Refractory hyponatremia.
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Brain Diseases↗
Biomedical subjects
H Y Lin
Publications and source records attributed to H Y Lin.
3D simulations of hydrodynamic drag forces on two porous spheres moving along their centerline.
This paper numerically evaluates the hydrodynamic drag force exerted on two highly porous spheres moving steadily along their centerline through a quiescent Newtonian fluid over a Reynolds number ranging from 0.1 to 40. At creeping-flow limit, the drag forces exerted on both spheres were approximately identical. At higher Reynolds numbers the drag force on the leading sphere (sphere #1) was higher than the following sphere (sphere #2), revealing the shading effects produced by sphere #1 on sphere #2. At dimensionless diameter beta<2 (beta=d(f)/2k(0.5), d(f) and k are sphere diameter and interior permeability, respectively), the spheres can be regarded as "no-spheres" limit. At increasing beta for both spheres, the drag force on sphere #2 was increased because of the more difficult advective flow through its interior, and at the same time the drag was reduced owing to the stronger wake flow produced by the denser sphere #1. The competition between these two effects leads to complicated dependence of drag force on sphere #2 on beta value. These effects were minimal when beta became low.
Journal Article↗
Weber-Christian disease presenting with intractable fever and periorbital swelling mimicking angioedema.
A 22-year-old male patient with Weber-Christian disease (WCD) presenting with periorbital swelling is a very rare occurrence. Lobular panniculitis in the periorbital and anterior tibial skin was diagnosed in this patient, based on the histological findings from biopsy specimens. The differential diagnosis was done before administering systemic corticosteroid. A dramatic response was achieved several days later, but relapse with intractable fever occurred 1 month later. The use of other immunosuppressive agents failed, and he died of septic shock 2 months later. The preceding infection may have been the immunopathologic factor in the development of WCD. Other effective treatments for WCD may be described in the future.
Adult↗
Expressions and regulation of endothelial and inducible nitric oxide synthases in mouse uterus during the estrous cycle and early pregnancy.
Nitric oxide (NO) has been implicated in many cellular processes. We examined the temporal and spatial expressions of endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in mouse uteri during the estrous cycle and early pregnancy, as well as the regulation of eNOS and iNOS by estradiol (E2) and progesterone (P4) in ovariectomized mouse uteri using in situ hybridization and immunohistochemistry. Our results showed that positive eNOS and iNOS signals were localized in the uterine luminal epithelium and glandular epithelium during the estrous cycle. In ovariectomized mice, both E2 and P4 regulated the expression of eNOS and iNOS. During early pregnancy, eNOS and iNOS were detected not only in epithelium, but also in the primary decidual zone surrounding implanting embryos on day 6 of pregnancy, and in the whole decidualized stroma on day 7 of pregnancy. In conclusion, the results demonstrated that two NOS isoforms were localized in mouse uteri in specific temporal and spatial patterns during the estrous cycle and early pregnancy, and ovarian hormones can regulate their expression. Furthermore, the data suggest that the expression of NOS during the peri-implantation period might lead to enhance NO production, which could promote embryo implantation.
Animals↗
Self-organized growth of nanopucks on Pb quantum islands.
Electronic Moirè patterns found on lead (Pb) quantum islands can serve as a template to grow self-organized cluster (nanopucks) arrays of various materials. These patterns can be divided into fcc- and hcp-stacked areas, which exhibit different binding strengths to the deposited adatoms. For Ag adatoms, the binding energy can differ substantially and the confined nucleation thus occurs in the fcc sites. Both the size distribution and spatial arrangement of the Ag nanopucks are analyzed and found to be commensurate with the characteristics of the template island, which exhibits a bilayer oscillatory behavior.
Journal Article↗
Analysis of polyglutamine-coding repeats in the TATA-binding protein in different neurodegenerative diseases.
