123rc/medical_text huggingface dataset:
Hypercalcemia in malignancy. The pathogenesis of hypercalcemia in malignancy has been enigmatic until recent years. Since the realization in 1980 that bioassays for parathyroid hormone detected a cross-reacting substance in malignancy, progress has been remarkably rapid. A parathyroid hormone-related protein was purified and identified by molecular cloning as a 141-amino acid peptide with limited homology to parathyroid hormone itself. Nonetheless, both peptides activate the parathyroid hormone receptor to produce hypercalcemia. It is now clear that the parathyroid hormone-related protein is the cause of hypercalcemia in most solid tumors, particularly squamous and renal carcinomas. New assays for the hormone as well as the related peptide have greatly simplified the differential diagnosis of hypercalcemia. At the same time, new agents for the treatment of hypercalcemia are becoming available, most notably the bisphosphonate drugs.
Foci of increased T2 signal intensity in MR images of healthy elderly subjects. A follow-up study. An 18-month follow-up study was conducted on 26 healthy elderly subjects with and without foci of increased T2 signal intensity on MR imaging. The subjects did not differ with respect to health status or cognitive performance as measured by the Cognitive Subscale of the Cambridge Mental Disorders of the Elderly Examination and the Mini Mental State Examination at follow-up. There was a significant decline in performance on the Digit Symbol Substitution Test in subjects who had evidence of T2 foci compared to the performance of subjects without T2 foci. This may indicate that the presence of T2 foci is correlated with subtle difficulties in learning and memory.
Tumor cell lines established in vitro: an independent prognostic factor for survival in non-small-cell lung cancer. OBJECTIVE: To determine the relation between in-vitro establishment of tumor cell lines and survival in patients with non-small-cell lung cancer. DESIGN: Cohort study. SETTING: Single-institution tertiary care center. PATIENTS: One hundred twenty-three consecutive patients with non-small-cell lung cancer from whom a viable tumor specimen could be obtained. INTERVENTION: Tumor tissue was removed at the time of entry into a therapeutic protocol. The tumor tissue was processed in the laboratory for attempted cell-line establishment. Patients classified as potentially curable (stages I, II, and IIIA) were treated with surgical resection, radiation therapy, or a combination. Patients suitable for palliative therapy only (stages IIIB and IV) were treated with radiation therapy with or without chemotherapy. Chemotherapy was based on in-vitro drug sensitivity when available. Cell-line establishment was correlated to clinical outcome. MEASUREMENTS AND MAIN RESULTS: Univariate analysis of survival was done using the log-rank test; multivariate analysis was done by Cox modeling step-up and step-down techniques. Cell lines were established from the tumor specimens of 25 patients (20%). Those patients experienced a median survival of 7 months compared with 18 months in patients from whom cell lines could not be established (P less than 0.001). In the 61 patients with potentially curable disease, 8 patients (13%) with cell lines established had a median survival of 8 months compared with 32 months for those without cell lines established (P = 0.001). In the 62 palliative group patients, the median survival of the 17 patients (27%) from whom tumor cell lines were established was 5 months compared with 7 months for those without cell lines (P = 0.15). Multivariate analysis in both groups showed cell-line establishment to be a significant indicator of prognosis (P less than 0.0001 for curable group; P less than 0.01 for palliative group). CONCLUSION: In-vitro tumor growth is related to decreased patient survival, which in turn reflects the biologic aggressiveness of cancers giving rise to these tumor cell lines.
Myocardial preservation using lidocaine blood cardioplegia. Prevention of ventricular fibrillation after aortic unclamping using lidocaine hydrochloride as an additive to cold potassium blood cardioplegia was studied prospectively in 46 patients undergoing elective myocardial revascularization. Patients were similar with respect to age, ventricular function, severity of coronary artery disease, cross-clamp time, completeness of revascularization, frequency of internal thoracic artery grafting, systemic temperature at the time of cross-clamp removal, and mean infusate volume and temperature. Patients receiving lidocaine blood cardioplegia (group 1, 23 patients) had a significant reduction in the incidence of ventricular fibrillation (22% versus 74%; p less than 0.0005) and in the mean number of cardioversion attempts required to defibrillate the heart (0.5 +/- 1.3 versus 1.9 +/- 0.97; p less than 0.0005) after cross-clamp removal compared with controls (group 2, 23 patients). There were no differences between the two groups postoperatively with regard to cardiac enzyme release, hemodynamic measurements, or clinical outcome. Patients receiving lidocaine blood cardioplegia tended to have a lower incidence of new postoperative atrial fibrillation (9% versus 26%). Ventricular function was preserved equally in both groups. We conclude that lidocaine is a safe additive to potassium blood cardioplegia and significantly reduces the incidence of ventricular fibrillation after aortic unclamping.
