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J P Xu

Publications and source records attributed to J P Xu.

At least 19 recordsLinked to original sources

Distribution and sources of surfzone bacteria at Huntington Beach before and after disinfection on an ocean outfall-- a frequency-domain analysis.

Fecal indicator bacteria (FIB) were measured approximately 5 days a week in ankle-depth water at 19 surfzone stations along Huntington Beach and Newport Beach, California, from 1998 to the end of 2003. These sampling periods span the time before and after treated sewage effluent, discharged into the coastal ocean from the local outfall, was disinfected. Bacterial samples were also taken in the vicinity of the outfall during the pre- and post-disinfection periods. Our analysis of the results from both data sets suggest that land-based sources, rather than the local outfall, were the source of the FIB responsible for the frequent closures and postings of local beaches in the summers of 2001 and 2002. Because the annual cycle is the dominant frequency in the fecal and total coliform data sets at most sampling stations, we infer that sources associated with local runoff were responsible for the majority of coliform contamination along wide stretches of the beach. The dominant fortnightly cycle in enterococci at many surfzone sampling stations suggests that the source for these relatively frequent bacteria contamination events in summer is related to the wetting and draining of the land due to the large tidal excursions found during spring tides. Along the most frequently closed section of the beach at stations 3N-15N, the fortnightly cycle is dominant in all FIBs. The strikingly different spatial and spectral patterns found in coliform and in enterococci suggest the presence of different sources, at least for large sections of beach. The presence of a relatively large enterococci fortnightly cycle along the beaches near Newport Harbor indicates that contamination sources similar to those found off Huntington Beach are present, though not at high enough levels to close the Newport beaches.

Bacteria↗

Diagnosis of human cytomegalovirus intrauterine infection using fetal cells from maternal blood.

OBJECTIVE: The sensitivity and specificity for the noninvasive prenatal diagnosis of human cytomegalovirus intrauterine infection were estimated by using isolating single fetal cells from maternal peripheral blood. METHODS: Micromanipulation techniques were employed to isolate single fetal nucleated erythroblasts from 273 maternal blood samples. SRY gene and HCMV-DNA in single fetal cells were detected by multiple primed in situ labeling (PRINS) from 76 HCMV-DNA positive samples of maternal peripheral blood. 273 samples of maternal peripheral blood were tested for SRY gene and HCMV-DNA in single fetal cells by primed extension preamplification (PEP) and polymerase chain reaction (PCR). RESULTS: The detection rate of fetal cells from maternal blood was 100% with micromanipulation techniques. The sensitivity of PRINS for SRY gene detection was 97.56% and its specificity was 100%. The sensitivity and specificity of PEP and PCR for SRY gene detection were 97.39% and 99.17%, respectively. The sensitivity of PRINS for HCMV-DNA detection was 92.68% and the specificity was 100%. The sensitivity and specificity of PEP and PCR for HCMV-DNA detection were 95.12%and 100%, respectively. CONCLUSION: The technique for noninvasive prenatal detection of intrauterine infection of HCMV using single fetal cells from maternal peripheral blood by using PRINS and PEP and PCR is more reliable than the CMV-DNA detection in peripheral maternal blood, amniocentesis or percutaneous umbilical blood sampling.

Cytomegalovirus↗

Fetal origin of single nucleated erythroblasts and free DNA in the peripheral blood of pregnant women.

OBJECTIVES: To investigate the feasibility of using single fetal nucleated erythroblasts (FNRBCs) and free DNA in maternal blood for non-invasive prenatal diagnosis. METHODS: Single FNRBCs were isolated from 51 of 116 samples of maternal blood analyzed by micromanipulation after density gradient centrifugation. Furthermore, the nested polymerase chain reaction (PCR) method was used to amplify the SRY gene of single FNRBCs. Primer extension pre-amplification and nested PCR were used to amplify the SRY gene of the plasma DNA extracted from 65 samples of maternal blood. RESULTS: The detection rate of single FNRBCs was 90.20% (46/51). The concordance rates between real fetal sex and sex determined by amplification of the SRY gene from single cells and from free DNA analysis were 82.61% (38/46) and 90.77% (59/65), respectively. CONCLUSIONS: Single nucleated erythroblasts and free DNA in maternal blood are of fetal origin and can be valuable fetal material sources for non-invasive prenatal diagnosis.

