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Biomedical subjects

C Y Lin

Publications and source records attributed to C Y Lin.

At least 163 records · Page 9Linked to original sources
PubMed1997

Defect of cell-mediated immune response against hepatitis B virus: an indication for pathogenesis of hepatitis-B-virus-associated membranous nephropathy.

To elucidate the questions of why not all patients with hepatitis B virus (HBV) infection develop HBV membranous nephropathy (HBVMN), we first measured serum HBe circulating immune complex (CIC) during the acute nephrotic phase of HBVMN and in HBV carriers. We found that the level of HBe CIC was low in the HBVMN patients and absent either in HBsAg+/HBeAg+ patients without HBVMN or HBsAg+/HBeAg- asymptomatic carriers. Second, we needed to characterize the cellular immune response to HBV in patients with HBVMN. However, lack of a suitable autologous effector/target cell system makes a precise study of HBVMN pathogenesis difficult. In the present study, we established a model system by using autologous HBcAg-expressing Epstein-Barr-virus-immortalized lymphoblastoid cell lines (LCL) as stimulator/target cells. Both proliferative response after stimulation with HBcAg and cytotoxic activity against autologous HBcAg-expressing LCL of the peripheral blood T cells obtained from the HBVMN patients and HBsAg carriers could be measured. Using autologous HBcAg-expressing LCL as stimulator/target cells for the study of HBcAg-specific cytotoxic T lymphocytes, we found that HBVMN patients had lower cytotoxic activity than did both HBV carriers and HBsAg-/HBsAb+, HBeAg-/HBeAb+ children. From the in vitro cytokine production study of peripheral blood T cells after stimulation with HBcAg, we found that T-helper-cell-1-related IL-2 and IFN-gamma productions were very low in HBVMN patients but T-helper-cell-2-related IL-10 production was higher in HBsAg+/HBeAg+ patients with HBVMN than in those without HBVMN. Based on these findings, we conclude that HBVMN children seem to have an inadequate cellular immune response to HBcAg.

Adolescent↗
PubMed1997

Maximal forced expiratory maneuver to measure airway obstruction in anesthetized guinea pigs.

Our purpose was to develop a method using a maximal forced expiratory flow (MFEF) for the study of airway hyperreactivity in guinea pigs induced by ovalbumin inhalation challenge. Eight guinea pigs (weight range 350-450 g) were sensitized by inhaled ovalbumin (group I) 2 times during a 1-week interval and then subjected to provocation with ovalbumin 1 week later. Pulmonary function tests at baseline and after acetylcholine challenge were performed 72 h later. Eight weight-matched normal guinea pigs served as controls (group II). All animals were anesthetized, paralyzed with gallamine, and ventilated via tracheostomy. They were given varying doses of acetylcholine (25, 50, 75, 100 micrograms/kg) injected through a jugular venous catheter. Five seconds after acetylcholine injections, pulmonary function was examined, including maximal forced expiratory maneuver, peak airway pressure (PaO) and total lung compliance. After completing the pulmonary function tests, bronchoalveolar lavage (BAL) was performed with 20 ml normal saline divided into two doses. Thereafter, the lungs were removed and examined histologically. The results showed that guinea pigs treated with ovalbumin had worse pulmonary function tests than normal controls, characterized by lower peak flow, MFEF 75%, MFEF 50% and vital capacity. The ovalbumin-presensitized guinea pigs also demonstrated severe bronchoconstriction in response to acetylcholine, characterized by larger decreases in peak flow, MFEF 75%, MFEF 50% and in vital capacity than the control group. Total cell count, the percentage and absolute number of eosinophils and lymphocytes were increased, and the percentage of macrophages was decreased in the BAL fluid of these animals. Finally, ovalbumin-sensitized guinea pigs had a severe inflammatory reaction in airway and lung tissue, characterized by congestion, edema and inflammatory cell infiltration (especially lymphocytes and eosinophils) and desquamation of bronchial epithelial cells. In conclusion, a forced expiratory maneuver can be used to perform pulmonary function tests in guinea pigs.

