shukoor65/lab-rag-model huggingface dataset:
Jejunal permeability to water and electrolytes in patients with chronic intrahepatic hypertension: evidence for a role of aldosterone. Acute prehepatic portal hypertension induces intestinal secretion in animal models. In the course of chronic liver disease, however, these changes are not observed, despite higher portal pressures than those found in experimental studies. Eight patients without diarrhoea and with chronic alcoholic liver disease were examined for evidence of increased jejunal secretion; their suprahepatic wedge pressure was raised from 21 to 45 mmHg (mean 34.6 mmHg). Jejunal perfusion with a triple lumen catheter and a proximal occluding balloon was used to study net flows of water and chloride as well as net and unidirectional flows of sodium and potassium. No statistical difference in intestinal flows of water and electrolytes was noted between cirrhotic patients and control subjects after infusion with a 30 mmol/l glucose solution. Infusion with a 30 mmol/l mannitol solution resulted in a lower absorption of water, Na, K, and Cl than with the glucose solution. A higher rate of Na secretion was observed in cirrhotic patients than control subjects after infusion with 30 mmol/l mannitol (p less than 0.01). In addition, the rate of Na secretion was higher in cirrhotic patients than in control subjects (p less than 0.05). There was no correlation between the net flow of Na and the suprahepatic wedge pressure. A second perfusion with a 30 mmol/l glucose solution was given 75 minutes after a bolus injection of spironolactone (400 mg). Net flows of Na and Cl were lower in cirrhotic patients than in control subjects (p less than 0.05) because of a lower absorption of Na. Patients with gradually developing portal hypertension have moderate jejunal secretions of H2O and electrolytes which we assume are partly masked by increased absorption resulting from hyperaldosteronism. In contrast to animal models, this mechanism may be part of the jejunal adaptation to permeability in acute portal hypertension.
Clinical significance of the large adrenal mass. Current clinical teaching indicates that large (greater than 5 cm in diameter) adrenal masses are often malignant. In a retrospective analysis of patients studied between 1977 and 1988 with computed tomography (CT), adrenal scintigraphy, and when available, magnetic resonance imaging (MRI) 45 were found to have adrenal masses greater than 5 cm (range 5-19 cm) in diameter. Thirty were benign (16 phaeochromocytomas, six adrenocortical adenomas, four adrenal cysts, two myelolipomas, an adrenal hematoma and a ganglioneuroma). Of 15 malignant masses, there were seven adrenocortical carcinomas, five adrenal metastases and three adrenal lymphomas. With the exception of the adrenal myelolipomas, cysts, and the ganglioneuroma neither CT nor MRI demonstrated sufficient diagnostic specificity to distinguish benign from malignant lesions. Functional scintigraphy with 131I-6-beta-iodomethyl-19-norcholesterol for suspected adrenocortical lesions and 131I-metaiodobenzylguanidine for suspected phaeochromocytomas frequently provided useful information.
Nd:YAG laser hyperthermia treatment of rat mammary adenocarcinoma in conjunction with surface cooling. Electromagnetic radiation ranging from radiofrequency to microwave has classically been used to induce hyperthermia for treatment of cancer. This paper presents a new technique using near infrared radiation from an Nd:YAG laser in conjunction with surface cooling to induce hyperthermia in a rat tumor model. A CW Nd:YAG laser hyperthermia system was used to induce hyperthermic temperatures in chemically (DMBA) induced rat mammary adenocarcinomas. The laser was interfaced to a computer and a thermometry unit that provided feedback to control the tumor temperature between 43.2-43.5 degrees C. A thermocouple was placed at the base of the tumor and its temperature was used to control laser exposure. All tumors were 10 to 20 mm in diameter. Surface cooling methods investigated included forced air flow from a fan, forced oxygen flow plus an IV drip, and forced moist oxygen flow from a nebulizer. Twelve rat mammary adenocarcinomas have been treated with Nd:YAG laser hyperthermia. In 4 treatments, no surface cooling was employed. In one treatment the surface was cooled using oxygen flow plus IV drip. In 7 treatments the skin was cooled using the nebulizer technique. The nebulization provided the most effective and reproducible surface cooling. Nd:YAG laser hyperthermia delivered in conjunction with nebulizer surface cooling produced efficient heating of rat mammary adenocarcinomas. A mean temperature of 42.1 degrees C was obtained at the base of the tumors while the mean surface temperature was 37.0 degrees C.