Adult↗

Effects of long-term enalapril and losartan therapy of heart failure on cardiovascular aldosterone.

Plasma aldosterone escape is found during long-term ACE inhibitor therapy of chronic heart failure. Evidence for aldosterone production in cardiovascular tissues raised the question of whether aldosterone escape occurs or not in these tissues. Rats with infarction-induced chronic heart failure were treated with enalapril (20 mg/kg/d) and losartan (15 mg/kg/d) for 20 weeks. Untreated chronic heart failure and sham-operated rats were used as positive and normal controls, respectively. Ex vivo mesenteric artery and heart perfusion, high performance liquid chromatography, and RIA for aldosterone were performed. Chronic heart failure due to myocardial infarction was associated with tissue-specific activation of cardiovascular aldosterone synthesis. In the mesenteric artery, enalapril significantly inhibited aldosterone production compared to untreated, chronic heart failure rats, and losartan lowered aldosterone production to that of sham rats. In myocardium, enalapril failed to significantly inhibit aldosterone production, and losartan significantly inhibited aldosterone production compared to untreated, chronic heart failure rats. These results provide the first evidence that long-term ACE inhibition therapy induces aldosterone escape in myocardium but not in mesenteric artery of chronic heart failure. The angiotensin II subtype 1 receptor blocker losartan tranquilized aldosterone levels in the cardiovascular tissues of chronic heart failure rats.

Aldosterone↗

Selenium, iodine and fungal contamination in Yulin District (People's Republic of China) endemic for Kashin-Beck disease.

We studied the status of selenium, iodine and fungal contamination in 353 school children (age 5-14 years) from four rural villages in the District of Yulin. In three villages Kashin-Beck disease (KBD) was endemic, whereas there were no cases of KBD in the fourth village. Clinical, biological and radiological examinations (right hand) were performed and KBD was established by X-ray diagnosis. The prevalence rate of KBD was 30.2%, 44.2% and 45.3% in the three endemic villages. Mean hair selenium and urine iodine concentrations were lower in affected than in unaffected children and fungal contamination in cereal grains stored in families with KBD was more elevated than in families without KBD. Low hair selenium concentration and presence of fungal cereal contamination were significantly associated with an increased risk of KBD, but low urine iodine was not.

Adolescent↗

[High-level expression of human calmodulin in E. coli and its effects on cell proliferation].

The gene coding for human CaM was amplified by PCR in which pUC/hCaM3 cDNA was usd as template. After inserting the hCaM III cDNA into the expression plasmid pBV220, we constructed the hCaM3 cDNA-recombinant expression vector(hCaM3/pBV220). The recombinant plasmid was then transformed into E. coli DH5 alpha. After heat induction, a high level expression of CaM protein was obtained. SDS-PAGE analysis showed that the recombinant E. coli could express a 17 kD protein which accounted for about 20% of the total cellular protein. Western blot analysis showed that anti-CaM monoclonal antibody(McAb) specifically bound to the 17 kD band of expression product. rhCaM was purified by Phenyl-sepharose CL-4B affinity chromatography from recombinant bacterial lysate. 3-4 mg of the purified protein were obtained from 1 liter of bacterial culture. The rhCaM was able to activate NAD kinase to the same extent as the standard human brain CaM (Sigma). K562 cells and SP2/0 cells were seeded in 24-well or 96-well plate and cultured for 48 h with rhCaM and CaM-antagonist trifluoperazine(TFP). Cell proliferation rates was determined by MTT assay. There was a significant positive correlation between the concentrations of rhCaM and the cell proliferation rates. CaM-antagonist TFP had an inhibitory effect on cell proliferation rate. The inhibition could be corrected by the addition of extracellular rhCaM.

Animals↗

[Inhibitory effects of melatonin on the development of 17-beta-estradiol induced prolactinoma in relation to plasma prolactin and peroxidative lipid contents].

