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Biomedical subjects

M L Wu

Publications and source records attributed to M L Wu.

At least 19 recordsLinked to original sources
PubMed2001

Arachidonic acid-induced H+ and Ca2+ increases in both the cytoplasm and nucleoplasm of rat cerebellar granule cells.

1. Arachidonic acid (AA) exerts multiple physiological and pathophysiological effects in the brain. By continuously measuring the intracellular pH (pH(i)) and Ca2+ levels ([Ca2+]i) in primary cultured rat cerebellar granule cells, we have found, for the first time, that 20 min treatment with 10 microM AA resulted in marked increases in Ca2+ and H+ levels in both the cytosol and nucleus. 2. A much higher concentration (40 mM) of another weak acid, propionic acid, was needed to induce a similar change in pH(i). The [Ca2+]i increase was probably caused by AA-induced activation of Ni2+-sensitive cationic channels, but did not involve NMDA channels or the Na+-Ca2+ exchanger. 3. AA-induced acidosis occurs by a different mechanism involving predominantly the passive diffusion of the un-ionized form of AA, rather than a protein carrier, as proposed by Kamp & Hamilton for fatty acids (FAs) in artificial phospholipid bilayers (the 'flip-flop' model). The following results, which are similar to those observed in lipid bilayers, support this conclusion: (1) FAs containing a -COOH group (AA, linoleic acid, alpha-linolenic acid, and docosahexaenoic acid) induced intracellular acidosis, whereas a FA with a -COOCH3 group (AA methyl ester) had little effect on pH(i), (2) a FA amine, tetradecylamine, induced intracellular alkalosis, and (3) the AA-/FA-induced pH(i) changes were reversed by bovine serum albumin. 4. Further evidence in support of a passive diffusion model, rather than a membrane protein carrier, is that: (1) there was a linear relationship between the initial rate of acid flux and the concentration of AA (2-100 microM), (2) acidosis was not inhibited by 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid, a potent inhibitor of the plasma membrane FA carrier protein, and (3) the involvement of most known H+-related membrane carriers and H+ conductance has been ruled out. 5. Since AA can be released under both physiological and pathophysiological conditions, the possible significance of the AA-evoked increases in H+ and Ca2+ in both the cytoplasm and nucleoplasm is discussed.

Acidosis↗
PubMed2001

Rhabdomyolysis: an unusual feature with mushroom poisoning.

Rhabdomyolysis resulting from mushroom poisoning previously has been unreported in the literature. We present an outbreak of Russula subnigricans poisoning with rhabdomyolysis. The most severely ill patient presented with rhabdomyolysis, severe electrolyte disturbance (hyperkalemia, hypocalcemia), respiratory failure, acute renal failure, pulmonary edema, ventricular tachycardia, and circulatory shock. Mycotoxin may be the cause of rhabdomyolysis. In areas where mushroom gathering is common, mushroom poisoning should be included in the differential diagnosis of rhabdomyolysis.

Female↗
PubMed2001

Food poisoning due to methamidophos-contaminated vegetables.

BACKGROUND: Organophosphate poisoning is well known for its characteristic symptoms and signs, but food poisoning caused by pesticide-contaminated food is seldom reported. CASE REPORT: We report three incidents of food poisoning that resulted from exposure to the organophosphate insecticide methamidophos in vegetables. These outbreaks caused a cholinergic syndrome in 4 patients. The cholinergic overactivity led as to suspect organophosphate food poisoning. All patients recovered well following appropriate therapy. The clinical diagnosis of organophosphate poisoning was confirmed by reduced levels of erythrocytes and plasma cholinesterase and the presence of methamidophos in the vegetable leftovers. The implicated vegetables and levels of methamidophos were: Ipomoea batatas 255 ppm, Gynura bicolor 110 ppm, and red cabbage 26.3 ppm. Since methamidophos is normally applied to vegetables during planting, improper selection and/or overuse of pesticide or improper harvest times may explain the occurrence of these high residue levels of methamidophos.

Adult↗
PubMed2001

Acute ethylene chlorohydrin poisoning: experience of a poison control center.

BACKGROUND: Ethylene chlorohydrin (CAS 107-07-3), a chemical once used in hastening grape vine sprouting in Taiwan, has caused severe toxicity upon acute exposure. Although such use of ethylene chlorohydrin is now prohibited in Taiwan, poisoning still occurs following its illegal use. Since data concerning human ethylene chlorohydrin poisoning remain rare, we report our experience in treating acute ethylene chlorohydrin-poisoned patients. METHODS: A retrospective analysis was conducted to evaluate patients with ethylene chlorohydrin poisoning reported to Taiwan Poison Control Center during 1985-1998. RESULTS: Seventeen patients with ethylene chlorohydrin poisoning were identified. There were 11 male and 6 female patients, ranging in age from 2 to 70 years (median 53 years). The intent of exposure was suicide in 5, accident in 9, and occupational exposure in 3 patients. Oral ingestion was the most common route of exposure (14 patients). Seven out of the 17 patients died within 24 hours due to metabolic acidosis and respiratory failure. Ethanol therapy, used in 2 patients, had no apparent benefit. Moderate or mild poisoning was characterized by gastrointestinal effects only and an uneventful recovery. CONCLUSIONS: Ethylene chlorohydrin can result in severe metabolic acidosis, respiratory failure, coma, and death after acute exposure.

