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Biomedical subjects

Jun Chen

Publications and source records attributed to Jun Chen.

At least 307 records · Page 17Linked to original sources
PubMed2003

Quality of life impact and treatment seeking of Chinese women with urinary incontinence.

The objective of this study was to investigate the quality of life (QOL) impact of urinary incontinence (UI) and to examine its relationship with treatment seeking in adult Taiwanese women. We conducted a cross-section in-person questionnaire interview of 1608 adult women living in the Taipei area. The characteristics and incontinence status were recorded. A short form incontinence impact questionnaire (IIQ-7) was used to evaluate the QOL impact of UI. Multiple logistic regression analysis was used to assess the determinative factors for treatment seeking. The mean IIQ-7 score of the 205 (12.7%) women who reported urinary leakage more than once per month in the preceding 12 months was 5.0 (range: 0-19), which showed a significant correlation with the severity of incontinence (r = 0.59, p < 0.001). Women with mixed type UI had a higher IIQ-7 score compared to those with stress or urge UI. Fifty-five (26.8%) incontinent women had sought medical help. Treatment seeking was highly related to IIQ-7 scores as 75% of incontinent women with an IIQ-7 score > 10 in contrast to 5% of those with an IIQ-7 score < or = 3 (p < 0.001) had sought medical care. On multiple logistic regression analysis, perceiving UI as a disease and a higher IIQ-7 score were independent factors predicting treatment seeking. We concluded that UI is a common problem that brings substantial QOL impact to Taiwanese women. The IIQ-7 questionnaire may provide a useful measurement to quantitate the degree of QOL impact, which is largely affected by the severity and type of incontinence. Women who perceive UI as a disease and those with a higher degree of QOL impact are more likely to seek medical help. Furthermore, treatment seeking in Taiwanese women with significant UI may be more common than thought as a great majority of women with higher IIQ-7 scores had sought medical help.

Adult↗
PubMed2003

OsBP-73, a rice gene, encodes a novel DNA-binding protein with a SAP-like domain and its genetic interference by double-stranded RNA inhibits rice growth.

The SAP domain is a recently defined DNA binding domain that forms a helix-extended-helix structure. SAP proteins have been implicated in nuclear architecture and/or RNA metabolism. In this paper, we describe the cloning and characterization of a rice gene, OsBP-73, encoding a 375 amino acid protein with a SAP-like domain. We identified the binding sequence of OsBP-73 by gel retardation assays and southwestern blotting. Northern blot analysis demonstrated that OsBP-73 is weakly expressed in root, leaf and immature seed. OsBP-73 gene expression was also examined by histochemical studies of transgenic rice plants carrying an OsBP-73 5'/GUS reporter gene. The reporter gene is mainly expressed in the tissues with high cell division activities, such as root tip, stem node, panicle and immature seed. Genetic interference of OsBP-73 gene expression by double-stranded RNA strikingly inhibits the whole plant growth but does not affect the passage from the juvenile to adult phase. These results suggest that OsBP-73 may play an important role in the regulation of cell proliferation.

Amino Acid Sequence↗
PubMed2003

Selenium and selenoproteins in the brain and brain diseases.

Over the past three decades, selenium has been intensively investigated as an antioxidant trace element. It is widely distributed throughout the body, but is particularly well maintained in the brain, even upon prolonged dietary selenium deficiency. Changes in selenium concentration in blood and brain have been reported in Alzheimer's disease and brain tumors. The functions of selenium are believed to be carried out by selenoproteins, in which selenium is specifically incorporated as the amino acid, selenocysteine. Several selenoproteins are expressed in brain, but many questions remain about their roles in neuronal function. Glutathione peroxidase has been localized in glial cells, and its expression is increased surrounding the damaged area in Parkinson's disease and occlusive cerebrovascular disease, consistent with its protective role against oxidative damage. Selenoprotein P has been reported to possess antioxidant activities and the ability to promote neuronal cell survival. Recent studies in cell culture and gene knockout models support a function for selenoprotein P in delivery of selenium to the brain. mRNAs for other selenoproteins, including selenoprotein W, thioredoxin reductases, 15-kDa selenoprotein and type 2 iodothyronine deiodinase, are also detected in the brain. Future research directions will surely unravel the important functions of this class of proteins in the brain.

