopathy coronary-dependent with MRI + RVI and secondary coronary thrombosis not obligatory. - Spain, DM and Bradess, VA (Circulation, 1960; 22: 816) recorded the increase of incidence of coronary thrombosis related with the increase of lifetime after AMI: < 1 hour = 16%, 1-14 hours = 37% and > 24 hours = 53%. MT explains: these numbers represent a clear demonstration that AMI is primary and the coronary thrombosis secondary, not obligatory and with slow formation. - Erhardt, LR et al (Lancet, 1973; 1:387; Am Heart J, 1976; 91:592) demonstrated the coronary thrombosis incorporating fibrinogen marked by I-125 and I-131, radioactive agents administered after 10-15 hours from the start of the clinical manifestations of AMI, fact that suggests coronary thrombosis as consequence of primary myocardial necrosis; and the record of the exclusion of I-125 in the thrombus of 1 case, when the radioactive agent was administered 47 hours after the start of clinical manifestations of AMI. MT explains: the radioactive agents I-125 and I-131 incorporated to the fibrinogen in the thrombus in progressive organization, not happened in the referred 1 case because the thrombus was already formed. - Hellstrom, HR (Circulation, 1970; 42 (Suppl III) : 165) demonstrated in a experimental manner, that AMI produced by surgical ligature of coronary artery without endothelial lesion was responsible by the vascular stasis and the consequent coronary thrombosis, recorded in the coronary artery after released. MT explains: significant coronary thrombosis formed as consequence of vascular stasis in the artery blocked by the AMI; such process is similar to the cerebral and cardiac infarctions coincident with the use of anticonceptives. - AMI coincident with rupture of atheromatous plaque and coronary thrombosis from coronary artery related with the infarcted region. MT explains: the coronary thrombosis watched in this way have been conveniently interpreted by the ortodoxy as primary. However, the coronary thrombosis can come late, subsequently to the AMI, whose rupture of the plaque should be provoked by the invasion of white blood cells identified as inflamatories and by its derived products providing the formation of coronary thrombosis. - Coronary arteries angiographically normal related with the infarction area without coronary thrombosis. MT explains: these arteries are widely compromised by the atherosclerotic process, exclusive of wall, apparently canalized but inelastic, what modifies the circulation from continuous to intermitent type which will endanger the dependent myocardium, taking it to the AMI according the MT model. - Case of UA interrupted by the cardiotonic, showing normal coronary arteries with slow flow and defined asynergy of the myocardial region coronary dependent and with systolic residual volume increased > (+/++); which, in the period of 2 years (still using cardiotonic), evolved to the total obstruction of the left descendent anterior artery and ventriculogram identical with systolic residual volume > (++), but without worsening the clinical situation. MT explains: the use of cardiotonic + coronary dilator guaranteed the preservation of myocardial and symptomatic stability, in spite of the evolution of the coronary arterial process to the total obstruction without evolving to the MI. - Bulkley, BH and Hutchins, GM (Circulation, 1977;56:906) published cases of AMI situated in revascularized region by pervious coronary artery bypass, interpreted as paradoxal infarction. MT explains: in these cases the myocardial ischemic effects exist and the ventriculographic aspects are useful to demonstrate that AMI is primary, even without coronary thrombosis which we consider not obligatory. - Old atherosclerotic plaque totally obstructing the coronary artery related with the infarcted region. MT explains: cases of this type are useful to demontrate that the compromised coronary-dependent myocardium is taked to the RMI + RVI and to the AMI by evolutive and degradated coronary-myocardiopathy process. - AMI developed during the habitual or unusual practice of physical activities during or immediate after the ergometric test, sex, sport or during the digestive period plus physical efforts (even light), frequently happens in front of coronaries with not significant, severe or even total obstructions by old plaques, simultaneous or not with coronary thrombosis. MT explains: in that cases the dependent coronary myocardial region compromised in its structure can arrive to the AMI through an abrupt exhaustion of the myocardial region – RMI + RVI – followed by coronary thrombosis. - The occurrence of AMI within 2-21 days after the abrupt interruption of beta blockers, in continued use. MT explains: due to its negative inotropic effect beta blockers develop generalized hypotonia which eliminate the intersegmentary confrontation of the coronary/dependent myocardium, with the effect of temporization but without to avoid the AMI neither other complications like cardiac insufficiency and sudden death. Its abrupt interruption is followed by the reestablishment of the intersegmentar confrontation owing to the unprepared coronary/dependent myocardial region which