shukoor65/lab-rag-model huggingface dataset:
Evaluation of antiarrhythmic drug effects with simultaneous analysis of single ventricular premature contractions, couplets and salvos. To improve the clinical value of ambulatory Holter electrocardiographic (ECG) monitoring as a tool of antiarrhythmic therapy control, a new statistical model was developed. In a patient group at increased risk of sudden cardiac death, the spontaneous variability of ventricular arrhythmias was assessed, with simultaneous consideration of single ventricular premature complexes, couplets and salvos. The study included 100 patients who suffered from coronary heart disease or idiopathic dilated cardiomyopathy and for whom greater than 30 ventricular premature complexes/h and couplets had been demonstrated on the last Holter ECG before the study. Between 3 and 12 Holter recordings were made for each patient in a drug-free state; the mean follow-up period was 260 days (maximum 1,403). The mean hourly values of the ectopic events (EE) were assessed separately for ventricular premature complexes, couplets and salvos. The spontaneous variability (SV) was calculated for single ventricular premature complexes, couplets and salvos as SV = log (EEday 2 + 0.01/EEday 1 + 0.01) and linked in one, two and three dimensions. Compared with the consideration of only one type of arrhythmia (one-dimensional model), the simultaneous use of two or three types of arrhythmia (two- or three-dimensional model) resulted in considerably lower reduction and aggravation rates as sufficient proof of drug effects. With control intervals up to 1 week, the one-dimensional model yielded reduction rates for ventricular premature complexes, couplets and salvos of -63%, -90% and -95%, respectively. In contrast, with the three-dimensional model, the rates were -28%, -72% and -88%. The corresponding aggravation values were +370, +1,114% and +2,189% versus +38%, +256% and +747%.
Impact of pretransplant conditioning and donor T cells on chimerism, graft-versus-host disease, graft-versus-leukemia reactivity, and tolerance after bone marrow transplantation. Graft rejection, mixed chimerism, graft-versus-host disease (GVHD), leukemia relapse, and tolerance are interrelated manifestations of immunologic reactivity between donor and host cells that significantly affect survival after allogeneic bone marrow transplantation (BMT). In this report, a mouse model of BMT, in which the donor and host were compatible at the major histocompatibility complex (MHC), was used (1) to examine the interrelationship of pretransplant conditioning and T-cell content of donor BM with regard to lymphoid chimerism and GVHD and (2) to determine how these factors affected graft-versus-leukemia (GVL) reactivity and donor-host-tolerance. AKR (H-2k) host mice were administered optimal or suboptimal total body irradiation (TBI) as pretransplant conditioning followed by administration of BM cells from B10.BR (H-2k) donor mice with or without added spleen cells as a source of T lymphocytes. Transplanted mice were injected with a supralethal dose of AKR leukemia cells 20 and 45 days post-BMT to assess GVL reactivity in vivo. The pretransplant conditioning of the host and T-cell content of the donor marrow affected the extent of donor T-cell chimerism and the severity of GVH disease. GVL reactivity was dependent on transplantation of mature donor T cells and occurred only in complete chimeras. Transplantation of T-cell-deficient BM resulted in the persistence of host T cells, ie, incomplete donor T-cell chimerism, even when lethal TBI was used. Mixed chimerism was associated with a lack of GVL reactivity, despite the fact that similar numbers of donor T cells were present in the spleens of mixed and complete chimeras. In this model, moderate numbers of donor T cells facilitated complete donor T-cell engraftment, caused only mild GVHD, and provided a significant GVL effect without preventing the subsequent development of tolerance after conditioning with suboptimal TBI. In contrast, severe, often lethal, GVHD developed when the dose of TBI was increased, whereas tolerance and no GVH/GVL reactivity developed when the T-cell content of the marrow was decreased.
