shukoor65/lab-rag-model huggingface dataset:
Angiosarcoma of the face and scalp. A case report with complete spontaneous regression. A wide, hemorrhagic lesion occurred on the face and scalp of a 75-year-old woman who had no history of previous trauma to the region. Histology showed features consistent with a diagnosis of angiosarcoma. Clinical and radiologic investigations failed to show any sign of internal involvement. The lesion completely regressed without any therapy within a few months from onset, and the patient is alive and free of disease 36 months after the first observation. Repeated clinicoradiologic investigations failed again to prove visceral diffusion of the tumor. Spontaneous regression of an angiosarcoma is an exceptional event, and only one similar case has been reported in the literature.
Mast cells are critical for the production of leukotrienes responsible for neutrophil recruitment in immune complex-induced peritonitis in mice. Mast cells are secretory cells strategically located in the vicinity of blood vessels where they can readily initiate and modulate various inflammatory processes, including plasma exudation and leukocyte infiltration. We have previously shown that 50% of the neutrophil influx during immune complex peritonitis in mice is due to mast cells. Eicosanoids are important mediators of various inflammatory processes including neutrophil infiltration. The possibility that mast cells are essential for the production of leukotrienes (LT) involved in the elicitation of neutrophils in immune complex peritonitis was investigated in mast cell-deficient, WBB6F1-W/WV, and normal, WBB6F(1-)+/+, mice. The time course and amounts of immunoreactive PGE2, 6-keto-PGF1 alpha, and TX3B2 released into the peritoneal exudates were similar in both sets of mice. LTB4 and LTC4 levels, however, were twofold higher in +/+ than in W/WV mice 2 h after stimulation. HPLC analysis of the peritoneal exudate confirmed the presence of leukotrienes. The 5-lipoxygenase inhibitor A-63162 blocked leukotriene production in a dose-dependent manner in both sets of mice. However, this compound caused a significant reduction (60%) of neutrophil infiltration only in WBB6F(1-)+/+ but not in the mast cell-deficient mice. Mast cell reconstitution of WBB6F1-W/WV mice restored the effect of A-63162 on PMN recruitment. These data suggest that mast cells in the vicinity of blood vessels are important for the synthesis of leukotrienes responsible for PMN recruitment.
Preliminary experience with magnetic resonance imaging in patients with third-trimester bleeding. Fifteen patients with third-trimester bleeding, in whom transabdominal ultrasound had failed to identify a definitive source of bleeding, underwent magnetic resonance imaging (MRI). Magnetic resonance imaging correctly identified three cases of placenta previa. In four patients, intrauterine blood was identified in hematomas. One hematoma was associated with a previa, two progressed to acute abruptions, and one was associated with a clot at the marginal cord insertion. Blood was seen leading away from the placenta in a case that progressed to an acute abruption. It was also seen in the region of the cervix in two patients with placenta previa. One patient had a normal MRI but had a fresh clot at delivery, which presumably formed after the imaging. In the remaining seven patients, MRI scans were negative and the placentas were normal at delivery. Our preliminary results suggest that MRI is helpful in evaluating patients with unexplained third-trimester bleeding.
Development of systemic lupus erythematosus after interferon therapy for chronic myelogenous leukemia. A 19-year-old man with Philadelphia-positive chronic myelogenous leukemia treated with interferon-alpha (IFN-alpha) therapy for 45 months had systemic lupus erythematosus disease features: malar rash, migratory arthralgias, elevated antinuclear antibodies, elevated antinative DNA, hypocomplementemia, lymphopenia, and proteinuria. After discontinuation of the IFN and initiation of corticosteroids, there was gradual recovery of symptoms, a decline in antinative DNA and antinuclear antibodies to normal levels, and a decrease in proteinuria. The potential association between IFN therapy and the development of systemic lupus erythematosus, and the role of IFN in other autoimmune diseases, is discussed.
Angioplasty of an oversized venous bypass graft using two fixed wire systems. Oversized saphenous vein bypass grafts may be inadequately dilated using currently available coronary angioplasty catheters. The hugging balloon technique has been previously described for lesions in large saphenous vein grafts. We report the initial use of the hugging balloon technique using two fixed wire angioplasty catheters in an oversized saphenous vein graft.