In the present study, we have examined inhibitory effects of melatonin on the development of pituitary prolactin-producing tumors (prolactinoma) induced by 17-beta-estradiol (E(2)) in vivo. The prolactinomas were established by implanting E(2)-laden silastic capsules subcutaneously in Sprague-Dawley male rats weighing 80 approximately 100 g. Melatonin (0.05, 0.25, 0.50, 1.00, and 2.00 mg/0.1 ml/rat) was administrated subcutaneously at l8:00 h for 90 days, beginning from d 7 prior to tumor induction. Controls were given equal volumes of 4 percent; alcohol in 0.9 percent; saline. Our results showed: (1) In control group and groups given respectively 0.05, 0.25, 0.50, 1.00 and 2.00 mg melatonin, the weight of prolactinoma was 115.0+/-71.0, 85.2+/-41.0, 58.9+/-24.1, 72.7+/-23.6, 79.3+/-56.1, 74.5+/-46.8 mg respectively; the plasma prolactin (PRL) content was 493.46+/-33.3, 373.78+/-26.5, 125.13+/-13.3, 201.79+/-11.2, 418.88+/-41.3, 281.94+/-36.4 ng/ml respectively; the plasma peroxidative lipid content was 1.21+/-0.23, 0.89+/-0.32, 0.92+/-0.27, 0.64+/-0.24, 0.41+/-0.14 and 0.43+/-0.21 delta233/ml respectively. (2) The correlation coefficients between tumor weight and plasma PRL content, tumor weight and plasma peroxidative lipid content, and plasma PRL content and plasma peroxidative lipid content were 0.8738, 0.5550 and 0.2141 respectively. These results indicate: (1) The dosages of 0.25 (P<0.01) and 0.50 (P<0.05) mg, but not 0.05 (P>0.05), 1.00 (P>0.05) and 2.00 (P>0.05) mg, melatonin significantly inhibited the development of the E(2)-induced prolactinoma and the secretion of PRL in comparison with the matched control. (2) The levels of 0.05 approximately 2.00 (P<0.05 approximately 0.00l) mg melatonin showed a dose-dependent antioxidative action. (3) There are positive correlation between tumor weight and plasma PRL content (P<0.05), but no correlation between tumor weight and plasma peroxidative lipid content (P>0.05), and plasma PRL content and plasma peroxidative lipid content (P>0.05). Therefore, our experiments demonstrate that the inhibition of the development of E(2)-induced prolactinoma by adequate dosage of melatonin may be related to the inhibitory effects of MLT on the secretion of PRL, but not to the antioxidative action of MLT.

Animals↗

[Inhibitory effect of melatonin on the development of pituitary prolactin-producing tumors induced by 17-beta-estradiol].

OBJECTIVE: To examine the inhibitory effect of melatonin (MLT) on the development of pituitary prolactin-producing tumors (prolactinoma) induced by 17-beta-estradiol (E2), in vivo, and explore MLT's oncostatic mechanisms. METHODS: The prolactinomas were established by implanting E2-laden silastic capsules subcutaneously in Sprague-Dawley male rats. MLT doses 0.05, 0.25, 0.50, 1.00, and 2.00 mg/rat were administrated separately to 5 groups subcutaneously starting seven days prior to tumor induction for 97 days. The matched controls were given equal volumes of 4% alcohol in saline. RESULTS: (1) The prolactinoma weights in 0.05, 0.25, 0.50, 1.00 and 2.00 mg MLT dose groups were 25.91% (P > 0.05), 48.78% (P < 0.01), 36.78% (P < 0.05), 31.04% (P > 0.05) and 35.22% (P > 0.05) respectively which were lower than that of control group; (2) The PRL mRNA levels of prolactinoma in 0.05, 0.25, and 0.50 mg MLT dose groups were 33.67% (P < 0.05), 25.51% (P < 0.05) and 41.84% (P < 0.01) respectively which were lower than that of control group as estimated by Northern Blot, and the in situ hybridization studies; (3) The DNA contents of prolactinoma in 0.05, 0.25 and 0.50 mg MLT dose groups were 40.73% (P < 0.001), 51.15% (P < 0.001) and 60.23% (P < 0.001) respectively which were lower than that of control group by laser scanning confocal microscopy; (4) Plasma peroxidative lipid contents in 0.05, 0.25, 0.50, 1.00 and 2.00 mg MLT dose groups were 26.45% (P < 0.05), 23.97% (P < 0.05), 47.11% (P < 0.001), 66.12%(P < 0.001) and 64.46% (P < 0.001) respectively which were lower than that of control group. The correlation coefficient between MLT doses and plasma peroxidative lipid contents was -0.8257 (P < 0.05). CONCLUSIONS: MLT in suitable doses is able to inhibit the development of E2-induced prolactinoma by inhibiting the expression of PRL gene and the DNA synthesis. The link between MLT antioxidative action and its inhibitory effect on development of prolactinoma should be further investigated.

