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Biomedical subjects

S Y Chou

Publications and source records attributed to S Y Chou.

At least 37 records · Page 2Linked to original sources

Prevalence of antibodies to hepatitis C virus in patients with nonalcoholic fatty liver.

BACKGROUND: Nonalcoholic fatty liver can be caused by obesity, diabetes mellitus, hyperlipidemia or nonalcoholic steatohepatitis. Hepatitis C viral infection can also cause macrovesicular steatosis and such inflammation of the liver as nonalcoholic steatohepatitis. To determine whether the prevalence of anti-HCV is higher in patients with nonalcoholic fatty liver, this clinical study was undertaken; we also tried to detect which factors predict the presence of anti-HCV in these patients. METHODS: The study included 205 nonalcoholic fatty liver patients (122 males and 83 females) with a mean age of 46.5 years, diagnosed by ultrasonic examination, on whom anti-HCV antibody tests were then done. RESULTS: Eleven cases (5.4%) were anti-HCV positive with a higher mean age of 56.4 +/- 11.1 years (p < 0.05). Anti-HCV positive patients had higher serum AST and ALT levels than negative patients (95 +/- 59 U/L, 166 +/- 116 U/L vs. 34 +/- 26 U/L, 51 +/- 43 U/L; p < 0.05), while anti-HCV negative patients had higher mean body weight (124 +/- 15% vs. 114 +/- 11% of IBW) and serum cholesterol levels (202 +/- 41 mg/dl vs. 159 +/- 45 mg/dl). There was no statistical difference between anti-HCV positive and negative groups in clinical parameters including gender, presence of HBsAg, history of DM, operation, blood transfusion, oral contraceptive usage, and cancer with or without chemotherapy. The prevalence of anti-HCV increased with age from 1.8% in the fourth and fifth decades to 25% in the eighth decade. The prevalence of anti-HCV was 1.4% (1 case) in 72 fatty liver with normal biochemical tests and 7.5% (10 cases) in 133 cases with abnormal biochemical tests, a difference which was statistically marginally significant (p = 0.055). Those with ALT levels greater than three-fold the normal limit had a significantly higher anti-HCV prevalence rate (25.9%) than those with normal (1.4%) or mildly (2.8%) elevated ALT levels (p < 0.001). Logistic regression analysis revealed that only age and serum ALT levels were independent predictive factors for the presence of HCV infection. CONCLUSIONS: Results revealed that the prevalence of anti-HCV in patients with nonalcoholic fatty liver was 5.4%, slightly higher than in the general population. Age and serum ALT level were the predictive factors for the presence of HCV infection.

Adult↗

Renal hemodynamics in acute unilateral ureteral obstruction: contribution of endothelium-derived relaxing factor.

The increase in ureteral pressure after acute unilateral ureteral obstruction (UUO) is associated with an initial increase in renal blood flow (RBF). The present study examines the role of nitric oxide, a major endothelium-derived relaxing factor (EDRF), in UUO-induced renal hyperemia in anesthetized dogs. In Group 1, vehicle solution was infused into the left renal artery. In Group 2, nitric oxide formation from L-arginine was competitively inhibited by intrarenal infusion of N omega-monomethyl-L-arginine (L-NMMA) (50 micrograms/kg./min.) before UUO. In Group 3, L-arginine (2 mg./kg./min.) was infused together with L-NMMA (50 micrograms/kg./min.) into the renal artery. After UUO, ureteral pressure increased in all groups, averaging 69 mm.Hg. In Group 1, RBF at 10 and 20 minutes after UUO increased 7.9 +/- 1.6% and 16.5 +/- 5.2%, respectively, significantly greater than in Group 2 (1.2 +/- 1.6% and 2.4 +/- 1.5%). After L-NMMA was discontinued in Group 2, RBF increased 17%, reaching a level similar to that in Group 1. In Group 3, L-arginine infusion abolished the effects of L-NMMA, and RBF was similar to that in Group 1 at all postobstructive intervals. Our data indicate that release of nitric oxide in the kidney is augmented by UUO and mediates the early renal hyperemia induced by UUO.

