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C Chen

Publications and source records attributed to C Chen.

At least 235 records · Page 13Linked to original sources

Hypothalamic dopaminergic receptor expressions in anorexia of tumor-bearing rats.

Our past microdialysis studies in ventromedial hypothalamic nucleus (VMN) and lateral hypothalamic area (LHA) of changes in dopamine concentrations in response to changes in food intake [characterized as feeding pattern (changes in meal number and size)] in anorexia of cancer show abnormal presynaptic dopaminergic neurotransmission. To determine postsynaptic receptor status, studies were done in tumor-bearing (TB) and non-tumor-bearing (NTB) free-feeding control rats while continuously measuring their food intake via a rat eater meter. When TB rats developed anorexia, TB and control rats were killed, and postsynaptic D(1)- and D(2)-receptor mRNA expression in LHA and VMN were measured via RT-PCR. At anorexia, food intake decreased initially by a decrease in meal number, whereas a concurrent increase in meal size occurred for 24 h in an attempt to maintain food intake constant. Then meal size also decreased. At this time, D(1)- and D(2)-receptor mRNA expressions in LHA and VMN of TB vs. controls were significantly upregulated. Verification of D(1)- or D(2)-receptor changes to changes in meal number and size at anorexia was made by injection of intra-VMN or -LHA dopaminergic receptor antagonists. Intra-VMN D(1)-receptor antagonist (SCH-23390) in TB rats decreased food intake mainly via a decrease in meal size. Intra-VMN D(2)-receptor antagonist (sulpiride) in TB rats increased food intake via an increase in meal number and in NTB free-feeding rats by an increase in meal size. Intra-LHA D(1)-receptor antagonist in TB rats had no effect on food intake or feeding pattern. Intra-LHA D(2)-receptor antagonist in TB and in NTB free-feeding rats increased food intake via an increase in meal number. Our data provide evidence that postsynaptic dopaminergic receptor subtypes in the hypothalamus are involved in the regulation of meal size, meal number, and thus food intake in anorectic TB rats.

Actins↗

Attenuated LTP in hippocampal dentate gyrus neurons of mice deficient in the PAF receptor.

Platelet-activating factor (PAF), a bioactive lipid (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) derived from phospholipase A(2) and other pathways, has been implicated in neural plasticity and memory formation. Long-term potentiation (LTP) can be induced by the application of PAF and blocked by a PAF receptor (PAF-R) inhibitor in the hippocampal CA1 and dentate gyrus. To further investigate the role of PAF in synaptic plasticity, we compared LTP in dentate granule cells from hippocampal slices of adult mice deficient in the PAF-R and their age-matched wild-type littermates. Whole cell patch-clamp recordings were made in the current-clamp mode. LTP in the perforant path was induced by a high-frequency stimulation (HFS) and defined as >20% increase above baseline of the amplitude of excitatory postsynaptic potentials (EPSPs) from 26 to 30 min after HFS. HFS-induced enhancement of the EPSP amplitude was attenuated in cells from the PAF-R-deficient mice (163 +/- 14%, mean +/- SE; n = 32) when compared with that in wild-type mice (219 +/- 17%, n = 32). The incidence of LTP induction was also lower in the cells from the deficient mice (72%, 23 of 32 cells) than in the wild-type mice (91%, 29 of 32 cells). Using paired-pulse facilitation as a synaptic pathway discrimination, it appeared that there were differences in LTP magnitudes in the lateral perforant path but not in the medial perforant path between the two groups. BN52021 (5 microM), a PAF synaptosomal receptor antagonist, reduced LTP in the lateral path in the wild-type mice. However, neither BN52021, nor BN50730 (5 microM), a microsomal PAF-R antagonist, reduced LTP in the lateral perforant path in the receptor-deficient mice. These data provide evidence that PAF-R-deficient mice are a useful model to study LTP in the dentate gyrus and support the notion that PAF actively participates in hippocampal synaptic plasticity.

