shukoor65/lab-rag-model huggingface dataset:
Hospital characteristics associated with adverse events and substandard care. To explore the epidemiology of adverse events (AEs), which were defined as injuries due to medical treatment, and that subset of AEs caused by negligence, we studied interhospital variation in these outcomes in a sample of 31,000 medical records drawn from a random selection of 51 hospitals in New York in 1984. We found a substantial variation in both AE rates (0.2% to 7.9%; mean, 3.2%) and the percentage of AEs due to negligence (1% to 60%; mean, 24.9%) among hospitals. Univariate analyses of AEs revealed that primary teaching institutions had significantly higher rates (4.1%) and rural hospitals had significantly lower ones (1.0%). The percentage of AEs due to negligence was lower in primary teaching (10.7%) and for-profit (9.5%) hospitals and was significantly higher in hospitals with predominantly (greater than 80%) minority patients who had been discharged (37%). These findings were corroborated by multivariate analysis. Our results suggest that AEs and negligence are not randomly distributed and that certain types of hospitals have significantly higher rates of injuries due to substandard care. These observations may represent an important improvement on existing measures of quality because they take into account the fact that some hospitals' populations may be at risk of suffering a poor outcome.
Dobutamine digital echocardiography for detecting coronary artery disease. To assess the value of dobutamine echocardiography for detecting coronary artery disease (CAD), 70 men (mean age 62 +/- 8 years) presenting for coronary angiography were prospectively studied. Dobutamine (2.5 to 40 micrograms/kg/min) was infused in 3-minute stages. Digital echocardiograms were recorded on-line at baseline, during low- and high-dose dobutamine infusion, and at recovery. An echocardiogram positive for CAD was defined as one showing a new wall motion abnormality induced by dobutamine. Compared with coronary angiography, the overall sensitivity of dobutamine echocardiography for detecting CAD was 86%, specificity 95% and accuracy 89%. The sensitivity for detecting 3-vessel CAD was 100%, 89% for 2-vessel and 69% for 1-vessel CAD. The accuracy of predicting multivessel disease by 2 methods was 71% and 84%, respectively. Heart rate at the echocardiographic ischemic threshold was lower in patients with 3- and 2-vessel CAD versus 1-vessel CAD (89 +/- 17, 95 +/- 18 and 118 +/- 18 beats/min, respectively, p less than 0.01); rate-pressure product was also lower in patients with 3- and 2-vessel CAD versus 1-vessel CAD (12.7 +/- 3.6, 13.7 +/- 2.8 and 18.9 +/- 44 x 10(3) beats/min x mm Hg, respectively, p less than 0.01). Heart rate was the most important physiologic determinant of ischemia induced by dobutamine. There were no major complications during the study. Thus, dobutamine digital echocardiography is an excellent test for identifying CAD and should be beneficial in patients unable to exercise.
Ifosfamide extrapyramidal neurotoxicity. Ifosfamide-associated central nervous system toxicity has been reported in 5% to 30% of patients treated with ifosfamide. Its pattern is characterized by metabolic encephalopathy with confusion, blurred vision, mutism, auditory or visual paranoid hallucinations, seizures, and rarely coma. The biochemical cause of the neurotoxicity is not understood completely, but it is thought to result from an accumulation of drug metabolites with direct central nervous system effects. A case of ifosfamide neurotoxicity is reported that had unusual extrapyramidal features in a patient treated with a 5-day course of infused ifosfamide. Although usually spontaneously reversible with cessation of drug administration, ifosfamide neurotoxicity occasionally has been associated with prolonged psychopathologic sequelae. Death from irreversible encephalopathy has also been reported rarely. The authors believe that classic extrapyramidal symptoms should be considered to be a part of the neurotoxic profile of ifosfamide.
