Search PubMed⌕ Search

Biomedical subjects

J Fang

Publications and source records attributed to J Fang.

At least 19 recordsLinked to original sources
PubMed1995

Pituitary adenylate cyclase activating polypeptide enhances rapid eye movement sleep in rats.

Pituitary adenylate cyclase activating polypeptide (PACAP), a member of the vasoactive intestinal polypeptide family, was tested for its effects on sleep in adult male Sprague-Dawley rats. PACAP was injected via intracerebro-ventricular cannula at light or dark onset; sleep and brain temperature (Tbr) were recorded for 12 h after injection. Rapid eye movement sleep (REMS) was significantly enhanced by 30 pmol, but not 3 or 300 pmol PACAP injected at dark onset. Non-REMS was not influenced by 3, 30, or 300 pmol PACAP Sleep and Tbr were not influenced by 3 or 30 pmol PACAP injected at light onset.

Animals↗
PubMed1995

A new approach to motor unit estimation with surface EMG triggered averaging technique.

A new method for estimating the number of motor units using a surface EMG triggered averaging technique is described. This method provides an estimation of mean motor unit potential (MUP) amplitude at different levels of contraction, which can be utilized to estimate the number of motor units in a given muscle. Motor unit count estimated in abductor pollicis brevis (APB) muscle of 11 normal healthy subjects ranged from 131 to 371 with a mean of 246 +/- 68. In our preliminary study of patients with lower motor neuron lesions, there was a significant reduction in the number of motor units. We believe our new noninvasive method of motor unit counting is a relatively simple and reproducible physiological technique.

Adult↗
PubMed1995

Inhibition of monoamine oxidases by haloperidol and its metabolites: pharmacological implications for the chemotherapy of schizophrenia.

The effect of haloperidol and its metabolites on human platelet monoamine oxidase B (MAO-B) and human placenta monoamine oxidase A (MAO-A) in vitro has been investigated. We found that 4-(4-chlorophenyl)-1-[4-(4-fluorophenyl)-4-oxobutyl]-pyridinium (HP+), 4-(4-chlorophenyl)-1-[4-(4-fluorophenyl)-4-oxobutyl]-1,2,3,6- tetrahydropyridine (HTP) and 4-chlorophenyl-1,2,3,6-tetrahydropyridine (CPTP) are potent inhibitors of MAO. HP+ appeared to be a reversible, uncompetitive and selective MAO-B inhibitor with a Ki of 0.83 microM. HTP was found to be an irreversible, uncompetitive and selective MAO-B inhibitor (Ki of 1.84 microM). CPTP inhibits both MAO-A and MAO-B. Some other haloperidol metabolites, i.e. 4-(4-chlorophenyl)-4-hydroxypyridine (CPHP), 4-(4-chlorophenyl)-1-[4-(4-fluorophenyl)-4-oxobutyl]-1,2,3,6- tetrahydropyridine N-oxide (HTPNO) and reduced haloperidol (RHAL), do not inhibit MAO to any appreciable degree at concentrations up to 100 microM. The results suggest that haloperidol metabolites may contribute to the reduction of platelet MAO-B activity in schizophrenic patients undergoing neuroleptic chemotherapy. An examination of the literature reveals that schizophrenic patients with low platelet MAO activity exhibit a strong association with the use of haloperidol. Other possible pharmacological implications of the inhibition of MAO activity are discussed.

Blood Platelets↗
PubMed1995

Lack of protective effect of R(-)-deprenyl on programmed cell death of mouse thymocytes induced by dexamethasone.

R(-)-Deprenyl, an archetypical MAO-B inhibitor, has been shown to delay the onset of the disabling syndrome of Parkinson's disease and to be useful in the treatment of Alzheimer's disease. Recently, R(-)-deprenyl has been claimed to be capable of preventing apoptosis of PC12 cells, which had been primed with nerve growth factor (NGF) and followed by withdrawal of serum. We investigated the effect of R(-)-deprenyl in a non-neuronal cell model, namely, apoptosis of mouse thymocytes induced by dexamethasone. Trypan blue exclusion and lactate dehydrogenase activity were applied to assess the cell survival. R(-)-Deprenyl did not exhibit any detectable protective effect to the thymocytes from apoptosis. The result is further confirmed by examining the apoptotic DNA fragmentation using gel electrophoresis and assessing the soluble DNA released by a spectrophotometric method.

