shukoor65/lab-rag-model huggingface dataset:
A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction. BACKGROUND. The independent contributions of subfractions of high-density lipoprotein (HDL) cholesterol (HDL2 and HDL3) and apolipoproteins in predicting the risk of myocardial infarction are unclear. Prospective data are sparse, but HDL2 is widely believed to be a more important predictor than HDL3. METHODS. Blood samples were collected at base line from 14,916 men (ages, 40 to 84 years) who were participants in the Physicians' Health Study. After five years of follow-up, plasma samples from 246 men with new myocardial infarction (case subjects) were analyzed together with specimens from 246 men matched to them for age and smoking status who had not had a myocardial infarction. RESULTS. The levels of total cholesterol and apolipoprotein B-100 were significantly associated with an increased risk of myocardial infarction (data on levels of low-density lipoprotein cholesterol were unavailable). Both HDL cholesterol and HDL2 levels were associated with a substantially decreased risk of myocardial infarction, but the HDL3 level was the strongest predictor; the relative risk was 0.3 (95 percent confidence interval, 0.2 to 0.6) for those in the fifth of the group with the highest HDL3 levels, as compared with the fifth with the lowest levels. The benefit of a higher HDL cholesterol level was most pronounced among those with lower total cholesterol levels. Levels of apolipoprotein A-I and apolipoprotein A-II were also associated with decreased risk. However, the levels of HDL subfractions and apolipoproteins did not add significantly to the value of a multivariate model that included the ratio of total to HDL cholesterol in predicting myocardial infarction, whereas that ratio remained a significant independent predictor of risk. After adjustment for other risk factors, a change of one unit in the ratio of total to HDL cholesterol was associated with a 53 percent change in risk (95 percent confidence interval, 26 percent to 85 percent). CONCLUSIONS. This study underscores the importance of HDL cholesterol in predicting the risk of myocardial infarction and demonstrates protective effects of both the HDL3 and HDL2 subfractions of HDL cholesterol. We found little or no predictive value for the levels of apolipoproteins A-I, A-II, and B or HDL subfractions after conventional risk factors and the ratio of total to HDL cholesterol were considered.
Tumor induction in a rat model for ureterosigmoidostomy without evidence of nitrosamine formation. Twenty rats were randomized into a vesicosigmoidostomy and an unoperated control group. In both groups the 24 hour excretion of secondary amines, nitrate, nitrite and nitrosamines was measured before and after gavage of proline and nitrate, piperazine and nitrate, N-nitrosoproline, mono-N-nitrosopiperazine. The urinary nitrosamine concentrations were not significantly different between both groups neither before nor after application of the several substances. Thirty rats were randomized into two vesicosigmoidostomy groups with and without antibiotic coverage and an unoperated control group. After ligation of distal rectum and mesosigmoid the rectosigmoids were removed. No significant concentrations of volatile nitrosamines could be measured in the rectosigmoid contents of the three groups. One hundred and twenty rats randomized into three groups following vesicosigmoidostomy received the potential nitrosamine antidotes sodium-2-mercaptoethane sulfonate or sodiumpentosan-polysulfate or acted as controls. 12/118 (10.2%) developed adenomas and 25/118 (21.2%) adenocarcinomas at the vesico-colonic anastomosis with no significant differences between the three groups concerning tumor incidence or mortality. The results show that colon carcinomas occur in a rat model for ureterosigmoidostomy without evidence for thus induced nitrosamine formation. This and the missing effect of nitrosamine antidotes suggest that other factors than nitrosation must be responsible for colon carcinogenesis following urinary diversion via intestine.