Accidents↗
PubMed2001

Cholestatic hepatitis caused by acute gold potassium cyanide poisoning.

INTRODUCTION: Poisoning after oral ingestion of gold potassium cyanide is rarely reported. A case of suicidal ingestion of gold potassium cyanide (potassium dicyanoaurate; CAS# 13967-50-5) is described. CASE REPORT: A 27-year-old man attempted suicide by ingesting 5 mL gold potassium cyanide solution. He developed vomiting, hyperamylasemia, and hepatic dysfunction. Cyanide poisoning was not detected but acute gold toxicity was noted. Pathologic findings of the liver showed centrilobular cholestasis with eosinophilic degeneration. The whole blood and serum gold were 4361 and 6011 microg/L, respectively, and the 24-hour urine gold was 429 microg/d in samples obtained on day 4. CONCLUSION: Gold-induced hepatotoxicity has been seen infrequently in patients receiving gold therapy. Reported agents include sodium aurothiomalate, sodium aurothiopropranol sulfonate, aurothioglucose, aurothiopolypeptide (Auro-detoxin), auric sulfide, and gold thiosulfate, our report adds gold potassium cyanide.

Acute Disease↗
PubMed2001

Identification and characterization of the three chitin-binding domains within the multidomain chitinase Chi92 from Aeromonas hydrophila JP101.

The gene (chi92) encoding the extracellular chitinase of Aeromonas hydrophila JP101 has been cloned and expressed in Escherichia coli. The mature form of Chi92 is an 842-amino-acid (89.830-kDa) modular enzyme comprised of a family 18 catalytic domain, an unknown-function region (the A region), and three chitin-binding domains (ChBDs; Chi92-N, ChBD(CI), and ChBD(CII)). The C-terminally repeated ChBDs, ChBD(CI) and ChBD(CII), were grouped into family V of cellulose-binding domains on the basis of sequence homology. Chitin binding and enzyme activity studies with C-terminally truncated Chi92 derivatives lacking ChBDs demonstrated that the ChBDs are responsible for its adhesion to unprocessed and colloidal chitins. Further adsorption experiments with glutathione S-transferase (GST) fusion proteins (GST-CI and GST-CICII) demonstrated that a single ChBD (ChBD(CI)) could promote efficient chitin and cellulose binding. In contrast to the two C-terminal ChBDs, the Chi92-N domain is similar to ChiN of Serratia marcescens ChiA, which has been proposed to participate in chitin binding. A truncated derivative of Chi92 that contained only a catalytic domain and Chi92-N still exhibited insoluble-chitin-binding and hydrolytic activities. Thus, it appears that Chi92 contains Chi92-N as the third ChBD in addition to two ChBDs (ChBD(CI) and ChBD(CII)).

Aeromonas hydrophila↗
PubMed2001

Peculiar artifacts mimicking carcinoma.

Artifacts that mimic malignancy may lead to diagnostic difficulty and can cause serious consequences. We present 2 cases received in consultation which demonstrated peculiar artifacts that closely mimicked carcinoma. In case 1, contaminating products of conception were confused with squamous cell carcinoma. In case 2, artifactual signet ring cells induced by procedural trauma were suspicious for signet ring cell carcinoma. In both cases, clinical correlation failed to completely exclude carcinoma, and limited tissue prevented use of ancillary studies. Our final resolution of these artifacts required lengthy and detailed morphologic analysis.

Aged↗
PubMed2001

A case of jellyfish sting.

Jellyfish sting may result in a wide range of symptoms from common erythematous urticarial eruptions to the rare box-jelly induced acute respiratory failure. In Taiwan, with the increasing frequency of international travel, cases of jellyfish sting to foreigners are on the rise. We report a case of jellyfish sting with the rare presentation of painless contact dermatitis. A 38-y-o man accidentally stepped on a sea urchin with his right foot during scuba diving in a beach in Thailand. Traditional therapy with vinegar was applied on the lesion. However, when he returned to Taiwan, erythematous patches on the left thigh with linear radiations to the leg were discovered. The skin lesions had bizzare shapes and showed progressive change. No pain or numbness was noticed. Jellyfish stingwas suspected, topical medications were applied, and the patient recovered without complication. Jellyfish stings usually result in a painful erythematous eruption. In this case, though the lesion involved a large surface, there was no pain. Delayed diagnosis of jellyfish sting was due to the atypical presentation and the physician's unfamiliarity to the Thai jellyfish sting. Awareness to the wide spectrum of jellyfish sting symptoms should be promoted.

