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Biomedical subjects

J Fang

Publications and source records attributed to J Fang.

At least 271 records · Page 15Linked to original sources
PubMed1996

Hyperactive behavioural effects induced by intranigral infusion of a pyridinium metabolite of haloperidol in rats.

Amphetamine-like behaviours such as sniffing and head movements were observed in rats intranigrally injected with a pyridinium metabolite of haloperidol (HP+). Photobeam interruptions by rats injected with HP+ were over 200 times more frequent than those of control rats 24 h after the operation. This apparent dopamine agonist effect of HP+ may be relevant to some of the clinical side effects of haloperidol such as acute dystonia and chronic tardive dyskinesia, which have been proposed to be the result of dopaminergic hyperactivity.

Animals↗
PubMed1996

Experimental study on spontaneous DNA synthesis of tonsillar lymphocytes in chronic recurrent tonsillitis and focal tonsillitis.

The immune function of tonsils and the immunological mechanisms of focal tonsillitis are still controversial. We do have some knowledge about the structure of tonsillar cells, but their functional status is still not clear. In 40 cases of chronic recurrent tonsillitis and 20 cases of focal tonsillitis with glomerular nephritis, cell culture of tonsillar lymphocytes was removed in vitro and 3H-tymidin incorporation applied to investigate the spontaneous DNA synthesis of tonsillar lymphocytes. The results demonstrated that: i) In chronic tonsillitis, spontaneous DNA synthesis of tonsillar lymphocytes in children is significantly stronger than that in adults (19,946 +/- 5,612 vs 9,216 +/- 5,702 cpm) (p <0.01). ii) Spontaneous DNA synthesis of tonsillar lymphocytes in focal tonsillitis is significantly stronger than that in the chronic recurrent tonsillitis in patients of the same age (25,307 +/- 12,231 cpm vs 12,455 +/- 7,914 cpm) (p <0.01). This indicates that the tonsillar lymphocytes are active in focal tonsillitis, can produce large amounts of memory B-cell clones, which reach other parts of the body through the blood and cause autoimmune reaction which can be blocked by tonsillectomy, thus curing the systemic disease.

Adolescent↗
PubMed1996

Alterations of level of total genomic DNA methylation and pattern of c-myc, c-Ha-ras oncogene methylation in human gastric carcinogenesis.

OBJECTIVE: To investigate the status of DNA methylation in gastric carcinogenesis. METHODS: We analysed methylation pattern of c-myc, c-Ha-ras oncogenes by southern blot hybridization. DNA from cancerous, paracancerous and non-cancerous area of surgically resected samples in 21 cases of advanced gastric cancer were digested with MspI/HpaII and hybridized with the two genomic 32P labelled probes. In addition, the level of total genomic DNA methylation was measured by incubating DNA with 3H-S-Adenosylmethionine (3H-SAM) in the presence of a methylase which methylates all the cytosine residues that are in the double CpG (cytosine-guanine). RESULTS: The results indicated that both c-myc and c-Ha-ras oncogene fragments containing CCGG sequence were hypomethylated in DNA samples from cancerous (10/21 and 5/10) and paracancerous (13/21 and 4/10) areas. Moreover, the level of total genomic DNA methylation in cancerous tissue was significantly lower than that in non-cancerous and paracancerous mucosa tissues (P < 0.05). The results from two methods are incompletely alike. CONCLUSION: These results supported a strong correlation between DNA hypomethylation and gastric carcinogenesis, particularly methylated pattern of c-myc and c-Ha-ras oncogenes fragments containing CCGG sequence was abnormal in gastric mucosa tissue from gastric cancerous and paracancerous areas.

Adult↗
PubMed1996

[Influence of different needling methods on fever caused by E. bacillus coli injection in rabbit].