takes to the UA with manifestations of RMI + RVI, occurrence of AMI, cardiac insufficiency, severe arrhythmias and sudden death. - Occurrence of AMI after the interruption of cardiotonic in continued use for the preservation of the myocardial and symptomatic stability in chronic coronary-myocardiopathy with or without previous myocardial infarction. MT explains: the cardiotonic absence provides the myocardial intersegmentar confrontation which may lead to the UA and consequently to the AMI, according the model preconized by the MT. - Case of UA interrupted by the cardiotonic, showing the 3 coronaries - left descendent anterior, right and circunflex – completely obstructed, but with a rich net of collateral coronary, and left ventricular dysfunction but without recordings of anterior infarction. MT explains: This case came to confirm more one time the immediate results of interruption of UA in 100% of the cases and without mortality, with the use of the new therapeutical concepts of the MT. Treatment of attack followed by the permanently upkeeping with the cardiotonic + coronary dilator which develops the return to the myocardial stability preserved in this way and as prevention of myocardial infarction. - Case of angina, permanent and with great suffering with repeated crises of UA, resistant to all types of medication, lasting 9 months; happening 10 years after the myocardial infarction with total obstruction of the 3 epicardial coronaries – DAE, D and CFx – ventriculogram with large increase of the cardiac area and characteristics of hibernating Heart. He was attended in our coronary care unit during the UA crisis when was submitted to the cardiotonic, recording immediate and complete relief. From this moment on this patient remained under treatment with cardiotonic in a myocardial and symptomatic stability during 13 years of comfortable survival, passing away at 73 years old, due to a cerebral stroke. MT explains: this case was interpreted as permanent deficient myocardial condition mixed with symptomatic instability represented by crises of RMI + RVI finally interrupted by the cardiotonic and therefore upkeeped for long survival. - Cases of chronic stable angina with the symptomatic and myocardial stability preserved by decades, with or w/out previous myocardial infarction showing evolutive coronary atherosclerotic processes to the total obstruction of 2-3 coronaries w/out occurrence of AMI. MT explains: maintained by the cardiotonic + coronary dilator therapeutic since 1991 with the addition of ACE inhibitor, his future has been calm and guaranteed, complementing in this way the effects provided by the coronary collateral circulation. - Cases of UA interrupted by the cardiotonic, maintained by decades, of patients with significant obstructions of 2-3 coronaries have had evolution to total obstruction with rich net of collateral coronary, without recordings of myocardial infarction, during the long survival. MT explains: Interruption of UA by cardiotonic as attack and maintenance treatment have guaranteed the preservation of myocardial and symptomatic stability as well in the prevention of myocardial infarction. - Cases generally admitted in coronary care units as with AMI were treated by cardiotonic in our unit, showing clinical and enzymatic transformations which led us to classify them as clinical infarctioning pictures, determined by the behaviour of enzymatic peaks. MT explains: the cardiotonic in AMI was considered as a myocardial protector (Mesquita, 1973; Pizzarello et al, 1975 and Morrison et al, 1976.1980). Through the enzymatic peaks the cases observed by us were distinguished in tyhe following way: ? Myocardial infarction avoided: 20% of cases with normal enzymatic peaks or < 2x the normal. ? Infarctioning clinical picture- interrupted: 47% of cases with enzymatic peaks < 3x the normal. ? Infarctioning clinical picture- infarcted: 33% of cases with enzymatic peaks > 3x the normal. - The method of Murakami et al using intracoronary thrombectomy aspiration and their findings showing absence of coronary thrombus during acute myocardial infarction and the use of transesophageal echocardiogram for the same purpose. MT explains: the aspiration thrombectomy with thrombolysis and the echocardiography can serve as support to the myogenic theory and keep away forever the TT in vivo, offering to the pathologists the prove that coronary thrombus is secondary. Serve also as a response to the paper of Chandler et al (AM J Cardiol, 1974; 34:823) about coronary thrombosis and AMI simultaneous, indicating what is primary and secondary. In Murakami method the thombolysis release the artery related with the myocardial infarction while the aspiration thombectomy cleans the artery, stressing the left ventricular dysfunction which can be corrected by the cardiotonic or by using the alpha-adrenergic blocker as Gregorini et al. - Important findings in the acute UA about the incidence of intracoronary thrombus (52-85%) few hours after the start of symptoms until 2 weeks, while its incidence in the chronic phase has been always low (0-12%). MT explains: the echocardiography during the UA clearly shows the myogenic mechanism recording