123rc/medical_text huggingface dataset:
Effect of increasing Helicobacter pylori ammonia production by urea infusion on plasma gastrin concentrations. It has been proposed that the hypergastrinaemia in subjects with Helicobacter pylori infection is caused by the action of the ammonia produced by the organism's urease activity on the antral G cells. To investigate this hypothesis we examined the effect on plasma gastrin of increasing the bacterium's ammonia production by infusing urea intragastrically to eight H pylori positive duodenal ulcer patients. After a 60 minute control intragastric infusion of dextrose solution at 2 ml/minute, a similar infusion containing urea (50 mmol/l) was continued for four hours. During the urea infusion, the median gastric juice urea concentration rose from 1.1 mmol/l (range 0.3-1.6) to 15.5 mmol/l (range 7.9-21.3) and this resulted in an increase in the ammonium concentration from 2.3 mmol/l (range 1.3-5.9) to 6.1 mmol/l (range 4.2-11.9) (p less than 0.01). This appreciable rise in ammonia production did not result in any change in the plasma gastrin concentration. The experiment was repeated one month after eradication of H pylori, at which time the median basal gastrin was 20 ng/l (range 15-25), significantly less than the value before eradication (30 ng/l range 15-60) (p less than 0.05). On this occasion, the gastric juice ammonium concentration was considerably reduced at 0.4 mmol/l (range 0.1-0.9) and the urea infusion did not raise the ammonium concentration or change the plasma gastrin concentration. In conclusion, augmenting H pylori ammonia production does not cause any early change in plasma gastrin.
An improved photochemical model of embolic cerebral infarction in rats. To provide further evidence that the multiple cerebral infarcts found in rats following photochemical damage to the carotid artery are caused by emboli and to eliminate the systemic hypotension and heating of the blood reported with the previous photochemical embolic stroke model (rose bengal and a green laser), I have modified the photochemical technique. Brain pathology was studied in 18 Wistar rats following carotid artery irradiation with a red laser (632 nm) at powers ranging from 100 to 800 mW/cm2 for 10 or 20 minutes following the injection of the photosensitizing dye Photofrin II. Multiple cerebral arterioles were occluded by platelet aggregates containing frequent erythrocytes and leukocytes, identical to the thrombotic material in the carotid artery but different from the platelet aggregates seen in the carotid artery and the brain in the rose bengal model. Eighty infarcts were distributed randomly throughout the brain ipsilateral to the nonocclusive carotid thrombus. Significant heating (0.5 degree C or more) of the blood occurred only with laser powers higher (1,600 mW/cm2) or laser irradiations longer (25 minutes) than those used in the improved model of embolic stroke. This model mimics one mechanism of stroke in humans and provides a means to study systematically the morphological evolution of small cerebral infarcts.
Mechanism of antitumor activity of tumor necrosis factor alpha with hyperthermia in a tumor necrosis factor alpha-resistant tumor. Cells from a radiation-induced fibrosarcoma (RIF-1) are exceedingly resistant to tumor necrosis factor alpha (TNF-alpha) in vitro. We tested whether the addition of mild hyperthermia (42.5 degrees C, 30 minutes) could enhance TNF-alpha activity against RIF-1 tumors growing in syngeneic hosts (C3H mice). TNF-alpha was administered intratumorally. Tumor cell killing essentially was not measurable following TNF-alpha, hyperthermia, or a combination of the two. Single-modality treatments also had no effect on tumor growth delay or on the x-ray dose (given 24 hours after the primary treatment) required to sterilize 50% of the tumors. The combination of TNF-alpha and hyperthermia, however, resulted in a marked increase in tumor doubling time and a highly significant reduction in the x-ray dose required to sterilize the tumors. Syngeneic lymph nodal lymphocytes and blood leukocytes did not appear to mediate the action of TNF-alpha on RIF-1 cells in vitro. Necrosis and hemorrhage were the most prominent histopathological alterations in the treated tumors. Electron microscopic studies 6 hours after therapy showed increased damage to capillary endothelial cells and accumulation of neutrophils in the capillaries of tumors treated with TNF-alpha with or without heat, suggesting that neutrophils may mediate the endothelial cell injury. These observations indicate a greater than additive tumoricidal effect of TNF-alpha with hyperthermia. Furthermore, they support the concept that the interaction between the two agents damages the vasculature, compromising the microcirculation and ultimately causing ischemic tumor necrosis.
