123rc/medical_text huggingface dataset:
Clinical and hemodynamic correlates of sympathetic nerve activity in normal humans and patients with heart failure: evidence from direct microneurographic recordings. To characterize the neural excitatory state of heart failure, simultaneous measurements of efferent sympathetic nerve activity to muscle (by microneurography) and rest hemodynamics were obtained in 10 normal subjects (age 25 +/- 2 years, mean +/- SEM) and 29 patients with heart failure (age 49 +/- 2 years; New York Heart Association functional class II to IV; left ventricular ejection fraction 21 +/- 1%; cardiac index = 2.16 +/- 0.13 liters/min per m2; pulmonary capillary wedge pressure 23 +/- 2 mm Hg). Sympathetic nerve activity was significantly higher in the patients with heart failure (54.7 +/- 4.5 bursts/min) than in normal subjects (16.7 +/- 2.2 bursts/min, p less than 0.001). Multiple linear regression analyses indicated that sympathetic activity in these human subjects was most strongly and inversely correlated with left ventricular stroke work index (r = -0.86, p less than 0.0001) and stroke volume index (r = -0.85, p less than 0.0001). There was a strong positive correlation between sympathetic nerve activity and pulmonary artery diastolic (r = 0.82, p less than 0.0001) and mean (r = 0.81, p less than 0.0001) pressures. Similar correlations were seen when patients with heart failure were analyzed separately. There was no significant correlation between sympathetic nerve activity and mean arterial pressure, left ventricular ejection fraction (by radionuclide ventriculography), cardiac chamber size (by echocardiography) or arterial oxygen tension in the patients with heart failure. Direct measurements of sympathetic nerve activity correlated closely with plasma norepinephrine (r = 0.72, p less than 0.0001) in patients with heart failure. Thus, sympathetic nerve activity at rest parallels impairment of cardiac performance in patients with heart failure.
Osteoid osteoma of the scapula. A case report and review of the literature. The scapula is a rare location for osteoid osteoma, which in most cases does not involve the flat bones. The en bloc excision in this uncommon location can be problematic since the surgical exposure is difficult, and shoulder joint function can be affected if the lesion is subchondral. In an 18-year-old man, an osteoid osteoma was located in the subchondral area of the glenoid. A guided needle biopsy of the nidus resulted in complete healing. This mode of treatment, with proper follow-up examination, is acceptable for a benign lesion situated in a problematic location.
High risk of severe bleeding in aged patients with chronic idiopathic thrombocytopenic purpura. The purpose of this study was to estimate the incidence and to establish which factors were associated with an increased risk of hemorrhagic complications in an historic cohort of 117 consecutive and unselected patients with chronic idiopathic thrombocytopenic purpura (ITP). Sixty-eight patients (58%) underwent medical treatment and/or splenectomy and 33 (48% of treated) achieved a complete stable remission. At equivalent platelet count the incidence of major hemorrhagic complications was significantly higher in aged (greater than 60 years) than in younger (less than 40 years) patients (10.4% v 0.4%/pt-y, relative risk = 28.9, P less than .01). A previous hemorrhagic event was identified as another major risk factor for hemorrhage (relative risk = 27.5, P less than .0005), while hypertension and underlying disorders had no influence. We conclude that age more than 60 years and a previous history of bleeding are major risk factors for severe hemorrhages in adults with ITP.