Fluctuation in timing of upper airway and chest wall inspiratory muscle activity in obstructive sleep apnea. An imbalance in the amplitude of electrical activity of the upper airway and chest wall inspiratory muscles is associated with both collapse and reopening of the upper airway in obstructive sleep apnea (OSA). The purpose of this study was to examine whether timing of the phasic activity of these inspiratory muscles also was associated with changes in upper airway caliber in OSA. We hypothesized that activation of upper airway muscle phasic electrical activity before activation of the chest wall pump muscles would help preserve upper airway patency. In contrast, we anticipated that the reversal of this pattern with delayed activation of upper airway inspiratory muscles would be associated with upper airway narrowing or collapse. Therefore the timing and amplitude of midline transmandibular and costal margin moving time average (MTA) electromyogram (EMG) signals were analyzed from 58 apnea cycles in stage 2 sleep in six OSA patients. In 86% of the postapnea breaths analyzed the upper airway MTA peak activity preceded the chest wall peak activity. In 86% of the obstructed respiratory efforts the upper airway MTA peak activity followed the chest wall peak activity. The onset of phasic electrical activity followed this same pattern. During inspiratory efforts when phasic inspiratory EMG amplitude did not change from preapnea to apnea, the timing changes noted above occurred. Even within breaths the relative timing of the upper airway and chest wall electrical activities was closely associated with changes in the pressure-flow relationship. We conclude that the relative timing of inspiratory activity of the upper airway and chest wall inspiratory muscles fluctuates during sleep in OSA.
Normalization of ventilation/perfusion relationships after liver transplantation in patients with decompensated cirrhosis: evidence for a hepatopulmonary syndrome. To examine the effect of liver transplantation on the respiratory and cardiovascular functions, ventilation/perfusion relationships were determined by multiple inert gas elimination technique in six patients with end-stage liver disease 1 to 19 mo before and 2 to 6 mo after liver transplantation. Cardiac output and pulmonary vascular pressures were measured after catheterization of the pulmonary artery. All patients had normal spirometry and chest x-ray films before transplantation. PaO2 before transplantation was 78.8 +/- 7.4 mm Hg (range = 51.8 to 102.8 mm Hg). All patients had perfusion of poorly ventilated lung regions (low ventilation/perfusion relationships) varying from 3% to 19% of cardiac output (mean = 8.5% +/- 2.4% of cardiac output) and two patients had intrapulmonary shunting (3% and 20% of cardiac output). Measured and calculated PaO2 agreed closely, indicating absence of pulmonary diffusion abnormality, as well as of extrapulmonary shunting. After transplantation, PaO2 normalized in all patients, and both shunting and low ventilation/perfusion relationships disappeared. Cardiac output decreased from 9.1 +/- 1.4 to 6.6 +/- 0.5 L/min (p less than 0.05), and the pulmonary vascular resistance increased from 0.69 +/- 0.14 to 1.64 +/- 0.43 mm Hg/L/min (p less than 0.05). The systemic vascular resistance also increased (before = 8.7 +/- 1.0; after = 15.3 +/- 1.1 mm Hg/L/min; p less than 0.001). Normalization of respiratory and cardiovascular alterations, after liver transplantation, in patients with end-stage liver disease indicates that these changes have a direct functional relationship to the diseased liver. It is hypothesized that this is part of a "hepatopulmonary syndrome,' which in similarity to the hepatorenal syndrome disappears with improved liver function.
