shukoor65/lab-rag-model huggingface dataset:
Oral leukoplakia and adolescent smokeless tobacco use. The recent increase in smokeless tobacco (ST) use has prompted investigators to assess the health effects of ST use. This study attempted to evaluate the prevalence of oral leukoplakia among adolescent users and to determine factors associated with its presence. During their annual physical examination, 1116 teenaged football players (567 black, 546 white) answered a 34-question survey and received an oral screening examination. Results indicated that 0.5% of nonusers, 1.5% of previous users, and 13% of current users had clinically evident oral leukoplakia. Factors statistically associated with higher leukoplakia rates included history of ST use, regular ST use, years of ST use, and the weekly quantity consumed. Factors not associated included use of alcohol, use of cigarettes, type of ST used, and hours of ST use. One brand of snuff was found to be associated with a relative risk of leukoplakia higher than that of another brand of snuff. Overall, in ST users oral leukoplakia was six times more likely to develop than in nonusers. Earlier ages of ST use may lead to greater periods of use (in years) and to possible increases in deleterious long-term health effects in current adolescents.
Evaluation of the effect of perineuronal morphine on the quality of postoperative analgesia after axillary plexus block: a randomized double-blind study. A randomized, double-blind study was performed on 50 patients scheduled for elective hand and forearm surgery under axillary plexus block to evaluate the effect of perineuronal morphine on the quality of postoperative analgesia. Patients were divided into two groups. In group A (n = 25) 5 mg of preservative-free morphine in 1.0 mL of 0.9% saline was added to the local anesthetic solution (20 mL of 1% plain lignocaine, 20 mL of 0.5% plain bupivacaine). They also received an intramuscular placebo injection of 1.0 mL of 0.9% saline in the upper thigh. In group B (n = 25), 1.0 mL of 0.9% saline was added to the local anesthetic solution and patients received an intramuscular injection of 5 mg of preservative-free morphine in 1.0 mL of 0.9% saline in the thigh. The addition of morphine to the local anesthetic solution for the axillary block did not shorten the onset time of the block, improve the quality of postoperative pain relief, or provide longer lasting analgesia than that obtained with intramuscular morphine.
Vascular renin-angiotensin system and neurotransmission in hypertensive persons. The existence of a vascular renin-angiotensin system and its role in modulating sympathetic activity were evaluated in forearm arterioles of hypertensive individuals. Isoproterenol (0.03, 0.01, 0.3 microgram/100 ml/min for 5 minutes each; n = 5) was infused into the brachial artery, and active and inactive renin, angiotensin II, and norepinephrine forearm balance (venous-arterial differences corrected for forearm blood flow by strain-gauge plethysmography) were measured. Isoproterenol caused vasodilation and a dose-dependent active and inactive renin, angiotensin II, and norepinephrine outflow, an effect blunted by propranolol (10 micrograms/100 ml/min). To evaluate the role of local angiotensin II on beta-mediated norepinephrine overflow, the experiment was repeated with captopril (2.5 micrograms/100 ml/min for 10 minutes; n = 5), which abolished angiotensin II release and significantly reduced norepinephrine overflow. To test whether angiotensin II facilitates both prejunctional norepinephrine release and its postjunctional action, we evaluated the effect of exogenous angiotensin II, infused into the brachial artery at low concentrations (0.001 microgram/100 ml/min), on forearm vasoconstriction and norepinephrine release induced by endogenous sympathetic activation (application of a lower body negative pressure: -10 and -20 mm Hg for 5 minutes, n = 10) and on the vasoconstrictor effect of local norepinephrine (0.0015, 0.005, 0.015, 0.05, 0.15 micrograms/100 ml/min for 3 minutes each; n = 6). Although angiotensin II increased the vasoconstricting effect and the norepinephrine release induced by lower body negative pressure, it failed to affect norepinephrine-mediated vasoconstriction. Our data indicate the existence in hypertensive individuals of a vascular renin-angiotensin system that seems to modulate sympathetic activity through the presynaptic facilitation of norepinephrine release.