Double-blind, placebo-controlled, cross-over trial of progabide as add-on therapy in epileptic patients. In a double-blind, cross-over trial, progabide (PGB) and placebo were compared as add-on therapy in 59 patients with moderate to severe epilepsy. Eight patients did not complete the study, 4 because of adverse drug reactions (elevation of liver transaminases, 2; gastritis, 1; and acute psychosis, 1) and 4 because of administrative reasons. Among the remaining 51 patients, seizure frequency was reduced greater than 50% in 18 patients with PGB treatment and in 8 patients with placebo (p less than 0.05). The number of days with seizures was significantly (p = 0.034) reduced during PGB treatment. Both patients' and physicians' preferences at the end of the trial were in favor (p less than 0.01) of PGB. Mild clinical side effects were present in 54.7% of the patients treated with PGB and in 37.7% with placebo. Increase in liver transaminases was observed in 2 patients during the double-blind study and in 1 during the follow-up period. Our data show that PGB, as previously reported, is useful in 30-40% of patients who are not responding completely to other antiepileptic drugs (AEDs). The compound is well tolerated, but liver function must be monitored.
A case of dyschondroplasia associated with brain stem glioma: diagnosis by stereotactic biopsy. We present a 24-year-old patient with multiple chondromas of both hands, the pelvis, the left leg, and an associated brain stem glioma. There was no evidence of hemangioma or dyschromia, and the condition was diagnosed as Ollier's disease, a special type of dyschondroplasia like Maffucci's syndrome and Kast's disease. An increased overall risk for development of malignant skeletal and nonskeletal tumors is associated with Maffucci's syndrome. The risk of malignant degeneration is lower in Ollier's disease. A glioma in the pons and the right lobe of the cerebellum was found in this patient. The literature describes an association with gliomas in only 12 cases of dyschondroplasia and an infratentorial localization in just one case. Signs of malignancy were histologically confirmed in 7 cases without significant preponderance of any one type. Our patient had a low-grade brain stem astrocytoma with fibrillar and gemistocytic components. A stereotactic serial biopsy made it possible to rule out malignant degeneration. Stereotactic brain tumor biopsy as a routine neurosurgical procedure is particularly valuable for deep space-occupying processes and forms the basis for therapy. In the present case, irradiation was not recommended.
Volumetric atrophy of the amygdala in Alzheimer's disease: quantitative serial reconstruction. The present study quantitatively assessed volumes of the amygdala and its subnuclei in autopsied cases of advanced Alzheimer's disease (AD) for comparison with age-matched controls. Amygdalar nuclei showed significant atrophy in AD with the exception of the paralaminar portion of the basal nucleus. The magnocellular regions of the amygdala showed proportionately greater size reductions as a fraction of total amygdala volume than did other areas. Computerized reconstruction of the amygdala provided three-dimensional views of a variety of structural alterations accompanying the volumetric declines with AD. The apparent selective vulnerability of the magnocellular amygdalar areas coincides with the loss of large nerve cells in AD.
Lymphocele: the spectrum of scintigraphic findings in lymphoceles associated with renal transplant. Lymphocele is a well recognized complication of renal transplant surgery. We performed a retrospective review of 305 renal transplant patients with over 2,500 scintigraphic exams to describe the pattern of activity on technetium-99m-DTPA blood flow and dynamic imaging, and iodine-131-OIH studies. Diagnostic criteria for a lymphocele were ultrasonic evidence of a perirenal fluid collection and analysis of that fluid that demonstrated BUN, creatinine, and electrolytes similar to the patient's plasma. Scintigraphic findings were attributed to a lymphocele if abnormalities were in the same area as the ultrasound fluid collection. Scintigraphic findings attributable to lymphocele resolved in all patients following surgical drainage or peritoneal window placement. Six of the 11 documented lymphoceles demonstrated a cold defect on initial dynamic images that "filled in" to equal background activity and another exceeded background. Three cases showed a rim of increased activity surrounding the lymphocele ("rim sign").
