shukoor65/lab-rag-model huggingface dataset:
Bronchial reactivity and allergy-promoting factors in monozygotic twins discordant for allergic rhinitis. Bronchial reactivity was studied twice in eight monozygotic twin pairs discordant for allergic rhinitis with pollen hypersensitivity, during the winter season (all eight pairs) and during the pollen season (seven pairs). On both occasions, the allergic twins showed significantly higher reactivity than their nonallergic siblings. The results indicate that moderate allergic rhinitis is associated with increased bronchial reactivity. This increased reactivity is an acquired trait; however, bronchial reactivity is not constantly increased in pollen rhinitis and may be normal even during the pollen season. The symptoms of allergic rhinitis usually started in childhood before the separation of the siblings. We could not demonstrate any major differences in exposure to allergens or airway irritants between the siblings. The allergic twins tended to have lower birth weight and insufficient weight increase just after birth.
Paraganglioma of the cauda equina: case report with magnetic resonance imaging description. The case of a 35-year-old white man with a cauda equina syndrome is presented. Magnetic resonance imaging confirmed the diagnosis, and radiation treatment successfully treated the condition.
Noninvasive estimation of the instantaneous first derivative of left ventricular pressure using continuous-wave Doppler echocardiography BACKGROUND. The complete continuous-wave Doppler mitral regurgitant velocity curve should allow reconstruction of the ventriculoatrial (VA) pressure gradient from mitral valve closure to opening, including left ventricular (LV) isovolumic contraction, ejection, and isovolumic relaxation. Assuming that the left atrial pressure fluctuation is relatively minor in comparison with the corresponding LV pressure changes during systole, the first derivative of the Doppler-derived VA pressure gradient curve (Doppler dP/dt) might be used to estimate the LV dP/dt curve, previously measurable only at catheterization (catheter dP/dt). METHODS AND RESULTS. This hypothesis was examined in an in vivo mitral regurgitant model during 30 hemodynamic stages in eight dogs. Contractility and relaxation were altered by inotropic stimulation and hypothermia. The Doppler mitral regurgitant velocity spectrum was recorded along with simultaneously acquired micromanometer LV and left atrial pressures. The regurgitant velocity profiles were digitized and converted to VA pressure gradient curves using the simplified Bernoulli equation. The instantaneous dP/dt of the VA pressure gradient curve was then derived. The instantaneous Doppler-derived VA pressure gradients, instantaneous Doppler dP/dt, dP/dtmax, and -dP/dtmax were compared with corresponding catheter measurements. This method of estimating dP/dtmax from the instantaneous dP/dt curve was also compared with a previously proposed Doppler method of estimating dP/dtmax using the Doppler-derived mean rate of LV pressure rise over the time period between velocities of 1 and 3 m/sec on the ascending slope of the Doppler velocity spectrum. Both instantaneous Doppler-derived VA pressure gradients (r = 0.95, p less than 0.0001) and Doppler dP/dt (r = 0.92, p less than 0.0001) correlated well with corresponding measurements by catheter during systolic contraction and isovolumic relaxation (pooled data). The Doppler dP/dtmax (1,266 +/- 701 mm Hg/sec) also correlated well (r = 0.94) with the catheter dP/dtmax (1,200 +/- 573 mm Hg/sec). There was no difference between the two methods for measurement of dP/dtmax (p = NS). Although Doppler -dP/dtmax was slightly lower than the catheter measurement (961 +/- 511 versus 1,057 +/- 540 mm Hg/sec, p less than 0.01), the correlation between measurements by Doppler and catheter was excellent (r = 0.93, p less than 0.0001). The alternative method of mean isovolumic pressure rise (896 +/- 465 mm Hg/sec) underestimated the catheter dP/dtmax (1,200 +/- 573 mm Hg/sec) significantly (on average, 25%; p less than 0.001). CONCLUSIONS. The present study demonstrated an accurate and reliable noninvasive Doppler method for estimating instantaneous LV dP/dt, dP/dtmax, and -dP/dtmax.