Impaired lipopolysaccharide-inducible tumor necrosis factor production in vitro by peripheral blood monocytes of patients with viral hepatitis. We investigated lipopolysaccharide-induced tumor necrosis factor production in vitro by peripheral blood monocytes from patients with various liver diseases. Tumor necrosis factor production was found to be significantly reduced in patients with chronic hepatitis B (n = 17; 135 +/- 30 pg tumor necrosis factor/ml; mean +/- S.E.M.) and patients with chronic non-A, non-B hepatitis (n = 15; 212 +/- 22 pg tumor necrosis factor/ml) compared with healthy control individuals (n = 47; 411 +/- 40 pg tumor necrosis factor/ml; p less than 0.0005 and p less than 0.01, respectively). This reduced tumor necrosis factor production was not only seen with an optimal stimulating concentration of lipopolysaccharide (100 ng/ml) but also with suboptimal concentrations (0.1 ng/ml). In contrast to patients with chronic viral hepatitis, monocytes from patients with alcohol-induced cirrhosis (n = 26; 444 +/- 49 pg tumor necrosis factor/ml), primary biliary cirrhosis (n = 7; 412 +/- 81 pg tumor necrosis factor/ml) and alcohol-induced fatty liver changes (n = 5; 401 +/- 62 pg tumor necrosis factor/ml) produced normal amounts of tumor necrosis factor when stimulated with an optimal concentration of lipopolysaccharide. Lipopolysaccharide (0.1 ng lipopolysaccharide/ml)-stimulated peripheral blood monocytes of patients with chronic hepatitis B (n = 15; 102 +/- 32 pg/ml) or non-A, non-B hepatitis (n = 13; 97+/- 16 pg/ml) could not be induced to produce more tumor necrosis factor either when prestimulated with gamma-interferon (170 +/- 45 pg/ml and 149 +/- 32 pg/ml, respectively), a lymphokine known to activate monocytes, or with the cyclooxygenase inhibitor indomethacin to reduce the suppressive effect of prostaglandin E2 (148 +/- 40 pg/ml and 153 +/- 45 pg/ml, respectively.
The burden of acute respiratory infection due to measles in developing countries and the potential impact of measles vaccine. Measles is a major cause of acute lower respiratory infection (ALRI) in developing countries. Hospital and community-based studies of ALRI have found that measles accounts for 6%-21% of the morbidity and 8%-93% of the mortality due to ALRI. Although live attenuated measles vaccine is one of the most effective vaccines in use today, measles has not been controlled in many parts of the world, primarily because the levels of vaccine coverage required to interrupt measles transmission have not been achieved. In addition, in some areas, a large percentage of cases of measles occur in infants who are younger than the age recommended for vaccination. Recent studies suggest that the Edmonston-Zagreb measles vaccine may be more immunogenic than other vaccine strains in young infants. A substantial proportion of ALRI could be prevented by increasing measles vaccine coverage and by the use of particular vaccine strains in younger children.
Adrenal and ovarian steroid hormone responses to gonadotropin-releasing hormone agonist treatment in polycystic ovary syndrome. It has been postulated that in polycystic ovary syndrome ovarian steroids can influence adrenal steroidogenesis. To test this hypothesis, basal and dexamethasone-suppressed-corticotropin-stimulated steroid hormone responses were compared among three groups of women before, during, and after gonadotropin-releasing hormone agonist treatment for 3 months. The groups were characterized as follows: (1) women with polycystic ovary syndrome with high dehydroepiandrosterone sulfate levels (greater than 400 micrograms/dl), (2) women with polycystic ovary syndrome with normal dehydroepiandrosterone sulfate levels (less than 300 micrograms/dl), and (3) normal ovulatory women. In response to gonadotropin-releasing hormone agonist, basal serum luteinizing hormone, follicle-stimulating hormone, estradiol, estrone, 17-hydroxyprogesterone, androstenedione, and testosterone in all three groups were suppressed to similar levels. Basal serum dehydroepiandrosterone sulfate levels in the group with high levels declined, but they did not reach the normal, unaltered concentrations in the other two groups. Two subjects with polycystic ovary syndrome in this group with high levels, who showed the greatest declines in basal serum dehydroepiandrosterone sulfate levels (34%, 40%), also had evidence of 3 beta-hydroxysteroid dehydrogenase deficiency before treatment, which was resolved by the end of treatment. In both groups with polycystic ovary syndrome, the increase in maximum incremental rise of dehydroepiandrosterone and dehydroepiandrosterone sulfate levels in response to a pharmacologic dose of corticotropin from a dexamethasone-suppressed baseline (adrenal androgen capacity) remained unaltered during gonadotropin-releasing hormone agonist administration. We conclude that ovarian steroids may promote excessive adrenal androgen secretion in women with polycystic ovary syndrome, may induce 3 beta-hydroxysteroid dehydrogenase deficiency as a mechanism for adrenal involvement in some women with polycystic ovary syndrome, and do not influence adrenal androgen capacity.