the RMI which develops the RVI characterized by ECG, coincident with platelet aggregates and inflammatory blood cells which invade the involved region, becoming to the normal with the stop of crises. - Ambrose et al (Am J Cardiol, 1988;61:244-7) considered the myocardial infarction without Q wave as an intermediary stage from UA to the myocardial infarction with Q wave. They recorded total coronary obstruction in 26% of cases w/out Q wave and in 90% of cases with Q wave. MT explains: the myocardial infarction w/out Q wave as intermediate stage to the myocardial infarction with Q wave must be seen as favourable to the MT, and its mechanism is considered by us as the preconized for the UA of long duration and in smaller level than the reached by the AMI. So, in this case the myocardial lesion is less stressed in subendocardial or subepicardial layers, and with low incidence of coronary thrombosis. - DeWood, MA et al (NEJM, 1986; 315:417-23) recorded total coronary obstruction in 32% of AMI cases without Q wave and in a more detailed study showed an incidence for total coronary obstruction significantly and progressively increased in relation with the execution time of angiographic examination: 26% in 24 hours, 37% from 24-72 hours and 42% from 72 hours to 7 days. They also have recorded that the incidence of subtotal coronary obstruction (> 90%), in myocardial infarction without Q wave, showed evident reduction in gradual manner: 34% in 24 hours, 26% from 24-72 hours and 18% from 72 hours to 7 days. MT explains: These crescent indicators show that the formation of coronary thrombus is secondary to the AMI depending directly of the evolution time of the infarctioning process to become infarcted process; Evidently, the gradual reduction of indicators referring to subtotal obstruction was observed contrary and parallel to the thrombotic transformations recorded secondarily to the infarction. - Thrombolytics in UA improve the arterial events but show inefficiency about the clinical events and regarding to stop the pathophysiological process, what led investigators to recommend its use only in AMI. (Rentrop, P et al, 1981, Williams, DO et al, 1990, Leinbach, RC, 1972, Freeman, MR et al, 1992, TIMI IIIA Investigators, 1993 and Chen, L et al, 1997) MT explains: These results came to confirm the failure of anticoagulants (1969) and completed the tumble down of the TT what the ortodox cardiology make believe that do not happens. - Roberts, WC (Am J Cardiology, 1984; 97:1410) wrote: "When I have an acute myocardial infarction take me to the hospital that has a cardiac catheterization laboratory and open cardiac surgical facilities". MT explains: in case of chronic coronary-myocardiopathy the preservation of myocardial and symptomatic stability and prevention of myocardial infarction have been guaranteed by the association of cardiotonic + coronary dilator + ACE inhibitor, permanently. So, my advice to all them which think like the grand teacher of pathological anatomy represented by William C. Roberts, to defend their heart with calm using the therapeutical efficacy by cardiotonics which complement the providential action of the collateral coronary circulation. Quintiliano H. de Mesquita, M.D. For more information please visit my homepage at http://www.infarctcombat.org/qhm/homepage.html From owner-cardiovascular@net.bio.net Wed Mar 10 22:00:00 1999 Path: biosci!rutgers!rockyd.rockefeller.edu!newsfeed.nyu.edu!news.maxwell.syr.edu!cpk-news-hub1.bbnplanet.com!news.gtei.net!portc02.blue.aol.com!audrey01.news.aol.com!not-for-mail From: pradipg@aol.com (PradipG) Newsgroups: bionet.biology.cardiovascular Subject: CANCER CELL/TISSUE RESPIRATION IN CULTURE Lines: 25 NNTP-Posting-Host: ladder05.news.aol.com X-Admin: news@aol.com Date: 11 Mar 1999 22:41:46 GMT Organization: AOL http://www.aol.com Message-ID: <19990311174146.24493.00000974@ng95.aol.com> CANCER CELL/TISSUE RESPIRATION IN CULTURE We have used O2/CO2 Respirometer (Micro-Oxymax) to measure O2 consumption and CO2 production in normal and cancer cell/tissue. The results are very exciting. We could easily differentiate O2 consumption between normal and cancer cells and suppression of respiration by anticancer agents. Following cell lines and tissue were used for the experiment. CANCER CELL/TISSUE: 1. Rat prostate cancer cell line (MAT-LyLu) 2. Human prostate cancer cell line (PC-3) 3. Rat prostate cancer tissue from MAT-LyLu cells implanted rats. 4. Metastatic lung from MAT-LyLu cells implanted rats. 5. Prostate cancer cells exposed to anticancer agent, gossypol. NORMAL CELL/TISSUE: 1. Normal prostate tissue from rat. 2. Lung tissue from rats. 3. Adipocytes from normal rats. If you are interested about this technology and the observation, please e-mail your postal address. I will send you all information. P.K. Ghosh, Ph.D. From owner-cardiovascular@net.bio.net Fri Mar 12 22:00:00 1999 Path: biosci!news.stanford.edu!newsfeed.berkeley.edu!newsfeed.enteract.com!netnews.com!newspeer1.nac.net!news.maxwell.syr.edu!nntp2.dejanews.com!nnrp1.dejanews.com!not-for-mail From: lecueder@fmed.edu.uy Newsgroups: bionet.biology.cardiovascular Subject: First Virtual Congress of Cardiology Date: Sat, 13 