Secreted or nonsecreted forms of acidic fibroblast growth factor produced by transfected epithelial cells influence cell morphology, motility, and invasive potential. Addition of exogenous acidic fibroblast growth factor (aFGF) to NBT-II epithelial carcinoma cells results in fibroblastic transformation and cell motility. We have generated aFGF-producing NBT-II cells by transfection with recombinant expression vectors containing human aFGF cDNA, or the human aFGF cDNA coupled to a signal peptide (SP) sequence. The effects of the nonsecreted and the secreted 16-kDa growth factor on the morphology, motility, and cell invasive potential (gelatinase activity) were compared. aFGF coupled to a SP was actively secreted out of the producing cells. The secretion of aFGF was not necessary for induction of gelatinase activity, as this was observed in NBT-II cells producing aFGF with or without SP. Production of aFGF, whether secreted or not secreted, resulted in increased in vitro motility of most isolated clones; however, there was no correlation between aFGF level and motility rate. The data suggest that expression of aFGF in NBT-II cells induces metastatic potential through an autocrine or intracrine mechanism.
Treatment of renal colic by prostaglandin synthetase inhibitors and avafortan (analgesic antispasmodic). In a study of the pain-relieving effect of 3 drugs commonly used to treat acute renal colic in this hospital, intravenous indomethacin and intramuscular diclofenac (prostaglandin synthetase inhibitors) were compared with intravenous Avafortan (analgesic antispasmodic). As first-line analgesics, prostaglandin synthetase inhibitors, if given intravenously, offer an effective alternative to Avafortan. Of 145 patients studied, 32 required a second injection for complete relief of pain. Administering a second dose of prostaglandin synthetase inhibitors resulted in equally significant pain relief rate even though the route was intramuscular.
Failure of surgery to improve outcome in hypertensive putaminal hemorrhage. A prospective randomized trial. Hypertensive putaminal hemorrhage remains a major cause of hemorrhagic stroke carrying extremely high morbidity. Considerable controversy remains regarding the optimal form of therapy. Between 1983 and 1989 we conducted a prospective randomized trial with three treatment strategies: best medical management, best medical management plus intracranial pressure monitoring, and surgical evacuation. Only patients with significant deficit harboring a putaminal hematoma at least 3.0 cm in diameter were entered. The study was interrupted after 21 patients had been studied (9, best medical management; 4, intracranial pressure monitoring; and 8, surgical evacuation). No differences were found among groups for age, admission blood pressure, and time interval between onset of symptoms and arrival at hospital. None of the subjects were capable of returning to prestroke activity. Fifteen (71%) died or remained vegetative at 6 months, and only 4 (19%) were capable of independent life at home. Of the 9 patients in the best medical management arm, 7 were dead or vegetative. In the surgical group, 4 patients died and only 2 were capable of independent life. These results suggest that current medical and neurosurgical therapies remain ineffective in preventing the devastating neurologic consequences of hypertensive putaminal hemorrhage.
A cellist with arm pain: thermal asymmetry in scalenus anticus syndrome. We report on a cellist with pain and coldness of the upper extremity. Abnormal thermographic studies were instrumental in uncovering intermittent compression of the subclavian artery, and this prompted us to study the effects of cello playing on skin temperature asymmetry. Temperature asymmetry was defined as the temperature difference (delta-T) from one hand to the other. In 57 controls, mean delta-T at rest was .309 +/- .254C. Exercising the upper extremities by prolonged elbow flexion or by movements mimicking cello playing in controls did not significantly affect delta-T. In our patient, delta-T was ten times control (3.6C). Angiography showed extrinsic compression of the subclavian artery occurring only after cello playing; sympathetic ganglion block relieved the pain. Our patient's abnormal skin temperature may have reflected sympathetic vasomotor hyperactivity. Intermittent neurovascular compression and sympathetic hyperactivity appear to be factors in scalenus anticus syndrome.
