123rc/medical_text huggingface dataset:
Expression of laminin and its receptor LBP-32 in human and rat hepatoma cells. Dramatic cellular changes that occur during hepatocarcinogenesis are associated with major alterations in extracellular matrix formation and in the relationships between cells and their microenvironment. We have studied the expression of laminin, the major noncollagenous glycoprotein of basement membrane, and the laminin receptor 32 kD laminin-binding protein in two rat (Faza 967 and HTC) and two human (HepG2 and HBGC2) hepatoma cell lines that express a variety of liver-specific functions. Laminin was found in the rough endoplasmic reticulum of these cells when the indirect immunoperoxidase method and electron microscopic examination were used. Radiolabeled laminin, immunoprecipitated from both media and cell extracts, was resolved by electrophoresis on sodium dodecyl sulfate gel in two major polypeptides that comigrated with the A and B subunits from Engelbreth-Holm-Swarm tumor laminin. Immunoblot analysis showed that the Mr = 400,000 polypeptide did not correspond to the A subunit of laminin. Northern blot analyses demonstrated large amounts of B1 and B2 mRNAs but no A chain mRNA. We conclude that the tumor cells produce the laminin B chains only. In contrast, normal adult hepatocytes from either man or rat lacked laminin mRNAs, whereas in 1-day primary culture, B chain mRNAs became detectable. The steady-state level of 32 kD laminin-binding protein mRNA was 10-fold and threefold higher in rat hepatoma cells than in freshly isolated and 1-day cultured normal rat hepatocytes, respectively. In human hepatocytes, the steady-state levels of 32 kD laminin-binding protein mRNAs varied depending on the donor and never reached the level of the human hepatoma cells.
Insulin as a mitogenic factor: role in the pathogenesis of cardiovascular disease. Evidence has been accumulating that insulin has actions that may promote the development of atherosclerosis. Research has involved three broad areas: actions of insulin on cultured arterial cells, the effect of insulin on isolated artery preparations, and the development of lipid-containing lesions in the arteries of experimental animals. Insulin, in concentrations similar to those found in physiologic conditions, stimulates proliferation of cultured arterial smooth muscle cells from a number of species, including humans. Insulin also stimulates migration of smooth muscle cells. Cholesterol synthesis and low-density lipoprotein interaction with its receptor in smooth muscle cells are stimulated by insulin. Insulin's mitogenic action appears to be mediated by the insulin-like growth factor receptor. Endothelial cells cultured from large vessels are resistant to the actions of insulin, but hyperglycemia inhibits their proliferation. Insulin deficiency protects animals from experimental atherosclerosis; this protection is lost with insulin treatment. Insulin administration results in lipid-containing lesions in chickens and rats fed a normal diet, and in increased lipid synthesis in the arteries of pigs and dogs. Isolated artery preparations from insulin-deficient or insulin-treated animals undergo lipid metabolism at a rate that correlates with the insulin concentrations in the donor animals. The biological actions of insulin (and glucose) on arterial tissue suggest that hyperglycemia and hyperinsulinemia may promote the development of atherosclerosis.
AAEM case report #1: ulnar neuropathy at the elbow. A patient with bilateral cubital syndrome complicated by anomalous innervation is presented. The electrodiagnostic approach to patients with this neuropathy is reviewed emphasizing new developments. The interpretation of the findings in this patient centers around issues of pathophysiology and methodology.
Observations on the haemopoietic response to critical illness. Peripheral blood cytopenias are common in patients receiving intensive care, particularly in those with multiple organ failure. To assess the contribution of bone marrow hypoplasia in such patients 44 bone marrow samples from 24 patients under intensive care were studied by standard morphological techniques and by the granulocyte-macrophage colony forming cell (GM-CFC) assay. Frequently observed morphological abnormalities in the bone marrow included the following: (i) a reduction in overall cellularity in seven patients, with a progressive decrease in most patients studied sequentially; (ii) an increase in the number of actively phagocytic macrophages; and (iii) a disruption of normal bone marrow architecture with the accumulation of intercellular hyaluronic acid glycosaminoglycan. Mean GM-CFC growth was significantly reduced when compared with that in a group of normal controls. In four of five patients studied sequentially GM-CFC growth became subnormal in association with a reduction in bone marrow cellularity. Inhibitory serum factors were not identified. These morphological abnormalities are similar to the changes observed in gelatinous degeneration of the bone marrow. In both situations disruption of the haemopoietic microenvironment, with the accumulation of hyaluronic acid proteoglycan, may be an important factor in the inhibition of haemopoietic progenitor cell growth. The proliferation of macrophages, by the release of a variety of cytokines or reactive oxygen intermediates, may also be implicated in impaired haemopoiesis and the development of disordered erythropoiesis.