The role of serotonin-1A receptor activation and alpha-1 adrenoceptor blockade in the hypotensive effect of 5-methyl-urapidil. Our study had three purposes: 1) to determine whether 5-methyl-urapidil, topically applied to the ventrolateral medulla, produces hypotension by activating serotonin-1A (5-HT1A) receptors, 2) to determine whether 5-methyl-urapidil given i.v. produces hypotension in part by activating 5-HT1A receptors in the ventrolateral medulla, and 3) to determine the specific site within the ventrolateral medulla where 5-methyl-urapidil elicits a hypotensive response. In terms of the first purpose, 5-methyl-urapidil applied bilaterally to the intermediate area of the ventral surface of the medulla (1.2 micrograms/side) of chloralose-anesthetized cats produced a decrease in mean arterial pressure of -39 +/- 4 mm Hg (N = 8). Prior blockade of 5-HT1A receptors at this site with bilateral application of spiperone (30 micrograms/side) prevented the hypotensive effect of 5-methyl-urapidil (mean blood pressure now increased by 5 +/- 4 mm Hg). Pretreatment with the alpha-1 adrenoceptor antagonist, prazosin, did not prevent the hypotensive effect of 5-methyl-urapidil. In terms of the second purpose, spiperone applied bilaterally to the ventral surface of the medulla counteracted a significant portion of the hypotensive effect of 5-methyl-urapidil given by the i.v. route. The dose of 5-methyl-urapidil given intravenously was below the dose that produces alpha-1 adrenoceptor blockade. In terms of the third purpose, microinjection of 5-methyl-urapidil into central nervous system sites associated with the intermediate area was found to have its greatest hypotensive effect at the subretrofacial nucleus. Mean arterial pressure decreased by 74 +/- 14 mm Hg (N = 3) after bilateral microinjection of 25 ng of the drug.
Initial staging of non-small cell lung cancer: value of routine radioisotope bone scanning. The exclusion of bone metastases is important in the initial staging of non-small cell lung cancer, though there is debate about whether bone scans should be performed routinely or restricted to patients who present with clinical or laboratory indicators suggesting skeletal metastases. In a prospective study of 110 consecutive patients referred for initial staging of non-small cell lung cancer, we assessed the sensitivity of a group of clinical indicators (chest pain, skeletal pain, bone tenderness on physical examination, serum alkaline phosphatase, and serum calcium) for the presence of skeletal metastases as determined by bone scanning. The final staging result was validated with follow up data over at least three years. At the initial staging 37 of 110 bone scans (34%) showed areas of increased uptake, of which only nine were confirmed to be metastases (by tomography, computed tomography, or biopsy). Half the patients (55) had at least one clinical indicator suggesting skeletal metastases, including all patients with proved skeletal metastases. Thus the sensitivity of these clinical indicators was 100% and the specificity 54%. Within one year three of 27 patients with non-confirmed positive bone scans had skeletal metastases, one of which was in the area that had shown increased uptake initially. All these patients had clinical indicators for skeletal metastases and all had inoperable advanced tumours. Four of 69 patients with an initially negative bone scan developed skeletal metastases within one year. It is concluded that in non-small cell lung cancer bone scanning can be restricted to patients with clinical indicators for skeletal metastases. This approach reduces the number of bone scans and consecutive investigations without loss of sensitivity in the detection of skeletal metastases.
Natural history of indeterminate colitis. The long-term outcome of patients with a pathological diagnosis of indeterminate colitis on a colectomy specimen was investigated. The case records of 46 such patients operated on for inflammatory bowel disease between 1960 and 1983 were reviewed. Using the preoperative clinical information, pathological and radiological reports, it was possible to divide the patients into three groups: group 1, probable Crohn's disease (19 cases); group 2, probable ulcerative colitis (11 cases); and group 3, indeterminate colitis (16 cases). The patients were followed for a minimum of 2.5 years (median 10, range 2.5-28 years). During this period the probable diagnosis changed in five cases only. One patient in group 1 (Crohn's disease) was subsequently considered to have ulcerative colitis (group 2). The other four patients were all in group 3. Three were reclassified as ulcerative colitis and the fourth as Crohn's disease on the finding of a single granuloma in a rectal biopsy. No case in group 3 required subsequent small bowel surgery. These data suggest that patients continuing with a diagnosis of indeterminate colitis in spite of careful preoperative and postoperative assessment are unlikely to show features of Crohn's disease in the long term. This may be important when considering a subsequent restorative proctectomy.
Ventricular tachycardia originating from the right ventricular free wall in a patient with an old myocardial infarction. A 64-year-old woman with right ventricular infarction had ventricular tachycardia (VT) with left bundle-branch block morphology. Pace-mapping during sinus rhythm and the earliest ventricular potential during VT suggested that the VT originated in the inflow-inferior site of the right ventricular free wall.
