Search PubMed⌕ Search

Biomedical subjects

Y Xu

Publications and source records attributed to Y Xu.

At least 1,135 records · Page 63Linked to original sources

Human relaxin decreases collagen accumulation in vivo in two rodent models of fibrosis.

The reproductive hormone, relaxin, inhibits collagen synthesis in vitro by normal human dermal fibroblast. In the present study, recombinant human relaxin is shown to modulate collagen accumulation and organization by mesenchymal cells in vivo in two rodent models of fibrosis: 1) fibrotic infiltration of polyvinyl alcohol sponge implants in rats, and 2) capsule formation around implanted osmotic pumps in mice. In the sponge, relaxin inhibits collagen accumulation, a measured by hydroxyproline content, in a dose-responsive manner by up to 25-29% in animals receiving 30 ng/ml relaxin, a finding supported by a decrease in collagen-specific trichrome staining in sections of sponges from relaxin-treated animals. In mice, the capsules surrounding relaxin-containing pumps are thinner and less dense than are capsules from control pumps. Ultrastructurally, control capsules are composed of densely packed parallel arrays of collagen fibrils, whereas fibrils more frequently are not packed in parallel arrays and are less abundant in treated capsules.

Animals↗

Protein kinase C inhibitors enhance endothelin-1 and attenuate vasopressin and angiotensin II evoked [Ca2+]i elevation in the rat cardiomyocyte.

Primary cultures of neonatal rat cardiomyocytes were pretreated for 16 h with either nonselective (staurosporine, 100 nM) or selective (NPC15437, 20 microM) protein kinase C (PKC) inhibitors. These inhibitors did not affect the basal cytosolic free calcium, [Ca2+]i, level (106 +/- 12 nM) as determined by fura-2 fluorescence methodology. Both agents significantly enhanced the maximal [Ca2+]i responses to endothelin-1 (ET-1) and attenuated the peak [Ca2+]i responses to arginine vasopressin and angiotensin II. They did not alter the EC50 values of any of these agonists. Since depletion of [Ca2+]o led to only partial attenuation of the enhanced response to ET-1 in the treatment groups, it is likely that PKC inhibition results in an exaggerated intracellular mobilization of Ca2+ to ET-1. It is concluded that PKC modulates agonist(s)-evoked intracellular Ca2+ mobilization and that the nature of regulation is governed by the agonist.

Alkaloids↗

Schistosoma japonicum-infected mice show reduced hepatic fibrosis and eosinophilia and selective inhibition of interleukin-5 secretion by CD4+ cells after treatment with anti-interleukin-2 antibodies.

Schistosoma japonicum-infected mice were injected with antibodies to interleukin-2 (IL-2) and/or IL-2 receptor to clarify the role of IL-2 on the granulomatous reaction around schistosome eggs in the liver. Granulomas were of normal or slightly increased size in animals subjected to IL-2 blockade, but hepatic fibrosis was markedly decreased in treated animals 10 weeks after infection. Anti-IL-2 treatment significantly decreased the in vitro secretion of IL-5 by antigen-stimulated spleen cells, and peripheral eosinophilia and tissue eosinophilia were diminished. Secretion of IL-2, IL-4, and gamma interferon was unaffected. Our results indicate that IL-2 is not an essential determinant of granuloma size in S. japonicum-infected mice but that, as in Schistosoma mansoni infection, the development of hepatic fibrosis is critically dependent on IL-2 levels and granuloma size and hepatic fibrosis are differentially regulated.

Animals↗

Cloning and characterization of ftsN, an essential cell division gene in Escherichia coli isolated as a multicopy suppressor of ftsA12(Ts).