Animals↗
PubMed2003

Determination of fatty acid levels in erythrocyte membranes of patients with chronic fatigue syndrome.

Chronic fatigue syndrome (CFS) is an illness characterized by persistent and relapsing fatigue, often accompanied by numerous symptoms involving various systems of whole body. The etiology of CFS remains unclear. Literature reported whether the concentrations of the essential fatty acids in red cell membranes of CFS patients were decreased is controversial. In our study, Forty-two patients who fulfilled the diagnostic criteria defined by Centers for Disease Control and Prevention (CDC). Thirty-seven age- and sex-matched controls were selected from healthy medical staffs and volunteers. After lipid analysis, we found that the levels of the arachidonic acid (ARA) and docosahexanoic acid (DHA) were decreased in patients suffered from CFS. However, the levels of the palmitic acid and oleic acid were increased. We speculated that there are two possible mechanisms--one of which is that oxidative stress has led to an excessive oxidation and resulting in the above fatty acids. Alternatively, insufficiency of ingestion of fatty acids might not be the major cause.

Adult↗
PubMed2003

Aging is associated with increased T-cell chemokine expression in C57BL/6 mice.

To better understand the contribution of the chemokine system in immune senescence, we determined the aging effect on CD4+ and CD8+ T-cell chemokine expression by microarray screening and ribonuclease protection assays. Compared with young C57BL/6 mice, freshly isolated CD4+ cells from aged mice express increased level of interferon-gamma-inducible protein 10 (IP-10), macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, regulated upon activation, normal T-cell expressed and secreted (RANTES), and lymphotactin (Ltn). T-cell receptor (TCR)/coreceptor stimulation up-regulates MIP-1alpha, MIP-1beta, and Ltn, and down-regulates IP-10 and RANTES expression in CD4+ T cells. A similar increase in chemokine expression was demonstrated in the CD8+ T cell. Enzyme-linked immunosorbent assays confirmed increased T-cell chemokine protein production in old CD4+ and CD8+ T cells. Finally, supernatant of cultured T cells from old animals caused an enhanced leukocyte chemotaxis response compared with that from young animals, suggesting that the age-related difference in T-cell chemokine expression has an important functional consequence.

Aging↗
PubMed2003

Supraspinal contribution to development of both tonic nociception and referred mirror hyperalgesia: a comparative study between formalin test and bee venom test in the rat.

BACKGROUND: The roles of descending facilitatory pathway from the rostral medial medulla (RMM) in development of persistent spontaneous nociception and hyperalgesia were evaluated in the bee venom (BV) test and the formalin test. METHODS: Bilateral lesions of the RMM with ibotenic acid, a soma-selective neurotoxin, were performed to study their effects on the spontaneous pain-related behaviors and hyperalgesia, which were determined by counting the number of flinching reflex per 5 min (1 h) and by measuring paw withdrawal thermal latency (PWTL) and mechanical threshold (PWMT) to radiant heat and von-Frey filaments to both hind paws in conscious rats, respectively. RESULTS: 1) Bilateral lesions of the RMM produced a similarly significant inhibition of persistent spontaneous flinching reflexes in the BV test and the formalin test; however, the inhibitory effect occurred in the late 50 min (11-60 min), but not the first 10 min (0-10 min) following intraplantar injection of either BV or formalin. 2) Bilateral lesions of the RMM prevented the development of the BV-induced referred mirror heat hyperalgesia occurred in the noninjected paw, but had no effect on the primary heat and mechanical hyperalgesia occurred in the injected paw. CONCLUSIONS: The present results provide a new line of behavioral evidence that tonic activation of descending facilitatory pathway contributes to the establishment of 1) the BV and formalin-induced persistent spontaneous nociception; and 2) the BV-induced referred mirror heat hyperalgesia and the central sensitization, but not the primary heat and mechanical hyperalgesia.