Animals↗
PubMed1995

Cytokines in sleep regulation.

The central thesis of this essay is that the cytokine network in brain is a key element in the humoral regulation of sleep responses to infection and in the physiological regulation of sleep. We hypothesize that many cytokines, their cellular receptors, soluble receptors, and endogenous antagonists are involved in physiological sleep regulation. The expressions of some cytokines are greatly amplified by microbial challenge. This excess cytokine production during infection induces sleep responses. The excessive sleep and wakefulness that occur at different times during the course of the infectious process results from dynamic changes in various cytokines that occur during the host's response to infectious challenge. Removal of any one somnogenic cytokine inhibits normal sleep, alters the cytokine network by changing the cytokine mix, but does not completely disrupt sleep due to the redundant nature of the cytokine network. The cytokine network operates in a paracrine/autocrine fashion and is responsive to neuronal use. Finally, cytokines elicit their somnogenic actions via endocrine and neurotransmitter systems as well as having direct effects neurons and glia. Evidence in support of these postulates is reviewed in this essay.

Acute-Phase Reaction↗
PubMed1995

Growth-hormone-releasing hormone mediates the sleep-promoting activity of interleukin-1 in rats.

The involvement of endogenous growth-hormone-releasing hormone (GHRH) in the sleep-promoting activity of interleukin-1 (IL1) was studied. The effects on sleep of intracerebroventricular injection of IL1 were tested in rats pretreated with intracerebroventricular antibodies to GHRH (GHRH-ab). One group of rats received two treatments each consisting of two injections, control IgG + physiological saline (IgG + Sal) and on another day GHRH-ab + Sal, whereas another group of rats received IgG + Sal, IgG + IL1 and GHRH-ab + IL1 on separate days with one day off between the various treatments. IgG or GHRH-ab was injected 6 h prior to dark onset; Sal or IL1 was administered at dark onset. Recording of sleep-wake activity and cortical brain temperature (Tcrt) was started with the injection of IgG or GHRH-ab and continued for 18 h. GHRH-ab (GHRH-ab + Sal) suppressed rapid eye movement sleep (REMS), non-REMS (NREMS) and EEG slow-wave activity (SWA) during NREMS throughout the recording period. IL1 treatment (IgG + IL1) enhanced NREMS and SWA, and induced fever for 6 h. Pretreatment with GHRH-ab (GHRH-ab + IL1) abolished the IL1-induced increases in NREMS, attenuated the enhancements in SWA, and suppressed fever for 6 hours after IL1. The results indicate that the sleep-promoting activity of IL1 is mediated at least in part via GHRH. The suppression of the IL1-induced fever by GHRH-ab might be attributed to an inhibition of hypothalamic somatostatin.

Animals↗
PubMed1995

Isolated diastolic hypertension. A favorable finding among young and middle-aged hypertensive subjects.

To identify pretreatment characteristics associated with subsequent myocardial infarction in young and middle-aged previously untreated hypertensive individuals, we examined the experience of 1560 participants in a work-site hypertension control program who were younger than 60 years. Subjects were categorized by initial blood pressure as having isolated diastolic hypertension (< 160/> or = 90 mm Hg, n = 965) or combined systolic and diastolic hypertension (> or = 160/> or = 90 mm Hg, n = 595). During 4.5 years of follow-up, there were 24 myocardial infarctions, yielding an overall incidence of 3.89 per 1000 person-years. Subjects with systolic/diastolic hypertension were older, had higher cholesterol and blood sugar levels, and included more smokers and people with left ventricular hypertrophy on electrocardiogram than those with isolated diastolic hypertension. Age-adjusted incidence rates for myocardial infarction were 5.20 and 2.21 per 1000 person-years in systolic/diastolic hypertension and isolated diastolic hypertension, respectively, and the relative risk of systolic/diastolic hypertension was 2.31 (95% confidence interval, 1.29-4.15). Among subjects with isolated diastolic hypertension, no myocardial infarction occurred in those with systolic pressure less than 140 mm Hg. Cox regression analysis including other known risk factors showed that pulse pressure, as a continuous variable (hazards ratio, 1.54; 95% confidence interval, 1.08-2.20), and type of hypertension, ie, systolic/diastolic hypertension versus isolated diastolic hypertension (hazards ratio, 2.11; 95% confidence interval, 1.08-4.13), were independently associated with myocardial infarction. These results suggest that young and middle-aged treated hypertensive individuals with normal pretreatment systolic pressure enjoy a more favorable prognosis than do those with systolic elevation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effects of Phytolacca acinosa polysaccharides I combined with interleukin-2 on the cytotoxicity of murine splenocytes against tumor cells.