Marked differences in immunocytological localization of [3H]estradiol-binding protein in rat pancreatic acinar tumor cells compared to normal acinar cells. [3H]Estradiol can bind to a specific protein in normal rat pancreatic acinar cells. Electron microscopic immunocytochemical analysis has shown this protein to be localized primarily in the rough endoplasmic reticulum and mitochondria. Rat exocrine pancreatic tumor cell lines, whether grown in tissue culture (AR42J) or as a tumor mass after sc injection into rats (DSL-2), lacked detectable amounts of this [3H]estradiol-binding protein (EBP), as determined by the dextran-coated charcoal assay. Furthermore, primary exocrine pancreatic neoplasms induced with the carcinogen azaserine contained little or no detectable [3H]estradiol-binding activity. However, electron immunocytochemical studies of transformed cells indicated the presence of material that cross-reacted with antibodies prepared against the [3H]EBP. The immunopositive reaction in transformed cells was localized almost exclusively in lipid granules. Such lipid organelles in normal acinar cells, although present less frequently than in transformed cells, have never been observed to contain EBP-like immunopositive material. Presumably, the aberrant localization of EBP in these acinar tumor cells results in loss of function of this protein, which in normal pancreatic acinar cells appears to exert a modulating influence on zymogen granule formation and the process of secretion.
Tissue-plasminogen activator for pulmonary embolism resulting in shock: two case reports and discussion of the literature. Two patients with significant relative contraindications to fibrinolysis, and with refractory shock caused by acute pulmonary embolism, who were successfully treated with recombinant tissue-type plasminogen activator (rt-PA) are reported. The role of rt-PA in the management of pulmonary embolism is discussed, and pertinent literature is reviewed.
Noninvasive radiological diagnosis of renal vein thrombosis in renal transplantation. Thrombosis of the allograft renal vein is a rare complication of renal transplantation. Of 557 consecutive renal transplants performed between January 1, 1985 and November 30, 1989, 3 cases occurred for an over-all incidence of 0.4%. In 2 cases the diagnosis was made preoperatively with renal scintigraphy and duplex Doppler sonography. No graft was salvaged, despite timely diagnosis in 2 patients. We conclude that the diagnosis of renal vein thrombosis in the renal allograft recipient should be suspected clinically and by the radiographic findings of absent perfusion on renal scintigraphy, and the detection of an arterial signal, albeit abnormal, on duplex Doppler sonography. When diagnosed, nephrectomy appears to be the only treatment.
Na+ transport in hypertension. Several different lines of argument lead to the conclusion that the Na+ ion is important in hypertension. These include dietary and epidemiological studies, studies on the isolated cells and tissues of hypertensive subjects, and the association of the genetic predisposition to hypertension with abnormalities of cellular Na+ handling. In isolated cells, the most convincing abnormalities have been shown in the Na+ pump, where there is also evidence of a circulating inhibitor of the pump in essential hypertension, although the nature of the agent is still uncertain. The genetic association between essential hypertension and Na+ transport is best represented by alterations in Na(+)-Li+ countertransport in hypertensive subjects and their near relatives, although interpretation is rendered more complex by the influence of nongenetic factors on this system. The demonstrated differences between hypertensive and nonhypertensive subjects in the cellular handling of Na+ have not been integrated into a totally convincing explanation of the ultimate mechanism of the condition. Attention has focused on the possible mechanisms whereby an increase in intracellular Na+ may increase the concentration of cytosolic Ca2+ in the vascular smooth muscle, which is presumed to be a necessary precondition to a chronically elevated peripheral vascular resistance.
