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Biomedical subjects

C S Lin

Publications and source records attributed to C S Lin.

At least 127 records · Page 7Linked to original sources
PubMed1998

Diffuse hyperplasia of the peribiliary glands.

Diffuse, severe, macroscopically recognizable dilatation and hyperplasia of the peribiliary glands of intrahepatic and extrahepatic bile ducts is an extremely rare condition. To our knowledge, this is the first such case reported in the literature. We encountered this condition in a patient with massive hepatic necrosis. The pathogenesis of the condition is discussed. Unfamiliarity with this pathology could lead to an erroneous diagnosis of a well-differentiated cholangiocarcinoma.

Adenocarcinoma↗
PubMed1998

Aeromonas hydrophila sepsis presenting as meningitis and necrotizing fasciitis in a man with alcoholic liver cirrhosis.

Aeromonas hydrophila is rarely reported as a causative organism of meningitis in humans. A 39-year-old man with alcoholic liver cirrhosis was admitted with a 2-day history of fever, chills, and confusion. Laboratory data revealed leukocytosis with granulocytosis, marked impairment of renal and liver function, and an elevated serum ammonia level. A. hydrophila was isolated from both blood and cerebrospinal fluid samples. Skin and soft-tissue lesions, consisting of bullae and necrotizing fasciitis, were found in the lower left leg 2 days after admission. Cultures of the bullous fluid, subcutaneous tissue, and fascia all yielded A. hydrophila. Pathologic examination revealed extensive necrosis. Although the patient was appropriately managed with antibiotics, debridement, and fasciotomies, his clinical status rapidly deteriorated, resulting in death 3 days after admission.

Adult↗
PubMed1998

Clinical manifestations and prognostic features of acute methamphetamine intoxication.

The prevalence of amphetamine abuse and the frequency of emergency department visits for amphetamine intoxication have increased dramatically worldwide. In this study, we retrospectively investigated the relationship between the prognostic features and clinical manifestations among patients admitted to the emergency department of a university hospital for acute methamphetamine intoxication during a 6-year period. Data collected included gender, age, route of abuse, time between drug exposure and arrival at the emergency department, estimated dose, signs and symptoms, laboratory values, and complications. Emergency therapy and cooling procedures were also recorded. After excluding 26 patients with multiple-drug intoxication, 18 patients (male-to-female ratio, 11:7) were include in the analysis. The mean age was 25.6 years. Thirteen patients survived and five died. Patients who died often presented with coma (80% vs 0%, p = 0.002), shock (60% vs 8%, p = 0.044), convulsions (100% vs 23%, p = 0.007), oliguria (80% vs 0%, p = 0.002), and high body temperature (41.4 +/- 0.5 degrees C vs 39.4 +/- 2.1 degrees C, p = 0.005). Furthermore, patients who died had significantly higher concentrations of blood urea nitrogen (8.7 +/- 2.1 vs 5.6 +/- 2.0 mmol/L, p = 0.01) and serum creatinine (212 +/- 71 vs 115 +/- 27 mumol/L, p = 0.033), and lower values of arterial pH (7.12 +/- 0.12 vs 7.34 +/- 0.10, p = 0.03), than those who survived. In the fatality group, the most common complication was rhabdomyolysis with acute renal failure (5 of 5); multiple organ failure resembling that from heatstroke was the leading cause of death from acute methamphetamine intoxication. In conclusion, the adverse prognostic features in patients with acute methamphetamine intoxication include coma, shock, convulsion, oliguria, and high core temperature. Acidosis, volume depletion, and ischemic renal damage were potential risk factors for development of acute renal failure in these patients.

Acute Disease↗
PubMed1998

Lecithin can be detected by volume-selected proton MR spectroscopy using a 1.5 T whole body scanner: a potentially non-invasive method for the prenatal assessment of fetal lung maturity.

The prenatal determination of fetal lung maturity is currently assessed by chemical analysis of surfactant associated lipids from aminotic fluid obtained by amniocentesis. This is an invasive procedure with rare but occasionally serious morbidity. Magnetic resonance spectroscopy (MRS) is a non-invasive method for the in vivo localization and identification of molecules with known resonance peaks at specified chemical shifts. In this report we examine the in vitro MRS of a lecithin/saline solution as well as term and preterm amniotic fluid samples with the use of a 1.5 T whole body scanner and a flexible surface coil. We found that amniotic fluid at term demonstrates a resonance peak at 3.2 ppm which was the same as the chemical shift of lecithin in saline. The lecithin peak is not observed in preterm amniotic fluid. This demonstrates the feasibility of using MRS with a whole body scanner to detect lecithin, one of the markers for fetal lung maturity.