Responsiveness of patients with advanced ovarian carcinoma to tamoxifen. A Gynecologic Oncology Group study of second-line therapy in 105 patients. One hundred five patients with Stage III or IV epithelial ovarian cancer whose disease had persisted or recurred after primary surgery and first-line chemotherapy were given tamoxifen (20 mg orally twice daily) and evaluated for response. Eighteen percent of the patients responded: 10% demonstrated a complete response (CR) and 8% showed a partial response (PR). Thirty-eight percent of the patients had short-term disease stabilization. CR had a median duration of 7.5 months, with the longest lasting 17 months. For patients with PR or stable disease, the median duration of response was 3 months (maximum duration, 9 months). When estrogen receptors of tumor tissue from patients demonstrating CR were evaluated, eight of nine (89%) had elevated estrogen receptor levels. This contrasts with patients who had stable or progressive disease as only 59% of them had measurable estrogen receptors (P = 0.16).
Meniscal tears: MR and arthrographic findings after arthroscopic repair. Magnetic resonance (MR) imaging was performed on 29 previously repaired menisci and one conservatively treated meniscus (total, 30 menisci). Intermediate- and T1-weighted MR sequences revealed persistent signal intensity extending to an articular surface (grade 3 signal intensity) in 27 of the 30 menisci. On T2-weighted images, seven of the 30 menisci were found to contain unequivocally higher signal intensity, defined by a full-thickness defect (grade 3 signal intensity involving two articular surfaces) increasing in signal intensity to a level equivalent to that of joint fluid. The MR imaging and arthrographic appearances of 23 of the 30 menisci were compared. Arthrographic examination revealed partial or complete healing in 13 menisci and tears in 10. The presence of grade 3 signal intensity on intermediate- and T1-weighted MR images did not reliably predict a tear seen at arthrography. Unequivocally higher signal intensity on T2-weighted images is a useful sign in the prediction of a persistent meniscal tear (sensitivity, 60%; specificity, 92%; P less than .02). Since presence of grade 3 signal intensity on intermediate- and T1-weighted images does not reliably predict a tear and unequivocal T2 increase in intensity has a sensitivity of only 60%, arthrography should be considered for assessment of the symptomatic, previously repaired meniscus.
Reduced vascular compliance as a marker for essential hypertension. In 38 patients with established essential hypertension and 32 age-matched normotensive control subjects proximal and distal arterial compliance were determined by computer-based assessment of the diastolic decay of a brachial arterial tracing and a modified Windkessel model of the circulation. In the hypertensive subjects compared to the normotensive subjects mean arterial pressure was 25% higher (P less than .001), systemic vascular resistance 23% higher (P less than .01), proximal compliance 19% lower (P less than .01), and distal compliance 72% lower (P less than .001). The reduction in distal compliance was highly age-dependent. In the youngest age range (45 to 54 years) little overlap appeared between hypertensive and normotensive groups, whereas in the oldest subjects studied (65 to 75 years) distal compliance was comparably low in the two groups. Thus, distal vascular compliance provides a sensitive and specific marker for the abnormal vasculature associated with hypertension and may be particularly useful in identifying the disease in young individuals with borderline blood pressure.