A new cell division gene, ftsN, was identified in Escherichia coli as a multicopy suppressor of the ftsA12(Ts) mutation. Remarkably, multicopy ftsN suppressed ftsI23(Ts) and to a lesser extent ftsQ1(Ts); however, no suppression of the ftsZ84(Ts) mutation was observed. The suppression of ftsA12(Ts), ftsI23(Ts), and ftsQ1(Ts) suggests that FtsN may interact with these gene products during cell division. The ftsN gene was located at 88.5 min on the E. coli genetic map just downstream of the cytR gene. ftsN was essential for cell division, since expression of a conditional null allele led to filamentation and cell death. DNA sequence analysis of the ftsN gene revealed an open reading frame of 319 codons which would encode a protein of 35,725 Da. The predicted gene product had a hydrophobic sequence near its amino terminus similar to the noncleavable signal sequences found in several other Fts proteins. The presumed extracellular domain was unusual in that it was rich in glutamine residues. A 36-kDa protein that was localized to the membrane fraction was detected in minicells containing plasmids with the ftsN gene, confirming that FtsN was a membrane protein.

Amino Acid Sequence↗

ETB receptors on aortic smooth muscle cells of spontaneously hypertensive rats.

The effect of the agonist sarafotoxin 6c (S6c), selective for endothelin (ET) receptor subtype B (ETB), on cytosolic free Ca2+ concentrations ([Ca2+]i) was determined by fura-2 methodology using aortic smooth muscle cells (ASMC) isolated from spontaneously hypertensive rats (SHR) and two normotensive strains, Wistar-Kyoto (WKY) and Sprague-Dawley (SD) rats. The basal [Ca2+]i was significantly higher in the ASMC of SHR (139 +/- 8 nM) than WKY (107 +/- 7 nM) and SD (102 +/- 4 nM) rats. S6c produced concentration-dependent elevations in [Ca2+]i in the ASMC of WKY and SHR, whereas it did not evoke significant increases in the [Ca2+]i levels in the ASMC of SD rats. The peak [Ca2+]i levels observed with maximal concentrations of S6c (500 nM) was higher (P < 0.01) in the SHR (346 +/- 36 nM) than the WKY group (148 +/- 19 nM). The natural nonselective agonist, ET-1, evoked maximal [Ca2+]i in the ASMC of SHR, WKY, and SD rats of 635 +/- 43, 304 +/- 19, and 289 +/- 24 nM, respectively. Depletion of extracellular Ca2+ concentration led to the reduction of the peak [Ca2+]i response to ET-1 by 60 and 40% in the WKY and SHR cells, respectively, whereas the response to S6c remained unaffected. The ETA-selective antagonist, BQ-123 (1 microM), did not affect the [Ca2+]i response to S6c, whereas it attenuated the response to ET-1 by 90 and 70% in the WKY and SHR cells, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

One systemic administration of transforming growth factor-beta 1 reverses age- or glucocorticoid-impaired wound healing.

The role of intravenously administered recombinant human transforming growth factor-beta 1 (rhTGF-beta 1) on the healing of incisional wounds in rats with impaired healing due to age or glucocorticoid administration was investigated. The administration of methylprednisolone to young adult rats decreased wound breaking strength to 50% of normal control. Breaking strength of incisional wounds from 19-mo-old rats was decreased approximately 27% compared with wounds from normal healing young adult rats. A single intravenous administration of rhTGF-beta 1 (100 or 500 micrograms/kg) increased wound breaking strength from old rats or young adult rats with glucocorticoid-induced impaired healing to levels similar to normal healing control animals when determined 7 d after injury. Even though the circulating half-life of systemically administered rhTGF-beta 1 is < 5 min, a sustained stimulatory effect on extracellular matrix secretion was evident in glucocorticoid-impaired rats when rhTGF-beta 1 was administered at the time of wounding, 4 h after wounding, or even 24 h before wounding. These observations indicate a previously unrecognized potential for the active form of TGF-beta 1 to profoundly influence the wound healing cascade after brief systemic exposure.

Aging↗

Regulation of hypothalamic preprogrowth hormone-releasing factor messenger ribonucleic acid expression in food-deprived rats: a role for histaminergic neurotransmission.