Adult↗
PubMed1997

Expression and characterization of the recombinant gene encoding chitinase from Aeromonas caviae.

The gene encoding a chitinase from Aeromonas caviae was cloned by PCR techniques. Its recombinant gene expression was performed using pET20b(+) in Escherichia coli BL21 (DE3). The recombinant chitinase with the extra 33 and 13 amino acids in its N- and C-termini, respectively, was purified to near homogeneity using His-Tag affinity chromatography. The recombinant chitinase was found to be present in both the culture medium and the cytoplasm. A single protein band on the native polyacrylamide gel was confirmed by both the activity staining and protein staining. The optimum pH and temperature of the recombinant chitinase were determined to be 6.25-6.5 and 42.5 degrees C, respectively. It was stable within the pH range of 5-7. Significant activity stimulation by Cu2+ and inhibition by Fe3+ and Hg2+ were observed. Detergents such as SDS and Triton X-100 strongly inhibited the enzyme activity. Substrates such as 4-methylumbelliferyl-N,N'-diacetylchitobioside and 4-methylumbelliferyl-N,N',N"-triacetylchitotriose were hydrolyzed by the recombinant chitinase; however, 4-methylumbelliferyl-N-acetylglucosaminide was not cleaved during the activity assay periods. When chitin power was suspended in buffer with the chitinase (pH 6.5 and 42.5 degrees C), N-acetylchitooligosaccharides [(GlcNAc)n, n = 1-4] were detected at 24 h.

Aeromonas↗
PubMed1997

A shortened life span of EKLF-/- adult erythrocytes, due to a deficiency of beta-globin chains, is ameliorated by human gamma-globin chains.

Using homologous recombination, both EKLF alleles in murine embryonic stem (ES) cells were inactivated. These EKLF-/- ES cells were capable of undergoing in vitro differentiation to form definitive erythroid colonies that were similar in size and number to those formed by wild-type ES cells. However, the EKLF-/- colonies were poorly hemoglobinized and enucleated erythrocytes in these colonies contained numerous Heinz bodies. Reverse transcriptase-polymerase chain reaction (RT-PCR) analyses revealed that adult and embryonic globin genes were appropriately regulated, with the exception of beta h1-globin, which continued to be expressed at a very low level. The ratio of adult beta-globin/alpha-globin mRNA in the mutant ES cells was 1/15 of that in wild-type ES cells. When the EKLF-/- cells were injected into blastocysts, they did not contribute at a detectable level to the mature erythrocyte compartment of the chimeric animals, based on analysis of glucose phosphate isomerase-1 (GPI-1) isozymes and hemoglobins that distinguish ES cell-derived erythrocytes from host blastocyst-derived erythrocytes. In contrast, semiquantitative RT-PCR analysis of RNA from reticulocytes of the same chimeric animals suggested that the ES cell-derived reticulocytes were present at a level of 6% to 8%. This indicated that the EKLF-/- erythrocytes in adult animals must be short-lived, apparently due to the imbalance of beta-versus alpha-globin chains, leading to the precipitation of excess alpha-globin chains to form Heinz bodies. Consistent with this hypothesis, the short life span was ameliorated by introduction into the EKLF-/- ES cells of a human LCR/gamma-globin gene, as evidenced by the presence of ES cell-derived reticulocytes as well as mature erythrocytes in the blood of the chimeric animals.

Animals↗
PubMed1997

Expression of the c-Met/HGF receptor in human breast carcinoma: correlation with tumor progression.

Hepatocyte growth factor/scatter factor (HGF/SF) induces cell motility and tissue remodeling of various epithelial cells through its receptor, the product of the proto-oncogene c-met. High levels of HGF/SF have been correlated with poor prognosis in human breast carcinoma. In this study, we examined the expression of the c-Met receptor in human breast-carcinoma cells in vivo and in cultured cell lines. Immunohistochemical analysis of biopsy samples of human breast carcinoma indicated that, in normal mammary gland, c-Met is localized in the ductal epithelium. The level of expression of c-Met in primary carcinomas was maintained in autologous metastatic lymph-node lesions in some cases, and in other cases was elevated. Frequently there was evidence of heterogeneity in cellular expression of c-Met within individual tumors, suggesting that micro-environmental factors may regulate receptor expression. In an analysis of a panel of human breast-carcinoma cell lines, we found that moderately differentiated cell lines did not express detectable levels of c-Met and were not responsive to HGF. In contrast, poorly differentiated and invasive cell lines did express high levels of the receptor and responded to HGF by increased motility and invasiveness. Sensitivity to HGF/SF also correlated with expression of the c-Met 9-kb mRNA. No correlation was found between gene copy number and the expression level of c-Met protein or mRNA. When the moderately differentiated and c-Met-negative T47D cell line was transfected with c-DNA for c-met, the transfectants showed delayed cell scattering and migratory response to HGF. Thus, over-expression of c-Met in moderately differentiated carcinoma cells may be one of several attributes that contribute to an invasive phenotype during the progression of breast cancer.