Activity of doxorubicin and cisplatin combination chemotherapy in patients with diffuse malignant pleural mesothelioma. An Italian Lung Cancer Task Force (FONICAP) Phase II study. Twenty-six symptomatic patients with diffuse malignant pleural mesothelioma (DMPM) were enrolled in a Phase II Italian Lung Cancer Task Force (FONICAP) study to assess the activity and toxicity of doxorubicin and cisplatin combination chemotherapy. The drug schedule was as follows; 60 mg/m2 of doxorubicin and 60 mg/m2 of cisplatin both given intravenously (IV) on day 1 every 3 to 4 weeks. Of the 24 evaluable patients, 6 objective partial responses (25%; 95% confidence limits, 9.77% to 46.71%) were observed. Twelve of 24 patients (50%), including 6 with no radiologic evidence of response, had a clinical improvement as demonstrated by an objective reduction of symptom or performance status scores along treatment. The overall median survival time was 10 months. Toxicity was mild and dose reductions or suspensions were not required. The combination of doxorubicin and cisplatin is effective and well tolerated. It might be considered for palliation of symptomatic patients with DMPM.
Effect of potassium intake on blood pressure. Epidemiologic, experimental, and clinical studies suggest that potassium is an important regulator of blood pressure. Surveys conducted in widely divergent geographic locations indicate higher prevalence of hypertension in populations ingesting diets low in potassium. Amelioration of hypokalemia lowers blood pressure in mineralocorticoid-induced hypertension in rats and in essential hypertensive patients receiving thiazide diuretics. We observed that in normotensive subjects ingesting normal amounts of sodium, short-term potassium depletion increases the mean arterial pressure from 90.9 +/- 2.2 mm Hg to 95.0 +/- 2.2 mm Hg (P less than 0.01). Furthermore, acute sodium loading increases blood pressure in potassium-depleted subjects but it had no effect in subjects ingesting normal amounts of potassium. Preliminary studies indicate that short-term potassium depletion also elevates blood pressure in hypertensive patients. Potassium supplementation lowers blood pressure in hypertensive patients ingesting normal amounts of sodium. Blacks appear to be more sensitive to the hypotensive effects of potassium. The mechanism of potassium-induced changes in blood pressure is not well understood. Potassium depletion consistently induces sodium retention. The hypertensive effects of potassium depletion and hypotensive effects of potassium supplementation are not observed when sodium intake is kept low. Direct vasoconstrictive effects of hypokalemia may contribute to the pressor effect of potassium depletion. The role of altered vascular sensitivity to vasoactive hormones and alterations in divalent cation metabolism in mediating the potassium-induced changes in blood pressure require further study.
Neurogenic sarcoma of the sinonasal tract. Five cases of a rare malignant sinonasal tumour of neurofibromatous nature are described. The term neurogenic sarcoma (or malignant peripheral nerve sheath tumour) is advocated instead of malignant schwannoma. The clinicopathological features of this tumour are described, and the different diagnosis are discussed. The necessity of using immunohistochemistry in the diagnosis of sinonasal tumours of fibromatous nature is emphasized. The clinical management consists of radical surgery and adjuvant radiotherapy. Clinically there seems to be a high-grade and a low-grade type of sinonasal neurogenic sarcoma, however, this could not be distinguished histologically in the present series.
Relative efficacy of antithrombin compared with antiplatelet agents in accelerating coronary thrombolysis and preventing early reocclusion. BACKGROUND. Optimal coronary thrombolysis should be prompt and persistent. Although activation of platelets and increased thrombin activity have been associated with clinical thrombolysis, the role of each in delaying thrombolysis or inducing early coronary reocclusion has been difficult to define. METHODS AND RESULTS. In conscious dogs with coronary thrombosis induced by electrical current, we assessed the impact on the rapidity of thrombolysis and the incidence of reocclusion of two types of adjunctive treatment given concomitantly with intravenous tissue-type plasminogen activator (t-PA): 1) inhibition of platelet function with a peptide mimetic antagonist of platelet glycoprotein IIb/IIIa receptors or with lysine acetylsalicylic acid (ASA) and 2) inhibition of thrombin activity with recombinant hirudin or with heparin. ASA but not the receptor antagonist shortened the time to thrombolysis with t-PA (20 +/- 13 [mean +/- SD] minutes with ASA, 36 +/- 15 minutes with receptor antagonist, and 43 +/- 16 minutes with the saline control). Reocclusion occurred promptly after completion of the infusion of t-PA in all seven dogs given saline. Reocclusion was delayed and prevented in some dogs within 90 minutes after the end of the infusion of t-PA by both antiplatelet agents but still occurred in 42% despite continued inhibition of platelet function (i.e., three of six dogs given ASA and two of six given receptor antagonist). In contrast, inhibition of thrombin activity with recombinant hirudin in a dose that prolonged the partial thromboplastin time modestly (1.5-2-fold) resulted in accelerated lysis (19 +/- 10 minutes) and prevention of reocclusion in each of six dogs. Heparin given in doses that elicited similar prolongation of the partial thromboplastin time did not accelerate lysis nor prevent reocclusion, which occurred in five of six dogs. CONCLUSIONS. Inhibition of thrombin by recombinant hirudin facilitates thrombolysis and maintains patency of coronary arteries recanalized with t-PA particularly effectively. The benefit conferred may reflect direct anticoagulant effects plus diminished activation of platelets secondary to decreased thrombin activity.
