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Biomedical subjects

J Chen

Publications and source records attributed to J Chen.

At least 163 records · Page 9Linked to original sources
PubMed2004

Further molecular characterisation of potyviruses infecting aroid plants for medicinal use in China.

Degenerate primers were used to detect and amplify 3'-terminal genome fragments of potyviruses from medicinal aroid plants growing at 16 sites in China. Virus was detected in 7 samples of which six, all of Pinellia ternata, contained a strain of soybean mosaic virus (SMV) similar to that previously reported from this host in China. The complete sequence of one isolate and the P1 protein coding region of the other isolates were also sequenced. In all cases, the P1 proteins resembled isolates of Dasheen mosaic virus (DsMV) more closely than SMV, confirming earlier suggestions of recombination in this region. In a phylogenetic analysis of SMV, DsMV and related sequences, the aroid sequences of SMV formed a distinct group which also included a sequence published as Zantedeschia symptomless virus (AF469171). One of the P. ternata samples was also infected with a second potyvirus, the 3'-terminal sequence of which was similar to DsMV and to some sequences published as Vanilla mosaic virus. The seventh infected sample was Typhonium flagelliforme and the virus from it was identified from its sequence as zantedeschia mosaic virus (ZaMV), providing the first report of this virus from mainland China.

China↗
PubMed2004

Poliovirus vaccination during pregnancy, maternal seroconversion to simian virus 40, and risk of childhood cancer.

Before 1963, poliovirus vaccine produced in the United States was contaminated with simian virus 40 (SV40), which causes cancer in animals. To examine whether early-life SV40 infection can cause human cancer, the authors studied 54,796 children enrolled in the US-based Collaborative Perinatal Project (CPP) in 1959-1966, 52 of whom developed cancer by their eighth birthday. Those children whose mothers had received pre-1963 poliovirus vaccine during pregnancy (22.5% of the children) had an increased incidence of neural tumors (hazard ratio = 2.6, 95% confidence interval: 1.0, 6.7; 18 cases) and hematologic malignancies (hazard ratio = 2.8, 95% confidence interval: 1.2, 6.4; 22 cases). For 50 CPP children with cancer and 200 CPP control children, the authors tested paired maternal serum samples from pregnancy for SV40 antibodies using a virus-like particle enzyme immunoassay and a plaque neutralization assay. Overall, mothers exhibited infrequent, low-level SV40 antibody reactivity, and only six case mothers seroconverted by either assay. Using the two SV40 assays, maternal SV40 seroconversion during pregnancy was not consistently related to children's case/control status or mothers' receipt of pre-1963 vaccine. The authors conclude that an increased cancer risk in CPP children whose mothers received pre-1963 poliovirus vaccine was unlikely to have been due to SV40 infection transmitted from mothers to their children.

Adult↗
PubMed2004

A new potyvirus from tuberose ( Polianthes tuberosa) in China.

Tuberose plants with mild mottle symptoms, growing in a glasshouse in Hangzhou, China, contained virions and inclusion bodies typical of a potyvirus. The virus was mechanically transmitted to tuberose but not to 14 other test plant species. A fragment of 4607 nucleotides, corresponding to the 3'-half of a typical potyvirus was amplified by RT-PCR using degenerate primers and sequenced. The most similar sequence in the databases was that of Tuberose mild mosaic virus (TuMMV) from Taiwan and this was the only virus significantly related to it in phylogenetic analyses. The new sequence had 71.1% nt and 76.6% aa identity to TuMMV in the coat protein. Western blot analyses using antisera raised to expressed coat protein showed that the two viruses were serologically related. Although there are no substantial biological data to distinguish the Hangzhou isolate from TuMMV, the molecular difference between the two virus isolates is similar to, or slightly greater than, that between several pairs of well-established potyvirus species. These results therefore suggest that the Hangzhou isolate should be regarded as a new member of the genus Potyvirus, and we have tentatively named it Tuberose mild mottle virus.

Amino Acid Sequence↗
PubMed2004

Observation of the decay psi(2S)-->K0SK0L.

