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Biomedical subjects

B Xu

Publications and source records attributed to B Xu.

At least 181 records · Page 10Linked to original sources
PubMed1999

[Morphological changes of external eyes before and after blepharoplasty].

OBJECTIVE: To discuss the morphological changes of external eyes before and after blepharoplasty. METHODS: A survey of 92 patients treated by blepharoplasty was carried out to compare the external eye morphology of pre-operation with that of post-operation. RESULTS: It was found significant differences in the post-operative patients, including the increased length and height of eyelids, and obvious changes of the length and angle of the exposed eyelashes. CONCLUSION: Blepharoplasty makes the eyelashes exposed and held up, and increases the up-to-low distance of eyelids. These changes promote the beauty of eyes.

Adolescent↗
PubMed1999

[Relationship between expression of estrogen receptor progestrone receptor and the biological characteristics of nasopharyngeal carcinoma].

OBJECTIVE: To Clarity the relationship between the expression of the estrogen receptor (ER), progestogen receptor (PR) and the biological characteristics of nasopharyngeal carcinoma (NPC). METHOD: The immuno-histochemical LSAB method was used to analyse the ER and PR in paraffin section specimen of 71 cases of nasopharyngeal carcinoma. CT scaning and clinic presentation were also put into consideration. RESULT: The expression of ER with (-), (+), (++) and (+++) in 71 cases were: 4(5.63%), 19(26.76%), 27(38.03%) and 21 (26.76%), respectively. The expression of PR with (-), (+) and (++) in 71 cases were: 41(57.75%), 29 (39.44%) and 2(2.82%), respectively. The encroaching of tumor to the tissue of parapharynx, the metastasis rate of lymphonode and clinic stage were related to the expression of ER (P < 0.01). The encroaching of tumor to the tissue of parapharynx, the metastasis rate of lymphonode were also assciated with the expression of PR (P < 0.05). CONCLUSION: NPC is a tumor of hightly expression of ER and PR. The positive intensity of ER and PR were associated with the encroaching extent of NPC, and the metastasis rate of lymphonode. It is significant to detarmine ER and PR of NPC in assessing the biological characterisitics of NPC and predicting the prognosis of NPC. It also suggests that the endocrine therapy can be put into consideration.

Adult↗
PubMed1999

[The research of distributed HRV analysis system based on DCOM].

This article introduces the meaning of Distributed Component Object Model(DCOM), which used network communication protocol to replace the local process communication to reach the aim of Distributed Computing, then it discusses the significance of HRV analysis, and finally it presents the system we developed.

Computer Communication Networks↗
PubMed1999

[Spectrophotometric determination of cinnarizine based on charge-transfer reaction].

The charge-transfer (CT) complex formed between cinnarizine as the donor and 7, 7, 8, 8-Tetracyanoquinodimethane (TCNQ) as the acceptor in acetone-methanol has been studied by spectrophotometric method. Beer's law is obeyed in the range of 0-18 microg x mL(-1) of cinnarizine. The apparent molar absorptivity of CT complex at 743 nm is 1.58 x 10(4) L x mol(-1) x cm(-1). The composition of CT complex is found to be 1 : 1 by Bent-French and Job's methods. The relative standard deviation is less than 3% (n = 10). The method has been applied to the determination of cinnarizine in tablets with satisfactory results.

Calcium Channel Blockers↗
PubMed1998

Increased appetite augments hypothalamic NPY Y1 receptor gene expression: effects of anorexigenic ciliary neurotropic factor.

Neuropeptide Y (NPY) is a potent endogenous appetite transducer but the NPY receptor subtype mediating the induction of appetite is unknown. Evaluation of hypothalamic NPY Y1 and Y5 receptor mRNA by RNase protection assay showed that appetite evoked either by fasting or food-restriction increased expression of Y1 mRNA. Suppression of appetite by the cytokine, ciliary neurotropic factor, blocked this increase in Y1 gene expression. In contrast Y5 mRNA levels were unchanged by these treatments. These findings suggest that NPY-induced stimulation of appetite requires signal transmission though Y1 receptor subtype in the hypothalamus.