A retroviral promoter is sufficient to convert proto-src to a transforming gene that is distinct from the src gene of Rous sarcoma virus. The src genes of four natural isolates of avian sarcoma viruses differ from cellular proto-src in two genetic substitutions: the promoter of the cellular gene is replaced by a retroviral counterpart, and at least six codons from the 3' terminus are replaced by retroviral or heterologous cell-derived elements. Since virus constructs with a complete proto-src coding region failed to transform avian cells but acquired transforming function by point mutations of various codons, it has been proposed that point mutation is sufficient to convert proto-src to a transforming gene. However, promoter substitution is sufficient to convert two other proto-onc genes, proto-ras and proto-myc, to retroviral transforming genes. In view of this, we have reexamined whether promoter substitution, point mutation, or both are necessary to convert proto-src into a retroviral transforming gene. It was found that a recombinant virus (RpSV), in which the src gene of Rous sarcoma virus (RSV) was replaced by the complete coding region of proto-src, transformed quail and chicken embryo cells. The oncogene of RpSV differs from the src gene of RSV in three genetic properties: (i) it is weaker--e.g., transformed cells are flatter; (ii) it is slower--e.g., focus formation takes 9 to 12 days compared to 4 days for RSV; and (iii) its host range is narrower than that of RSV--e.g., only subsets of heterogeneous embryo cells are transformed by RpSV even after weeks or months. Replacement of the proto-src 3' terminus of RpSV by that of src from RSV generates a recombinant virus (RpvSV) that equals RSV in transforming function. It is concluded that a retroviral promoter, naturally substituted via illegitimate recombination with retroviruses, is sufficient to convert at least three proto-onc genes, src, myc, and ras, to retroviral transforming genes.
Two types of abnormal somatosensory evoked potentials in chronic cerebellar ataxias. To investigate subclinical sensory impairment in spinocerebellar degenerations, median nerve somatosensory evoked potentials (SEPs) were examined in 16 patients with chronic cerebellar ataxia who were originally diagnosed by clinical neurologists as having olivopontocerebellar atrophy (OPCA). Two types of abnormal SEP patterns were found in six patients. Two patients had the SEP pattern of peripheral neuropathy, which was also detected by peripheral sensory nerve conduction studies. Four patients had abnormal SEPs seen in patients with the lesions in the central nervous system (dorsal column, medial lemniscus). Magnetic resonance imaging (MRI) showed multiple sclerosis (MS). It is possible that clinically diagnosed OPCA sometimes includes a similar form of Friedreich's ataxia with subclinical sensory fiber neuropathy detected by SEPs and peripheral sensory conduction studies. In cases of lesions in the central nervous system demonstrated by both SEPs and MRI, there must be a follow-up in order to make a final diagnosis. In those cases, an alternative diagnosis of MS must be considered when the temporal profile of symptoms and signs characteristic of MS is observed.
Late outcome of survivors of out-of-hospital cardiac arrest with left ventricular ejection fractions greater than or equal to 50% and without significant coronary arterial narrowing. In a retrospective survey of 1,195 survivors of out-of-hospital ventricular fibrillation, 43 patients were identified in whom left ventricular ejection fraction was greater than or equal to 0.50 and in whom no coronary artery stenosis of greater than or equal to 50% luminal diameter were present. Thirteen (30%) of these patients had hypokinesia on left ventriculography, and 20 patients (47%) had a persistently abnormal electrocardiogram. Seven patients (16%) had recurrent out-of-hospital cardiac arrest during an average follow-up of 86 +/- 54 months. The presence of either wall motion or electrocardiographic abnormalities defined patients with a several-fold higher risk of recurrent cardiac arrest than those without such abnormalities. The risk for recurrent cardiac arrest within 5 years was 30% in those with abnormal electrocardiograms versus 5% in the others (p less than 0.03). Age was an independent predictor of recurrent cardiac arrest in this group (p less than 0.01); surprisingly, recurrent cardiac arrest was occurring more often among younger patients. Although cardiac arrest is unusual in patients without major structural heart disease, its recurrence in such survivors is common. Patients at relatively high risk for recurrent ventricular fibrillation can be identified by their youth and by abnormalities detected on the surface 12-lead electrocardiogram or by contrast left ventriculography.
Management of premature removal of the percutaneous gastrostomy. Percutaneous endoscopic gastrostomy (PEG) has become the preferred method of enteral access for nutritional support. With increased use of this modality, complications are encountered more frequently. Premature withdrawal, inadvertent removal of the gastrostomy tube within the first seven days after insertion, before adherence of the gastric serosa to the parietal peritoneum, has been an indication for laparotomy. This report describes the treatment of premature withdrawal by immediate endoscopic replacement. Over an 18-month period, 271 patients underwent insertion of a PEG. Five patients (1.8%) who inadvertently removed their gastrostomy tube within seven days of insertion were treated with immediate replacement using the retrograde string technique, avoiding laparotomy. All five PEGs were successfully replaced through the same gastrostomy site. Despite the presence of pneumoperitoneum, no patient developed peritonitis or other septic complications. Premature gastrostomy tube withdrawal is safely managed by endoscopic replacement and observation. Laparotomy is unnecessary and potentially meddlesome.