Trinucleotide repeat (TNR) expansion in the gene for TATA binding protein (TBP) has recently been described as causal for spinocerebellar ataxia type 17. The normal number of repeats has been considered to be 42 or less. An intermediate range with reduced penetrance has been assumed to be 43-47 CAA/CAG repeats. We examined this gene in 30 patients with autosomal-dominant cerebellar ataxia (ADCA), 35 patients with sporadic ataxia, 11 patients with Huntington's disease (HD), 351 patients with idiopathic Parkinson's disease (PD), 105 patients with Alzheimer's disease (AD), and 291 controls with no history of neurodegenerative disease. Three patients (one with sporadic PD and two with AD) carrying more than 42 TNRs in the TBP gene were identified. This reveals that the phenotype associated with CAG/CAA expansion in the TBP gene may be heterogeneous.
Aged↗
Multiple oxidative stress-response members of the Adapt78 family.
Adapt78 is an oxidative and calcium stress-response gene. Its protein product is a potent natural inhibitor of the intracellular calcium signaling protein calcineurin. Much of what is known about Adapt78 protein is based on cell-transfection studies. Toward understanding natural endogenous Adapt78, we used an antibody raised against cellular Adapt78 and recently determined that endogenous Adapt78 protein, like its mRNA, is oxidative and calcium stress responsive. Here we report the identification of a second endogenous form of this protein family of 41 kDa. Subcellular fractionation of human HeLa cells revealed that in contrast to results of previous transfection studies, most endogenous Adapt78, characterized as 29 and 41 kDa electrophoretic doublets, resides in the cellular cytosol. The 41 kDa form of Adapt78 was abundant and found to exhibit many characteristics in common with the previously reported oxidative stress-responsive 29 kDa form, including hypo- and hyperphosphorylation variants, rapid loss of the hypophosphorylated form following oxidative stress, response to various kinase and phosphatase inhibitors, and localization. However, it also exhibited some unique characteristics, most notably the lack of calcium inducibility. Finally, the 29 kDa form exhibited a much shorter half-life and strong stabilization following oxidant exposure compared with the 41 kDa Adapt78 form. These data reveal the presence of a novel oxidative stress-responsive 41 kDa Adapt78 species, lend further insight into the Adapt78 family of proteins and their distribution, and challenge previous conclusions obtained using transfection protocols.
Blotting, Western↗
Arsenic accumulation and acute toxicity in aquacultural juvenile milkfish (Chanos chanos) from blackfoot disease area in Taiwan.
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Animals↗
Regulation of matrix metalloproteinases (MMPS) and their inhibitors (TIMPS) during mouse peri-implantation: role of nitric oxide.
Nitric oxide (NO) is believed to play pivotal roles in embryo implantation. The purpose of this study was to investigate the effect of NO on matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs), as well as the mechanism of NO during mouse implantation. Nitric oxide synthase (NOS) inhibitor, L-NAME was administered with or without sodium nitroprusside (SNP), NO donor, into one uterine horn on day 3 of pregnancy, and the contralateral uterine horn served as the control. We collected the uteri on days 5, 6, and 7 of pregnancy and examined the mRNA expression of MMP-2, -9, and TIMP-1, -2, -3, as well as the activities of MMP-2 and -9 by using in situ hybridization and gelatin zymography, respectively. The results showed that, compared with the control, the expression of MMP-2 and -9 mRNAs was decreased in L-NAME-treated uteri during peri-implantation. Treatment of mice with L-NAME had slight effect on the expression of TIMP-1 mRNA on day 5 of pregnancy, and no effect on TIMP-2 mRNA expression during peri-implantation. However, the expression of TIMP-3 mRNA was increased. The gelatin zymography results indicated that the activity of MMP-9 was decreased during peri-implantation, but the activity of MMP-2 did not change significantly in these time points examined. The L-NAME-mediated effect on MMPs and TIMPs were significantly reversed when SNP was co-administered with L-NAME. These data suggest that inhibition of NO production regulates the gene expression of MMP-2, -9, and TIMP-3, together with the activity of MMP-9 during peri-implantation, which may have serious consequence on embryo implantation.