The decay psi(2S)-->K(0)(S)K(0)(L) is observed using psi(2S) data collected with the Beijing Spectrometer at the Beijing Electron-Positron Collider; the branching fraction is determined to be B(psi(2S)-->K(0)(S)K(0)(L))=(5.24+/-0.47+/-0.48)x10(-5). Compared with J/psi-->K(0)(S)K(0)(L), the psi(2S) branching fraction is enhanced relative to the prediction of the perturbative QCD "12%" rule. The result, together with the branching fractions of psi(2S) decays to other pseudoscalar meson pairs (pi(+)pi(-) and K+K-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.

Journal Article↗
PubMed2004

Prostaglandin ethanolamides (prostamides): in vitro pharmacology and metabolism.

We investigated whether prostaglandin ethanolamides (prostamides) E(2), F(2alpha), and D(2) exert some of their effects by 1) activating prostanoid receptors either per se or after conversion into the corresponding prostaglandins; 2) interacting with proteins for the inactivation of the endocannabinoid N-arachidonoylethanolamide (AEA), for example fatty acid amide hydrolase (FAAH), thereby enhancing AEA endogenous levels; or 3) activating the vanilloid receptor type-1 (TRPV1). Prostamides potently stimulated cat iris contraction with potency approaching that of the corresponding prostaglandins. However, prostamides D(2), E(2), and F(2alpha) exhibited no meaningful interaction with the cat recombinant FP receptor, nor with human recombinant DP, EP(1-4), FP, IP, and TP prostanoid receptors. Prostamide F(2alpha) was also very weak or inactive in a panel of bioassays specific for the various prostanoid receptors. None of the prostamides inhibited AEA enzymatic hydrolysis by FAAH in cell homogenates, or AEA cellular uptake in intact cells. Furthermore, less than 3% of the compounds were hydrolyzed to the corresponding prostaglandins when incubated for 4 h with homogenates of rat brain, lung, or liver, and cat iris or ciliary body. Very little temperature-dependent uptake of prostamides was observed after incubation with rat brain synaptosomes or RBL-2H3 cells. We suggest that prostamides' most prominent pharmacological actions are not due to transformation into prostaglandins, activation of prostanoid receptors, enhancement of AEA levels, or gating of TRPV1 receptors, but possibly to interaction with novel receptors that seem to be functional in the cat iris.

Amides↗
PubMed2004

Methotrexate for ankylosing spondylitis.

BACKGROUND: Ankylosing spondylitis (AS) is a chronic inflammatory disease of unknown cause, characterized by sacroiliitis and spondylitis. To date, treatment of AS has been limited to the alleviation of symptoms, mainly using non-steroidal anti-inflammatory drugs (NSAIDs). For patients refractory or intolerant to NSAIDs, the disease modifying antirheumatic drugs (DMARDs) have been used as a second line approach. Methotrexate (MTX) is currently one of the most widely used DMARDs and its efficacy in rheumatoid arthritis (RA) has been confirmed (Suarez-Almazor 2003). There is uncertainty whether MTX works in the treatment of AS. OBJECTIVES: To evaluate the efficacy and toxicity of methotrexate in the treatment of ankylosing spondylitis. SEARCH STRATEGY: Relevant randomised and quasi-randomised trials in any language were sought using the following sources: CENTRAL (Cochrane Central Register of Controlled Trials, Issue 2, 2003), MEDLINE (1966 to June Week 4 2003), EMBASE (1980 to 2003 Week 26), CINAHL (1982 to June Week 3 2003) and the reference section of retrieved articles. SELECTION CRITERIA: We evaluated randomised and quasi-randomised trials examining the efficacy of methotrexate on AS. DATA COLLECTION AND ANALYSIS: Unblinded trial reports were reviewed independently by two reviewers according to the selection criteria. Disagreements on the inclusion of the studies were resolved, where necessary, by recourse to a third reviewer. The methodological quality of included trials were independently assessed by the same reviewers on randomization, concealment, blindness (participants, care providers and outcome investigators), description of withdrawals and drop-outs and intention-to-treat analysis. The same reviewers independently entered the data extracted from the included trials, using RevMan's double entry facility. In the absence of significant heterogeneity, results were combined using weighted mean difference or standardised mean difference for continuous data, and relative risk for dichotomous data. MAIN RESULTS: Two trials met the inclusion criteria. Altan 2001compared naproxen plus MTX (7.5 mg/week orally) with naproxen alone and Roychowdhury 2002 compared MTX (10 mg/week orally) with placebo. The duration of the trials were 12 months and 24 weeks, respectively. They assessed different outcomes except for C-reactive protein (CRP). The included trials treated a total of 81 patients and assessed more than 10 outcomes relevant to the review, covering function, pain, peripheral arthritis/enthesitis, morning stiffness, patient and physician global assessment, CRP and erythrocyte sedimentation rate (ESR). No significant difference between intervention groups was found favouring MTX over no MTX. No serious side effect was reported in either trial. REVIEWERS' CONCLUSIONS: There was no statistically significant benefit of MTX in the examined outcomes for AS patients. High quality, larger sample and longer period of randomized controlled trials (possibly with higher dosage of MTX) are needed to verify the uncertainty about the efficacy and toxicity of MTX for the treatment of AS.