Animals↗
PubMed2003

Translocation of apoptosis-inducing factor in vulnerable neurons after transient cerebral ischemia and in neuronal cultures after oxygen-glucose deprivation.

Loss of mitochondrial membrane integrity and the resulting release of apoptogenic factors may play a critical role in mediating hippocampal neurodegeneration after transient global ischemia. In the present study, the authors have cloned and characterized the rat cDNA encoding apoptosis-inducing factor (AIF), an intramitochondrial protein that promotes cell death in a caspase-independent manner upon release into nonmitochondrial compartments. In contrast to the expression patterns of a number of apoptosis-regulatory gene products during brain development, the expression of AIF protein increases gradually with brain maturation and peaks in adulthood. In a rat model of transient global ischemia, AIF was found to translocate from mitochondria to the nucleus in the hippocampal CA1 neurons after ischemia and to manifest a DNA-degrading activity that mimicked the purified AIF protein and was inhibitable by AIF immunodepletion. The temporal profile of AIF translocation after ischemia (24 to 72 hours) coincided with the induction of large-scale DNA fragmentation at the size of 50 kbp, a well-characterized hallmark of AIF-like activity but preceded the formation of internucleosomal DNA fragmentation (72 hours), a DNA degradation associated with the terminal stage of cell death. Further, the nuclear translocation of AIF after ischemia was not blocked by inhibiting caspase-3/-7 activities, but, as shown in neuronal cultures that were challenged with transient oxygen-glucose deprivation, it can be prevented by intracellular delivery of the mitochondria-associated antiapoptotic protein Bcl-xL. The results presented here strongly suggest that mitochondrial release of AIF may be an important factor, in addition to the previously reported cytochrome c and Smac, which could contribute to the selective vulnerability of CA1 neurons to transient global ischemic injury.

Amino Acid Sequence↗
PubMed2003

Inducible repair of oxidative DNA lesions in the rat brain after transient focal ischemia and reperfusion.

To determine the role of oxidative DNA damage and repair in brain injury after focal ischemia and reperfusion, the authors investigated DNA base damage and DNA base excision repair (BER) capacity, the predominant repair mechanism for oxidative DNA lesions, in the rat model of temporary middle cerebral artery occlusion. Contents of 8-hydroxyl-2'-deoxyguanosine (8-oxodG) and apurinic/apyrimidinic abasic site (AP site), hallmarks of oxidative DNA damage, were quantitatively measured in nuclear DNA extracts from brains 0.25 to 72 hours after 1 hour of middle cerebral artery occlusion. In parallel to the detection of DNA lesions, the capacity for 8-oxodG- or AP site-dependent DNA repair synthesis was measured in nuclear protein extracts using specific in vitro DNA repair assays. After postischemic reperfusion, the levels of 8-oxodG and AP sites were markedly increased in ischemic tissues. In frontal/parietal cortex, regions that survived ischemia, 8-oxodG and AP sites were efficiently repaired during reperfusion. However, in the caudate, a region that was destined to infarct, the DNA lesions were poorly repaired. In consistent with the patterns of endogenous lesion repair, a markedly induced and long-lasting (at least 72 hours) BER activity was detected in the cortex but not in the caudate after ischemia. The induced BER activity in ischemic cortex was attributed to the upregulation of gene expression and activation of selective BER enzymes, particularly DNA polymerase-beta and OGG1. These results strongly suggest that inducible DNA BER constitutes an important endogenous mechanism that protects brain against ischemia-induced oxidative neuronal injury.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2003

Identification of CYP1A2 as the main isoform for the phase I hydroxylated metabolism of genistein and a prodrug converting enzyme of methylated isoflavones.