Animals↗
Do patients with acute liver failure have a better chance to receive liver grafting?
OBJECTIVE: Patients with acute hepatic failure (AHF) were always given first priority on the transplant waiting list. We investigated whether AHF patients will deprive other patients on the waiting list of the chance of liver transplantation (LTx). METHODS AND RESULTS: From January 1999 to March 2003, a total of 423 patients were on the transplant waiting list at the National Taiwan University Hospital. Sixty-five of the patients had AHF caused by hepatitis-B-related disease (HBV, n = 52, 80%), Wilson disease (n = 3, 4.6%), drug-induced AHF (n = 3, 4.6%), and other causes (n = 7, 10.8%).Thirty-three patients died and 16 survived by medical treatment. Two received LTx abroad and 14 underwent LTx at our hospital (7 living-related; 7 cadaver). A total of 140 patients died while waiting for a transplant during the period studied. Of them, 107 were among 358 non-AHF patients (30%), and time-to-death interval was 133 +/- 175 days (median: 62); 33 were among 65 AHF patients (51%); time to death was 19 +/- 28 days (median: 8). There were 35 cadaver donor livers available during the period; 28 of 358 non-AHF patients (7.8%), and 7 of 65 AHF patients (10.7%) received cadaveric LTx. Their waiting time totaled 342 +/- 316 and 12 +/- 9 days, respectively (P < .0001). CONCLUSION: Most AHF patients died unless they received liver grafts. Even with a higher priority assigned to them, AHF patients still have little chance to get a cadaver donor liver in Taiwan, and non-AHF patients have an even slimmer chance. Therefore, we need to encourage liver donation from living-related donors.
Cadaver↗
Influence of UNOS status on chance of heart transplantation and posttransplant survival.
UNLABELLED: This study was designed to compare the chance of heart transplantation (HTx) and survival among patients in different UNOS statuses in Taiwan. METHODS AND RESULTS: From 1996 to 2002, among 203 patients on the heart transplant waiting list, 127 patients had undergone HTx up to December 2002 with 71 dead while waiting, and 5 still alive without transplantation. This study included those 198 patients who had either undergone HTx or who died. At the time of registry, 40 patients were at status IA, 57 at IB, and 101 at II. Nineteen (47.5%) of 40 status IA patients underwent HTx with a mean waiting time of 92 +/- 116 days and median waiting time of 35 days. The 1-month survival was 84%, and 1-year survival was 58%. Seven (64.9%) of 57 status IB patients underwent HTx with a mean waiting time of 85 +/- 100 days and a median waiting time of 40 days. Both 1-month and 1-year survivals were 92%. Seventy-one (70.3%) patients among 101 status II patients underwent HTx. Their mean waiting time was 134 +/- 135 days and median waiting time was 86 days. Their 1-month survival was 95%, and 1-year survival was 85%. CONCLUSION: Although UNOS status IA patients had a shorter waiting time, their chance to undergo HTx was lower than those in either status IB or status II. The UNOS status IA heart-waiting patients showed lower posttransplant 1-month and 1-year survival rates.
ABO Blood-Group System↗
Genetic testing in spinocerebellar ataxia in Taiwan: expansions of trinucleotide repeats in SCA8 and SCA17 are associated with typical Parkinson's disease.
