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L Yin

Publications and source records attributed to L Yin.

At least 91 records · Page 5Linked to original sources
PubMed1999

Testosterone inhibits apoptosis of Leishmania donovani-infected macrophages.

AIM: Investigate the effect of the male sex hormone, testosterone (Te), on apoptosis of bone marrow derived macrophages (BMMs) from female C57BL/6j mice METHODS: Propidium iodide (PI) staining and transmission electron microscopy (TEM) techniques were used to investigate apoptosis specific-morphological changes. BMMs derived from Te-treated mice and Oil-treated mice were challenged with Leishmania donovani (L. d.), Oligo-nucleosomal DNA were extracted 24 h post infection to detect apoptosis. RESULTS: The removal of M-CSF from the medium could induce BMM apoptofsis. And the DNA fragmentation assay also indicated that: 1. there was no difference in the amount of apoptotic cells between Te and Oil group; 2. Te + L. d. group had significantly less dead cells than Oil + L. d. group demonstrating that Te could prevent apoptosis of macrophage infected with L. d. to a greater extent. CONCLUSION: Te inhibits apoptosis of the macrophages infected with L. d., however, this inhibition did not occur in the macrophages uninfected with L. d. Te-induced macrophage apoptosis-inhibition may play an important role in Te-induced immunosuppression.

Animals↗
PubMed1998

Disruption of the Jak1 gene demonstrates obligatory and nonredundant roles of the Jaks in cytokine-induced biologic responses.

Herein we report the generation of mice lacking the ubiquitously expressed Janus kinase, Jak1. Jak1-/- mice are runted at birth, fail to nurse, and die perinatally. Although Jak1-/- cells are responsive to many cytokines, they fail to manifest biologic responses to cytokines that bind to three distinct families of cytokine receptors. These include all class II cytokine receptors, cytokine receptors that utilize the gamma(c) subunit for signaling, and the family of cytokine receptors that depend on the gp130 subunit for signaling. Our results thus demonstrate that Jak1 plays an essential and nonredundant role in promoting biologic responses induced by a select subset of cytokine receptors, including those in which Jak utilization was thought to be nonspecific.

Animals↗
PubMed1998

Risk of connective tissue disease and related disorders among women with breast implants: a nation-wide retrospective cohort study in Sweden.

OBJECTIVE: To examine the relation between connective tissue disease and related conditions and breast implants. DESIGN: Retrospective cohort study of all women in the Swedish national inpatient registry who underwent breast augmentation surgery with artificial implants during 1964-93, compared with women who underwent breast reduction surgery during the same period. SETTING: Sweden. SUBJECTS: 7442 women with implants for cosmetic reasons or for reconstruction after breast cancer surgery and 3353 women with breast reduction surgery. MAIN OUTCOME MEASURES: Subsequent hospitalisation for definite connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, dermatomyositis, and Sjögren's syndrome) or related disorders. RESULTS: 29 women with implants were hospitalised for definite connective tissue disease compared with 25.5 expected based on general population rates (standardised hospitalisation ratio 1.1 (95% confidence interval 0.8 to 1.6)). There were no diagnoses of systemic sclerosis, and no significant excess in risk for polymyalgia rheumatica, fibromyalgia, and several related disorders. Among women who underwent breast reduction surgery, 14 were hospitalised for definite connective tissue disease compared with 10.5 expected (standardised hospitalisation ratio 1.3 (0.7 to 2.2)). Compared with the breast reduction group, women with breast implants showed a slight reduction for all definite connective tissue disease (relative risk 0.8 (95% confidence interval 0.5 to 1.4)). CONCLUSIONS: This large nationwide cohort study shows no evidence of association between breast implants and connective tissue disease.

Adult↗
PubMed1998

Control of mouse hepatocyte proliferation and ploidy by p53 and p53ser246 mutation in vivo.

