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Biomedical subjects

M Hong

Publications and source records attributed to M Hong.

At least 127 records · Page 7Linked to original sources
PubMed1995

Effects of dehydroepiandrosterone (DHEA) on pituitary prolactin and arcuate nucleus neuron tyrosine hydroxylase mRNA levels in the rat.

It is well documented that dehydroepiandrosterone (DHEA), an adrenal androgen, is converted into potent androgens and/or estrogens in peripheral tissues. Since sex steroids are involved in the regulation of prolactin (PRL) secretion, we have studied the effect of DHEA administration on PRL mRNA levels in both adult male and female rats. Since tuberoinfundibular dopaminergic (TIDA) neurons are involved in the negative regulation of PRL, we have also evaluated the effects of DHEA on the genetic expression of tyrosine hydroxylase (TH), the limiting enzyme in catecholamine biosynthesis in TIDA neurons. Sham-operated and castrated animals of both sexes received during 2 days DHEA at the dose of 6 mg/kg/day, starting on the first day after castration. PRL and TH mRNA levels were measured by quantitative in situ hybridization. In the male rat, orchiectomy performed 3 days earlier did not modify PRL mRNA levels. DHEA administration increased the hybridization signal in both sham-operated and orchiectomized animals. In the female, ovariectomy decreased PRL mRNA levels and, as observed in the male, DHEA treatment induced an increase in the hybridization signal in both control and ovariectomized rats. In TIDA neurons, castration increased TH mRNA levels as evaluated by number of grains over labelled neurons and the number of TH-labelled cells per section in both male and female animals. In both sham-operated male rats and orchiectomized animals, DHEA decreased the hybridization signal. In the female, DHEA administration completely prevented the increase in TH mRNA levels due to ovariectomy. In sham-operated female rats, the treatment had no effect. These data clearly indicate that in both male and female rats DHEA exerts an estrogenic influence on both PRL and TH gene expression. Although these in vivo experiments do not allow to establish whether the stimulation of PRL gene expression is due to an action of the steroid on the pituitary or at the hypothalamic level or alternatively at both sites, it is likely that one of the mechanisms of action of DHEA might be related to a decrease in dopamine release following a depression of TIDA neuron activity.

Animals↗
PubMed1995

Role of neuropeptide Y in the regulation of tyrosine hydroxylase gene expression in rat adrenal glands.

It is well known that the adrenal medulla contains high concentrations of neuropeptide Y (NPY) where it coexists with epinephrine and norepinephrine. In order to evaluate the possible involvement of NPY in the regulation of the chromafin cells of the rat adrenal medulla, we have studied the effects of NPY and some NPY analogs on the concentrations of tyrosine hydroxylase (TH) mRNA. The following peptides, NPY, PYY, [Leu31, Pro34]-NPY (a Y1 receptor agonist) and NPY13-36 (a Y2 receptor agonist) were administered intravenously at the dose of 40 micrograms/100 g body weight. All the animals were perfused with 4% paraformaldehyde 4 h after injection and cryostat sections of adrenals were processed for in situ hybridization using a 35S-labelled oligonucleotide probe encoding for rat TH. Optical density measurements performed in adrenal medulla demonstrated that the administration of NPY, PYY, and [Leu31, Pro34]-NPY induced a marked increase in the hybridization signal while the Y2 receptor agonist NPY13-36 did not affect TH mRNA levels. Then, these data clearly indicate that NPY positively regulates the genetic expression of TH probably via the Y1 NPY receptor subtype. They suggest that variations in the levels of circulating NPY or in the release of NPY by the chromaffin cells themselves (in autocrine and/or paracrine way) can increase the biosynthesis of catecholamines in rat adrenals.

Adrenal Medulla↗
PubMed1995

[Study on expression and regulation of atrial natriuretic factor (ANF) gene in nasal mucosa].