Acute Disease↗

Evidence that inactive p42 mitogen-activated protein kinase and inactive Rsk exist as a heterodimer in vivo.

Mitogen-activated protein kinases (MAP kinases) are active only when phosphorylated. Here we examine whether the activation of Xenopus p42 MAP kinase might involve changes in its association with other proteins as well as changes in its phosphorylation state. We find that when p42 MAP kinase is phosphorylated and active, it is monomeric, and that when p42 MAP kinase is nonphosphorylated and inactive, about half of it is monomeric and half is a component of a 110-kDa complex. We identify Rsk, an 82-kDa protein kinase that can be phosphorylated and partially activated by p42 MAP kinase, as being specifically associated with inactive p42 MAP kinase. It is possible that the complex of inactive p42 MAP kinase and inactive Rsk acts as a single signal reception particle and that the activation of the two kinases may be better described as a fork in a bifurcating signal transduction pathway than as successive levels in a kinase cascade.

Animals↗

Occupational hand dermatoses of hairdressers in Tainan City.

OBJECTIVES: To determine the prevalence, clinical features, and patterns of hand dermatosis in hairdressers in Tainan, Taiwan, and to examine the associations between patterns of dermatosis and risk factors such as job description, work exposure, and sensitisation to common allergens. METHODS: Interviews, examinations, and patch tests of the hairdressers from nine hairdressing stores randomly selected from Tainan City. Patch test agents included 41 substances with common allergens, shampoo preservatives, hair dyes, permanent waving and bleaching agents. RESULTS: 98 hairdressers finished the examination, 83% of them had occupational dermatosis and 32% had scissor induced scars or wounds. Most of the dermatoses belonged to either dry metacarpophalangeal dermatitis or eczema of the fingers. 44% of the hairdressers showed positive skin reaction to one or more patch test agents. The patch test results were different from previous reports in that the most common allergens were nickel, thimerosal, Captan, Kathon CG, and fragrance mix, and that the sensitivity to hair dye and permanent wave ingredients were low. The dry metacarpophalangeal dermatitis was associated with exposure to shampoo, and the eczema of the fingers with skin sensitivity to patch test agents. CONCLUSION: Hairdressers in Tainan City had a high prevalence of dermatoses including traumatic wounds, and allergic and irritant contact dermatitis. The rates of sensitivity to some of the common sensitising agents were different from previous reports.

Adolescent↗

Spontaneous rupture of the liver associated with pregnancy: a report of two cases.

Spontaneous rupture of the liver associated with pregnancy is a rare and grave complication, usually occurring in preeclampsia or eclampsia. Two cases of ruptured subcapsular hematoma of the right liver during pregnancy are reported. The first case was a 19-year-old woman who had suffered from epigastralgia and absent fetal heart beat in the 32nd week of gestation. The second case was a 31-year-old female who complained of nausea and right upper quadrant pain in the 35th week of pregnancy. Both had preeclampsia, and developed shock with disseminated intravascular coagulation soon after admission. Both received surgery and were found to have ruptured hematoma over the right liver. Finally, the first patient died of renal failure, but the second survived because preoperative diagnosis had been exact. Greater suspicion, then awareness of diagnosis can lead to better timing of surgery and an improved prognosis for mother and child.

Adult↗

Inflammatory fibroid polyp of the jejunum causing intussusception: a case report.

Inflammatory fibroid polyp is a rare benign lesion of the gastrointestinal tract. This report concerns a 56-year-old female who presented with intermittent abdominal pain, vomiting and diarrhea; she had had partial intestinal obstruction over a period of two months. Plain abdomen showed dilatation of the small bowels. Abdominal echo revealed intussusception of the small intestine. During exploratory laparotomy a polypoid dumb-bell shaped polyp was noted as the leading point of the jejunojejunal intussusception, segmental resection of the jejunum was performed. Histological features of the polyp met the diagnosis of inflammatory fibroid polyp.

Female↗

Trimethoprim-sulfamethoxazole induces reversible hyperkalemia.