The effect of expression of the p53 gene, in the presence or absence of the p53ser246 mutation (p53*), on ploidization (image cytometry), proliferation (expression of proliferating cell nuclear antigen and radioactive thymidine histoautoradiography), and apoptosis (in situ detection of DNA fragments) is determined in hepatocytes of p53-null and p53*-transgenic mice. The mouse p53ser246 mutation is equivalent to the p53ser249 mutation found in human hepatomas associated with hepatitis B virus infection and aflatoxin exposure. The hepatocytes of heterozygous or homozygous p53-knockout mice (p53+/-; p53-/-), as well as knockout mice expressing one allele of p53ser246 (p53+/-, p53*; p53-/-, p53*), do not undergo normal polyploidization with aging and show an increase in the number of cycling (G1-, S-, and M-phase) cells. In addition, p53ser246-transgenic mice (p53+/+, p53*; p53+/-, p53*; and p53-/-, p53*) have a greatly increased number of hepatocytes in the G1 phase. No differences in rates of apoptotic hepatocytes are found among any of the mouse groups studied, so the increased proliferation results in a hyperplasia manifested by a increased number of small periportal cells. We conclude that loss of p53 removes blocks in the cell cycle, leading to increased proliferation, whereas expression of the p53ser246 mutation stimulates G0 to G1 and/or M to G1 transition of hepatocytes. Increased proliferation of hepatocytes, combined with no concomitant increase in apoptosis, may in part explain the enhanced development of hepatocellular carcinomas in p53-knockout and p53*-transgenic mice exposed to aflatoxin.

Amino Acid Sequence↗
PubMed1998

Continuing quality improvement procedures for a clinical PACS.

The University of California at San Francisco (USCF) Department of Radiology currently has a clinically operational picture archiving and communication system (PACS) that is thirty-five percent filmless, with the goal of becoming seventy-five percent filmless within the year. The design and implementation of the clinical PACS has been a collaborative effort between an academic research laboratory and a commercial vendor partner. Images are digitally acquired from three computed radiography (CR) scanners, five computed tomography (CT) scanners, five magnetic resonance (MR) imagers, three digital fluoroscopic rooms, an ultrasound mini-PACS and a nuclear medicine mini-PACS. The DICOM (Digital Imaging and Communications in Medicine) standard communications protocol and image format is adhered to throughout the PACS. Images are archived in hierarchical staged fashion, on a RAID (redundant array of inexpensive disks) and on magneto-optical disk jukeboxes. The clinical PACS uses an object-oriented Oracle SQL (systems query language) database, and interfaces to the Radiology Information System using the HL7 (Health Languages 7) standard. Components are networked using a combination of switched and fast ethernet, and ATM (asynchronous transfer mode), all over fiber optics. The wide area network links six UCSF sites in San Francisco. A combination of high and medium resolution dual-monitor display stations have been placed throughout the Department of Radiology, the Emergency Department (ED) and Intensive Care Units (ICU). A continuing quality improvement (CQI) committee has been formed to facilitate the PACS installation and training, workflow modifications, quality assurance and clinical acceptance. This committee includes radiologists at all levels (resident, fellow, attending), radiology technologists, film library personnel, ED and ICU clinician end-users, and PACS team members. The CQI committee has proved vital in the creation of new management procedures, providing a means for user feedback and education, and contributing to the overall acceptance of, and user satisfaction with the system. Well developed CQI procedures have been essential to the successful clinical operation of the PACS as UCSF Radiology moves toward a filmless department.

Computer Communication Networks↗
PubMed1998

Two pimarane diterpenoids from Ephemerantha lonchophylla and their evaluation as modulators of the multidrug resistance phenotype.

Two new pimarane diterpenoids, lonchophylloids A (1) and B (2), were isolated from the stems of Ephemerantha lonchophylla. The structures of 1 and 2 were established predominantly through the application of extensive 1H-and 13C-NMR, 1D- and 2D-homonuclear and heteronuclear correlation NMR experiments, and X-ray diffraction methods. Consistent with structure--activity predictions, both compounds were capable of sensitizing cells that expressed the multidrug resistance phenotype to the toxicity of the anticancer drug doxorubicin.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1998

Host response to EBV infection in X-linked lymphoproliferative disease results from mutations in an SH2-domain encoding gene.

