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Biomedical subjects

C Shu

Publications and source records attributed to C Shu.

At least 37 records · Page 2Linked to original sources
PubMed1997

Regenerative changes in median nerve defects using various rabbit skeletal muscles.

We examined the morphological changes of median nerve regeneration which situated to pass through degenerative latissimus dorsi and brachial triceps muscles in rabbits. Morphological observation was performed at 7, 14, 28, 45, 60 and 180 days after the creation of defect of the bilateral median nerves. Regenerative nerve fibers were observed in the residual tubes of left degenerative muscle bridges. In this respect the regenerative effect of the latissimus dorsi was better than that of the brachial triceps. These results suggest that regular and longer muscle fibers as those of latissimus dorsi may contribute to the effective regeneration of nerve.

Animals↗
PubMed1997

[Genetic divergence of Cordyceps sinensis as estimated by random amplified polymorphic DNA analysis].

Random amplified polymorphic DNA(RAPD) has been used in analyzing 13 winter worm, summer grasses (Cordyceps sinensis [Berk.], Sacc.) from 5 areas in Qingzang plateau. For 19 arbitrary primers, each individual showed about 65 RAPD markers. The genetic distances among those 13 winter worm, summer grasses were correlated to their geographic distances. Molecular phylogenetic tree constructed by UPGMA and NJ suggested that 13 winter worm, summer grasses could be divided into 3 clusters: east cluster, north cluster and middle cluster, in consistence with their origins and genetic divergence among different clusters. Furthermore, our results implied that the RAPD markers of winter worm, summer grasses showed a geographic specificity and could be a better genetic marker in studying genetic diversity and phylogeny of winter worm, summer grasses.

Genetic Variation↗
PubMed1996

Lipid peroxidation of mitochondrial membrane induced by D1: an organic solvent extractable component isolated from a crude extract of burn eschar.

D1, an organic solvent extractable component of an extract from burn eschar was characterized and the mechanism of its inhibitory effect on mitochondrial respiratory functions was investigated. Using silicic acid column chromatography, it was found that D1 consisted of two parts: a toxic simple lipid and a non-toxic complex lipid. Six subunits were obtained by further silicic acid column chromatography, among them, the no. 4 and no. 6 were toxic. Infrared spectrometric studies showed that no. 4 consisted of esters, while no. 6 were peroxides. D1 also contained large amounts of malonaldehyde (MDA) and lipid hydroperoxides (ROOH). Vitamin E was found to prevent the inhibitory action of D1 on mitochondrial function and to reduce the amount of MDA produced. However, if vitamin E was introduced after the addition of D1 the inhibition could not be prevented, although there was still a reduction in MDA production; therefore, MDA per se was probably not the cause of the inhibition. D1 induced ROOH formation in mitochondrial membranes. Cumene hydroperoxide, an organic hydroperoxide, was capable of inhibiting the mitochondrial function. This inhibitor action was blocked by vitamin E. It is speculated that ROOH in D1 is probably the element that inhibits mitochondrial function. That D1 caused lipid peroxidation of membrane lipid was also proved by analysing the fatty acid composition of mitochondrial membranes before and after treatment with D1. It was found that the amount of polyunsaturated fatty acids decreased and that of saturated fatty acids increased after incubation with D1, a direct proof that lipid peroxidation has occurred. Lipid peroxidation of the membrane lipid was the result of the action of oxygen free radicals. This process was best shown by a chemiluminescence study. In this experiment, D1 induced chemiluminescence which was dose-dependently related to the amount of D1 used. This was probably the most direct proof that D1 caused lipid peroxidation of membrane lipid resulting in damage of the mitochondria.

Burns↗
PubMed1996

[The role of Ca2+ in the pathogenesis of human pituitary GH-secreting adenomas].