Therapeutic benefits of calcium channel blockers in cyclosporine-treated organ transplant recipients: blood pressure control and immunosuppression. Cyclosporine has dramatically improved the success rates for all forms of organ transplantation. However, its use is complicated by the frequent occurrence of hypertension and reversible nephrotoxicity. The iatrogenic hypertension induced by cyclosporine resembles a low-renin, salt-sensitive form of essential hypertension, which is often controlled with salt restriction and therapies counteracting renal salt acquisition, e.g., diuretics and calcium channel blockers (CCBs). CCBs may also counteract the direct vasoconstrictive effects of cyclosporine, as well as the effects of other vasoconstrictors, such as endothelin or thromboxane, that may be stimulated by cyclosporine. Additionally, CCBs may potentiate the immunosuppression of cyclosporine, yet minimize nephrotoxicity. We demonstrated that the in vitro combination of verapamil and cyclosporine had an additive inhibitory effect on the activation and function of human peripheral blood mononuclear cells in several assays of the afferent and efferent limbs of immunologic responses. This additive immunosuppression was not likely to have been related to these drugs' effects on interleukin-2 (IL-2) circuitry, since no additive inhibition of IL-2 production or IL-2 responsiveness was found. There was some additive inhibition of IL-2 receptor expression at the higher concentrations of verapamil and cyclosporine that were tested. Although the combination of verapamil and cyclosporine additively inhibited mitogen-induced 45Ca uptake, the inhibitory effect of cyclosporine appears to be due to an inhibition of lymphocyte activation rather than direct inhibition of calcium flux through the slow calcium channel, suggesting that the two drugs do not have additive effects in depressing the transmembrane flux of calcium. More recently, we have demonstrated that the inactive enantiomer of verapamil, which does not block the slow calcium channel, has identical immunosuppressive capabilities as the active enantiomer. Thus, the antiproliferative effect of verapamil is probably slow-calcium-channel independent and may represent the ability of the drug to interfere with muscarinic, alpha 1-adrenergic, or even opiate receptors on lymphocytes or to block lymphocyte potassium channels. An even better possibility is that verapamil may diminish necessary precursor molecule uptake into lymphocytes, since both the inactive and active isomeric forms of verapamil are capable of diminishing thymidine, uridine, and leucine incorporation into stimulated lymphocytes--necessary for DNA, RNA, and protein synthesis, respectively. These in vitro observations may have clinical applicability, as early studies demonstrate reduced rejection rates of cyclosporine-treated transplant patients receiving CCBs. Consequently, CCBs are important medications to be considered for use in cyclosporine-treated organ transplant recipients.
Beneficial effect of long-term beta blockade after acute myocardial infarction in patients without anterograde flow in the infarct artery. Previous studies have shown that long-term survival after acute myocardial infarction (AMI) is improved by beta-adrenergic blockade and anterograde flow in the infarct artery. This study was done to assess the influence of beta blockade on mortality in survivors of AMI without anterograde flow. Over 9.5 years, 113 subjects (87 men and 26 women, aged 26 to 66 years) with AMI and no anterograde flow in the infarct artery and no disease of the other arteries were medically treated for 48 +/- 28 (mean +/- standard deviation) months. Forty-six patients received long-term beta blockade (group I), whereas 67 did not (group II). The groups were similar in age, sex, cardioactive medications, left ventricular performance and infarct artery. Of the 46 group I subjects, 1 (2%) died of cardiac causes; in contrast, 20 (30%) of the group II patients died of cardiac causes (p = 0.007 compared with group I). Thus, in survivors of AMI without anterograde flow in the infarct artery, mortality is markedly reduced by long-term beta blockade.
Intensive sequential chemotherapy with mitoxantrone and continuous infusion etoposide and cytarabine for previously treated acute myelogenous leukemia. Intensive sequential chemotherapy with mitoxantrone, 12 mg/m2/d on days 1 through 3, etoposide, 200 mg/m2/d as a continuous infusion on days 8 through 10, and cytarabine, 500 mg/m2/d as a continuous infusion on days 1 through 3 and 8 through 10 was administered to 72 patients aged less than 60 years with previously treated acute myelogenous leukemia (AML). Forty patients had refractory AML (nonresponse to prior therapy, early first relapse, or multiple relapse) and 32 had late first relapse. Sixty-one percent of patients, with a 95% confidence interval (CI) ranging from 49% to 72%, achieved complete remission (CR), including 45% (CI: 30% to 62%) of refractory patients and 81% (CI: 64% to 93%) of late first relapse patients. Twenty-nine percent of patients (CI: 19% to 41%) did not respond to therapy and 10% (CI: 4% to 19%) died from therapy-related toxicity. Median duration of aplasia was 30 days. Nonhematologic WHO grade 3 or more toxicity included sepsis (57% of patients), vomiting (10%), mucositis (35%), diarrhea (7%), skin rash (6%), and hyperbilirubinemia (11%). Postinduction therapy was attempted in 36 of 44 CR patients: 16 of them received a second course of the same regimen, 7 received maintenance chemotherapy, 4 underwent autologous bone marrow transplantation (BMT), and 9 allogeneic BMT. At a median follow-up of 20 months, 23 of the 44 complete remitters have relapsed, 1 to 14 months after achievement of CR, including 19 of 31 patients not undergoing BMT. Median survival is 7 months with 16% (CI: 4% to 28%) projected survival at 47 months. Median disease-free survival is 6 months with 21% (CI: 3% to 39%) of CR patients projected to remain disease-free at 46 months. Twenty-six percent (CI: 13% to 43%) of the evaluable patients who did not receive transplantation had inversion of CR duration. Among patients younger than 50 years, there was no significant difference in disease-free survival between patients receiving postinduction chemotherapy and those receiving BMT. We conclude that this chemotherapy regimen is highly efficient and could be used as first-line therapy in young patients with AML.