X-linked lymphoproliferative syndrome (XLP or Duncan disease) is characterized by extreme sensitivity to Epstein-Barr virus (EBV), resulting in a complex phenotype manifested by severe or fatal infectious mononucleosis, acquired hypogammaglobulinemia and malignant lymphoma. We have identified a gene, SH2D1A, that is mutated in XLP patients and encodes a novel protein composed of a single SH2 domain. SH2D1A is expressed in many tissues involved in the immune system. The identification of SH2D1A will allow the determination of its mechanism of action as a possible regulator of the EBV-induced immune response.

Antigens, CD↗
PubMed1998

Association of multiple endocrine neoplasia type 2 and Hirschsprung disease.

In a few patients with Hirschsprung disease (HSCR) and no clinical symptoms of multiple endocrine neoplasia type 2 (MEN-2A) or medullary thyroid carcinoma (MTC), missense mutations in the cysteine residues 609 and 620 of the Ret gene have been identified. In several pedigrees with either MEN-2A or familial MTC (FMTC) a documented germline mutation in cysteine 618 or 620 follows the segregation of the disease phenotype. The appearance of the HSCR phenotype in such patients and pedigrees cannot be easily reconciled with the gain of function which is associated with the dominant oncogenic effect of MEN-2A mutations. Gastrointestinal manifestations are known to occur also in association with MEN-2B but, to the best of our knowledge, in only very few cases the intestinal phenotype of MEN-2B has been investigated by enzymo-histochemical techniques, as in the present work. We report an extensive molecular study of patients, two with HSCR and FMTC carrying a Cys620Arg or Ser mutation and two with MEN-2B and gastrointestinal symptoms carrying a Met918Thr mutation. One of the latter two patients showed aganglionosis of the last 5 cm of rectum which caused a congenital megacolon leading to the diagnosis and operation for HSCR. The mutation screening of all the exons of Ret in 3 of these patients did not reveal any additional mutation. Therefore these results do not support the hypothesis of additional constitutional Ret mutations in patients showing association of MEN-2 and HSCR, whilst the histochemical and clinical data in one of these patients indicate that MEN-2B can be associated with a true form of short segment HSCR.

Drosophila Proteins↗
PubMed1998

The epitope spreading cascade during progression of experimental autoimmune encephalomyelitis and multiple sclerosis.

We have made the following observations regarding self-recognition during the development and progression of murine experimental autoimmune encephalomyelitis (EAE) and human multiple sclerosis (MS): 1) chronic progression of EAE is accompanied by a sequential, predictable cascade of neo-autoreactivity, commonly referred to as epitope spreading, presumably caused by endogenous self-priming during autoimmune-mediated tissue damage; 2) there is an invariant relationship between the progression of EAE and the emergence of epitope spreading; 3) progression of EAE can be inhibited by the induction of antigen-specific tolerance to spreading determinants after onset of initial neurologic symptoms; 4) CD4+ Th 1 cells responding to spreading determinants are autonomously encephalitogenic; 5) epitope spreading occurs during the development of MS and in some cases involves HLA-DP class II-restricted self-recognition; and 6) progression of both EAE and MS is accompanied by the decline of primary T-cell autoreactivity associated with disease onset and by the concurrent emergence of the epitope spreading cascade. Our studies directly challenge the traditional view that EAE and MS are initiated and maintained by autoreactivity directed against a single predominant myelin protein or determinant. Our results indicate that progression of EAE and MS involves a shifting of T-cell autoreactivity from primary initiating self-determinants to defined cascades of secondary determinants that sustain the inflammatory self-recognition process during disease progression.