Pituitary gonadal functioning in male alcoholics in an Indian psychiatric hospital. Serum levels of luteinizing hormone (LH), testosterone and hepatic functions were measured in 38 male alcoholics and in 24 male control subjects. Significant elevation of serum LH and a trend of low serum testosterone were noted with scant evidence of advanced liver disease. None of the alcoholics had clinical stigmata of hypogonadism and feminization.
Insular carcinoma: a distinct thyroid carcinoma with associated iodine-131 localization Insular carcinoma, once considered a poorly-differentiated thyroid cancer, has been reclassified as a distinct thyroid neoplasm. Since this neoplasm is composed of follicular epithelial cells, it may concentrate radioiodide (131I) making postoperative 131I imaging for detection of metastases and radiotherapy possible. A 20-yr review of 35 cases diagnosed as anaplastic or undifferentiated thyroid carcinoma at this medical center revealed five patients with insular carcinoma. Four patients showed postoperative 131I localization and received therapeutic doses of 131I. Three of the four showed extrathyroidal 131I localization in neoplastic lesions. In one patient, the resolution of metastatic lesions by magnetic resonance and 131I imaging suggests that 131I may have an important therapeutic role in this aggressive neoplasm.
Role of endothelium-derived prostanoid in angiotensin-induced vasoconstriction. To test the hypothesis that prostanoids contribute to angiotensin II-induced vascular contraction, we compared the effect of angiotensin II on isometric tension development by rings of descending thoracic aorta bathed in Krebs' bicarbonate buffer with and without indomethacin (10 microM) to inhibit cyclooxygenase, CGS13080 (10 microM) to inhibit thromboxane A2 synthesis, or SQ29548 (1 microM) to block thromboxane A2/prostaglandin endoperoxide receptors. The comparisons were made in rings of aorta taken from normotensive rats and from rats with aortic coarctation-induced hypertension at 12 days and 90-113 days after coarctation. These rings released thromboxane B2, which was found to be endothelium dependent, increased in hypertensive rats, and stimulated by angiotensin II (10(-6) M) in normotensive rats and in hypertensive rats at 12 days after coarctation. The angiotensin II (10(-6) to 10(-5)M)-induced contraction of aortic rings was increased by about 30% at 12 days after coarctation and decreased at 90-113 days after coarctation. Removal of the endothelium increased the contractile effect of angiotensin II (10(-6) M) in aortic rings of normotensive rats and hypertensive rats at 90-113 days after coarctation but decreased the effect in aortic rings of hypertensive rats at 12 days after coarctation. In rats at 12 days after coarctation, the angiotensin II (10(-6) M)-induced contraction of aortic rings with endothelium was attenuated by indomethacin and SQ29548 but not by CGS13080. These data suggest that a prostanoid-mediated and endothelium-dependent mechanism of vasoconstriction contributes to the constrictor effect of angiotensin II in aortic rings of rats in the early phase of aortic coarctation-induced hypertension.
Temporary closure of the abdominal wall by use of silicone rubber sheets after operative repair of ruptured abdominal aortic aneurysms. Management of patients after operative repair of abdominal aortic aneurysms can be further complicated if primary closure of the abdominal wall cannot be technically accomplished or is associated with profound increases in intraabdominal and peak inspiratory pressures. We recently treated five patients with ruptured abdominal aortic aneurysms and one patient with a ruptured thoracoabdominal aneurysm whose abdominal incisions had to be closed with a Dacron reinforced, silicone sheet. All patients were hemodynamically unstable either at admission to the hospital or became so during operation. Four patients required the insertion of a silicone rubber sheet at the primary operation because of massive retroperitoneal hematoma or edema of the bowel wall or both. Incisions in two patients were closed primarily, but the patients required reexploration and secondary closure with silicone rubber sheets because of the development of marked increases in peak inspiratory pressures, intraabdominal pressures, and decreased urinary output. Four of the six patients subsequently underwent successful removal of the silicone rubber sheets with delayed primary closure of the abdominal wall, and two others died before removal. The patient with the ruptured thoracoabdominal aneurysm died on postoperative day 20 because of pulmonary sepsis but had a healed abdominal incision. The three surviving patients have been discharged. A silicone rubber sheet may be necessary for closure of the abdominal wall after repair of ruptured abdominal aortic aneurysm in patients where primary abdominal wall closure is impossible or where it results in compromise in respiratory or renal function.
