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T B Reynolds

Publications and source records attributed to T B Reynolds.

At least 19 recordsLinked to original sources

Bakers' yeast, a model for fungal biofilm formation.

Biofilms are formed by the aggregation of microorganisms into multicellular structures that adhere to surfaces. Here we show that bakers' yeast Saccharomyces cerevisiae can initiate biofilm formation. When grown in low-glucose medium, the yeast cells adhered avidly to a number of plastic surfaces. On semi-solid (0.3% agar) medium they formed "mats": complex multicellular structures composed of yeast-form cells. Both attachment to plastic and mat formation require Flo11p, a member of a large family of fungal cell surface glycoproteins involved in adherence. The ability to study biofilm formation in a tractable genetic system may facilitate the identification of new targets for antifungal therapy.

Agar↗

Hyperfibrinolytic activity in hospitalized cirrhotic patients in a referral liver unit.

OBJECTIVE: Increased frequency of hyperfibrinolytic activity was reported in patients with cirrhosis. However, the incidence, clinical presentation, and the parameters related to hyperfibrinolysis remain largely unknown in these patients. By utilizing euglobulin lysis time (ELT) and other clinical coagulation tests, the present study investigated the incidence of and clinical parameters related to hyperfibrinolytic activity, and assessed predicting factors to epsilon-aminocaproic acid (EACA) treatment in cirrhotic patients with hyperfibrinolysis in a liver unit. METHODS: The study included 86 consecutive patients who were referred and admitted to a referral liver unit for various liver diseases. The mean age was 50.0 yr, with a male: female ratio of 60:26. Sixty-six patients (76.7%) were Hispanic and 75 (87.2%) were cirrhotic. The etiologies of liver diseases included alcoholic liver disease (n = 68, 79.1%), hepatitis B (n = 2, 2.3%), hepatitis C (n = 6, 7.0%), autoimmune hepatitis (n = 3, 3.5%), cryptogenic liver disease (n = 4, 4.7%), and hepatocellular carcinoma (n = 3, 3.5%). Coagulation studies included ELT, PT, PTT, fibrinogen, D-dimer, and fibrin degradation product levels. RESULTS: Hyperfibrinolytic activity as reflected by shortened ELT was present in 27/75 cirrhotic (31.3%) but 0/11 noncirrhotic patients, which was significantly correlated with higher Child-Pugh (C-P) class, abnormal levels of PT, PTT, fibrinogen, platelet count, and total bilirubin. Shortened ELT was more frequently seen in patients with hepatic decompensation and mucocutaneous bleeding, although these relationships were not statistically significant. In 27 patients with hyperfibrinolysis, five (18.5%) required EACA treatment for progressive mucocutaneous bleeding and/or hematoma. EACA treatment was significantly associated with higher C-P scores; greatly shortened ELT (< or =50% of normal value); and abnormal levels of fibrinogen, total bilirubin, and PT, indicating that these factors may serve as predictors for EACA treatment. CONCLUSION: Hyperfibrinolytic activity was seen in 31.3% of patients with cirrhosis, which is correlated with higher C-P scores; abnormal PT, PTT, fibrinogen level, and platelet count; and hyperbilirubinemia. Patients who received EACA treatment usually have a more severe hyperfibrinolytic activity as indicated by shortened ELT and low level of fibrinogen, and more severe liver disease as indicated by higher C-P scores and hyperbilirubinemia.

Aged↗

Ascites.

This article reviews the progress made during the last century in understanding and managing ascites. The list of known causes of ascites has lengthened considerably. There is improved understanding of the mechanism of ascites formation and the pathophysiology of the renal sodium retention that accompanies portal hypertensive ascites. Management of ascites has become substantially easier with the advent of new diuretics, and new procedures such as peritoneovenous shunting, transjugular intrahepatic portosystemic stent placement, and liver transplantation.

Ascites↗

Reversible peripartum liver failure: a new perspective on the diagnosis, treatment, and cause of acute fatty liver of pregnancy, based on 28 consecutive cases.