To determine the component(s) of dietary protein that regulates GH-releasing factor (GRF) synthesis, we measured hypothalamic prepro-GRF mRNA by solution hybridization/nuclease protection analysis in food-deprived rats refed protein-free diets (PF) supplemented with individual amino acids. Adult male Sprague-Dawley rats were allowed free access to food (Fed), food deprived for 72 h (FD), or FD then refed for 72 h with a normal (NF) diet, a protein-free (PF) diet, or PF diets containing tyrosine, tryptophan (Trp), glutamic acid, or histidine (His). Food-deprived rats displayed the expected 80% reduction in hypothalamic prepro-GRF mRNA. Upon refeeding, levels were normalized in rats refed a normal diet, but not in those refed a PF diet alone or with tyrosine, Trp, or glutamic acid. In contrast, prepro-GRF mRNA was restored to 70% of Fed values by a PF diet with His. Supplementing a PF diet with His was sufficient to maintain hypothalamic prepro-GRF mRNA expression, as 3 days of feeding replete rats with PF diet or PF diet with added Trp resulted in a 50% reduction in prepro-GRF mRNA, whereas levels were reduced 25% by feeding animals a PF diet with His. Groups of rats allowed free access to food were treated for 72 h with two daily injections of 100 mg/kg alpha-fluoremethylhistidine, a specific irreversible inhibitor of histidine decarboxylase, to determine if the effect of His on prepro-GRF mRNA depended on neural conversion to histamine. alpha-Fluoremethylhistidine-treated rats showed a 40% reduction in hypothalamic prepro-GRF mRNA, with no concomitant change in preproneuropeptide-Y or preprosomatostatin. These data indicate that decreased hypothalamic prepro-GRF mRNA in FD rats is due in part to the lack of dietary and provide clear evidence for a role of the histaminergic neural system in the regulation of hypothalamic GRF expression.

Animals↗

Tissue distribution of somatostatin receptor subtype messenger ribonucleic acid in the rat.

The tissue distribution of mRNA encoding five somatostatin receptor subtypes, SSTR1, SSTR2, SSTR3, SSTR4, and SSTR5, was determined in adult rat tissues by solution hybridization/nuclease protection analysis using sequence-specific cRNA probes. In the central nervous system, SSTR1 and SSTR2 mRNA were expressed widely, with highest levels in hippocampus, hypothalamus, cortex, and amygdala and expression of both isoforms in cerebellum and spinal cord. Expression of SSTR3 was also widespread, occurring in all brain regions examined, with the highest level of expression in the cerebellum. SSTR4 mRNA was detected in most brain regions, with highest levels occurring in the hippocampus, cortex, and olfactory bulb. No detectable levels were found in cerebellum. SSTR5 showed a unique pattern of expression in the central nervous system, being found primarily in the hypothalamus and preoptic area. In peripheral tissues, high levels of SSTR1 and SSTR2 mRNA were found in pituitary and spleen. SSTR1 mRNA was also found in the heart and intestine, SSTR2 was detected in pancreas, and both isoforms were expressed in stomach. Expression of SSTR3 was noted in heart, liver, stomach, intestine, kidney, spleen, and pituitary. The patterns of expression were similar for SSTR4 and SSTR3 mRNA; however, SSTR4 was not expressed in liver. SSTR5 was expressed predominantly in the pituitary, but detectible levels were observed in spleen and intestine. Thus, the SSTR subtype mRNA showed both a tissue-specific and overlapping pattern of expression. Taken together with SSTR-specific signal transduction systems, this probably explains the diverse physiological actions of somatostatin.

Animals↗

Tenascin expression in the mouse: in situ localization and induction in vitro by bFGF.

