Biomedical subjects

J P Chang

Publications and source records attributed to J P Chang.

At least 19 recordsLinked to original sources

PubMed1992

Usefulness of predischarge electrophysiologic study in predicting late outcome after surgical ablation of the accessory pathway in the Wolff-Parkinson-White syndrome.

A predischarge electrophysiologic study was performed in 113 patients with the Wolff-Parkinson-White (WPW) syndrome who had undergone surgical ablation of the accessory pathway. The study was performed 5 to 20 (mean 10 +/- 3) days after surgery. There were 82 male and 31 female patients (aged 4 to 58 years, mean 36 +/- 13). Sixty-one patients (54%) had manifest, 52 (46%) had concealed and 12 (11%) had multiple accessory pathways. All but 1 patient had atrioventricular reentrant tachycardia incorporating single or multiple accessory pathways during the control electrophysiologic study. The accessory pathways were located in the left ventricular free wall in 60% of cases, right ventricular free wall in 22%, posteroseptum in 13%, and anteroseptum in 5%. The predischarge electrophysiologic study showed that the accessory pathway was capable of anterograde and retrograde conductions in 4 patients (all with manifest WPW syndrome). Four patients showed induction of supraventricular tachycardia, including 2 with atrioventricular reentrant tachycardia, and 2 with atrioventricular nodal reentrant tachycardia. Recurrence of supraventricular tachycardia was noted in 5 patients during a follow-up of 28 +/- 26 months. Of these 5 patients, 2 had inducible and 3 had no inducible supraventricular tachycardia during the predischarge electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1992

One-stage operation for treatment after delayed diagnosis of thoracic esophageal perforation.

Perforation of the thoracic esophagus can be fatal unless diagnosed promptly and treated effectively. The high mortality with delayed treatment is due principally to an inability to effectively close the perforation and prevent leakage. From 1982 to 1988, 7 consecutive patients (aged 16 to 73 years) were treated after a delayed diagnosis (26 hours to 25 days) of thoracic esophageal perforation. In all patients, the perforation was closed after debridement with total exclusion of the esophagus (T-tube cervical esophagostomy plus absorbable ligatures applied to the esophagogastric junction and the cervical esophagus distal to the esophagostomy). Radical decortication and wide mediastinal and pleural drainage were also done. Nutritional supply was given through a feeding gastrostomy. Antibiotics were administered according to the results of cultures. All patients survived. Continuity of the esophagus was established by removal of the T tube and spontaneous absorption of the ligatures. Endoscopy and esophagography performed 4 weeks after the initial operation showed a well-healed esophagus without stenosis or leakage in all patients. No secondary thoracotomy or esophageal reconstruction was necessary. No dysphagia was noted during follow-up (range, 12 to 50 months; mean follow-up, 23 months). We conclude that primary closure of the perforation and total esophageal exclusion with the use of absorbable ligatures and T-tube esophagostomy can provide a one-stage operation with good results for repair of thoracic esophageal perforation diagnosed late.

Adolescent↗

PubMed1992

Relationship between cyclic AMP-stimulated and native gonadotropin-releasing hormone-stimulated gonadotropin release in the goldfish.

