shukoor65/lab-rag-model huggingface dataset:
Can esmolol manage surgically-induced tachycardia? Bolus esmolol treatment of intra-operative tachycardia due to surgical stimulation. A double-blind, randomised study was conducted to examine the efficacy of a single bolus dose of esmolol in treating surgically-induced tachycardia. Anaesthetic technique was identical in all patients, and consisted of premedication with midazolam and glycopyrronium, induction with thiopentone followed by suxamethonium, tracheal intubation, and maintenance with isoflurane 0.6% (end-tidal) and 60% nitrous oxide in oxygen. Forty-eight patients developed a heart rate of greater than 95 beats/minute or 20% more than pre-induction values at an average time of 34 minutes after tracheal intubation and received placebo (15 patients), esmolol 50 mg (16 patients), or esmolol 100 mg (17 patients). Controlled intervention was instituted if heart rate or blood pressure was not adequate. Both 50 and 100 mg of esmolol resulted in lower heart rates compared to placebo (p less than 0.05), with no difference between the two esmolol groups (p greater than 0.05). Patients who received placebo had more episodes of medical intervention than those given esmolol (p less than 0.05). No adverse effects occurred in any patient.
Transient loss of consciousness: the value of the history for distinguishing seizure from syncope. We studied 94 consecutive patients (age 15 or over) to investigate which aspects of the history and clinical findings help to distinguish seizures from syncope and related conditions. Clonic movements or automatism observed by an eyewitness classified an event as a seizure. The seizure group consisted of 41 patients and the syncope group of 53 patients. The likelihood ratio was used to calculate the predictive power of single findings and logistic regression to analyse combinations of findings. The best discriminatory finding was orientation immediately after the event according to the eyewitness and the age of the patient in the absence of an eyewitness report (P less than 0.001). We found a seizure five times more likely than syncope if the patient was disoriented after the event and three times more likely if the patient was less than 45 years of age. Nausea or sweating before the event were useful to exclude a seizure. Incontinence and trauma were not discriminative findings.
Fc receptor function and circulating immune complexes in gluten sensitive enteropathy--possible significance of serum IgA. The capacity to clear IgG containing immune complexes from the circulation was studied in patients with coeliac disease (n = 13), dermatitis herpetiformis (n = 8), and coeliac disease with concomitant serum IgA deficiency (n = 4). A small group of patients with active ulcerative colitis (n = 4) was included as a bowel disease control group. Clearance was estimated by measuring the disappearance rate of a bolus dose of intravenously injected IgG coated autologous erythrocytes. The mean T1/2 of clearance was prolonged in both coeliac disease (86 (24) minutes) and dermatitis herpetiformis (111 (35) minutes), compared with healthy subjects (20 (5) minutes) and coeliac patients with concomitant serum IgA deficiency (T1/2 = 17 (6) minutes). Patients with ulcerative colitis had a prolonged clearance, with a T1/2 of 195 (63) minutes. Values of circulating immune complexes were measured by four assays; C1q binding and C3, IgG, and IgA containing immune complexes. C1q binding immune complexes were detected only in IgA deficient gluten sensitive enteropathy. Patients with coeliac disease and dermatitis herpetiformis had higher values of C3, IgG, and IgA containing immune complexes than control subjects and serum IgA deficient patients with coeliac disease. The clearance rate was inversely correlated to the amount of immune complexes for the subgroups of gluten sensitive enteropathy.
Glandular excision in total glandular mastectomy and modified radical mastectomy: a comparison. Total glandular mastectomy and modified radical mastectomy were compared for the amount of breast tissue remaining after surgery. Multiple biopsies were taken from the anterior chest walls of women following total glandular mastectomy (N = 27) and modified radical mastectomy (N = 28) to try to detect any residual glandular tissue. Regardless of procedure performed, breast tissue was identified histologically in 5 percent of all biopsy specimens (159 and 161, respectively). One of every five operative fields was shown to have glandular elements in at least one of the biopsy sites; the positive biopsies did not form a discernible pattern. The residual breast tissue in each of these patients averaged less than 1 gm. On the basis of this study, modified radical mastectomy and total glandular mastectomy appear to be equally effective in removing most of the breast.