Animals↗

Mechanisms of lectin (phytohemagglutinin)-induced growth in small intestinal epithelial cells.

BACKGROUND/AIMS: The lectin phytohemagglutinin is a mitogen for intestinal epithelial cells in vivo. The mechanisms of action are unknown and were therefore analyzed in vitro. METHODS: Human (Intestine-407) and rat (IEC-6; IEC-18) intestinal epithelial cell lines were stimulated with phytohemagglutinin. Proliferation was assayed by (3)H-thymidine incorporation, activation of mitogen-activated protein kinase (MAPK) by Western blotting, and induction of c-fos mRNA expression by semiquantitative polymerase chain reaction. Control experiments were performed with phenyl-N-acetyl-alpha-D-galactosaminide or the tyrosine kinase inhibitor tyrphostin A25. RESULTS: Phytohemagglutinin (0.1 microg/ml) significantly stimulated proliferation in all three cell lines after 48-72 h. MAPK activation was detected after 15-30 min, and an induction of c-fos mRNA expression after 15- 30 min of stimulation. Mitogenic effects were blocked by preincubation with phenyl-N-acetyl-alpha-D-galactosaminide or tyrphostin A25. CONCLUSION: Phytohemagglutinin stimulated proliferation, MAPK activation and induction of c-fos mRNA expression. The lectin may contribute to intestinal mucosal growth and regeneration thereby preventing gut atrophy.

Animals↗

Association of asthma with beta(2)-adrenergic receptor gene polymorphism and cigarette smoking.

Recent studies have suggested that two polymorphisms of the beta(2)-adrenergic receptor (beta(2)AR) gene at codons 16 (arginine to glycine) and 27 (glutamine to glutamate) affect an individual's airway responsiveness, or response to acute or chronic beta(2)-agonist therapy but are not risk factors for asthma. We hypothesize that there is an interaction effect on asthma between the beta(2)AR gene polymorphisms and cigarette smoking. A case-control study was conducted in 128 asthma cases and 136 control individuals identified from 10,014 studied subjects in rural Anqing, China. Allele-specific polymerase chain reaction (PCR) was used to genotype beta(2)AR gene polymorphisms. Multiple logistic regression was used to adjust for potential confounding factors. We found a marginally significant interaction between cigarette smoking and beta(2)AR-16 genotype after adjusting for important confounding factors (p = 0.06). Specifically, we found that compared with never-smoking Gly-16 homozygotes, those ever-smokers who are Arg-16 homozygotes had a significantly increased risk of asthma (odds ratio [OR] = 7.81; 95% confidence interval [CI]: 2.07 to 29.5). This association showed a clear dose-response relationship with the number of cigarettes smoked. However, there was no significant association of asthma with polymorphisms of the beta(2)AR at position 27 (OR = 1.38; 95% CI: 0.69 to 2.73). Our study suggests a gene-environment interaction between the Arg-16 genotype and ever cigarette smoking with respect to the susceptibility of an individual to asthma.

Adult↗

Direct modification of somatotrope function by long-term leptin treatment of primary cultured ovine pituitary cells.

Leptin is produced primarily in adipocytes and regulates body energy balance. A close link between leptin and pituitary hormones, including GH, has been reported. The mechanisms employed by leptin to influence somatotropes are not clear, however. Here we report a direct action of recombinant ovine leptin on primary cultured ovine somatotropes by analyzing the levels of mRNA encoding for GH or the receptors for GHRH (GHRH-R) and GH-releasing peptides (GHRP). Treatment of ovine somatotropes with leptin (10(-7)-10(-9) M) for 1-3 d reduced the mRNA levels encoding GH and GHRH-R, but increased GHRP receptor mRNA levels in a time- and dose-dependent manner. Three-day treatment of cells with leptin decreased the GH response to GHRH stimulation, but the GH response to GHRP-2 stimulation was increased. The combined effect of GHRH and GHRP-2 on GH secretion was not altered by treatment of the cells with leptin. These results demonstrated a direct action of leptin on ovine pituitary cells, leading to a reduced sensitivity of somatotropes to GHRH. It is also suggested that GHRP may be useful to correct the decrease in GHRH-induced GH secretion by leptin.