OBJECTIVE: We sought to describe our experience with the clinical diagnosis, management, and course of patients with acute fatty liver of pregnancy. STUDY DESIGN: Twenty-eight cases of acute fatty liver of pregnancy at the Los Angeles County and University of Southern California Medical Center from 1982 to June 1997 were identified, and presenting symptoms, clinical course, laboratory values, maternal complications, and neonatal outcomes were studied. RESULTS: The incidence of acute fatty liver of pregnancy was 1 in 6659 births. There were no maternal deaths. Initial presentation was at an average of 37 weeks of gestation with a characteristic prodrome of malaise, nausea, vomiting, and abdominal pain. No patient was admitted with the diagnosis of acute fatty liver of pregnancy. The condition was diagnosed most commonly on the second hospital day after laboratory results indicated coagulopathy, renal insufficiency, and liver function abnormalities. One patient underwent liver biopsy at cesarean delivery. Radiologic studies did not aid with the diagnosis. Twenty-one patients were admitted in spontaneous labor, and 16 labors were complicated by abnormal fetal heart rate patterns or meconium. There was 1 stillbirth and 1 neonatal death as a result of perinatal asphyxia. Maternal morbidity consisted of hypoglycemia, infection, renal insufficiency, coagulopathy, encephalopathy, and wound complications. All patients had evidence of disseminated intravascular coagulopathy with profoundly decreased antithrombin levels. All patients recovered normal liver function post partum. CONCLUSIONS: Reversible peripartum liver failure may be diagnosed and managed on the basis of clinical and laboratory criteria. With adequate support, these patients may have full recovery of hepatic function.

Acute Disease↗

The high osmolarity glycerol response (HOG) MAP kinase pathway controls localization of a yeast golgi glycosyltransferase.

The yeast alpha-1,3-mannosyltransferase (Mnn1p) is localized to the Golgi by independent transmembrane and lumenal domain signals. The lumenal domain is localized to the Golgi complex when expressed as a soluble form (Mnn1-s) by exchange of its transmembrane domain for a cleavable signal sequence (Graham, T. R., and V. A. Krasnov. 1995. Mol. Biol. Cell. 6:809-824). Mutants that failed to retain the lumenal domain in the Golgi complex, called lumenal domain retention (ldr) mutants, were isolated by screening mutagenized yeast colonies for those that secreted Mnn1-s. Two genes were identified by this screen, HOG1, a gene encoding a mitogen-activated protein kinase (MAPK) that functions in the high osmolarity glycerol (HOG) pathway, and LDR1. We have found that basal signaling through the HOG pathway is required to localize Mnn1-s to the Golgi in standard osmotic conditions. Mutations in HOG1 and LDR1 also perturb localization of intact Mnn1p, resulting in its loss from early Golgi compartments and a concomitant increase of Mnn1p in later Golgi compartments.

Calcium-Calmodulin-Dependent Protein Kinases↗

Nephrogenic ascites. Analysis of 16 cases and review of the literature.

Nephrogenic ascites is an entity that manifests as refractory ascites in patients with end-stage renal disease, where portal hypertensive, infectious, and malignant processes have been excluded. Most of these patients are undergoing hemodialysis. Hypoalbuminemia may predispose these uremic patients to ascites formation. The characteristics of the ascitic fluid suggest that the pathogenesis of the ascites is an alteration in peritoneal membrane permeability or impaired resorption due to peritoneal lymphatic channel obstruction. The ascitic fluid has a high protein content, low serum-ascites albumin gradient (SAAG), and low leukocyte count. Daily hemodialysis should be the initial therapy and is successful in one-third to three-fourths of patients within 3 weeks. Continuous ambulatory peritoneal dialysis or insertion of a peritoneovenous shunt are alternative treatments. Other therapies include instillation of intraperitoneal corticosteroids and binephrectomy, which have less predictable outcomes. Renal transplantation is the definitive treatment for nephrogenic ascites. Control of ascites reverses the progressive cachexia associated with uncontrolled disease, resulting in improved quality of life and survival approaching that of end-stage renal disease patients without ascites.

Adult↗

Transjugular intrahepatic portosystemic shunt: a successful treatment for hepatopulmonary syndrome.

Hepatopulmonary syndrome is a well described complication of chronic liver disease. Though uncommon, it carries a high morbidity and mortality. The pathogenesis of the syndrome has not been clearly defined. Portal hypertension seems to play a crucial role in the pathogenesis of the syndrome, probably by enhancing nitric oxide production. As yet, no pharmacological therapy has been proven effective. Many reports of successful reversal of the syndrome after liver transplantation have been published. We report a patient with hepatopulmonary syndrome who showed a significant and durable (4 months') improvement in his symptoms, arterial oxygenation, and intrapulmonary shunts, as calculated by radionuclide studies after transjugular intrahepatic portosystemic shunt placement. Transjugular intrahepatic portosystemic shunt may represent a durable treatment option for patients with hepatopulmonary syndrome.

Dilatation, Pathologic↗

Evaluation of pleural fluid in patients with cirrhosis.