Effects of Ca2+ channel blockers (nicardipin and nifedipin) and Ca2+ ionophore A23187 on the basal secretion and on the secretion stimulated by GRH or inhibited by SMS, a SRIF analogne of GH were investigated in monolayer cell cultures of 23 cases of human pituitary GH-secreting adenomas. The roles of GRH and SMS in 45Ca influx were investigated also. The GH secretion of most GH adenomas was depended on Ca2+, but the abnormality in different link of GH secretion mediated by Ca2+ was observed. The defects of receptor and post-receptor including Ca2+ channel and Ca(2+)-GH secretion couple regulated by GRH and SRIF were found in 66.7% and 55.6% of GH adenomas respectively. These abnormalities may contribute to GH hypersecretion in GH adenomas.

Adenoma↗
PubMed1996

[Morphological studies of the adrenal zona glomerulosa cells and the thyroid and pituitary glands in streptozocin-induced experimental diabetic rats].

Changes in pathological morphology in the adrenal glomerulosa, the thyroid and pituitary glands in streptozotocin-induced experimental diabetic rats were studied by histologic, ultrastructural examination and morphometry. Experimental diabetes provoked atrophy and retrograde degeneration of organelles in the adrenal zona glomerulosa cells and the thyroid follicular epithelium. In the pituitary of diabetic rats, organelles in thyrotrophs were the same as the controls in morphometry, but TSH release was impaired. These studies indicate that pathological changes in the zone glomerulsa cells and the thyroid of diabetic rats appear to be responsible for the impaired function of these two glands. Moreover, reduced TSH release in the pituitary glands is also associated with impaired function of the thyroid gland.

Animals↗
PubMed1995

Extracellular accumulation of potently microbicidal bactericidal/permeability-increasing protein and p15s in an evolving sterile rabbit peritoneal inflammatory exudate.

To what extent the host defense role of granule-associated antibacterial proteins and peptides of PMN includes extracellular action has not been established. To address this question, we have analyzed the antibacterial activity of cell-free (ascitic) fluid (AF) obtained from glycogen-induced sterile inflammatory rabbit peritoneal exudates in which > 95% of the accumulating cells are PMN. AF, but not plasma collected in parallel, exhibits potent activity toward serum-resistant Gram-negative and Gram-positive bacteria. Total and specific antibacterial activity of AF increases during the first 12 h after injection of glycogen in parallel with the influx of PMN. At maximum, > 99% of 10(7) encapsulated Escherichia coli and Staphylococcus aureus are killed in 30 min/ml of AF. Neutralizing antibodies against the bactericidal/permeability-increasing protein (BPI) of PMN abolishes activity of AF toward encapsulated E. coli but has no effect on activity vs staphylococci. However, BPI alone (approximately 1 microgram/ml in AF) can only account for < or = 20% of AF activity toward E. coli. AF also contains 15 kD PMN proteins (p15s) that act in synergy with BPI. Purified BPI and p15s, in amounts present in AF, reconstitute the growth-inhibitory activity of AF toward encapsulated E. coli. These findings show for the first time an extracellular function of endogenous BPI, providing, together with the p15s, a potent microbicidal system toward Gram-negative bacteria resistant to plasma-derived proteins and phagocytes in inflammatory exudates.

Animals↗
PubMed1995

[Preliminary studies on protective effects of selenium on human fetal hepatocyte in vitro injured by lipid peroxidation].

A selenium protection model of human fetal hepatocyte in vitro injured by lipid peroxidation was established. It was found that survival rate and secretion of albumin of the injured cells decreased, and release of alanine transaminase (ALT) and its activities in the cells increased, as compared with those in controls, with a very significant difference. Under electronic microscope, ultrastructure of the injured cells appeared obscure, their membrane and membranous organella swelling, or membranous structure breaking. Injuries mentioned above in cells pre-treated with selenium were obviously decreased and activities of glutathione peroxidase increased. But protective effects of selenium supplement were weaker. It suggested that preventive supplement with selenium could reduce injury to human hepatocyte caused by lipid peroxidation.

Cell Survival↗
PubMed1994

Effect of chronic tobacco smoke exposure on the function of alveolar macrophages in mice.