Animals↗

Parathyroid hormone stimulates fra-2 expression in osteoblastic cells in vitro and in vivo.

PTH and PTH-related protein (PTHrP) are key mediators of skeletal development and homeostasis through their activation of the PTH-1 receptor. Previous studies have found that several AP-1 family members are regulated by PTH, such as c-fos, fra-1, and c-jun. There are numerous genes in the bone microenvironment that contain AP-1 sites, and different Fos family members are reported to have opposing transcriptional activities at AP-1 sites. The purpose of this study was to identify the effects of PTH on expression of the AP-1 protein complex member, fra-2, to extend our understanding of transcriptional regulators of PTH action. PTH induction of fra-2 messenger RNA (mRNA) levels in MC3T3-E1 preosteoblastic cells was maximal with 0.1 microM PTH (1-34). The expression in vitro was greatest 1 h after treatment and was present with N-terminal PTH but not PTH (7-34) or (53-84). Cycloheximide treatment induced fra-2 expression, and actinomycin D inhibited basal and PTHrP-induced expression. AP-1 protein in nuclear extracts of MC3T3-E1 cells was increased with PTH treatment at 3 h and consisted of high levels of Fra-2 protein, as evidenced by a supershift in an electrophoretic mobility shift assay and Western blot analysis. Up-regulation of steady-state fra-2 mRNA was also noted in vivo, where injection of PTH (1-34) (20 microgram) resulted in a more-than-7-fold maximal increase in fra-2 mRNA expression in the calvaria of mice, after 1 h of treatment. These data add to the transcriptional mediators induced by PTH and suggest that the interplay of AP-1 family members will provide insight into regulatory pathways of PTH and PTHrP for their anabolic and catabolic actions in bone.

Animals↗

Association of airway responsiveness with asthma and persistent wheeze in a Chinese population.

STUDY OBJECTIVES: Data from a cross-sectional study were analyzed to examine the association of increased airway responsiveness with physician-diagnosed asthma and persistent wheeze. DESIGN: Two methods for calculating the provocative dose that decreases the airflow rate by 20% (PD(20)) were used as indexes for increased airway responsiveness: (1) a 20% drop in FEV(1) calculated from baseline FEV(1) (PD(20)b), and (2) a 20% drop in FEV(1) from FEV(1) measurements after inhalation of saline solution (PD(20)s). Both PD(20)b and PD(20)s were measured through induction by varying doses of methacholine. SETTING: Anqing, Anhui Province, China. PARTICIPANTS: Study subjects were 8 to 74 years of age and were classified into four groups: children (< 15 years old), young adults (15 to 29 years old), adults (30 to 44 years old), and older adults (> or 5 years old). INTERVENTIONS: The differences in estimated odds ratios of airway hyperresponsiveness with asthma and wheeze, sensitivity and specificity, and coefficients of variation were compared between PD(20)b and PD(20)s. The sample for analysis consisted of 10,284 subjects from 2,663 nuclear families with complete data on wheeze, asthma, and major potential confounding factors. MEASUREMENTS AND RESULTS: The prevalence of asthma in this sample was lowest in subjects with no demonstrable PD(20) and had a reverse dose-response relationship with PD(20) across all age groups. Using the receiver operating characteristic, the sensitivity and specificity of the PD(20)s or PD(20)b were found to be almost identical. A similar trend was found for persistent wheeze, although the estimated odds ratios for persistent wheeze appeared slightly smaller than those for physician-diagnosed asthma. CONCLUSIONS: This study demonstrates a dose-response relationship between increased airway responsiveness and asthma and wheeze in this Chinese population. PD(20)s or PD(20)b yielded virtually indistinguishable results, which indicated that either of the two tests could serve as an index of airway hyperresponsiveness.