Primary CNS lymphoma treated with osmotic blood-brain barrier disruption: prolonged survival and preservation of cognitive function. Combination chemotherapy with or without radiotherapy has had only modest efficacy in the treatment of primary CNS lymphoma. Median survival of these patients, treated primarily with radiotherapy, is 13 months; 5-year survival is less than 5%. Thirty consecutive non-acquired immune deficiency syndrome patients with primary CNS lymphoma were treated with barrier-dependent chemotherapy using intraarterial mannitol to open the blood-brain barrier (BBB). Follow-up included extensive neuropsychologic testing of all patients. Thirteen patients received cranial radiation 1 to 9 months before referral (group 1). Seventeen patients received initial BBB disruption chemotherapy with subsequent radiation only for tumor progression or recurrence (group 2). The difference in median survivals from diagnosis--17.8 months for group 1 and 44.5 months for group 2--was statistically significant (P = .039). Group 1 survival is comparable with the 20-month median survival of a historical series of patients (n = 208) treated with radiotherapy with or without chemotherapy. Group 2 patient survival represents an advance in the survival of CNS lymphoma and was associated with preservation of cognitive function in six of seven nonirradiated complete responders observed for 1 to 7 years. Patient toxicity was manageable in this intensive therapeutic regimen. In this series, a plateau in survival curves suggests that a major portion of these patients may be cured without the neuropsychologic sequelae associated with cranial radiation.
Modulation of neuropathic pain behavior in rats by spinal disinhibition and NMDA receptor blockade of injury discharge. When a peripheral nerve is severed, damaged sensory fibers emit a barrage of impulses that lasts for many seconds, or even several minutes ('injury discharge'). We have shown in rats that local anesthetic blockade of this discharge suppresses autotomy (a behavioral model of neuropathic pain). Correspondingly, mimicking prolonged injury discharge with electrical stimulation, especially of C-fibers, increased autotomy. These data support the hypothesis that injury discharge plays a role in the triggering of neuropathic pain. The mechanism of triggering autotomy was investigated using intrathecal injection of agents affecting glutamatergic transmission. A single intrathecal injection at the lumbar enlargement of the NMDA receptor blockers MK-801 and 5-APV, just prior to neurectomy, significantly suppressed autotomy. Blocking glycinergic inhibition just prior to neurectomy with a single strychnine injection strikingly enhanced autotomy. Strychnine enhancement of autotomy was prevented by prior injection of MK-801 or 5-APV. These results suggest that the expression of autotomy in rats, and by inference neuropathic pain in humans, is affected by injury discharge, possibly mediated by long-lasting, NMDA receptor-related, spinal disinhibition.
Plasmapheresis. A therapeutic option in the management of heparin-associated thrombocytopenia with thrombosis. Heparin-associated thrombocytopenia with thrombosis (HATT) is an uncommon syndrome that is estimated to occur in 1-5% of patients with heparin-induced thrombocytopenia. Early diagnosis requires careful clinical surveillance, and the management of these patients can be complex. Cessation of heparin therapy and substitution or addition of oral anticoagulants, antiplatelet agents, dextrans, and prostacyclin analogues have been advocated. The authors are aware of only two case reports in the literature that examine the use of plasmapheresis as a therapeutic alternative. The authors report a case of a 53-year-old white man who developed HATT after a single protamine-reversed exposure to heparin. Controlled platelet aggregation studies performed before and after apheresis sessions documented a dramatic response and rapid normalization of platelet number and function in the patient. The authors conclude that plasmapheresis could be a valuable adjunct in the successful management of patients with HATT. When done in conjunction with platelet aggregation studies, an objective measurement of therapeutic efficacy can be achieved.
Nutritional support in the critically ill surgical patient. Aggressive nutritional support in the critically ill surgical patient is essential if improved outcome is to be realized. An understanding of the metabolic alterations of trauma and sepsis provides the foundation for a nutritional prescription for the individual patient. Careful nutritional assessment; titration of fluid, electrolytes, and micronutrients; provision of adequate calories and nitrogen to meet metabolic needs; and the selective use of specialized formulations are important components of nutritional management in the ICU.
Patellofemoral pain. An arthroscopic perspective. Patellofemoral pain should be approached as thoroughly as any other musculoskeletal disease. A careful patient history and physical examination are mandatory. These are followed by appropriate imaging studies such as radiographs, bone scans, CT scans, CT arthrograms, and MRI, as each individual case demands. Finally, arthroscopy is employed in its proper sequence. This article has been developed as an attempt to define a classification scheme of anterior knee pain and then to narrow this down to pain localized to the patellofemoral joint. The authors have attempted to isolate further the clinical entities to those that can be diagnosed and treated arthroscopically. Arthroscopy and arthroscopic surgery allow recognition and treatment of these disorders with minimal invasiveness and patient morbidity.
