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Biomedical subjects

W H Hsu

Publications and source records attributed to W H Hsu.

At least 19 recordsLinked to original sources
PubMed1992

Impalpable thoracic bony lesions diagnosed by sonographically guided needle aspiration biopsy.

Impalpable osteolytic lesions may be detected and diagnosed by ultrasonography and sonographically guided needle aspiration biopsy. Eleven cases with bone destruction found on chest radiographs were proved to be malignant by sonographically guided needle aspiration biopsy. The bony lesions were all hypoechoic and could be demonstrated easily. No complications or discomfort occurred after needle aspiration. Bony lesions can be detected by ultrasonography only when pathologic changes have occurred. Ultrasonography and sonographically guided needle aspiration biopsy provide a simple, convenient, and non-invasive method for detecting and diagnosing impalpable osteolytic lesions.

Aged↗
PubMed1992

Intrathoracic schwannoma of vagus nerve.

Intrathoracic neurogenic tumors are relatively common mediastinal tumors generally located in the posterior mediastinum. The most common origin is the intercostal nerve or the sympathetic chain. These tumors rarely arise from vagus nerve in the anterior mediastinum. The English literature demonstrates a total of 29 cases, which are more often on the left than the right. Here, we present another case: a 41-year-old man with a history of chronic cough for 10 years, whose chest radiograph showed a homogenous mass in the right anterosuperior mediastinum. The chest CT scan revealed a well-defined mass, 4-cm in diameter, located at the right side of trachea. Marked compression and lateral displacement of the R't innominate vein were noted. The mass was heterogenous with partial area of relative lower density and only mild enhancement was noted after contrast medium infusion. Sternotomy with tumor resection from the right vagus nerve was done. The histological diagnosis was schwannoma.

Adult↗
PubMed1992

Detection of mass lesions in the collapsed lung by ultrasonography.

Ultrasonography is useful in the detection of mass lesions in the collapsed lung, using the collapsed lungs as a "sonic window". Twenty-four patients suspected of having a tumor causing lung collapse, as shown on their chest radiographs, were examined by ultrasonography. Eighteen out of 24 patients were found to have mass lesions in their collapsed lungs. Thoracic computed tomography (CT) was also performed in 12 of these 18 patients; of those, 11 showed compatibility with sonographic findings in the detection of mass lesions in their collapsed lungs. The remaining six of these 24 patients with no mass lesions detected by ultrasonography were proven to have collapsed lung due to sputum impaction (n = 2) and lung cancer (n = 4). The fact that four patients had lung cancer that was not detectable by ultrasonography, might have been due to relatively small mass lesions at deep locations (main or intermediate bronchus) and narrowing of the "sonic window" (partial lung collapse). Though it has some limitations, ultrasonography is helpful in detecting mass lesions in collapsed lungs. Sono-guided fine needle aspiration biopsy (SGFNAB) can also be performed simultaneously, smoothly and without any major complications. In our series, SGFNAB was performed in eight out of 18 patients to make a cytopathologic diagnosis. We recommend this safe, convenient, and noninvasive method to screen for lesions in the collapsed lung, especially when bronchoscopic examination is impossible.

Aged↗
PubMed1991

The nucleotide sequence of Schwanniomyces occidentalis alpha-amylase gene.

The nucleotide sequence of the coding and regulatory regions of the alpha-amylase-encoding gene (AMY) of Schwanniomyces occidentalis has been determined. This sequence contained an open reading frame of 512 codons, from which a protein with Mr of 53,723 could be predicted. A putative signal sequence encoding for 25 amino acids was proposed for the 5' end of the open reading frame. Regulatory sequences, such as TATA box, CCAAT box and a signal sequence for polyadenylation and transcription termination could be found in the flanking regions of AMY gene. The deduced amino acid sequence also contained four common conserved regions characteristic of other alpha-amylase proteins.

Amino Acid Sequence↗
PubMed1991

Somatostatin inhibits insulin secretion by a G-protein-mediated decrease in Ca2+ entry through voltage-dependent Ca2+ channels in the beta cell.