Clinical features and treatment of obstructive sleep apnea. OBJECTIVE: To review the clinical features and treatment of obstructive sleep apnea (OSA). DATA SOURCE AND SELECTION: All articles on OSA published in French and English between 1970 and 1990 and indexed in Index Medicus were reviewed. Studies addressing the epidemiologic features and clinical aspects of OSA were selected, and special emphasis was given to articles reporting the effects of treatment on morbidity and mortality rates. MAIN RESULTS: OSA is characterized by episodes of upper airway obstruction during sleep that result in repetitive hypoxemia and sleep disruption. OSA leads to various neuropsychologic and cardiovascular complications, including daytime hypersomnolence, cognitive impairment, systemic and pulmonary hypertension and cardiac arrhythmias. There is suggestive evidence that the death rate among affected people is increased. The true incidence of OSA is unknown, but estimates have varied from 1% upwards among men. The current treatment with the greatest overall effectiveness and acceptability is nasal continuous positive airway pressure. CONCLUSION: This common, readily treatable disorder is associated with serious complications and therefore must be widely recognized by health professionals.
Ultrasonography in patients with suspected acute appendicitis: a prospective study. The diagnostic accuracy of high-resolution real-time ultrasonography was prospectively studied in 240 patients admitted to the hospital with suspected acute appendicitis. The criteria for ultrasound diagnosis of appendicitis included a sausage-shaped, aperistaltic, hypoechoic structure when imaged along its longitudinal axis, with a target-like appearance on transverse section. The ultrasonographic findings were correlated with surgical-pathological outcome in 82 cases with proven appendicitis, with laparotomy findings in another 21 patients and with clinical follow-up in the remainder. The overall sensitivity, specificity and accuracy of ultrasonography in the diagnosis of acute appendicitis were 78%, 92% and 87%, respectively. The positive predictive value was 84% and the negative predictive value was 88%. Ultrasonography may significantly improve the diagnostic accuracy in patients with suspected acute appendicitis and should be performed in all patients in whom the clinical diagnosis is equivocal. The ultrasonographic findings must be interpreted in light of the clinical findings.
Endoscopic palliative intubation of the esophagus invaded by lung cancer. Thirty-two patients with esophageal involvement by lung cancer were managed by endoscopic intubation. In 22 patients with extrinsic esophageal strictures, the success rate of intubation was 91%, and 82% were discharged with their dysphagia relieved and esophageal patency restored. The mean survival rate was 4.4 months. In 10 patients with esophago-bronchial fistulas, 3 had the fistulous tract obliterated and lived a mean of 5 months. This low success rate of closing fistulas is due to failure to seal off the space between the stent and the fistula because of absence of tumor-associated stenosis. The overall morbidity rate was 28.1% (18.8% perforation, 6.3% hemorrhage, and 3.1% tracheal obstruction). The overall mortality rate was 18.8%. Although complications were more frequent than in primary esophageal tumors, endoscopic intubation was the only way to palliate this desperate condition and provided 66.6% of patients with relief of symptoms, nutritional improvement, and a mean survival time of 4.5 months.