Combined laryngeal framework medialization and reinnervation for unilateral vocal fold paralysis. The laryngeal framework-Silastic implant technique has become an increasingly attractive alternative to Teflon injection, particularly when there is fixation of the cricoarytenoid joint or the defect to be corrected is larger than usual; but it does not restore ability to change tension in the vocal fold. Unilateral vocal fold reinnervation can overcome this drawback and, when used in conjunction with surgical medialization, may offer return of function very close to normal. Twenty-nine patients with unrecovered unilateral vocal fold paralysis and/or fixation of the cricoarytenoid joint have been managed by use of a Silastic implant combined with unilateral vocal fold reinnervation with no complications. Voice improvement has been assessed on preoperative and postoperative voice recordings. The combined surgical techniques for reinnervation and a modification of Silastic implantation via the laryngeal framework approach are reported.
Beneficial effect of 1,3-butanediol on cerebral energy metabolism and edema following brain embolization in rats. We assessed the effect of 1,3-butanediol on cerebral energy metabolism and edema after inducing multifocal brain infarcts in 108 rats by the intracarotid injection of 50-microns carbonized microspheres. An ethanol dimer that induces systemic ketosis, 25 mmol/kg i.p. butanediol was injected every 3 hours to produce a sustained increase in the plasma level of beta-hydroxybutyrate. Treatment significantly attenuated ischemia-induced metabolic changes by increasing the concentrations of phosphocreatine, adenosine triphosphate, and glycogen and by reducing the concentrations of pyruvate and lactate. Lactate concentration 2, 6, and 12 hours after embolization decreased by 13%, 44%, and 46%, respectively. Brain water content increased from 78.63% in six unembolized rats to 80.93% in 12 saline-treated and 79.57% in seven butanediol-treated rats 12 hours after embolization. (p less than 0.05). The decrease in water content was associated with significant decreases in the concentrations of sodium and chloride. The antiedema effect of butanediol could not be explained by an osmotic mechanism since equimolar doses of urea or ethanol were ineffective. Our results support the hypothesis that the beneficial effect of butanediol is mediated through cerebral utilization of ketone bodies arising from butanediol metabolism, reducing the rate of glycolysis and the deleterious accumulation of lactic acid during ischemia.
Anatomy of anal sphincters and related structures in continent women studied with magnetic resonance imaging. Five anally continent nulliparas of reproductive age were studied with magnetic resonance imaging. The internal and external anal sphincters could be easily delineated, as could the intervening longitudinal musculature, puborectalis muscle, anococcygeal raphe, anorectal lumen, vagina, uterus, bladder, urethra, coccyx, and pubis. The shape of the sphincters was nearly cylindrical, with an anterior component averaging 18.3 mm thick and 28.0 mm long. Fifty-four percent of this anterior thickness was attributable to the internal sphincter. The anorectal angle varied considerably, with a mean of 86.8 +/- 19.1 degrees (range 60-112). The angle between the portion of the rectal lumen supported by the anococcygeal raphe, or levator plate, and the plane of the puborectalis muscle was consistent at 149.0 +/- 6.3 degrees (138-154). The finding of anterior anal sphincters with substantial thickness and length contrasts markedly with a view often pictured in the literature of a female anal sphincter that narrows anteriorly to half its posterior length and forms a small bundle of muscle rather than a broad band. Knowledge of these relationships is important in primary repair of obstetric sphincter lacerations as well as in surgical correction of anal incontinence.