Antirheumatic Agents↗
PubMed2004

Novel regulatory mechanisms of mTOR signaling.

As a master regulator of cellular processes ranging from cell growth and proliferation to differentiation, the mammalian target of rapamycin (mTOR) is critically involved in a complex signaling network. mTOR appears to govern an amino acid sensing pathway that integrates with a phosphatidylinositol 3-kinase-dependent mitogenic pathway to activate the downstream effectors. Recent findings have revealed some unexpected regulatory mechanisms of mTOR signaling. A direct link between mTOR and mitogenic signals is found to be mediated by the lipid second messenger phosphatidic acid. In addition, cytoplasmic-nuclear shuttling of mTOR appears to be required for the cytoplasmic functions of this protein. A new picture of the rapamycin-sensitive signaling network is emerging, with implications in putative upstream regulators and additional downstream targets for mTOR.

Animals↗
PubMed2004

Involvement of lymphocytes with a Th1 cytokine profile in bone cell damage associated with MMP-9 production in collagen-induced arthritis.

OBJECTIVE: To investigate whether lymphocytes could directly cause the destruction of bone cells in collageninduced arthritis (CIA) mice and the mechanism of this destruction. METHODS: Arthritis was induced with chick type II collagen in Kunming mice. The activities of TNF-alpha and IFN-gamma were measured by biological methods. The mRNA of TNF-alpha, IFN-gamma, T-bet, a Th1 specific transcription factor and Fas was detected by reverse transcript-polymerase chain reaction (RT-PCR). Matrix metalloproteinase (MMP)-9 was measured by gelatin zymography assay. The cytotoxicity of spleen cells to bone cell populations and the proliferation of spleen cells against chick type II collagen (CII) were examined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2H-tetrazolium bromide (MTT) method. RESULTS: Arthritis was successfully induced by chick CII in Kunming mice, which had remarkable paw swelling and typical features of arthritis. Compared with naive mice, the arthritic mice showed an increased IFN-gamma and TNF-alpha production in serum, and the spleen cells from the arthritic mice displayed a Th1 cytokine profile and directly damaged bone cells in vitro. Interestingly, naive spleen cells treated by phorbol 12-myristate 13-acetate (PMA) also damaged bone cells as did spleen cells from CIA mice. Cyclosporine A blocked the cytotoxicity of spleen cells from CIA mice to bone cells. Only anti-CD4 and complement system together inhibited the effect of spleen cells from CIA mice on bone cells. Only the spleen cells from arthritic mice could proliferate against chick CII. In addition, the culture supernatants from spleen cells of arthritic mice contained a higher activity of MMP-9 and production of NO than those of naive mice. PMA elevated the activity of MMP-9 but not the production of NO in naive spleen cells. Moreover, the activities of TNF-alpha, IFN-gamma and MMP-9 but not the production of NO were higher in joint tissues of arthritic mice than those of naive mice. TNF-alpha and IFN-gamma significantly elevated the activity of MMP-9 in spleen cells from both arthritic and naive mice in vitro. Moreover, only anti-MMP-9 but not anti-MMP-2 antibody inhibited the cytotoxicity of spleen cells from CIA mice to bone cells. CONCLUSIONS: The elevated proinflammatory factors such as TNF-alpha and IFN-gamma may promote the MMP-9 activity in local inflammatory cells that are actually involved in the bone cell damage in CII-induced arthritis.

