Biomedical subjects

Y H Su

Publications and source records attributed to Y H Su.

At least 37 records · Page 2Linked to original sources

PubMed1996

Responses of somatostatin, beta-endorphin and dynorphin A to a glucose load in two groups of women with polycystic ovarian syndrome.

To investigate the relationship between elevated LH, hyperinsulinemia and neuropeptides in polycystic ovarian syndrome (PCOS), we measured the endogenous levels of insulin, somatostatin (SS), beta-endorphin (beta-EP) and dynorphin A (Dyn A) before and after a glucose load in three groups: group 1 (LH/ FSH > or = 3, n = 30); group 2 (LH/FSH < 3, n = 25), and controls (n = 15). In the basal state, significantly negative correlations were found between LH and SS (r = -0.51, p < 0.05) in group 1 and between LH and beta-EP (r = -0.49, p < 0.05) in group 2. After a glucose load, PCOS women had greater beta-EP and Dyn A responses in group 1 and impaired SS response in group 2 as compared with the control. The data suggest endogenously lower SS, higher beta-EP and Dyn A may contribute to the elevation of LH and insulin secretions in PCOS.

Adult↗

PubMed1995

[Protective effect of "wei tong ling" on gastric mucosa and influence on quality of gastric ulcer healing].

The acute gastric ulcer rat models were induced by dehydrated alcohol, 0.6 N hydrochloric acid and 0.6 N sodium hydroxide, and the chronic gastric ulcer rat models were established by means of acetic acid, the protective effect of Chinese medicine "Wei Tong Ling" (WTL) on gastric mucous membrane was studied. Using histochemical mucin stain, AgNOR stain and immunohistochemical technique the regenerated mucosa of healed gastric ulcer induced by acetic acid in rats was observed quantitatively. They were compared with that of WTL. The results showed that the regenerated mucosa of healed gastric ulcer might be the morphological basis for the recurrence of gastric ulcer and be associated with canceration. WTL could not only accelerate the healing of ulcer but also raise the quality of gastric ulcerous healing which was beneficial for the prevention of ulcer recurrence and canceration. The protective effect of WTL on gastric mucosa was confirmed by various assays.

Animals↗

PubMed1994

[Light and electron microscopic histochemical studies of alkaline phosphatase (ALP) isoenzymes in gastric cancer].

By using light and electron microscopic histochemical techniques, the activities and distributions of ALP isoenzymes in gastric cancers and benign gastric diseases were examined. The results showed: Nagao, Regan and Kasahara isoenzymes, which were not expressed in normal gastric mucosae and non-malignant lesions, may be considered as the tumor markers of gastric cancer. The epithelium of intestinal metaplasia exhibited intestinal-type ALP only, which was one of the markers of well-differentiated intestinal metaplasia. In the view-point of the gene expression of ALP isoenzymes, two mutation hypothesis and recessive-gene mutation hypothesis may be proper for gastric cancer.

Adenocarcinoma↗

PubMed1993

Mapping the genetic region coding for herpes simplex virus resistance to mouse interferon alpha/beta.

Herpes simplex virus (HSV) ocular virulence has been associated with strain sensitivity to mouse interferon (IFN)-alpha/beta. To identify the region of the virus genome associated with heightened resistance to this cytokine, intertypic recombinants were constructed using the intact genome of avirulent, IFN-sensitive HSV type 1 (strain 35) and XbaI-digested DNA from virulent, IFN-resistant HSV type 2 (strain 186). An intertypic recombinant, designated HSV-R4, was isolated which grew to titres 10- to 100-fold higher than HSV-1(35) in mouse ocular tissue in vivo, and induced stromal keratitis. The recombinant which was several orders of magnitude more resistant to mouse IFN-alpha/beta than HSV-1(35) had a genome composed of HSV-1(35) DNA except for a 12 kb fragment (0.15 to 0.23 map units) derived from HSV-2(186). To define the IFN resistance locus further, three overlapping subclones of this 12 kb fragment were constructed from the HSV-2(186) genome and subjected to marker rescue experiments. The cloned BamHI D fragment was the only subclone that promoted HSV-1(35) ocular growth in vivo. An intertypic recombinant, designated HSV-R(BD), was isolated from the 35 x 186 BamHI D transfection progeny pool. This recombinant, in contrast to HSV-1(35), was several orders of magnitude more resistant to mouse IFN-alpha/beta inhibition in vitro, grew 10- to 100-fold better in mouse ocular tissue in vivo, and caused severe necrotizing stromal keratitis in BALB/c mice. Analysis of the recombinant genome indicated that the HSV-2 genetic information responsible for IFN resistance of HSV-R(BD) was located within the BamHI D fragment, most likely mapping to that region containing three partial open reading frames designated UL14, UL15 and UL16. The products encoded by this region remain to be identified.