Animals↗
PubMed1998

Immunostimulatory action of L-4-oxalysine counteracts immunosuppression induced by alpha-fetoprotein.

We have previously reported that L-4-oxalysine, a natural product in China, exhibits marked antitumor and immunoregulatory activities. The present study was set up to investigate the effect of L-4-oxalysine on the immunological activity of alpha-fetoprotein. It was observed in in vitro experiments that concanavalin A reactivity, one-way mixed lymphocyte reaction and interleukin-6 activity of spleen cells from hepatoma-22-bearing mice were significantly inhibited by various concentrations of alpha-fetoprotein. However, L-4-oxalysine functionally antagonized the alpha-fetoprotein-induced suppression of the mitogen- and one-way mixed lymphocyte culture-induced proliferation of spleen lymphocytes and interleukin-6 production by these cells in mice bearing the hepatoma-22 tumor. The results indicate that L-4-oxalysine has immunostimulatory activity and this effect of the agent counteracts the immunosuppression induced by alpha-fetoprotein, although L-4-oxalysine does not directly antagonize alpha-fetoprotein.

Adjuvants, Immunologic↗
PubMed1998

Neural substrates for leptin and neuropeptide Y (NPY) interaction: hypothalamic sites associated with inhibition of NPY-induced food intake.

Intracerebroventricular (i.c.v.) injection of leptin, the adipocyte hormone, inhibits neuropeptide Y (NPY)-induced feeding in the rat. To identify the neural substrate for leptin and NPY interaction in the hypothalamus, we evaluated the expression of c-fos-like immunoreactivity (FLI), an early marker of neuronal activation, in response to icv administration of leptin, NPY and leptin plus NPY. As expected, leptin significantly decreased NPY-induced feeding in leptin plus NPY-treated rats. A comparative evaluation of the number of FLI-positive neurons in hypothalamic sites showed that both leptin and NPY activated FLI in the parvocellular subdivision of the paraventricular nucleus (pPVN), dorsomedial nucleus (DMN) and ventromedial nucleus (VMN). NPY also augmented the FLI response in the magnocellular PVN (mPVN) and supraoptic nucleus (SON), two sites where leptin alone was ineffective. Combined leptin and NPY treatment significantly decreased the number of FLI-positive neurons in the magnocellular PVN but increased their number in the dorsomedial nucleus as compared to the number of FLI-expressing neurons in these sites after NPY and leptin alone. Because there is morphologic evidence of a link between magnocellular PVN and dorsomedial nucleus, these results suggest the functional involvement of leptin plus NPY responsive elements in these sites in reduction of NPY-induced feeding by leptin.

Animals↗
PubMed1998

Stimulation of tumor-cell growth by alpha-fetoprotein.

It has been recognized that alpha-fetoprotein (AFP), as an oncofetal antigen, is re-expressed in large amounts in adult tumor cells and serves clinically useful purposes in tumor-marker assays. However, its biological activities are still undefined. In the present study, the ability of AFP to stimulate tumor-cell growth was observed by an in vitro experimental system. Mouse ascites cancer cells derived from hepatoma-22(H-22) or Ehrlich ascites carcinoma(EAC) were extracted intraperitoneally and cultured in RPMI 1640 medium containing 10% newborn calf serum for 48 hr. Cell growth was quantitated by a colorimetric assay using a MTT microculture tetrazolium dye. The results demonstrated that AFP significantly increased H-22-cell proliferation, with stimulation per cents of 122 to 156%. A similar growth-promoting effect of AFP was observed using EAC cells, with stimulation per cents of 86 to 210%. Moreover, the growth-stimulatory activity of AFP could be abrogated with anti-AFP antibodies. In addition, 5-fluorouracil could obviously inhibit AFP-induced proliferation of H-22 or EAC cells in vitro. These results suggest that AFP is associated with tumor-cell growth and may serve as an important target of tumor therapy.