Animals↗
PubMed1998

Human immunodeficiency virus type 1 replication is modulated by host cyclophilin A expression levels.

Human immunodeficiency virus type 1 (HIV-1) Gag and the cellular protein cyclophilin A form an essential complex in the virion core: virions produced by proviruses encoding Gag mutants with decreased cyclophilin A affinity exhibit attenuated infectivity, as do virions produced in the presence of the competitive inhibitor cyclosporine. The A224E Gag mutant has no effect on cyclophilin A affinity but renders HIV-1 replication cyclosporine resistant in Jurkat T cells. In contrast, A224E mutant virus is dead in H9 T cells, although replication is rescued by cyclosporine or by expression in cis of a Gag mutant that decreases cyclophilin A-affinity. The observation that disruption of the Gag-cyclophilin A interaction rescues A224E mutant replication in H9 cells prompted experiments which revealed that, relative to Jurkat cells, H9 cells express greater quantities of cyclophilin A. The resulting larger quantity of cyclophilin A shown to be packaged into virions produced by H9 cells is presumably disruptive to the A224E mutant virion core. Further evidence that increased cyclophilin A expression in H9 cells is of functional relevance was provided by the finding that Gag mutants with decreased cyclophilin A affinity are dead in Jurkat cells but capable of replication in H9 cells. Similarly, cyclosporine concentrations which inhibit wild-type HIV-1 replication in Jurkat cells stimulate HIV-1 replication in H9 cells. These results suggest that HIV-1 virion infectivity imposes narrow constraints upon cyclophilin A stoichiometry in virions and that infectivity is finely tuned by host cyclophilin A expression levels.

Alanine↗
PubMed1998

High-resolution mapping of the X-linked lymphoproliferative syndrome region by FISH on combed DNA.

X-linked lymphoproliferative syndrome is an inherited immunodeficiency for which the responsible gene is currently unknown. Several megabase-sized deleted regions mapping to Xq25 have been identified in XLP patients, and more recently a 130-kb deletion has been reported (Lamartine et al., 1996; Lanyi et al., 1996). To establish a physical map of this deleted region and to identify the XLP gene, two cosmid contigs were established (Lamartine et al., 1996). However, the physical map of this region is still uncompleted and controversial and three points remain unsolved: (1) the centromeric-telomeric orientation of the whole region, (2) the relative orientation of the two contigs, and (3) the size of the gap between the two contigs. To provide a definitive answer to these questions, high-resolution mapping by fluorescence in situ hybridization on combed DNA and molecular approaches were combined to establish the physical map of the XLP region over 600 kb. Our results identified a gap of 150 kb between the two contigs, established the relative orientation of one contig to the other, and determine the centromeric-telomeric orientation of the whole region. Our results show that the order of the marker over this region is: cen.1D10T7-DF83-DXS982.tel.

Chromosome Mapping↗
PubMed1998

Cytotoxicity of xenobiotics and expression of glutathione-S-transferases in immortalised rat hepatocyte cell lines.

1. Immortalised rat hepatocyte cell lines are more sensitive to the cytotoxicity of 1-chloro-2,4-dinitrobenzene and ethacrynic acid than primary cultures of hepatocytes. 2. Class alpha glutathione S-transferases are not expressed in immortalised hepatocyte cell lines. Class pi glutathione S-transferase expression is elevated in the immortalised cell lines compared with freshly isolated hepatocytes, but it is not as high as in the HTC rat hepatoma cell line. 3. Immortalised hepatocyte cell lines may provide a sensitive model system for detecting cytotoxicity associated with xenobiotics which are detoxified by glutathione S-transferases.

Animals↗
PubMed1998

Breast implants and risk of neurologic disease: a population-based cohort study in Sweden.