OBJECTIVE: To determine the effect of trimethoprimsulfamethoxazole (Tmp-Smx) on serum potassium concentration. DESIGN: Retrospective cohort study. SETTING: An urban teaching hospital. PATIENTS: Fifty-one persons hospitalized for symptomatic infection with human immunodeficiency virus (HIV). Twenty-five patients who were taking high-dose Tmp-Smx (trimethoprim 20 mg/kg per day; sulfamethoxazole, 100 mg/kg per day) for Pneumocystis carinii pneumonia were the study group. Twenty-six patients who had not received the drug were the control group. Patients who received potassium supplements, those taking medications known to alter potassium homeostasis or renal function, or those with a serum creatinine level more than 186 mumol/L were excluded. MEASUREMENTS AND MAIN RESULTS: Serum potassium concentration in the study group was 4.1 +/- 0.1 mmol/L (mean +/- SE) and increased by 1.1 mmol/L (Cl, 0.8 to 1.5 mmol/L) (P < 0.0001) 9.8 +/- 0.5 days after starting Tmp-Smx therapy. Patients followed longitudinally showed a progressive increase in serum potassium levels during therapy and a progressive decline after discontinuing Tmp-Smx. Blood urea nitrogen and serum creatinine levels increased mildly from 4.3 +/- 0.5 mmol/L and 85 +/- 6 mumol/L to 6.4 +/- 0.7 mmol/L and 113 +/- 8 mumol/L, respectively. The serum potassium level in the control group was 4.3 +/- 0.1 mmol/L and remained unchanged during hospitalization. CONCLUSIONS: High-dose Tmp-Smx therapy used for the treatment of P. carinii pneumonia in HIV-infected patients leads to an increase in the serum potassium concentration and may result in life-threatening hyperkalemia. Patients receiving high doses of Tmp-Smx require close monitoring of their serum potassium concentration, particularly 7 to 10 days after the start of therapy.

AIDS-Related Opportunistic Infections↗

The renal hemodynamic response to endothelin in chronic cyclosporine-treated dogs.

Use of the immunosuppressive agent cyclosporine A (CyA) is limited by its associated nephrotoxicity, characterized by an increase in renal vascular resistance (RVR) and reductions in renal blood flow (RBF) and glomerular filtration rate (GFR). The vascular endothelium produces vasoactive substances including endothelium derived relaxation factor (EDRF) and endothelin (ET), which modulate vascular tone. Since CyA has been shown to damage the endothelium, we examined the renal hemodynamic response to intrarenal ET infusion (4 micrograms./kg./minute) in chronic cyclosporine-treated dogs. Prior to ET infusion, CyA-treated dogs had a lower RBF and a greater RVR than normal dogs. In normal dogs, after ET infusion RVR increased from 30.24 +/- 0.64 to 44.60 +/- 1.66 mmHg./ml./minute (p < 0.001), RBF decreased from 4.26 +/- 0.28 to 2.90 +/- 0.30 ml./min./g. (p < 0.001) and GFR decreased from 50.20 +/- 5.90 to 36.50 +/- 7.90 ml. per minute (p < 0.001). In contrast, there was no change in RBF, GFR and RVR after intrarenal ET infusion in CyA-treated dogs. Prior to ET infusion, arterial plasma ET concentration was 5.0 +/- 1.1 pg./ml. in CyA-treated dogs, similar to 7.5 +/- 1.4 pg./ml. in normal dogs, and was not significantly altered in either group after intrarenal ET infusion. We conclude that ET may not contribute to the increased RVR in chronic cyclosporine nephrotoxicity, and suggest a vascular toxicity of CyA, rendering renal vessels unresponsive to the vasoconstrictive effect of ET.

Animals↗

Hyperkalemia with high-dose trimethoprim-sulfamethoxazole therapy.