Estimates of radiation absorbed dose for intraperitoneally administered iodine-131 radiolabeled B72.3 monoclonal antibody in patients with peritoneal carcinomatoses. Using a newly available model for determining estimates of radiation absorbed dose of radioisotopes administered intraperitoneally, we have calculated absorbed dose to tumor and normal tissues based on a surgically controlled study of radiolabeled antibody distribution. Ten patients with peritoneal carcinomatosis received intraperitoneal injections of the murine monoclonal antibody B72.3 radiolabeled with 131I. Biodistribution studies were performed using nuclear medicine methods until laparotomy at 4-14 days after injection. Surgical biopsies of normal tissues and tumor were obtained. The marrow was predicted to be the critical organ, with maximum tolerated dose [200 rad (2 Gy) to marrow] expected at about 200 mCi (7.4 GBq). In patients with large intraperitoneal tumor deposits, the tumor itself is an important source tissue for radiation exposure to normal tissues. Local "hot-spots" for tumor-absorbed dose were observed, with maximum tumor-absorbed dose calculated at 11,000 rad (11 Gy) per 100 mCi (3.7 GBq) administered intraperitoneal; however, tumor rad dose varied considerably. This may pose serious problems for curative therapy, especially in patients with large tumor burdens.
The clinical course of perimesencephalic nonaneurysmal subarachnoid hemorrhage We studied the early clinical course of 65 patients with perimesencephalic (nonaneurysmal) subarachnoid hemorrhage. None of the patients rebled; none had delayed cerebral ischemia; and only 3 patients (5%) developed clinical signs of acute hydrocephalus, 2 requiring ventricular shunting. Hyponatremia and electrocardiographic changes were found in the same proportions as in patients with aneurysmal rupture. All patients had a good outcome after 3 months. To control for the influence of the relatively small amount of cisternal blood in perimesencephalic hemorrhage on the absence of delayed cerebral ischemia, we compared these 65 patients with 49 patients who had aneurysmal subarachnoid hemorrhage. This control group with aneurysms was selected according to a similar amount of cisternal blood, a comparable level of consciousness on admission, and absence of other factors known to increase the risk for delayed cerebral ischemia. We found that 4 of the 49 patients with aneurysmal hemorrhage developed delayed cerebral ischemia (Fisher's exact test, p = 0.03); therefore the relatively small amount of blood does not account for the absence of delayed cerebral ischemia in perimesencephalic hemorrhage. Patients with a perimesencephalic pattern of hemorrhage and a normal angiogram should be considered to have a distinct subset of subarachnoid hemorrhage and should be excluded from future treatment trials of patients with subarachnoid hemorrhage.
The hyperekplexias and their relationship to the normal startle reflex. The startle response to unexpected auditory and somaesthetic stimulation was studied in 8 patients with hereditary or symptomatic hyperekplexia. It was abnormal in its resistance to habituation and in its exaggerated motor response. Both noise and taps to the face and head elicited a normal early blink response, separate from the subsequent true startle reflex. The earliest reflex EMG activity recorded after the blink was in sternocleidomastoid. EMG activity in masseter, and trunk and limb muscles followed later. This pattern of muscle recruitment suggests a brainstem origin for the abnormal startle responses. In addition, the abnormal startle responses exhibited disproportionately long latencies to the intrinsic hand and foot muscles and relatively slow recruitment of caudal muscles. The pattern of muscle recruitment was similar between patients, irrespective of the absolute latency of the response, and regardless of whether stimulation was auditory or somaesthetic. This suggests that auditory and somaesthetic afferents converge on a common brainstem efferent system, and that this system forms the final common pathway for abnormal startle responses of differing latency. The characteristics of this efferent system differ from those previously described in brainstem reticular reflex myoclonus, but are similar to those described in the normal auditory startle reflex in man. This suggests that the abnormal startle response in hyperekplexia, and the normal startle reflex represent pathological and physiological activity in the same brainstem efferent system.