Extended aortic valvuloplasty: a new approach for the management of congenital valvar aortic stenosis. A new technique for the treatment of congenital valvar aortic stenosis is described. It consists of augmenting the aortic cusp by extending the commissurotomy incision into the aortic wall around the leaflet insertion, mobilizing the valve cusp attachment at the commissures, and freeing the aortic insertion of the rudimentary commissure. The results of standard valvotomy performed on 48 patients (group 1) were compared with those of the new extended valvuloplasty carried out on 16 patients (group 2). The two groups were comparable in age at operation (2.7 +/- 2.1 years for group 1 versus 2.1 +/- 1.7 years for group 2; p = not significant) and in preoperative pressure gradient (58 +/- 25 mm Hg for group 1 versus 61 +/- 36 mm Hg for group 2; p = not significant). There was no operative mortality in either group. Follow-up is available on all patients, with a mean of 4.3 +/- 2.6 years for group 1 versus 1.7 +/- 0.5 years for group 2 (p = 0.05). There was one late death in group 1. Postoperative gradient was 47 +/- 13 mm Hg in group 1 versus 19 +/- 13 mm Hg in group 2 (p = 0.05). Moderate or severe regurgitation was present in 18 patients (38%) in group 1 and 2 patients (13%) in group 2 (p = not significant). Reoperation was needed in 8 patients (17%) in group 1 versus 2 patients (13%) in group 2 (p = not significant). The described valvuloplasty procedure addresses the unique pathological features of valvar aortic stenosis and provides better relief of the obstruction than the presently available techniques. Longer follow-up is needed to determine the late results of this approach.
Cocaine and indomethacin: fetal anuria, neonatal edema, and gastrointestinal bleeding. A case is reported in which exposure to cocaine and indomethacin was associated with development of fetal anuria, anasarca, and neonatal gastrointestinal hemorrhage. Cocaine and indomethacin may act synergistically to adversely affect renal, cardiovascular, and platelet function. It may be prudent to obtain a drug history and urine screen for cocaine before instituting indomethacin therapy for preterm labor or polyhydramnios.
Pathologic and hemodynamic sequelae of unilobar biliary obstruction and associated liver atrophy. A patient is presented with unilobar biliary obstruction associated with marked liver atrophy and compensatory hypertrophy. Characteristically she was not jaundiced and had no portal hypertension. Quantitative measurements of the degree of hepatocyte hyperplasia showed that over 50% of cells in the hypertrophied lobe were hyperplastic. Surprisingly, a similar percentage of cells in the atrophied lobe were also hyperplastic. No difference was found in the size of hepatocytes between the two lobes or among the hepatocyte subpopulations in the atrophied lobe. The findings in this case suggest (1) lobar atrophy induces a hyperplastic response in more than one half of the cells of the contralateral lobe; (2) the development of atrophy consequent on biliary obstruction is likely the result of destruction of whole cells rather than cytoplasmic loss; (3) the development of a hyperplastic response within the atrophied lobe is a new finding and is consistent with the hormonal theory of hepatic regeneration; and (4) striking compensatory hypertrophy of the liver is associated with normal portal venous pressure.
Is reversal of left ventricular hypertrophy in hypertension beneficial? The left ventricle increases its mass and wall thickness in hypertension as a result of the progressive increase in hemodynamic overload offered by increasing arterial blood pressure and total peripheral resistance. However, evidence is increasing that nonhemodynamic factors may also be important in the development of left ventricular hypertrophy (LVH). This LVH resulting from hypertensive disease conveys an independent risk of premature cardiovascular morbidity and mortality. The specific mechanisms accounting for this increased risk are not known with assurance, although several mechanisms are under active study; they include more prominently ventricular dysrhythmias and myocardial ischemia. It is possible to diminish the increased left ventricular mass with pharmacological agents, although currently it is not known whether this reversal also diminishes the risk associated with LVH. Therefore, at the present time the best means for preventing the risk of LVH is to prevent its development in the first place, and this seems to be preventable through control of arterial blood pressure at the earliest stages of hypertension. Risk may also be diminished in patients with existing LVH who are receiving digitalis or diuretics or who have chronic fluid- and electrolyte-disturbing diseases. Under these circumstances, the careful use and selection of antihypertensive therapy and control of electrolyte balance no doubt will prevent unnecessary morbidity and mortality.