Phytolacca acinosa polysaccharides I (PAP-I), a kind of purified polysaccharides, isolated from Phytolacca acinosa Roxb was found to significantly augment the cytotoxicity of murine splenocytes and interleukin-2 (IL-2) activated splenocytes against P815 tumor cells in vitro. The optimal concentration of PAP-I was 1 microgram.ml-1 and the peak level of the cytotoxicity against P815 tumor cells was reached on d 3-5. The supernatants collected from splenocytes cultured with PAP-I alone or in combination with IL-2 showed no effect on the cytotoxicity against P815 tumor cells. Splenocytes from mice injected ip with PAP-I, 5, 10 and 50 mg.kg-1, thrice a week produced more cytotoxicity against P815 and L929 tumor cells compared with the control group. PAP-I ip was shown to significantly increase IL-2 activated killer cell activity (LAK) against P815 tumor cells. The higher the dosage of PAP-I, the more potent the LAK activity was observed. These results confirmed that PAP-I can augment the cytotoxicity of murine splenocyte against tumor cells and LAK activity and warranted further evaluation of its clinical usefulness.

Animals↗
PubMed1995

Differential expression of neural cell adhesion molecule (NCAM) during osteogenesis and secondary chondrogenesis in the embryonic chick.

Progenitor cells in the periosteum-perichondrium of the posterior hook of the quadratojugal (QJ, a membrane bone) in the embryonic chick are bipotential for osteogenesis and chondrogenesis. These cells switch from osteogenesis to chondrogenesis between 10 to 11 days in normal (mobile) embryos but not in paralyzed (immobile) embryos. Expression of neural cell adhesion molecule (NCAM) was studied using a monoclonal antibody in QJ hooks from normal and paralyzed chick embryos between 10 and 21 days of incubation. NCAM is expressed in osteoprogenitor cells and osteoblasts but not in chondroprogenitor cells, chondroblasts, or chondrocytes. The switch of progenitor cell differentiation from an osteogenic to a chondrogenic pathway between 10 and 11 days of incubation coincides with down-regulation of NCAM expression. Both initiation of secondary chondrogenesis and down-regulation of NCAM depend on biomechanical stimulation. In embryos paralyzed at 9 days, secondary cartilage fails to form and progenitor cells remain positive for NCAM. Furthermore, paralysis influences NCAM expression in progenitor cells before secondary chondrogenesis morphologically begins, indicating that NCAM may play a role in the initiation of secondary chondrogenesis. In 15-day normal embryos, NCAM-positive cells accumulate between the perichondrium and secondary cartilage in a position that prevents further cartilage formation in the hook. In 19-day embryos, these cells lose their NCAM expression and restart chondrogenesis in a second phase of differentiation, forming an articular cartilage. Loss of NCAM expression in this cell layer and re-commencement of chondrogenesis do not occur in embryos paralyzed at 13 days, and therefore also require biomechanical stimulation. Hence, down-regulation of NCAM expression correlates with two phases of secondary chondrogenesis in embryonic life, both of which are dependent upon embryonic movement.

Animals↗
PubMed1995

[Effect of xiaopiling granules on muscular histochemistry of gastric precancerous changes in rats].

The effect of Xiaopiling Granules on muscular histochemistry of gastric precancerous changes in rats was observed quantitatively. The activity of SDH and M-ATPase as well as the content of muscular glycogen in model groups were found significantly lower than those of the normal groups (p < 0.01), and in this decrease Xiaopiling Granules had markedly played a preventive and therapeutic role.

Animals↗
PubMed1995

Measures of blood pressure and myocardial infarction in treated hypertensive patients.