Endocarditis prophylaxis in a primary care clinic. BACKGROUND. Primary care physicians often make decisions about the use of endocarditis prophylaxis (EP). Compliance with American Heart Association (AHA) recommendations has been found to be poor in hospitalized patients and in a dental school clinic. The purpose of this study was to examine the use of endocarditis prophylaxis in a primary care clinic. METHODS. The problem list of all adult patients seen in a primary care clinic in 1989 was reviewed for diagnoses that might require EP. Eighty-four charts were identified and reviewed. RESULTS. Sixty-five percent of the study patients had documentation in their charts about the need for EP. Mitral valve prolapse was the most frequent diagnosis. The physicians recommended EP for most patients with mitral valve prolapse regardless of whether there was documented mitral insufficiency. Endocarditis prophylaxis was most commonly prescribed for dental procedures. Six patients received prophylaxis for procedures for which the AHA does not recommend prophylaxis. Only 19% of the antibiotic regimens prescribed were entirely consistent with the AHA 1984 guidelines. The most common deviation from the AHA guidelines was continuing oral antibiotics too long. CONCLUSIONS. Compliance with the AHA 1984 recommendations, although better than reported in other settings, was less than optimal in this primary care clinic. Family physicians should consider whether EP is indicated in any patient with cardiac disease. If prophylaxis is indicated, then such a recommendation should be clearly documented in the chart. Family physicians need to be familiar with the 1990 AHA recommendations.
Lightning and its effects on the auditory system. Patients struck by lightning can present with a wide variety of unusual otologic problems including burns to the external auditory canal, tympanic membrane rupture, middle ear injury, and sensorineural hearing loss. Four patients who incurred various otologic problems, including one patient with previously unreported bilateral oval window fistulas following lightning injury, are presented. Audiologic, otologic, and surgical findings are reviewed as well as patient follow-up and outcome.
High levels of p19/nm23 protein in neuroblastoma are associated with advanced stage disease and with N-myc gene amplification. The gene encoding a novel protein designated nm23-H1, which was recently identified as identical to the A subunit of nucleotide diphosphate kinase from human erythrocytes, has been proposed to play a role in tumor metastasis suppression. We report that untreated neuroblastoma tumors contain a cellular polypeptide (Mr = 19,000) designated p19, identified in two-dimensional electrophoretic gels, which occurs at significantly higher levels (P = 0.0001) in primary tumors containing amplified N-myc gene. The partial amino acid sequence obtained for p19 is identical to the sequence of the human nm23-H1 protein. An antibody to the A subunit of erythrocyte nucleotide diphosphate kinase reacted exclusively with p19. In this study, significantly higher levels of p19/nm23 occurred in primary neuroblastoma tumors from patients with advanced stages (III and IV) relative to tumors from patients with limited stages (I and II) of the disease. Even among patients with a single copy of the N-myc gene, tumors from patients with stages III and IV had statistically significantly higher levels of p19/nm23 than tumors from patients with stages I and II. Our findings indicate that, in contrast to a proposed role for nm23-H1 as a tumor metastasis suppressor, increased p19/nm23 protein in neuroblastoma is correlated with features of the disease that are associated with aggressive tumors. Therefore, nm23-H1 may have distinct if not opposite roles in different tumors.
Atrial natriuretic factor modulates the plasma levels of a Na+/K+ATPase inhibitor in volume expanded borderline hypertensives. To evaluate the existence of a relationship between atrial natriuretic factor (ANF) and plasma Na+/K+ATPase inhibitory activity in humans, we examined the hemodynamic and humoral response to volume expansion in 41 borderline hypertensive patients (BHT) with either normal (n = 33) or low plasma renin activity (n = 8). The study was carried out by measuring blood pressure, forearm circulation, plasma renin activity (PRA), ANF, and plasma levels of an endogenous Na+/K+ATPase inhibitor before and after 2 h of acute intravenous NaCl infusion (0.22 mL/min/kg bodyweight). The early (45 min) changes of ANF and those of Na+/K+ATPase inhibitory activity attained at the end of saline infusion were inversely related in BHT with normal PRA and directly related in the low-PRA population (r = 0.64). The time-course of ANF response to sodium loading was significantly delayed in BHT characterized by normal venous distensibility. They also showed a greater increase in plasma Na+/K+ATPase inhibitory activity occurring with an hypertensive, vasoconstrictive, and sodium retaining response as well. We conclude that in normal PRA borderline hypertensives, ANF may modulate the release of a plasma Na+/K+ATPase inhibitor in a setting where extracellular volume is acutely expanded. Our findings also suggest that dissimilarities in peripheral venous distensibility are able to influence the time-course of ANF response. The blunted ANF increase observed in response to NaCl loading in a subset of BHT could represent an early marker of the attitude of such patients to develop high blood pressure leading to the release of a Na(+)-pump inhibitor and influencing individual salt-sensitivity.