Nonketotic hyperglycinemia: treatment with NMDA antagonist and consideration of neuropathogenesis. Patients with neonatal-onset nonketotic hyperglycinemia have high-glycine content in cerebrospinal fluid (CSF) which is believed to be a cause of intractable neurologic manifestations. The glycine receptor was believed to be inhibitory in the central nervous system; however, a newly discovered glycine receptor is of the excitatory N-methyl-D-aspartate (NMDA) receptor type, which cannot be antagonized by strychnine. The NMDA receptor antagonist, ketamine, was administered to a patient with nonketotic hyperglycinemia; he demonstrated some improvement in hyperirritability, voluntary movement, and electroencephalographic findings. Strychnine therapy had been administered before this trial of NMDA antagonist, but without improvement. The respiratory condition improved with the reduction of the CSF glycine level after withdrawal of sodium valproate. Our findings indicate that high-glycine content in CSF may affect the brain in different ways via NMDA and classic glycine receptors.
Differences of pathophysiology in experimental meningitis caused by three strains of Streptococcus pneumoniae. Differences in cytochemical and pathophysiologic abnormalities in experimental meningitis caused by pneumococcal strains A, B, and C were determined. Strain C produced the most severe abnormalities of cerebrospinal fluid (CSF) concentrations of lactate (P less than .01), protein (P less than .02), and glucose (P less than .01), CSF white blood cell count (P less than .04), cerebral blood flow (P less than .02), and clinical signs (P less than .05). Brain edema occurred only with strains A anc C, with no association with disease severity; intracranial hypertension was also independent of disease severity. Strain B, not C, achieved the highest bacterial titers in the CSF (P less than .005). The widely different abilities of strains of Streptococcus pneumoniae to induce intracranial abnormalities suggest that virulence determinants affect not only evasion of defense during colonization and invasion, as shown in other models, but also determine the course of disease once infection has been established. Differences of cell-wall metabolism among pneumococcal strains may play a role in this latter phase of the development of meningitis.
Lack of correlation between histologic findings and response to chemotherapy in metastatic breast cancer. A retrospective analysis was undertaken to assess the prognostic role of histologic findings in response to chemotherapy and survival in patients with metastatic breast cancer. Histologic material was available for 395 of 1587 patients treated for metastatic breast cancer at the M.D. Anderson Cancer Center between 1973 and 1984. Chemotherapy consisted of 5-fluorouracil, doxorubicin, and cyclophosphamide or similar drugs, with or without tamoxifen. Maintenance cyclophosphamide, methotrexate, and 5-fluorouracil was continued for 2 years after a cumulative doxorubicin dose of 450 mg/m2 was administered. The histologic distribution was as follows: infiltrating ductal carcinoma, 353; invasive lobular, 14; mixed histology, ten; mucinous, seven; signet ring, four; tubular, three; papillary, two; sarcomatoid, one; and apocrine, one. Because individual histologic types occurred infrequently, the patients were divided into infiltrating ductal and nonductal groups. Baseline patient characteristics included age, performance status, estrogen-receptor status, prior hormone response, disease extent, and levels of alkaline phosphatase, bilirubin, and lactate dehydrogenase. These were similar in the two groups. Significantly more patients with nonductal histology had greater than three metastatic sites. There were also more patients with hemoglobin less than 10 mg/dl and albumin less than 3.5 mg/dl in the nonductal group of patients. However, statistically these factors did not have an impact on the results. There was a 63% response rate (17% complete and 46% partial) for the ductal group and a 60% response rate (12% complete and 48% partial) for the nonductal group. The time from initiation of chemotherapy to disease progression was identical (12 months) for the two groups. Survival from initiation of chemotherapy was not significantly different (22 months for ductal and 27 months for nonductal). Based on this study, the authors conclude that histologic findings have no bearing on patient response to chemotherapy or survival in metastatic breast cancer.
Thromboembolism prophylaxis. Choosing the proper method for surgical patients. The primary care physician can play a major role in preoperative consultation in terms of assisting the surgical team to reduce the risk of thromboembolism. A preoperative risk assessment takes into account the type and duration of surgery as well as the existence of risk factors such as age and underlying medical conditions. With careful communication, the consulting physician and surgical team can together select a method of preventing thromboembolism that will prove both safe and effective.