The relationship between drugs elevating intracellular cAMP levels and gonadotropin (GTH)-releasing hormone (GnRH) in the stimulation of GTH secretion in the goldfish was investigated using dispersed goldfish pituitary cells in primary culture. In static incubation experiments, activation of adenylyl cyclase by forskolin and the inhibition of cAMP phosphodiesterase by 3 isobutyl-1-methylxanthine (IBMX) increased cAMP release and stimulated GTH secretion. The addition of membrane permeant cAMP analogs, 8-bromoadenosine 3':5'-cyclic monophosphate (8Br-cAMP), and dibutyryl cAMP also increased GTH release, suggesting that elevation of cAMP levels can induce GTH secretion. In the goldfish, dopamine is a physiological inhibitor of GTH release. Application of the dopamine agonist apomorphine decreased the GTH responses to forskolin, 8Br-cAMP, and salmon GTH-releasing hormone (sGnRH). The ability of agents that elevate cAMP levels to mimic GnRH action on GTH release suggests that cAMP may mediate GnRH-stimulated GTH secretion in the goldfish; however, this possibility was not substantiated by results from further experiments. In 2-hr static incubation studies, the GTH responses to sGnRH and chicken GnRH-II (cGnRH-II) were enhanced by coincubations with forskolin, IBMX, and 8Br-cAMP. The magnitudes of these enhancements were at least additive, if not synergistic. The levels of cAMP released into the media were unaffected by treatment with sGnRH and cGnRH-II, either in the absence or in the presence of IBMX. Replacement of normal testing media with Ca(2+)-deficient media (without Ca2+ salts and in the presence of 0.1 mM EGTA) decreased sGnRH and cGnRH-II stimulation of GTH release but did not affect forskolin and 8Br-cAMP actions. These results indicate that sGnRH and cGnRH-II stimulation of short term (less than or equal to 2-h) GTH release in the goldfish is not mediated by cAMP. The kinetics of the interactions between sGnRH, forskolin, and IBMX were also investigated in cell column perifusion studies. Applications of 5-min pulses of forskolin and IBMX stimulated rapid increases in GTH release; the latencies of these responses were similar to that observed with sGnRH. The simultaneous applications of sGnRH with either forskolin or IBMX resulted in GTH responses that were of greater magnitude and longer duration than those in response to sGnRH alone. These results together indicate that elevation of cAMP levels can potentiate the GTH response to the native GnRHs by increasing the magnitude of the acute GTH release and by prolonging the duration of GnRH action; however, cAMP does not appear to be involved directly in mediating GnRH stimulation of GTH release.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Methyl-3-isobutylxanthine↗

PubMed1992

Exposure to bleached kraft pulp mill effluent disrupts the pituitary-gonadal axis of white sucker at multiple sites.

Our recent studies have demonstrated reproductive problems in white sucker (Catostomus commersoni) exposed to bleached kraft pulp mill effluent (BKME) at Jackfish Bay on Lake Superior. These fish exhibit delayed sexual maturity, reduced gonadal size, reduced secondary sexual characteristics, and circulating steroid levels depressed relative to those of reference populations. The present studies were designed to evaluate sites in the pituitary-gonadal axis of prespawning white sucker affected by BKME exposure. At the time of entry to the spawning stream, plasma levels of immunoreactive gonadotropin (GtH)-II (LH-type GtH) in male and female white sucker were 30- and 50-fold lower, respectively, than the levels in fish from a reference site. A single intraperitoneal injection of D-Arg6, Pro9N-Et sGnRH (sGnRH-A, 0.1 mg/kg) increased plasma GtH levels in male and female fish at both sites, although the magnitude of the response was greatly reduced in BKME-exposed fish. Fish at the BKME site did not ovulate in response to sGnRH-A, while 10 of 10 fish from the reference site ovulated within 6 hr. Plasma 17 alpha,20 beta-dihydroxy-4-pregnen-3-one (17,20 beta-P) levels were depressed in BKME-exposed fish and unlike fish at the reference site, failed to increase in response to sGnRH-A. Testosterone levels in both sexes and 11-ketostestosterone levels in males were elevated in fish from the reference site but were not further increased by GnRH treatment. In contrast, BKME-exposed fish exhibit a transitory increase in testosterone levels in response to the GnRH analog. In vitro incubations of ovarian follicles obtained from fish at the BKME site revealed depressed basal secretion of testosterone and 17,20 beta-P and reduced responsiveness to the GtH analog human chorionic gonadotropin and to forskolin, a direct activator of adenylate cyclase. By comparison, ovarian follicles from fish collected at BKME and reference sites produced similar levels of prostaglandin E basally and in response to a phorbol ester and calcium ionophore A23187, suggesting that BKME effects on ovarian function are selective and do not reflect a general impairment of ovarian function. BKME-exposed fish had plasma levels of testosterone glucuronide proportionately lower than those of reference fish, suggesting that there are site differences in the peripheral metabolism of steroids. These studies demonstrate that BKME exposure affects reproduction by acting at multiple sites in the pituitary-gonadal axis.

Animals↗

PubMed1992

Actions of two native GnRHs and protein kinase C modulators on goldfish pituitary cells. Studies on intracellular calcium levels and gonadotropin release.