The theory of reinforcement and reduction with acupuncture is one of the important contents of the needling techniques in acupuncture. In order to verify the theory, experimental fever caused by venous injection of E. Bacillus coll in rabbits were treated by acupuncture at Quchi(LI 11) with different needling methods (reinforcing or reducing) and stimulations (acupuncture or electroacupuncture). The results showed that each of the three reducing techniques with simple rotating of needle, rotation with lifting-thrusting needle and electroacupuncture presented the fever-subduing effects, especially obtaining the immediate effect and lowering the peak of fever. Among them, the former two had the better result than electroacupuncture. The reinforcing technique with rotating needle did not give rise to the significant effect on lowering fever. The result indicates that there exist significant differences in the effect on fever-subduing between reinforcing and reducing methods with acupuncture and between acupuncture and electroacupuncture. The simple reducing needling technique share the same therapeutic result with compound one. The work provides avaluable example for further laboratory study of reinforcing-reducing theory of acupuncture.

Acupuncture Therapy↗
PubMed1996

[Study of nitric oxide synthases, nitric oxide and tumor necrosis factor in different types of ascites].

The purpose of this study was to elucidate the clinical significance of nitric oxide synthases (NOS), nitric oxide (NO) and tumor necrosis factor (TNF) in different types of ascites. NOS, NO and TNF in ascitic transudates of 21 patients with liver cirrhosis, ascitic exudate of 32 patients with liver cirrhosis and carcinogenesic ascites of 19 patients were measured by Griess, ELISA and colorimetric methods. Compares to the value in ascitic transudate of 21 patients with liver cirrhosis, NOS (7.32 +/- 3.13 nmol.min-1.g-1), NO (15.4 +/- 7.6 mumol/L) and TNF (331.7 +/- 121.2 mumol/L) in ascitic exudate of 32 patients with liver cirrhosis were significantly higher (P < 0.01). The NO (10.7 +/- 3.2 mumol/L) and TNF (185.6 +/- 84.1 mumol/L) in carcinogenesic ascites of 19 patients were between those in ascitic exudates and those in ascitic transudates of patients with liver cirrhosis (P < 0.05 or 0.01). The NOS activity was highest in carcinogenesic ascites. The decrease of 24h urine volume in patients with cirrhosis was relative to the increase of NO level in ascites. Those suggested that measurements of NOS, NO and TNF in ascites are helpful in differential diagnosis of ascites. The separation between NO level and NOS activity in ascites indicates that the ascites is carcinogenesis.

Adolescent↗
PubMed1996

[Effect of xiaopiling granules on the treatment of gastric precancerous changes as detected by image analyzer and electronic microscope].

Therapeutic effect of Xiaopiling Granules on gastric precancerous changes was observed, using image analyzer and electronic microscope. The result indicated that the Granules could efficiently eliminate gastric mucositis, nourish gastric mucosa, soften or restrain dysplasia, ameliorate structure atypism and cell atypism of dysplasia, promote elimination of dysplasia and efficiently ameliorate the ultrastructure of gastric precancerous changes.

Adult↗
PubMed1995

An anti-tumor necrosis factor antibody suppresses sleep in rats and rabbits.

It is hypothesized that tumor necrosis factor (TNF) is an endogenous sleep-promoting substance. In the present experiments we studied the effects of a monoclonal anti-TNF antibody in rats and rabbits. Seven rats and 14 rabbits were implanted with electroencephalographic electrodes, a brain thermistor and an intracerebroventricular guide cannula. The animals were injected with saline, control IgG, and monoclonal hamster anti-murine-TNF antibodies (TNFab) on 3 separate days. Ten micrograms TNFab suppressed non-rapid-eye-movement sleep (NREMS) in rats. In rabbits, 2.5 micrograms TNFab did not affect sleep but decreased brain temperature; in contrast, 25 micrograms TNFab suppressed NREMS without affecting brain temperature. These results are consistent with the hypothesis that endogenous TNF plays an important role in sleep regulation.

Analysis of Variance↗
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 tumor necrosis factor in the brain suppresses rabbit sleep.