We evaluated the effect of chronic tobacco smoke exposure on the function of the alveolar macrophage (AM) in mice. Tumor necrosis factor-alpha production of the AM triggered by lipopolysaccharides was smaller in smoke-exposed mice as compared to control mice but did not reach statistical significance (27.3 +/- 4.0 vs. 34.8 +/- 4.9 U/ml). The percentage of AM which did not phagocytize latex particles in the smoke-exposed mice was significantly larger than that in control mice (33.9 +/- 2.3 vs. 20.8 +/- 2.1%; p < 0.05). Ia antigen expression of the AM was significantly larger in smoke-exposed mice (cytotoxicity index: 0.180 +/- 0.033 vs. 0.038 +/- 0.0118; p < 0.01). The asialo-GM1 antigen expression was similar in both groups (0.949 +/- 0.007 vs. 0.961 +/- 0.011). Although the precise mechanisms of these functional changes of the AM by tobacco smoke exposure are not clear, they may have some immunological effects on the alveolar space.

Animals↗
PubMed1994

The bactericidal/permeability increasing protein of neutrophils is a potent antibacterial and anti-endotoxin agent in vitro and in vivo.

The Bactericidal/Permeability Increasing protein (BPI) is a major constituent of the azurophilic granules of human and rabbit polymorphonuclear leukocytes (PMN). The cDNA of the highly conserved protein has been isolated from man, rabbit and cow. The ca. 50 kDa BPI and a ca. 25 kDa bioactive N-terminal fragment are cytotoxic only for Gram-negative bacteria (GNB). This target-cell specificity reflects the strong attraction of the highly cationic protein for the negatively charged lipopolysaccharides (LPS) in the bacterial envelope. Native and recombinant (r) holo-BPI and the N-terminal fragment (rBPI-23) bind with high affinity (apparent Kd 1-10 nM) to all forms of isolated LPS so far examined, and inhibit the numerous biological effects of LPS in vitro (including in whole blood ex vivo) as well as in animals. Under the same conditions the antibacterial activities of holo-BPI and rBPI-23 against GNB with rough chemotype LPS are the same, but against serum-resistant and smooth chemotype GNB rBPI-23 is up to 30-fold more potent than holo-BPI. Holo-BPI and rBPI-23 protect mice, rats and rabbits against lethal cytotoxic effects of LPS and in some cases against lethal inoculations with live GNB.

Animals↗
PubMed1993

The effects of aging on the function of alveolar macrophages in mice.

In order to determine whether the function of alveolar macrophages (AM) is modulated by aging, we measured the TNF-alpha production, phagocytic function, and surface antigen expression of AM from young and old mice. When AM were primed by IFN-gamma (500 units/ml) and triggered by LPS (100 micrograms/ml), TNF-alpha production by AM was significantly smaller in old mice as compared with young mice (young mice: 161.7 +/- 28.2 units/ml; old mice: 89.3 +/- 13.6 units/ml, P < 0.05). The percentage of AM which phagocytosed latex particles (more than one particle) in old mice was significantly lower than in young mice (young: 78.1 +/- 2.5%; old: 62.8 +/- 3.4%, P < 0.05). Ia antigen expression of the AM was significantly higher and asialo-GM1 antigen expression was significantly lower in old mice than in young mice (Ia: young, 0.030 +/- 0.005; old, 0.092 +/- 0.024, P < 0.05; asialo-GM1: young, 0.-9 +/- 0.01; old, 0.75 +/- 0.07, P < 0.01). These results suggest that alveolar macrophage function is at least decreased in part with aging in mice.

Aging↗
PubMed1993

The long-term observation of the transplantation of encapsulated rat islets to the diabetic mice.

Rat islets encapsulated in the immuno-isolated membrane were transplanted intraperitoneally into 11 streptozotocin induced diabetic mice. The effective rate was 91% while all rejected in the 11 nonencapsulated xenograft group. 4 mice showed complete remission and longest normoglycemic period in those mice was 360 days. The pathological changes of islets of the long-term successful xenograft group were studied and showed atrophy. It proved that the immuno-isolated membrane can protect rejection during xeno-transplantation.