Adolescent↗

Effects of micromolar concentrations of manganese, copper, and zinc on alpha1-adrenoceptor-mediating contraction in rat aorta.

To determine the influences of the Mn, Cu, and Zn on alpha1-adrenoceptor (AR)-mediated vasoconstriction, we investigated their effects on vasoconstriction produced by the alpha1-AR agonist phenylephrine in isolated rings of rat thoracic aorta. The cumulative concentration-contraction curves for phenylephrine were obtained in the absence and presence of Mn (0.3, 1, 3 microM), Cu (1, 10, 16 microM), and Zn (0.3, 1, 10 microM). Mn, Cu, and Zn each inhibited phenylephrine-mediated contraction in a dose-dependent manner. The maximal phenylephrine-induced contraction was significantly reduced by the pretreatment of the arterial rings with 10 and 16 microM Cu (p<0.05). The results suggest that variations in the plasma concentrations of metal might lead to changes in alpha1-AR-mediated constrictive response.

Adrenergic alpha-1 Receptor Agonists↗

The in vitro effect of leptin on growth hormone secretion from primary cultured ovine somatotrophs.

Although existing data suggest an influence of leptin on circulating levels of growth hormone (GH), the action site and properties of leptin are still controversial. Using primary cultured ovine pituitary cells, we studied the direct effect of leptin on the secretion of GH. Pituitary cells were dissociated by collagenase and subjected to Percoll gradient centrifugation to enrich the somatotroph population to 60-80% of cells. Treatment of primary cultured ovine somatotrophs with leptin (10(-9)-10(-7) M) for 30 min did not affect basal, GH-releasing hormone (GHRH) (10(-7) M)- or GH-releasing peptide-2 (GHRP-2)(10(-7) M)-stimulated GH secretion. Following treatment of cells for 1-3 d with leptin, GHRH-stimulated GH secretion was reduced and GHRP-2-stimulated GH secretion increased. The combined effect of GHRH and GHRP-2 on GH secretion was not altered by the treatment of cells with leptin for 3 d. GHRH receptor mRNA levels in cultured somatotrophs were decreased but GHRP receptor mRNA levels were increased by 3-d leptin treatment. These results suggest that leptin has a long-term effect on somatotrophs to reduce GHRH receptor synthesis leading to a decrease in GHRH-stimulated GH secretion. Leptin appears, however, to have an opposite effect on GHRP receptor synthesis leading to an increase in GHRP-stimulated GH secretion.

Animals↗

Administration of unmodified prolactin (U-PRL) and a molecular mimic of phosphorylated prolactin (PP-PRL) during rat pregnancy provides evidence that the U-PRL:PP-PRL ratio is crucial to the normal development of pup tissues.

During rat pregnancy initial high concentrations of prolactin (PRL) decline by about day 9, concomitant with an increase in the ratio of unmodified to phosphorylated PRL. The physiological significance of both the decline in total PRL and the change in ratio of the two PRLs is unknown. To test the importance of each, either unmodified PRL (U-PRL) or a molecular mimic of phosphorylated PRL (PP-PRL) were continuously administered to rats throughout pregnancy. A dose of 6 microg/24 h resulted in circulating concentrations of 50 ng/ml of each administered PRL and had little effect on the pregnancy itself. After birth, pups were killed and various tissues examined. In the pup lungs, exposure to additional PP-PRL caused a reduction in epithelial integrity and an increase in apoptosis, whereas exposure to additional U-PRL had beneficial, anti-apoptotic effects. In the heart, PP-PRL caused an apparent developmental delay, whereas U-PRL promoted tissue compaction. In the blood, U-PRL increased the number of mature red blood cells at the expense of white blood cell production. Within the white blood cell population, myelopoiesis was favored at the expense of lymphopoiesis. PP-PRL, in contrast, had a less dramatic influence on the hematopoietic compartment by promoting red blood cell maturation and granulocyte production. In the thymus, exposure to PP-PRL caused accumulation of apoptotic thymocytes in enlarged glands, whereas exposure to U-PRL resulted in smaller thymi. In the spleen, exposure to U-PRL increased cellularity, with the majority of cells belonging to the erythroid series - a finding consistent with increased red blood cells in the circulation. Exposure to PP-PRL was without discernible effect. In all of these tissues, the contrasting effects of the two PRLs indicate that the absolute concentration of PRL is not crucial, but that the ratio of U-PRL to PP-PRL has a profound effect on tissue development. In brown fat, both PRL preparations decreased the number of lipid droplets. This result is therefore probably a consequence of the increase in total PRL. The results of this study attest to the importance of the U-PRL:PP-PRL ratio normally present during pregnancy and have provided clues as to the possible pathogenesis of a variety of neonatal problems.