Hypoxic events in the surgical intensive care unit. An oxygen-monitoring protocol was established in the surgical intensive care unit (SICU) at the Denver General Hospital in July 1988. A 3-month surveillance audit ending March 1989 prospectively documented 100 consecutive hypoxic events in 51 of 241 (21%) SICU patients. These episodes occurred during mechanical ventilation in 46 patients, during spontaneous ventilation in 15 patients with artificial airways, and the remaining 39 occurred in nonintubated patients. Hypoxemia was recognized by pulse oximetry in 59, arterial blood gas analysis in 24, mixed venous oximetry in 15, and transcutaneous oxygen monitoring in 2. These events were due to problems with the ventilator or airway in 42, recent interventions in 21, new pulmonary process in 19, progression of underlying disease in 11, and unknown causes in 7. Two thirds resulted from mechanical problems amenable to simple intervention; there were two adverse outcomes. In conclusion, acute hypoxia is a frequent potentially morbid SICU event. Advances in continuous oxygen monitoring permit early identification and thereby may limit adverse outcomes, but should not prompt an expensive diagnostic work-up.
Immunosuppressive acidic protein in malignant diseases. Clinical relevance? The immunosuppressive acidic protein (IAP) has been described as a tumor associated marker in some solid tumors and hematologic diseases. To define the clinical relevance the authors determined the serum IAP levels in 194 patients with malignancies before initiation of therapy, 14 patients with idiopathic thrombocytopenic purpura (ITP), 28 patients with bacterial pneumonia, and 23 healthy volunteers. Immunosuppressive acidic protein was measured by radial immunodiffusion. The mean value of our controls was 405 +/- 48 micrograms/ml. This is consistent with published data. The mean values for patients with malignancies varied from 554 micrograms/ml to 698 micrograms/ml. These are only marginally higher than those observed for the controls. In contrast patients with bacterial pneumonia demonstrated significantly elevated values (1038 +/- 261 micrograms/ml). The authors conclude that IAP cannot be used as a diagnostic marker for the malignant diseases examined in this study.
Tumor necrosis factor regulates the expression of granulocyte-macrophage colony-stimulating factor and interleukin-3 receptors on human acute myeloid leukemia cells. Tumor necrosis factor (TNF) acts as a potent enhancer of granulocyte-macrophage colony-stimulating factor (GM-CSF)- and interleukin-3 (IL-3)-induced human acute myeloid leukemia (AML) growth in vitro. We have analyzed the effects of TNF alpha on the expression of GM-CSF and IL-3 receptors on AML cells. Incubation of blasts from seven patients with AML in serum-free medium with TNF (10(3) U/mL) and subsequent binding studies using 125I-GM-CSF and 125I-IL-3 show that TNF increases the specific binding of GM-CSF (30% to 280%) and IL-3 (40% to 600%) in all cases. From Scatchard plot analysis it appears that TNF upregulates (1) low-affinity GM-CSF binding sites, (2) common high-affinity IL-3/GM-CSF binding sites, and (3) unique (non-GM-CSF binding) IL-3 binding sites. The effect of TNF is dose dependent and is half maximal at a concentration of 100 U/mL, and becomes evident at 18 hours of incubation with TNF at 37 degrees C, but not at 0 degree C. The GM-CSF dose-response curve of AML-colony-forming units plateaus at a higher level in the presence of TNF, which indicates that additional numbers of cells become responsive to GM-CSF. Incubation of AML blasts with the phorbol ester 12-0-tetradecanoylphorbol-13-acetate or formyl-Met-Leu-Phe (protein kinase C activators) does not influence GM-CSF receptor expression, suggesting that receptor upregulation by TNF is not mediated through activation of protein kinase C. On the other hand, the protein synthesis inhibitor cycloheximide abrogates receptor upregulation induced by TNF. In contrast to these findings in AML, TNF does not upregulate GM-CSF receptor numbers on blood granulocytes or monocytes. We conclude that TNF exerts positive effects on growth factor receptor expression of hematopoietic cells.
Endoscopic ultrasonography in staging rectal cancer. Endoscopic ultrasonography (EUS) was used to stage rectal cancer by assessing depth of invasion through bowel wall layers and/or involvement of lymph nodes. EUS findings were correlated with histopathologic findings to discern the usefulness of this modality in predicting which patients could be candidates for sphinctersaving procedures and the avoidance of abdominoperineal resection. The Olympus EU-M3 endoscopic ultrasound system was used to assess depth of penetration through rectal wall layers and to identify lymph nodes. Comparison of EUS findings to histopathologic findings was possible in 13 patients. EUS agreed with histopathology in 9 of 13 cases (69.3%) ( p = 0.07, kappa statistic). EUS agreed with histopathology as the presence or absence of lymph nodes in 9 of 13 cases (69.3%) (p = 0.07). However, the presence of lymph nodes could not necessarily predict metastatic involvement of these nodes. In one patient, invasion of vaginal cuff was correctly predicted. In nine cases, computed tomographic analysis (CT) was available for comparison to EUS in detection of penetration beyond the bowel wall. CT agreed with histopathology in 3 of 9 (33%), whereas EUS agreed with histopathology in 7 of 9 (78%).