Using 32P labelled rat ANF cDNA probe, the ANF gene transcripts in rat nasal mucosa and the effect of glucocorticoid and estrogen on the ANF gene transcripts was examined by Dot blot and Northern blot hybridization. Further more, the gene expression of ANF in nasal mucosa tissues of some patients with nasal diseases were also examined. The results showed that nasal mucosa contained ANF mRNA which could synthesize ANF. Both estrogen and glucocorticoid could enhance ANF gene expression in nasal mucosa with dose dependance. The gene expression of ANF in nasal polyps and inferior turbinate mucosa of patients with nasal polyps was more evident than that in other pathological conditions. The clinical significance of ANF in nasal mucosa was also discussed.

Adolescent↗
PubMed1995

[Identification of transcription start site of waxy gene in O. sativa subsp. indica 232].

Analysis of Northern blot and the cDNA sequence of rice waxy gene showed that the transcript of rice waxy gene may extend beyond 1.2kb upstream of the tranlation start site. So a 21 nts oligonucleotide was designed as primer. The transcription start site of the waxy gene in O. sativa subsp. indica 232 cultiva was determined by primer extension reaction with the endosperm RNA of indica 232 as template. The context sequence of transcription start site, CTCACCA, fits well with the consensus sequence CTCATCA from higher plant genes with only one base change. The transcription start site of F. spontanea No. 1 waxy gene and the putative TATA boxs of two rices are discussed by comparison of sequence.

Base Sequence↗
PubMed1994

The role of excitatory amino acids in the expression of precipitated acute and chronic clonidine withdrawal: an in vivo voltammetric study in the rat locus coeruleus.

It has been previously shown that activation of excitatory amino acid (EAA) pathways contributes to hyperactivity of the locus coeruleus (LC) in antagonist precipitated opioid withdrawal. In this study, using differential normal pulse voltammetry to monitor catechol oxidation as an index of the activity of the LC, the role of EAA pathways in antagonist precipitated withdrawal after acute and chronic clonidine treatment was examined. Intracerebroventricular clonidine (10 micrograms i.c.v.) significantly reduced LC activity to 54.4 +/- 3.1% of baseline 45 minutes following the injection. Subsequent systemic injection of the selective alpha 2 receptor antagonist atipamezole (0.2 mg/kg i.v.) or yohimbine (0.5 mg/kg i.v.) resulted in a rapid reversal of the depressant effects and a significant increase in LC activity above baseline. Pretreatment with the non-selective EAA receptor antagonist gamma-D-glutamylglycine (DGG) (50 micrograms i.c.v.) attenuated the atipamezole-induced rebound response of the LC but not the reversal of clonidine action. However, both the yohimbine-induced rebound and reversal of clonidine effects were attenuated by DGG treated animals. In chronic clonidine treated animals (2, 5, 7, 10 micrograms/h i.c.v., 5 days), a challenge with atipamezole (0.2 mg/kg i.v.) produced an immediate increase in LC activity, blood pressure and heart rate. The magnitude of these responses was dependent on the dose of clonidine. The atipamezole-induced increase in LC activity and blood pressure was significantly attenuated by pretreatment with DGG (200 micrograms i.c.v.). These findings suggest that LC hyperactivity and blood pressure increases elicited during clonidine withdrawal are mediated in part by activation of EAA receptors. In this regard, the mechanisms underlying clonidine withdrawal closely resembles those underlying opioid withdrawal.

Acute Disease↗
PubMed1994

A new staging system for nasopharyngeal carcinoma in China.

PURPOSE: An accurate and rational nasopharyngeal carcinoma (NPC) stage based on images is proposed. METHODS AND MATERIALS: Four hundred and twenty-one cases of NPC, treated in the Cancer Hospital, Sun Yat-sen University of Medical Sciences (SUMS), with computed tomography scanning before initial radiotherapy, are analyzed. Important prognostic factors that form the basis of the new staging system are screened out by means of Cox model and clinical experiences. Survival curves of various kinds of T and N stages are compared by computer simulation. A new staging system is proposed by studying the traditional staging systems such as the AJC, UICC, Ho's and Changsha systems. RESULTS: According to the new staging criteria, the 5-year survival rates for Stages I-IV are 89.7%, 75.9%, 51.3%, and 22.2%, respectively. CONCLUSION: This new clinical staging for NPC based on a large amount of cases multivariate analysis is satisfactory and widely used in China.