Animals↗
PubMed1998

Leptin and ciliary neurotropic factor (CNTF) inhibit fasting-induced suppression of luteinizing hormone release in rats: role of neuropeptide Y.

Periods of chronic undernutrition and short periods of fasting suppress pituitary luteinizing hormone (LH) secretion and upregulate hypothalamic neuropeptide Y (NPY), the orexigenic peptide. The effect of suppression of NPY upregulation with ciliary neurotropic factor (CNTF), a cytokine, and leptin, an adipocyte hormone, on pituitary LH secretion was evaluated in fasted rats. In the first experiment, daily injection of CNTF (0.2 nmol) intracerebroventricularly (i.c.v.) for 4 days drastically reduced food intake and body weight gain similar to the weight loss seen in pair-fed rats. Food deprivation (FD) also decreased body weight. Despite drastic loss in body weight, plasma LH was reduced in FD and pair-fed rats, but not in CNTF-treated rats. In the second experiment, FD rats received either control vehicle, CNTF (0.2 nmol) or leptin (0.2 nmol) daily for 4 days. FD increased steady state levels of preproNPY mRNA in the hypothalamus over the control freely-fed rats. However, both CNTF and leptin suppressed hypothalamic gene expression and significantly attenuated LH suppression in response to FD. Taken together, these results support the hypothesis that the upregulation of hypothalamic NPY system may underlie diminution in pituitary gonadotropin secretion and that the NPYergic pathway may serve as a communication bridge between the neural processes that regulate reproduction and those that maintain energy balance.

Adipocytes↗
PubMed1998

Evidence that dark-phase hyperphagia induced by neurotoxin 6-hydroxydopamine may be due to decreased leptin and increased neuropeptide Y signaling.

Hyperphagia and obesity can be experimentally induced in rodents by microinjection of 6-hydroxydopamine (6-OHDA) into the ventral noradrenergic bundle (VNAB) to interrupt efferent catecholaminergic pathways to the hypothalamus. Since hypothalamic neuropeptide Y (NPY) is implicated in the control of ingestive behavior, we evaluated hypothalamic NPY activity in this model of obesity. Adult male rats injected bilaterally with 12 microg of 6-OHDA in the VNAB displayed an enhanced rate of body weight gain and selective dark-phase hyperphagia that started at about 10 days postinjection and persisted for the entire duration of the experiment. NPY gene expression, assessed by ribonuclease protection assay, was significantly higher in the hypothalami of 6-OHDA-treated hyperphagic rats during the dark phase (p < 0.01 vs. levels during the light phase and in control, vehicle-injected rats). We also evaluated gene expression of NPY Y and Y5 receptors, receptor subtypes reported to mediate NPY-induced feeding. The dark-phase increase in NPY mRNA was accompanied by the concomitant upregulation of NPY Y5R gene expression, but not of Y1R mRNA levels. Leptin, the peripheral hormone secreted by adipocytes, is believed to maintain body weight and inhibit food intake, most likely by suppressing hypothalamic NPY activity. Evaluation of leptin gene expression in the epididymal fat revealed that the upregulation of leptin mRNA noted during the dark phase in control rats did not occur in 6-OHDA-treated rats. These observations implied that the normal restraint on NPY and feeding exercised by leptin in control rats may be abrogated in 6-OHDA-treated hyperphagic rats due to insufficient levels of leptin. If so, administration of leptin should inhibit food intake in these rats. Indeed, injection of leptin (2 mg/kg, intraperitoneally (i.p.)) on 2 consecutive days reduced 24-h food intake by 25% and significantly reduced body weight. These results suggest that the nocturnal hyperphagia and resultant obesity induced by 6-OHDA injected into the VNAB may be attributed to leptin deficiency concomitant with increased hypothalamic NPY.

