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Biomedical subjects

Z J Yang

Publications and source records attributed to Z J Yang.

At least 19 recordsLinked to original sources
PubMed2001

Hyperbaric O2 reduces intestinal ischemia-reperfusion-induced TNF-alpha production and lung neutrophil sequestration.

Treatment with hyperbaric O2 (HBO) ameliorates ischemia-reperfusion (I/R) injury. Since tumor necrosis factor-alpha (TNF-alpha) plays an important role in I/R injury, we hypothesized that the effect of HBO in I/R injury may be due to its ability to inhibit TNF-alpha production. In this study, one group of rats received HBO during 60 min of ischemia (HBO group, n = 9), while control rats endured the same procedure but did not receive HBO (non-HBO, n = 9). A group of sham-operated control rats (SHAM, n = 6) underwent laparotomy without occlusion of the artery and HBO treatment. Intestinal I/R led to an increase in serum TNF-alpha concentration to [mean (SEM)] 165 (32) pg/ml (P < 0.01 vs SHAM rats). HBO attenuated this increase [34 (9) pg/ml; P<0.05 vs non-HBO group]. Intestinal I/R also resulted in a marked increase in lung myeloperoxidase content [0.62 (0.04) U/g vs 0.17 (0.02) U/g of SHAM rats, P<0.01]. HBO suppressed this increase [0.40 (0.04) U/g, P<0.05 vs non-HBO rats]. HBO ameliorated the injury to the intestine and lung. The number of neutrophils sequestered in the lung was reduced in HBO rats compared to non-HBO rats [6.4 (0.9) neutrophils/per oil field and 10.9 (2) neutrophils/per oil field, respectively; P < 0.05]. These findings demonstrate that HBO inhibits TNF-alpha production during intestinal I/R, and this reduced TNF-alpha production may be attributed to the beneficial effects of HBO.

Acute Disease↗
PubMed2001

Environmental stress on diving-induced platelet activation.

Platelet activation has been suggested to play an important role in the pathogenesis of prethrombotic states and thus may be responsible for decompression illness during compressed air (scuba) diving. To investigate the effect of physical, mental, and environmental stress on platelet activation during immersion in ice-cold water, we examined 10 male breath-hold divers (BHD), 10 elite BHD (eBHD), and 10 scuba divers during immersion in an ice-covered lake at moderate altitude. Platelet activation was examined by surface expression of activation-dependent glycoproteins CD62p, CD63, and CD42a with flow cytometry 10 min before and 1 min and again 24 h after diving. Plasma epinephrine level was also measured. In addition, the relationship between the activated platelets and the epinephrine level was evaluated. The percentage of platelet activation increased from 2.1 +/- 0.4 to 5.7 +/- 0.3, 1.8 +/- 0.3 to 12.9 +/- 0.8, and 3.7 +/- 0.9 to 31.2 +/- 0.8 in BHD, eBHD, and scuba divers, respectively. The percentage of platelet activation returned to pre-immersion levels in BHD and eBHD divers 24 h after diving, but was still higher in scuba divers. A positive relationship exists between the plasma epinephrine level and the percentage of the platelet activation. This study suggests that physical and mental stress enhance platelet activation during diving in ice-cold water.

Adult↗
PubMed2000

Dopamine and serotonin VMN release is related to feeding status in obese and lean Zucker rats.