Acetylcholine↗
PubMed1997

Detection of human papillomavirus mRNA and cervical cancer cells in peripheral blood of cervical cancer patients with metastasis.

PURPOSE: To determine the presence of cervical cancer cells in circulating peripheral blood of stage IVb cervical cancer patients with metastasis to distant organs. PATIENTS AND METHODS: Cervical cancer tissue from 15 stage IVb cervical cancer patients with metastasis were analyzed for the presence of human papillomavirus (HPV) type 16 DNA by nested polymerase chain reaction (PCR). The presence of transcriptional products of the HPV type 16 E6-transforming gene in the peripheral blood of the same 15 cancer patients was analyzed by reverse transcription and PCR. Cervical tissues and peripheral-blood specimens from 12 normal healthy individuals served as controls. RESULTS: Thirteen of 15 (86.7%) cervical cancer tissues from same number of patients were found to contain HPV type 16 DNA. Peripheral-blood specimens from 12 of 13 (92.3%) cervical HPV DNA-positive patients were found to contain HPV-specific mRNA detectable by reverse transcription (RT) and PCR. Cervical tissues from all 12 normal controls were HPV-free. None of the peripheral-blood specimens from two cervical HPV-negative cancer patients and 12 normal controls contained detectable amounts of mRNA of HPV type 16 E6-transforming gene. CONCLUSION: The most likely source of the HPV-specific mRNA detected in the peripheral blood of cervical cancer patients with metastasis is the cervical cancer cells derived from or shed from the cervix. The presence of HPV E6 mRNAs in peripheral blood may be a sensitive indicator of circulating cervical cancer cells. If PCR positivity is proven to be able to predict disease progression reliably, these findings may have clinical applications in the treatment of cervical and many other cancers.

DNA, Viral↗
PubMed1997

Differential expression of telomerase activity in human cervical cancer and cervical intraepithelial neoplasia lesions.

PURPOSE: Telomeres are tandem arrays of repeated DNA sequences located at the ends of eukaryotic chromosomes, and are synthesized by the enzyme telomerase. Loss of telomeric DNA may play an important role in the development of human cancers. However, very little is known about the status of telomerase during human cervical cancer development. PATIENTS AND METHODS: Telomerase activity was measured by telomere repeat amplification protocol (TRAP) assay in 24 cervical cancers, one carcinoma in situ (CIS), and 20 cervical intraepithelial neoplasia (CIN) lesions. Adjacent nontumor cervical tissue from the same 24 cervical cancer patients and normal cervical tissues from 11 control individuals also were examined for the presence of telomerase activity. RESULTS: Twenty two of the 24 (91.7%) cervical cancer specimens and the single CIS tissue were strongly positive for telomerase activity. Relatively weak but distinctive telomerase activity also was detectable in one of four CIN-I (25%), two of eight CIN-II (25%), and two of eight CIN-III (25%), respectively. However, telomerase activity was not found in the 24 corresponding nontumor cervical tissues from the same cervical cancer patients and the 11 normal cervical tissues from control individuals. CONCLUSION: The majority of cervical cancers contain strong telomerase activity. Significant proportions of noncancerous CIN tissues also contain telomerase activity, although weaker than that in cervical cancer. It seems that there is a progressive increase of telomerase activity in association with an increased degree of cervical malignancy. These results seem to suggest that the expression of telomerase may play a crucial role in cervical cancer carcinogenesis.

Carcinoma in Situ↗
PubMed1997

Bronchoconstriction and eosinophil recruitment in guinea pig lungs after platelet activating factor administration.