OBJECTIVE: To examine the risk of neurologic disorders among women with breast implants. BACKGROUND: Case reports in the literature have raised concern about a possible link between silicone breast implants and some types of neurologic disorders, but there is a dearth of epidemiologic studies in this area. METHODS: Through the nationwide Swedish hospital discharge register, we identified a population-based cohort of 7433 women with breast implants. A similarly identified cohort of 3351 women who underwent breast reduction surgery served as a comparison. The women were followed from 1972 (or date of breast surgery if it occurred later) through 1993 by means of record linkages and review of inpatient medical records. Ratios of observed to expected numbers, and relative risks (RR) with 95% confidence intervals (CI), were calculated as measures of the risk of neurologic diseases among women with implants. RESULTS: A direct comparison of the exposed (implant) versus comparison (breast reduction) groups, after exclusion of patients with pre-existing disease or incorrect neurologic diagnoses, showed no excess risk among implant patients (RR = 0.8; 95% CI = 0.5 to 1.4). When external rates derived from the background population were used as comparison, we found a small, statistically nonsignificant excess of neurologic disorders both in the breast implant (RR = 1.3; 95% CI = 0.9 to 1.9) and the breast reduction (RR = 1.5; 95% CI = 0.9 to 2.4) cohorts. CONCLUSION: Our results provide no support for the conjecture that breast implants cause neurologic disease.

Adult↗
PubMed1998

[Placental morphometriological study on prolonged and delayed pregnancy and its relationship to pregnancy outcome].

OBJECTIVE: To study the morphological characteristics of the placental villous vessels and uteroplacental spiral arteries in the prolonged and delayed pregnancy and its relationship to pregnancy outcome. METHODS: Placentae from 20 cases of prolonged pregnancy (PP), 15 cases of delayed pregnancy (DP), and 29 cases of normal term pregnancy (NTP) were examined by morphometriological feature image analysis. RESULTS: Significant differences were found between PP and NTP groups (P < 0.05) in the following findings: the placental weights, the numbers of the placental villus with the syncytial knots, cytotrophoblasts, thickening of basal lamina, fibrinoid necrosis, vasculosyncytial membranes, and the diameter, perimeter and area of the villi the spiral artery wall thickening of the uteroplacental bed, and the incidences of the oligoamnios and amniotic fluid meconium staining. Significant differences of the villus perimeter and oligoamnios were only found between DP and NTP (all P < 0.05). There was no significant differences in the indices between PP and DP. As the pregnancy delayed and prolonged, the placental weights gradually decreased and the low Apgar score of neonates gradually increased. CONCLUSION: After term pregnancy the placental function is gradually lowered especially in PP. The situations of the placenta, amniotic fluid, and fetus should be frequently monitored after 40 gestational weeks.

Female↗
PubMed1998

[Uterine and placental vascular lesions in pregnancy induced hypertension and its relationship to pregnancy outcome].

OBJECTIVE: To study the vascular lesions of the uterus and placenta in severe pregnancy induced hypertension (SPIH) and its relationship to pregnancy outcomes. METHODS: 29 cases of SPIH and 29 cases of normal term pregnancies (NTP) were examined to observe the expressions of IgA, IgG, IgM and C3 in the vascular walls of placental villus and uterus placental bed by immunohistochemical technique. RESULTS: (1) In SPIH, the positive expression rates of the IgA, IgG, IgM and C3 in the vascular wall of placental villus (20.1%, 24.1%, 72.4%, and 65.5%) and uterus placental bed (20.0%, 20.0%, 70.0% and 60.0%) were significantly higher than those of NTP (all P < 0.05), while there were no expression in NTP. (2) The thickening of endangium angiostenosis, fibronoid necrosis and acute arterial atherosis were found at the sites of positive expressions in SPIH. (3) In SPIH complicated by intrauterine growth retardation (IUGR), the positive expressions of the immunocomplex and complement in the vessel walls (76.2%) were significantly higher than those of the SPIH without IUGR (50%, all P < 0.05). CONCLUSION: In SPIH, there are depositions of immunocomplex and complement on the vessel walls of placental villus and uteroplacenta. Immunological factor plays an important role in the development of PIH.

Adult↗