Animals↗

Adsorption of colostral antibodies against classical swine fever, persistence of maternal antibodies, and effect on response to vaccination in baby pigs.

OBJECTIVE: To determine kinetics of antibody absorption, persistence of antibody concentrations, and influence of titers on vaccination of baby pigs with a vaccine against classical swine fever (CSF). ANIMALS: 15 sows and their litters. PROCEDURE: Farrowings were supervised. Initial time of suckling was recorded. In the first experiment, blood samples were collected at farrowing, 2 and 4 hours after suckling, and hourly until 10 hours after initial suckling. Samples were assayed for CSF antibodies, using a serum neutralizing (SN) test. A second experiment included 33 baby pigs vaccinated as follows: 10 prior to ingestion of colostrum, 18 between 1 and 4 hours after ingestion of colostrum, and 5 at 12 hours after ingestion of colostrum. Fourteen pigs were vaccinated when 7 weeks old, and 15 pigs were not vaccinated. At 10 weeks of age, pigs were challenge-exposed with virulent CSF virus. Blood samples were collected and assayed for CSF antibodies and p125 antigen and p125 antibodies. RESULTS: CSF antibodies were detected in pigs beginning 2 hours after suckling. Colostral antibodies persisted for > 7 weeks (half-life, 79 days). Vaccination of pigs before suckling provided effective protection from severe disease after challenge-exposure. However, vaccination of neonates with antibody titers was not effective, because 19 of 23 (82%) pigs succumbed after challenge-exposure. All pigs vaccinated when 7 weeks old resisted challenge-exposure, whereas all unvaccinated control pigs succumbed. CONCLUSIONS AND CLINICAL RELEVANCE: Vaccination before ingestion of colostrum conferred good protection against CSF in baby pigs. Vaccination of 7-week-old pigs that had decreasing concentrations of passively acquired antibodies was efficacious.

Adsorption↗

Nuclear magnetic resonance study of water mobility in pasta filata and non-pasta filata mozzarella.

Changes in molecular mobility of water in pasta filata and non-pasta filata Mozzarella cheeses were investigated during the first 10 d of storage using nuclear magnetic resonance (NMR) relaxation techniques. Water in pasta filata Mozzarella was classified into two fractions by spin-spin relaxation times, T21 and T22, and corresponding proton intensities, A1 and A2, representing low and high molecular mobility, respectively. Increase in A1 (and decrease in A2) suggested that, there was a redistribution of water from more- to less-mobile fraction (from T22 to T21 fraction) during the first 10 d of storage. The NMR data did not indicate the two-state behavior of water molecules in non-pasta filata Mozzarella. However, the T2 values of non-pasta filata Mozzarella were comparable to the T21 values of pasta filata Mozzarella indicating that the molecular mobility of water in non-pasta filata Mozzarella is comparable to that of the less mobile water fraction in pasta filata Mozzarella. Generally, T2 and T1 values of pasta filata and non-pasta filata Mozzarella cheeses increased during the 10-d storage. This is believed to be due to structural changes in the protein matrix.