Tumor necrosis factor (TNF) is a cytokine that possesses many biological activities, including enhancement of non-rapid-eye-movement sleep (NREMS). The role of endogenous TNF in the regulation of spontaneous sleep is unknown. If TNF is involved in sleep regulation, then reduction of endogenous TNF should suppress spontaneous sleep. A soluble TNF-binding protein I (TNF-BP I) and a synthetic fragment of TNF-BP I, TNF-R-(159-178), that contains the biologically active region of TNF-BP I, were used. These substances bind TNF and possess TNF-inhibitory activity; their effects on rabbit sleep after intracerebroventricular injection were determined across a 6-h recording period. Two doses of TNF-BP I (0.05 micrograms and 0.5 micrograms) were administered; the higher dose of TNF-BP I significantly decreased NREMS. Four doses of TNF-R-(159-178) (0.25 micrograms, 2.5 micrograms, 25 micrograms and 50 micrograms) were used. The 25 micrograms and 50 micrograms doses significantly suppressed NREMS. The highest dose (50 micrograms) also decreased REM sleep. These results are consistent with the hypothesis that endogenous brain TNF is involved in the regulation of normal sleep.

Animals↗
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

Comparison of cytotoxicity of a quaternary pyridinium metabolite of haloperidol (HP+) with neurotoxin N-methyl-4-phenylpyridinium (MPP+) towards cultured dopaminergic neuroblastoma cells.

Haloperidol has recently been found to be metabolized to its pyridinium ion (HP+). This conversion of haloperidol to HP+ appears to be similar to the activation of the dopaminergic neurotoxin N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to N-methyl-4-phenyl pyridinium ion (MPP+). MPP+ is responsible for the damage of striatal dopaminergic neurons induced by MPTP in humans and animals. It seemed sensible to investigate whether or not HP+ might be toxic towards dopaminergic neurons and perhaps associated with some of the residual moto-function side effects of haloperidol. We therefore investigated the neurotoxicity of HP+ toward cultured human dopamine neuroblastoma cells (SH-SY5Y) and compared it with that of MPP+. HP+ reduced the viability as measured by MTT and [3H]thymidine incorporation methods in SH-SY5Y cells. Cell membrane integrity is reduced by the treatment of HP+ as measured by intracellular LDH levels. The toxicity was concentration and time dependent. Interestingly, HP+ appeared to be more toxic than MPP+ towards the SH-SY5Y cells in early phase in cultures. The toxicity of MPP+ appear to be progressive and subsequently become more than HP+ with prolonged cultivation. In contrary to MPP+, the toxic effect of HP+ towards a dopamine transporter transfected SK-N-MC cell line is not different from its wild type. This indicates that dopamine uptake system is probably not involved in the cytotoxicity caused by HP+.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1995

Effect of haloperidol and its metabolites on dopamine and noradrenaline uptake in rat brain slices.

The effects of haloperidol and its metabolites on dopamine (DA) and noradrenaline (NA) uptake were investigated. Both direct uptake of [3H]DA and [3H]NA into the rat striatal and hippocampus slices and binding of a specific DA uptake inhibitor [3H]GBR-12935 were employed in the present study. Haloperidol pyridinium (HP+), haloperidol 1,2,3,6-tetrahydropyridine (HTP), 4-(4-chlorophenyl)-1,2,3,6-tetrahydropyridine (CPTP) and reduced haloperidol (RHAL) are potent inhibitors of DA uptake. HTP N-oxide (HTPNO) exhibits a relatively weak effect on DA uptake. Other metabolites of haloperidol, i.e. 4-(4-chlorophenyl)-4-hydroxypyridine (CPHP) and haloperidol N-oxide (HNO), as well as haloperidol itself possess negligible inhibitory effect on DA uptake. HP+ has been shown to be an amine releaser. It is possible that HP+ may induce amphetamine-like neurotoxicity. The effects of the metabolites of haloperidol on [3H]NA uptake are similar to those on [3H]DA uptake. HP+ appears to be different from MPP+, which is a more potent [3H]NA uptake blocker than on [3H]DA uptake. Although haloperidol exhibits no DA uptake inhibitory effect, it has a high affinity for the [3H]GBR-12935 binding site. The possible pharmacological implications such inhibitory effects on amine uptake are discussed.

Animals↗
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↗