Animals↗

Human 3'-phosphoadenosine 5'-phosphosulfate synthetase 1 (PAPSS1) and PAPSS2: gene cloning, characterization and chromosomal localization.

Sulfae conjugation is an important pathway in the metabolism of a large number of exogenous and endogenous compounds. These reactions are catalyzed by sulfotransferase (SULT) enzymes that utilize 3'-phosphoadenosine 5'-phosphosulfate (PAPS) as a sulfate donor. PAPS is synthesized from ATP and inorganic sulfate by PAPS synthetase (PAPSS). Two separate PAPSS cDNAs, PAPSS1 and PAPSS2, have been identified in human tissues. We have cloned and characterized the genes for human PAPSS1 and PAPSS2 to make it possible to study the pharmacogenomics of these enzymes. Both genes consisted of 12 exons with virtually identical exon-intron splice junction locations. All splice junctions conformed to the "GT-AG" rule. The total length of PAPSS1 was approximately 108 kb, while that of PAPSS2 was greater than 37 kb. The 5'-flanking region of PAPSS1 did not include a TATA box sequence near the site of transcription initiation, but PAPSS2 had a TATA motif located 21 bp upstream from the site of transcription initiation. Northern blot analysis showed that the major PAPSS1 and PAPSS2 transcripts were approximately 2.7 and 4.2 kb in length, respectively. PAPSS1 mapped to human chromosome band 4q24 while PAPSS2 mapped to 10q22-23 by fluorescence in situ hybridization analysis. Cloning and structural characterization of PAPSS1 and PAPSS2 will make it possible to perform molecular genetic and pharmacogenomic studies of these important enzymes in humans.

Blotting, Northern↗

Synthesis of the marine sponge cycloheptapeptide phakellistatin 5(1).

Phakellistatin 5 (1), a constituent of The Federated States of Micronesia (Chuuk) marine sponge Phakellia costada, was synthesized by solution-phase and solid-phase techniques. Because the linear peptide bearing (R)-Asn resisted cyclization, the synthesis of this peptide was repeated using the PAL resin attachment proceeding from N-Fmoc-D-Asp-alpha-OCH(2)CH=CH(2). After addition of the final unit (Ala), the allyl ester was removed under neutral conditions with Pd(o) [P(C(6)H(5))(3)](4). Removal of the final Fmoc-protecting group and cyclization with PyAOP provided (R)-Asn-phakellistatin 5 (2) in 28% overall yield. The same synthetic route from (S)-Asp led to natural phakellistatin 5 (1) in 15% overall recovery. The solution-phase and solid-phase synthetic products derived from (S)-Asp were found to be chemically but not biologically identical with natural phakellistatin 5 (1). This important fact suggested that a trace, albeit highly cancer-cell growth inhibitory, constituent accompanied the natural product or that there is a subtle conformational difference between the synthetic and natural cyclic peptides.

Animals↗

Regulation of nitric oxide synthase to promote cytostasis in ovarian follicular development.

Our own recent studies have demonstrated that inducible nitric oxide synthase (iNOS) is predominantly localized in granulosa cells of healthy immature follicles in the rat ovary, whereas granulosa cells of either healthy mature follicles or follicles destined to be atretic are devoid of iNOS. These findings suggest that iNOS is pivotal for immature follicles to remain dormant. To test this hypothesis, we examined the effects of a GnRH agonist (buserelin), a proapoptotic substance, and epidermal growth factor (EGF), a mitogenic and, consequently, antiapoptotic factor, on the amount of iNOS mRNA in rat granulosa cells. Administration of buserelin in immature female rats transiently diminished iNOS mRNA levels in the ovaries as determined by Northern blot analysis. In cultured rat granulosa cells, buserelin and EGF increased the incidence of apoptosis and DNA synthesis, respectively, whereas both reduced iNOS mRNA levels as determined by reverse transcription-coupled polymerase chain reaction. The concomitant addition of S-nitroso-N-acetyl-DL-penicillamine, an NO donor, together with buserelin or EGF eliminated the observed effects of these substances (i.e., induction of apoptosis and stimulation of DNA synthesis, respectively). These results suggest that the changes in developmental status of immature follicles either into development or atresia are associated with reduced iNOS levels in granulosa cells, thus reinforcing the notion of NO as a cytostatic factor in ovarian follicles.