The nature and course of olfactory deficits in Alzheimer's disease. OBJECTIVE: The aim of this study was to determine the specific nature and course of olfactory deficits in Alzheimer's disease. Previous studies had noted impaired odor identification, but there was no unanimity about the presence of odor detection deficits. METHOD: Odor identification was tested in 55 patients with Alzheimer's disease and 57 elderly control subjects by using the University of Pennsylvania Smell Identification Test. Odor detection was assessed in 46 subjects with Alzheimer's disease and 40 control subjects by using a forced-choice threshold test with geraniol as the odorant. RESULTS: Significant deficits in olfactory identification were present in subjects who were in the earliest stages of cognitive impairment, and these deficits increased as Alzheimer's disease progressed. There was some overlap in individual smell identification test scores between cognitively impaired patients and normal elderly subjects. On the other hand, odor detection deficits did not appear until Alzheimer's disease was relatively advanced. Smell identification test scores were correlated with Mini-Mental State scores, but geraniol detection was not. CONCLUSIONS: Odor identification is impaired early in Alzheimer's disease and may be more influenced by cognitive status than is acuity of odor detection, which is not altered until later in the disorder. The pattern of hyposmia in Alzheimer's disease suggests that the disorder may not "begin in the nose," as has been theorized previously. Further refinement of olfactory testing may be useful in the diagnostic evaluation of early dementia.
Comparison between perindopril and nifedipine in hypertensive and normotensive diabetic patients with microalbuminuria. Melbourne Diabetic Nephropathy Study Group OBJECTIVE--To compare the efficacy of angiotensin converting enzyme inhibition with calcium antagonism in diabetic patients with microalbuminuria. DESIGN--Randomised study of diabetic patients with microalbuminuria treated with perindopril or nifedipine for 12 months and monitored for one or three months after stopping treatment depending on whether they were hypertensive or normotensive. Patients were randomised separately according to whether they were hypertensive or normotensive. SETTING--Diabetic clinics in three university teaching hospitals. PATIENTS--50 diabetic patients with persistent microalbuminuria. In all, 43 completed the study: 30 were normotensive and 13 hypertensive; 19 had type I diabetes and 24 had type II diabetes. INTERVENTIONS--For 12 months 20 patients were given perindopril 2-8 mg daily and 23 were given nifedipine 20-80 mg daily. MAIN OUTCOME MEASURES--Albumin excretion rate, blood pressure, and glomerular filtration rate. RESULTS--Both perindopril and nifedipine significantly reduced mean blood pressure. During treatment there was no significant difference between those treated with perindopril and those treated with nifedipine with respect to albuminuria or mean blood pressure. Stopping treatment with both drugs was associated with a sustained increase in albuminuria and mean blood pressure. There was a significant correlation between mean blood pressure and albuminuria and also between the reduction in mean blood pressure and the decrease in albuminuria during treatment with both drugs. In hypertensive patients both drugs caused significant decreases in mean blood pressure and albuminuria. In normotensive patients there was no significant reduction in albuminuria with either regimen. CONCLUSIONS--In diabetic patients with microalbuminuria blood pressure seems to be an important determinant of urinary albumin excretion. Perindopril and nifedipine have similar effects on urinary albumin excretion, both preventing increases in albuminuria in normotensive patients and decreasing albuminuria in hypertensive patients.
Acetazolamide-responsive vestibulocerebellar syndrome: clinical and oculographic features. Five patients who presented with long-standing episodic vertigo had ocular motor signs localizing to the vestibulocerebellum. In each patient, the episodic vertigo was either abolished or markedly decreased in frequency and severity with acetazolamide therapy. In 4, other family members had identical symptoms and signs. This syndrome is 1 of the few treatable causes of chronic episodic vertigo.