Blotting, Western↗
PubMed1997

TNF receptor-2-triggered apoptosis is associated with the down-regulation of Bcl-xL on activated T cells and can be prevented by CD28 costimulation.

Stimulation of recently activated T cells results in apoptosis of the responding cells, a process referred to as activation-induced cell death. This process is believed to play an important role in the regulation of immune homeostasis and is suggested to be mediated mainly by interactions between Fas and Fas ligand. Recent evidence indicates that TNF-alpha and TNFR2 interaction plays an important role in down-regulating activated T cells. The role of TNFR2 signaling in activation-induced cell death, however, has not been directly examined. We demonstrate here that 48-h activated T cells are most sensitive to TNFR2-induced apoptosis. Cross-linking of TNFR2 on activated T cells results in down-regulated protein and mRNA expression of Bcl-xL. Furthermore, CD28 costimulation can prevent anti-TNFR2-induced apoptosis and restore Bcl-xL expression. These results have potential implications for understanding the role of TNFR2 signaling in the regulation of T cell responses.

Animals↗
PubMed1997

Prothymosin alpha promotes cell proliferation in NIH3T3 cells.

Thymic hormones have immunomodulatory effects on T cells and hence have been used clinically to restore the immunity of immunodeficient patients as well as to enhance the cellular immunity of cancer patients. Prothymosin alpha, which is a member of the thymic hormone family, has recently been suggested to act as a nuclear protein participating in the stimulation of cell proliferation. To characterize the biological activities ofprothymosin alpha in vitro, we established NIH3T3 cell transformants that constitutively express higher prothymosin alpha protein and its mRNA compared with the wild-type counterpart. Cells that overexpressed prothymosin alpha increased the proliferative activity assayed by the [3H]-thymidine incorporation or by the cell cycle analysis with the fluorescent-activated cell sorter. The results provide direct evidence that prothymosin alpha plays a role in cell proliferation by shortening the duration of the G1 phase.

3T3 Cells↗
PubMed1997

Alteration of endogenous antioxidant enzymes in naturally occurring hypertrophic cardiomyopathy.

We have recently developed a porcine model with naturally occurring hypertrophic cardiomyopathy (HCM). Similar to humans, occluded intramural coronary artery and damaged mitochondria are frequently observed in these animals in which the disease is thought to be associated with the local ischemia of myocardium. In view of antioxidant functions involved in the ischemic injury, we measured the expression of endogenous antioxidant enzymes in the tissues with and without HCM. The results showed a significant increase of Cu,Zn-superoxide dismutase (SOD), but not Mn-SOD, and decrease of catalase (CAT) activities in the various areas of HCM hearts. It was demonstrated that SOD/CAT ratios in the HCM hearts were significantly higher than those in normals and were found to be dramatically correlated with the severity of cardiac hypertrophy. The altered SOD/CAT ratio was also consistent with increase in lipid damage. We hypothesize that the elevated SOD combined with an inadequate amount of H2O2 scavenging enzyme may lead HCM heart at oxidative stress risk. However, the pathogenic role of imbalanced antioxidant enzyme needs to be further explored.

Animals↗
PubMed1997

The murine L-plastin gene promoter: identification and comparison with the human L-plastin gene promoter.