Using a forced expiratory maneuver to measure flow volume loops, we evaluated the ability of platelet activating factor (PAF) to induce acute bronchospasm and in histological changes associated with bronchial asthma in guinea pigs. We determined both the dose-response curve and the time course of PAF-induced bronchoconstriction. Eight guinea pigs with weights ranging from 350 to 450 g were anesthetized, tracheotomized, and then paralyzed with gallamine. Baseline pulmonary function tests (PFT) were done. Different doses (25, 50, 100, 200, and 500 ng/kg) of PAF were injected through the jugular vein, and serial PFTs were done at 30 sec, 2, 5, and 20 min after each dose of PAF. Acetylcholine provocation testing was done following the 200 ng/kg dose of PAF. The PFTs included a forced expiratory maneuver, airway opening pressure (PaO), and total lung compliance (TLC). After all PFTs were completed, cell counts were done on fluid obtained from bronchoalveolar lavage (BAL) and the lungs were removed for histological study. Eight other guinea pigs were used as controls. The results showed that with increasing doses of PAF from 25 ng/kg to 200 ng/kg, all lung function parameters, including vital capacity, peak flow, MFEF 75%, MFEF 50%, MFEF 25%, and total lung compliance, gradually decreased. However, a further increase of the dose of PAF up to 500 ng/kg did not result in continued worsening of PFTs. The most severe bronchoconstriction occurred 30 sec after PAF was injected, and it gradually resolved thereafter. PAF injection also induced a severe inflammatory reaction of the airway and lung tissue, characterized by congestion, edema, inflammatory cell (especially lymphocytes and eosinophils) infiltration, and desquamation of bronchial epithelial cells. In conclusion, in the guinea pig model, PAF can induce acute reversible bronchospasm and bronchial hyperreactivity, as well as the typical histological changes of bronchial asthma.

Acetylcholine↗
PubMed1997

[Simple, practical closed-circuit anesthesia].

The practice of closed-circuit anesthesia provides many advantages, including conservation of body heat and airway humidity, hemodynamic stability, minimization of operating room as well as environmental pollution, and a saving of up to 90% in consumption of anesthetics. However, the misunderstanding of the theory of the uptake of inhalation anesthetics has hampered the clinical practice of closed-circuit anesthesia. With proper recognition of the existence of the functional residual capacity and the alveolar membrane, a new concept of uptake of inhalation anesthetics has been developed: (1) uptake is dependent on the inspired concentration; (2) the functional residual capacity is a part of the anesthetic circuitry; and (3) uptake should be represented by 1-FA/FI. This physiologic and common-sense approach to understanding the processes of uptake of inhalation anesthetics greatly facilitates the practice of closed-circuit anesthesia. This new approach not only provides for a simple calculation of the minute to minute requirement for anesthetic vapors, depending on the desired inspired anesthetic concentration, but also enables one to practice closed-circuit anesthesia easily and safely with the currently existing anesthetic equipment.

Anesthesia, Closed-Circuit↗
PubMed1997

Uptake of charged liposomes by the rat liver.

The influences of liposomal surface charge on hepatic uptake of liposomes in vivo and in vitro were studied in rats. 3H-inulin was entrapped in positively charged, negatively charged or neutral liposomes composed of phosphatidylcholine, cholesterol, and a charge lipid at a molar ratio of 4:4:1, or without a charge lipid. Plasma and liver concentrations of inulin were measured 5, 15, 30, and 60 minutes after an intravenous bolus dose of liposome. The in vitro study comprised incubation of liposomes with primary culture of isolated rat hepatocytes. The incubation was terminated at 30, 60, 90, 120, and 180 minutes, and cellular uptake of inulin was determined. The results showed that the positively charged liposomes resulted in the highest plasma liposome concentration. The negatively charged liposomes gave the highest liver liposome concentration, among the three liposomes. In vitro study also demonstrated that cellular uptake of a negatively charged liposome was higher than positively charged or neutral liposomes. These results suggest that positively charged liposomes might be preferable for maintaining higher plasma concentrations, while negatively charged liposomes might be more efficient for drug delivery to the liver.

Analysis of Variance↗
PubMed1997

Factors affecting delection of bleeding lesions in the stomach by initial emergency endoscopy.