Probability of appendicitis before and after observation. STUDY OBJECTIVE: To examine patients with abdominal pain for changes in probability of appendicitis during observation. STUDY DESIGN: Retrospective cohort study. SETTING: University-affiliated community hospital. METHODS: 252 patients with abdominal pain who were examined underwent short-term (10.4 hours) observation (95% confidence interval [CI], 8.7, 12.1) before the decision to operate during a one-year period. Alvarado's scoring system and a probability-of-diagnosis nomogram were used to assign scores and estimate probability of appendicitis. MEASUREMENTS AND RESULTS: In the study group, mean score of patients with appendicitis increased after observation from 6.8 (95% CI, 6.2, 7.4) to 7.8 (95% CI, 7.3, 8.3), corresponding to a change in probability of appendicitis from 50% to 65%. Mean score of patients without appendicitis decreased from 3.8 (95% CI, 3.5, 4.1) to 1.6 (95% CI, 1.58, 1.62), corresponding to a change in probability from 35% to 22%. The difference between mean scores for patients with and without appendicitis increased from 2.6 (95% CI, 2.0, 3.2) to 6.2 (95% CI, 6.15, 6.25) during observation. The study group initially had intermediate probability of appendicitis (score, 4.35; 95% CI, 4.04, 4.66) compared with high probability for patients who went directly to surgery after their initial evaluation (63 patients; score, 7.59; 95% CI, 7.05, 8.73) and low probability for patients with abdominal pain who were sent home after their initial evaluation without observation or surgery (2,097 patients; score, 1.87; 95% CI, 1.48, 2.26). CONCLUSION: In this group of patients with intermediate initial probability of appendicitis, observation improved the ability to distinguish patients with from those without appendicitis.
Cardiac epinephrine synthesis. Regulation by a glucocorticoid. BACKGROUND. The heart can synthesize epinephrine. Homogenates of rat heart, which contain the enzymes phenylethanolamine N-methyltransferase (PNMT) and nonspecific N-methyltransferase (NMT), methylate norepinephrine to form epinephrine. The cardiac atrium contains primarily PNMT and the cardiac ventricle contains both PNMT and NMT. METHODS AND RESULTS. Rats were given the glucocorticoid dexamethasone at doses ranging from 0.2 to 20 mg/kg. Twenty-four hours later, cardiac atria, ventricle, skeletal muscle, and adrenal had increases in PNMT activity to as much as 230% of baseline. NMT activity was unchanged. Longer-term treatment with 1 mg/kg dexamethasone daily for 12 days increased cardiac PNMT activity about fivefold and also increased atrial epinephrine levels. Dexamethasone did not alter ventricular epinephrine levels but increased levels of both PNMT and catechol-O-methyltransferase, the major catabolic enzyme for epinephrine. After dexamethasone treatment, greater volumes of anti-PNMT antiserum were needed to decrease PNMT enzymatic activity, indicating that dexamethasone treatment resulted in greater amounts of PNMT and did not just activate existing PNMT molecules. Denervation of the masseter muscle of rats by unilateral superior cervical ganglionectomy markedly diminished tissue norepinephrine and epinephrine levels but had no effect on masseter PNMT or NMT levels. We have previously shown that chemical sympathectomy with 6-hydroxydopamine increases cardiac PNMT levels. These findings suggest that PNMT is an extraneuronal enzyme in both cardiac and skeletal muscle. CONCLUSIONS. Glucocorticoids have several cardiovascular effects, including increased cardiac output and blood pressure. Enhanced cardiac epinephrine synthesis may mediate some of these glucocorticoid effects.