In a patient with the acquired immunodeficiency syndrome, a progressive increase in the serum potassium concentration occurred with high-dose trimethoprim-sulfamethoxazole (TMP-SMX) therapy for Pneumocystis carinii pneumonia. In this patient, factors known to alter transcellular potassium shifts to induce hyperkalemia were not present. There was no evidence of glucocorticoid or mineralocorticoid insufficiency at the time of hyperkalemia, while the transtubular potassium gradient decreased. The hyperkalemia resolved spontaneously on discontinuation of TMP-SMX therapy, suggesting that this electrolyte abnormality is related to altered renal tubular secretion of potassium as a consequence of the high-dose TMP-SMX therapy.

AIDS-Related Opportunistic Infections↗

The stimulatory effect of insulin on diacylglycerol generation in adipocyte membranes from ob/ob mice is impaired by growth hormone.

Physiologically, the action of insulin on carbohydrate and lipid metabolism is opposed by several hormones, including glucocorticoids, glucagon, catecholamines, and pituitary GH. Perhaps least is known about the mechanism(s) involved in the antiinsulin action of GH. Since the generation of diacylglycerol (DAG) appears to be an early event in the insulin-signaling cascade, it was of interest to determine whether GH would interfere with this effect of insulin. Experiments were conducted to determine whether insulin would stimulate the generation of DAG in adipocytes of the obese (ob/ob) mouse, and whether this response could be blocked by the diabetogenic GH derivative S-carboxymethylated human GH (RCM-hGH). Isolated adipocytes of the ob/ob mouse were used for these studies, because unlike normal rodents, the ob/ob mouse responds predictably to the antiinsulin action of GH. Insulin produced a rapid biphasic increase in the amount of DAG in a crude membrane fraction of the adipocytes. The first peak in DAG mass occurred within 5 min of exposure of the cells to insulin, and the second peak occurred after 30 min. The first peak in DAG mass did not occur in adipocytes that had been incubated with pertussis toxin before exposure to insulin. Also, adipocytes isolated from ob/ob mice that had been treated with RCM-hGH failed to respond to insulin with an increase in DAG mass. RCM-hGH blocked both the first and second insulin-induced peaks in DAG mass within 6 h of its administration. This is the time at which ob/ob mouse adipocytes exhibit increased insulin resistance in response to RCM-hGH. Neither exposure to insulin nor treatment with RCM-hGH had any appreciable effect on the fatty acid composition of the DAG present in the adipocyte membranes. These findings are compatible with the idea that GH produces some defect in the insulin-signaling cascade that is proximal to the events that result in the generation of DAG in the adipocyte.

Adipose Tissue↗

The cellular and molecular regulation of 1,25(OH)2D3 production.

The synthesis of 1,25(OH)2D3 is a critical control point in the regulation of calcium metabolism, and possibly in the growth and differentiation of a number of cell types. This paper reviews our current understanding of the regulation of this process at the cellular and molecular levels, with the emphasis on the mechanisms of feedback control 1,25(OH)2D3 itself, control of parathyroid hormone, the roles of cyclic AMP dependent protein kinase and protein kinase C, and the interaction between the various intracellular regulators of 1,25(OH)2D3 production.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

Failure of atrial natriuretic peptide to induce natriuresis in aortocaval fistula dogs.

Creation of an aortocaval fistula (ACF) in dogs induces salt and water retention, activation of the renin-angiotensin and adrenergic nervous systems and renal papillary ischemia associated with high levels of circulating atrial natriuretic peptide (ANP). The effects of intrarenal ANP (1.2 micrograms/min) infusion on systemic and renal hemodynamics, renal excretory function, renal output of renin and norepinephrine (NE) and papillary plasma flow (PPF) were studied in both normal and ACF dogs. ANP did not alter systemic hemodynamics in either group, but led to a significant increase in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (V), sodium excretion (UNaV) and fractional excretion of sodium (FENa), and a significant decrease in renal vascular resistance (RVR) and urine osmolality (UOsm) in normal dogs. GFR, RBF, RVR, V, UNaV, FENa and UOsm remained unchanged, however, in ACF dogs. In ACF dogs, both renal renin and NE output were significantly greater during baseline and remained significantly greater following ANP infusion, associated with a significantly lower PPF compared with normal dogs. These data suggest that ACF dogs are resistant to the renal effects of ANP, which can neither mitigate the hormonal mediators of sodium retention nor reverse the papillary ischemia observed in this model.