Psychological stress and susceptibility to the common cold BACKGROUND. It is not known whether psychological stress suppresses host resistance to infection. To investigate this issue, we prospectively studied the relation between psychological stress and the frequency of documented clinical colds among subjects intentionally exposed to respiratory viruses. METHODS. After completing questionnaires assessing degrees of psychological stress, 394 healthy subjects were given nasal drops containing one of five respiratory viruses (rhinovirus type 2, 9, or 14, respiratory syncytial virus, or coronavirus type 229E), and an additional 26 were given saline nasal drops. The subjects were then quarantined and monitored for the development of evidence of infection and symptoms. Clinical colds were defined as clinical symptoms in the presence of an infection verified by the isolation of virus or by an increase in the virus-specific antibody titer. RESULTS. The rates of both respiratory infection (P less than 0.005) and clinical colds (P less than 0.02) increased in a dose-response manner with increases in the degree of psychological stress. Infection rates ranged from approximately 74 percent to approximately 90 percent, according to levels of psychological stress, and the incidence of clinical colds ranged from approximately 27 percent to 47 percent. These effects were not altered when we controlled for age, sex, education, allergic status, weight, the season, the number of subjects housed together, the infectious status of subjects sharing the same housing, and virus-specific antibody status at base line (before challenge). Moreover, the associations observed were similar for all five challenge viruses. Several potential stress-illness mediators, including smoking, alcohol consumption, exercise, diet, quality of sleep, white-cell counts, and total immunoglobulin levels, did not explain the association between stress and illness. Similarly, controls for personality variables (self-esteem, personal control, and introversion-extraversion) failed to alter our findings. CONCLUSIONS. Psychological stress was associated in a dose-response manner with an increased risk of acute infectious respiratory illness, and this risk was attributable to increased rates of infection rather than to an increased frequency of symptoms after infection.
Chronic pain and substance abuse: a pilot study of opioid maintenance. Recent reports suggest that opioid maintenance may be appropriate for treatment-resistant patients with chronic nonmalignant pain syndromes. However, a history of substance abuse is thought to be a contraindication for such treatment. We present a pilot study of a methadone maintenance-type treatment for patients with both chronic pain and substance abuse, evaluating the ability to attract and hold patients, the methodology for assessing change, and the potential problems and pitfalls. Weekly random urinalysis, weekly psychotherapy, and quarterly self-report tests of pain, mood, and function were used to evaluate change. Three out of 4 patients remained in treatment for 19-21 months, stopped needle use, and/or markedly decreased substance abuse, and appear to have improved functionally. Surprisingly, all 3 patients had significant psychopathology requiring treatment with psychotropic medication. This treatment may warrant further research.
Ciprofloxacin: drug of choice in the treatment of malignant external otitis (MEO). Ciprofloxacin, a fluorinated quinolone with high efficacy against Pseudomonas aeruginosa, was used in the treatment of 10 consecutive patients with malignant external otitis. All patients had skull base osteomyelitis documented by nuclear and computed tomography (CT) scans. Dosages of 1.5 g of ciprofloxacin daily were used for a mean average of 10 weeks. All patients were considered cured with a minimum follow-up of 18 months after completion of therapy. A new classification of malignant external otitis (MEO) is presented.