Characterization of the structure of the erythropoietin receptor by ligand blotting. Erythropoietin (Epo) regulates the growth and differentiation of erythroid cells by binding to a specific receptor. We characterized the native Epo receptor on erythroleukemia cell lines by ligand blotting. Solubilized cell membrane proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred onto nitrocellulose, and probed with 125I-Epo. Specificity was demonstrated by inhibition of 125I-Epo binding by unlabeled excess Epo but not other peptide growth factors and by the cellular distribution of the Epo binding protein. A single membrane protein of 61 Kd +/- 4 Kd was sufficient to bind 125I Epo in both human (OCIM2, K562) and murine (GM979, Rauscher, DA-1) cell lines. This finding is consistent with the predicted size of the Epo receptor from the murine cDNA clone. However, chemical crosslinking of 125I-Epo to its receptor has identified two Epo binding proteins of 105 Kd and 85 Kd. This difference may occur because the receptor is size fractionated before Epo binding in the ligand blot, but after Epo binding in crosslinking studies. Ligand blotting demonstrates that the native Epo receptor is composed of a single 61-Kd Epo binding protein, and suggests the presence of additional proteins of 20 to 25 Kd that associate with the receptor after Epo binding.
Activation signals leading to proliferation of normal and leukemic CD3+ large granular lymphocytes. The activation signals leading to proliferation of normal and leukemic CD3+ large granular lymphocytes (LGL) were studied in vitro. Anti-CD3 monoclonal antibody (MoAb) alone (P less than .01) and recombinant interleukin-2 (IL-2) alone (P less than .01) caused significant stimulation of peripheral blood mononuclear cells (PBMC) from four CD3+ LGL leukemia patients, as measured in a 3H-thymidine incorporation assay. Recombinant interleukin-4 (IL-4) alone had no effect (P = .11). The combination signals of anti-CD3 MoAb and either IL-2 or IL-4 produced a proliferative response greater than anti-CD3 MoAb alone (P less than .01) or lymphokine alone (P less than .01). Leukemic LGL, purified by two-color sorting, were subsequently activated by anti-CD3 MoAb and IL-2 and assessed for DNA content by viable Hoechst No. 33342 (HO) staining. Results of these studies demonstrated that leukemic LGL were stimulated directly by anti-CD3 MoAb and IL-2, with the percentage of cells in cell cycle (S + G2/M) ranging from 16% to 72%. Normal CD3+ LGL were also stimulated to enter the cell cycle by anti-CD3 and IL-2. These results show that leukemic LGL proliferate in vitro after activation through the T-cell receptor and/or lymphokine.
Circulatory adaptation to orthostatic stress in healthy 10-14-year-old children investigated in a general practice. 1. The magnitude and time course of circulatory adaptation to active standing were investigated in healthy premenarchic girls and boys (n = 24; 10-14 years old) by non-invasive measurement of heart rate and continuous finger blood pressure (Finapres). 2. Four subjects (two girls, two boys) showed presyncopal symptoms after 4-9 min of free standing. 3. In the 20 non-fainting subjects, changes in blood pressure and heart rate upon standing did not differ between girls (n = 10) and boys (n = 10). In the initial phase of standing (first 30 s) systolic and diastolic blood pressures dropped by 22 +/- 14 (mean +/- SD) and 16 +/- 7 mmHg, respectively, at 8 +/- 2 s. Blood pressure subsequently recovered and showed an overshoot in all subjects. The transient drop in blood pressure was accompanied by an increase in heart rate of 40 +/- 7 beats/min. These characteristic transient changes were not observed with passive head-up tilt. During the early steady-state phase (2 min), systolic blood pressure was similar to the supine value and diastolic blood pressure rose by 11 +/- 5 mmHg. Heart rate increased by 25 +/- 11 beats/min. In six of the subjects (three girls, three boys) the increase in heart rate exceeded 30 beats/min (postural tachycardia). Little further changes were observed during prolonged (10 min) standing.