Animals↗
PubMed2004

Role of Akt/protein kinase B in the activity of transcriptional coactivator p300.

Akt/protein kinase B is a downstream target of the phosphatidylinositol 3-kinase (PI3K) pathway and plays a critical role in promotion of cell survival. The function of transcriptional coactivator p300 is required by many transcription factors to either activate or repress gene expression. Here, we show that induction of PI3K enhances the metabolic stability of endogenous p300 protein. On the other hand, repression of PI3K by LY294002 induces p300 degradation through the 26S proteasome pathway and impedes the transcriptional activity of the coactivator. In addition, Akt interacts with the coactivator and the activity of Akt is required to maintain the steady-state level of p300. Our study provides a new insight into the molecular mechanisms by which the critical concentration of p300 protein is regulated and suggests a role for Akt in control of various cellular activities through the transcriptional coactivator p300.

Acetyltransferases↗
PubMed2004

Neuronal expression of the drug efflux transporter P-glycoprotein in the rat hippocampus after limbic seizures.

In the brain, the efflux transporter P-glycoprotein (Pgp) is predominantly located on the luminal membrane of endothelial cells lining brain microvessels and forming the blood-brain barrier. Many lipophilic drugs, including antiepileptic drugs, are potential substrates for Pgp. Overexpression of Pgp in endothelial cells of the blood-brain barrier has been determined in patients with drug resistant forms of epilepsy such as temporal lobe epilepsy and rodent models of temporal lobe epilepsy and suggested to lead to reduced penetration of antiepileptic drugs into the brain. Expression of Pgp after seizures has also been described in astrocytes, whereas it is not clear whether neurons can express Pgp. In the present study, Pgp expression was studied by immunohistochemistry in rats 24 h after a status epilepticus induced by either pilocarpine or kainate, widely used models of temporal lobe epilepsy. Unexpectedly, in addition to endothelial Pgp staining, intense Pgp staining was found in neurons in the CA3c/CA4 sectors and hilus of the hippocampus formation, but not in other brain regions examined. The neuronal Pgp staining was confirmed by two different Pgp antibodies. Double immunolabeling and confocal microscopy showed that Pgp was colocalized with the neuronal marker neuronal nuclear antigen, but not with the glial marker glial fibrillary acidic protein. No neuronal Pgp staining was seen in control rats. The expression of Pgp in neurons after limbic seizures was substantiated by determining Pgp encoding genes (mdr1a, mdr1b) in neurons by real time quantitative RT-PCR. Increased Pgp expression in hippocampal neurons is likely to affect the action of drugs with intraneuronal targets and, in view of recent evidence from other cell types, could be associated with prevention of apoptosis which is involved in neuronal damage developing after seizures such as produced by pilocarpine.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed2004

Injection of okadaic acid into the meynert nucleus basalis of rat brain induces decreased acetylcholine level and spatial memory deficit.

Abnormal hyperphosphorylation of tau and cholinergic deficit occur in the early stage of Alzheimer's disease (AD) and relate to the dementia symptom. Hyperphosphorylation of tau, neurofilament (NF) and other proteins in AD brain appears to be caused by a down-regulation of protein phosphatase 2A (PP2A), but the mechanism leading to cholinergic deficit is still unknown. In this study, we selectively inhibited PP2A by injection of okadaic acid (OA) into the Meynert nucleus basalis of rats. We found that injection of OA induced hyperphosphorylation of tau and NF and decreased acetylcholine (ACh) level in the nucleus basalis of Meynert. These alterations were accompanied by spatial memory deficit in OA-injected rats. We also demonstrated that the OA-induced ACh reduction may be due to a failure of intraneuronal transport of choline acetyltransferase (ChAT) from cell body to the neuronal terminals rather than an alteration of activity of ChAT or acetylcholinesterase. This study suggests that a down-regulation of PP2A may underlie both abnormal hyperphosphorylation of cytoskeletal proteins leading to neurofibrillary degeneration and cholinergic deficiency in AD.

Acetylcholine↗
PubMed2004

Altered pain-related behaviors and spinal neuronal responses produced by s.c. injection of melittin in rats.