Previous results indicate that the two native gonadotropin (GtH)-releasing hormones of the goldfish, sGnRH and cGnRHII, stimulate GtH secretion in an extracellular Ca2+ ([Ca2+]o) dependent manner. In the present study, sGnRH, cGnRHII, KCI and the protein kinase C (PKC) activators TPA and DiC8, stimulated increases in intracellular Ca2+ ([Ca2+]i) levels in goldfish pituitary cells. Testing in Ca(2+)-deficient medium abolished the [Ca2+]i responses to cGnRHII, TPA and KCI and attenuated responses to sGnRH and DiC8. These results are the first to demonstrate that in teleost pituitary cells both native GnRHs stimulate increases in [Ca2+]i levels via [Ca2+]o entry. sGnRH- and DiC8-stimulated increases in [Ca2+]i also appear to be partially due to mobilization of Ca2+ from intracellular stores. Other results are consistent with a role for PKC in mediating GnRH action especially extracellular Ca2+ entry. Firstly, the PKC inhibitor staurosporine decreased GnRH- and TPA-induced [Ca2+]i responses. Secondly, incubation with Ca(2+)-deficient medium attenuated TPA- and DiC8-stimulated GtH release. Thirdly, GtH release responses to PKC activators were enhanced and reduced by an agonist and an antagonist of Ca2+ channel function, respectively. However, differences in the sensitivity of DiC8- and TPA-elicited responses to manipulations of [Ca2+]o entry indicate that these two PKC activators may have different actions in the goldfish pituitary. A difference in action of the two GnRHs on mobilization of Ca2+ from intracellular stores is also indicated.

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

PubMed1992

Differences in extracellular calcium involvement mediating the secretion of gonadotropin and growth hormone stimulated by two closely related endogenous GnRH peptides in goldfish pituitary cells.

Two endogenous gonadotropin-releasing hormone (GnRH) peptides, salmon GnRH (sGnRH) and chicken GnRH II (cGnRH II), stimulate gonadotropin (GtH) and growth hormone (GH) secretion in the goldfish. The extracellular calcium (e-Ca2+) dependence of the GtH and GH response to the two GnRH peptides were compared using static incubations of dispersed goldfish pituitary cells. Incubation with Ca(2+)-depleted medium (without the addition of Ca2+ salts and in the presence of EGTA) did not alter basal GtH secretion, but reduced the GtH response to sGnRH, and abolished the cGnRH II-induced GtH release. Blockade of e-Ca2+ entry by low concentrations of CoCl2 had no effect on basal GtH secretion but reduced cGnRH II and sGnRH stimulated GtH release when applied at 0.1 and 0.5 mM concentrations, respectively. In general, treatments with voltage-sensitive Ca2+ channel (VSCC) antagonists, verapamil, nifedipine and nicardipine, did not alter basal GtH release but attenuated GnRH-stimulated GtH responses. cGnRH II-induced GtH release was decreased by 10 nM verapamil and 1 nM nifedipine, whereas the reduction of GtH responses to sGnRH required 100 times higher concentrations of these VSCC antagonists. cGnRH II but not sGnRH stimulation of GtH secretion was also abolished by 10 microM nicardipine. In contrast to GtH release, exposure to Ca(2+)-depleted medium reduced basal GH release and abolished the GH responses to both GnRH peptides. sGnRH and cGnRH II-stimulated GH responses were both abolished by 0.1 mM CoCl2, decreased by 1 nM verapamil, and reduced by 10 nM nicardipine. Addition of 0.1 and 10 microM nifedipine inhibited the GH responses to sGnRH and cGnRH II, respectively. Basal GH release was not affected by the VSCC antagonists tested. Results from this study indicate that entry of e-Ca2+, in part through VSCC, is involved in GnRH stimulation of GtH and GH release from goldfish gonadotropes and somatotropes; however, the e-Ca2+ dependence of the GtH and GH responses to the two endogenous GnRHs differ. The stimulatory effects of cGnRH II on GtH secretion is more dependent on and sensitive to e-Ca2+ than sGnRH. Whereas the sensitivity of GH responses to manipulations of e-Ca2+ availability is, in most instances, similar for both GnRH peptides. These results further suggest that basal secretion of GH is more sensitive to e-Ca2+ than basal GtH release; however, VSCC are not involved in the maintenance of basal release of either hormone.

Animals↗

PubMed1992

Influence of GABA on gonadotrophin release in the goldfish.