The elusive cause of instability in unstable angina. The causes of unstable angina are still largely unknown. However, some facts deriving from angiographic, postmortem, and pathophysiologic studies are well established. Angiographic findings: coronary thrombi and complicated stenoses are more frequent in unstable than in stable angina. Conversely, the severity of coronary atherosclerosis and the development of collateral circulation is similar in both coronary syndromes. Postmortem findings: the following features are more frequent in unstable than in stable angina: (1) mural thrombi, which often represent out-growth from the inside of a fissured plaque; (2) inflammatory cells at the site of plaques and in perivascular nerves; and (3) contraction bands in smooth muscle cells of the media surrounding plaques. However, fissured plaques can be found in 10% of individuals dying of noncardiac causes, and fissured plaque may occasionally be missing under the coronary thrombus in unstable angina. Pathophysiologic findings: patients with unstable angina compared with those with stable angina exhibit: (1) higher levels of serotonin in the coronary sinus; (2) higher systemic levels of fibrino-peptide A; (3) higher urinary levels of thromboxane A2 metabolites; and (4) a greater coronary reactivity to constrictor stimuli. A critical analysis of these established facts is required to set the stage for a better comprehension of the causes which can cause a coronary segment to progress in a stuttering way toward acute persistent coronary occlusion and myocardial infarction. Plaque fissure is likely to be an important background thrombogenic stimulus in many cases.
Antitumor effect of synthetic derivatives of lipid A in an experimental model of colon cancer in the rat. Colon carcinoma is one of the most frequent causes of cancer death in industrialized countries. The patients generally die of the metastases. In a colon cancer rat model, the authors have shown that lipopolysaccharides from Escherichia coli induced the regression of carcinomatosis and cured 20%-30% of the rats. Some synthetic derivatives of lipid A, which are less toxic than lipopolysaccharides, were injected 14 days after the tumor cells. They induced the complete regression of peritoneal carcinomatosis consisting of numerous nodules measuring 1-5 mm in 20%-30% of rats. Only compounds with three or more hydroxymyristic acid residues were effective. In vivo effects were correlated with the capacity to induce the production of interleukin 1 and tumor necrosis factor but not with the capacity to induce macrophage-mediated cytolysis. It is therefore possible to synthesize weakly toxic derivatives of lipopolysaccharides retaining their antitumoral property in vivo.
Diurnal variation of essential and physiological tremor. Evaluations were made of the diurnal variations of tremor power at rest, after fatigue and after mass loading, and plasma norepinephrine in patients with familial essential tremor and normal subjects. Diurnal tremor power rhythms for both essential and physiological tremor pursued identical temporal profiles. Plasma norepinephrine levels followed a congruent diurnal pattern with later peak values than the peak values of tremor power. Sympathetic nervous system activity is unlikely to be the cause of diurnal tremor power variation. The consistent diurnal rhythm of tremor power may affect dosage schemes of tremorolytic drugs.
Recent developments in the diagnosis and management of patients with transient ischaemic attacks and minor ischaemic strokes. Appropriate management of the patient with transient focal neurological symptoms must start with accurate clinical diagnosis. Wider use of clear diagnostic criteria and symptom checklists, and better knowledge of the clinical features of the 'funny turns' which are not related to transient focal cerebral ischaemia could reduce the present variability in clinical diagnosis of transient ischaemic attacks. More accurate clinical diagnosis contributes to better selection of the most appropriate investigation strategy for each patient. A basic minimum standard of investigation is outlined and perhaps provides a suitable template for audit. Patients with transient ischaemic attacks which are definitely in the carotid distribution may be eligible for entry in trials of carotid endarterectomy. Prudent use of duplex ultrasound studies of the carotid arteries in patients with appropriate symptoms is an effective way to reduce the costs of investigations and their complications (i.e. the number of strokes associated with cerebral angiography). Digital venous subtraction angiography has, by comparison, many disadvantages as a screening tool. Advances in management include: recent statistical overviews which have emphasized the need to consider blood pressure and plasma cholesterol reduction in a large proportion of patients, and the value of long term anti-platelet therapy in reducing the risks of stroke, myocardial infarction and vascular death in both males and females. The value of anticoagulants in patients with atrial fibrillation and transient ischaemic attacks or minor stroke is being tested in current trials.