We tested the hypothesis that somatostatin (SRIF) inhibits insulin secretion from an SV40 transformed hamster beta cell line (HIT cells) by an effect on the voltage-dependent Ca2+ channels and examined whether G-proteins were involved in the process. Ca2+ currents were recorded by the whole cell patch-clamp method, the free cytosolic calcium, [Ca2+]i, was monitored in HIT cells by fura-2, and cAMP and insulin secretion were measured by radioimmunoassay. SRIF decreased Ca2+ currents, [Ca2+]i, and basal insulin secretion in a dose-dependent manner over the range of 10(-12)-10(-7)M. The increase in [Ca2+]i and insulin secretion induced by either depolarization with K+ (15 mM) or by the Ca2+ channel agonist, Bay K 8644 (1 microM) was attenuated by SRIF in a dose-dependent manner over the same range of 10(-12)-10(-7) M. the half-maximal inhibitory concentrations (IC50) for SRIF inhibition of insulin secretion were 8.6 X 10(-12) M and 8.3 X 10(-11) M for K+ and Bay K 8644-stimulated secretion and 1 X 10(-10) M and 2.9 X 10(-10) M for the SRIF inhibition of the K+ and Bay K 8644-induced rise in [Ca2+]i, respectively. SRIF also attenuated the rise in [Ca2+]i induced by the cAMP-elevating agent, isobutylmethylxanthine (1 mM) in the presence of glucose. Bay K 8644, K+ and SRIF had no significant effects on cAMP levels and SRIF had no effects on adenylyl cyclase activity at concentrations lower than 1 microM. SRIF (100 nM) did not change K+ efflux (measured by 86Rb+) through ATP-sensitive K+ channels in HIT cells. SRIF (up to 1 microM) had no significant effect on membrane potential measured by bisoxonol fluorescence. Pretreatment of the HIT cells with pertussis toxin (0.1 microgram/ml) overnight abolished the effects of SRIF on Ca2+ currents, [Ca2+]i and insulin secretion implying a G-protein dependence in SRIF's actions. Thus, one mechanism by which SRIF decreases insulin secretion is by inhibiting Ca2+ influx through voltage-dependent Ca2+ channels, an action mediated through a pertussis toxin-sensitive G-protein.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Activation of alpha 2-adrenergic receptors decreases Ca2+ influx to inhibit insulin secretion in a hamster beta-cell line: an action mediated by a guanosine triphosphate-binding protein.

Activation of the sympathetic nervous system inhibits insulin secretion. We tested the hypothesis that activation of alpha 2-adrenergic receptors on the beta-cell by epinephrine or clonidine attenuates insulin release by an effect on the voltage-dependent Ca2+ channel (VDCC) and examined the role of G-proteins in this signal transduction pathway. Using a cultured SV40-transformed hamster beta-cell line (HIT cells) as a model system, we determined the effect of alpha 2-adrenergic agonists on insulin secretion, 86Rb+ efflux (a marker for K+ channel flux), and the free cytosolic Ca2+ level [( Ca2+]i) monitored in fura-2-loaded cells. In a dose-dependent manner, epinephrine and clonidine (10(-8)-10(-5)M) attenuated the increase in [Ca2+]i and insulin secretion induced by either K+ depolarization or stimulation of the VDCC with the agonist Bay K 8644. Epinephrine failed to affect the rise in [Ca2+]i induced by carbamylcholine, an agent that mobilizes intracellular Ca2+. Epinephrine also did not changes 86Rb+ efflux from HIT cells. The inhibitory effects of epinephrine were prevented by the alpha 2-adrenergic antagonist idazoxan, but were unaffected by the alpha 1-adrenergic antagonist phenoxybenzamine. Pretreatment of HIT cells with pertussis toxin (0.1 micrograms/ml) overnight abolished the inhibitory effects of epinephrine and clonidine on both [Ca2+]i and insulin secretion. These data suggest that one mechanism by which alpha 2-adrenergic agonists inhibit insulin secretion is by inhibiting Ca2+ influx through VDCC, an action that is mediated through a pertussis toxin-sensitive G-protein.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1991

Antagonistic effect of atipamezole on xylazine-induced sedation, bradycardia, and ruminal atony in calves.