The glycoprotein tenascin is found in the extracellular matrix in regions of cell motility, cell proliferation, and tissue modelling. We have used novel tenascin cDNA probes to localize tenascin transcripts in the developing mouse and to study the regulation of tenascin expression by growth factors in vitro. At postnatal day 1 tenascin mRNAs are abundant in regions of bone and cartilage formation, as well as in the ependymal layer of the central nervous system. Previous studies have demonstrated that transforming growth factor-beta type 1 (TGF-beta 1) can induce tenascin expression in vitro. As TGF-beta 1 is absent or scarce in the developing brain, it is likely that other growth factors, alone or in addition to TGF-beta 1, may regulate tenascin expression during development. Therefore, we have compared the effects of TGF-beta 1 and a growth factor that is found in both developing connective tissue and the central nervous system, basic fibroblast growth factor (bFGF), on tenascin expression in a mouse embryo fibroblast cell line (Swiss 3T3 cells). Immuno-slot blot analysis of Swiss 3T3 cell-conditioned culture medium demonstrates that bFGF is a more potent inducer of tenascin expression than TGF-beta 1. Furthermore, bFGF and TGF-beta 1 have an additive effect on levels of tenascin, but not fibronectin, in the conditioned medium. Western blots revealed that different forms of tenascin are induced by bFGF and TGF-beta 1: the tenascin induced by the former has a molecular mass of approximately 250 kDa, the latter induces an approximately 200 kDa form of tenascin. The induction of large tenascin by bFGF was confirmed by northern blot analysis, which revealed increased levels of an 8 kb tenascin transcript after 24 h by as little as 4 ng/ml of bFGF in serum-free medium. Thus bFGF, alone or in combination with TGF-beta 1, is a potential regulator of tenascin expression in vitro. bFGF may alter not only the relative abundance of tenascin and fibronectin in the extracellular matrix, but also the splice variant of tenascin expressed by a given cell type.

3T3 Cells↗

Preferential survival of mice expressing the Qa-2 antigen.

The Ped gene, a gene that influences the rate of embryonic cleavage division, birth weight, litter size and weaning weight, is at least partially encoded by gene(s) that specify the Qa-2 antigen. Two congenic strains of mice, B6.K1 (Qa-2 negative) and B6.K2 (Qa-2 positive), which differ only at the Q region of the mouse major histocompatibility complex (MHC), were tested for the effect of the presence or absence of Qa-2 antigen on litter size, duration of gestation and embryo survival. It was confirmed that B6.K1 (Qa-2 negative) mice have smaller litters than do B6.K2 (Qa-2 positive) mice. In addition, the duration of gestation for the B6.K1 mice was found to be longer than the duration of gestation for the B6.K2 mice. Finally, a comparison of the relative survival of Qa-2-positive and Qa-2-negative mice in a single uterine environment showed the preferential survival of mice expressing the Qa-2 antigen. Thus, the presence of Qa-2 antigen appears to be advantageous for reproductive success.

Animals↗

[Intratesticular subcapsular assay, a simple method for the preliminary screening of male contraceptives].

The MB-50 protocol worked out for long by the World Health Organization has been widely employed for the screening of male contraceptives. With this method, 40-80 rats will be used for 1 sample and the course of study will be about 3 months. In view of the high expenses and long duration of time needed, it seems to be not suitable for a preliminary screening. We have exploited a much simpler method, the intratesticular subcapsular assay. The method is as follows: Puncture the scrotal skin and the tunica albuginea at the equatorial plane of the testis just opposite to the epididymis with an intradermal needle fixed at a tuberculin syringe. Then push on the needle for 3-4 mm along the equator parallel to the tunica albuginea. Inject 100 microliters of solution containing 0.1-5 mg of the sample to each testis. To the controls, only the vehicle is injected. One week later the same procedure is repeated and 2 more weeks later, the animals are sacrificed and the data are observed (see Table 1 and 2). In this paper, 7 samples screened with this method were compared with results of the MB-50 method, no positive sample was missed except one false positive sample. These results indicate the coincidence between these two methods.

Animals↗

Synthesis, cloning and sequencing of glucoamylase cDNA from Aspergillus niger mutant T21.