Fetal cephaloceles: diagnosis with US. The prenatal sonograms of 15 fetuses with cephaloceles (13 occipital, one ethmoidal, and one frontoparietal) were retrospectively reviewed. The prognosis for fetuses with cephaloceles was poor: Only three of 14 with follow-up were born alive (21%), and all are likely to be handicapped. Karyotypes were abnormal in four of nine fetuses tested (44%). Associated cranial abnormalities observed in various numbers of fetuses included ventriculomegaly, the "lemon" sign, a flat basioccipital, "beaked" tectum, and bone defect. A wide variety of neural and nonneural anomalies were associated with cephaloceles. At least one sonographically observed concomitant neural or nonneural axis abnormality or an abnormal karyotype was present in nine of 15 fetuses (60%). Some associated neural malformations noted pathologically were not observed prenatally. Cranial meningoceles were not accurately distinguished from encephaloceles sonographically, and they also were associated with a poor prognosis. Comparison of findings in fetuses with cephaloceles with those of 15 fetuses with cystic hygromas revealed that the two abnormalities can usually be distinguished by the relationship of the mass with the neck and by other cranial findings present in fetuses with cephaloceles but absent in association with cystic hygromas.
Classification and natural history of clinically identifiable subtypes of cerebral infarction. We describe the incidence and natural history of four clinically identifiable subgroups of cerebral infarction in a community-based study of 675 patients with first-ever stroke. Of 543 patients with a cerebral infarct, 92 (17%) had large anterior circulation infarcts with both cortical and subcortical involvement (total anterior circulation infarcts, TACI); 185 (34%) had more restricted and predominantly cortical infarcts (partial anterior circulation infarcts, PACI); 129 (24%) had infarcts clearly associated with the vertebrobasilar arterial territory (posterior circulation infarcts, POCI); and 137 (25%) had infarcts confined to the territory of the deep perforating arteries (lacunar infarcts, LACI). There were striking differences in natural history between the groups. The TACI group had a negligible chance of good functional outcome and mortality was high. More than twice as many deaths were due to the complications of immobility than to direct neurological sequelae of the infarct. Patients in the PACI group were much more likely to have an early recurrent stroke than were patients in other groups. Those in the POCI group were at greater risk of a recurrent stroke later in the first year after the index event but had the best chance of a good functional outcome. Despite the small anatomical size of the infarcts in the LACI group, many patients remained substantially handicapped. The findings have important implications for the planning of stroke treatment trials and suggest that various therapies could be directed specifically at the subgroups.
Hepatocellular expression of lymphocyte function-associated antigen 3 in chronic hepatitis. T lymphocyte-mediated cytolytic immune reactions are considered a major cause of hepatocyte injury in chronic viral and autoimmune hepatitis. To further investigate local immune responses, we studied the expression of lymphocyte antigens and cell-cell interaction molecules known to be involved in effector-target cell interactions by light and electron microscopy in liver biopsy specimens from patients with chronic viral and autoimmune hepatitis. CD8+ lymphocytes were found to be the predominant population of cells in the inflammatory infiltrate in chronic hepatitis B and non-A, non-B hepatitis. In contrast, CD4+ cells constituted a comparably higher proportion of cells and were more numerous than CD8+ cells in chronic autoimmune hepatitis. In both viral and autoimmune hepatitis, a substantial portion of lymphocytes expressed activation antigens such as T11/3 (CD2R) and IL-2-R (CD25). Lymphocyte function-associated antigen-3 (CD58), which mediates lymphocyte adhesion and activation and is the natural ligand of the CD2/T11 lymphocyte surface receptor, could be demonstrated on endothelial cells and hepatocytes. Hepatocellular lymphocyte function-associated antigen-3 expression in chronic hepatitis showed membranous and cytoplasmic staining of hepatocytes and had a positive correlation with the degree of inflammatory activity. These results suggest that effector-target interactions between hepatocytes and lymphocytes mediated by the lymphocyte function-associated antigen-3/CD2 pathway play a role in chronic inflammatory liver disease. Possible functional consequences of this interaction include enhancement of antigen-specific immune reactions and antigen-independent mechanisms of T cell activation, which may contribute considerably to the degree of inflammatory activity and tissue damage in chronic hepatitis.