The influence of GABA on pituitary gonadotrophin (GTH) release in the goldfish was studied by means of in vivo and in vitro techniques. It was found that GABA injected intraperitoneally caused an increase of serum GTH levels in regressed or early maturing fish, but not in late maturing animals. Moreover, injection of a GABA transaminase inhibitor caused a significant increase of GABA within the hypothalamus and pituitary, and a dose-dependent increase in serum GTH levels. To determine if this effect could be exerted directly at the level of the pituitary, dispersed pituitary cells in static incubation or in perifusion were exposed to increasing concentrations of GABA or its agonists muscimol and baclofen. None of these drugs was able to modify the spontaneous or GnRH-induced secretion of GTH, indicating that the in vivo effect of GABA was most likely mediated via another hypothalamic factor. Using in vitro incubation of pituitary slices, it was found that GABA caused a dose-related stimulation of GnRH release at the level of the pituitary, providing a possible explanation for the observed in vivo stimulatory effect of GABA on GTH release. Since the seasonal effect of GABA in vivo indicated a possible interaction of GABA with sexual steroids, GABA was given intraperitoneally to female goldfish implanted with either testosterone or estradiol. We found that the stimulatory effect of GABA on GTH release was abolished in estradiol-treated females but was still observed in testosterone-implanted fish. Moreover, estradiol but not testosterone caused a decrease of the GABA concentration within the telencephalon.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminobutyrate Transaminase↗

PubMed1992

Isolation and characterization of hypothalamic growth-hormone releasing factor from common carp, Cyprinus carpio.

A growth hormone-releasing factor (GRF)-like peptide was isolated from the hypothalamus of common carp, Cyprinus carpio, by acid extraction, gel filtration chromatography, immunoaffinity chromatography using antiserum directed against rat GRF, and multiple steps of HPLC using octadecyl columns. Based on Edman degradation and peptide mapping, this teleost GRF was established to be a 45-residue peptide with the following primary structure: His-Ala-Asp-Gly-Met-Phe-Asn-Lys-Ala-Tyr-Arg-Lys-Ala-Leu-Gly-Gln-Leu-Ser- Ala-Arg - Lys-Tyr-Leu-His-Thr-Leu-Met-Ala-Lys-Arg-Val-Gly-Gly-Gly-Ser-Met-Ile-Glu- Asp-Asp-Asn-Glu-Pro-Leu-Ser. Carp GRF is closely related structurally to peptides of the glucagon-secretin superfamily, and more particularly to mammalian vasoactive intestinal peptide (VIP) precursors and the N-terminal portion of mammalian GRFs. A synthetic replicate of this peptide is highly potent [50% effective dose (ED50) approximately 0.08 nM] in stimulating GH release from cultured goldfish pituitary glands and in elevating serum GH levels 30 min after injection (0.1 micrograms/g) in goldfish.

Amino Acid Sequence↗

PubMed1992

Dopamine stimulates growth hormone release from the pituitary of goldfish, Carassius auratus, through the dopamine D1 receptors.

Previously, we have demonstrated that ip injection of apomorphine, a nonselective dopamine (DA) agonist, increases serum GH levels in the goldfish, suggesting a possible role of DA in GH regulation. In the present study, the effects of DA on GH release in the goldfish were further characterized using an in vitro perifusion system for pituitary fragments. DA increased GH release in a dose-dependent manner with an ED50 of 0.26 +/- 0.06 microM. SKF38393, a DA D1 agonist, mimicked the GH-releasing effect of DA with an ED50 of 0.41 +/- 0.12 microM. Stereoselectivity consistent with mammalian DA D1 systems was demonstrated for the GH response to SKF38393; only the (+)- but not (-)-enantiomer of SKF38393 induced a dose-dependent GH release. Two other D1 agonists, SKF77434 and SKF82958, were also found to have GH-releasing activity. In contrast, high doses (up to 1 microM) of the DA D2 agonists, bromocriptine and LY171555, did not affect basal GH levels. The receptor specificity for DA-stimulated GH release was further investigated by using D1 and D2 antagonists; the D1 antagonists SCH23390 and SKF83566 completely abolished the GH response to DA or the D1 agonist SKF38393, whereas the D2-specific antagonists domperidone and (-)-sulpiride were not effective in this respect. Taken together, the present study demonstrates that DA is stimulatory to GH release from the pituitary of goldfish, and its action is mediated through receptors resembling the mammalian DA D1 receptors. The apparent similarities of the DA D1 receptor pharmacology between the goldfish and the mammals also indicate that D1 receptor is highly conserved during vertebrate evolution.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1992

Effects of porcine follicular fluid, inhibin-A, and activin-A on goldfish gonadotropin release in vitro.