Adrenergic Agents↗
PubMed1998

The anti-gonadotropic effects of cytokines: the role of neuropeptides.

The inhibitory effect of inflammation and endotoxins on the secretion of reproductive hormones from the hypothalamo-pituitary axis is well documented. A comparison of the luteinizing hormone (LH) suppressing effects of several pro-inflammatory cytokines revealed that centrally administered IL-1 beta was the most potent inhibitor of pituitary LH secretion; interleukin (IL)-1 alpha and tumor necrosis factor (TNF) alpha were relatively less effective, whereas IL-6 was ineffective. This order of potency suggested that the anti-gonadotropic effects of an immune challenge are most likely attributable to the action of centrally released IL-1 beta, and this was supported by the demonstration that IL-1 beta suppressed hypothalamic luteinizing hormone releasing hormone (LHRH) release. We used a multifaceted approach to identify the afferent signals in the brain that convey immune messages to hypothalamic LHRH neurons. Pharmacological studies with specific antagonists of opioid receptor subtypes demonstrated that activation of the mu 1 receptor subtype was required to transmit the cytokine signal. Furthermore, icv IL-1 beta upregulated hypothalamic POMC mRNA and increased the concentration and release of beta-endorphin, the primary ligand of mu 1 receptors. We have obtained evidence that IL-1 beta also enhanced the gene expression and concentration of tachykinins, a family of nociceptive neuropeptides in the hypothalamus. Blockade of tachykinergic NK2 receptors attenuated IL-1 beta induced inhibition of LH secretion. Collectively, these results demonstrate that IL-1 beta, generated centrally in response to inflammation, upregulates the opioid and tachykinin peptides in the hypothalamus. These two groups of neuropeptides are critically involved in relaying the cytokine signal to neuroendocrine neurons and causing the suppression of hypothalamic LHRH and pituitary LH release.

Animals↗
PubMed1998

The contribution of poly-L-lysine, epidermal growth factor and streptavidin to EGF/PLL/DNA polyplex formation.

High-level targeted gene delivery has been demonstrated by molecular conjugates in vitro; however, in vivo delivery has been limited. The complexity of the resulting protein/DNA polyplex and a lack of understanding of its formation are persistent limitations. In this report, we show the effect of the DNA-binding agent poly-L-lysine (PLL), the ligand epidermal growth factor (EGF), and the coupling protein streptavidin on particle size, charge and gene delivery. Smaller (< 80 nm) and more stable polyplexes were obtained with PLL1116 than with shorter versions of PLL, especially in 0.15 M NaCl. Stability was increased by adding streptavidin to the polyplex; however, EGF increased particle size (> 1000 nm) and decreased gene delivery when > 300 EGF molecules per polyplex were used, indicating that a critical number of EGF molecules was needed for efficient gene delivery. The correct combination of these components resulted in the most efficient gene delivery in vitro and now provide for testing a more stable protein/DNA polyplex to aid in enhancing gene delivery in vivo.

Biotinylation↗
PubMed1998

Intercellular trafficking of VP22-GFP fusion proteins is not observed in cultured mammalian cells.

Herpes simplex virus type 1 (HSV-1) VP22 was recently reported to mediate intercellular trafficking of a protein fused to the C-terminus of VP22. To explore the application of such trafficking, we constructed plasmids expressing green fluorescent protein (GFP) fused to the C-terminus of either wild-type VP22 or a 160 amino acid peptide from VP22. In vitro studies showed that the majority of both fused proteins were localized to the nuclei of transfected cells. Quantitative analysis of GFP-positive cells, however, showed no significant increase in intercellular protein trafficking for cells transfected with either fusion protein compared with a lacZ-expressing plasmid. Our results suggest that the use of HSV-1 VP22 for mediating intercellular trafficking of transgene products is limited.

Animals↗
PubMed1998

Neuropeptide Y (NPY) Y1 receptor mRNA is upregulated in association with transient hyperphagia and body weight gain: evidence for a hypothalamic site for concurrent development of leptin resistance.