Granulocyte function in coronary artery disease. Granulocytes defend the body against invading microbes by producing a complex armamentarium of toxic substances, such as proteolytic enzymes, oxygen radicals and arachidonic acid metabolites. Under certain circumstances, however, such compounds may be released in the absence of phagocytosable particles, resulting in injury to normal cell and connective tissue degradation. Recent experimental studies have emphasized the potential role of granulocytes in the pathogenesis of myocardial ischemia. Clinical investigations have also shown alterations in neutrophil function in stable and unstable clinical manifestations of ischemic heart disease. "Priming" of granulocytes in stable forms of coronary disease may predispose to the subsequent development of acute coronary events, whereas activation of neutrophils may lead to alterations in vascular permeability and coronary flow regulation, leading to further myocardial and endothelial injury in acute myocardial infarction, unstable angina and coronary angioplasty.
Severe lactic acidosis related to acute thiamine deficiency. The authors report a case of severe lactic acidosis in a 3-year-old boy, after 20 days of total parenteral nutrition without vitamin supplementation. This child with acute lymphoblastic leukemia underwent a period of severe refractory lactic acidosis (pH between 6.81 and 7.00 and a serum lactate level up to 38 mmol/liter) leading to cardiac arrest. After the initial resuscitation and the subsequent treatment of shock and vitamin K deficiency, acute peritoneal dialysis was instituted to correct the severe lactic acidosis. Initial low plasma thiamine levels confirmed the diagnosis of thiamine deficiency. An associated transient pancreatic dysfunction was also noted. The patient's overall course with thiamine replacement therapy led to a complete recovery within 5 days and no sequelae were noted after 12 months.
Assessment of aortic regurgitation by the acceleration flow signal void proximal to the leaking orifice in cinemagnetic resonance imaging. BACKGROUND. The proximal acceleration flow region is a laminar flow field that is located immediately upstream from the leaking orifice. The purpose of this study was to evaluate whether cinemagnetic resonance imaging can provide information regarding the proximal acceleration flow region in patients with aortic regurgitation and to analyze the relation between the area of the proximal acceleration flow delineated by cinemagnetic resonance imaging and the severity of aortic regurgitation delineated by angiography. METHODS AND RESULTS. Thirty-eight consecutive patients who underwent aortography were examined by cinemagnetic resonance imaging. The region of proximal flow acceleration was identified as a semicircular-shaped signal void in the aorta during diastole. Cinemagnetic resonance imaging detected the proximal acceleration flow region in 26 of the 30 patients who were proved to have this lesion (sensitivity, 87%). In eight patients without aortic regurgitation according to aortography, no proximal acceleration flow region was detected (specificity, 100%). The area of the acceleration flow signal void from the long-axis view was well correlated with angiographic degree of aortic regurgitation. CONCLUSIONS. Cinemagnetic resonance imaging is useful in detecting the proximal acceleration flow region and permits noninvasive assessment of the severity of aortic regurgitation.
Neutrophil activation is confined to the maternal circulation in pregnancy-induced hypertension. The aim of this study was to determine whether neutrophil activation occurs in the fetal circulation in pregnancy-induced hypertension and to correlate this with evidence of neutrophil activation in the maternal circulation. Twenty-one normal pregnancies and 23 complicated by pregnancy-induced hypertension were studied in the third trimester. The mean length of gestation at delivery was significantly shorter (P less than .01) and the mean birth weight percentile was significantly lower (P less than .05) in the hypertensive group; otherwise the groups were comparable. Blood was obtained before cesarean delivery or established labor in the mothers and immediately after delivery from the umbilical vein. Plasma neutrophil elastase, which is released after neutrophil activation, was measured by radioimmunoassay as a marker for neutrophil activation. The mean (+/- standard error) concentration of neutrophil elastase in maternal plasma in the hypertensive group (35.9 +/- 4.7 ng/mL) was significantly higher than in the normal group (20.8 +/- 0.87 ng/mL) (P less than .005). The concentration of neutrophil elastase in umbilical venous plasma was not significantly different between the normal and hypertensive groups. However, significantly higher concentrations of neutrophil elastase were found in the umbilical venous plasma of pregnancies delivered vaginally compared with those delivered by cesarean (P less than .05) regardless of diagnosis. There was no correlation between maternal venous and umbilical venous plasma neutrophil elastase concentrations, birth weight percentile, plasma urate, or platelet count. These data suggest that neutrophil activation is confined to the maternal circulation in pregnancy-induced hypertension where it may contribute to vascular damage and dysfunction in areas such as the placental bed.