OBJECTIVE: To identify entry characteristics associated with subsequent myocardial infarction in treated hypertensive patients. DESIGN: Nested case-control study and cohort study. SETTING AND PATIENTS: The 5730 participants (mean age 53 years; 61% male and 45% Caucasian) were selected from a worksite-based, union-sponsored, systematic hypertension control program from 1973 to 1992. METHODS: In the case-control study myocardial infarction cases were matched by age, sex, year of entry to the program, years of follow-up and previous treatment status (treated or untreated) with non-event subjects. Baseline clinical and biochemical characteristics were analyzed with regard to the outcome of myocardial infarction, using univariate and multivariate analyses, respectively, in case-control and cohort studies. RESULTS: During 5.43 years of follow-up the incidence of myocardial infarction was 6.75/1000 person-years. Univariate analysis indicated that myocardial infarction cases had higher cholesterol level and were more likely to have a previous history of diabetes than controls. The initial systolic blood pressure and pulse pressure of cases were significantly higher than in controls. Logistic regression models indicated that initial pulse pressure, either as a continuous or as a categorical variable, was the only measure of blood pressure independently associated with myocardial infarction after adjustment for other risk factors. Analysis of the experience of the total 5730 as well as 2445 previously untreated patients with a cohort study generated identical results. CONCLUSION: A large pulse pressure difference appears to be the most powerful measure available of initial blood pressure to identify, in advance, those hypertensive patients at greatest risk for a subsequent myocardial infarction.

Blood Glucose↗
PubMed1995

[Effects of 3 kinds of decoction on serum gastrin, gastrin cell density and the content of PGE2 of gastric antral mucosa in experimental chronic gastritis in rats].

Experimental chronic gastritis (ECG) models were established in rats by inserting a spring into pyloric canal as well as feeding sodium deoxycholate. An experiment was undertaken to observe the therapeutic effects of three formulas of traditional Chinese medicine "Shipitong" (SPT), "Ganpingyangwei" (GPYW) and "Weile" (WL). The experimental results show that all of the three decoctions can make serum gastrin, gastrin cell density and amount of antral mucosal PGE2 of the ECG rats return to normal levels.

Animals↗
PubMed1995

[Antitumor activities of 8-chloroadenosine in vivo and in vitro].

8-chloroadenosine showed marked activity against mice solid tumor hepatoma 22 (H22) and ascitic leukemia L-1210. At 100mg. Kg-1. /d x 7, the inhibition rate of H22 was 71.7 +/- 13.3% (P < 0.01) and 66.1 +/- 4.46% (P < 0.01), i.p. and i.v., respectively; at the same dose, the life-prolonging rate of mice bearing L-1210 was 124.0 +/- 22.1% (P < 0.01) and 104.2 +/- 20.1% (P < 0.01), i.p. and i.v., respectively. 8-chloroadenosine also showed activity against 3 human cancer cell lines in vitro. The IC50 values were determined by measuring cell growth using trypan blue dye exclusion. The results showed that HL-60 and K562, and human gastric cancer cell line MGc80-3 and IC50 values of 1. 8 mumol/L, 4.2 mumol/L and 1.56 mumol/L, respectively. The toxicity of 8-chloroadenosine was low, with LD50 of 1025.0 +/- 52.4 mg/kg for mice and 793.4 +/- 70.1 mg/kg for rats by single i.p. injection.

2-Chloroadenosine↗
PubMed1995

Crossed inhibition in the human motor system.

We used transcranial magnetic stimulation in humans to investigate the effect of focal unilateral stimulation of the motor cortex on the function of the contralateral motor cortex. Surface-recorded, rectified, averaged electromyography (EMG) showed relative silent periods in small hand muscles at 35-64 and 123-158 ms following ipsilateral cortical stimulation over the hand area. The first inhibitory phase started 11 ms after the minimum corticospinal conduction time from the contralateral cortex, appropriate for transcallosal conduction. Foot muscles (with focal stimulation over the ipsilateral hand area) also showed silent periods at 61-104 ms, indicating a marked spread of the inhibitory effect throughout the opposite motor cortex. H-reflex studies in the upper limb showed that this inhibitory effect was not mediated at the level of the alpha motoneuron. Single motor unit peristimulus time histogram studies in upper limb muscles showed inhibition similar to that seen in the surface recordings and no evidence of excitation following ipsilateral motor cortex stimulation. Transcranial magnetic stimulation performed with large circular coils centered at the vertex activates both excitatory and inhibitory processes bilaterally so that focal unilateral stimulation is preferable in detailed studies of motor system physiology.

Adult↗
PubMed1994

Inhibition of nitric oxide synthesis inhibits rat sleep.