BACKGROUND: Accurate endoscopic diagnosis of acute gastric bleeding can be problematic and missing diagnoses are not uncommon. However, the causes of diagnostic difficulty and the most common locations of bleeding resulting in missed diagnosis are not well known. METHODS: To determine the causative factors of incomplete study, we analyzed the medical records and performed follow-up on 64 patients for whom initial emergency endoscopy had failed to identify the sites of acute gastric bleeding. The bleeding sites were confirmed by the findings of subsequent endoscopic examination or operation in these cases. RESULTS: Excessive blood covering the examination field was the most frequent cause of incomplete endoscopic study (60/64). Underlying gastric lesions which were later identified as sources of gastric bleeding included: 30 gastric ulcers, 9 gastric varices, 6 acute gastric mucosal lesions, 3 Dieulafoy's lesions, 3 portal hypertensive gastropathies, 2 gastric tumors, 1 Mallory-Weiss tear and 2 unidentified bleeding sites. Eight patients refused further evaluation. The locations of the bleeding sites included: 1 esophagocardiac junction, 8 cardia, 5 fundus, 21 body, 9 antrum, 7 stoma, 3 diffuse pattern. The 42-day mortality rate of these patients was 20%. Of these patients, decompensated liver cirrhosis (8/13) and hepatic failure (7/13) were the most common underlying diseases. CONCLUSION: Inadequate preparation was the most frequently procedural problem associated with missed diagnosis. Lesions located in the body of the stomach were most likely to go undiagnosed. Gastric ulcers were the most common type of unidentified bleeding ulcer site. Hepatic failure was the most common cause of death. The high mortality rate of these patients appeared to be related to underlying diseases rather than to the nature of the lesions responsible for gastric bleeding.

Adult↗
PubMed1997

Allogeneic bone marrow transplantation for Gaucher disease--a case report.

A Chinese patient who presented painful disability of right hip was diagnosed as having type 1 Gaucher disease four years later when hepatosplenomegaly was found. Splenectomy was performed but her condition did not improve. So human leukocyte antigen (HLA)-matched sibling allogeneic bone marrow transplantation (BMT) was performed. The transplantation course was smooth. Although her bone marrow was in mixed chimeric state, symptoms disappeared and her growth caught up with normal level after BMT. Gaucher disease should be considered in cases with hepatosplenomegaly and bone disorder of unknown causes. Allogeneic BMT is an effective treatment, but the treatment-related risk should be seriously evaluated and the late complications should be closely monitored.

Bone Marrow Transplantation↗
PubMed1997

Persistent transforming growth factor beta 1 expression may predict peritoneal fibrosis in CAPD patients with frequent peritonitis occurrence.

The efficiency of continuous ambulatory peritoneal dialysis (CAPD) depends on the permeability of the peritoneal membrane. Peritoneal fibrosis (PF) causes the loss of dialytic function. Several studies have indicated that PF is closely related to the proliferation of peritoneal fibroblasts and the deposition of extracellular matrix (ECM). Transforming growth factor beta 1 (TGF beta 1) plays a major role in stimulating ECM deposition. Frequent peritonitis occurrence may cause persistent TGF beta 1 mRNA expression. In an attempt to search for a factor related to PF, we designed a longitudinal study to measure TGF beta 1 levels in dialysate and TGF beta 1 mRNA expression in peritoneal mononuclear cells (PMNCs) from peritoneal dialysate before, at the onset of and once a week during peritonitis and after peritonitis in patients with high peritonitis occurrence (HPO) and patients with low peritonitis occurrence (LPO). Fifteen patients with a LPO rate and 5 patients with a HPO rate were followed up longitudinally. Meanwhile, TGF beta 1 levels and TGF beta 1 mRNA expression were augmented in peritoneal dialytic fluid before, during, and after the episodes of peritonitis. Peritoneal permeability was evaluated by the peritoneal equilibration test (PET). The results revealed that in the LPO group, TGF beta 1 and TGF beta 1 mRNA were detectable at early stages of peritonitis, but the levels decreased rapidly and were undetectable 2 weeks after peritonitis. On the other hand, in the HPO group, TGF beta 1 and TGF beta 1 mRNA persisted for a long time. We could detect TGF beta 1 and TGF beta 1 mRNA in dialytic fluid and PMNCs even 2, 3, and 4 weeks after episodes of peritonitis. When compared with that of the first or second episode of peritonitis, peritoneal function evaluated with the PET was found to obviously deteriorate at the third episode of peritonitis. These findings were confirmed by an in situ hybridization technique to evaluate the relationship between TGF beta 1 mRNA expression and PF from biopsied peritoneal specimens. These findings suggest that the high TGF beta 1 levels in the dialysate are related to an increased expression of TGF beta 1 in the peritoneum. Persistent TGF beta 1 expression in the peritoneum may serve as a useful parameter in predicting PF in CAPD patients with frequent peritonitis occurrence.