Prenatal alcohol exposure and language development. The effects of fetal alcohol exposure on language and speech acquisition were investigated in a cohort of socioeconomically disadvantaged urban children. Language development was assessed by instruments derived from the Expressive and Receptive Scales of the Sequenced Inventory of Communication Development (SICD) at 1, 2, and 3 years, and by indices constructed from a taped speech sample at age 2 years. Three indices of maternal drinking were supplemented with birth weight and a tally of craniofacial anomalies as early indicators of fetal alcohol damage. No statistically significant relationships were found between the alcohol and language indices after statistical control for confounding variables. The anomalies tally was marginally related to reduced language scores. The statistical significance of this relationship, depended, however, on a single child with the characteristics of fetal alcohol syndrome. The pattern of results suggested that the anomalies tally, and to a lesser extent birth weight, are more sensitive indicators of fetal alcohol exposure than subsequent language development.
Acute and chronic poisoning from residential exposures to elemental mercury--Michigan, 1989-1990. From May 1989 through November 1990, eight episodes of elemental mercury exposure in private residences or schools in the United States were reported to the Agency for Toxic Substances and Disease Registry (ATSDR). The case studies in this report document two of these episodes (both in Michigan) of residential mercury poisoning--one involving acute mercury exposure, and the other, chronic exposure to elemental mercury. These episodes illustrate the differing clinical and toxicologic manifestations of acute and chronic mercury poisoning.
Recognition of UGA as a selenocysteine codon in type I deiodinase requires sequences in the 3' untranslated region. Selenocysteine is incorporated cotranslationally at UGA codons, normally read as stop codons, in several bacterial proteins and in the mammalian proteins glutathione peroxidase (GPX), selenoprotein P and Type I iodothyronine 5' deiodinase (5'DI). Previous analyses in bacteria have suggested that a stem-loop structure involving the UGA codon and adjacent sequences is necessary and sufficient for selenocysteine incorporation into formate dehydrogenase and glycine reductase. We used the recently cloned 5'DI to investigate selenoprotein synthesis in eukaryotes. We show that successful incorporation of selenocysteine into this enzyme requires a specific 3' untranslated (3'ut) segment of about 200 nucleotides, which is found in both rat and human 5'DI messenger RNAs. These sequences are not required for expression of a cysteine-mutant deiodinase. Although there is little primary sequence similarity between the 3'ut regions of these mRNAs and those encoding GPX, the 3'ut sequences of rat GPX can substitute for the 5'DI sequences in directing selenocysteine insertion. Computer analyses predict similar stem-loop structures in the 3'ut regions of the 5'DI and GPX mRNAs. Limited mutations in these structures reduce or eliminate their capacity to permit 5'DI translation. These results identify a 'selenocysteine-insertion sequence' motif in the 3'ut region of these mRNAs that is essential for successful translation of 5'DI, presumably GPX, and possibly other eukaryotic selenocysteine-containing proteins.
Mitochondrial DNA and Parkinson's disease. Two major lines of evidence support the hypothesis that an impairment of mitochondrial function may underlie neuronal death in Parkinson's disease. First, the neurotoxicity of the parkinsonism-inducing compound 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is due to the generation of its 1-methyl-4-phenylpyridinium (MPP+) metabolite in the central nervous system; the toxicity of MPP+ is likely to result from its ability to block mitochondrial electron flow at the level of complex I. Second, recent studies have revealed a deficiency of mitochondrial complex I activity in the brain as well as other tissues of parkinsonian patients. This enzyme activity reduction might be explained by a defect in one or more of the genes coding for the subunits of complex I. Since seven of these genes are localized in the mitochondrial genome, it is conceivable that abnormal mitochondrial DNA (mtDNA) might play a role in the pathogenesis of Parkinson's disease. The entire sequence of the human mitochondrial genome is known, and human mtDNA can be isolated and rapidly analyzed using techniques such as the polymerase chain reaction. Therefore, identification of an easily detectable mtDNA alteration might ultimately be used as a marker for the diagnosis and screening of Parkinson's disease.