This study determined the cytochrome P450 (P450) isoforms responsible for metabolism of isoflavones using human liver microsomes (HLM) and expressed P450s. The primary metabolite of genistein is 3'-OH-genistein, as identified with an authentic chemically synthesized standard. CYP1A2 was predominantly responsible for 3'-OH-genistein formation since its formation was inhibited (>50%, p < 0.05) by a monoclonal antibody specific for CYP1A2, was correlated with CYP1A2 activities of HLM, and was catalyzed by expressed CYP1A2. In addition to CYP1A2, CYP2E1 also catalyzed, although to a lesser extent, its formation. The contribution of these P450s to the formation of 3'-OH-genistein was also confirmed with a panel of expressed enzymes. Methylated isoflavones biochanin A, prunetin, and formononetin (10-100 microM) were rapidly converted by HLM and expressed CYP1A2 to more active genistein and daidzein. The conversion of biochanin A to genistein appears to be mainly mediated by CYP1A2 because of the strong correlation between the conversion rates and CYP1A2 activities in HLM. Thus, CYP1A2 is an effective prodrug-converting enzyme for less active methylated isoflavones. CYP1A2-catalyzed conversion of biochanin A to genistein (Km, 7.80 microM; Vmax, 903 pmol/min/mg of protein; Vmax/Km, 116 microl/min/mg of protein) was much faster than 3'-hydroxylation of genistein (Km, 12.7 microM and Vmax, 109 pmol/min/mg of protein; Vmax/Km, 8.6 microl/min/mg of protein). The interaction studies showed that genistein inhibited formation of acetaminophen from phenacetin with an IC50 value of 16 microM. Additional studies showed that phenacetin and genistein were mutually inhibitory. In conclusion, CYP1A2 and CYP2E1 metabolized genistein and CYP1A2 acted as prodrug-converting enzymes for other less active methylated isoflavones.

Acetophenones↗
PubMed2003

Metabolism of flavonoids via enteric recycling: role of intestinal disposition.

The purpose of this study was to determine the importance of intestinal disposition in the first-pass metabolism of flavonoids. A four-site perfused rat intestinal model, rat liver and intestinal microsomes, Caco-2 cell microsomes, and the Caco-2 cell culture model were used. In the four-site model, approximately 28% of perfused aglycones are absorbed (approximately 450 nmol/30 min). Both absorption and subsequent excretion of metabolites were rapid and site-dependent (p < 0.05). Maximal amounts of intestinal conjugates excreted per 30 min were 61 and 150 nmol for genistein and apigenin, respectively. Maximal amounts of biliary conjugates excreted per 30 min were 50 and 30 nmol for genistein and apigenin, respectively. Microsomes, prepared from Caco-2 cells, rat intestine, and rat liver, always glucuronidated apigenin faster than genistein (p < 0.05). In addition, rat jejunal microsomes glucuronidated both flavonoids faster (p < 0.05) than rat intestinal microsomes prepared from other regions. When comparing glucuronidation in different organs, jejunal microsomes often but not always glucuronidated both flavonoids faster than liver microsomes. In the Caco-2 model, both flavonoids were rapidly absorbed and rapidly conjugated, and the conjugates were excreted apically and basolaterally. Similar to the four-site perfusion model, apigenin conjugates were excreted much faster than genistein conjugates (>2.5 times for glucuronic acid, >4.5 times for sulfate; p < 0.05). In conclusion, intestinal disposition may be more important than hepatic disposition in the first-pass metabolism of flavonoids such as apigenin. In conjunction with enterohepatic recycling, enteric recycling may be used to explain why flavonoids have poor systemic bioavailabilities.

Animals↗
PubMed2003

Molecular determinants of KCNQ1 channel block by a benzodiazepine.