Three doses of an alpha 2-adrenoreceptor antagonist, atipamezole, were administered to reverse xylazine-induced sedation, bradycardia, and ruminal atony in calves. Once a week for 4 weeks, each of 6 calves was administered IV 1 treatment of: 0.3 mg of xylazine/kg of body weight, followed in 10 minutes by 1 ml of 0.9% NaCl; 0.3 mg of xylazine/kg, followed in 10 minutes by 3 micrograms of atipamezole/kg; 0.3 mg of xylazine/kg, followed in 10 minutes by 10 micrograms of atipamezole/kg; or 0.3 mg of xylazine/kg, followed in 10 minutes by 30 micrograms of atipamezole/kg. The order of the 4 treatments in each calf was selected at random. Xylazine alone caused lateral recumbency for 33.6 +/- 7.1 minutes (mean +/- SEM). Atipamezole administered at dosages of 3, 10, and 30 micrograms/kg shortened xylazine-induced lateral recumbency to 20.5 +/- 3.0, 10.2 +/- 0.2, and 9.3 +/- 0.5 minutes, respectively. Calves given xylazine alone stood at greater than 60 minutes after the onset of recumbency. Atipamezole given at 3, 10, and 30 micrograms/kg shortened the time from onset of lateral recumbency to standing to 40.2 +/- 6.9, 12.8 +/- 1.1, and 10.0 +/- 0.7 minutes, respectively. Drowsiness was found in calves given the lowest dosage of atipamezole (3 micrograms/kg) after the calves stood. Atipamezole given at dosages of 10 and 30 micrograms/kg reversed xylazine-induced ruminal atony in a dose-dependent manner. In addition, 30 micrograms of atipamezole/kg reversed xylazine-induced bradycardia, but the lower dosages of this antagonist did not. Results indicated that 30 micrograms of atipamezole/kg should be a useful antidote for xylazine overdose in cattle.

Adrenergic alpha-Antagonists↗
PubMed1991

Retrograde flow of spermatozoa into the urinary bladder of cats during electroejaculation, collection of semen with an artificial vagina, and mating.

The effect of methoxamine on retrograde flow of spermatozoa into the urinary bladder of domestic cats during electroejaculation and the incidence of retrograde flow during the collection of semen with an artificial vagina, or during mating was examined. In experiment 1, urine collected by cystocentesis prior to electroejaculation was azoospermic or contained few, nonmotile spermatozoa, whereas urine collected after electroejaculation contained more (P = 0.002) spermatozoa, and motile spermatozoa were evident in urine obtained from 6 of 8 cats. Administration of methoxamine hydrochloride (200 micrograms/kg of body weight, IV) did not affect spermatozoal output or percentage of retrograde flow. Percentage of retrograde flow for control cats ranged from 61.18 to 92.95% (mean +/- SD, 80.00 +/- 14.28%) and for methoxamine-treated cats, ranged from 15.25 to 92.49% (mean +/- SD, 58.10 +/- 32.28%), but the difference was not significant. In experiment 2, an artificial vagina was used to collect semen from 5 of the 8 cats used in experiment 1. Urine collected by cystocentesis after ejaculation contained spermatozoa, and motile spermatozoa were evident in the urine from 4 of 5 cats. The mean (+/- SD) percentage of retrograde flow for these 5 cats was 46.82 +/- 31.67% (range, 14.56 to 90.32%). In experiment 3, each of the 5 cats that were used in experiments 1 and 2 were mated. Spermatozoa were recovered from the vagina of each mated female, and motile spermatozoa were also present in postejaculation urine obtained by cystocentesis from each of the 5 male cats. Mean total number of spermatozoa in the postmating urine was 29.42 +/- 33.58 x 10(6) (range, 0.22 x 10(6) to 76.05 x 10(6) spermatozoa).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Nucleotide sequence and expression of the isoamylase gene from an isoamylase-hyperproducing mutant, Pseudomonas amyloderamosa JD210.