The Western Washington Myocardial Infarction Registry and Emergency Department Tissue Plasminogen Activator Treatment Trial. This study comprised a registry and an emergency department treatment trial using recombinant tissue plasminogen activator. During 1 year, 1,028 patients with documented acute myocardial infarction (AMI) were evaluated for eligibility for thrombolytic therapy. Of these, 221 patients (22%) were eligible for thrombolytic therapy under currently accepted criteria, 175 (79%) of them were correctly identified by emergency department physicians for thrombolytic therapy, and 160 were enrolled in the trial. Only 3 patients (2%) enrolled by emergency department physicians did not subsequently evolve documented AMI. In all, 807 patients (78%) were ineligible for thrombolytic therapy: 335 (33%) because of greater than or equal to 1 contraindications, 364 (36%) because of nondiagnostic electrocardiograms on presentation, and 105 (10%) because of age greater than 75 years, or greater than 6 hours of chest pain at presentation, or both. Mortality in treated patients at 14 days was 5.6%, and survival at 1 year was 92%. The mean time from hospital arrival to thrombolytic treatment was 55 +/- 27 minutes. Initial management of AMI with recombinant tissue plasminogen activator in the emergency department provided rapid and safe treatment comparable to that reported in trials that started treatment in the coronary care unit. The proportions of eligible patients could be increased from 1 in 5 to 1 in 3, if patients currently excluded only because of age greater than 75 years or because of greater than 6 hours of chest pain were offered treatment.
Liver viability after ischemia-reperfusion. Lack of a reproducible model to quantitatively assess hepatocellular injury following ischemia has made it difficult to assess new strategies for minimizing hepatic injury. We studied the progression of hepatocellular injury after ischemia and ischemia with reperfusion in rats. Irreversible injury was quantitated using a triphenyltetrazolium chloride assay that was shown to correlate with ultrastructural changes. Adenosine triphosphate decreased to 36% of basal values after 30 minutes, but returned to normal with reperfusion with no decrease in viability. In contrast, viability fell by 30% after 60 minutes of ischemia, and by 64% when 60 minutes of ischemia was followed by reperfusion. We conclude that reperfusion of ischemic liver increases the degree of irreversible damage. The model employed here seems to be useful for studying ischemic and reperfusion injury in the liver.
Assessment of systolic thickening with thallium-201 ECG-gated single-photon emission computed tomography: a parameter for local left ventricular function. We measured left ventricular (LV) systolic thickening expressed as a systolic thickening ratio in 28 patients, using 201Tl ECG-gated SPECT. Five normals, 15 patients with prior myocardial infarction, 5 with hypertrophic cardiomyopathy, and 3 with dilated cardiomyopathy were studied. The systolic thickening ratio was calculated as [(end-systolic--end-diastolic pixel counts) divided by end-diastolic pixel counts], using the circumferential profile technique of both end-diastolic and end-systolic short axial images. Functional images of the systolic thickening ratio were also displayed with the "bull's-eye" method. The mean systolic thickening ratio thus calculated were as follows: normals, 0.53 +/- 0.05 (mean +/- 1 s.d.); non-transmural prior myocardial infarction, 0.33 +/- 0.09; transmural prior myocardial infarction, 0.14 +/- 0.05; hypertrophic cardiomyopathy in relatively nonhypertrophied areas, 0.56 +/- 0.11; hypertrophic cardiomyopathy in hypertrophied areas, 0.23 +/- 0.07; and dilated cardiomyopathy, 0.19 +/- 0.02. The systolic thickening ratio analysis by gated thallium SPECT offers a unique approach for assessing LV function.
Two-dimensional Doppler echocardiographic correlation of dipyridamole-thallium stress testing with isometric handgrip. To determine how frequently new wall-motion abnormalities that are indicative of ischemia accompany thallium redistribution, 47 consecutive patients underwent two-dimensional echocardiography during routine dipyridamole-thallium stress testing. A secondary aim of the study was to determine whether the addition of isometric handgrip exercises to the standard dipyridamole imaging protocol increased the frequency of wall-motion abnormalities or thallium redistribution. Echocardiograms and thallium scans were independently interpreted, and wall-motion abnormalities that appeared with dipyridamole, handgrip exercise, or both were compared with results of thallium imaging. Five of 24 patients with thallium redistribution had new wall-motion abnormalities, and the extent (number of segments) of thallium redistribution in these five patients was significantly greater than in those who did not have well-motion abnormalities (p less than 0.03). The addition of isometric handgrip exercises to the imaging protocol did not distinguish between patients with and without new wall-motion abnormalities or thallium redistribution. Thus new wall-motion abnormalities infrequently accompany thallium redistribution in routine dipyridamole stress testing in spite of the addition of handgrip exercises, but when new wall-motion abnormalities are present, they are associated with a greater area of thallium redistribution.