Analysis of programmed stimulation methods in the evaluation of ventricular arrhythmias in patients 20 years old and younger. The purpose of this study was to systematically evaluate programmed ventricular stimulation in patients less than 21 years of age undergoing electrophysiologic testing. A standardized protocol was applied in 55 consecutive patients (mean age 14 years) with the following clinical presentations: sustained ventricular tachycardia (VT) (n = 17); ventricular fibrillation (VF) (n = 7); syncope with heart disease (n = 10); nonsustained VT (n = 6); and syncope with an ostensibly normal heart (n = 15). The stimulation protocol consisted of 1 and 2 ventricular extrastimuli during sinus rhythm, followed by 1 to 4 (S2, S3, S4, S5) extrastimuli during pacing at 2 ventricular sites. Of the 17 patients with sustained VT, 12 had induction of the arrhythmia (sensitivity = 71%). Overall, 18 of 55 patients had inducible sustained VT, with this response significantly enhanced by use of S4 or S5 protocols (p = 0.02). Although no syncope patients with an ostensibly normal heart had inducible sustained VT, 7 had polymorphic nonsustained VT in response to ventricular stimulation. The mean number of extra-stimuli preceding the induction of nonsustained or sustained VT or VF did not differ. The induction of VF in 5 cases during this study was preceded in each case by extrastimuli intervals less than or equal to 190 ms. Thus, data indicate that aggressive stimulation protocols appear to be required for induction of sustained VT in most young patients, nonsustained polymorphic VT as a response to aggressive programmed stimulation is of uncertain significance, and that coupling intervals less than or equal to 190 ms may correlate with the induction of VF.
Gallbladder varices: imaging findings in patients with portal hypertension. A retrospective review of the medical and imaging records of 50 patients with portal hypertension examined in the authors' department during a 2-year period identified six patients with gallbladder wall varices. Imaging studies performed in these patients included computed tomography (CT) (four patients), duplex and color Doppler flow (five patients), and magnetic resonance (MR) (four patients). Five of six patients with gallbladder varices had portal vein thrombosis. Anechoic areas within the gallbladder wall detected with ultrasonography could be distinguished from intramural edema by using duplex or color Doppler flow imaging in all five patients in whom it was used. Contrast material enhancement of these varices was detected with CT in three patients, two of whom also had adjacent mesenteric collaterals. Gradient-echo MR imaging (fast imaging in steady precession/fast low-angle shot) showed flow-related enhancement within the gallbladder wall in two patients. The presence of gallbladder wall varices may imply the presence of portal vein thrombosis. Since these varices can be a source of major blood loss, surgeons must be made aware of them when operating on patients with portal hypertension.
Spontaneous perinephric hemorrhage: imaging and management. We report on 10 patients with spontaneous perinephric hemorrhage associated with underlying disease, including renal cell carcinoma (5), angiomyolipoma (2), malignant melanoma (1), periarteritis nodosa (1) and severe portal hypertension (1). The etiology could not be identified with computerized tomography (CT) in 5 cases (50%), including 2 renal cell carcinomas, 1 angiomyolipoma, 1 periarteritis nodosa and 1 portal hypertension. Arteriography demonstrated underlying lesions in 4 of these 5 cases (80%) including the case of vasculitis. CT combined with magnetic resonance imaging is accurate for the diagnosis of spontaneous perinephric hemorrhage but the underlying pathological condition is often undetectable in the acute phase due to the perinephric blood. CT should be the first study performed if this diagnosis is suspected. Arteriography is recommended if a renal mass is not detected. If a mass is not identified with these 2 imaging studies and the patient is clinically stable, followup thin slice CT should be performed.
Hypothalamic-pituitary-adrenal function in patients with the premenstrual syndrome. Patients with primary affective disorders, such as melancholic depression and anorexia nervosa, frequently have a hyperactive hypothalamic-pituitary-adrenal (HPA) axis, characterized by hypersecretion of CRH and a blunted ACTH response to exogenous CRH. Premenstrual syndrome (PMS) is a luteal phase dysphoric disorder characterized by primarily affective and behavioral disturbances. HPA axis function was compared in PMS patients and control women, respectively, diagnosed by DSM3-R criteria or found to have no current psychiatric disorders, determined by the Schedule for Affective Disorders and Schizophrenia-Lifetime Interview. Urinary free cortisol excretion was the same in PMS and normal women, and no differences in urinary free cortisol excretion between the follicular and luteal phases occurred in either group. Two HPA axis abnormalities, however, were noted when PMS patients were compared to normal women. First, basal evening cortisol concentrations in plasma were significantly decreased, while the time-integrated response of plasma cortisol to ovine (o) CRH was significantly increased. Second, the negative correlation between time-integrated plasma ACTH and cortisol responses to oCRH and basal luteal progesterone concentrations present in normal control women was not seen in the PMS patients. These changes in basal and oCRH-stimulated plasma cortisol levels in association with normal urinary free cortisol excretion suggest that women with PMS might have transient or episodic disturbances of their HPA axis, which appear adequately corrected by this system's servomechanisms. This probably explains the maintenance of regular menstrual cycles in PMS patients, which contrasts with the irregular menses observed in patients with depression, anorexia nervosa, or women who participate in chronic strenuous exercise.