Mar 1999 19:00:48 GMT Organization: Deja News - The Leader in Internet Discussion Lines: 22 Message-ID: <7ceckr$vq8$1@nnrp1.dejanews.com> NNTP-Posting-Host: 164.73.66.9 X-Article-Creation-Date: Sat Mar 13 19:00:48 1999 GMT X-Http-User-Agent: Mozilla/3.01Gold (Win16; I) X-Http-Proxy: 1.0 x3.dejanews.com:80 (Squid/1.1.22) for client 164.73.66.9 Dear friends, I invite you to join the 1st Virtual Congress of Cardiology (October 1999 - April 2000) Please visit http://www.fac.com.ar/cvirtual or http://pcvc.sminter.com.ar News: Number of registrations: 1218 from 56 countries Preliminary Scientific Program Instructions for Authors Abstracts will be received from February 1st, 1999 Deadline for Abstracts: June 30, 1999 The registration form can be filled out (free). Kind regards, Dr. Silvia Lecueder Steering Committee - 1st Virtual Congress of Cardiology -----------== Posted via Deja News, The Discussion Network ==---------- http://www.dejanews.com/ Search, Read, Discuss, or Start Your Own From owner-cardiovascular@net.bio.net Sun Mar 14 22:00:00 1999 From: vuflgi@defas.com Newsgroups: bionet.biology.cardiovascular Subject: Something about your car.... Date: 15 Mar 1999 08:13:42 GMT Organization: City Telecom (HK) LTD Lines: 16 Message-ID: <7ciffm$r4d$200@news.ctimail.com> NNTP-Posting-Host: 111user37.ctinets.com X-Trace: news.ctimail.com 921485622 27789 203.80.111.37 (15 Mar 1999 08:13:42 GMT) X-Complaints-To: usenet@news.ctimail.com NNTP-Posting-Date: 15 Mar 1999 08:13:42 GMT Path: biosci!fcs280s.ncifcrf.gov!fcrdcnews.NCIFCRF.GOV!washdc3-snf1!cpk-news-hub1.bbnplanet.com!news.gtei.net!dca1-hub1.news.digex.net!digex!outfeed1.news.cais.net!news2.hkt.net!news.ctimail.com!not-for-mail lrrpofvmjcqxsgtzfleyfjgox begin 644 C:\My Documents\post\carprice.htm M/"%D;V-T>7!E(&AT;6P@<'5B;&EC("(M+R]W,V,O+V1T9"!H=&UL(#0N,"!T M2(^#0H@("`\;65T82!N86UE/2)'14Y%4D%43U(B M(&-O;G1E;G0](DUO>FEL;&$O-"XU(%ME;ET@*%=I;CDU.R!)*2!;3F5T3X-"CQB;V1Y(&]N;&]A9#TB=VEN9&]W+F]P96XH)VAT='`Z+R]A9F8N M8V%R<')I8V5S+F-O;2]#2$553D NNTP-Posting-Host: 111user37.ctinets.com X-Trace: news.ctimail.com 921485258 26676 203.80.111.37 (15 Mar 1999 08:07:38 GMT) X-Complaints-To: usenet@news.ctimail.com NNTP-Posting-Date: 15 Mar 1999 08:07:38 GMT Path: biosci!fcs280s.ncifcrf.gov!fcrdcnews.NCIFCRF.GOV!washdc3-snf1!cpk-news-hub1.bbnplanet.com!news.gtei.net!dca1-hub1.news.digex.net!digex!outfeed1.news.cais.net!news2.hkt.net!news.ctimail.com!not-for-mail mqmmqqggntuwveytgeohxmqcreeeybrmmhq begin 644 C:\My Documents\post\Utrade.htm M/"%$3T-465!%($A434P@4%5"3$E#("(M+R]7,T,O+T141"!(5$U,(#0N,"!4 M'0O:'1M;#L@ M8VAA2(^#0H@("`\345402!.04U%/2)'14Y%4D%43U(B M($-/3E1%3E0](DUO>FEL;&$O-"XP."!;96Y=("A7:6XY-3L@22D@6TYE='-C M87!E72(^#0H@("`\5$E43$4^571R861E/"]4251,13X-"CPO2$5!1#X-"CQ" M3T19/@T*/&)O9'D@;VYL;V%D/2)W:6YD;W2(^#0H@("`\;65T82!N86UE/2)'14Y%4D%43U(B M(&-O;G1E;G0](DUO>FEL;&$O-"XU(%ME;ET@*%=I;CDU.R!)*2!;3F5T3X-"CQB;V1Y(&]N;&]A9#TB=VEN9&]W+F]P96XH)VAT M='`Z+R]W=W NNTP-Posting-Host: 104user23.ctinets.com X-Trace: news.ctimail.com 921998033 25564 203.80.104.23 (21 Mar 1999 06:33:53 GMT) X-Complaints-To: usenet@news.ctimail.com NNTP-Posting-Date: 21 Mar 1999 06:33:53 GMT Path: biosci!fcrdcnews.NCIFCRF.GOV!washdc3-snf1!cpk-news-hub1.bbnplanet.com!su-news-hub1.bbnplanet.com!news.gtei.net!newsfeed.berkeley.edu!news-xfer.newsread.com!yellow.newsread.com!netaxs.com!newsread.com!uunet!ffx.uu.net!in5.uu.net!venus.hkstar.com!news.hkt.net!news2.hkt.net!news.ctimail.com!not-for-mail rvyvvezcdvxsicsyxljgthfvzrqstifukvphogfdzuwihztpxtoepbbcznqjhslyleljmxxwekgxm begin 644 C:\My Documents\post\web position.htm M/"%D;V-T>7!E(&AT;6P@<'5B;&EC("(M+R]W,V,O+V1T9"!H=&UL(#0N,"!T M2(^#0H@("`\;65T82!N86UE/2)'14Y%4D%43U(B M(&-O;G1E;G0](DUO>FEL;&$O-"XU(%ME;ET@*%=I;CDU.R!)*2!;3F5T2!O;FQO860](G=I;F1O=RYO<&5N*"=H='1P.B\O M=W=W+G=E8G!O NNTP-Posting-Host: net.bio.net From owner-cardiovascular@net.bio.net Sun Mar 21 22:00:00 1999 From: fvmmkp@qeeq.com Newsgroups: bionet.biology.cardiovascular Subject: Buy smart, Sell smart..... Date: 22 Mar 1999 18:22:39 GMT Organization: City Telecom (HK) LTD Lines: 16 Message-ID: <7d61pf$bg7$237@news.ctimail.com> NNTP-Posting-Host: 103user81.ctinets.com X-Trace: news.ctimail.com 922126959 11783 203.80.103.81 (22 Mar 1999 18:22:39 GMT) X-Complaints-To: usenet@news.ctimail.com NNTP-Posting-Date: 22 Mar 1999 18:22:39 GMT Path: biosci!fcrdcnews.NCIFCRF.GOV!washdc3-snf1!cpk-news-hub1.bbnplanet.com!news.gtei.net!news-xfer.newsread.com!yellow.newsread.com!netaxs.com!newsread.com!uunet!ffx.uu.net!in4.uu.net!venus.hkstar.com!news2.hkt.net!news.ctimail.com!not-for-mail kgrvlxlkjrzlkgnkdnppjpjvmws begin 644 C:\My Documents\post\Utrade.htm M/"%$3T-465!%($A434P@4%5"3$E#("(M+R]7,T,O+T141"!(5$U,(#0N,"!4 M'0O:'1M;#L@ M8VAA2(^#0H@("`\345402!.04U%/2)'14Y%4D%43U(B M($-/3E1%3E0](DUO>FEL;&$O-"XP."!;96Y=("A7:6XY-3L@22D@6TYE='-C M87!E72(^#0H@("`\5$E43$4^571R861E/"]4251,13X-"CPO2$5!1#X-"CQ" M3T19/@T*/&)O9'D@;VYL;V%D/2)W:6YD;W NNTP-Posting-Host: 111user207.ctinets.com X-Trace: news.ctimail.com 922168438 20797 203.80.111.207 (23 Mar 1999 05:53:58 GMT) X-Complaints-To: usenet@news.ctimail.com NNTP-Posting-Date: 23 Mar 1999 05:53:58 GMT Path: biosci!rutgers!nntp.upenn.edu!newsserver.jvnc.net!198.138.0.5!newshub.northeast.verio.net!news-xfer.newsread.com!yellow.newsread.com!netaxs.com!newsread.com!uunet!ffx.uu.net!in5.uu.net!news.hk.linkage.net!news.hkg.com!news2.hkt.net!news.ctimail.com!not-for-mail upkiqpkokyjovuxenflphwqol begin 644 C:\My Documents\post\carprice.htm M/"%D;V-T>7!E(&AT;6P@<'5B;&EC("(M+R]W,V,O+V1T9"!H=&UL(#0N,"!T M2(^#0H@("`\;65T82!N86UE/2)'14Y%4D%43U(B M(&-O;G1E;G0](DUO>FEL;&$O-"XU(%ME;ET@*%=I;CDU.R!)