Effect of systemic fibrinogen depletion on intraabdominal abscess formation. Deposition of fibrin within the peritoneal cavity is an integral host response to local infection. To directly assess the role of fibrin deposition in the pathogenesis of intraabdominal abscess formation, the ability to induce abscesses in fibrinogen-depleted mice was examined. We hypothesized that systemic defibrinogenation with ancrod would limit the availability of fibrinogen for deposition within the peritoneal cavity and would therefore impair intraabdominal abscess formation. A gelatin capsule containing 50% sterile feces plus Bacteroides fragilis 1 x 10(9) CFU was inserted IP into control or defibrinogenated mice. System defibrinogenation resulted in alteration of the character of abscess formation, as manifested by reduced abscess size and degree of purulence. Abscesses were significantly smaller (0.18 +/- 0.02 gm [n = 29] vs. 0.09 +/- 0.02 gm [n = 11], p less than 0.01) and less purulent (p less than 0.001) in the ancrod-treated mice than in control animals, despite equal numbers of bacteria in the abscesses recovered from both groups. The effect of ancrod was specific for defibrinogenation, because IP repletion with fibrinogen reversed the ancrod effect on abscess size. In addition to its local effects, systemic fibrinogen depletion resulted in a significant elevation in mortality following IP infection (1 of 30 control animals vs. 10 of 23 ancrod-treated animals, p less than 0.01). However, this was not due to an increase in the magnitude of the B. fragilis bacteremia. These studies demonstrate that fibrin deposition contributes to the pathogenesis of purulent abscess formation and that systemic depletion of fibrinogen may alter host susceptibility to the consequences of infection.
Role of gastric colonization in the development of pneumonia in critically ill trauma patients: results of a prospective randomized trial. Critically ill trauma patients were entered in a prospective, randomized trial to determine the role of gastric colonization in the development of pneumonia. Trauma patients admitted to the SICU were randomized to receive antacids (n = 27), continuous IV cimetidine (n = 32), or sucralfate (n = 30). Quantitative nasogastric tube (NGT) cultures were obtained biweekly and correlated with gastric pH, the incidence of pneumonia, and the incidence of pneumonia caused by an organism previously isolated from the stomach (percentage of gastric source of pneumonia--% GSP). Patients receiving antacids had a significantly greater pH than those receiving cimetidine (5.6 +/- 1.03 vs. 4.7 +/- 1.03; p = 0.006). However, there was no significant difference between the overall incidence of pneumonia, the percentage of NGT isolates greater than 10(6)/ml, or the % GSP. The gastric bacteriology of the three subgroups was nearly identical, with Candida albicans, Enterococci, and beta-hemolytic Streptococci being the most frequently isolated organisms. Gastric growth of organisms preceding their appearance in the blood occurred in 5 of 89 (5.6%) patients. These results suggest that 1) in trauma patients, the incidence of pneumonia is not increased by the use of stress ulcer prophylactic agents that elevate gastric pH; 2) increases in gastric pH progressively increased the number of intragastric bacteria but this did not correlate with an increased incidence of % GSP; and 3) while organisms in the upper intestinal tract may be pathogens for pneumonia, they are uncommonly a source of bacteremia in seriously injured patients.