The anterior inferior cerebellar artery in the internal auditory canal. It has been proposed that compression of the auditory and vestibular nerve trunks by vascular loops might be the cause of otherwise unexplained hearing loss, tinnitus, and vertigo, as well as Meniere's disease. We studied the human temporal bone histological collection at the Massachusetts Eye and Ear Infirmary to determine whether audiovestibular symptoms could be correlated with the presence of the anterior inferior cerebellar artery within the internal auditory canal. Anterior inferior cerebellar artery loops were found within the internal auditory canals of 12.3% of 1327 temporal bones, about half the number found when preparations with intact brains are studied. This difference can be attributed to avulsion of the anterior inferior cerebellar artery during removal of the brain at autopsy. There were 5 cases of unexplained unilateral hearing loss with anterior inferior cerebellar artery loops: 3 in the opposite ear and 2 in both ears. There were 2 cases with unilateral unexplained tinnitus with anterior inferior cerebellar artery loops: 1 in the involved ear and 1 in the opposite ear. A case with bilateral tinnitus had an anterior inferior cerebellar artery loop in 1 ear. There were 29 cases of vertigo with no peripheral histopathological correlate or central nervous system disorder; anterior inferior cerebellar artery loops were found in the internal auditory canals of 7 (12.5%) of the 56 ears in this group, which is not significantly different from the 12.3% incidence recorded for the entire collection. In 23 cases of unilateral Meniere's disease, there were anterior inferior cerebellar artery loops in the hydropic ears in 3, the opposite ear in 1, and both ears in 1. We can find no correlation between unexplained hearing loss, tinnitus, vertigo, or Meniere's disease and the presence of the anterior inferior cerebellar artery in the internal auditory canal.
Identification and characterization of a low-affinity granulocyte-macrophage colony-stimulating factor receptor on primary and cultured human melanoma cells. Hematopoietic growth factor receptors are present on cells of normal nonhematopoietic tissues such as endothelium and placenta. We previously demonstrated functional human granulocyte-macrophage colony-stimulating factor (GM-CSF) receptors on small cell carcinoma of the lung cell lines, and others have reported that certain solid tumor cell lines respond to GM-CSF in clonogenic assays. In the current study, we examine human melanoma cell lines and fresh specimens of melanoma to determine whether they have functional GM-CSF receptors. Scatchard analyses of 125I-GM-CSF equilibrium binding to melanoma cell lines showed a mean of 542 +/- 67 sites per cell with a kd of 0.72 +/- 0.14 nmol/L. Cross-linking studies in the melanoma cell line, M14, showed a major GM-CSF receptor species of 84,000 daltons. Under the conditions tested, the M14 cells did not have a proliferative response to GM-CSF in vitro, nor was any induction of primary response genes detected by Northern analysis in response to GM-CSF. Studies to determine internal translocation of the receptor-ligand complex indicated less than 10% of the 125I-GM-CSF internalized was specifically bound to receptors. Primary melanoma cells from five surgical specimens had GM-CSF receptors; Scatchard analysis was performed on one sample, showing 555 sites/cell with a kd of 0.23 nmol/L. These results indicate that human tumor cells may express a low-affinity GM-CSF receptor protein that localizes to the cell surface and binds ligand, but lacks functional components or accessory factors needed to transduce a signal.
Primary anterior mediastinal B-cell lymphoma. A clinicopathologic and immunohistochemical study of 16 cases. Sixteen cases of primary anterior mediastinal B-cell lymphoma were characterized by morphologic, immunophenotypic, and clinical profiles. Twelve were men and four were women. The median age was 42 years. Virtually all tumors were of large cell type. Three main morphologic categories were identified, with one rare exception. In some tumors, the cells were compatible with centrocytes and centroblasts (four). Others had cells readily identifiable as centroblasts (six). Both these groups had a variable proportion of cells with multilobed nuclei. A third group was composed mainly of unclassifiable cells with multilobed nuclei (five). All had discernible sclerosis of varying intensity. A wider range of morphologic features and different sex distribution was noticed in comparison with previously reported clear cell features and younger women. The dominant phenotype of these B-cell lymphomas was CD19+, CD22+, CD37+, CD21-, CD30-, CD10-, CD5-, and Ig-negative. The finding of CD21-, Ig-negative phenotype, as observed by the authors and others, overlaps with some high-grade lymphomas of follicular center cell origin but is thought to bear similarity to a noncirculating population of thymic medullary B-cells. The tumors attained large size without peripheral dissemination and responded to chemotherapy as well as radiotherapy.