Alginates↗
PubMed1992

Comparison between the interaction of steroids with [35S]TBPS binding to cerebral cortical and to pituitary membranes: correlation with inhibition of prolactin release.

It has been shown previously that 5 alpha-pregnan-3 alpha-ol-20-one (5 alpha 3 alpha P) can inhibit prolactin release from anterior pituitary gland cells in culture through an interaction with a specific modulatory site on the GABAA receptor complex in anterior pituitary gland membranes. In the present work, this receptor site has been labelled with [35S]t-butylbicyclophosphorothionate ([35S]TBPS) to enable a study of the relative binding affinities (RBA) of different steroids for the GABAA receptor complex to be made. We have found a high correlation (r = +0.88) between the inhibition of [35S]TBPS binding to anterior pituitary membranes and the inhibition of [35S]TBPS binding to cerebral cortical membranes by nine different steroids. There was also a high correlation between the inhibition of prolactin release from anterior pituitary gland cells in culture by these steroids and the inhibition of [35S]TBPS binding to anterior pituitary membranes (r = +0.99) or to cortical membranes (r = +0.81). These observations suggest that the measurement of prolactin release from anterior pituitary gland cells in culture is a good indicator of the functional activity of drugs that bind to the allosteric modulatory TBPS-binding site on the GABAA-receptor complex.

Animals↗
PubMed1992

Inhibition of mouse alveolar macrophage production of tumor necrosis factor alpha by acute in vivo and in vitro exposure to tobacco smoke.

We investigated the effects of tobacco smoke exposure on the production of tumor necrosis factor alpha (TNF alpha) by alveolar macrophages (AM) in mice (C57BL/6). The results obtained are as follows: (1) In vivo tobacco smoke exposure caused a significant decrease in the production of TNF alpha by AM with the stimulation of lipopolysaccharide (LPS; control group: 19.32 +/- 5.52 U/ml, smoked group: 4.28 +/- 0.98 U/ml; p less than 0.05). (2) In vitro exposure of AM to tobacco smoke extracts (water-soluble extracts) also caused a decrease in the production of TNF alpha up to 93% of control with stimulation of LPS (p less than 0.05) without any decrease in cellular viability. We concluded that the production of TNF alpha by AM was impaired by smoking via direct action of the factors present in tobacco smoke.

Animals↗
PubMed1992

Human bactericidal/permeability-increasing protein and a recombinant NH2-terminal fragment cause killing of serum-resistant gram-negative bacteria in whole blood and inhibit tumor necrosis factor release induced by the bacteria.

The bactericidal/permeability-increasing protein (BPI) of neutrophils and BPI fragments neutralize the effects of isolated Gram-negative bacterial lipopolysaccharides both in vitro and in vivo. Since endotoxin most commonly enters the host as constituents of invading Gram-negative bacteria, we raised the question: Can BPI and its bioactive fragments also protect against whole bacteria? To determine whether the bactericidal and endotoxin-neutralizing activities of BPI/fragments are expressed when Gram-negative bacteria are introduced to the complex environment of whole blood we examined the effects of added BPI and proteolytically prepared and recombinant NH2-terminal fragments on: (a) the fate of serum-resistant encapsulated Escherichia coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa that survive the antibacterial actions of whole blood and (b) the ability of these bacteria to trigger cytokine release. Added BPI in nanomolar concentrations killed each of three encapsulated strains of E. coli and in closely parallel fashion inhibited tumor necrosis factor (TNF) release. Holo-BPI and its NH2-terminal fragment were equipotent toward a rough LPS chemotype K1-encapsulated strain, but the fragment was substantially more potent than holo-BPI toward two encapsulated smooth LPS chemotype strains. TNF release induced by K. pneumoniae and P. aeruginosa was also inhibited by both holo-BPI and fragment but, at the protein concentrations tested, P. aeruginosa was killed only by the fragment and K. pneumoniae was not killed by either protein. The bactericidal action of BPI/fragment toward E. coli is inhibited by C7-depleted serum, but accelerated by normal serum, indicating that BPI, acting in synergy with late complement components, enhances extracellular killing of serum-resistant bacteria. Thus, BPI and an even more potent NH2-terminal fragment may protect against Gram-negative bacteria in the host by blocking bacterial proliferation as well as endotoxin-mediated effects, not only as components of the intracellular antibacterial arsenal of the neutrophil, but also as potentially therapeutic extracellular agents.