Animals↗

Inhibition of c-Jun DNA binding by mitogen-activated protein kinase.

Here we demonstrate that partially purified Xenopus p42 mitogen-activated protein (MAP) kinase phosphorylates bacterially expressed human c-Jun at a single site, serine 243. Several lines of evidence argue that this phosphorylation is due to p42 MAP kinase itself rather than some contaminating species. Phosphorylation of serine 243 markedly decreases the binding of c-Jun to oligonucleotides containing the 12-O-tetradecanoylphorbol-13-acetate response element. These findings suggest that MAP kinase may play a role in the down-regulation of c-Jun or in the cycle of transcriptional initiation and elongation.

Amino Acid Sequence↗

Reversal of Na+ retention in chronic caval dogs by verapamil: contribution of medullary circulation.

The effects of verapamil on papillary plasma flow (PPF) and Na+ excretion were studied in anesthetized chronic caval dogs with low cardiac output and Na+ retention. Infusion of verapamil into the left renal artery (5 and 10 micrograms.kg-1.min-1) caused a dose-dependent ipsilateral increase in renal blood flow and Na+ excretion (from 10 +/- 2 to 171 +/- 32 and 225 +/- 35 mu eq/min, respectively). PPF in the left kidney was 26.6 +/- 4.4 and was significantly greater than that measured in the contralateral kidney (13.3 +/- 2.4 ml.min-1.100 g-1) (P < 0.01). The natriuresis occurred independent of changes in cardiac output and peripheral vascular resistance. In a separate group of caval dogs in which stimulation of the renin-angiotensin and adrenergic systems was intensified with a tighter caval constriction, verapamil failed to induce renal vasodilation or natriuresis and PPF was not altered. Despite the disparate hemodynamic responses, verapamil stimulated renal production of both renin and prostaglandin E2 in both groups of caval dogs. We conclude that the ability of verapamil to induce papillary vasodilation may contribute to the natriuresis seen in the caval dog, in which the site of Na+ retention includes the loop of Henle.

Animals↗

Growth hormone inhibits activation of phosphatidylinositol phospholipase C in adipose plasma membranes: evidence for a growth hormone-induced change in G protein function.

Pituitary growth hormone (GH) functions physiologically to oppose the actions of insulin on carbohydrate and lipid metabolism by interfering with metabolic events that occur after insulin binds to its receptor. Which postreceptor effects are involved is presently unknown. Recently, we found that insulin rapidly stimulates a phosphatidylinositol phospholipase C (PI-PLC) in adipose tissue of obese (ob/ob) mice and that this effect of insulin is blocked by treatment of the animals with S-carboxymethylated human GH (RCM-hGH), a derivative having mainly anti-insulin activity. The activation of this PI-PLC by insulin is also inhibited by pertussis toxin. Thus, this study was performed to examine whether the inhibitory effect of GH on the activation of this PI-PLC is exerted at the level of signal transmission by guanine nucleotide binding proteins (G proteins). We found that the nonhydrolyzable GTP analogue, guanosine 5'-[gamma-thio]triphosphate, stimulated basal PI-PLC activity in plasma membranes of adipose tissue of saline-treated ob/ob mice, but it did not stimulate the enzyme in adipose membranes from RCM-hGH-treated mice. Also, RCM-hGH treatment markedly inhibited pertussis toxin-catalyzed ADP ribosylation of G protein alpha subunits in the membranes, suggesting some modification of the G proteins by GH. Immunoblot analysis of adipose membranes from saline- and RCM-hGH-treated mice using antiserum AS/7 (anti-Gi1 alpha and anti-Gi2 alpha) or antiserum EC/2 (anti-Gi3 alpha) showed no difference in the amount of Gi alpha-like protein between the groups. These findings suggest that GH interferes with the ability of a putative Gi-like protein to mediate the activation of PI-PLC in adipose membranes without altering the expression of the G protein.

Adipose Tissue↗

Hemodynamic function in dogs with chronic obstructive jaundice: effects of radiocontrast medium.