KCNQ1 channels underlie the slow delayed rectifier K+ current, mediate repolarization of cardiac action potentials, and are a potential therapeutic target for treatment of arrhythmia. (E)-(+)-N-[(3R)-2,3-dihydro-1-methyl-2-oxo-5-phenyl-1H-1,4-benzodiazepin-3-yl]-3-(2,4-dichlorophenyl)-2-propenamide [L-735821 (L-7)] is a potent blocker of KCNQ1 channels. Here we describe the structural determinants of KCNQ1 that are critical for high-affinity block by L-7 using site-directed mutagenesis to alter specific residues and voltage clamp to record channel currents in Xenopus laevis oocytes. Chimeric channels were constructed by combination of regions from L-7-sensitive KCNQ1 and L-7-insensitive KCNQ2 channel subunits. This approach localized the drug interaction site to the pore and S6 domains of KCNQ1. Substitution of single amino acids identified Thr-312 of the pore domain and Ile-337, Phe-339, Phe-340, and Ala-344 of the S6 domain as the most important molecular determinants of channel block. Some mutations also altered the inactivation properties of KCNQ1, but there was no correlation between extent of inactivation and sensitivity to block by L-7. Modeling was used to simulate the docking of L-7 to the KCNQ1 channel pore. The docking was consistent with our experimental data and predicts that L-7 blocks K+ conductance by physically precluding the occupancy of a K+ ion to a pore helix-coordinated site within the central hydrated cavity, a crucial step in ion permeation.

Amino Acid Sequence↗
PubMed2003

[Studies on the relationship between vitamin D receptor gene polymorphism and osteoporosis in postmenopausal women].

OBJECTIVE: To determine the relationship between vitamin D receptor (VDR) gene polymorphism and osteoporosis in postmenopausal women. METHODS: The polymerase chain reaction-restriction fragment length polymorphism was used to detect VDR genotype in 40 patients with osteoporosis and 21 healthy postmenopausal women. RESULTS: In the patients with osteoporosis, the bb, Bb, and BB genotype accounted for 82.5%, 17.5% and 0, respectively; in healthy groups, they were 85.71%, 14.29% and 0, respectively (P>0.05). CONCLUSION: Significant association between VDR genotype and osteoporosis in Chinese women was observed in this study.

DNA↗
PubMed2003

[Effects of burn serum on the viscoelasticity and the structure of rat intestinal epithelial cells].

OBJECTIVE: To investigate the effects of burn serum on the viscoelasticity and the structure of rat intestinal epithelial cells. METHODS: The rat intestinal epithelial cell strain (IEC-6) was cultured and stimulated by burn serum. The changes of IECs before and after the stimulation were dynamically observed by cytoskeleton immunohistochemistry, ELISA and the measurement of cytomembranous viscoelasticity. RESULTS: During the early stage of burn serum stimulation, the skeleton protein expression in IEC decreased obviously with weakened positive signals of microfilaments and microtubules and with decreased cellular elasticity. CONCLUSION: The cytoskeleton injury could cause the increase of cellular fragility and the decrease of the viscoelasticity, which ultimately lead to the change of cellular biodynamics. These changes might directly participate the development of postburn intestinal epithelial injury.

Actins↗
PubMed2003

[Organochlorine residues of sediments in Taihu Lake and its risk evaluation].

This study analyzed chlorinated pesticides of sediments in Taihu Lake. The DDT, DDE, DDD, HCH isomers, Aldrin, Diddrin, Hexachlorobenze, Heptachlor were measured in all samples. beta-HCH, p, p'-DDE and Hexachlorobenze had higher concentrations than others. The average values of them were 6.572 ng/g, 1.432 ng/g and 2.158 ng/g, respectively. HCHs in sediments were higher than DDTs. The organochlorine residues in sediments mainly originated form the runoff, atmospherically deposition and industrial sewage. HCHs and DDTs of sediments in Taihu Lake were higher than those of sediments in Chinese rivers, but lower than those of bays reported in some papers. According to the ERL and ERM value of risk evaluation for ocean which can also be applied for lake, sediments in Taihu Lake pose a low risk to consumers of bottom feeders.