Study of neurotransmitter role in food intake regulation in a leptin signaling deficient model, such as the Zucker rat, would benefit in the understanding of mechanisms of human obesity, in which leptin resistance is a common syndrome. We studied dopamine (DA) and serotonin (5-HT) concentrations in vivo in the ventromedial nucleus (VMN) of the hypothalamus, as they relate to eating after food deprivation in obese and lean 9-week-old male Zucker rats. DA and 5-HT concentrations were measured by HPLC via microdialysis before and during refeeding in 24-h food-deprived rats. Before food was provided, mean baseline DA and 5-HT levels were lower in obese than in lean rats (9.2 +/- 0.9 vs 15.1 +/- 1.9 pg/10 microl, p < 0.01, and 0.68 +/- 0.05 vs 1.17 +/- 0.02 pg/10 microl, p < 0.001, respectively). Food intake was accompanied by a decrease in DA levels in both obese and lean rats to 64% (p < 0.01) and 65% (p < 0.02) of their baseline levels respectively. 5-HT levels were significantly increased during eating by 41% in obese and 35% in lean rats (p < 0.01) from the baseline levels. Thus in obese rats with altered leptin signaling we found an unaltered pattern of DA and 5-HT release associated with food deprivation and refeeding, but with presence of their low levels. This points to an impaired postsynaptic monoaminergic action to produce an adequate metabolic response in obese Zucker rats in response to feeding state.

Animals↗
PubMed2000

Evidence for the medullary visceral zone as a neural station of neuroimmunomodulation.

The aim of the present study was to test the possibility that the catecholaminergic projectional pathway from the vagus nerve to the medullary visceral zone (MVZ) thence to the paraventricular nucleus of hypothalamus (PVN) was involved in the cytokine-to-brain communication. A triple labeling method in which WGA-HRP retrograde tracing was combined with anti-Fos and -TH immunohistochemical staining was used. WGA-HRP was stereotaxically injected into unilateral PVN in the rat, after a survival of 48 h, animals received intraperitoneal injection of lipopolysaccharide (LPS). The distribution of the HRP retrogradely labeled neurons, Fos protein positive and catecholaminergic neurons (tyrosine hydroxylase as marker) in the MVZ was observed. Subdiaphragmatic vagotomy (SDV) and sham surgery were also used to observe the different Fos expression in the MVZ after intraperitoneal administration of lipopolysaccharide (LPS) or pyrogen-free saline (NS). Under light microscope, seven types of positively stained neurons could be distinguished within the MVZ, namely neurons single-labeled with Fos, HRP or TH, respectively; neurons double-labeled with Fos/TH, Fos/HRP or HRP/TH separately; and neurons triple-labeled with Fos, HRP and TH staining. Intraperitoneal LPS caused lots of robust Fos expression within the MVZ in the sham surgery groups and this response in the MVZ was markedly inhibited in the vagotomized rats. The results suggested that some catecholaminergic neurons in the MVZ could send projections to the PVN and this pathway might be involved in the relay of peripheral immune information via vagus nerve. MVZ was a neural relay station in the immune-to-brain communication and might play a significant role in the neuroimmunomodulation via vagus-MVZ-PVN pathway.

Animals↗
PubMed2000

Effects of intra-VMN mianserin and IL-1ra on meal number in anorectic tumor-bearing rats.

BACKGROUND: Tumor growth in animals and humans is associated with the onset of anorexia and reduced food intake. We previously demonstrated that the ventromedial nucleus of hypothalamus (VMN) plays a contributory role in mediating cancer anorexia. Because serotonin and interleukin-1 (IL-1) are putative mediators of cancer anorexia, we hypothesized that their influence on food intake during tumor growth might occur via their action within the VMN. METHODS: To test this hypothesis, 12 Fischer rats injected subcutaneously with 10(6) viable MCA sarcoma cells (TB rats) and their nontumor-bearing controls (NTB, n = 13) were studied. When anorexia developed, TB and NTB rats received bilateral intra-VMN microinjections of the serotonin antagonist mianserin (200 nmol) or the IL-1 receptor antagonist (IL-1ra, 25 ng). Food intake and its determinants of meal number and size were continuously recorded via a computerized device. RESULTS: In NTB rats, intra-VMN mianserin did not affect food intake, whereas after IL-1ra or vehicle a momentary decrease in food intake due to a predominant reduction of meal size occurred. In TB rats, intra-VMN mianserin or IL-1ra selectively increased meal number, leading to improved food intake. CONCLUSIONS: Data suggest that intra-VMN serotonin and IL-1 are involved in influencing cancer related anorexia.