Adult↗
PubMed1994

Role of neuropeptide Y in the regulation of gonadotropin-releasing hormone gene expression in the rat preoptic area.

It is well documented that neuropeptide Y (NPY) is involved in the regulation of the hypothalamo-pituitary gonadal axis. In order to determine the influence of NPY on the biosynthesis of GnRH, we have studied the effects of NPY and some NPY analogs on GnRH gene expression in neurons in the male rat preoptic area (POA). The following peptides NPY, peptide YY (PYY), [Leu31,Pro34]NPY (a Y1 receptor agonist) and NPY13-36 (a Y2 receptor agonist) were injected into the left lateral ventricle of adult castrated male rats. In another series of experiments, the same peptides were administered intravenously (IV). All the animals were perfused with 4% paraformaldehyde 4 hours after injection. Cryostat sections through the POA were processed for quantitative in situ hybridization. The intracerebroventricular injection of PYY, NPY and [Leu31,Pro34]NPY induced a marked increase in the number of grains overlying the labelled neurons (20 to 45% over control). On the other hand, the Y2 receptor agonist NPY13-36 did not influence mRNA levels. Similar results were obtained following the i.v. administration although the magnitude of the stimulating effect was less important (12 to 20% over control). These data then strongly suggest that NPY positively regulates the genetic expression of GnRH in neurons via the Y1 NPY receptor subtype.

Animals↗
PubMed1994

Severe osteoarthrosis after fracture of the mandibular condyle: a clinical and histologic study of seven patients.

The factors that induce complications subsequent to fractures of the mandibular condyle have long been controversial. A clinical and histologic study of seven patients (nine temporomandibular joints [TMJs]) who suffered from severe TMJ problems subsequent to condylar fractures showed that the complications were related to comminution of the condyle, sagittal fracture of the condyle, and subcondylar fracture dislocation. Alterations in these TMJs all involved secondary osteoarthrosis. Additionally, aseptic necrosis, bifid deformity of the condyle (two of the three sagittally fractured condyles), and TMJ ankylosis occurred in these patients. It is suggested that the involved fracture patterns be given more attention by clinicians.

Adult↗
PubMed1993

Evidence for the involvement of excitatory amino acid pathways in the development of precipitated withdrawal from acute and chronic morphine: an in vivo voltammetric study in the rat locus coeruleus.

Previous studies have demonstrated that activation of excitatory amino acid (EAA) pathways projecting to the locus coeruleus may be involved in the increased firing of locus coeruleus (LC) neurons during opioid withdrawal. Using differential normal pulse voltammetry to monitor catechol oxidation current (CA.OC), an index of neuronal activity in the LC, the role of EAA pathways in naloxone precipitated withdrawal after acute and chronic morphine treatment was examined. Acute morphine treatment (10 micrograms i.c.v.) significantly reduced the CA.OC signal in the LC to 54.3 +/- 3.1% of baseline. Naloxone challenge (1 mg/kg i.v.) completely reversed the morphine effect and produced a significant increase in the CA.OC signal above baseline, peak 145.4 +/- 10.1% of baseline. This naloxone-induced rebound response was attenuated by pretreatment with the EAA receptor antagonists gamma-D-glutamylglycine (DGG) (2, 20, 200 micrograms i.c.v.) and (-)-2-amino-7-phosphonoheptanoic acid (D-APH), but not L-APH (25 micrograms i.c.v.). In chronically morphine-treated rats (25 micrograms/h i.c.v., 5 days), naloxone challenge (1 mg/kg i.v.) produced a significant increase in CA.OC signal, peak 466.5 +/- 112.7% of baseline. This naloxone-induced response was attenuated by pretreatment with DGG (200 micrograms i.c.v.) or D-APH (25 micrograms i.c.v.). To the extent that CA.OC reflects locus coeruleus neuronal activity, the present findings further suggest that increases in locus coeruleus activity during naloxone precipitated withdrawal after both acute and chronic morphine treatment are mediated at least in part by activation of EAA pathways.