Inhibin and activin are important reproductive regulators in mammalian species and have been demonstrated to be highly conserved in structure. The present study examines the effects of porcine follicular fluid (pFF; a crude inhibin and activin preparation) and purified porcine inhibin-A and activin-A on goldfish gonadotropin-II (GTH-II) release. In studies using primary cultures of dispersed goldfish pituitary cells in static incubation, treatments with pFF, inhibin-A, and activin-A for 10 h caused dose-dependent increase in GTH-II release. In perifusion studies using goldfish pituitary fragments, basal GTH-II release was significantly elevated after 12-h exposure to 500 micrograms/ml pFF. Furthermore, GnRH-induced GTH-II secretion was potentiated by pretreatment with pFF. When pFF was applied in the form of 5-min pulses, a rapid dose-related stimulation of GTH-II was observed. Similarly, challenges with 2-min pulses of 15, 150, and 1500 pM inhibin-A and activin-A stimulated GTH-II release by goldfish pituitary fragments in a rapid and dose-dependent manner. This acute stimulatory action of inhibin on goldfish GTH-II release was completely abolished after pretreatment with specific inhibin antibodies. The acute actions of inhibin and activin on GTH-II release are probably not due to the release of endogenous GnRH from nerve terminals in the pituitary fragments or binding to the GnRH receptors. First, a specific GnRH antagonist did not block the actions of inhibin and activin. Second, dopamine, a potent inhibitor of GnRH-stimulated GTH-II secretion in goldfish, was only partially effective in decreasing inhibin- and activin-induced GTH-II release. Third, the stimulatory effects of inhibin and GnRH on GTH-II release were additive. These lines of evidence also indicate that the mechanisms mediating inhibin and activin stimulation of goldfish GTH-II release may be somewhat different from those of GnRH. These results demonstrate that in contrast with the usual inhibitory effects of inhibin on GTH release in mammals, both inhibin and activin exert long term and acute stimulatory actions on GTH-II release in the goldfish.

Activins↗

PubMed1992

Prognosis of thymic carcinoma: analysis of 16 cases.

Primary thymic carcinoma is a rare malignant neoplasm which arises from the thymic epithelium. Between May 1982 and September 1990, 16 patients with thymic carcinomas, diagnosed at Chang Gung Memorial Hospital, were reviewed. Their ages ranged from 19 to 75 years, with a median of 40 years. Males predominated (male to female ratio was 11:5). The most common presenting symptoms were chest pain, cough, body weight loss and dyspnea. No paraneoplastic syndromes were seen. Chest roentgenograms of 15 patients revealed a mediastinal mass, but a definitive diagnosis could not be made until surgery. Adjacent mediastinal tissues were invaded, or adhered to, by all the tumors. Six distinct histologic types were found, squamous cell carcinoma being the most common (seven cases). The primary treatment of surgical resection was attempted in 14 patients, but only in five cases could the tumors be completely resected; two had a biopsy only. Radiotherapy, with or without chemotherapy, given postoperatively, achieved additional local control in seven of the nine partially resected patients (77%). Distant metastasis occurred in nine of 16 patients (56%). Lymph nodes, bone and lung were the most common metastatic sites. Chemotherapy with cisplatin and/or adriamycin-based regimens was given to patients who had distant metastasis, but the responses were unsatisfactory. The overall survival at one, three and five years was 88%, 51% and 31%, respectively. The median survival was 30 months. The median survival of patients with pure squamous cell carcinoma (> 49 months) was superior to that of patients with other histologic types (18 months; p < 0.01).

Adult↗

PubMed1992

[Valve replacement for aortic stenosis].