Role of early fluid resuscitation in pediatric septic shock. OBJECTIVE. To examine the association of the volume of fluid administered at 1 and 6 hours after presentation, with survival and the occurrence of the adult respiratory distress syndrome, cardiogenic pulmonary edema, and persistent hypovolemia during the resuscitation of children with septic shock. SETTING AND PATIENTS. All pediatric patients with septic shock presenting to the emergency department over a 6-year period and having a pulmonary artery catheter inserted by 6 hours after presentation were identified. METHODS. Patients were analyzed together and in three groups based on fluid volume in the first hour: group 1, less than 20 mL/kg; group 2, 20 to 40 mL/kg; and group 3, more than 40 mL/kg. Adult respiratory distress syndrome was diagnosed by the presence of alveolar infiltrates, hypoxemia, and a pulmonary capillary wedge pressure of 15 mm Hg or less. Cardiogenic pulmonary edema was diagnosed similarly, except the pulmonary capillary wedge pressure was greater than 15 mm Hg. Hypovolemia was diagnosed by the presence of oliguria, hypotension, and a pulmonary capillary wedge pressure of 8 mm Hg or less 6 hours after presentation. RESULTS. We identified 34 patients (median age, 13.5 months). At 1 and 6 hours, respectively, group 1 (n = 14) received 11 +/- 6 and 71 +/- 29 mL/kg (mean +/- SD) of fluid; group 2 received 32 +/- 5 and 108 +/- 54 mL/kg of fluid; and group 3 received 69 +/- 19 and 117 +/- 29 mL/kg of fluid. Survival in group 3 (eight of nine patients) was significantly better than in group 1 (six of 14 patients) or group 2 (four of 11 patients). Adult respiratory distress syndrome developed in 11 patients (32%) and cardiogenic pulmonary edema developed in five patients (15%). Having adult respiratory distress syndrome was associated with increased mortality, but adult respiratory distress syndrome was not increased in any group. Similarly, cardiogenic pulmonary edema was not associated with the fluid volume received or with decreased survival. Hypovolemia occurred in six patients in group 1 and two patients in group 2; all eight subsequently died. CONCLUSION. Rapid fluid resuscitation in excess of 40 mL/kg in the first hour following emergency department presentation was associated with improved survival, decreased occurrence of persistent hypovolemia, and no increase in the risk of cardiogenic pulmonary edema or adult respiratory distress syndrome in this group of pediatric patients with septic shock.
Vigabatrin and psychosis. We report a series of 14 cases of psychosis occurring in patients with severe intractable epilepsy, following the prescription of vigabatrin, a new antiepileptic drug. Nine patients had no previous history of psychosis. In eight patients the psychosis occurred following a change in the habitual pattern of seizure activity; in four it developed after a period of seizure freedom followed by a cluster of seizures, and in the other four patients an alternating psychosis was observed. In five patients there was no clear relationship to seizure pattern. Another patient developed psychosis after taking an overdose of between eight and 12 g of vigabatrin. A further three patients, who developed psychosis following vigabatrin withdrawal, were not included in this series. The mean dose at onset of the psychosis (excluding the patient who took an overdose) was 2580 mg, and the period from initiation of therapy to the onset of psychosis varied from five days to 32 weeks (and occurred 24 hours after the overdose of vigabatrin). In all cases the psychosis resolved, but necessitated the withdrawal of vigabatrin, except in the single patient who took the overdose. The mechanism of this behaviour change is unclear, but in some instances may reflect vigabatrin's powerful anti-epileptic action. This is clearly not the case for all patients. Vigabatrin should be started with caution in patients with severe epilepsy, particularly in the presence of a previous history of psychosis, and such patients should be carefully monitored.
Peripheral adaptations in congestive heart failure: a review. In congestive heart failure, peripheral adaptive mechanisms play a significant and largely underestimated role. In acute heart failure, sympathetic-mediated peripheral vasoconstriction together with chronotropic and inotropic actions serves to maintain perfusion pressure and blood supply to the vital organs. In chronic heart failure, activation of the renin-angiotensin system increases peripheral vascular resistance and arterial tone and decreases arterial compliance and vasodilator capacity. Endothelium-mediated, flow-dependent vasodilation is reduced as a consequence of reduced blood flow. Deconditioning renders the blood vessels incapable of dilating in response to increased flow. Simultaneously, reduced blood flow and inactivity are induced by deconditioning, with functional and structural consequences within the skeletal muscle. Exercise performance is limited by reduced overall blood flow, reduced conductance of the feeding arteries, elevated tone of the resistance vessels, reduced vasodilator capacity, impaired dissipation of heat from the working muscle, and functional and structural changes of the skeletal muscle due to underperfusion and inactivity. The adaptive mechanisms operate at different time scales. Under therapeutic intervention, their reversibility also follows different time constants. Restoration of the vasodilator capacity of the large arteries and of the abnormalities of skeletal muscle in heart failure requires time. Vasodilation with reduced pre- and/or afterload will retard progression of the superimposed ventricular dilation and hypertrophy, and therefore retard the progress of the disease. However, restoration of the peripheral blood flow and of organ function will require time. Restoration of the vascular compliance and of the full amplitude of adaptive flow-dependent vasodilation in the large arteries requires weeks or months. Similarly, restoration of functionally and morphologically altered skeletal muscle can be expected to be reversible over a longer time period.