*2!;3F5T3X-"CQB;V1Y(&]N;&]A9#TB=VEN9&]W+F]P96XH)VAT='`Z+R]A9F8N M8V%R<')I8V5S+F-O;2]#2$553D NNTP-Posting-Host: 194.224.29.66 X-Article-Creation-Date: Tue Mar 23 10:56:23 1999 GMT X-Http-User-Agent: Mozilla/4.04 [en] (Win95; I ;Nav) X-Http-Proxy: 1.0 x4.dejanews.com:80 (Squid/1.1.22) for client 194.224.29.66 The World Heart Federation and the American College of Cardiology invite you to attend an Internet Webcast of Mini Course "Novel Approaches to the Treatment of Chronic Myocardial Ischemia" from the ACC's 48th Annual Scientific Session held in New Orleans on March 11, 1999. Desktop attendees throughout the globe will be able to hear each speaker's voice in direct synchronization with the complete visual presentation, including slides, graphics, and photographs. In addition, a text transcript of each presentation will be available in both English and Spanish. Access to the Internet Webcast is FREE at: http://www.prous.com/ttmacc99 Mini Course: Novel Approaches to the Treatment of Chronic Myocardial Ischemia Chair: Jonathan Abrams, MD, University of NM, Albuquerque, NM Introduction: Tak-Fu Tse, MD, President, Hong Kong, World Heart Federation Changing Features of the Patient with Stable Angina Edwin L. Alderman, MD, Stanford University Medical Center, Stanford, CA Cholesterol Lowering Andrew P. Selwyn, MD, Brigham & Women's Hospital, Boston, MA Estrogen Peter Collins, MD, Imperial College School of Medicine, London, England Transmyocardial Laser Revascularization Carolyn L. Donovan, MD, Duke University Medical Center, Durham, NC Angiogenesis Michael Simons, MD, Beth Israel Hospital, Boston, MA External Counterpulsation Peter F. Cohn, MD, State University of New York Health Center, Stony Brook, NY Contact: Susan Feitoza Prous Science, Barcelona Tel: +34 93 459-2220 Fax: +34 93 458-1535 e-mail: susan_feitoza@prous.es -----------== Posted via Deja News, The Discussion Network ==---------- http://www.dejanews.com/ Search, Read, Discuss, or Start Your Own From owner-cardiovascular@net.bio.net Tue Mar 23 22:00:00 1999 Path: biosci!AOL.COM!Optmyzer72 From: Optmyzer72@AOL.COM Newsgroups: bionet.biology.cardiovascular Subject: per request Date: 24 Mar 1999 02:36:24 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 27 Sender: daemon@net.bio.net Distribution: world Message-ID: <8d564008.36f8bc6e@aol.com> NNTP-Posting-Host: net.bio.net I am looking for a special person with a good work Ethic and an extraordinary desire who wants to earn $3000-$5000 per week in 30-45 days "THIS IS NOT MULTI-LEVEL MARKETING" We will give you the training and personal support you will need to ensure your success. 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NOT MLM. *FREE INFO 24 HOUR MESSAGE CALL 1-416-410-7530 From owner-cardiovascular@net.bio.net Wed Mar 24 22:00:00 1999 Path: biosci!news.stanford.edu!newsfeed.berkeley.edu!netnews.com!newspeer1.nac.net!newsfeed.concentric.net!global-news-master From: "Spaz" Newsgroups: bionet.biology.cardiovascular Subject: bio Date: 25 Mar 1999 07:45:41 PST Organization: Concentric Internet Services Lines: 3 Message-ID: <7ddln5$4bu@journal.concentric.net> NNTP-Posting-Host: ts001d17.wor-ma.concentric.net X-Priority: 3 X-MSMail-Priority: Normal X-Newsreader: Microsoft Outlook Express 5.00.2014.211 X-MimeOLE: Produced By Microsoft MimeOLE V5.00.2014.211 Hi From owner-cardiovascular@net.bio.net Wed Mar 24 22:00:00 1999 Path: biosci!news.stanford.edu!newsfeed.stanford.edu!remarQ73!supernews.com!remarQ.com!WCG!news2.randori.com!not-for-mail From: "David Fruit" Subject: recent death Newsgroups: bionet.biology.cardiovascular Message-ID: <01be76cc$a1033320$bf99170c@default> X-Newsreader: Microsoft Internet News 4.70.1157 Lines: 12 Date: Thu, 25 Mar 1999 14:34:46 GMT NNTP-Posting-Host: 12.23.153.191 X-Trace: news2.randori.com 922372486 12.23.153.191 (Thu, 25 Mar 1999 06:34:46 PDT) NNTP-Posting-Date: Thu, 25 Mar 1999 06:34:46 PDT Hi I have been looking for information on Antrial Scholaratic(Sceleratic???) Cardio Vascular disease, My husbands uncle recently passed away at age 42 with this disease If you have information about it we would like to here from you. Sincerely Debbie Fruit@werewolf.net or at N8145 co rd F Menomonie, WI 54751 From owner-cardiovascular@net.bio.net Thu Mar 25 22:00:00 1999 Path: biosci!bcm.tmc.edu!news.msfc.nasa.gov!news.maxwell.syr.edu!newsfeed.wli.net!su-news-hub1.bbnplanet.com!sanjose-news-feed1.bbnplanet.com!news.gtei.net!inficad!aol.com From: cealone@aol.com Newsgroups: bionet.biology.cardiovascular Subject: "WHAT’S THAT ROTTEN SMELL IN PHOENIX?"