End stage renal disease serum contains a specific renal cell growth factor. End stage renal disease (ESRD) kidneys display abnormal growth characterized by a continuum of cystic disease, adenoma and carcinoma. This study evaluates the hypothesis that serum of patients with ESRD contains increased amounts of a growth factor which specifically induces proliferation of renal cells. ESRD sera compared to sera from normal controls induced a two to three-fold increase in the proliferative rate of renal cell carcinoma cell lines and normal kidney explants compared to cell lines from other sites. The increased proliferative activity of ESRD sera on renal cells was paralleled by an increase in cytosolic free calcium. The growth factor activity was encoded by a polypeptide of between 15 and 30 kd. The activity of ESRD sera on renal cells was not mimicked or inhibited by epidermal growth factor, basic fibroblast growth factor and platelet derived growth factor indicating that the renal cell specific growth factor activity in ESRD is different from these factors.
Substantia nigra: a site of action of muscle relaxant drugs. Sites of action of centrally active muscle relaxant drugs are not well defined. Clinical experience with such drugs suggests that the spinal cord may be one of the important regions from which pathologically increased muscle tone may be relieved. Supraspinal centers that may also be involved in the expression of muscle relaxant action have not yet been defined. We report here that microinjections of therapeutically relevant muscle relaxants into the midbrain tegmentum of genetically spastic rats decrease muscle tone. The substantia nigra is the region from which midazolam, baclofen, and tizanidine (drugs used clinically in the treatment of spasticity), or gamma-vinyl-GABA, (-)-2-amino-7-phosphonoheptanoate, and [D-pro2-D-phe7-D-trp9]-substance P (experimental drugs active in animal models of spasticity), reduce muscle tone in genetically spastic rats and Hoffmann reflexes in normal rats. The effects of muscle relaxant drugs are topographically restricted to the substantia nigra pars reticulata and are receptor specific. These observations disclose a previously unknown function of the substantia nigra in mediating muscle relaxation.
Critical analysis of neoadjuvant therapy for Stage IIIa non-small cell lung cancer [corrected] [published erratum appears in Am Rev Respir Dis 1991 Jun;143(6):1473] Lung cancer is the major cause of cancer mortality. Locally advanced (Stage III) disease constitutes 30 to 40% of the entire group of non-small cell lung cancer (NSCLC). Surgical resection offers the best opportunity for cure, but resection of disease is possible in only a minority of patients with Stage IIIa disease. Even among patients who have "successful" surgery systemic relapse is common, and the 5-yr survival after complete resection is only 30%. Preoperative (neoadjuvant) chemotherapy is under investigation in an attempt to improve the bleak outcome of patients with Stage IIIa NSCLC. Preliminary trials have shown that this approach is feasible: neoadjuvant treatment can be administered with moderate toxicity and in most cases without compromising the possibility for surgical resection. In some instances, neoadjuvant treatment has produced pathologic complete responses, and in others it has decreased tumor bulk so that inoperable patients became surgical candidates. Whether this latter phenomenon has an impact on survival is unknown. Therefore, the role of neoadjuvant treatment for locally advanced lung cancer will not be known until properly designed randomized trials are conducted.
Brain and spinal cord hemorrhage in long-term survivors of malignant pediatric brain tumors: a possible late effect of therapy. Three children with malignant primary CNS tumors treated with craniospinal radiotherapy developed intraparenchymal hemorrhages a median of 5 years following therapy in sites distant from the primary tumor. Radical surgical procedures disclosed fresh and old hematoma, gliosis, and necrosis in all 3 patients and an aggregation of abnormal microscopic blood vessels in two. No tumor was found. All 3 patients remain in long-term (greater than 10 years) continuous remission.