Scirrhous carcinoma of the stomach versus hypertrophic gastritis: findings at endoscopic US. To differentiate scirrhous carcinoma from hypertrophic gastritis, 16 patients with scirrhous carcinoma of the stomach and seven patients with hypertrophic gastritis were examined with endoscopic ultrasonography (US) between August 1987 and October 1990. US images of the normal gastric walls of 16 patients with gastric ulcers served as controls. Characteristic features of scirrhous carcinoma included an irregular hypoechoic enlargement of the third (submucosa) and fourth (muscularis propria) layers. The mean thickness of the third and fourth layers was increased sixfold and threefold, respectively, compared with thickness in healthy subjects. In the patients with scirrhous carcinoma, the mucosal layer remained normal in appearance at US, and it was possible to distinguish the five-layer structure of the gastric wall. These findings were prospectively correlated with histopathologic findings in the resected specimens. In contrast, only the mucosal layer was thickened in cases of hypertrophic gastritis. Recognition of these patterns at US can aid in the differential diagnosis of scirrhous carcinoma and such benign diseases as hypertrophic gastritis with a thickened gastric wall.
Enhanced detection of intracardiac sources of cerebral emboli by transesophageal echocardiography. We performed transesophageal echocardiography in 50 consecutive hospitalized patients with recent transient ischemic attack or stroke of embolic origin to determine whether transesophageal echocardiography is more sensitive than transthoracic echocardiography in detection of possible intracardiac sources of embolism. Twenty-six of 50 patients with a negative transthoracic echocardiogram for potential source of emboli had a transesophageal echocardiography study that demonstrated at least one intracardiac abnormality. Abnormalities noted by transesophageal echocardiography included five of 50 patients with either a left atrial or left atrial appendage clot, four patients with a patent foramen ovale, and nine patients with spontaneous echocardiographic contrast. In 11 of 50 patients with no other source of embolism, we found highly mobile filamentous strands on the mitral valve, which have not been described previously. These mitral valve echo strands may represent a fissured surface or fibrosis that can serve as a nidus for thrombus formation. We detected no unexpected left ventricular thrombus or left atrial myxoma. Factors significantly associated with a greater likelihood of a positive transesophageal echocardiography study included left atrial enlargement, atrial fibrillation, and a calcified or thickened mitral valve. Our study suggests that transesophageal echocardiography is a valuable addition to transthoracic echocardiography in investigating potential intracardiac sources of embolism.
Ependymoma: internal correlations among pathological signs: the anaplastic variant. In a series of 298 cases of ependymoma, survival analysis identified some prognostic histological factors but failed to demonstrate a worse survival for the anaplastic variant diagnosed with the common criteria used for assessing anaplasia in primitive brain tumors. This finding suggests that either anaplastic ependymoma does not exist, or that the established criteria are not useful in its identification. To solve these problems, the association of histological, immunohistochemical, and ultrastructural signs in 173 intracranial cases was investigated and analyzed by means of contingency tables. Many signs had only focal distribution. Some signs, meaningful for anaplasia, such as very high cell density and number of mitoses, were found to be associated, whereas other signs usually considered indicative of anaplasia, such as endothelial hyperplasia, glomeruli, and necrosers, were not. In addition, pseudorosettes, mesodermic areas, and incomplete formation of perivascular pseudorosettes were signs associated with very high cell density and number of mitoses. Distribution of glial fibrillary acidic protein and vimentin, as well as other immunohistochemical and ultrastructural features, were not helpful, with the exception of microsettes found by electron microscopy. Our conclusion is that the anaplastic variant of ependymoma is recognizable only when some histological prognostic factors, such as cell density and number of mitoses, are maximally expressed.