Animals↗
PubMed2000

[grp75 protects cells from injuries caused by glucose deprivation].

To elucidate the functions of grp75, CHL cells over-expressing grp75 are cultured in glucose-free medium in order to simulate energy metabolic stress. Their susceptibilities to injuries caused by glucose deprivation are assessed by trypan blue exclusion, LDH leakage measurement and cytometry analysis. Data shows a stronger resistance to glucose deprivation among cells over-expressing grp75 than among cells constitutively expressing grp75. The outcome suggests that grp75 can protect cells from injuries caused by glucose deprivation.

Animals↗
PubMed2000

Comparison of early feeding pattern dynamics in female and male rats after reversible ventromedial nucleus of hypothalamus block.

BACKGROUND: In the hypothalamus, a number of interconnected foci, including the ventromedial nucleus of hypothalamus (VMN), interact to control food intake (FI). FI is a function of meal number (MN) and meal size (MZ). Because gender differences exist in feeding patterns, we aimed at investigating the role of the VMN in determining the relationship of MZ and MN in female and male rats. METHODS: FI and feeding patterns of 10 female and 12 male Fischer-344 rats were studied after VMN block, achieved via stereotaxically located intra-VMN microinjection of the neuronal blocker, colchicine (0.32 microgram dissolved in 50 nL of isotonic injectate and instilled on each side into the VMN). RESULTS: After colchicine injection in normal female rats, an immediate and significant increase in FI occurs as a result of the following: 1) increased MZ in dark and light phases and 2) increased light phase MN with consequent loss of the normal diurnal cycle in FI. Recovery of feeding cycle and normal vaginal smear pattern occurred by study's end. In normal male rats, VMN block resulted in the following: 1) an increase in FI resulting from increased MN occurring predominantly during the light phase, thereby 2) disrupting the usual light/dark feeding cycle. CONCLUSIONS: Sexual differences in regulation of FI occur after temporary reversible VMN block: in female rats, MZ is more sensitive to experimental modulation, whereas in male rats it is MN.

Animals↗
PubMed1999

Prototypic G protein-coupled receptor for the intestinotrophic factor glucagon-like peptide 2.

Glucagon-like peptide 2 (GLP-2) is a 33-aa proglucagon-derived peptide produced by intestinal enteroendocrine cells. GLP-2 stimulates intestinal growth and up-regulates villus height in the small intestine, concomitant with increased crypt cell proliferation and decreased enterocyte apoptosis. Moreover, GLP-2 prevents intestinal hypoplasia resulting from total parenteral nutrition. However, the mechanism underlying these actions has remained unclear. Here we report the cloning and characterization of cDNAs encoding rat and human GLP-2 receptors (GLP-2R), a G protein-coupled receptor superfamily member expressed in the gut and closely related to the glucagon and GLP-1 receptors. The human GLP-2R gene maps to chromosome 17p13.3. Cells expressing the GLP-2R responded to GLP-2, but not GLP-1 or related peptides, with increased cAMP production (EC50 = 0.58 nM) and displayed saturable high-affinity radioligand binding (Kd = 0.57 nM), which could be displaced by synthetic rat GLP-2 (Ki = 0.06 nM). GLP-2 analogs that activated GLP-2R signal transduction in vitro displayed intestinotrophic activity in vivo. These results strongly suggest that GLP-2, like glucagon and GLP-1, exerts its actions through a distinct and specific novel receptor expressed in its principal target tissue, the gastrointestinal tract.

Amino Acid Sequence↗
PubMed1999

Interleukin-1alpha injection into ventromedial hypothalamic nucleus of normal rats depresses food intake and increases release of dopamine and serotonin.