The isoamylase gene (ISO) of Pseudomonas amyloderamosa JD210, an isoamylase-hyperproducing mutant, was cloned in an isoamylase-deficient and transformable mutant strain K31. By deletion analysis, the ISO gene was found to be located within a 3.3 kilobases BamHI fragment. Its nucleotide sequence contained an open reading frame of 2328 nucleotides (776 amino acids) encoding a secreted isoamylase precursor. The ISO gene fragment was inserted into plasmids pKT230 and pBR 322 in opposite orientations. The expression of the ISO gene in the constructed plasmids was compared in P. amyloderamosa K31, Pseudomonas aeruginosa PAO1-161, Pseudomonas putida mt-2 and Escherichia coli HB101. In all transformed cells, the majority of the isoamylase produced was secreted and higher isoamylase activities were obtained in transformats with the transcriptional direction of the ISO gene similar to the nearby drug-determinant gene of the vector.

Amino Acid Sequence↗
PubMed1990

Molecular cloning of a novel splice variant of the alpha subunit of the mammalian Go protein.

We screened a HIT (hamster insulin-secreting tumor) cell cDNA library constructed in lambda gt11 with a Go-specific oligonucleotide probe and isolated six recombinant phages. The inserts of these phages encoded two forms of alpha o, called here alpha o1 and alpha o2. The deduced amino acid sequence of alpha o1 is identical in all of its 354 amino acids to that reported previously for rat and bovine alpha o; that of alpha o2, also of 354 amino acids, is identical to alpha o1 up to and including amino acid 248 and differs thereafter in 26 amino acids. At the nucleotide level, alpha o1 and alpha o2 are identical up to and including the second base of the codon that specifies amino acid 243 and differs thereafter in 88 nucleotides of the remaining open reading frame and has no similarity to alpha o1 in its 3'-untranslated region. We propose that alpha o1 and alpha o2 result as a consequence of alternative splicing of a single alpha o transcript. Northern analysis with specifically designed oligonucleotides indicates that both forms of alpha o are expressed in normal tissues, e.g. brain. After in vitro transcription and translation, the peptides encoded in the alpha o1 and alpha o2 cDNAs could be ADP-ribosylated by pertussis toxin in the presence of added beta gamma dimers. The count of distinct G proteins keeps increasing.

Adenosine Diphosphate Ribose↗
PubMed1990

Amitraz-induced glucose intolerance in rats: antagonism by yohimbine but not by prazosin.

Amitraz (N'-[2,4-dimethylphenyl]-N-[(2,4-dimethylphenyl)imino]-N- methylmethanimidamide) is a formamidine insecticide/acaricide that increases plasma glucose and decreases plasma insulin concentrations in dogs when applied topically. Because amitraz activates alpha 2-adrenoceptors in numerous tissues, in this study we used rats as a model to determine whether these effects of amitraz are mediated by alpha 2-adrenoceptors. The i.v. injection of amitraz (0.1, 0.3, and 1 mg/kg) followed by i.v. glucose injection (1 g/kg) induced a dose-dependent glucose intolerance characterized by hypoinsulinemia. At 1 mg/kg, amitraz completely blocked the insulin release induced by i.v. glucose administration. The alpha 2-adrenoceptor antagonist yohimbine (1 mg/kg, i.v.) prevented the effects of amitraz, but the alpha 1-adrenoceptor antagonist prazosin (0.3 mg/kg, i.v.) did not. The results suggested that one mechanism by which amitraz prolongs glucose-induced hyperglycemia is via inhibition of insulin release and this effect is mediated by alpha 2-adrenoceptors.

Animals↗
PubMed1990

The effects of yohimbine and four other antagonists on amitraz-induced depression of shuttle avoidance responses in dogs.

The ability of five antagonists to prevent the central nervous system's depressant effects of amitraz in dogs was evaluated using a shuttle avoidance paradigm. All drugs were injected iv into six male dogs trained to avoid a 1-mA shock by jumping over a hurdle within 10 sec of the start of a tone. Dogs were given an antagonist or saline followed in 5 min by 3 mg/kg amitraz dissolved in dimethyl sulfoxide (DMSO) or DMSO alone. After pretreatment with saline, amitraz decreased significantly the means number of avoidance responses and increased significantly the means latencies of avoidance responses. After pretreatment with the alpha 2-adrenoreceptor antagonist yohimbine (0.1 mg/kg), amitraz no longer decreased the means number of avoidance responses or lengthened the means latencies of avoidance responses. The nonselective alpha-adrenoreceptor antagonist tolazoline (3.3 mg/kg) prevented amitraz-induced increases in means latencies, but did not prevent the decreases in the means number of avoidances. The alpha 1-adrenoreceptor antagonist prazosin (1 mg/kg), the muscarinic receptor antagonist atropine (0.04 mg/kg), and the opioid receptor antagonist naloxone (1 mg/kg) did not prevent either of amitraz's effects. The data suggest that the amitraz-induced suppression of avoidance responding is mediated by alpha 2-adrenoreceptors rather than by alpha 1-adrenergic, muscarinic, or opioid receptors.