2-Amino-5-phosphonovalerate↗
PubMed1993

Inhibition of spinal opioid antinociception by intrathecal beta-endorphin1-27 in the rat.

1. The effects of intrathecal (i.t.) administration of beta-endorphin and two shorter fragments, human and ovine beta-endorphin1-27, were examined for antinociceptive activity in the tail-flick and paw-pressure tests in the rat. Additionally, the ability of ovine beta-endorphin1-27 to influence the action of i.t. beta-endorphin, morphine and [D-Pen2-D-Pen5]enkephalin (DPDPE) was also examined in these tests. 2. After i.t. injection, beta-endorphin produced potent dose-related antinociception in the tail-flick and paw-pressure tests. Shorter endorphins produced much weaker effects. The order of antinociceptive efficacy was beta-endorphin > human beta-endorphin1-27 > ovine beta-endorphin1-27. 3. Administration of ovine beta-endorphin1-27 (0.72, 1.44 nmol, i.t.) significantly attenuated the antinociceptive effect of beta-endorphin (2.88 nmol, i.t.) in the tail-flick and paw-pressure tests. 4. Both i.t. morphine and DPDPE produced dose-related antinociception in the tail-flick and paw-pressure tests. The potency of DPDPE was lower than that of morphine in both tests; however, the effect of DPDPE was weaker in the paw-pressure test. 5. Administration of ovine beta-endorphin1-27 (1.44 nmol, i.t.) significantly attenuated the antinociceptive effect of morphine (14.9 nmol, i.t.) in both tests and the effect of DPDPE (38.7 nmol) in the tail-flick test. 6. The results show that beta-endorphin1-27 acts as an opioid antagonist at the spinal level in the rat. Its ability to inhibit the action of morphine and DPDPE suggests that it may attenuate beta-endorphin action by an interaction with mu- and/or delta-opioid receptors.

Analgesics↗
PubMed1992

Stereoselective effects of central alpha 2-adrenergic agonist medetomidine on in vivo catechol activity in the rat rostral ventrolateral medulla (RVLM).

The stereoselective central effects of a novel, highly potent and selective alpha 2-agonist medetomidine on adrenergic neuronal activity, reflected by changes in catechol oxidation current, in the rostral ventrolateral medulla of the halothane-anesthetized rat were examined using in vivo differential normal pulse voltammetry. Dexmedetomidine, the active isomer, significantly decreased catechol oxidation current to 33.4 +/- 4.5% of baseline when given centrally (1 microgram, i.c.v.) and to 10.3 +/- 3.9% of baseline when given systemically (50 micrograms/kg, i.v.). Dexmedetomidine also significantly reduced mean arterial blood pressure by 19.9% following central administration but significantly increased mean arterial blood pressure by 59.9% following systemic administration. Levomedetomidine, the inactive isomer, had no effect on catechol oxidation current or blood pressure. The depressant effects of dexmedetomidine on catechol oxidation current were reversed by the selective alpha 2-adrenoceptor antagonist atipamezole (2 micrograms, i.c.v. or 200 micrograms/kg, i.v.). The results of the present study demonstrate, to our knowledge, for the first time the central stereoselective effects of medetomidine and antagonism by atipamezole on rostral ventrolateral medulla activity in the anesthetized rat.

Adrenergic alpha-Agonists↗
PubMed1992

In vivo catechol activity in the rat locus coeruleus following different nociceptive stimuli and naloxone.