Recently, we have reported that following s.c. injection of a solution containing the whole bee-venom (BV; Apis mellifera), into one hind paw of a rat, the experimentally produced honeybee's sting, the animal shows altered pain-related behaviors and inflammation relevant to pathological pain state. To see whether melittin, the major (over 50%) toxic component of the BV, is responsible for the above abnormal pain behavioral changes, the present study was designed to investigate the effects of s.c. melittin on either nociceptive behaviors in conscious rats or spinal dorsal horn neuronal responses in anesthetized rats. In the behavioral surveys, s.c. injection of three doses of both melittin (5, 25 and 50 microg) and BV (10, 50 and 100 microg) into the posterior surface of one hind paw of rats produced an immediate tonic nociceptive response displaying as persistent spontaneous paw flinching reflex. Similar to the BV test, the melittin response was also monophasic and dose-dependent in terms of both intensity and time course. As an accompanied consequence, both heat and mechanical hypersensitivity (hyperalgesia and allodynia) and inflammatory responses (paw swelling and plasma extravasation) were induced by s.c. melittin injections. In the electrophysiological recordings, s.c. injection of the same three doses of melittin into the cutaneous receptive field produced an immediate, dose-dependent increase in spontaneous spike discharges of spinal dorsal horn wide-dynamic-range (WDR) neurons which are believed to be responsible for the spinally-organized nociceptive flexion reflex. The melittin-induced ongoing spike responses are similar to the behavioral flinching reflex in terms of both duration and frequency. Furthermore, the responsiveness of the WDR neurons to both heat (42 degrees C, 45 degrees C, 47 degrees C and 49 degrees C) and mechanical (brush, pressure and pinch) stimuli was significantly enhanced by s.c. injection of melittin shown as a leftward shift of the stimulus-response functional curves. Taken together, the present results suggest that melittin, the major toxin of the whole BV, is likely to be responsible for production of the long-term spinal neuronal changes as well as persistent spontaneous nociception, heat/mechanical hypersensitivity and inflammatory responses that are produced by experimental honeybee's sting.

Animals↗
PubMed2004

Comparative analysis of transcriptional profiles between two apoptotic pathways of light-induced retinal degeneration.

Light exposure can exacerbate the condition of a variety of human retinal diseases by increasing the rate of photoreceptor cell death. How light negatively affects photoreceptor cell survival is not yet fully understood. Previous studies involving light damage models have revealed two independent apoptotic pathways: low levels of light induce retinal degeneration in the arrestin -/- mouse via constitutive activation of the phototransduction cascade, whereas strong light exposure to the retina, such as in an albino eye, elicits photoreceptor cell death via activator protein (AP-1) induction. In order to better understand the initial gene expression changes underlying light damage, dark-reared arrestin -/- and albino BALB/c mice were exposed to constant white light (2000 lux), and their retinal morphology was assessed as a function of time. The expression profiles of retinal transcripts were then compared between dark-adapted and light-exposed arrestin -/-, pigmented wild-type and BALB/c mice at a time point when morphological changes were minimal. As expected, the dark-adapted samples showed little difference in expression pattern between the three genotypes. Among the genes differentially regulated by light in BALB/c, but not arrestin -/- retinas, were c-fos and other stress-induced early response genes. In both mouse models, a marked increase in expression of the bZIP family of transcription factors was observed. Our results show a select group of unique and overlapping sets of genes induced by light in the two mouse models. These expression changes may constitute the underlying initiating events leading to the two distinct mechanisms of light damage.

Animals↗
PubMed2004

Transitional cell carcinoma in renal transplant recipients.

We describe our experience in managing transitional cell carcinoma (TCC) in renal transplant (RTx) recipients. Nineteen RTx recipients (7 men; 12 women) presented with hematuria or hydronephrosis of native kidneys and were suspected with TCC were reviewed retrospectively; 17 of them proved to have TCC. The mean interval of the occurrence of TCC was 58.7 months (range, 3-144 months) after RTx. The patients with suspected upper tract lesions received bilateral nephroureterectomies (BNU) and bladder cuff resection. Transurethral resection of the bladder tumor (TUR-BT) was performed in patients with concomitant or solitary superficial bladder lesions. Of the 15 patients with upper tract TCC, 8 had bilateral lesions pathologically, but only 2 of them were suspected preoperatively on image study. With a mean follow-up of 28 months (range, 1-57 months) both the overall graft and patient survival rates were 76%; 4 patients with advanced diseases at presentation died. Bladder recurrence was noted in 6 patients (35%). Transplant patients with hematuria warrant detailed study of the whole urinary system and periodic ultrasonography of the native kidneys is recommended in all RTx recipients. Simultaneous BNU for the native kidneys is mandatory if there is any evidence of TCC in either renal/ureteral unit.