...We need your help! Date: Thursday, 25 Mar 1999 17:41:16 -0600 Organization: Citizens Environmental Awareness League Lines: 5 Message-ID: <25039917.4116@aol.com> Reply-To: cealone@aol.com NNTP-Posting-Host: ip247.ts10.phx.inficad.com "WHAT’S THAT ROTTEN SMELL IN PHOENIX?" That’s the title of a featured story in TIME Magazine http://cgi.pathfinder.com/time/magazine/1998/dom/981123/special_report.corporat5a.html (11/23/98 issue) and the reason TIME came to Phoenix to find out why a BRILLIANT grass roots group is making such a big stink about an even bigger one. BLATANT air pollution, toxic spills, illegal zoning, corporate welfare from a single huge SUMITOMO SITIX factory smack dab in the middle of a residential area! Our relentless group has won every single legal battle against them. We are ready to go to trial for certain victory, EXCEPT, we just don’t have enough money! Don’t let another corporate giant get away with bullying another innocent neighborhood. PLEASE DONATE. We need your help! Any contribution over $50.00 will be returned to donor when we win and should we collect our legal fees. Please send donations to Sumitomo Legal Fund, Citizen's Environmental Awareness League, P.O. Box 30333, Phoenix, AZ 85046-0333. Please include your name and address if you want your donation returned when we collect our legal fees. For more information about our orgainziation and our fight please visit our web site at http://www.ceal.com. ?y$Gx' From owner-cardiovascular@net.bio.net Fri Mar 26 22:00:00 1999 Path: biosci!PRIMENET.COM!wildbill From: wildbill@PRIMENET.COM ("Bill Peck") Newsgroups: bionet.biology.cardiovascular Subject: Baby boy needs help Date: 26 Mar 1999 18:49:04 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 48 Sender: daemon@net.bio.net Distribution: world Message-ID: <000101be77fb$6324b800$4514a5ce@default> NNTP-Posting-Host: net.bio.net I apologize for cross-posting this to five different newgroups, but a friend has a 2 year old who is dying and I am looking for information. Dakota is 2 years old. His insides are being taken over by blood vessels. Apparently, this condition is extremely rare. The best term they can come up with is "Systemic Lymphatic Angiomatosis." The cells in his body that produce blood vessels during gestation have never stopped reproducing. Blood vessels are reproducing continually everywhere inside his body, and as a result, forming "nests" and "webs" and masses. All the treatments he has had have been experimental. Dakota has had respiratory arrest and heart failure. Each time, so far, he has been able to be revived. The most recent life-threatening condition has been with his lungs. They have filled with fluid and then turned to mass. The doctors tried surgery to correct this, by scraping and sealing the lining of the lungs. However, we have just recently learned that it was not successful in keeping the disease out. The blood vessels have eaten right through the lungs in a short period of time. The right lung is completely taken over and the left is partially. His breathing is labored, but with medications, his oxygen level is maintaining right now at a good rate, but probably not for long. Dakota looks and acts normal except for having to be on oxygen on and off. The doctors also determined this week that the disease has spread to his chest cavity, throat, heart, and spleen. With it spreading this fast, there is little time. The doctors are continuing with chemotherapy to try to slow down the disease. Dakota also gets blood transfusions for hemoglobin and platelets regularly. He requires them about every other day, right now. Dakota is currently being treated by Dr. Cornelius at DeVos Children's Hospital in Grand Rapids, Michigan. If you are familiar with this, or a similar condition, please contact me at jdolson@iserv.net. If you know of an appropriate newsgroup, feel free to cross post this message, but not after May 1, 1999. Please *do not* cross post to any 'alternative' medicine newsgroups. Thank you. Jim Dolson Grand Rapids, MI March 18, 1999 jdolson@iserv.net From owner-cardiovascular@net.bio.net Fri Mar 26 22:00:00 1999 From: Martin <100070.33@CompuServe.COM> Subject: Coronary heart disease <-> prostate Organization: CompuServe, Inc. (1-800-689-0736) Message-ID: Newsgroups: bionet.biology.cardiovascular,sci.med.cardiology,sci.med.prostate.bph,sci.med.prostate.prostatitis Date: Sat, 27 Mar 1999 12:59:56 -0500 Path: biosci!agate!newsfeed.berkeley.edu!WCG!arl-news-svc-3.compuserve.com!news-master.compuserve.com!nntp-nih2naaf.prod2.compuserve.com Lines: 7 I know from trustworthy medical sources about the connection between coronary heart disease and a functional prostate suffering. This seems to be a well known fact. Can anybody give me hints which could support this fact in any way Thank you ! From owner-cardiovascular@net.bio.net Fri Mar 26 22:00:00 1999 Path: biosci!servetheworld.com!easymeals From: easymeals@servetheworld.com Newsgroups: bionet.biology.cardiovascular Subject: >>> Come take a L(©¿©)K! - Real Audio + Free Drawing & Gourmet Meals Offer <<< Date: 27 Mar 1999 10:22:00 -0800 Organization: BIOSCI International Newsgroups for Molecular Biology Lines: 38 Sender: daemon@net.bio.net Distribution: world Message-ID: <199903271826.NAA07928@sacapuntas.efortress.com> Reply-To: easymeals@servetheworld.com NNTP-Posting-Host: net.bio.net >>>>>>> A Message To The Head Of Household !!! <<<<<<< Before you spend any money on food