Poly(A)+ RNA was isolated from Aspergillus niger T21, a glucoamylase overproducing strain and was used as template to synthesize double stranded cDNA. A cDNA library was then constructed. The E. coli transformants were screened for the glucoamylase cDNA by in situ colony hybridization with P-labeled fragment of glucoamylase gene as probe. The positive rate was 1.6%. Restriction analysis proved that 32% of the positive clones carried the inserts of 2.1 kb of full length glucoamylase cDNA. Sequence of the glucoamylase cDNA was determined and the result showed that the sequence of glucoamylase gene of the mutant T21 was almost the same as that reported previously. The high rate of glucoamylase cDNA-containing clones in the cDNA library of strain T21 provided evidence of high steady state level of glucoamylase mRNA in mycelium of mutant T21. Most likely it is one of the major causes for the high glucoamylase productivity of mutant T21.

Aspergillus niger↗

[Histochemical studies on the glycoconjugates of experimental alkali burned cornea in rabbit].

The model of experimental alkali burn of cornea in rabbit was obtained using 1 mol/L NaOH solution. After being burned for 1, 3, 7 and 14 days, the histochemical changes of these models were studied by using labelled concanavalin A (ConA-FITC) and wheat germ agglutinin (WGA-FITC). The results showed that after being burned, the amount of glycoconjugates interacted with these lectins decreased, and increased gradually after 7 days, then reached the level higher than that in the normal cornea. These changes were related to the recovery of alkali burned cornea.

Animals↗

[Ensure treatment for IUGR].

A prospective study on Ensure and amino acid infusion treatment for IUGR was carried out in 1989 and 1990 in PUMC Hospital. The patients were divided into two groups. Subjects in group 1 received Ensure, and those in group 2 received amino acid treatment. Each group included 40 subjects. The incidence of SGA was found to decrease from 2.18% in 1989 to 1.59% in 1990. The cure rate of IUGR reached 41.7% and 21.9% in groups 1 and 2, respectively. The average birth weights were 2,820g and 2,656g in groups 1 and 2 (t = 19.15, P < 0.001), respectively. Our conclusion is that Ensure is an effective nutritional drug for treatment of IUGR.

Birth Weight↗

[Cytogenetic studies of brown field-mouse].

The karyotype of Brown Field-Mouse (Microtus mandarinus) is reported in this paper. The formula of karyotypes is:2n = 50 = 2 (M,T)+2SM+44T+XX(M,SM)XY(SM,ST). The first pair of the autosomes and the X-chromosomes show polymorphism. Only one X-chromosome can be found in the seven out of the fifteen female specimens studied. The formula of its karyotypes is 2n = 49 = 2(M,ST)+2SM+44T+X O. The X-chromosomes of these seven specimens are metacentric, and are different from the X (that is SM) of normal male, these are the type M. Three kinds of karyotypes of Microtus mandarinus studied in this paper are different from the karyotypes (XO,OY,XY) of M. oregoni studied by Brown et al. (1964). The mechanism of generation of chromosomal polymorphism is discussed. Individual ontogenesis mechanism of the type XO and its reproduction are also discussed.

Animals↗

Effect of subconjunctival daunorubicin on glaucoma surgery in rabbits.

Daunorubicin (DNR), an antibiotic-antimetabolite, was used as an adjunct to standardized partial-thickness filtration surgery in 21 rabbits to determine its effects on that surgery. Postoperatively, one of the eyes of each rabbit received subconjunctival injections of DNR 25 micrograms or 50 micrograms, while the fellow eyes received only diluent, daily for 2 to 14 days. Bleb survival, fistula patency, the thickness of the subconjunctival connective tissue, and postoperative complications were investigated. The filtration blebs lasted significantly longer (P < .005), the rate of fistula closure was significantly lower (P < .005), and the subepithelial connective tissue was much looser and thicker in the experimental eyes than in the control eyes. Corneal toxicity occurred more frequently in the eyes treated with the higher-dose DNR than in those treated with the lower dose and in the control eyes.

Animals↗