DNA tests in normal subjects and patients with ataxia and Parkinson's disease (PD) were carried out to assess the frequency of spinocerebellar ataxia (SCA) and to document the distribution of SCA mutations underlying ethnic Chinese in Taiwan. MJD/SCA3 (46%) was the most common autosomal dominant SCA in the Taiwanese cohort, followed by SCA6 (18%) and SCA1 (3%). No expansions of SCA types 2, 10, 12, or dentatorubropallidoluysian atrophy (DRPLA) were detected. The clinical phenotypes of these affected SCA patients were very heterogeneous. All of them showed clinical symptoms of cerebellar ataxia, with or without other associated features. The frequencies of large normal alleles are closely associated with the prevalence of SCA1, SCA2, MJD/SCA3, SCA6, and DRPLA among Taiwanese, Japanese, and Caucasians. Interestingly, abnormal expansions of SCA8 and SCA17 genes were detected in patients with PD. The clinical presentation for these patients is typical of idiopathic PD with the following characteristics: late onset of disease, resting tremor in the limbs, rigidity, bradykinesia, and a good response to levodopa. This study appears to be the first report describing the PD phenotype in association with an expanded allele in the TATA-binding protein gene and suggests that SCA8 may also be a cause of typical PD.
Age of Onset↗
Oxidative and calcium stress regulate DSCR1 (Adapt78/MCIP1) protein.
DSCR1 (adapt78) is a stress-inducible gene and cytoprotectant. Its protein product, DSCR1 (Adapt78), also referred to as MCIP1, inhibits intracellular calcineurin, a phosphatase that mediates many cellular responses to calcium. Exposure of human U251 and HeLa cells to hydrogen peroxide led to a rapid hyperphosphorylation of DSCR1 (Adapt78). Inhibitor and agonist studies revealed that a broad range of kinases were not responsible for DSCR1 (Adapt78) hyperphosphorylation, including ERK1/2, although parallel activation of the latter was observed. Phosphorylation of both DSCR1 (Adapt78) and ERK1/2 was attenuated by inhibitors of tyrosine phosphatase, suggesting the common upstream involvement of tyrosine dephosphorylation. The hyperphosphorylation electrophoretic shift in DSCR1 (Adapt78) mobility was also observed with other oxidizing agents (peroxynitrite and menadione) but not nonoxidants. Calcium ionophores strongly induced the levels of both hypo- and hyper-phosphorylated DSCR1 (Adapt78) but did not alter phosphorylation status. Calcium-dependent growth factor- and angiotensin II-stimulation also induced both DSCR1 (Adapt78) species. Phosphorylation of either or both serines in a 13-amino acid peptide made to a calcineurin-interacting conserved region of DSCR1 (Adapt78) attenuated inhibition of calcineurin. These data indicate that DSCR1 (Adapt78) protein is a novel, early stage oxidative stress-activated phosphorylation target and newly identified calcium-inducible protein, and suggest that these response mechanisms may contribute to the known cytoprotective and calcineurin-inhibitory activities of DSCR1 (Adapt78).
Angiotensin II↗
Metabolic load of recombinant protein production: inhibition of cellular capacities for glucose uptake and respiration after induction of a heterologous gene in Escherichia coli.
The strong expression of recombinant proteins in bacteria affects the primary carbon and energy metabolism resulting in growth inhibition and acetate formation. By applying glucose pulses to fed-batch fermentations performed for production of a heterologous (alpha-glucosidase in Escherichia coli, we show that the induction of the recombinant gene strongly inhibits the maximum specific uptake capacities for glucose and the respiration capacity. The accumulation of glucose in the fermentation medium promotes the growth of plasmid-free cells. These inhibition effects are well described by including the kinetics of product formation into a recently published dynamic model (Lin et al. [2001] Biotechnol Bioeng 73:349-357). The new model also includes the population characteristics and gives a good fit to the measured data describing growth, production, substrate consumption, by-product formation, and respiration.
Bioreactors↗
Role of the general stress response during strong overexpression of a heterologous gene in Escherichia coli.