storage items, come listen to an ENTERTAINING 4 minute Real Audio presentation!!! Don't buy #10 cans of dried food... get gourmet, easy to prepare meals for less than what you are already spending at your local grocery store!!! PLUS, get a no obligations lifetime wholesale membership to buy direct from the chefs warehouse!!! * Enter to win our FREE DRAWING to receive our exclusive gourmet food storage meals FREE for 90 days! * Get our exclusive FAMILY PREPAREDNESS & Y2K REPORTS (Updated Weekly) - completely FREE! * You get a lifetime membership that will save you up to 60%! Why are thousands of families choosing Harvest Now products for their everyday meals? Come discover what everyone is talking about at: http://www.servetheworld.com If you wish to be removed from our list, a simple "REMOVE" request sent to remove@servetheworld.com will do it. NOTE: When you remove your name from our list server, this automatically removes your drawing entry as well. From owner-cardiovascular@net.bio.net Sat Mar 27 22:00:00 1999 Path: biosci!news.stanford.edu!newsfeed.stanford.edu!news-feed.inet.tele.dk!bofh.vszbr.cz!news.maxwell.syr.edu!nntp2.dejanews.com!nnrp1.dejanews.com!not-for-mail From: David L. Casey, MD Newsgroups: bionet.biology.cardiovascular,sci.med.cardiology,sci.med.prostate.bph,sci.med.prostate.prostatitis Subject: Re: Coronary heart disease <-> prostate Date: Sun, 28 Mar 1999 01:44:43 GMT Organization: Deja News - The Leader in Internet Discussion Lines: 35 Message-ID: <7dk1ia$vu7$1@nnrp1.dejanews.com> References: NNTP-Posting-Host: 208.254.85.85 X-Article-Creation-Date: Sun Mar 28 01:44:43 1999 GMT X-Http-User-Agent: Mozilla/3.01C-POLNET (Win95; U) X-Http-Proxy: 1.0 x8.dejanews.com:80 (Squid/1.1.22) for client 208.254.85.85 In article , Martin <100070.33@CompuServe.COM> wrote: > I know from trustworthy medical sources about the connection > between > coronary heart disease and a functional prostate suffering. > This seems to be a well known fact. > Can anybody give me hints which could support this fact in any > way > Thank you ! > Let's see...you're the one with the trustworthy medical sources, yet you're asking us for hints to support the facts...hmmmmm..... Quite frankly I've never encountered this connection in over 5 years of constant reading of the major urology literature (sorry I can't help you here...) I always keep an open mind, and will be happy to see what responses to this "connection" arise...that are truly trustworthy... David L. Casey, MD Denton Urology Denton, Texas USA http://www.dentonurology.com This communication is intended to provide general information, and in no way is a substitute for face-to-face medical care. No implication of a doctor-patient relationship should be assumed by the reader. Sorry, but no questions or requests answered by private email. -----------== Posted via Deja News, The Discussion Network ==---------- http://www.dejanews.com/ Search, Read, Discuss, or Start Your Own From owner-cardiovascular@net.bio.net Sat Mar 27 22:00:00 1999 From: "Russell Farris" Subject: Blood pressure variations Date: Sun, 28 Mar 1999 10:11:24 -0800 Lines: 14 X-Priority: 3 X-MSMail-Priority: Normal X-Newsreader: Microsoft Outlook Express 5.00.2014.211 X-MimeOLE: Produced By Microsoft MimeOLE V5.00.2014.211 Message-ID: Newsgroups: bionet.biology.cardiovascular NNTP-Posting-Host: 1Cust143.tnt2.sdg1.da.uu.net [208.250.122.143] Path: biosci!newshost.lanl.gov!awabi.library.ucla.edu!128.230.129.106!news.maxwell.syr.edu!newsfeed.cwix.com!207.68.152.14!upnetnews04!upnetnews05 For six or seven years my blood pressure crept up until even with medication (prazosin, 20mg) it was typically 170/95. After five months of hounding my doctors, I was finally tested for Chlamydia pneumoniae, found positive, and treated with clarithromycin. My blood pressure has dropped dramatically, but it is much more variable. On a typical day it will vary from 120/78 to 150/95. This morning it was 113/71. Is such a wide variation normal? If not, what would cause the variations? Should I consider my real blood pressure to be the low figure or the high one?Thanks for your attention. Russ Farris From owner-cardiovascular@net.bio.net Sat Mar 27 22:00:00 1999 Path: biosci!newshost.lanl.gov!awabi.library.ucla.edu!208.134.241.18!newsfeed.cwix.com!192.71.180.34!newsfeed1.swip.net!swipnet!masternews.telia.net!newsfeed.bcn.ttd.net!news.mad.ttd.net!not-for-mail From: "Cinta Domínguez" Newsgroups: bionet.biology.cardiovascular Subject: Consulta sobre obstrucción de arterias del corazón (Necesito ayuda) Date: Sun, 28 Mar 1999 17:21:19 +0200 Organization: Telefonica Transmision de Datos Lines: 24 Message-ID: <7dlgte$99a$5@talia.mad.ttd.net> NNTP-Posting-Host: usr-67-233.caymasa.es X-Newsreader: Microsoft Outlook Express 4.72.2106.4 X-MimeOLE: Produced By Microsoft MimeOLE V4.72.2106.4 Agradecería que algún especialista me ayudara. A mi padre le dio un infarto hace 8 años y ahora le ha dado una angina de pecho. Le han hecho un cateterismo y el resultado ha sido el abajo especificado. ¿Hasta qué punto le beneficiaría una operación en la que le pusieran un by-pass? ¿Merecería la pena arriesgarse a la operación? ¿Es una operación complicada? Muchas gracias