Animals↗

[Expression of 2.1 kb enhancin gene fragment from Helicoverpa armigera granulosis virus in Escherichia coli].

The 2.1 kb fragment of enhancin gene from Helicoverpa armigera granulosis virus was inserted into vector pQE-30 and expressed successfully in E. coli M15(pREP4). The synergy of expression product(P78) on AcMNPV against the larvae of Plutella xylostella was also studied. The results indicated that the percentage of correct mortality of the larvae increased 27.88%-32.92% in 10 post-infection days.

Baculoviridae↗

Expression of Fas-Fas ligand in murine testis.

PROBLEM: During spermatogenesis, it has been suggested that the number of germ cells to be matured is regulated and restricted through the apoptotic mechanism. In the present study, we investigated the expression and apoptotic role of Fas and Fas ligand (L) in the murine testis. METHOD OF STUDY: The expression of Fas-FasL in the murine testis was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR)-Southern blot hybridization, in situ hybridization, and Western blot methods. The terminal deoxynucleotide transferase mediated dUTP-nick end label (TUNEL) and DNA fragmentation methods were applied to detect the generation of apoptosis in germ cells. RESULTS: By means of RT-PCR-Southern blot hybridization, we demonstrated the positive expression of Fas in testicular germ cells, and of FasL in testicular cells. supporting the findings with in situ hybridization that Fas was localized in germ cells, whereas FasL was localized in Sertoli cells of murine testis. A specific band at 45 kDa was obtained in the lysates from testis and germ cells with Western blot analysis. Then, the co-incubation of germ cells with Spodoptera frugiperda (Sf9)-FasL cells in vitro resulted in the induction of apoptosis in germ cells detected by the TUNEL method. Furthermore, DNA fragmented ladders were also demonstrated in germ cells co-incubated with Sf9-FasL cells. CONCLUSION: Fas-FasL system seemed to play an apoptotic role in spermatogenesis by the molecular interaction between FasL on Sertoli cells and Fas on germ cells.

Animals↗

Effects of hypoxia/reoxygenation and cytokines on adhesion of leukocytes to cerebral microvascular endothelial cells.

AIM: To study the influence of hypoxia/reoxygenation (H/R) on the adhesion of neutrophils (Neu) and monocytes (Mon) to cultured bovine cerebral microvascular cells induced by tumor necrosis factor alpha (TNF-alpha) or interleukin 1-alpha (IL-1 alpha). METHODS: Bovine cerebral microvascular endothelial cells (CMEC) and smooth muscle cells (CMSMC) were exposed to normoxia or H/R in the presence or absence of TNF-alpha (IL-1 alpha). The number of adhesions of Mon and Neu to CMEC and CMSMC was measured by flow cytometry. RESULTS: CMEC were subjected to hypoxia for 2 h followed by reoxygenation with TNF-alpha (2 micrograms.L-1) for 2 h, the adhesion rate of CMEC for Mon and Neu were increased to 35.0% +/- 0.9% and 36.0% +/- 0.6% (the TNF-alpha treated group was 28.9% +/- 1.1% and 28.8% +/- 1.3%), respectively. CMSMC were treated as above, the adhesion rate of Mon and Neu was enhanced to 49.9% +/- 0.4% and 43.9% +/- 1.4% (the TNF-alpha treated group was 34.0% +/- 1.9% and 34.0% +/- 1.3%), respectively. CMEC and CMSMC were treated by IL-1 alpha, similar results were obtained. CONCLUSION: H/R enhanced the adhesion of Mon and Neu to CMEC and CMSMC induced by TNF-alpha or IL-1 alpha.

Animals↗

Antagonistic effects of Ginkgo biloba extract on adhesion of monocytes and neutrophils to cultured cerebral microvascular endothelial cells.