IgG reactivity in the spinal cord and motor cortex in amyotrophic lateral sclerosis. The spinal cord and motor cortex of patients with amyotrophic lateral sclerosis (ALS) were examined with immunohistochemical methods for the presence of IgG. In 13 of 15 spinal cords, a population of motoneurons stained positively for IgG in a granular pattern, characteristic of binding to the rough endoplasmic reticulum. In 6 of 11 motor cortices, a proportion of pyramidal cells also stained positively for IgG. No such reactivity was noted in motoneurons of control human tissues, although positive IgG staining was present in astrocytes of ALS and control specimens. Reactive microglia and/or macrophages were detected in the territory of degenerating pyramidal tracts and ventral horns. The surface of most of these cells stained positively for IgG, and 50% stained positively for HLA-DR. The accumulation of IgG in motoneurons and the presence of immunologically active macrophages provide additional evidence for the participation of immunologic factors in the pathogenesis of ALS.
Survival of patients with well-differentiated astrocytomas diagnosed in the era of computed tomography. We report 25 verified cases of well-differentiated cerebral astrocytomas in adults treated between 1978 and 1988. All patients were diagnosed by computed tomographic (CT) scans, with 5 undergoing a craniotomy for debulking and 20 undergoing a biopsy alone. The median survival for the entire group was 8.2 years, the longest survival yet reported for a series of patients with these tumors. A review of the literature suggests that the longer survival observed in more recent series is the result of the earlier diagnosis of tumors afforded by modern brain imaging. Twenty of our patients presented with seizures in the absence of any other focal findings and would probably not have had a biopsy in the era before CT scans until their tumors had progressed. Only 8% of our patients had papilledema at the time of presentation, in contrast to almost half of the patients with low-grade astrocytomas reported before 1975, supporting the hypothesis that patients in the CT era are diagnosed earlier. None of our patients died from progressive low-grade disease. One patient died from a squamous cell cancer, and 7 died as a consequence of their tumors dedifferentiating into a more malignant astrocytoma or glioblastoma multiforme, with a median time of approximately 5 years after the diagnosis. Our findings, together with the available data in the literature, suggest that death from a focal low-grade astrocytoma, in the absence of malignant degeneration, may be a rare event. Consequently, future therapeutic efforts should be targeted at preventing dedifferentiation.
A comparison of adenocarcinoma and squamous cell carcinoma of the cervix. A comparison and survival analysis of 203 patients (21%) with adenocarcinoma and 756 (79%) with squamous cell cancer of the cervix for the time period 1970-1985 is reported. The mean number of new cases of adenocarcinoma (N = 12) remained the same, while squamous cell cases decreased from 57 to 32. The clinical features were compared; oral contraceptive usage, node status, diabetes, and symptoms of bleeding were not related to cell type. Nulliparity was more frequent in patients with adenocarcinoma, whereas obesity and smoking were more frequent in patients with squamous cell cancer. Survival in stage I was significantly influenced by the cell type. Patients with stage I squamous cell disease had a 90% 5-year survival, compared with 60% for adenocarcinoma (P less than .0001). Other features that influenced survival included node status (P = .001), poor differentiation of tumor histology (P = .001), diabetes (P = .001), and Papanicolaou smear interval (P = .001). Patients undergoing radical hysterectomy were analyzed separately, and adenocarcinoma cell type significantly influenced survival (P = .0008). Patients with stage II squamous cell disease had a 62% survival, compared with 47% for adenocarcinoma (P = .01); patients with stage III squamous cell disease had a 36% survival, compared with 8% for adenocarcinoma (P = .002). The percentage of adenocarcinoma has increased because of the decreased number of patients with squamous cell disease. Stage-for-stage survival is significantly decreased for patients with adenocarcinoma as opposed to squamous cell disease.
Renoduodenal fistula in a patient with chronic nephrostomy drainage: a case report. We describe the occurrence of a renoduodenal fistula related to a nephrostomy tube in a patient with xanthogranulomatous pyelonephritis and renal calculi. The patient was successfully treated by nephrectomy. Etiological, diagnostic and therapeutic aspects are discussed.