Cheese↗

Increased expression of the pro-inflammatory enzyme cyclooxygenase-2 in amyotrophic lateral sclerosis.

Mutations in the copper/zinc superoxide dismutase (mSOD1) gene are associated with a familial form of amyotrophic lateral sclerosis (ALS), and their expression in transgenic mice produces an ALS-like syndrome. Recent observations suggest a role for inflammatory-related events in the progression and propagation of the neurodegenerative process in ALS. Consistent with this view, the present study demonstrates that, during the course of the disease, the expression of cyclooxygenase type 2 (Cox-2), a key enzyme in the synthesis of prostanoids, which are potent mediators of inflammation, is dramatically increased. In both early symptomatic and end-stage transgenic mSOD1 mice, neurons and, to a lesser extent, glial cells in the anterior horn of the spinal cord exhibit robust Cox-2 immunoreactivity. Cox-2 mRNA and protein levels and catalytic activity are also significantly increased in the spinal cord of the transgenic mSOD1 mice. The time course of the spinal cord Cox-2 upregulation parallels that of motor neuronal loss in transgenic mSOD1 mice. We also show that Cox-2 activity is dramatically increased in postmortem spinal cord samples from sporadic ALS patients. We speculate that Cox-2 upregulation, through its pivotal role in inflammation, is instrumental in the ALS neurodegenerative process and that Cox-2 inhibition may be a valuable therapeutic avenue for the treatment of ALS.

Amyotrophic Lateral Sclerosis↗

[The transference and distribution of tritium water in the soybean-soil system].

The isotope trace techniques of simulation contamination were applied to explore the rule of transference and distribution of tritium water in a simulated soybeam-soil ecosystem. The activity ratio of two forms of tritium in plant and soil sample were measured by 50 days simulation experiment. The results showed that when tritium water was entered the soil, it not only was transferred to other compartments in the system, but also vaporized into atmosphere rapidly. Both free water tritium and bound tritium were found in the soybean and the soil. The activity ratio of free water tritium reduced after reaching the maximum (19.4 Bq.g-1 in root, 12.3 Bq.q-1 in stem and leaf) at 6th hour in the soybean. The bound tritium increased slowly. The activity ratio of total tritium in soybean root was upper than those in stem and leaf in the earlier stage, they reach equipoise each other in the later stage. The activity ratio of two tritium in the surface soil reduced continuously. The compartment model of tracer kinetic was applied to imitate the experimental data. The activity ratio of soil Cs = 88.37e-11.847t + 7.38e-0.030t and the activity ratio of soybean Cb = 10.30(e-0.030t - e-11.847t) were gained.

Soil↗

Periodontitis as a biofilm infection.

Microbial biofilms are a major concern of infections associated with implantable medical devices as well as with many non-implant related chronic infectious diseases in humans. Dental plaque is also a biofilm. Dental plaque is probably one of the best characterized biofilms occurring on the surface of human tissues. This article will examine the impact of biofilm research on concepts of microbial etiology and the treatment implications for periodontitis.

Bacteria↗

[Study on the effects of DNA and natural killer cell damage induced by microcystins LR].

OBJECTIVE: Microcystin is a group of algae toxin which causes liver cancer. In this paper we tried to study the carcinogenic and tumor promotion mechanism of Microcystin LR (MCLR). METHODS: The single cell microgel electrophoresis assay (MGE) and 3H-TdR releasing assay were used to study the effects of on DNA damage and natural killer cell (NK cell) activity. RESULTS: The different doses of MCLR caused DNA damage in rat lymphocytes compared to 0.85% NaCl. However, no time-dependent relationship and dose dependent relationship between MCLR and DNA migration were observed, and the DNA damage was recovered rapidly after MCLR treatment. At the same time MCLR reduced NK cells activity in mice. CONCLUSION: The above results provide some evidence on the mechanisms of carcinogenicity and promotional effects of MCLR at cellular and molecular levels.

Animals↗