Experimental hypertension. Several interventions are used to induce hypertension in the experimental animal. The three most used interventions are renal ischemia, mineralocorticoid excess, and genetic manipulation. The sequence of events leading from these initiating manipulations to the elevated arterial pressure is being explored to define the mechanism responsible for hypertension. The following mechanisms are currently extensively evaluated: Pressor and depressor factors of renal origin, neurogenic regulation, circulating humoral factors, vessel wall hypertrophy, and membrane transport abnormality. The experimental models of hypertension hold great promise in providing an understanding of the mechanisms and developing effective treatment in clinical hypertension.
Group C streptococcal bacteremia: analysis of 88 cases. Eighty-eight cases of group C streptococcal bacteremia were reviewed retrospectively. Most patients had underlying diseases (72.7%), predominantly cardiovascular disease (20.5%) or malignancy (20.5%). The infection originated most often from the upper respiratory tract (20.5%), the gastrointestinal tract (18.2%), or the skin (17.1%). Prior exposure to animals or animal products was reported in 23.9% of cases. The most common clinical manifestations of group C streptococcal bacteremia were endocarditis (27.3%), primary bacteremia (22.7%), and meningitis (10.2%). Of streptococcal isolates, 61.4% were not speciated, 19.3% were Streptococcus equisimilis, 17.1% were Streptococcus zooepidemicus, and two (2.3%) were Streptococcus equi. The isolates were sensitive to most antibiotics, and most patients were treated with beta-lactam agents. Mortality was high (25.0%), especially among older patients and patients with endocarditis, meningitis, and disseminated infection. Group C streptococcal bacteremia does not differ from bloodstream infection caused by other beta-hemolytic streptococci with regard to clinical presentation, treatment, or outcome.
Chordoma of the petrous bone. We have presented two cases of chordoma arising from an unusual location within the skull. Chordomas in the skull usually arise from within the body of the clivus, reputedly from notochordal remnants. The first case, which was diagnosed both with CT and MRI, had its origin from the petrous bone, with extension into the left cerebellopontine angle. Chordoma was not considered high on the list of differential diagnoses. A right pontine hemorrhage, which was evacuated surgically, was diagnosed in the second case both from its clinical appearance and from that on CT scan. Only when bone windowing technique was used with CT was a lytic lesion of the right petrous bone evident. Chordoma was only diagnosed on autopsy. In reviewing these two cases and the literature, it is evident that chordoma must be considered in the differential diagnosis of erosive lesions of the petrous bone.
Anaesthesia for Proteus syndrome. A 14-year-old boy with Proteus syndrome presented for orthopaedic surgery to his legs. No report in the literature exists on anaesthesia for this condition. Our patients posed airway problems that were managed by tracheal intubation under sedation using a fibreoptic bronchoscope. Anaesthesia was induced with thiopentone and maintained with nitrous oxide and isoflurane in oxygen. His lungs were ventilated mechanically throughout surgery, which was uneventful.
Arrhythmias in heart failure--therapeutic challenges. Electrophysiologic disorders are common at all stages of heart failure due to myocardial mechanical factors, neuroendocrine disturbances, electrolyte abnormalities, or ischemia, and also because of cardiovascular drugs. The prevalence of various forms of heart block, bradycardias, and arrhythmias in heart failure is largely unknown, as is their relationship to the etiology of the syndrome. Complex and multiform ventricular premature beats and nonsustained ventricular tachycardia are common, and their frequency is broadly related to the severity of heart failure. Supraventricular arrhythmias are also common features of the syndrome. The heart failure syndrome has an ominous prognosis. Approximately half the patients die suddenly, but the causal relationship between preexisting arrhythmias and sudden death is not known. Equally vital is knowledge of the influence of drug therapy on the arrhythmias of heart failure, but at present this is scarce and needs further study.
Mastoid obliteration with the temporoparietal fascia flap. Obliteration of persistently discharging open mastoid cavities is one surgical option to achieve a dry ear. All the currently described techniques involve the use of random pattern local tissue flaps or free grafts. Ten patients have undergone obliteration procedures using the vascularized temporoparietal fascia flap. This resulted in rapid epithelialization by six weeks in seven out of 10 cases. The remaining three patients have persistent non healed areas over the medial attic wall, but are not troubled by otorrhoea. The indications, technique and complications of mastoid obliteration by this axial pattern flap are described.