Mucosal intussusception to avoid ascending cholangitis. Many methods have been devised to prevent ascending cholangitis following Kasai's hepatic portoenterostomy for biliary atresia. To investigate the effectiveness of mucosal intussusception in preventing ascending cholangitis, 20 mongrel dogs were randomized to undergo Roux-en-Y cholecystjejunostomy and common bile duct ligation with or without mucosal intussusception. Aeromonas hydrophila was instilled into the gastrointestinal tract. Bacterial cultures were grown from samples taken from the gallbladders and lower jejunum, and blood chemistry and barium studies were performed. The barium studies showed satisfactory lack of reflux in all ten dogs with mucosal intussusception. Only two of them had positive cultures for Aeromonas from the gallbladder 3 days after bacterial instillation into the jejunum. All ten dogs in the control group had positive cultures for Aeromonas from the gallbladder. Our results showed that the mucosal intussusception group had a significantly lower rate of recovery of organisms from the gallbladder compared with the control group when the organisms were instilled into distal intestine (P less than 0.05). The method is worthy of clinical trial as a means of preventing or treating ascending cholangitis.
Biphasic effects of doxorubicin on the calcium release channel from sarcoplasmic reticulum of cardiac muscle. To define the mechanism of doxorubicin cardiotoxicity, the effects of doxorubicin and caffeine were examined on calcium release channels from cardiac sarcoplasmic reticulum. We found that calcium release from cardiac sarcoplasmic reticulum vesicles was induced by both compounds. When sarcoplasmic reticulum vesicles were incorporated into planar lipid bilayers, calcium-permeable channels were observed. Addition of caffeine (2.5-10 mM) increased channel open probability from less than 0.1% to 40%, and this effect persisted for a mean of 44 minutes. In contrast, doxorubicin (2.5-10 microM) had a biphasic effect; initially, doxorubicin activated the channel, whereas after a mean of 8 minutes, the channel became irreversibly inhibited. Although the degree of channel activation by doxorubicin was concentration dependent, the time needed to inactivate the channel was concentration independent. Pretreatment with dithiothreitol (0.2 mM) prevented doxorubicin-induced channel inactivation, and channel activity persisted for an average of 58 minutes. Dithiothreitol alone did not alter channel open probability. Our results support the hypotheses that 1) the integrity of sulfhydryl groups is important for some aspects of calcium release channel function and 2) activation and inactivation of the channel are separable processes. The biphasic effect of doxorubicin on channel function may also correspond to the clinically observed adverse effects of doxorubicin, a widely used chemotherapeutic agent that, after prolonged usage, causes a dilated cardiomyopathy.
Mapping the distribution of amobarbital sodium in the intracarotid Wada test by use of Tc-99m HMPAO with SPECT. The intracarotid amobarbital sodium, or Wada, test has been used to localize speech and memory function prior to surgical treatment of temporal lobe seizures. The authors mixed technetium-99m hexamethyl-propyleneamine oxime (HMPAO) with amobarbital sodium and injected the mixture in 25 patients with epilepsy. Single photon emission computed tomography (SPECT) of the brain was then performed to determine intracerebral distribution of the amobarbital sodium. Results of SPECT were compared with those of conventional and digital subtraction angiography (DSA). The distribution of Tc-99m HMPAO and, presumably, amobarbital sodium varied from patient to patient. SPECT revealed a statistically different distribution from that predicted with conventional angiography. The distribution also often differed from that of DSA, although the difference was not significant. SPECT revealed infrequent delivery to mesial temporal lobe structures. This emphasizes the need for caution in the use of the intracarotid amobarbital sodium test to predict the outcome of removal of these areas.
Muscle fibre type and habitual snoring. Although anatomical abnormalities of the upper airway have been recorded in some patients with obstructive sleep apnoea (OSA), a muscle tone dysregulation also seems to have an important role in this disorder. Since habitual snoring is the initial stage of OSA, the structural characteristics of upper airway muscles (medium pharyngeal constrictor muscle [MPCM]) from 13 men (9 non-snorers and 4 habitual snorers) were studied. MPCM fibre structure in non-snorers was broadly similar to that in normal limb muscles, with the exception that fibre diameters were smaller for all fibre types. Compared with limb muscles, MPCM had a smaller proportion of type IIb fibres and a higher proportion of types I and IIa fibres. MPCM in habitual snorers had an abnormal distribution of fibre types (low percentage of type I and type IIb fibres and high percentage of type IIa fibres) compared with non-snorers (p less than 0.001) and the type IIa fibres were hypertrophic. No myopathic or neurogenic changes were seen. Two possible hypotheses explain the abnormal distribution of fibre types in snorers. First, a constitutionally determined reduction of slow alpha-motor neurons induces an adaptive transformation of type IIb to type IIa fibres and a hypertrophy of type IIa fibres; or, second, motor neurons change their patterns of discharge and, hence, of activation, and modify fibre-type distribution of MPCM as an adaptation to the anatomical characteristic of upper airway and habitual snoring.