Animals↗
PubMed1990

Xylazine enhances porcine myometrial contractility in vitro: possible involvement of alpha 2-adrenoceptors and Ca2+ channels.

The effects of xylazine on porcine myometrial contractility were studied in vitro using uterine strips to determine the alpha 2-adrenergic influences during the diestrous stage of the estrous cycle. Xylazine (10(-8)-10(-5) M) caused a dose-dependent increase in the amplitude of myometrial contractility. The alpha 2-adrenoceptor antagonists idazoxan and yohimbine (10(-8)-10(-6) M) blocked the effects of xylazine in a dose-dependent manner. Yohimbine was approximately 10 times more potent than idazoxan in this regard. In contrast, an alpha 1-adrenoceptor antagonist prazosin (10(-7) and 10(-6) M) did not block the xylazine-induced increase in myometrial contractility, but a higher dose of prazosin (10(-5) M) did reduce the effects of xylazine. When the porcine uterine strips were pretreated with Ca2(+)-free Tyrod's solution or verapamil, a Ca2+ channel blocker, the effects of xylazine on myometrial contractility were completely abolished, whereas those of carbachol were only moderately reduced. The results suggest that the xylazine-induced myometrial contractility is mediated by alpha 2-adrenoceptors and that this effect is mediated, at least in part, by Ca2+ channels, whereas the effect of carbachol is attributed to an increase in both Ca2+ entry and release of Ca2+ from intracellular pools.

Adrenergic alpha-Antagonists↗
PubMed1990

Ion channels and insulin secretion.

We review the role of ion channels in regulating insulin secretion from pancreatic beta-cells. By controlling ion permeability, ion channels at the membrane play a major role in regulating both electrical activity and signal transduction in the beta-cell. A proximal step in the cascade of events required for stimulus-secretion coupling is the closure of ATP-sensitive K+ channels, resulting in cell depolarization. Of particular relevance is the finding that this channel is directly regulated by a metabolite of glucose, which is the primary insulin secretagogue. In addition, this channel, or a closely associated protein, contains the sulfonylurea-binding site. Another K+ channel, the Ca2(+)-activated K+ channel, may be involved in cell repolarization to create homeostasis. Voltage-dependent Ca2+ channels are activated by cell depolarization and regulate Ca2+ influx into the cell. By controlling cytosolic free-Ca2+ levels ([Ca2+]i), these channels play an important role in transducing the initial stimulus to the effector systems that modulate insulin secretion. The link between a rise in [Ca2+]i and the terminal event of exocytosis is the least-understood aspect of stimulus-secretion coupling. However, phosphorylation studies have identified substrate proteins that may correspond to those involved in smooth muscle contraction, suggesting an analogy in the processes of stimulus secretion and excitation contraction. The advent of new methodology, particularly the patch-clamp technique, has fostered a more detailed characterization of the beta-cell ion channels. Furthermore, biochemical and molecular approaches developed for the structural analysis of ion channels in other tissues can now be applied to the isolation and characterization of the beta-cell ion channels. This is of particular significance because there appear to be tissue-specific variations in the different types of ion channels. Given the importance of ion channels in cell physiology, a knowledge of the structure and properties of these channels in the beta-cell is required for understanding the abnormalities of insulin secretion that occur in non-insulin-dependent diabetes mellitus. Ultimately, these studies should also provide new therapeutic approaches to the treatment of this disease.

Animals↗
PubMed1990

Effects of tetramethylpyrazine on heart rate and pupil diameter in rats.