Animals↗

PubMed1991

Evidence endogenous interferon production contributed to the lack of ocular virulence of an HSV intertypic recombinant.

An intertypic recombinant isolated from rabbit kidney cells following co-transfection of HSV-1(17) and HSV-2(186) DNA failed to induce overt ocular pathology when inoculated onto the murine sacrificed cornea at concentrations as high as 10(7) PFU per eye. In contrast, both parents induced corneal disease at a 1000-fold lower dose. The reason(s) for the failure of the intertypic recombinant, designated RO25X, to induce corneal pathology was investigated. It was found that the recombinant was 100-fold more sensitive to the inhibitory effects of interferon (IFN) alpha/beta than the parent strains in corneal button growth studies in vitro. R025X readily grew in cultured mouse corneal fibroblasts at a low multiplicity of infection. However, the peak titer was approximately 8-fold lower than that of strain 17. Addition of rabbit anti-IFN alpha/beta to the culture medium resulted in a 4 to 5-fold increase in infectious titer compared to its growth in the absence of antiserum. Most significantly, when mice were pre-treated in vivo with anti-IFN alpha/beta 24 hours prior to virus corneal infection, 67% of the recipients developed moderate to severe stromal keratitis, whereas none of the controls developed corneal pathology. Blepharitis was also significantly increased in incidence and severity in the antiserum treated hosts. We conclude that the inability of R025X to induce ocular disease was due, at least in part, to the inhibitory effects of interferon produced in response to infection.

Animals↗

PubMed1991

[Autoimmune reaction factors of infertility in patients with endometriosis].

The presence of immunoprotein depositions in endometrium and antiendometrial autoantibodies in serum was detected in 59 infertile patients with endometriosis, 45 infertile patients without endometriosis and 11 fertile women by the methods of immunohistochemistry determination and immunodiffusion assay. The immunoprotein depositions in endometrium of endometriosis were significantly increased. The antiendometrial auto-antibodies in serum were positive in 32.2% for infertile patients with endometriosis, 6.7% for infertile patients without endometriosis and 0% for fertile women. This suggested that an autoimmune response might be an etiologic factor of infertility in patients with endometriosis.

Adult↗

PubMed1990

Ocular avirulence of a herpes simplex virus type 1 strain is associated with heightened sensitivity to alpha/beta interferon.

BALB/c mice infected on the scarified cornea with herpes simplex virus type 1 strain 35 [HSV-1(35)] rarely developed ocular disease even at challenge doses as high as 10(7) PFU per eye. In contrast, HSV-1(RE) consistently induced stromal keratitis at an inoculum of 2 x 10(4) PFU. The goal of this study was to determine the reason for the difference in virulence between the two HSV strains. Both HSV-1 strains replicated to similar titers in excised corneal "buttons." However, after in vivo infection of the cornea, the growth of strain 35 was evident only during the first 24 h postinfection, whereas the replication of strain RE persisted for at least 4 days. In vitro tests revealed that HSV-1(35) was greater than 10 times more sensitive to alpha/beta interferon (IFN-alpha/beta) than HSV-1(RE). Both strains induced comparable serum levels of IFN after intraperitoneal inoculation. The kinetics of HSV-1(35) clearance from the eye was markedly altered by treatment with rabbit anti-IFN-alpha/beta. Virus titers exceeding 10(4) PFU per eye could be demonstrated 4 to 5 days postinfection in mice given a single inoculation of antiserum 1 h after infection. Furthermore, anti-IFN treatment in 3-week-old mice infected with HSV-1(35) led to the development of clinically apparent corneal disease which subsequently progressed to stromal keratitis in the majority of recipients. These results indicate that the striking difference in the capacity of HSV-1(35) and HSV-1(RE) to induce corneal disease was related to the inherently greater sensitivity of strain 35 to IFN-alpha/beta produced by the host in response to infection.

Animals↗

PubMed1988