An increased number of gamma/delta T-cells and gastric epithelial cell expression of the groEL stress-protein homologue in Helicobacter pylori-associated chronic gastritis of the antrum. Numerous studies have shown that the presence of Helicobacter pylori in the stomach is linked to the development of chronic gastritis most commonly seen in the antrum. However, the pathogenic mechanisms are unclear. In 23 of 31 patients, examined due to symptoms from the upper gastrointestinal tract, H. pylori-associated chronic gastritis of the antrum was diagnosed histologically and by growth of H. pylori. Immunoperoxidase staining on gastric biopsy specimens from these patients showed an increased number of gamma/delta T-cells within the epithelium. Furthermore, the Mab ML30 (raised against the 65 kDa heat shock protein of mycobacteria) demonstrated positive staining in the gastric epithelial cells in all H. pylori-positive but not in H. pylori-negative biopsy specimens. H. pylori also reacted with ML30, as detected by immunoperoxidase staining as well as by immunoblotting. Intraepithelial gamma/delta T cells may play a role in host defense against invading H. pylori, and the bacteria may trigger an autoimmune response to stress proteins expressed by the gastric epithelial cells.
Effects of lidocaine on reperfusion arrhythmias and electrophysiological properties in an isolated ventricular muscle model of ischemia and reperfusion. Transmembrane electrical activity was recorded from endo- and epicardium of isolated segments of guinea pig right ventricles with standard microelectrode techniques. An ECG was also recorded by two electrodes placed at opposite ends of the tissue bath. Regular stimulation was delivered to the endocardium. Tissues were exposed to simulated ischemia for 15 min and then were reperfused with "normal" Tyrode's solution. Rapid sustained or nonsustained ventricular tachycardia, bigeminy or trigeminy with characteristics of transmural reentry occurred in early reperfusion in 14 of 20 hearts (70%). Arrhythmias were accompanied by prolongation of transmural conduction time and abbreviation of endocardial effective refractory period. With lidocaine, at 1, 5, 10 and 50 microM, reperfusion arrhythmias occurred in 53.3, 22.2, 20.8 and 14.3% of hearts, respectively. The decreased incidence of arrhythmias was statistically significant for 5 to 50 microM lidocaine (P less than .01). The antiarrhythmic effect did not correlate with changes in transmural conduction time, endocardial effective refractory period, or endocardial excitability. However, antiarrhythmic concentrations of lidocaine selectively depressed epicardial excitability and significantly increased endo- to epicardial conduction block during late ischemic and early reperfusion periods. Epicardial inexcitability extended to late diastole and conduction block was not restricted to premature beats. Thus, in transmural reentry in which the epicardium is an essential component of the circuit, lidocaine may interrupt the circuit by selectively rendering this component inexcitable.
An outbreak of Escherichia coli O157:H7 colitis associated with consumption of precooked meat patties. An outbreak of Escherichia coli O157:H7 hemorrhagic colitis at a Minnesota junior high school in October 1988 comprised 32 cases among 1562 students (attack rate, 2.0%). Four children were hospitalized; none developed hemolytic-uremic syndrome. Case children were more likely than controls to have eaten heat-processed meat patties (odds ratio, 6.2; 95% confidence interval, 2.0-20.1; P less than .001) in the school cafeteria on a specific day. The minimum estimated attack rate among students who ate these patties was 8%. The patties should have been sufficiently cooked by the manufacturer to destroy enteric pathogens before they were frozen and distributed. E. coli were cultured from frozen patties that were manufactured at the same plant on the same dates as the implicated patties, but serotype O157:H7 was not isolated. Heat-processed meat patties may serve as vehicles for E. coli O157:H7 infection, and currently there are no federal or state regulatory standards to ensure the safety of these products.