A microdialysis injector probe administered IL-1alpha into ventromedial hypothalamus (VMN) and concurrently measured release of dopamine (DA), DOPAC, 5-HT, and 5-HIAA. After baseline dialyses, six rats received 2-ng IL-1alpha and six rats received vehicle (1 microl saline) into VMN. Sixty minutes later, food was provided for 40 min while VMN monoamines were measured every 20 min. Vehicle had no significant effect on monoamines, their metabolites, or food intake. Food intake was significantly lower in IL-1alpha rats vs. controls (p < 0.01). Baseline levels of VMN monoamines (pg/10 microl dialysate) in IL-1alpha and vehicle groups were similar. DA and 5-HT rose immediately on injecting IL-1alpha and remained higher (p < 0.05) than basal during the first 60 min and 40 min sampling period, respectively. Levels of 5-HIAA also increased (p < 0.01). Eating decreased VMN DA in controls, and decreased VMN DOPAC in IL-1alpha-treated rats. During eating, VMN 5-HT in control rats significantly increased while increasing VMN 5-HIAA occurred in IL-1alpha rats. Findings show that an IL-1alpha pathophysiological dose injected into the VMN was associated with anorexia and significantly increased dopaminergic and serotonergic activities and suggest that enhanced VMN DA and 5-HT activities may be part of an IL-1alpha-initiated cascade involved in IL-1alpha-associated anorexia.

Animals↗
PubMed1999

Infusion of nicotine into the LHA enhances dopamine and 5-HT release and suppresses food intake.

Nicotine administration induces hypophagia. Because of the involvement of hypothalamic neurotransmitters in food intake control, we hypothesized that increased activity of the lateral hypothalamic dopamine (LHA-DA) and/or serotonin (LHA-5-HT) may be responsible for nicotine-induced hypophagia. Either 4 mM nicotine or vehicle was administered via reverse microdialysis technique into the LHA of overnight food-deprived rats for 60 min; then food was provided for 40 min. The LHA-DA, 5-HT and their intermediate metabolites, DOPAC and 5-HIAA, were continuously measured during 20-min intervals before, during, and after nicotine administration. Continuous nicotine administration for 60 min increased LHA-DA and DOPAC concentrations during the first 40 min, and induced a long-lasting increase in LHA-5-HT release, until 120 min after the start nicotine administration, even when nicotine administration was stopped. The food intake during the 40-min refeeding period was significantly lower when rats received nicotine. Eating induced a significant and short-lasting increase in the LHA-DA and a long-lasting increase in the LHA-5-HT. These findings indicate that nicotine enhances dopaminergic and serotonergic activity in the LHA, and that the enhanced LHA-5-HT activity may contribute to nicotine-induced hypophagia.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1999

Effect of operative stress on food intake and feeding pattern in female rats.

Effects of operative stress on food intake, meal size, and meal number were measured in 15 female rats before and after jugular vein catheterization. All rats had 5-d estrous cycles which correlated with cyclical feeding patterns that were most prominent during dark phase eating. In proestrous, meal number peaked (30.3+/-1.32), and meal size reached a nadir (0.33+/-0.02 g) with some corresponding change in food intake (9.8+/-0.38 g). Following operation on day 11, the cyclical variation of food intake, meal number, and meal size with estrous cycle was lost for the first 3 d, as was the diurnal rhythm in food intake. Eight rats recovered their dark phase feeding pattern by day 17 (recovered group), while 7 had not done so even by day 24 (non-recovered group). Food intake decreased to 40% of baseline in the recovered group and to 25% in the non-recovered group on day 11, increasing to 70% by day 14 in both groups and matching preoperative levels by day 17. Similar postoperative decreases were observed in meal number and meal size. Light phase feeding was increased, the ratio of day to night food intake being three times preoperative levels even at day 24. Preoperatively, non-recovered rats were similar to the recovered rats in all feeding indexes and continued to have estrous cycling in vaginal smears postoperatively. In the non-recovered rats, meal size more than doubled and meal number was depressed by 47% of preoperative levels and remained low until the end of the study. We conclude that operative stress disrupted cyclical and diurnal rhythms in food intake. In female rats, meal size is the first index to recover, increasing temporarily to maintain food intake.