Microinjection of colchicine (COL), a neurotoxin that blocks axoplasmic flow in the neurons, bilaterally into the ventromedial nucleus (VMN) evokes transient hyperphagia and body weight gain. These shifts in energy balance occurred in conjunction with development of increased sensitivity to neuropeptide Y (NPY), the endogenous orexigenic signal. In order to trace the aetiology of NPY supersensitivity, we have evaluated (1) NPY Y1 and Y5 receptor (R) gene expression in the hypothalamus and (2) the possibility of alterations in the inhibitory action of leptin, a hormone produced by lipocytes. Adult male rats were rendered hyperphagic with bilateral microinjections of COL (4 microg/side) into the VMN. We observed that hypothalamic NPY Y1 mRNA levels, as measured by RNAase protection assay, were significantly increased on day 2 and returned to the control level on day 4 in COL-injected rats. The effects on NPY Y5R mRNA were not as clear cut. Interestingly, serum leptin levels increased in association with the hyperphagia and body weight gain, thereby raising the likelihood of development of resistance to the suppressive effect of endogenous leptin on food intake. Indeed, intracerebroventricular injection of 7 microg human recombinant leptin, a dose that attenuated daily food intake in normal and fasted rats, was completely ineffective in attenuating hyperphagia in COL-treated rats. These results show that transient hyperphagia induced by interruption of signalling in the VMN may be caused by increased sensitivity to NPY, which may be caused, in part, by increased expression of NPY Y1R in hypothalamic sites involved in regulation of ingestive behaviour. Additionally, the observation of increased leptin release and concurrent development of leptin resistance suggest that a normally functioning VMN may be necessary for the central inhibitory effects of leptin on food intake.

Animals↗
PubMed1998

Role of branched-chain aminotransferase isoenzymes and gabapentin in neurotransmitter metabolism.

Because it is well known that excess branched-chain amino acids (BCAAs) have a profound influence on neurological function, studies were conducted to determine the impact of BCAAs on neuronal and astrocytic metabolism and on trafficking between neurons and astrocytes. The first step in the metabolism of BCAAs is transamination with alpha-ketoglutarate to form the branched-chain alpha-keto acids (BCKAs). The brain is unique in that it expresses two separate branched-chain aminotransferase (BCAT) isoenzymes. One is the common peripheral form [mitochondrial (BCATm)], and the other [cytosolic (BCATc)] is unique to cerebral tissue, placenta, and ovaries. Therefore, attempts were made to define the isoenzymes' spatial distribution and whether they might play separate metabolic roles. Studies were conducted on primary rat brain cell cultures enriched in either astroglia or neurons. The data show that over time BCATm becomes the predominant isoenzyme in astrocyte cultures and that BCATc is prominent in early neuronal cultures. The data also show that gabapentin, a structural analogue of leucine with anticonvulsant properties, is a competitive inhibitor of BCATc but that it does not inhibit BCATm. Metabolic studies indicated that BCAAs promote the efflux of glutamine from astrocytes and that gabapentin can replace leucine as an exchange substrate. Studying astrocyte-enriched cultures in the presence of [U-14C]glutamate we found that BCKAs, but not BCAAs, stimulate glutamate transamination to alpha-ketoglutarate and thus irreversible decarboxylation of glutamate to pyruvate and lactate, thereby promoting glutamate oxidative breakdown. Oxidation of glutamate appeared to be largely dependent on the presence of an alpha-keto acid acceptor for transamination in astrocyte cultures and independent of astrocytic glutamate dehydrogenase activity. The data are discussed in terms of a putative BCAA/BCKA shuttle, where BCATs and BCAAs provide the amino group for glutamate synthesis from alpha-ketoglutarate via BCATm in astrocytes and thereby promote glutamine transfer to neurons, whereas BCATc reaminates the amino acids in neurons for another cycle.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