Although fluid analysis usually is the first step toward identifying the cause of pleural effusion in patients with cirrhosis and ascites, there are no available data on the reliability of this approach, therefore, we retrospectively evaluated hematologic and biochemical parameters from pleural fluid analysis in 21 patients with hepatic hydrothorax (with proven peritoneal-pleural communication) and 6 patients with primary pleural disease (2 with tuberculosis, 3 with parapneumonic effusion, and 1 with empyema). The criteria developed by Light were diagnostic of pleural "exudate" in only one of six patients with primary pleural disease, concentrations of leukocytes, total protein (TP), albumin, and lactic dehydrogenase (LDH) in both fluids were measured and pleural fluid-to-ascites ratios of these measurements were calculated. Only ratio values for leukocytes and TP were higher in the group of patients with primary pleural disease compared with those with hepatic hydrothorax. Ratio values for leukocytes and TP overlapped between both groups during baseline conditions and during episodes of spontaneous bacterial peritonitis and pleuritis. We conclude that pleural fluid analysis has limited diagnostic efficacy in the patient with cirrhosis. Data collected by other methods--clinical and radiologic--should assist in arriving at the correct diagnosis.

Adult↗

Hyponatremia of cirrhosis: role of vasopressin and decreased 'effective' plasma volume.

BACKGROUND: The mechanism(s) of hyponatremia of cirrhosis is not completely clarified. Although increased vasopressin activity has been proposed in some studies, there have been reports disputing its role in the pathogenesis of profound hyponatremia in patients with decompensated liver disease. Methodologic flaws and lack of correlation with indices of circulatory dysfunction may have contributed to these discrepancies. The aims of the present study were to measure levels of vasopressin both in plasma and in urine and to correlate them with the volume-dependent hormonal systems of plasma renin activity (PRA) and atrial natriuretic factor (ANF). METHODS: Plasma vasopressin, ANF, and PRA were measured by radioimmunoassay in 19 patients with cirrhosis, ascites, and severe hyponatremia (mean serum sodium, 121.8 mmol/l) and 11 patients with cirrhosis and normal serum sodium (mean, 137.6 mmol/l). Vasopressin levels were also assessed by radioimmunoassay in urine. RESULTS: Patients with hyponatremia had higher plasma and urine vasopressin levels than patients with normal serum sodium concentrations (plasma, 2.9 versus 1.0 pg/ml, P = 0.0009; urine, 38.3 versus 12.3 ng/g creatinine, P = 0.0008). PRA was higher (4.8 versus 1.0 ng/ml/h, P = 0.0004) and plasma ANF lower (111.1 versus 148.7 pg/ml, P = 0.01) in patients with hyponatremia. CONCLUSIONS: These results indicate that plasma and urine vasopressin levels are inappropriately increased in patients with cirrhosis and severe hyponatremia. The concomitant increase of PRA and decrease of plasma ANF suggest that decreased 'effective' plasma volume generates nonosmotic stimuli for vasopressin hypersecretion in these patients.

Adult↗

Salmonella hepatitis: analysis of 27 cases and comparison with acute viral hepatitis.

The liver is commonly involved in patients with typhoid fever. However, severe hepatic derangement simulating acute viral hepatitis is rare. Our aim was to characterize the clinical picture, biochemical features, and prognosis of Salmonella hepatitis. Retrospective case-control analysis of medical records included 27 patients with Salmonella hepatitis and 27 inpatients with acute viral hepatitis from 1973 to 1993. Travel history, clinical picture, a standard battery of 18 biochemical tests, complete blood counts, disease complications, duration of hospital admission, and final outcome were analyzed. Eleven patients with Salmonella hepatitis (40%) travelled abroad within 1 month of illness. A greater proportion of Salmonella hepatitis patients developed fever > 104 degrees (44% vs. 4%, respectively; P < .0001), and had relative bradycardia (42% vs. 4%, respectively; P < .002) than viral hepatitis patients. Salmonella hepatitis was associated with lower peak serum alanine transaminase (ALT), aspartate transaminase, and higher peak serum alkaline phosphatase (296 vs. 3,234 U/L, 535 vs. 2,844 U/L, and 500 vs. 228 U/dL, respectively; P < .0001, <.0003, and <.004). The admission ALT/lactic dehydrogenase (LDH) ratio, when levels of both enzymes were expressed as multiples of upper limit of normal value for each, was significantly lower in Salmonella hepatitis. All Salmonella hepatitis cases had a ratio < 4, and all viral hepatitis cases had a ratio > 5, P < .0001. Left shift of white blood cells was more common in Salmonella hepatitis (83% vs. 37%; P < .004). Patients with Salmonella hepatitis had a longer hospitalization (14.8 vs. 6.5 days, respectively; P < .0001). All 54 patients survived their illness. The clinical picture of Salmonella hepatitis is frequently indistinguishable from viral hepatitis. The admission ALT/LDH ratio is the best discriminator between both entities. Other clues that raise the possibility of Salmonella hepatitis include high fever, relative bradycardia, and left shift of WBCs. Despite long hospitalization, Salmonella hepatitis responds to proper antibiotic therapy and has an excellent prognosis.