Animals↗
PubMed1999

Use of orchiectomy and testosterone replacement to explore meal number-to-meal size relationship in male rats.

Because food intake is a function of meal number and meal size and because gender-related hormones are involved in feeding regulation, we explored effects of orchiectomy and testosterone replacement on the relationship between meal number and size and changes in resulting feeding patterns in adult male rats, randomized into orchiectomy and sham-operation groups. A rat eater meter measured feeding indexes for 1 wk before and 2 wk after castration and during 8 days of testosterone replacement. Orchiectomy leads to an immediate change in the meal number-to-size relationship, resulting in 1) change in pattern of feeding; 2) a significant decrease in dark-phase meal number; 3) a significant increase in dark-phase meal size, but insufficient to offset decrease in meal number, so total food intake significantly decreased during dark phase; 4) no significant change in light-phase meal number; and 5) an increase in meal size leading to an increased food intake during light phase, which offset decreased food intake in dark cycle and resulted in no net significant change in food intake after orchiectomy. Testosterone replacement acutely reversed effects of orchiectomy on meal number-to-meal size relationship, restoring feeding pattern. Data suggest that androgens immediately influence the meal number-to-meal size relationship. The speed of onset seen after orchiectomy suggests that the influence of testosterone on food intake may also occur partially via a nongenomic effect.

Animals↗
PubMed1999

Preliminary study on HA coating percutaneously implanted in bone.

A comparative investigation on the possibility of hydroxyapatite (HA) coating and pure Ti column to form biological sealing with skin tissue was completed in this study. HA coating and pure Ti column were percutaneously implanted in the tibia of rabbits. Compared with titanium (Ti) implant, HA coating forms epithelial sealing with skin tissue at 6 weeks postoperatively, while the Ti implant may loosen from the implanted site and be lost. The Ti column loosing rate at this time was 50%. However, once the Ti implant becomes fixed with the bone tissue, it can form epithelial sealing with skin tissue just like the HA coating, at 8 weeks postoperatively. At 8 weeks postoperatively, the epithelial sealing is not destroyed in spite of the fact that the HA coating is biodegraded. Our results show that the HA coating can become fixed with the bone faster than the Ti, which is beneficial for epithelial sealing formation. The main role of HA coating for epithelial sealing is beneficial for sealing at the initial period after it is implanted.

Animals↗
PubMed1998

Despite its homology to angiostatin apolipoprotein(a) does not affect angiogenesis.

Apolipoprotein(a) [apo(a)] contains a kringle domain(IV) homologous to that of angiostatin, a natural angiogenic inhibitor. Because of this structural similarity we suspected that apo(a) could be an inhibitor of angiogenesis. The possible role of apo(a) in microvascular proliferation was studied in an in vivo quantitative model, the disc angiogenesis system (DAS) and compared to angiostatin. Apo(a) and other test compounds were placed in the center of a polyvinyl alcohol foam disc that was implanted subcutaneously in mice. After 14 days, the disc was removed and vascular growth into the disc was measured. Apo(a) did not affect spontaneous vessel growth into the disc, while angiostatin suppressed this growth and basic fibroblast growth factor (bFGF) increased it. Additionally, apo(a) did not modify the vascular growth induced by bFGF. Transgenic mice expressing the human apo(a) gene were used to study the systemic effect of apo(a): neither an increase nor a decrease in vascular growth was detected. Our results suggest that apo(a) is unlikely to play a significant role in the control of angiogenesis. Furthermore, our experiments confirm the inhibitory effect of angiostatin not only on induced angiogenesis but also on baseline, spontaneous angiogenesis.

Angiostatins↗
PubMed1998

Ventromedial nucleus of hypothalamus is related to the development of cancer-induced anorexia: in vivo microdialysis study.