A long-term study of doxazosin in the treatment of mild or moderate essential hypertension in general medical practice. This study assessed the long-term (54 weeks) antihypertensive efficacy and safety of doxazosin in the treatment of mild or moderate essential hypertension, defined as sitting and standing diastolic blood pressure of 95 to 114 mm Hg. Of the 153 patients who successfully completed an initial 14-week trial, 61 continued uninterrupted into a 40-week extension study. Optimal antihypertensive efficacy was achieved by week 12 and maintained in all patients for the duration of 1 year. The final mean sitting blood pressure was 148/84 mm Hg and was reduced from a mean baseline level of 173/102 mm Hg. Occasional decreases in heart rate were observed, but these were not considered to be clinically relevant (1 to 3 beats/min). The mean final dose of doxazosin for patients evaluable for efficacy was 2.4 mg/day; 91.7% of patients were taking less than or equal to 4 mg/day. No increase in daily maintenance dose was observed from the initial phase to the long-term extension study. After 1 year of treatment, 93.3% of patients were considered a therapeutic success (sitting diastolic blood pressure greater than or equal to 10 mm Hg reduction from baseline or less than or equal to 90 mm Hg with greater than or equal to 5 mm Hg reduction). In no patients was there a worsening in the severity category of the hypertension. Total serum cholesterol concentrations were reduced significantly (6.6% p = 0.03) at the end of week 14. Reductions in total serum cholesterol levels persisted throughout the extension study, with a final reduction of 5.4%.
Coffee, caffeine, and cardiovascular disease in men BACKGROUND. For many years, an association between coffee consumption and the risk of coronary heart disease has been suspected. Although based on small numbers of end points, a prospective study has suggested a particularly strong association between recent coffee drinking and the incidence of cardiovascular disease. METHODS. We examined prospectively the relation of coffee consumption with the risk of myocardial infarction, need for coronary-artery bypass grafting or angioplasty, and risk of stroke in a cohort of 45,589 U.S. men who were 40 to 75 years old in 1986 and who had no history of cardiovascular disease. RESULTS. During two years of follow-up observation, 221 participants had a nonfatal myocardial infarction or died of coronary heart disease, 136 underwent coronary-artery surgery or angioplasty, and 54 had a stroke. Total coffee consumption was not associated with an increased risk of coronary heart disease or stroke. The age-adjusted relative risk for all cardiovascular disease among participants who drank four or more cups of coffee per day was 1.04 (95 percent confidence intervals, 0.74 to 1.46). Increasing levels of consumption of caffeinated coffee were not associated with higher risks of cardiovascular disease. Higher consumption of decaffeinated coffee, however, was associated with a marginally significant increase in the risk of coronary heart disease (relative risk, 1.63; 95 percent confidence interval, 1.02 to 2.60). Finally, we observed no pattern of increased risk across the subgroups of participants with increasing intakes of caffeine from all sources. Adjustment for major cardiovascular-risk indicators, dietary intake of fats, and cholesterol intake did not materially alter these associations. CONCLUSIONS. These findings do not support the hypothesis that coffee or caffeine consumption increases the risk of coronary heart disease or stroke.
Management of hypertension by reduction in sympathetic activity. The sympathetic nervous system may initiate or maintain hypertension, and a range of approaches that reduce sympathetic activity is often of value in management. These may include nonpharmacological methods, such as the various forms of behavioral therapy (e.g., meditation, relaxation, and biofeedback techniques); weight reduction and avoidance of particular foods and agents that stimulate sympathetic activity (including caffeine and alcohol), and regular physical exercise. Pharmacological therapy includes centrally acting drugs such as alpha-methyldopa, clonidine, and reserpine; ganglionic blockers such as hexamethonium; agents acting on sympathetic nerve terminals such as guanethidine and debrisoquine; and drugs that may act at multiple sites, such as the beta-adrenergic blockers. The role of reducing sympathetic activity in the current management of hypertension and its complications is considered in this overview.