Previous findings indicate that nitric oxide (NO) may play a role in the regulation of sleep-wake activity. In rabbits, blocking the production of endogenous NO by a nitric oxide synthase inhibitor, N omega-nitro-L-arginine (L-NAME) suppresses spontaneous sleep and interferes the somnogenic actions of interleukin 1. In the present experiments we extended our earlier work by studying the long-term effects of L-NAME treatment on sleep-wake activity including power spectra analyses of the electroencephalogram (EEG) in rats. Rats implanted with EEG electrodes, brain thermistor, and intracerebroventricular (i.c.v.) guide cannula were injected i.c.v. with vehicle or 0.2, 1, or 5 mg L-NAME at light onset. In separate experiments, rats were injected intraperitoneally (i.p.) with L-NAME three times (50, 50, 100 mg/kg), 12-12 h apart. Both i.c.v. and i.p. injections of L-NAME elicited decreases in time spent in NREMS and REMS. After i.c.v. injection of 5 mg L-NAME the sleep responses were long-lasting; NREMS did not return to baseline even 72 h after injection. EEG delta-wave activity during NREMS (slow wave activity) was also suppressed after 0.2 and 5 mg L-NAME. Brain temperature was slightly increased after the two lower doses of L-NAME, whereas there was a transient decrease in Tbr after 5 mg L-NAME. Acute i.p. injection of 50 mg/kg L-NAME elicited an immediate decrease in NREMS which lasted for approximately 2 h. The second injection of 50 mg/kg L-NAME and the following injection of 100 mg/kg L-NAME induced biphasic decreases in NREMS but not REMS.

Amino Acid Oxidoreductases↗
PubMed1994

Increase of prolactin mRNA in the rat hypothalamus after intracerebroventricular injection of VIP or PACAP.

Vasoactive intestinal peptide (VIP), the structurally homologous pituitary adenylate cyclase-activating peptide (PACAP) and the pituitary hormone, prolactin (PRL) enhance rapid eye movement sleep (REMS). VIP and PACAP are both inducers of PRL gene expression and release in the pituitary gland. Little is known about PRL regulation in the brain although it is hypothesized that the REMS-promoting activity of i.c.v. administered VIP may be mediated via the activation of cerebral PRL. To test whether VIP or PACAP in fact increase intracerebral mRNA, the peptides (VIP: 30 or 300 pmol; PACAP: 220 pmol) were injected i.c.v. into rats at dark onset. 1 h later, cDNA was synthesized from purified hypothalamic mRNA. Standardized amounts were analysed for PRL using the polymerase chain reaction followed by Southern blotting and hybridization. Compared with beta-actin mRNA levels, both VIP and PACAP increased PRL mRNA levels in a dose-dependent fashion though VIP was more effective on a molar basis. The previously reported alternatively spliced PRL mRNA (lacking exon 4) was not detected. The data support the hypothesis that the REMS-promoting activity of central VIP and PACAP might be mediated by cerebral PRL.

Animals↗
PubMed1994

Effect of L-deprenyl, its structural analogues and some monoamine oxidase inhibitors on dopamine uptake.

The effect on dopamine uptake by L-deprenyl, its structural analogues and different types of monoamine oxidase (MAO) inhibitors was investigated. Both direct [3H]dopamine uptake into rat striatal slices and binding of a specific dopamine uptake inhibitor [3H]GBR-12935 were used in the present study. L-Deprenyl exhibits a relatively weak dopamine uptake inhibitory effect in vitro, while D-deprenyl possesses a very potent inhibitory effect. The potent effect of D-deprenyl on dopamine uptake may be responsible, at least in part, for its behavioral effects and abuse liability. L-Methamphetamine, a metabolite of L-deprenyl, does not inhibit [3H]GBR-12935 binding but it reduces the retention of [3H]dopamine in striatal tissues, suggesting that it may enhance dopamine release. The MAO-A inhibitors clorgyline and brofaromine also exhibit dopamine uptake inhibitory effects. Irreversible and reversible MAO-B inhibitors, however, such as pargyline, aliphatic N-methylpropargylamines, Ro 19-6327 and MDL-72974A and MAO-A inhibitor moclobemide do not possess any appreciable inhibitory effects on dopamine uptake. Dopamine uptake is probably unrelated to the pharmacological actions of L-deprenyl.

Animals↗