Prognosis of Wilsonian chronic active hepatitis. Twenty of 320 patients with Wilson's disease initially presented with chemical and laboratory features of chronic active hepatitis, confirmed histologically in 17. When first seen, cirrhosis was present in all 20 and was complicated by ascites and/or jaundice in 11. Within 1 week to 8 years of the onset of over liver disease the diagnosis of Wilson's disease was established, and treatment with D-penicillamine was promptly initiated in 19 patients. One man refused treatment and died 4 months later. Treated patients received D-penicillamine or trientine for a total of 264 patient-years (median, 14 patient-years). Abnormal water retention, for which salt restriction and diuretics were added to penicillamine or trientine, disappeared in all but 1 of the patients so affected. Symptomatic improvement and virtually normal levels of serum albumin, bilirubin, aspartate aminotransferase, and alanine aminotransferase followed within 1 year in the majority of subjects. One woman died after 9 months of treatment. Two patients, who became noncompliant with the therapeutic regimen after 9 and 17 years of successful pharmacological treatment, required liver transplants. These results indicate that the prognosis of specifically treated Wilsonian chronic active hepatitis is very good in spite of the presence of cirrhosis.
Microalbuminuria in essential hypertension. Clinically apparent proteinuria in essential hypertension is associated with increased cardiovascular and total mortality and is an independent risk factor for cardiovascular and cerebrovascular disease. Subclinical elevation of urinary albumin excretion is seen more frequently than clinical proteinuria in essential hypertension and the levels of microalbuminuria (excretions of 30 to 300 mg/24 h) correlate with blood pressure. The increased urinary albumin excretion in hypertension may be explained by several factors such as renal hemodynamic changes, permselectivity changes of the glomerular filter, and structural arteriolar and glomerular changes due to nephrosclerosis. It has been clearly demonstrated that microalbuminuria is a risk factor for the development of clinical proteinuria, renal failure and increased cardiovascular mortality in insulin-dependent diabetes mellitus. It is still not known whether microalbuminuria also predicts development of proteinuria and decline in renal function in hypertension but there is some evidence indicating that microalbuminuria may be a marker of increased cardiovascular risk in hypertensives.
Childhood stroke after minor neck trauma: case report. Cerebral infarction after minor trauma to the neck has rarely been reported. A case is presented of a child with trauma to the vertebrobasilar artery resulting in stroke. Computerized tomography scan and angiography results are presented. Despite two subsequent, separate transient episodes of vertigo, the child had good functional recovery with complete restoration of language and cognitive function. After 28 months, residual impairments identified were a mild right-sided ataxia and hemiparesis.
Pancreatic duct abnormalities in gall stone disease: an endoscopic retrograde cholangiopancreatographic study. This study was carried out to assess pancreatic duct abnormalities in gall stone disease. Endoscopic retrograde cholangiopancreatograms of 50 patients with gall stone disease were analysed and the results compared with those obtained in 33 patients investigated for cholestatic jaundice who were found to have a normal biliary tree (control group). Abnormal pancreatograms were obtained in 24 (48%) patients with gall stone disease and in only two (6%) in the control group; the differences were statistically significant (chi 2 = 14.3; p less than 0.001). The patients in the control group showed mild abnormalities as did those in the gall stone group. The frequency of various abnormalities were: mild 16 (32%), moderate five (10%), and severe three (6%). Pancreatic duct abnormalities were more severe and occurred more frequently in patients with gall stones who had stones in the biliary tree than in patients with a normal biliary tree (postcholecystectomy patients, 55% v 25%) but the difference between the two groups just failed to be significant (chi 2 = 3.34). In conclusion, nearly half of all patients with gall stone disease have pancreatic duct abnormalities and in 16% these were severe enough to be labelled as chronic pancreatitis.