UNLABELLED: Based on reports that increased hypothalamic ventromedial nucleus (VMN)-serotonin (5-HT) is associated with cancer anorexia and recent findings in our laboratory that low levels of dopamine (DA) in the VMN are associated with prolonged inter meal intervals thus decreased food intake, and reports that setting up satiation is concomitant with descending levels of DA in the rostromedial hypothalamus, we hypothesized that an elevated 5-HT to low DA ratio in the VMN modulates food intake in cancer anorexia. METHODS: In Expt 1: A microdialysis cannula guide was placed stereotactically into the VMN of methylcholanthrene (MCA) sarcoma tumor-bearing (TB) Fischer rats and in non-tumor-bearing (NTB) and pair-fed (PF) controls. When TB rats manifested anorexia by a decrease in food intake, VMN-5-HT, its metabolite 5-hydroxyindolacetic acid (5-HIAA), and DA with its metabolite 3,4,-dihydroxyphenylacetic acid (DOPAC) were measured by in vivo microdialysis using HPLC during baseline, in response to food, and after feeding. In Expt 2: TB rats had tumor removed and VMN microdialysis performed 7 days later. RESULTS: Increased 5-HT release and turnover, and significantly reduced DA release with increased DOPAC occurred in TB vs NTB or PF rats. When food was offered, intake in TB rats was significantly lower than in NTB control rats. During eating, VMN-5-HT rose and peaked significantly earlier in TB vs NTB rats, while DA release was significantly reduced. With eating, the 5-HT and DA metabolism became reduced in all rats. Seven days after surgical removal of the tumor, 24 h food intake had increased to the level of controls; and when food was offered during microdialysis, intake in TB rats increased (ns relative to control), but was not yet normal. VMN microdialysis showed that 5-HT was normal at baseline, as well as during and after eating, while DA remained depressed. The metabolic turnover of 5-HT and DA was significantly lower in TB-r and PF vs NTB rats. We conclude that increased 5-HT/DA ratio is related to the development of cancer-induced anorexia.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1998

Systemic nicotine administration suppresses food intake via reduced meal sizes in both male and female rats.

The appetite suppressing effect of tobacco products, via the main pharmacological agent nicotine, is a major reason for its usage both by woman and man. Food intake (FI) could be changed by altering either meal size (MZ) or meal number (MN), which are regulated dependently in a reciprocal manner. The present study investigated the effect of systemic nicotine administration on the rat feeding pattern. Because of gender differences in the effects of nicotine, both male and female rats were studied. Alzet mini-osmotic pumps (Model 2001) and the automated rat eatometer were used to evaluate the feeding pattern of male and female Fischer 344 rats during seven days of systemic nicotine infusion (6 mg/kg b.w. s.c.). The main findings are: 1) systemic nicotine infusion decreased food intake in both sexes; 2) the decreased food intake was due to significantly reduced meal sizes while meal numbers were not altered significantly in either males or females; 3) the cyclical pattern of vaginal smears, food intake, meal number and meal size of female rats was not affected by nicotine administration. We conclude that the feeding suppressive effect of nicotine, which is due to reduced meal sizes and thus satiation, is not sex-hormones related.

Animals↗
PubMed1997

Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice.

Lipoprotein(a) contributes to the development of atherosclerosis through the binding of its plasminogen-like apolipoprotein(a) component to fibrin and other plasminogen substrates. Apolipoprotein(a) contains a major lysine binding site in one of its kringle domains. Destruction of this site by mutagenesis greatly reduces the binding of apolipoprotein(a) to lysine and fibrin. Transgenic mice expressing this mutant form of apolipoprotein(a) as well as mice expressing wild-type apolipoprotein(a) have been created in an inbred mouse strain. The wild-type apolipoprotein(a) transgenic mice have a fivefold increase in the development of lipid lesions, as well as a large increase in the focal deposition of apolipoprotein(a) in the aorta, compared with the lysine binding site mutant strain and to nontransgenic littermates. The results demonstrate the key role of this lysine binding site in the pathogenic activity of apolipoprotein(a) in a murine model system.

Animals↗