We retrospectively reviewed 122 consecutive patients with aortic stenosis from January 1977 to December 1990. There were 68 male and 54 female patients. Their age ranged from 5 to 73 years old (47 +/- 16, mean +/- SD). Sixty eight patients also had associated mitral valve lesion, 13 patients had tricuspid valve lesion, and 3 patients had coronary artery disease. Aortic valve replacement was performed on all patients. Mechanical valves were implanted in 86 cases and tissue valves in 36 cases. Associated procedures were performed in 54 cases: mitral valve replacement in 34 cases, mitral valve repair in 18 cases and coronary artery bypass grafting in 2 cases. A bicuspid aortic valve was found in 20 cases (16.4%). Hospital mortality was 4.9% (6 cases). Follow-up was completed in 95% of the surviving cases (110 cases). The survival rate was 82 +/- 3% at 13 years and redo-free rate was 73 +/- 8% at 13 years. Seven cases required redo operation, due to tissue valve degeneration in 5 and thrombosis of the mechanical valve in 2. All 7 patients survived. Late death occurred in 6 cases: 3 from malignancy, 2 from stroke and 1 from ventricular arrhythmia. We concluded that valve replacement for aortic stenosis is a safe and satisfactory procedure with good long-term results.

Adolescent↗

PubMed1992

[Migration of Kirschner wire from the right sternoclavicular joint into the main pulmonary artery. A case report].

The use of Kirschner wires (K-wires) for bone and joint fixation carries the risk of migration of the wire from the fixation site over time. However, review of the literatures disclosed rather few reports on this issue. We describe such a case in order to emphasize the potential complication and serious hazard that migration of such metallic devices can result in, especially when the fixation site is close to the thoracic cavity.

Adult↗

PubMed1991

Demonstration of gonadotropin releasing-hormone receptors on gonadotrophs and somatotrophs of the goldfish: an electron microscope study.

Dispersed pituitary cells of the goldfish were incubated with biotinylated [D-Lys6, Pro9-N-ethylamide] salmon gonadotropin-releasing hormone (sGnRH-A) then avidingold (10 nm), and were fixed, embedded and sectioned. Cells were identified as gonadotrophs, somatotrophs, or prolactin cells using specific hormone antisera and protein-A gold (20 nm) as a marker. Attachment of the biotinylated sGnRH-A to the pituitary cell sections was determined by scanning cell surfaces for the smaller gold particles using the transmission electron microscope. Attachment was observed on gonadotrophs and somatotrophs, but was negligible on prolactin cells. Preincubation with unlabelled salmon gonadotropin-releasing hormone or chicken II gonadotropin-releasing hormone, or omission of the salmon gonadotropin-releasing hormone analog, prevented the reaction. The direct visualization of specific gonadotropin-releasing hormone receptors on gonadotrophs and somatotrophs supports the existence of direct stimulatory actions of gonadotropin-releasing hormone on gonadotropin and somatotropin release in gold-fish.

Animals↗

PubMed1991

Intrapericardial pheochromocytoma.

In a 34-year-old man with hypertension and increased urinary catecholamine excretion for 12 years, an m-[131I]iodobenzylguanidine scan and chest computed tomography located an intrapericardial pheochromocytoma in the left atrium. The tumor was excised through a left thoracotomy with cardiopulmonary bypass and circulatory arrest. At 34-month follow-up, blood pressure and urine catecholamine levels were normal. In the 15 cases of intrapericardial pheochromocytoma treated by resection reported in the literature, all 11 survivors were symptom-free except 1 who had residual left atrial tumor and multiple skeletal metastatic lesions. Computed tomography directed by the m-[131I]iodobenzylguanidine scan can be used for detailed location of the tumor. Appropriate surgical approach and use of cardiopulmonary bypass are critical in the resection of these highly vascular tumors.

Adult↗

PubMed1991

Traumatic asphyxia.

During a 5-year period, we treated 14 cases of traumatic asphyxia. There were 12 male and 2 female patients ranging in age from 2 to 32 years. Most suffered crushing injuries at work or were run over by motor vehicles. Mild to severe cervicofacial cyanosis and petechiae developed in all patients. A fear response was reported by 12 of the patients. Subconjunctival hemorrhage was also found in 12 patients. Nine patients had tachypnea and 7 complained of dyspnea. Most of the patients suffered some associated injuries including 8 head injuries, 7 pulmonary contusions, and 6 cases of blunt abdominal trauma. Less-associated injuries were rib fractures, brachial and radial nerve injuries, hemothorax, and pneumothorax. The hospital stay ranged from 4 to 28 days (mean, 14 days) and follow-up from 10 to 60 months (mean, 32 months). Treatment for traumatic asphyxia included measurement of arterial blood gases, oxygen supplementation, and intubation with mechanical ventilation. The patients' recovery conditions were relative to the severity of injury and the associated injuries.