Plastins (or fimbrins) are a family of actin-binding proteins that are conserved from yeast to humans. In mammals, three tissue-specific plastin isoforms have been identified. The L isoform (L-plastin) is normally expressed only in leukocytes but is also found in >90% of neoplastic nonleukocyte human cells. Because L-plastin expression in tissue-specifically regulated in both humans and rodents, it is likely that similar mechanisms regulate L-plastin gene expression in human and rodent cells and that they could be identified by comparing the function and nucleotide sequences of the human and murine L-plastin gene promoters. Previously, we reported the isolation and characterization of the human L-plastin gene promoter. In this study, we isolated a murine L-plastin 5' end cDNA and used it as a probe to isolate several murine genomic clones. A representative clone contained 7 kb of the flanking region, 0.1 kb of the first exon, and 9.9 kb of the first intron. A continuous 1,354-bp sequence was identified around the first exon. Five transcription initiation sites were found 40 to 73 bp downstream from a perfect TATA box. Alignment of the sequence with its human counterpart revealed approximately 60% homology in a 1-kb region spanning the first exon and the flanking region. The TATA box, one ER binding site, and two ETS binding sites were completely conserved. An Sp1 binding sequence in the human promoter was partially conserved in the murine promoter but could still bind to Sp1. A second ER binding sequence, lying 5' adjacent to the TATA box in the human promoter, was conserved only at the 3' half-site in the murine promoter; the 5' half-site was changed into a potential AP1 binding site. This AP1/ER hybrid sequence was incapable of binding to ER. However, both human and murine promoters were found to function equally well in either human or murine leukocytes.

3T3 Cells↗
PubMed1997

Identification of the human alpha6 integrin gene promoter.

The alpha6 integrin subunit couples with either the beta1 or the beta4 subunit to form a laminin receptor. alpha6 expression is cell-type-specific and generally is present at high levels in epithelial and endothelial cells. To study its gene regulation, we isolated a genomic clone containing the human alpha6 integrin gene promoter. It includes 3 kb of the upstream flanking region, the first exon (385 bp), and 9 kb of the first intron. The alpha6 promoter directs transcription initiation from a primary site 202 nucleotides from the translation initiation codon. Unlike most other integrin gene promoters, the alpha6 promoter has a TATA box (GATAAA), which is located 22 nucleotides upstream from the primary transcription initiation site. A 190-bp region upstream from the TATA box is highly rich (78%) in C and G nucleotides and contains several Sp1 and AP2 binding sequences. However, full promoter activity (in the presence of the SV40 enhancer) requires only 78 bp of this C/G-rich sequence upstream from the TATA box. Slightly upstream from the C/G-rich region are a steroid receptor binding homolog and an epithelial-cell-specific E-pal sequence. Another possible epithelial cell-specific binding sequence (Ker1) is found immediately downstream from the TATA box. Cell-type-specific activities of the promoter paralleled the alpha6 mRNA levels in four tested cell lines. In the presence of the SV40 enhancer, alpha6 promoter activity increased approximately four-fold in primary keratinocytes and in HT1080 fibrosarcoma cells and 30-fold in T47D breast carcinoma cells, but remained undetectable in K562 leukemia cells. Genomic analysis that compared alpha6-expressing with non-alpha6-expressing cells suggested that DNA methylation is not involved in the silencing of the alpha6 gene in alpha6-negative cells. DNase I footprint analysis confirmed the binding of Sp1 and AP2 to their cognate sequences. A nuclear extract of high-alpha6-expressing HBL-100 cells also produced significant binding to these sites, suggesting that the two transcription factors are probably involved in the positive regulation of the alpha6 promoter.

Amino Acid Sequence↗
PubMed1997

Cantrell's syndrome in an infant.

Cantrell's syndrome is a rare combination of congenital midline thoracoabdominal defects and congenital heart disease. surgical repair can correct many of the anomalies. We report a neonate who presented with a short sternum, defective upper abdominal muscle, ectopic umbilicus, anterior diaphragmatic defect, ventricular septal defect and an intra-abdominal left ventricular diverticulum. Initially, the infant was treated with digoxin and diuretics for 5 months. Due to poor control of heart failure, one-stage surgical correction was performed with patch repair of the ventricular septal defect, ligation of left ventricular diverticulum and closure of the defects of the diaphragm and upper abdominal wall.

Abnormalities, Multiple↗
PubMed1997

The role of nitrogenase in a cyanide-degrading Klebsiella oxytoca strain.