AIM: To study the action of Ginkgo biloba extract (GbE) on tumor necrosis factor (TNF-alpha)-induced adhesion of monocytes (Mon) and neutrophils (Neu) to cultured cerebral microvascular endothelial cells. METHODS: TNF-alpha-induced endothelial adhesivity toward Mon and Neu was studied using bovine cerebral microvascular endothelial cells (BCMEC) in vitro. The number of Mon and Neu adhering to the BCMEC monolayers was determined by flow cytometry. RESULTS: Pretreatment of BCMEC with TNF-alpha increased Mon and Neu adhesion to BCMEC from 12.5% +/- 0.2% to 31.3% +/- 0.5% and from 13.8% +/- 0.4% to 32.1% +/- 0.5%, respectively. GbE (1-100 mg.L-1) inhibited the effect of TNF-alpha in a concentration-dependent manner. E-selectin mAb (1 mg.L-1) blocked Mon and Neu adhesion to BCMEC induced by TNF-alpha. CONCLUSION: The inhibition of GbE on Mon and Neu adhesion to BCMEC was mediated through the suppression of E-selection expression.

Animals↗

Ureaplasma urealyticum infection and apoptosis of spermatogenic cells.

AIM: To study the relationship between Ureaplasma urealyticum (UU) infection and apoptosis of human spermatogenic cells. METHODS: Spermatogenic cells were observed under light microscope with Wright-Giemsa staining and by means of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (dUTP)-biotin nick-end labeling (TUNEL) technique. RESULTS: Apoptotic rate of UU-infected males (15.5% +/- 6.8%) was significantly higher than that of controls (5.2% +/- 2.3%). CONCLUSION: Apoptosis of spermatogenic cells can be caused by UU infection, which provides further evidence for UU-induced male infertility.

Adult↗

Studies on apoptosis of spermatogenic cells in normal fertile men treated with supraphysiological doses of testosterone undecanoate.

AIM: To study the anti-spermatogenic mechanism of supra-physiological doses of testosterone undecanoate (TU). METHODS: Twenty fertile adult men received four intramuscular injections of TU at monthly intervals, 1000 mg upon admission and 500 mg for the subsequent injections. The apoptotic germ cells in the semen were studied under light microscope with terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) and Wright-Giemsa staining methods. RESULTS: After treatment, the sperm density and the number of spermatogenic cells in the semen were significantly decreased (P < 0.01), while the apoptotic ratios of spermatocytes and spermatids increased significantly (P < 0.01) as compared with the pretreatment levels. Apoptosis was found to be augmented in the whole series of castoff spermatogenic cells. CONCLUSION: Besides its suppressive effect on spermatogenesis through a negative feed-back mechanism, TU enhances apoptosis of spermatogenic cells, which may be an additional mechanism of its anti-spermatogenic activity.

Apoptosis↗

[Expression of prolactin, TGF alpha and TGF beta 1 genes in estrogen-induced eutopic and ectopic pituitary prolactin-secreting tumors of rats].

The Sprague-Dawley (SD) rat bearing a heteroplasted pituitary underneath renal capsule was used to observe differential expression of prolactin (PRL), transforming growth factor alpha (TGF alpha) and transforming growth factor beta 1 (TGF beta 1) genes during the formation of pituitary prolactin-secreting tumor (prolactinoma) induced by 17 beta-estradiol (E2). Our results indicated that in both eutopic and ectopic pituitaries disconnected from hypothalamus formed simultaneously PRL-secreting tumors after the rats treated with E2 for 120 days in vivo, which was accompanied by overexpression of PRL gene (P < 0.05-0.01). The PRL mRNA level was higher in eutopic prolactinoma than that in ectopic prolactinoma (P < 0.05). Overexpression of TGF alpha and TGF beta 1 genes were also detected in eutopic prolactinoma. However, the expression of TGF alpha and TGF beta 1 genes in ectopic prolactinoma was similar to that in normal pituitary. It is suggested that TGF alpha and TGF beta 1 may be involved in prolactinoma tumorigenesis of eutopic pituitary. However, the mechanism mediating eutopic and ectopic prolactin-secreting tumor formation seems different.

Animals↗