Platelet-activating factor (PAF) stimulates the production of PAF acetylhydrolase by the human hepatoma cell line, HepG2. The human hepatoma cell line, HepG2, secreted an activity that degrades platelet-activating factor (PAF) by the hydrolysis of the sn-2 acetyl group. This activity was Ca++ independent, inhibited by diisopropylfluorophosphate but not by p-bromophenacyl bromide, and resistant to treatment with trypsin or pronase. Separation of HepG2-conditioned medium by gel filtration disclosed that the activity was associated with lipoproteins. An antiserum against PAF acetylhydrolase immunoprecipitated this activity. It was not recognized by an antibody against lecithin:cholesterol acyltransferase (LCAT), which also is secreted by HepG2 cells. Therefore the phospholipase A2 activity of LCAT was excluded as a source of the observed activity. PAF added to the culture medium stimulated the secretion of the PAF-degrading activity by HepG2 cells, while lyso-PAF was inactive. Maximal stimulation was observed with 5 ng/ml PAF, which induced a fivefold increase. The presence of 5 ng/ml PAF, enhanced the secretion of [35S]methionine-labeled PAF acetylhydrolase and cycloheximide inhibited both the basal and PAF-stimulated secretion of the labeled enzyme. We conclude that HepG2 cells produce PAF acetylhydrolase. The liver may be a major source of plasma PAF acetylhydrolase, and PAF may induce the production of its inactivating enzyme by the liver.
Prognosis in familial non-polyposis colorectal cancer. Familial cases of non-polyposis colorectal cancer have attracted much interest but little is known of their natural history. Using a population based study we have determined whether a positive family history of bowel cancer is an independent prognostic factor. All patients under 55 years with histologically confirmed colorectal cancer in Northern Ireland during the period 1976-8 were studied. The family history was validated in 95% of all nonpolyposis cases (n = 205). Medical history or cause of death were verified for 98% of 1811 first degree relatives. The strength of the family history was assessed using a score that compares the mortality from bowel cancer in the family against the average population mortality, taking account of family size and age structure. The family history score was not predictive of survival neither in univariate analysis or in a Cox's proportional hazards multivariate analysis controlling for age, sex, stage, site, and duration of symptoms. In conclusion, a positive family history does not independently influence prognosis in patients with bowel cancer.
Carboxyhaemoglobin concentrations, pulse oximetry and arterial blood-gas tensions during jet ventilation for Nd-YAG laser bronchoscopy. Oxygen saturation measured with pulse oximetry (SpO2) is overestimated in the presence of carboxyhaemoglobin (COHb). Smoke produced during laser resection of tracheobronchial malignancies may increase concentrations of COHb. We have measured COHb concentrations in 14 patients undergoing laser resection and compared SpO2 with functional oxygen saturation (SaO2) to ascertain if pulse oximetry is an accurate monitor of oxygen saturation. During the procedure frequent changes occur in ventilatory mechanics. Arterial blood-gas tensions were measured to see if gas exchange was satisfactory. Mean preoperative COHb was 1.4%. There was no significant change in COHb in any patient at any stage during treatment. The highest value was 2.05%. The mean difference between SaO2 and SpO2 was 1.13% (95% confidence interval 0.70-1.56%). Oxygen saturation may therefore safely be monitored by pulse oximetry in patients managed by our technique. Empirical setting of a jet ventilator provided acceptable blood-gas tensions, although sometimes it was necessary to increase the FlO2 to greater than 0.3 to maintain oxygenation.
Immunologic abnormalities accompanying acute and chronic viral infections. A number of viral infections induce profound alterations in immune function; these changes may or may not be related to direct infection of lymphoid cells. The immunologic abnormalities that occur during acute systemic viral infections such as measles or infectious mononucleosis include suppression of responses to tuberculin skin tests in vivo and suppression of mitogen responses in vitro, evidence of activation of the immune system with up-regulation of activation-associated cell-surface markers and soluble cellular products, and evidence of altered immune regulation with autoimmune disease and elevated IgE. These abnormalities are likely to be interrelated and can become chronic when the viral infection is not cleared and persists.