Acute Disease↗

Diagnostic features of tuberculous peritonitis in the absence and presence of chronic liver disease: a case control study.

PURPOSE: To determine diagnostic features of tuberculous peritonitis (TBP) in the absence and presence of chronic liver disease. PATIENTS AND METHODS: Thirty-four patients with TBP (13 without [Group I] and 21 with chronic liver disease [Group II] and 26 controls with cirrhosis and uninfected ascites (Group III) were studied. RESULTS: The clinical features in Groups I and II were similar and all patients had elevated ascitic fluid total mononuclear cell count. In Groups I, II, and III, respectively, ascitic fluid protein was > 25 g/L in 100% (13/13), 70% (14/20), and 0% (0/26); serum-ascites albumin gradient (SAAG) was > 11 g/L in 0% (0/13), 52% (11/21), and 96% (25/26), (0% [0/13], 71% [15/21], and 96% [25/26] after correction for serum globulin); and ascitic fluid lactate dehydrogenase (LDH) level was > 90 U/L in 100% (12/12), 84% (16/19), and 0% (0/20), respectively. In Groups I and II combined, ascitic fluid acid-fast stain was negative in all but Mycobacterium tuberculosis culture was positive in 45% (10/22); peritoneal nodules occurred in 94% (31/33), granulomas in 93% (28/30), and positive peritoneal M tuberculosis culture in 63% (10/16). CONCLUSIONS: In patients with suspected TBP, ascitic fluid protein of > 25 g/L, SAAG of < 11 g/L and LDH of > 90 U/L have high sensitivity for the disease. With coexistent chronic liver disease, a lower protein level and higher SAAG are usually not helpful but LDH > 90 U/L is a useful parameter for screening. Diagnosis is best confirmed by laparoscopy with peritoneal biopsy and M tuberculosis culture.

Aged↗

Selective management of hepatic adenomas.

Hepatic adenomas are uncommon hepatic neoplasms that may be identified after life-threatening hemorrhage, or as an incidental radiologic finding. The incidence of malignant transformation is unknown, and the correct treatment strategy is unclear. We examined our 10-year experience in the management of 12 patients with hepatic adenomas. Eleven adults (mean age of 37.6 years) and one 3-month-old were identified. Nine of 10 adult females (90%) were taking a hormonal preparation at the time of diagnosis. Four patients with tumor sizes of 1.0 to 4.0 cm were observed after cessation of oral contraceptives. Four patients with lesions of 5.5 to 13 cm underwent surgical resection. Three had malignant transformation, and two of the three had increased Alpha-fetoprotein levels. Four patients presented with acute hemorrhage and were treated initially by hepatic arterial embolization. We conclude that management of adenomas should be individualized based on their size and mode of presentation. Patients with lesions less than 5 cm and normal alpha-fetoprotein can be safely observed off oral contraceptives and followed by radiologic imaging. Lesions >5 cm should be considered for surgical resection due to the risk of malignancy. Hepatic arterial embolization is a new approach for acute hemorrhage.

Adenoma↗

Large bloody ascites in association with pelvic endometriosis: case report and literature review.

Endometriosis is only rarely the cause of massive bloody ascites. This entity simulates gynecological malignancy and is seldom recognized before surgical exploration of the abdomen. It is more commonly seen in black nulliparous females. Hormonal modulation has obviated the need for surgical resection, in some cases. We report a case of such an entity and review the medical literature.

Adult↗

Carbohydrate-deficient transferrin and false-positive results for alcohol abuse in primary biliary cirrhosis: differential diagnosis by detection of mitochondrial autoantibodies.

Primary biliary cirrhosis (PBC) is one of the few nonalcohol-induced liver pathologies that causes false positives in assays of carbohydrate-deficient transferrin (CDT) for diagnosing alcohol abuse. CDT was quantified by isoelectric focusing-immunoblotting-laser densitometry (IEF-IB-LD) analysis of serum from 117 women: 57 PBC patients, 20 alcohol abusers, and 40 healthy donors. Only 5% (3 of 57) of PBC patients were positive at the densitometric cutoff value chosen (> 90% specificity). Serum samples from 15 PBC patients were further evaluated by IEF-IB-LD and CDTect chromatography-RIA. Receiver-operating characteristic (ROC) analysis showed that IEF-IB-LD better discriminated between PBC and alcohol abuse than CDTect did. By ROC analysis, mitochondrial autoantibodies to pyruvate dehydrogenase antigen M2 detected by enzyme immunoassay yielded optimal test performance for diagnosing PBC. Of six patients falsely positive for CDT by CDTect, five (83%) tested M2-positive. Thus, abnormal CDT results should be further evaluated by mitochondrial antibody testing in patients with findings compatible with PBC.