Antimicrobial Cationic Peptides↗
PubMed1991

Tyrosine hydroxylase and POMC mRNA in the arcuate region are increased by castration and hyperprolactinemia.

We have examined the changes which occur in neuronal expression of tyrosine hydroxylase (TH) and proopiomelanocortin (POMC) mRNA in response to castration and hyperprolactinemia (HP) in male rats. Steady-state mRNA levels were determined by quantitative in situ hybridization histochemistry (ISHH) using 35S-labeled synthetic 48-base oligodeoxynucleotide probes. Castration produced a 27% increase in TH mRNA in the periventricular and arcuate nuclei. PRL-exposed rats exhibited a further 27% increase in the level of TH mRNA and a striking 48% increase in POMC mRNA in periarcuate region cell bodies. These results indicate that gonadal steroids and PRL are involved, either directly or indirectly, in regulating the biosynthesis of TH and POMC in the hypothalamus.

Analysis of Variance↗
PubMed1991

Effects of tumor-induced hyperprolactinemia on LH secretion following stimulation of the medial preoptic area, pituitary responsiveness and the estrogen-induced LH surge.

In the present study we utilized the 7315a PRL- and ACTH-secreting tumor to induce a hyperprolactinemic (HP) state sufficient to profoundly suppress the postcastration LH rise in female rats. Tumor-induced prolactin levels which ranged 2,000-3,000 ng/ml substantially reduced the LH rise in both ovariectomized (OVX) and OVX + estradiol-17 beta (E2)-treated rats. Bilateral electrochemical stimulation (ECS, 100 microA DC for 60 s) of the ventral diagonal band of Broca-medial preoptic area (DBB-MPOA) resulted in comparable LH responses in control and HP rats in the presence of absence of estradiol. Transient decreases in PRL release occurred following ECS of the DBB-MPOA. Pituitary responsiveness was assessed with two LHRH challenges spaced 60 min apart at doses of 25 and 50 ng LHRH/100 g body weight. The mean maximal LH increments (delta LH) to some of these LHRH challenges were decreased in HP rats. Finally, the LH surge induced in the afternoon in OVX + E2-treated rats was diminished 71% by the presence of the PRL-secreting tumor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Single cell levels of hypothalamic messenger ribonucleic acid encoding luteinizing hormone-releasing hormone in intact, castrated, and hyperprolactinemic male rats.

We have examined the changes that occur in neuronal expression of LHRH mRNA in response to castration and hyperprolactinemia in male rats. Single cell levels of LHRH mRNA were determined by quantitative in situ hybridization histochemistry using an 35S-labeled synthetic 48-base oligodeoxynucleotide probe and quantitative autoradiography. Nine days postcastration, a 10.4-fold increase in mean plasma LH titers was observed which was associated with significantly increased LHRH mRNA in rostral hypothalamic neuronal cell bodies. Both increases were blocked in rats rendered hyperprolactinemic by the presence of the 7315a PRL-secreting pituitary tumor. The location and number of neurons expressing LHRH mRNA were unchanged, indicating that these differences were attributable to amounts of mRNA expressed per neuron. Experimental differences occurred in LHRH perikarya situated throughout the rostral hypothalamus from the organum vasculosum of the lamina terminalis to the caudal extent of the medial preoptic nucleus. These results suggest that gonadal steroids and PRL are involved, either directly or indirectly, in regulating the biosynthesis of LHRH in the rostral hypothalamus.

Animals↗