Iliofemoral venous thrombectomy followed by percutaneous closure of the temporary arteriovenous fistula. Iliofemoral venous thrombosis treated by anticoagulants alone almost invariably results in postthrombotic sequelae with deep venous reflux alone or combined with an outflow obstruction. This study evaluates the result of iliofemoral venous thrombectomy with temporary proximal arteriovenous fistula (AVF) performed on 48 consecutive patients. In 10 patients the thrombus extended in the inferior vena cava, and the thrombectomy was combined with inferior vena cava interruption. The AVF closed spontaneously in 8 of 48 patients (patency rate, 84%). An attempt to close the AVF by placing a detachable balloon percutaneously under radiographic control was made 6 to 12 weeks later (success rate, 87%; complications, rare). A preclosure arteriovenography of the femoro-iliaco-caval segment revealed 34 of 38 segments open (patency rate, 89%). Four patients had severe stenosis of the iliac segment, and a transvenous percutaneous dilatation was successfully performed in three of the four patients, keeping the fistula. At AVF closure 4 weeks later the arteriovenography showed sustained dilatation in only two patients. Thirty-seven patients were followed for 3 to 48 months (median, 24 months) and 30 of 37 patients (81%) who had no symptoms were not using compression stockings. Doppler investigation revealed patent and competent femoral and popliteal veins and normal photoplethysmography in 56% of the patients. Four iliac veins were occluded (patency rate, 88%). No recurrence of fistula had occurred. Venous iliofemoral thrombectomy seems to better preserve valve function. The percutaneous balloon closure of the AVF has decreased the complication rate, facilitated venographic evaluation of the result, and made possible the performance of percutaneous interventions under the protection of the AVF.
Occupational carpal tunnel syndrome in Washington State, 1984-1988. BACKGROUND: There are no published population-based studies of occupational carpal tunnel syndrome (OCTS) using a strict case definition. Most studies are either industry specific or present patient self-report of symptoms. METHODS: We conducted a population-based incidence study of OCTS using the Washington State Workers' Compensation database. Incident OCTS claims were identified with paid bills for physician reported ICD codes 354.0 and 354.1. RESULTS: There were 7,926 incident OCTS claims identified for the years 1984-1988, which yields an industry-wide incidence rate of 1.74 claims/1,000 FTEs. The mean age (37.4 years) and female/male ratio (1.2:1) in this population differ from those reported in nonoccupational carpal tunnel studies (mean age, 51 years; female/male ratio, 3:1). The female-specific OCTS incidence rate increased significantly during the study period. The highest industry specific OCTS rates were found in the food processing, carpentry, egg production, wood products, and logging industries. CONCLUSION: Demographic differences and industry-specific rates consistent with workplace exposures suggest that OCTS is distinct from CTS occurring in nonoccupational settings. Workers' compensation data proved useful in identifying high risk industries.
Obesity and hypertension. There is a close association of obesity with hypertension through mechanisms not now understood. Hypertension occurs frequently in industrialized societies where weight gain with advancing years is a common feature and is rare in primitive societies where weight and age are negatively correlated. Hemodynamically, obesity is characterized by an expanded blood volume and increased cardiac output. Hypertension results if/when systemic vascular resistance fails to decrease as cardiac output increases. When calorie restriction leads to weight loss, both blood volume and cardiac output decrease; when the blood pressure falls, this is because peripheral resistance is unchanged. Weight-loss programs are helpful for the obese hypertensive because when hypertension is mild, blood pressure often (but not always) normalizes. Also, weight loss has been shown to decrease antihypertensive drug requirements. Interest in obesity-associated hypertension focuses on hyperinsulinemia/insulin resistance as causative factors. Although the evidence is tempting, it is far from conclusive and it seems likely that the mechanism of this type of hypertension is as multifactorial as those of other types.
Maternal plasma level of endothelin is increased in preeclampsia. Endothelin is a potent vasoconstrictor that is reportedly increased in conditions characterized by endothelial damage. Maternal plasma endothelin levels were compared between 27 women with preeclampsia (23 without and 4 with the hemolysis, elevated liver enzymes, and low platelet count syndrome) and 14 women with normotensive pregnancies. The mean +/- SEM plasma endothelin values were significantly higher in patients with preeclampsia uncomplicated by the hemolysis, elevated liver enzymes, and low platelet count syndrome (5.48 +/- 0.30 fmol/ml vs 3.86 +/- 0.28, p less than 0.001). In addition, the preeclamptic group with the hemolysis, elevated liver enzymes, and low platelet count syndrome had significantly higher endothelin levels than those without the syndrome (8.30 +/- 1.62 fmol/ml vs 5.48 +/- 0.30, p less than 0.05). There was no correlation between plasma endothelin values and either systolic or diastolic blood pressure. We conclude that plasma endothelin levels are significantly increased in women with preeclampsia and particularly in those with the hemolysis, elevated liver enzymes, and low platelet count syndrome, suggesting an association with widespread endothelial damage.