Quantitative comparison of aromatase induction by dexamethasone in fibroblasts from a patient with familial cortisol resistance and a patient with cortisol hyperreactive syndrome. The ability of dexamethasone to induce aromatase activity was tested in fibroblasts from a patient with familial cortisol resistance, a patient with cortisol hyperreactive syndrome, and five normal subjects. Dexamethasone increased enzyme activity in all cases in a concentration-dependent manner (over a range of 1-1000 nmol/L). In fibroblasts from a patient with familial cortisol resistance, the response curve of dexamethasone-induced aromatase activity was shifted to the right compared to that of normal cells. However, the maximal induction of the enzyme at 1 mumol/L dexamethasone was unchanged in cortisol-resistant fibroblasts. On the other hand, in fibroblasts from the patient with the cortisol hyperreactive syndrome, the half-maximal effect of dexamethasone was similar to that in normal cells, but maximum induction of aromatase activity was 2 times greater than that in normal cells. The glucocorticoid antagonist RU 486 inhibited dexamethasone-induced aromatase activity in these patients' cells and in normal cells in a concentration-dependent manner, indicating that the altered effects of dexamethasone on aromatase induction observed in each cell type were mediated through glucocorticoid receptors.
Prevention of stress-induced erosive gastritis by parenteral administration of arachidonic acid. Stress-induced mucosal ulcerations are associated with a decreased synthesis of mucosal prostaglandin (PG) E2. This phenomenon is poorly understood. To investigate whether it is due to a decreased availability of the necessary substrates to the mucosa, four groups of 10 Holtzman rats were studied: group 1 received normal saline by intraperitoneal (ip) injection; group 2 also received ip normal saline, then were submitted to stress, by the cold restraint method; group 3 received a solution of arachidonic acid (AA) ip; and group 4 also received ip AA, then were submitted to stress. After sacrifice, the number of gastric ulcerations were counted and specimens of nonulcerated mucosa were assayed for PGE2 by high-performance liquid chromatography; the mean numbers of ulcers were 0, 5.8, 0.8, and 3 and the mean levels of PGE2 were 55, 41, 125, and 62 pg/mg of wet tissue for groups 1, 2, 3, and 4, respectively. It is concluded that parenteral administration of AA reduces but does not completely eliminate stress-induced gastric ulcerations and that the stressed animals synthesized half as much PGE2 as the nonstressed ones after ip administration of equal amounts of AA, suggesting that stress reduces the availability of AA to the gastric mucosa, possibly by vascular spasm.
Mitral valve replacement combined with coronary artery operation: determinants of early and late results. Mitral valve replacement combined with coronary artery bypass grafting has been reported as being associated with a higher mortality than either mitral valve replacement or coronary artery bypass grafting alone. Cause of mitral valve disease and severity of mitral regurgitation have been reported as related to mortality. To study the correlation of the cause of mitral valve disease and severity of mitral regurgitation to hospital mortality and long-term survival, we analyzed the results of 135 patients undergoing mitral valve replacement and coronary artery bypass grafting between June 1974 and August 1989. The hospital mortality was 11.8% (16/135). Fifteen preoperative and operative variables were tested for correlation with hospital or late mortality using univariate tests and multivariate regression. Advanced age (greater than 60 years), New York Heart Association functional class, and wall motion score were independently associated with hospital mortality (p less than 0.05). The cause of mitral valve disease and severity of mitral regurgitation were not related to hospital mortality or long-term survival (p greater than 0.05). The follow-up rate was 96.6% for the hospital survivors (115/119). Mean follow-up was 52.6 +/- 4.1 months. There were 35 late deaths. Survival was 91.9%, 89.9%, 78%, and 49.9% at 1, 2, 5, and 10 postoperative years, respectively. Preoperative New York Heart Association functional class and use of catecholamines during the postoperative intensive care period were independently related to late survival (p less than 0.05).