Adult↗
PubMed2000

Assessment of caspase activities in intact apoptotic thymocytes using cell-permeable fluorogenic caspase substrates.

To detect caspase activities in intact apoptotic cells at the single cell level, cell-permeable fluorogenic caspase substrates were synthesized incorporating the optimal peptide recognition motifs for caspases 1, 3/7, 6, 8, and 9. Caspase activities were then assessed at various times after in vitro treatment of mouse thymocytes with dexamethasone or anti-Fas antibody. Dexamethasone induced the following order of appearance of caspase activities as judged by flow cytometry: LEHDase, WEHDase, VEIDase, IETDase, and DEVDase. Since the relative order of caspases 3 (DEVDase) and 6 (VEIDase) in the cascade has been controversial, this caspase activation order was reexamined using confocal microscopy. The VEIDase activity appeared before DEVDase in every apoptotic cell treated with dexamethasone. In contrast, anti-Fas stimulation altered this sequence: IETDase was the first measurable caspase activity and DEVDase preceded VEIDase. In an attempt to determine the intracellular target of the potent antiapoptotic agent carbobenzoxy-valyl-alanyl-aspartyl(beta-methyl ester)-fluoromethyl ketone (Z-VAD[OMe]-FMK), we examined its ability to inhibit previously activated intracellular caspases. However, no significant reductions of these activities were observed. These fluorogenic caspase substrates allow direct observation of the caspase cascade in intact apoptotic cells, showing that the order of downstream caspase activation is dependent on the apoptotic stimulus.

Amino Acid Chloromethyl Ketones↗
PubMed2000

Possible mechanism(s) of arachidonic acid-induced intracellular acidosis in rat cardiac myocytes.

Arachidonic acid (AA) and other nonesterified fatty acids (FAs) have been shown to exert harmful effects during cardiac ischemia. By continuously measuring intracellular pH (pH(i)) changes in neonatal and adult cardiac myocytes, we have found, for the first time, that 10 micromol/L AA induces a substantial intracellular acidosis (0.3 to 0.4 pH units). We have ruled out the possibilities that the AA-induced acidosis is caused by (1) inhibition or stimulation of the pH(i) regulators, (2) protein kinase C activation or the generation of AA metabolites or free radicals, or (3) activation of NADPH oxidase or an inward H(+) current. The AA-induced acidosis fits to a simple diffusion mechanism, as proposed by Kamp and Hamilton (flip-flop model) for artificial phospholipid bilayers. The important properties found in the cardiac myocyte are that (1) the initial rate of acid flux (J(H)) increases with the AA concentration (2 to 50 micromol/L), (2) FAs with a (-)COOH group (eg, AA, oleic acid, and linoleic acid) induce intracellular acidification, but FAs with a (-)COOCH(3) group (eg, AA methyl ester) have little effect on the pH(i), (3) tetradecylamine (FA amine) induces intracellular alkalosis, and, most importantly, (4) both the AA- and tetradecylamine-induced pH(i) changes can be reversed by 0.3% BSA. Because a low concentration of AA (10 micromol/L) can induce a substantial acidosis, the possible involvement of the FA-evoked acidosis in the negative inotropic effect during cardiac ischemia is discussed. The full text of this article is available at http://www. circresaha.org.

Acidosis↗
PubMed2000

Identification of the indoleamine 2,3-dioxygenase nucleotide sequence in a rat liver transplant model.

A tryptophan catabolizer, indoleamine 2,3-dioxygenase (IDO) is highly expressed in the placenta and plays an essential role in maternal tolerance. Recent data have shown that the administration of an IDO inhibitor blocked not only maternal tolerance but also liver allograft tolerance. However, little is known about the induction of IDO in liver allografts, although a gene specific for tryptophan 2,3-dioxygenase (TDO) is believed to be expressed in the liver. In the present study, we investigated whether IDO is induced in liver allografts. Synthetic oligonucleotide primers based on the mouse IDO cDNA sequence were used to amplify RNA derived from livers of donor, syngeneic or allogeneic OLT rats. RNA encoding IDO was induced in the rat allogeneic liver after orthotopic liver transplantation (OLT), but not in syngeneic OLT. The rat nucleotide sequence of the RT-PCR products obtained from OLT livers revealed identities of 89% homology to the mouse IDO and of 68% to the human IDO. This study demonstrated the presence of RNA encoding IDO in allogeneic OLT livers, which may be involved in the immune response after liver transplantation.

Amino Acid Sequence↗