Carcinoma, Transitional Cell↗
PubMed2004

Pharmacokinetic variability of sirolimus in Taiwanese renal transplant recipients.

To evaluate the pharmacokinetic variability of sirolimus (Rapamycin, SRL) in our renal transplant (RTx) recipients, dose-normalized trough concentration (C(0)) of SRL, and their intrasubject coefficients of variation (%CV) were analyzed. Thirty-eight patients were enrolled in regimens containing SRL. Concomitant immunosuppression included steroids (n = 38), cyclosporine (n = 33), tacrolimus (n = 3), and mycophenolate mofetil (n = 7). The mean dose-normalized C(0) was 2.13 +/- 0.91 ng/mL/mg. The intrasubject %CV of the dose-normalized C(0) ranged from 14% to 88% and averaged 42% in our series. The mean dose-normalized C(0) of SRL in our RTx recipients was much lower than that reported in Phase III trials. The intrasubject variation of dose-normalized C(0), even after administrating SRL for 6 months, could still be quite prominent. Thus, we suggest that, to maintain adequate therapeutic concentrations, periodic (monthly or bimonthly) SRL C(0) measurement is necessary in Taiwanese (Oriental) patients receiving SRL.

Cyclosporine↗
PubMed2004

The utility of resistance index of distal interlobular arteries in evaluating renal graft function.

The correlations of the mean values of resistance index (RI) of the distal interlobular, arcuate, and interlobal arteries of the kidneys were evaluated with HDI 5000 ultrasonographic system using a 2- to 5-mHz scan probe under the power Doppler detection mode in 60 patients with various native renal conditions and 70 renal allografts. The mean values of RIs of the distal interlobular arteries and those of the interlobal arteries in the renal allografts were significantly correlated with the recipients' renal functions (P = .015 and .030, respectively), whereas those of arcuate arteries were not.

Creatinine↗
PubMed2004

Intrasplenic transplantation of allogeneic hepatocytes modified by BCL-2 gene protects rats from acute liver failure.

BACKGROUND: Apoptosis of donor hepatocytes may be induced by recipient cytotoxic T lymphocytes (CTLs) during acute rejection, representing a major impediment for these cell transplants. Because the mechanisms of transplanted hepatocyte loss involve Fas-mediated pathways, BCL-2 genetic modification may protect liver cells. In the present study, we further investigated whether BCL-2 transfer into transplanted liver cells rendered them resistant to Fas ligand-induced apoptosis, and protected rats from acute liver failure. MATERIALS AND METHODS: Hepatocytes isolated from Sprague-Dawley rats were infected with an adenovirus vector encoding human BCL-2 gene (AdCMVBCL-2) or a control AdCMVLacZ vector. Forty-eight hours later, cells challenged with recombinant Fas ligand (rhsFasL) were assayed for apoptosis using TUNEL staining and caspase 3 activity. Other cells were transplanted into the spleens of Wistar rats with a 90% hepatectomy 12 hours later. RESULTS: Western blot analysis and RT-PCR confirmed the expression of hBcl-2 in AdCMVhBcl-2-infected hepatocytes. Recombinant FasL produced a dose-dependent increase in TUNEL-positive percentage and caspase-3 activity in uninfected hepatocytes, but did not influence these features in AdCMVhBcl-2-infected cells. On challenge with 90% hepatectomy, the survival of Wistar rats receiving transplantation of AdCMVhBCL-2-infected hepatocytes was significantly prolonged compared with the controls. CONCLUSION: Adenovirus-mediated BCL-2 gene transfer protects transplanted hepatocytes from Fas-mediated cytolysis, thus holding promise for a new avenue of acute liver failure treatment.

Adenoviridae↗