The nucleus locus coeruleus (LC) has been implicated in the processing of spinal reflexes following noxious stimuli. It has been demonstrated that noxious stimuli activate LC neuronal firing, but little is known about the neurochemical changes that might occur following such activation. To determine the effects of different noxious stimuli on LC neuronal activity, anaesthetized rats were exposed to mechanical (tail pinch), thermal (55 degrees C water), and chemical (5% Formalin injected in the hind paw) stimuli; the catechol oxidation current (CA.OC), an index of noradrenergic neuronal activity, in the locus coeruleus was monitored using differential normal pulse voltammetry. In addition, the effect of the opioid antagonist naloxone on the CA.OC in the LC was examined. Exposure to both mechanical and chemical stimuli significantly increased CA.OC indicating an increase in LC noradrenergic neuronal activity, while the thermal stimulus had no effect. Treatment with naloxone (1 mg/kg i.v.) had no effect on CA.OC in the LC. The results show a differential responsiveness of LC noradrenergic neurons to different modes of noxious stimuli and fail to demonstrate a tonic opioid regulation of these neurons in the anaesthetized rat.

Animals↗
PubMed1992

Estradiol, progesterone and testosterone exposures affect the atrial natriuretic peptide gene expression in vivo in rats.

To clarify the effects of sex hormones on the expression of atrial natriuretic peptide (ANP), ovariectomized and intact female rats were subcutaneously injected with estradiol, progesterone, a mixture of them or olive oil solvent; castrated and untouched male rats were subcutaneously injected with estradiol, testosterone or olive oil, once a day for 7 days. The relative rANP-mRNA contents of rat atrial were measured by molecular hybridization. rANP-cDNA was labeled with 32P as a probe. The results revealed that estradiol and progesterone increased ANP gene expression. Furthermore their effects were associated with administration dose of these hormones and it was shown that they are probably coordinated. The physiological amounts of estradiol and progesterone may maintain suitable levels of rANP-mRNA and androgen may also increase the ANP gene expression in vivo. These experiments suggested that female sex hormone may have a dual purpose in fluid balance.

Animals↗
PubMed1992

[Effects of female sex hormones on atrial natriuretic factor gene expression in rats].

To clarify the effects of female sex hormones on ANF gene expression, emasculated and intact female rats were subcutaneously injected with estradiol (E2), progesterone (P) and olive oil solvent (O) respectively, once a day for 7 days. The relative rANF-mRNA contents of rat atria were measured by molecular hybridization, and rANF-cDNA was labeled with alpha-32P as probe. The groups and hormone doses per 100 g body weight were: (1) sham, 0.2 ml O; (2) rats were bilaterally ovariectomized(OVX), 0.2 ml O; (3) OVX, 80 ng E2; (4) OVX, 80 micrograms E2; (5) OVX, 0.2 mg P; (6) OVX, 2 mg P; (7) OVX, 80 ng E2, 0.2 mg P. The results showed that the rANF-mRNA of group (2) was the lowest, it was 75% of that in group (1), while the rANF-mRNA levels in groups (3)-(7) were 1.1, 2.0, 1.9, 2.3 and 2.1 folds of that in group (2) respectively. The results revealed that E2 and P increased ANF gene expression. Their effects were associated with the dosage. The two may have synergistic actions. Physiological amount of E2 and P may maintain suitable level of rANF-mRNA. This experiment suggested that female sex hormone may have dual effects in body fluid balance.

Animals↗
PubMed1992

Effect of gluco- and mineralocorticoids on gene expression of atrial natriuretic peptide by rat atria in vivo.

The effect of gluco- and mineralocorticoids on atrial natriuretic peptide (ANP) gene expression as well as plasma sodium and potassium concentrations was studied in both intact and adrenalectomized Wistar rats. Atria total RNA was extracted with cold phenol method and hybridized to alpha-32P labeled rat ANP-cDNA probe. The ANP gene transcripts in intact rats receiving dexamethasone and in adrenalectomized rats receiving both dexamethasone and deoxy-corticosterone increased by twofold, while there were no significant changes in the other groups. There were no parallel correlations between the rise of corticoid hormones-induced plasma Na+ concentration and the enhancement of rANP-mRNA level. The results suggest that glucocorticoids, when used together with mineralocorticoids, may directly increase ANP gene expression, whereas administration of mineralocorticoids alone has no effect on ANP gene expression.

Adrenalectomy↗