Adolescent↗

PubMed1991

Possible involvement of protein kinase C in gonadotropin and growth hormone release from dispersed goldfish pituitary cells.

Static incubation with tumor-promoting 4 beta-phorbol esters, activators of the Ca2(+)- and phospholipid-dependent protein kinase C enzyme (PKC), caused dose-dependent increases in gonadotropin (GTH) and growth hormone (GH) secretion in primary cultures of dispersed goldfish pituitary cells. The estimated half-maximal effective doses (ED50) for stimulating GTH and GH release were 0.35 +/- 0.17 and 0.32 +/- 0.13 nM 12-O-tetradecanoyl phorbol 13 acetate (TPA), 3.71 +/- 1.30 and 1.37 +/- 0.76 nM 4 beta-phorbol 12,13-dibutyrate, 6.90 +/- 4.84 and 1.89 +/- 0.25 nM 4 beta-phorbol 12,13-dibenzoate, and 455 +/- 258 and 311 +/- 136 nM 4 beta-phorbol 12,13-diacetate, respectively. In contrast, treatments with up to 10 microM of the inactive 4 alpha-phorbol 12,13-didecanoate ester did not alter GTH and GH release. Additions of the synthetic diacylglycerol, dioctanoyl glycerol, also enhanced GTH and GH secretion in a dose-dependent manner and with ED50s of 1.73 +/- 0.83 and 1.73 +/- 1.19 microM, respectively. The GTH and GH responses to stimulation by TPA were attenuated by incubation with Ca2(+)-depleted medium containing EGTA or by treatment with the Ca2+ channel blocker verapamil. Coincubation with the PKC inhibitor H7 reduced the GTH and GH responses to TPA. As in previous studies, additions of salmon gonadotropin-releasing hormone (sGnRH) or chicken GnRH-II (cGnRH-II) induced GTH and GH release; these hormone responses to sGnRH and cGnRH-II were also decreased by the addition of H7. These results indicate that activation of PKC may stimulate GTH and GH release in goldfish and suggest that sGnRH and cGnRH-II actions on goldfish pituitary GTH and GH secretion are also mediated, at least partially, by PKC.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1991

Lack of involvement of arachidonic acid metabolism in chicken gonadotropin-releasing hormone II (cGnRH-II) stimulation of gonadotropin secretion in dispersed pituitary cells of goldfish, Carassius auratus. Identification of a major difference in salmon GnRH and chicken GnRH-II mechanisms of action.

Gonadotropin (GTH) release in static incubations of dispersed goldfish pituitary cells was stimulated by chicken GTH-releasing hormone II (cGnRH-II), salmon (s)GnRH, phospholipase A2, phospholipase C, phospholipase D, and arachidonic acid (AA). Coincubations with nordihydroguaiaretic acid (NDGA), 5,8,11,14-eicosatetraenoic acid, and indomethacin did not alter the GTH responses to cGnRH-II. In contrast, NDGA reduced sGnRH-stimulated GTH release. Incubation with Ca(2+)-deficient medium abolished the GTH responses to cGnRH-II, reduced sGnRH-stimulated GTH release, but did not alter AA actions on GTH secretion. Apomorphine, a dopamine agonists that had been shown to partially inhibit the GTH responses to sGnRH and to abolish those induced by cGnRH-II, did not affect the hormone response to AA. However, the partial inhibitory actions of NDGA and apomorphine on sGnRH-induced GTH release were additive. These findings suggest the existence of a major difference in cGnRH-II and sGnRH stimulation of GTH release--AA metabolism is not involved in cGnRH-II, as opposed to sGnRH actions. This difference in second messenger activation may also explain the differential sensitivity of the two GnRH peptides to dopamine inhibition and manipulations of extracellular Ca2+ availability. The results further suggest that dopamine and AA affect GTH release via non-overlapping signal transduction pathways.

Animals↗