China↗
PubMed2003

ARMER, apoptotic regulator in the membrane of the endoplasmic reticulum, a novel inhibitor of apoptosis.

We have identified a novel protein, apoptotic regulator in the membrane of the endoplasmic reticulum (ARMER), which protects HT1080 fibrosarcoma cells from apoptosis induced by various stimuli. We demonstrate that ARMER is an endoplasmic reticulum (ER) integral membrane protein with four predicted transmembrane domains and a COOH-terminal KKXX ER retrieval motif. We used an inducible expression system (pIND) to study the effects of regulated ARMER overexpression. Cells in which ARMER was overexpressed exhibited protection from multiple apoptotic inducers including serum starvation, doxorubicin, UV irradiation, tumor necrosis factor alpha, and the ER stressors brefeldin A, tunicamycin, and thapsigargin. Analysis of the caspase proteolytic cascade reveals that ARMER inhibits proteolysis of the caspase-9-specific fluorogenic substrate LEHD-AFC as well as endogenous substrates downstream of caspase-9; however, it does not inhibit cytochrome c release or cleavage of caspase-9 itself. Apoptotic stimuli cause endogenous levels of ARMER protein and RNA to decrease, leading to cell death; however, sustaining ARMER protein levels through exogenous expression inhibits apoptosis. These data suggest that ARMER is a novel ER integral membrane protein which protects cells by inhibiting caspase-9 activity and reveal a possible role for ARMER in cell survival.

Adaptor Proteins, Signal Transducing↗
PubMed2003

[Autotrophic biofilters for oxidation of nitric oxide].

Carbon foam, a kind of new engineering material as packing material was adopted in three fi 50.8 mm biofilters with different pore dimension and a domesticated autotrophic nitrite nitrobacteria to investigate the purification of nitrie oxide(NO) in air stream. The biofilm was developed on the surface of carbon foams using nitrite as its only nitric source. The moisture in the filter was maintained by ultrasonic aerosol equipment, which can also minimize the thickness of the liquid film. The liquid phase nitrification test was conducted to determine the variability and the potential of performance among the three carbon foam-based biofilters. The investigation showed that during the NO influent concentration of 200 to 800 g/(L.min), the 24PPC (Pores Per Centimeter) carbon foam-based biofilters had the greatest potential, achieving removal efficiencies of 94% to 98%. The 8PPC and 18PPC carbon foam-based biofilters achieved removals efficiencies of 15% to 21% and of 30% to 40%, respectively. Further research showed the potential for this system to remove NO from an air stream on the base of a steady removal efficiency of 41% to 52% was attained for the 24PPC carbon foam-based biofilter at specified NO influent concentrations of 66.97 to 267.86 mg/m3 and an empty-bed residence time of 3.5 minutes.

Air Pollutants↗
PubMed2003

Human Chk1 expression is dispensable for somatic cell death and critical for sustaining G2 DNA damage checkpoint.

Mammalian Chk1 is an essential kinase for embryonic development and plays an important role in the cellular response to DNA damage. However, it remains unclear whether inhibition of Chk1 induces apoptosis in somatic cells. The uncertainty has become a critical issue for rationale design of Chk1 mechanism-based anticancer drugs. Here we show that Chk1 small interfering RNA (siRNA) effectively eliminates Chk1 protein expression without altering the cell cycle profile or inducing apoptosis in various human cancer cell lines under normal conditions. In the presence of DNA-damaging agents, however, Chk1 siRNA alone is sufficient to abrogate the DNA damage-induced G(2) checkpoint and significantly enhance apoptosis. Cell cycle kinetic profiles show that abrogation of G(2) arrest is mediated through shortening of the checkpoint. We also demonstrate that Chk1 siRNA enhances DNA damage-induced apoptosis in p53-deficient cancer cell lines and augments the growth inhibition conferred by DNA-damaging agents. These findings imply that Chk1 inhibitors will have low cytotoxicity on their own and can enhance the efficacy of DNA-damaging drugs.

Apoptosis↗