Alcoholism↗

Serum lactic dehydrogenase in the differential diagnosis of acute hepatocellular injury.

Acute hepatocellular injury, whether due to viral hepatitis, hepatic ischemia, or drug hepatotoxicity, results in elevated levels of serum aminotransferases (AST and ALT). Serum lactate dehydrogenase (LD) is reported to be markedly elevated in ischemic hepatitis. Thus, comparisons of the degree of elevation of serum levels of LD, ALT, and AST may be helpful in the differential diagnosis of acute liver injury. To study this, we reviewed serum enzyme patterns early in the course of acute liver injury in patients with acute viral hepatitis A and B (n = 51), ischemic hepatitis (n = 20), and acetaminophen injury (n = 26). All patients had serum ALT and/or AST at least five times the upper limit of normal. For a given ALT and AST level, LD was higher in ischemic hepatitis and acetaminophen injury than in viral hepatitis. The mean ALT/LD ratio for acute viral hepatitis was 4.65, for ischemic hepatitis 0.87, and for acetaminophen injury 1.46. Mean ALT/LD ratio for viral hepatitis was significantly higher (p < 0.0001) than for the other two groups combined. An ALT/LD ratio of 1.5 differentiated acute viral hepatitis from ischemic hepatitis and acetaminophen injury with a sensitivity of 94% and a specificity of 84%.

Acetaminophen↗

Ultrasonographic diagnosis of acute alcoholic hepatitis 'pseudoparallel channel sign' of intrahepatic artery dilatation.

BACKGROUND: In an ultrasound pilot study of acute alcoholic hepatitis (AAH), parallel tubular structures within the liver subsegments were observed. Pulse-Doppler flowmetry revealed that these structures were formed by a dilated hepatic arterial branch and an adjacent portal venous branch. This finding was termed the "pseudoparallel channel sign" (PPCS). The aims of this study were to assess the significance of this sign and show the characteristic ultrasound findings of AAH. METHODS: PPCS was specifically searched for on ultrasonography by two physician operators in consecutive patients (77 AAH, 119 other alcoholic liver disease, 49 nonalcoholic liver disease, and 15 healthy patients). RESULTS: PPCS was observed in 90% of patients with AAH and in 23% of patients with other alcoholic liver disease. This sign was not detected in nonalcoholic liver disease or healthy patients. Biopsy specimens were available in 100 patients, 51 of whom were patients with alcoholism. In those 51 patients, PPCS gave a sensitivity of 82%, a specificity of 87%, and an accuracy of 84% in diagnosing AAH. Patients with criteria of AAH had more segments involved with PPCS than patients without. CONCLUSIONS: PPCS may be an important diagnostic finding in AAH.

Acute Disease↗

Hyperthyroidism and hepatic dysfunction. A case series analysis.

Liver dysfunction in hyperthyroid patients has not been well characterized. We analyzed the clinical records of 43 patients with hyperthyroidism to define the spectrum of clinical and liver test abnormalities. The patients were divided into three categories: (a) 18 patients with uncomplicated hyperthyroidism (HT) (b) 19 with hyperthyroidism and congestive heart failure (HT/CHF), and (c) 6 with hyperthyroidism and concomitant unrelated liver disease (HT/ULD). Hepatomegaly and/or spenomegaly were noted in 15 of 19 (79%) patients with HT/CHF as compared to 6 of 18 (33%) patients with HT and 3 of 6 (50%) patients with HT/ULD. Four patients with HT/CHF had ascites. Serum aminotransferase levels greater than 250 IU/L were noted in only 1 of 37 (3%) patients without unrelated liver disease. Patients with HT/ULD or HT/CHF had markedly low prothrombin time. Serum bilirubin levels as high as 323 microM were noted in patients with HT. No characteristic liver histology due to hyperthyroidism was noted. Severe liver test abnormalities, including deep jaundice and prolonged prothrombin time, can occur in patients with hyperthyroidism alone or with HT/CHF. This makes the diagnosis of concomitant, unrelated liver disease difficult until the hyperthyroidism has been controlled.

Adult↗