Apical hypertrophic cardiomyopathy in a non-Oriental man. Japanese investigators first described apical HCM in 2.9% of patients who had diagnostic left ventricular catheterization for suspected ischemic heart disease or cardiomyopathy. This entity was initially thought to be limited to individuals of Asian origin and has been uncommonly described in patients of Western origin. Patients of Western origin differ in several ways from those in the original description of Yamaguchi et al, but they both share the same classic criterion of hypertrophy of the left ventricular apex. The major differences probably relate to the anatomic variation in the distribution of the left ventricular hypertrophy as described by Maron et al. It is not known whether racial, genetic, or environmental factors account for the variation of disease expression in Asian and Western patients. Our case illustrates that this diagnosis should be considered in patients who have chest pain (anginal or atypical) and markedly abnormal findings on electrocardiograms in the absence of hypertension or significant coronary artery disease.
Clinical trials. A family physician's perspective. Primary care specialists diagnose and manage a wide variety of problems. Cancer is one relatively small part of the practice of these clinicians. Patients with newly diagnosed cancer usually are referred to surgical specialists. Primary care physicians often determine future events after surgical care. Oncologists may or may not be consulted depending on tumor type and past experiences of the physician, patient, and patient's family. Many primary care physicians think that chemotherapy regimens given empirically have little if any scientific evidence to support their use. Side effects of cancer treatment regimens often cause suffering and profoundly effect quality of life. There is a lack of communication between oncologists and primary care physicians. Dialogue between oncologists and primary care doctors may help solve communication problems. Clinical trials help determine which treatments are effective. Many clinical trials are conducted at the community hospital level. Most primary care physicians support clinical trials once they know about them. Education activities should be directed at promoting patient referral for participation in clinical trials.
Growth factor expression after stroke. Fibroblast growth factors are polypeptides with potent trophic effects on central nervous system cells. Both acidic and basic forms of fibroblast growth factor are found in the mammalian brain. We have examined the expression of these factors after focal brain injury or stroke. After infarction of the lateral cerebral cortex in the mature rat brain, we found a twofold to threefold increase during the first 3 weeks after stroke in levels of fibroblast growth factors in tissue surrounding infarcts. This increase persisted for at least 2 months and appeared mainly to be due to increased levels of basic, but not acidic, fibroblast growth factor. Because of its gliotrophic, angiogenic, and neuronotrophic properties, basic fibroblast growth factor may play an important role in the cascade of cellular reactions that contributes to wound healing and functional recovery after stroke.
The role of beta-blockade therapy for ventricular tachycardia induced with isoproterenol: a prospective analysis. Isoproterenol is sometimes required for ventricular tachycardia (VT) induction. However, the role of beta-blockade for treatment of such VT has not been critically assessed. The use of beta-blockade was evaluated prospectively in 14 consecutive patients who required isoproterenol 2.4 +/- 1.3 (+/- S.D.) micrograms/min to induce sustained monomorphic VT (greater than 30 seconds, or requiring termination due to hemodynamic collapse) after a negative baseline study. The VT mechanisms were enhanced automaticity (group A, six patients), triggered automaticity (group B, three patients), and reentry (group C, five patients). Groups A and B had serial intravenous electropharmacologic tests with propranolol alone (0.2 mg/kg), verapamil alone (0.15 mg/kg), and propranolol plus verapamil, and group C had serial tests with propranolol alone, procainamide or quinidine (class Ia drug) alone, and propranolol plus a class Ia drug until VT could no longer be induced. All six patients in group A responded to propranolol alone. In group B, one patient responded to verapamil alone, and two patients responded to propranolol plus verapamil. In group C, three patients responded to propranolol alone, one patient responded to a class Ia drug alone, and one patient responded to propranolol plus a class Ia drug. During a follow-up of 7 to 37 (17.9 +/- 10.7) (+/- S.D.) months, VT has not recurred in any patient. Three patients treated initially with propranolol alone have required substitution of amiodarone due to refractory congestive heart failure. In patients requiring isoproterenol for VT induction, beta-blockade alone appears to be effective in preventing reinduction of VT caused by enhanced automaticity. A heterogeneous response occurs when the VT mechanisms are triggered automaticity or reentry.