The strong overexpression of heterologous genes in Escherichia coli often leads to inhibition of cell growth, ribosome destruction, loss of culturability, and induction of stress responses, such as a heat shock-like response. Here we demonstrate that the general stress response, which is connected to the stress response regulator sigmas (sigma38, rpoS gene product), is suppressed during strong overproduction of a heterologous alpha-glucosidase. The mRNA levels of the rpoS and osmY stress genes drastically decrease after induction of the strong overexpression system. It is shown that an rpoS mutation causes a significant loss of cell viability after induction of the expression system. Furthermore, it is demonstrated that an E. coli c/pP mutant, which could be suggested to improve heterologous protein production, is not a good production host if a tac-promoter is used to control the expression of the recombinant gene. Data from this study suggest that the overexpression of the alpha-glucosidase was greatly decreased by sigma factor competition in the clpP mutant, due to the increased sigmas level in this mutant background.
Bacterial Proteins↗
The context framing the changes in health-related quality of life and working competence before and after lung transplantation: one-year follow-up in Taiwan.
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Adult↗
Mammalian resistance to oxidative stress: a comparative analysis.
Changes in gene expression represent a major protective mechanism, and enforced overexpression of individual genes has been shown to protect cells. However, no large-scale comparison of genes involved in mammalian oxidative stress protection has yet been described. Using filter microarray and restriction fragment differential display technology, hydrogen peroxide (H2O2)-resistant variants of hamster HA-1 fibroblasts and human HL-60 promyelocytes were found to possess a surprising lack of commonality in specific modulated genes with the single exception of catalase, supporting the hypothesis that catalase overexpression is critical for resistance to H2O2. Comparison of two cell lines from the same species (hamster) selected with an exogenous oxidative stressing agent (H2O2) and an endogenous metabolic oxidative stressing agent (95% O2) also revealed little commonality in modulation of specific mRNAs with the exception of glutathione S-transferase enzymes and catalase. Acute oxidative stress in HL-60 led to the modulation of a limited subset of the genes associated with chronic oxidative stress resistance. Overall, these results suggest that mammalian resistance to oxidative and perhaps other stress does not require a significant number of common genes but rather only a limited number of key genes (e.g., catalase in our model systems) in combination with others that are cell type and stress agent specific.
Animals↗
Dual regulation of glycogen synthase kinase-3beta by the alpha1A-adrenergic receptor.
Catecholamines, acting through adrenergic receptors, play an important role in modulating the effects of insulin on glucose metabolism. Insulin activation of glycogen synthesis is mediated in part by the inhibitory phosphorylation of glycogen synthase kinase-3 (GSK-3). In this study, catecholamine regulation of GSK-3beta was investigated in Rat-1 fibroblasts stably expressing the alpha1A-adrenergic receptor. Treatment of these cells with either insulin or phenylephrine (PE), an alpha1-adrenergic receptor agonist, induced Ser-9 phosphorylation of GSK-3beta and inhibited GSK-3beta activity. Insulin-induced GSK-3beta phosphorylation is mediated by the phosphatidylinositol 3-kinase/Akt signaling pathway. PE treatment does not activate phosphatidylinositol 3-kinase or Akt (Ballou, L. M., Cross, M. E., Huang, S., McReynolds, E. M., Zhang, B. X., and Lin, R. Z. (2000) J. Biol. Chem. 275, 4803-4809), but instead inhibits insulin-induced Akt activation and GSK-3beta phosphorylation. Experiments using protein kinase C (PKC) inhibitors suggest that phorbol ester-sensitive novel PKC and Gö 6983-sensitive atypical PKC isoforms are involved in the PE-induced phosphorylation of GSK-3beta. Indeed, PE treatment of Rat-1 cells increased the activity of atypical PKCzeta, and expression of PKCzeta in COS-7 cells stimulated GSK-3beta Ser-9 phosphorylation. In addition, PE-induced GSK-3beta phosphorylation was reduced in Rat-1 cells treated with a cell-permeable PKCzeta pseudosubstrate peptide inhibitor. These results suggest that the alpha1A-adrenergic receptor regulates GSK-3beta through two signaling pathways. One pathway inhibits insulin-induced GSK-3beta phosphorylation by blocking insulin activation of Akt. The second pathway stimulates Ser-9 phosphorylation of GSK-3beta, probably via PKC.
Adrenergic alpha-Agonists↗