Chronic obstruction of the biliary tract alters circulatory function. The effects of radiocontrast medium (iothalamate meglumine) on systemic and renal hemodynamics were studied in normal dogs and dogs with chronic common bile duct ligation (CBDL). After intravenous injection of radiocontrast, cardiac output and stroke volume were not altered in normal and CBDL dogs; arterial pressure was stable in normal dogs but decreased significantly in CBDL dogs and was accompanied by reduced systemic vascular resistance. In normal and CBDL dogs the renal hemodynamic responses to radiocontrast medium were characterized by initial vasoconstriction (independent of renal renin release) and later vasodilation. This vasodilatation in CBDL dogs was particularly striking as it occurred despite reduced renal perfusion pressure and the augmented renin-angiotensin system. Inhibition of prostaglandin synthesis with indomethacin in CBDL dogs abolished both the hypotensive and the renal vasodilator responses to radiocontrast medium. We conclude that enhanced prostaglandin activity contributes to the labile hemodynamic function noted in obstructive jaundice.

Animals↗

Renal medullary circulation: hormonal control.

It is now becoming apparent that the medullary circulation in the kidney can be regulated separately from overall renal blood flow. This characteristic of the medullary circulation plays an important role in the kidney's ability to excrete a dilute or concentrated urine in concert with changes in water and sodium transport in the distal nephron secondary to the action of vasopressin, prostaglandins, the renal nerves, and other hormones without significant other renal hemodynamic changes. There is strong evidence that renal autocoids such as angiotensin II and prostaglandins uniquely affect regional blood flow in the inner medulla because of the special structure and organization of the microvasculature in this region. There is also evidence that this regional blood flow is in part regulated by circulating hormones, such as vasopressin and atrial natriuretic peptide, which are released in response to changes in extracellular fluid volume or osmolality. In addition, data are emerging to suggest that the kallikrein-kinin system, acetylcholine, the renal nerves and adenosine participate in this regulation. In addition to the role of the medullary circulation in the urinary concentrating operation, there are data to suggest that the medullary circulation either directly (by changes in physical forces) or indirectly (by regulating medullary toxicity) may influence sodium excretion in a variety of conditions. In this regard, activation of the renin-angiotensin system locally reduces blood flow in the papilla which may be necessary before sodium retention is fully expressed in salt retaining states. Future research looking at the microvasculature of the medulla and papilla and those factors that control the contractility of these vessels are necessary before a clearer picture emerges. Nevertheless, from the data already available it seems reasonable to suggest that the medullary circulation may be as important to kidney function during physiological and pathophysiological states as is the cortical circulation.

Acetylcholine↗

Renal actions of endothelin: interaction with prostacyclin.

The renal actions of endothelin were examined by infusing it intrarenally in anesthetized dogs at 4 ng.min-1.kg-1 without affecting arterial blood pressure or cardiac output. Endothelin infusion caused a transient and significant increase in renal blood flow (RBF) by 13 +/- 2%, followed by large decreases in RBF and glomerular filtration rate (GFR; by 26 +/- 2 and 23 +/- 7%, respectively) but did not alter urine flow rate or absolute sodium excretion. After endothelin infusion, renal venous and arterial plasma 6-ketoprostaglandin F1 alpha increased from 250 +/- 58 and 117 +/- 31 to 1,044 +/- 249 and 617 +/- 211 pg/ml, respectively, and its renal output increased from 339 +/- 99 to 963 +/- 202 pg.min-1.g-1 (P less than 0.01 for all). The renal prostacyclin synthesis was augmented by endothelin without stimulating the renal renin release or norepinephrine output. Inhibition of prostaglandin synthesis with indomethacin partially prevented the early renal vasodilation induced by endothelin, which then caused a more pronounced decline in RBF and GFR (by 65 +/- 7 and 54 +/- 8%, respectively). With suppression of prostacyclin synthesis, inhibition of renin release by endothelin was observed. Thus the vasoconstrictive effects of endothelin on renal hemodynamics are significantly modified by its ability to enhance production of vasodilators, including prostacyclin.

6-Ketoprostaglandin F1 alpha↗