Safety, stability, and effectiveness of immunoadsorption under membrane plasmapheresis treatment for myasthenia gravis. Nine patients (five women and four men, average age 50.4 years) with refractory myasthenia gravis (MG) underwent thymectomy and were then treated with immunoadsorption under membrane plasmaphersis (IAP). Thymic histology showed hyperplasia in nine patients. An immunoadsorption column (ASAHI, Med, Co) was made with tryptophan. A Plasouto 1,000 (ASAHI, Med, Co) was used as the machine. The plasma separator was a first filter (ASAHI, Med, Co), and immunoadsorption columns were used for plasma perfusion. IAP treatment was performed three times weekly for a total of six times, after which IAP was done every 3 weeks. The removal rate of anti-Ach-R titer was 54 +/- 12%; IgG, IgA, and IgM levels improved in nine of nine patients after IAP treatment, and improvement of gait disturbances were seen in two of two. Muscle strength improved in all nine patients, whereas speech disturbances improved in two of three. Eye ptosis improved in nine of nine patients. Subjective improvement was reported by nine of nine patients, and none had severe side effects with IAP. In conclusion, IAP is a safe, stable, effective, and clinically useful treatment. for MG.
Interactions between N-methyl-D-aspartate and CGS 19755 administered intramuscularly and intracerebroventricularly in pigeons. Behavioral effects of N-methyl-D-aspartate (NMDA) and the competitive NMDA antagonist cis-4-phosphonomethyl-2-piperidine-carboxylic acid (CGS 19755) were studied in pigeons. NMDA decreased responding under a fixed-ratio schedule of food presentation and was 8000 times more potent administered intracerebroventricularly (i.c.v.) as compared to intramuscularly (i.m.). CGS 19755 was 870 times more potent in producing catalepsy when administered i.c.v.; however, the duration of catalepsy was similar by the two routes of administration. Administered i.m. CGS 19755 decreased response rates only at doses that also produced catalepsy; administered i.c.v. some doses of CGS 19755 decreased responding without producing other behavioral effects. Rate-decreasing effects of i.m. NMDA were attenuated by i.m. CGS 19755; however, when CGS 19755 was administered i.c.v., there was little or no antagonism of NMDA. Rate-decreasing effects of i.c.v. NMDA were not attenuated by i.m. or i.c.v. CGS 19755 up to doses that produced catalepsy or eliminated responding. The large difference in potency between i.m. and i.c.v. administration for NMDA and for CGS 19755, as well as the slower onset of catalepsy when CGS 19755 was administered i.m., suggests these compounds do not readily cross the blood-brain barrier when administered parenterally. The inability of CGS 19755 to attenuate the rate-decreasing effects of NMDA when CGS 19755 or NMDA was administered i.c.v. suggests NMDA might decrease responding by different mechanisms when administered i.m. or i.c.v. in pigeons. Together these results indicate antagonism of NMDA in this study, and perhaps in other studies, when both NMDA and CGS 19755 were administered parenterally, might result from a peripherally mediated interaction. Moreover, this agonist-antagonist interaction is not a simple, competitive antagonism.
Factors related to and consequences of weight loss in patients with stomach cancer. The Norwegian Multicenter experience. Norwegian Stomach Cancer Trial. Of 1165 patients with stomach cancer included in a national, prospective multicenter study with 51 surgical units participating, information about weight loss before diagnosis was available for 855 patients (73%). Median weight loss was 5 kg; 259 patients (31%) experienced no weight loss. By logistic regression analysis the authors found that weight loss increased with age and advancing stages of disease (TNM Stage I-IV), with decreasing Karnofsky index, in Lauren's diffuse versus intestinal tumor type, and with tumors located at the cardia/esophagus. Increasing weight loss reduced the resectability rate significantly, but no association between weight loss and postoperative complication rate was found. The odds ratio for postoperative mortality was 2.5 to 1 for the weight loss group 5 to 10kg versus 0 kg. In conclusion, weight loss reflects a less favorable tumor status. Weight loss did not increase postoperative morbidity but did lead Weight to a higher death rate after surgery.