Motor neuron disease in a patient with a monoclonal IgMk directed against GM1, GD1b, and high-molecular-weight neural-specific glycoproteins. In a patient with motor neuron disease and benign IgMk monoclonal gammopathy, the M protein reacted with the glycolipids GM1, GD1b, and asialo GM1 and, by immunoblot, with some high-molecular-weight neural-specific glycoproteins. The main reactive bands had an approximate molecular weight of 250 and 400 kd, were most concentrated in the spinal cord, and were also bound by the lectin peanut agglutinin. The presence of the Ga1(beta 1-3)Ga1NAc epitope on these neural-specific glycoproteins may help to explain the selective neurological impairment of the patient.
Relationship between plasma atrial natriuretic factor and urinary kallikrein excretion in essential hypertensives. In order to seek possible relationships between renal kallikrein and atrial natriuretic factor (ANF), we measured urinary kallikrein (UK) and ANF in 84 normal subjects (NS) and in 104 uncomplicated essential hypertensives (HP). Atrial natriuretic factor was significantly higher in HP than in NS (38.5 +/- 1.3 vs 29.0 +/- 1.3 pg/mL, P less than .01), whereas UK was significantly lower in HP than in NS (11.1 +/- 0.9 v 15.3 +/- 0.6 nkatal/24 h, P less than .01). Calculating the 95% of the percentile distribution of the single values of UK in the group of NS we were able to show that 24 out of 104 HP had a UK which fell below the lowest limit (4.5 nkat/24 h) of the normal range. We therefore divided our HP into two subgroups: patients with normal kallikrein excretion (NK) (n = 80; mean UK 13.8 +/- 0.8 nkat/24 h) and patients with low kallikrein excretion (LK) (n = 24; mean UK 2.3 +/- 0.3 nkat/24 h). Normal kallikrein patients had a mean plasma ANF value of 31.9 +/- 1.2 pg/mL which was almost superimposable to that found in NS; on the contrary, the mean plasma level of ANF in LK patients (50.7 +/- 2.2 pg/mL) was significantly higher than that measured in NK patients and in NS (P less than .01 v NK patients and NS, respectively). Since a low urinary kallikrein excretion may represent a marker of an impaired production of renal kallikrein, the high levels of ANF found in the LK subgroup could be the result of a compensatory response of the atrium attempting to maintain sodium and volume homeostasis.
Evidence that genetic emphysema in tight-skin mice is not caused by neutrophil elastase. Mutant tight-skin mice that had severe pulmonary emphysema were crossed with beige mice that contained neutrophils deficient in elastase activity. The resultant tight skin-beige cross mice were deficient in neutrophil elastase activity, yet they were still afflicted with the same degree of severe emphysema as the tight-skin mice. The results indicate that neutrophil elastase does not cause the emphysematous lesions found in tight-skin mice.
Randomized, controlled trial comparing long-term sulfonamide therapy to ventilation tubes for otitis media with effusion. Several studies have indicated that either the surgical insertion of ventilation tubes (VTs) or long-term treatment with sulfonamide-based antibacterials is effective in the management of otitis media with effusion (OME; otherwise known as serous otitis media, secretory otitis media, and glue ear) when compared with a no-treatment control or placebo. This controlled trial is the first to compare directly the effectiveness of these two treatments for long-standing OME. Outcome variables are treatment success rates, hearing thresholds, recurrent acute otitis media episodes, and side effects of medication or complications of VT placement. One hundred twenty-five children (aged 2.5 to 7 years) who met the usual indications for surgery (long-standing [greater than 3 months] OME and conductive hearing loss) were randomly assigned to "medical" treatment (sulfisoxazole 75 mg/kg per day for 6 months) or "surgical" treatment (bilateral insertion of VTs). Subjects underwent pure-tone audiometry (500, 1000, 2000, 4000 Hz) and otomicroscopic examination at 2, 4, 6, 12, and 18 months. A significantly greater proportion of medical subjects (67%) than surgical subjects (48%) were treatment failures at 6, 12, or 18 months (P = .0208). Surgical subjects had significantly better hearing at 2 and 4 months (P values less than .01) but not at 6, 12, and 18 months (P values greater than .2). A significantly greater proportion of surgical subjects (50%) experienced complications of treatment than did medical subjects (9%) (P less than .001). Thirty-three percent of candidates for VT placement did not require surgery when treated with a 6-month course of sulfisoxazole.