Adolescent↗
PubMed1997

Linkage analysis of families with autosomal dominant polycystic kidney disease by KG8-CA marker.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic diseases of human. Traditionally, ADPKD is diagnosed by ultrasonography, computed tomography (CT) or magnetic resonance imaging (MRI) of kidneys for the presence of renal cysts. Individuals who carry the defective gene but have not yet developed cysts in kidney may not be diagnosed. Genetic analysis reveals it to be caused mostly by a single-gene disorder of a genetic locus, designated PKD1. Recently, the genetic locus involving PKD1 has been identified on chromosome 16p13.3, and has been cloned and completely sequenced. METHODS: A pair of primers, KG8-CA, located between D16S84 and D16S125, was selected and synthesized for the polymerase chain reaction (PCR) to identify individuals who may carry the defective locus. The sequence of KG8-CA primers, was 5'-CTCCCAGGGTGGAGGAAGGTG-3' and 5'-GCAGGCACAGCCAGCTCCGAG-3'. PCR products were analyzed in denaturing condition, using gel containing 8% acrylamide and 7M urea. Autoradiography was carried out to interpret the results. RESULTS: Four Chinese families with history of ADPKD showed different DNA patterns in individuals with ADPKD and in normal individuals. Among the members in four families with history of ADPKD, every individual shared a common DNA band, suggesting that this band was derived from normal PKD1 allele. On the other hand, individuals diagnosed to have ADPKD showed one or two additional DNA bands which migrated differently from the common DNA band and should therefore be derived from defective ADPKD allele. Previous studies have shown that the ADPKD allele is highly polymorphic, as was evident in these family studies. CONCLUSIONS: Among the members from these four families, some were clinically normal and had DNA pattern that was typical to patients with ADPKD. These individuals might carry the defective PKD1 allele but have not yet developed the ADPKD symptoms. Therefore, the method described in this study has diagnostic values for pre-symptomatic individuals as well as for patients already diagnosed with ADPKD.

Female↗
PubMed1996

Galpha12 differentially regulates Na+-H+ exchanger isoforms.

Activation of several GTPases stimulates Na+-H+ exchange, resulting in an increased efflux of intracellular H+. These GTPases include alpha subunits of the heterotrimeric G proteins Gq and G13, as well as the low molecular weight GTP-binding proteins Ras, Cdc42, and Rho (Hooley, R., Yu, C.-Y., Simon, M., and Barber, D. L. (1996) J. Biol. Chem. 271, 6152-6158). GTPases coupled to the inhibition of Na+-H+ exchange, however, have not been identified. Several neurotransmitters, including somatostatin and dopamine, inhibit Na+-H+ exchange through a guanine-nucleotide-dependent mechanism, suggesting the involvement of a GTPase. In this study we determined that mutational activation of the alpha subunit of G12 inhibits the ubiquitously expressed Na+-H+ exchanger isoform, NHE1. Transient expression of mutationally activated Galpha12 inhibited serum- and Galpha13-stimulated NHE1 activity in HEK293 cells and CCL39 fibroblasts. In addition, in NHE-deficient AP1 cells stably expressing specific NHE isoforms, mutationally activated Galpha12 inhibited NHE1 activity but stimulated activities of the Na+-H+ exchanger (NHE) isoforms NHE2 and NHE3. In contrast, mutationally activated Galpha13, another member of the Galpha12/13 family, stimulated all three NHE isoforms. Although previous studies have identified a parallel action of Galpha12 and Galpha13 in regulating MAP (mitogen-activated protein) kinases and cell growth, these GTPases have opposing effects on NHE1 activity.