Cell-surface ganglioside GD2 in the immunohistochemical detection and differential diagnosis of neuroblastoma. The expression of the disialoganglioside GD2 was analyzed in 67 solid tumors and normal tissues from children by using the GD2-specific murine monoclonal antibody 3A7 and the indirect immunoperoxidase method. GD2 was expressed in all of 28 neuroblastomas and was most abundant in stroma-poor tumors. In differentiating stroma-rich neuroblastomas, neuroblastic clusters, neurofibrils, and most ganglion-like cells were positive, whereas Schwann's-cell stroma did not express GD2. In ganglioneuromas, only a few ganglion-like cells showed GD2, whereas all other structures were negative. Scattered foci of ganglioside GD2 also were found in some non-neuronal tumors, such as rhabdomyosarcomas and osteosarcomas, but not in lymphomas, Askin tumors, or most Wilms' tumors. The monoclonal antibody 3A7 is a useful aid in the immunohistochemical diagnosis of neuroblastoma. In addition, the intense cell surface staining of neuroblastoma cells by this reagent makes it potentially useful for detecting residual neuroblastoma in bone marrow samples and lymph node biopsies.
Objective antitumor activity of acivicin in patients with recurrent CNS malignancies: a Southwest Oncology Group trial. Acivicin (AT-125) is a glutamine antagonist with dose-limiting, schedule-dependent CNS toxicity and predictable CSF penetration after intravenous administration. Because of these properties, a trial in CNS malignancies was initiated. Thirty-two patients with recurrent or residual malignant astrocytomas were treated with AT-125. The majority of patients had glioblastoma multiforme (24) and had received prior nitrosoureas (21). The median age was 50 years, and Southwest Oncology Group (SWOG) performance status was 2. The major determinant of response was based upon radiologic criteria using computed tomographic (CT) scanning and/or magnetic resonance imaging (MRI) scans. The tumor mass was measured in two perpendicular planes, which yielded the largest cross-sectional area. Standard solid tumor criteria for response were used. All responding patients also had a stable or tapered dose of corticosteroids with stable or improved performance status and neurologic examination. There were four objective responses (12%): one complete remission (3 1/2+ years) and three partial remissions (57, 86, and 322 days). Two patients had improvement in disease that did not meet requirements for a partial remission. Toxicity was mild and primarily consisted of nausea, vomiting, and lethargy. Two patients were removed from study due to neurotoxicity (depression and hallucinations). The strict response criteria used in this trial were not those that have been used in testing other active agents such as carmustine (BCNU). We conclude that AT-125 has objective antitumor activity in malignant astrocytomas and warrants further study.
Lovastatin inhibits gallstone formation in the cholesterol-fed prairie dog. The efficacy of lovastatin, an inhibitor of hepatic cholesterol synthesis in the prevention of cholesterol gallstone formation, was evaluated in the prairie dog model. Two groups of animals were maintained on either nonlithogenic or 1.2% cholesterol-enriched chow for 21 days. Seven of the animals in each group received lovastatin, and the remaining six received only distilled water. All of the cholesterol-fed/water-treated animals had crystals and 83% had gallstones, but none of the cholesterol-fed/lovastatin-treated animals had gallstones and only three had microscopic crystals. These data indicate that lovastatin inhibits cholesterol gallstone formation in a diet-induced model of gallstone disease.