It is well known that the major function of nitrogenase is to fix atmospheric nitrogen. However, cyanide can also serve as a subtrate for nitrogenase and can be reduced to CH4 and NH4+. A cyanide-degrading Klebsiella oxytoca strain was isolated from cyanide contaminated water. This isolate was also found to have a nitrogen-fixation capability. Nitrogenase activities in this organism could be induced by KCN. However, there was no significant difference of the induction effect between 1 mM KCN and 5 mM KCN. It was found that the cyanide-degrading ability of this isolate could be inhibited by multicopy hybrid pGR112 nif-containing plasmids. Comparing the wild type K. oxytoca strain with the pGR112 plasmid transformed strain, a typical diauxic growth of the wild type strain was observed in a medium containing NH4Cl and KCN. Although the nif plasmid transformed strain also exhibited diauxic growth in the same medium, a much longer second lag phase was noted. In addition, methane, the nitrogenase reduction end product of cyanide, could be detected on cyanide-containing growth cultures. Ammonium chloride, a repressor of nitrogenase gene expression, was consumed prior to KCN in both strains. Again, the degradation of KCN in the pGR112 transformed strain occurred only under loose control of the nitrogenase gene. These findings strongly suggest that nitrogenase may be the sole cyanide-degrading enzyme in this organism.

Bacterial Proteins↗
PubMed1997

Trifascicular block with intermittent complete atrioventricular block in a child.

Trifascicular block, which consists of impaired conduction in the three main fascicles of the ventricular conduction system, may progress to high-grade or complete atrioventricular block. It rarely occurs in children with a structurally normal heart. We report a case of trifascicular block in a previously healthy 9-year-old girl. The patient presented with repetitive seizures. The electrocardiogram showed a complete right bundle branch block, left axis deviation, PR interval prolongation, and intermittent high-degree and complete atrioventricular block. She was successfully treated with a temporary pacemaker and her electrocardiogram returned to a normal sinus rhythm in 3 days. She has remained well over a 4-year follow-up. Although her cardiac enzyme levels were normal, the clinical course and electrocardiography findings suggested myocarditis. We emphasize the diagnosis of trifascicular block using electrocardiography; clinical outcome is good, if the patient is managed properly.

Child↗
PubMed1996

Differential effects of an erythropoietin receptor gene disruption on primitive and definitive erythropoiesis.

Although the hormone erythropoietin (Epo) and its receptor (EpoR) are known to play important roles in the regulation of erythropoiesis, several questions remain concerning the developmental role of Epo/EpoR signaling. As the functions of Epo have been defined primarily through studies of definitive erythroid cells, its importance for primitive, embryonic erythropoiesis remains uncertain, as does the significance of EpoR expression in several nonerythroid cell types. To address these questions, mouse embryonic stem cells and embryos lacking a functional EpoR gene were produced by gene targeting. The effects of the mutation were examined in embryos developing in vivo, in chimeric adult mice produced with homozygous mutant embryonic stem cells, and in hemopoietic cells cultured in vitro. No defects were apparent in nonerythroid cell lineages in which the EpoR normally is expressed, including megakaryocytes and endothelial cells. In the mutant yolk sac, primitive erythrocytes were produced in normal numbers, they underwent terminal differentiation, and expressed near normal levels of embryonic globins, although they were reduced in size and their proliferation was severely retarded after E9.5. In contrast, in the fetal liver, definitive erythropoiesis beyond the late progenitor (CFU-E) stage was drastically inhibited by the EpoR mutation, and virtually no definitive erythrocytes were produced in vivo, leading to embryonic death by E13.5. Thus, our results suggest a fundamental difference in the molecular mechanisms stimulating primitive and definitive erythropoiesis. It was also observed that a few mutant definitive erythroid cells could terminally differentiate when cultured with additional cytokines, demonstrating that although Epo/EpoR signaling is important for definitive erythroid cell survival and proliferation, it is not an obligatory step in differentiation.

Animals↗
PubMed1996

Laminin-binding integrins in tumor progression and metastasis.

Interactions between tumor cells and extracellular matrix occur at several points during the metastatic cascade. Epithelial tumors, which represent nearly 90% of human neoplasia, must invade their underlying basement membrane to enter the interstitial stroma. For distant metastasis, malignant cells must penetrate basement membranes to gain access to blood vessels and organ parenchyma. Integrin receptors that bind to multiple laminin isoforms appear to mediate tumor cell adhesion to basement membranes before and during invasion. It is notable that changes in several laminin-binding integrins occur during tumor progression. These changes may include increased or decreased expression, or changes in distribution from a polarized to a dispersed pattern. Integrins not only mediate cell adhesion and motility but also transduce important downstream signaling events that regulate cell growth, survival, and gene expression. During tumor progression, the development of variant cells with changes in integrin expression and the associated signaling pathways could result in cells with a highly invasive and metastatic phenotype.

Disease Progression↗