The alpha-adrenergic nature of tetramethylpyrazine (TMPZ), a commonly used cardiovascular drug in China, was studied with a combined bradycardia and mydriasis model in the pentobarbital anesthesized rat. Intravenous injections of TMPZ at 1-30 mg/kg failed to change heart rate or pupil size, whereas iv injections of both clonidine (alpha 2-adrenoceptor agonist, 1-30 micrograms/kg) and methoxamine (alpha 1-adrenoceptor agonist, 10-300 micrograms/kg) caused dose-dependent bradycardia and mydriasis. Pretreatment of rats with TMPZ (30 mg/kg) did not significantly change clonidine- or methoxamine-induced bradycardia or mydriasis. However, when TMPZ was injected 2 min after clonidine administration (30 micrograms/kg), while the mydriasis reached a maximum, it slightly but significantly reversed the clonidine-induced mydriasis for 15-20 s. In contrast, the alpha 2-adrenoceptor antagonist idazoxan (6 micrograms/kg) caused the same degree of reduction of the clonidine-induced mydriasis for greater than 2 min. Our results suggested that TMPZ at the doses studied did not have alpha-adrenoceptor agonistic activities, but may have slight alpha 2-adrenoceptor antagonistic activities.

Animals↗
PubMed1990

Retrograde flow of spermatozoa into the urinary bladder of dogs during ejaculation or after sedation with xylazine.

Retrograde flow of spermatozoa into the urinary bladder of dogs during ejaculation or after administration of xylazine was examined. In experiment 1, the mean (+/- SD) spermatozoal concentration in urine collected by cystocentesis before ejaculation was 0.322 +/- 0.645 X 10(6)/ml. After ejaculation, motile spermatozoa were present in the urine collected by cystocentesis from 12 of 15 dogs, and the concentration of spermatozoa in the urine (5.139 +/- 7.014 X 10(6)/ml) was higher (P less than 0.025) than the concentration in the urine collected before ejaculation. The percentage of the total number of spermatozoa that were displaced during ejaculation and flowed into the urinary bladder (retrograde flow) ranged from 0 to 99.75% (24.67 +/- 33.98%). In experiments 2 and 3, administration of xylazine to sexually rested dogs induced retrograde flow of spermatozoa into the urinary bladder. In experiment 2, all dogs had spermatozoa in urine collected after xylazine administration, with motile spermatozoa present in the urine from 9 of 10 dogs. In experiment 3, urine collected from dogs before administration of xylazine was azoospermic or contained few, nonmotile spermatozoa (0.063 +/- 0.135 X 10(6)/ml), whereas urine collected after administration of xylazine had more (P less than 0.025) and motile spermatozoa (3.717 +/- 4.273 X 10(6)/ml). In experiment 4, administration of xylazine to dogs after ejaculation did not increase the concentration of spermatozoa in the urine. Results indicate that spermatozoa flow into the urinary bladder of dogs during ejaculation or after administration of xylazine to sexually rested dogs.

Animals↗
PubMed1989

Reconstruction of the esophagus with the left colon.

This report reviews our experience with 96 patients with benign or malignant stricture of the esophagus who underwent interposition of the left colon with or without esophageal resection from July 1982 to June 1987. There were 67 male and 29 female patients ranging in age from 8 to 80 years. Thirty-seven patients had fibrotic stricture secondary to corrosive injury of the esophagus, 42 had cancer of the esophagus, and 17 had cancer of the gastric cardia. The incidence of postoperative complications and surgical mortality, respectively, was 16.2% and 2.7% for patients with corrosive stricture of the esophagus, 35.7% and 11.9% for patients with cancer of the esophagus, and 35.2% and 5.8% for patients with cancer of the gastric cardia. Reconstruction resulted in good function in 75.6% of the patients with corrosive stricture of the esophagus, 66.6% of the patients with cancer of the esophagus, and 70.5% of patients with cancer of the gastric cardia. The morbidity and mortality were higher in the group with malignant esophageal strictures because of advanced age, poor general condition of the patient, and extent of the surgical procedure needed. Cervical anastomotic leakage was the most frequently encountered complication (13.5%), and all the poor-function results were caused by this complication. In our experience, reconstruction of the esophagus with left colon is a satisfactory method that can be accomplished with acceptable morbidity and mortality. The left colon is a durable and functional substitute.

Adolescent↗