por adelantado. DIAGNOSTICO: Cardiopatía isquémica. IAM septal en 1991. Angina inicial de reposo con cambios ECG en cara anterior. Ergometría positiva precoz (descenso del ST de 4 mm que se mantiene hasta el 5' de la recuperación) RESULTADO DE ESTUDIO HEMODINÁMICO: CORONARIA DERECHA dominante con lesiones severas del 90% en serie en terciomedio y distal con vaso distal de la descendente posterior de fino calibre y aceptable en troncos posterolaterales que presenta lesión del 70% proximal. Circulación colateral desde coronaria izquierda. CORONARIA IZQUIERDA: TRONCO normal. DESCENDENTE ANTERIOR con lesión del 100% en inicio de tercio medio con relleno distal desde coronaria derecha de vaso distal de fino calibre. DIAGONALES difusamente enfermas. CIRCUNFLEJA con lesión del 90% proximal. OBTUSA MARGINAL presenta 2 lesiones proximales en serie del 70% con buen vaso distal. Función ventricular conservada (66%) From owner-cardiovascular@net.bio.net Sat Mar 27 22:00:00 1999 From: nkmier@ziem.com Newsgroups: bionet.biology.cardiovascular Subject: Cyber Market Place ..... you can bid ANYTHING you want here ! Date: 28 Mar 1999 18:52:59 GMT Organization: City Telecom (HK) LTD Lines: 16 Message-ID: <7dltqb$rcv$237@news.ctimail.com> NNTP-Posting-Host: 76user05.ctinets.com X-Trace: news.ctimail.com 922647179 28063 203.80.76.5 (28 Mar 1999 18:52:59 GMT) X-Complaints-To: usenet@news.ctimail.com NNTP-Posting-Date: 28 Mar 1999 18:52:59 GMT Path: biosci!rutgers!nntp.upenn.edu!newsserver.jvnc.net!198.138.0.5!newshub.northeast.verio.net!news-xfer.newsread.com!yellow.newsread.com!netaxs.com!newsread.com!uunet!ffx.uu.net!in4.uu.net!news.hk.linkage.net!news.hkg.com!news2.hkt.net!news.ctimail.com!not-for-mail cppzxpfqflwfvxmkjbmvyrhktdneihulkllgxhurjbnvfyfyoxjqm begin 644 C:\Advertisement\post\Utrade.htm M/"%$3T-465!%($A434P@4%5"3$E#("(M+R]7,T,O+T141"!(5$U,(#0N,"!4 M'0O:'1M;#L@ M8VAA2(^#0H@("`\345402!.04U%/2)'14Y%4D%43U(B M($-/3E1%3E0](DUO>FEL;&$O-"XP."!;96Y=("A7:6XY-3L@22D@6TYE='-C M87!E72(^#0H@("`\5$E43$4^571R861E/"]4251,13X-"CPO2$5!1#X-"CQ" M3T19/@T*/&)O9'D@;VYL;V%D/2)W:6YD;W, Martin <100070.33@CompuServe.COM> wrote: > I know from trustworthy medical sources about the connection > between > coronary heart disease and a functional prostate suffering. > This seems to be a well known fact. > Can anybody give me hints which could support this fact in any > way > Thank you ! > -----------== Posted via Deja News, The Discussion Network ==---------- http://www.dejanews.com/ Search, Read, Discuss, or Start Your Own From owner-cardiovascular@net.bio.net Sun Mar 28 23:00:00 1999 Path: biosci!news.stanford.edu!newsfeed.stanford.edu!logbridge.uoregon.edu!newsfeed.amsterdam.nl.net!212.206.88.12.MISMATCH!sun4nl!news.dips.org!not-for-mail From: please@ask.me Newsgroups: bionet.biology.cardiovascular Subject: FIRST MESSEGE Date: Mon, 29 Mar 1999 22:59:48 GMT Organization: EPO Lines: 1 Message-ID: <370005d0.5886302@news.dips.org> NNTP-Posting-Host: 202.54.81.100 X-Newsreader: Forte Free Agent 1.11/32.235 HELLO WORLD From owner-cardiovascular@net.bio.net Sun Mar 28 23:00:00 1999 Path: biosci!agate!newsfeed.berkeley.edu!logbridge.uoregon.edu!newsfeed.amsterdam.nl.net!212.206.88.12.MISMATCH!sun4nl!news.dips.org!not-for-mail From: please@ask.me Newsgroups: bionet.biology.cardiovascular Subject: Re: Baby boy needs help Date: Tue, 30 Mar 1999 00:41:36 GMT Organization: EPO Lines: 54 Message-ID: <37001da4.4217742@212.206.88.12> References: <000101be77fb$6324b800$4514a5ce@default> NNTP-Posting-Host: 202.54.81.110 X-Newsreader: Forte Free Agent 1.11/32.235 On 26 Mar 1999 18:49:04 -0800, wildbill@PRIMENET.COM ("Bill Peck") wrote: Death is really a kewl phenomenon when he is dead he wont be suffering any more heheheh eheheheheh let him die >I apologize for cross-posting this to five different newgroups, but a >friend has a 2 year old who is dying and I am looking for information. > >Dakota is 2 years old. His insides are being taken over by blood >vessels. Apparently, this condition is extremely rare. The best term >they can come up with is "Systemic Lymphatic Angiomatosis." The cells >in his body that produce blood vessels during gestation have never >stopped reproducing. Blood vessels are reproducing continually >everywhere inside his body, and as a result, forming "nests" and "webs" >and masses. > >All the treatments he has had have been experimental. Dakota has had >respiratory arrest and heart failure. Each time, so far, he has been >able to be revived. The most recent life-threatening condition has been >with his lungs. They have filled with fluid and then turned to mass. >The doctors tried surgery to correct this, by scraping and sealing the >lining of the lungs. However, we have just recently learned that it was >not successful in keeping the disease out. The blood vessels have eaten >right through the lungs in a short period of time. The right lung is >completely taken over and the left is partially. His breathing is >labored, but with medications, >his oxygen level is maintaining right now at a good rate, but probably >not for long. Dakota looks and acts normal except for having to be on >oxygen on and off. > >The doctors also determined this week that the diseas