Opiates suppress carrageenan-induced edema and hyperthermia at doses that inhibit hyperalgesia. This study determined whether opiates alter vascular components of inflammation (hyperthermia, edema and plasma extravasation) in addition to the suppression of hyperalgesia. Rats were administered carrageenan into one hind paw and saline into the other hind paw, followed by i.p. injection of morphine (0.2-5.0 mg/kg) or saline at 60 min, and testing at 90 min after hind paw injections. Morphine produced a dose-dependent reduction in carrageenan-induced hyperalgesia (17-53%), hyperthermia (39-53%) and edema (24-36%). Morphine treatment did not alter the temperatures of the contralateral saline-injected paws, indicating that opiate suppression of hyperthermia was not confounded by alterations in systemic body temperature or blood flow. The opiate effects on inflammation were stereospecific since levorphanol (1 mg/kg), but not dextrorphan (1 mg/kg), suppressed carrageenan-evoked hyperalgesia, hyperthermia and edema. Pre-treatment with naltrexone (1.5 mg/kg) blocked the effects of a 5 mg/kg dose of morphine sulfate on hyperalgesia, hyperthermia and edema. In a separate study, i.v. injection of morphine sulfate (2 mg/kg) reduced plasma extravasation by 41% (P less than 0.01). Morphine administration resulted in significantly greater increases in paw withdrawal latencies in the inflamed (38-139%) than the contralateral, saline-treated paws (4-19%). The results indicate that opiates exert a moderate, though significant, reduction in the vascular signs of inflammation in addition to their reduction of hyperalgesia. The mechanisms for this vascular effect involve inhibition of both vasodilation (as indicated by a decrease in hyperthermia) and inhibition of vascular permeability. In addition, opiates exhibit enhanced antinociceptive effects in inflamed paws, even when compared to uninjured paws in the same animal.
Dopamine and high-dose insulin infusion (glucose-insulin-potassium) after a cardiac operation: effects on myocardial metabolism. Myocardial insulin resistance, in association with surgical stress, restricts the availability of carbohydrates and increases the load of free fatty acids (FFAs) on the heart. On theoretical grounds adrenergic drugs may be expected to aggravate this situation, whereas the opposite is expected from insulin. The influence of dopamine and a combination of dopamine (7 micrograms/kg body weight/min) and high-dose insulin (7 IU/kg) on myocardial energy metabolism was studied in 19 patients 4 to 6 hours after a coronary operation. Infusion of dopamine (7 micrograms/kg body weight/min) induced metabolic changes that may be unfavorable to the strained myocardium. There was an increase of the myocardial FFA load and a rise in myocardial oxygen expenditure by 60% to 70%. There changes were, however, not matched by an increase in myocardial substrate uptake. "Oxygen wastage" of FFA metabolism at high circulating catecholamine levels is suggested. There were also signs suggesting an amplified systemic trauma response: systemic oxygen consumption increased by 15%, and an increase in the arterial levels of FFAs, glucose, and ketones was observed. Divergent metabolic effects of dopamine and insulin were demonstrated. The most prominent metabolic effects of adding high-dose insulin to dopamine were a marked reduction of arterial FFA levels and a shift toward myocardial carbohydrate utilization at the expense of FFAs. Myocardial uptake of FFAs ceased. Myocardial insulin resistance may thus to a significant extent be overcome by supraphysiological doses of insulin, even during infusion of adrenergic drugs.
Learning disabilities in epilepsy: neurophysiological aspects. Subclinical generalized spike-wave discharges are often accompanied by transitory cognitive impairment, demonstrable by psychological testing during EEG recording. Transitory cognitive impairment is demonstrated most readily by difficult tasks and during generalized regular spike-wave bursts lasting for more than 3 s, but can also be found during briefer and even focal discharges. That this is not simply a consequence of global inattention is shown by the fact that focal discharges exhibit some specificity: left-sided focal spiking is more likely to produce errors on verbal tasks, for instance, whereas right-sided discharges are more often accompanied by impairment in handling nonverbal material. Both learning difficulties in general and specific abnormal patterns of cognitive functioning are well documented in children with epilepsy and are most pronounced in those with frequent interictal discharges. However, there is now evidence that intermittent cognitive impairment due to the discharges themselves contributes significantly to such neurophysiological abnormalities. The significance of transitory cognitive impairment accompanying subclinical EEG discharges for everyday functioning is uncertain, but there is experimental evidence that subclinical discharges may be accompanied by disruption of educational skills in children or by impairment of driving performance in motorists. In some individuals, suppression of discharges by antiepileptic drugs has demonstrably improved psychological function, but further work is required to determine the indications for such treatment.