Animals↗
PubMed1996

Genomic aberrations of human papillomavirus recovered from cervical cancers.

Human papillomaviruses (HPV) contribute to the development of malignancies of the uterine cervix and the viral E6 and E7 oncogenes are invariably retained and expressed in cervical cancer tissues. Minor, but not major, structural aberrations have been found quite frequently in viral DNA recovered from cervical cancer tissues. We examined the presence of the DNA sequence of HPV type 18 in 33 cervical cancer tissues by polymerase chain reaction. HPV type 18 DNA sequences was found in 24 of these 33 cervical cancer tissue specimens, and at least 21 of these 24 specimens did not appear to retain all the region and open reading frames examined. Twelve of these 24 tissues seemed to harbor only the E6 and/or E7 genes. These results can be construed to suggest that the absence of viral genes other than E6 and E7 is quite frequent in HPV recovered from cervical cancer tissues and that the E6 and E7 genes are important in the carcinogenesis of cervical carcinoma. It is possible that the E6 and/or E7 alone may be sufficient to maintain the transformed phenotype of cervical cancer.

DNA, Viral↗
PubMed1996

Identification of a small deletion in one allele of patients with infantile form of glycogen storage disease type II.

Glycogen storage disease type II (GSD II, Pompe's disease) is an autosomal recessive inherited disease caused by the deficiency of acid alpha-D-glucosidase. In this paper we report two unrelated Chinese patients with infantile form of GSD II who had compound heterozygotes containing a small deletion in one of the acid alpha-D-glucosidase alleles. In both of these compound heterozygotes, one allele contains the C1935A transversion which is the most common mutation in Chinese patients and the other allele contains the newly identified 4 nt deletion of coding sequence (deletion nt 1411-1414). This small deletion causes a reading frameshift and translational premature termination signal in exon 9.

Alleles↗
PubMed1996

In vivo immunosuppressive effect and the decreasing expression of MHC class II antigens by purine nucleoside phosphorylase inhibitor 8-amino-9-benzylguanine in recipient tissues of canine renal allograft rejection.

8-Amino-9-benzylguanine (8-ABG), a potent purine nucleoside phosphorylase inhibitor, was administered to dogs for 10 days following single renal transplantation. A significant prolongation of graft survival was observed in the groups treated with 100 and 150 mg kg/day of 8-ABG per os compared with the control group that was not treated with any immunosuppressant. Expression of major histocompatibility complex (MHC) class II antigens (Ag) was investigated in the normal kidney(s) and renal allografts of mongrel dogs after single renal transplantation. The 8-ABG was administered to the normal and renal allografted dogs and no detectable MHC class II Ag in the normal kidneys was found. During acute rejection, the MHC class II Ag was expressed on the renal tubular epithelium and glomerular vascular endothelium in graft kidneys. The intensity of the MHC class II Ag expression was correlated to the severity of rejection. This abnormal expression of MHC class II Ag on allograft kidney was suppressed by 8-ABG treatment. Our results suggest that MHC class II Ag expression can be induced on the renal allografts during acute rejection. This abnormal expression of MHC class II Ag may serve as a specific index for diagnosis of kidney allograft rejection. That 8-ABG can suppress abnormal expression of MHC class Ag on allografted kidney and prolong graft survival indicates that 8-ABG may provide an alternative approach for the development of a potential new immunosuppressant.

Animals↗