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Biomedical subjects

J Q Pan

Publications and source records attributed to J Q Pan.

13 recordsLinked to original sources

Effects of early feed restriction and cold temperature on lipid peroxidation, pulmonary vascular remodelling and ascites morbidity in broilers under normal and cold temperature.

Two experiments were conducted to evaluate the effects of early feed restriction on lipid peroxidation, pulmonary vascular remodelling and ascites incidence in broilers under normal and low ambient temperature. In experiment 1, the restricted birds were fed 8h per day either from 7 to 14 d or from 7 to 21 d, while the controlled birds were fed ad libitum. In experiment 2, the restricted birds were fed 80 or 60% of the previous 24-h feed consumption of full-fed controls for 7 d from 7 to 14 d. On d 14, half of the birds in each treatment both in experiment 1 and experiment 2 were exposed to low ambient temperature to induce ascites. Body weight and feed conversion ratio were measured weekly. The incidences of ascites and other disease were recorded to determine ascites morbidity and total mortality. Blood samples were taken on d 14, 21, 28, 35 and 42 to measure the plasma malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). On d 42, samples were taken to determine the right/total ventricular weight ratio (RV/TV), vessel wall area/vessel total area ratio (WA/TA) and mean media thickness in pulmonary arterioles (mMTPA). Low-temperature treatment increased plasma MDA concentration. When broilers were exposed to a cool environment for 3 weeks, plasma SOD and GSH-Px activity were decreased compared with normal-temperature chicks. RV/TV, WA/TA and mMTPA on d 42 were increased in birds exposed to cold, consistent with the increased pulmonary hypertension and ascites morbidity. Early feed restriction markedly decreased plasma MDA concentration. The plasma SOD and GSH-Px activity of feed-restricted birds were markedly higher than those fed ad libitum on d 35 and d 42. All early feed restriction treatments reduced ascites morbidity and total mortality. On d 42, the RV/TV, WA/TA and mMTPA of feed-restricted broilers were lower than that of the ad libitum-fed broilers. The results suggested that early feed restriction alleviated the lipid peroxidation, promoted the activity of enzymatic antioxidant and inhibited pulmonary vascular remodelling. These changes might be associated with reduced ascites incidence.

Animals↗

Alternative splicing in the cytoplasmic II-III loop of the N-type Ca channel alpha 1B subunit: functional differences are beta subunit-specific.

Structural diversity of voltage-gated Ca channels underlies much of the functional diversity in Ca signaling in neurons. Alternative splicing is an important mechanism for generating structural variants within a single gene family. In this paper, we show the expression pattern of an alternatively spliced 21 amino acid encoding exon in the II-III cytoplasmic loop region of the N-type Ca channel alpha(1B) subunit and assess its functional impact. Exon-containing alpha(1B) mRNA dominated in sympathetic ganglia and was present in approximately 50% of alpha(1B) mRNA in spinal cord and caudal regions of the brain and in the minority of alpha(1B) mRNA in neocortex, hippocampus, and cerebellum (<20%). The II-III loop exon affected voltage-dependent inactivation of the N-type Ca channel. Steady-state inactivation curves were shifted to more depolarized potentials without affects on either the rate or voltage dependence of channel opening. Differences in voltage-dependent inactivation between alpha(1B) splice variants were most clearly manifested in the presence of Ca channel beta(1b) or beta(4), rather than beta(2a) or beta(3), subunits. Our results suggest that exon-lacking alpha(1B) splice variants that associate with beta(1b) and beta(4) subunits will be susceptible to voltage-dependent inactivation at voltages in the range of neuronal resting membrane potentials (-60 to -80 mV). In contrast, alpha(1B) splice variants that associate with either beta(2a) or beta(3) subunits will be relatively resistant to inactivation at these voltages. The potential to mix and match multiple alpha(1B) splice variants and beta subunits probably represents a mechanism for controlling the plasticity of excitation-secretion coupling at different synapses.

Alternative Splicing↗

Alternative splicing of a short cassette exon in alpha1B generates functionally distinct N-type calcium channels in central and peripheral neurons.

The N-type Ca channel alpha1B subunit is localized to synapses throughout the nervous system and couples excitation to release of neurotransmitters. In a previous study, two functionally distinct variants of the alpha1B subunit were identified, rnalpha1B-b and rnalpha1B-d, that differ at two loci;four amino acids [SerPheMetGly (SFMG)] in IIIS3-S4 and two amino acids [GluThr (ET)] in IVS3-S4. These variants are reciprocally expressed in rat brain and sympathetic ganglia (). We now show that the slower activation kinetics of rnalpha1B-b (DeltaSFMG/+ET) compared with rnalpha1B-d (+SFMG/DeltaET) channels are fully accounted for by the insertion of ET in IVS3-S4 and not by the lack of SFMG in IIIS3-S4. We also show that the inactivation kinetics of these two variants are indistinguishable. Through genomic analysis we identify a six-base cassette exon that encodes the ET site and with ribonuclease protection assays demonstrate that the expression of this mini-exon is essentially restricted to alpha1B RNAs of peripheral neurons. We also show evidence for regulated alternative splicing of a six-base exon encoding NP in the IVS3-S4 linker of the closely related alpha1A gene and establish that residues NP can functionally substitute for ET in domain IVS3-S4 of alpha1B. The selective expression of functionally distinct Ca channel splice variants of alpha1B and alpha1A subunits in different regions of the nervous system adds a new dimension of diversity to voltage-dependent Ca signaling in neurons that may be important for optimizing action potential-dependent transmitter release at different synapses.

Action Potentials↗

Inhibitory effects of nitric oxide and interleukin-10 on production of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 in mouse alveolar macrophages.

AIM: To observe the effects of nitric oxide and interleukin-10 (IL-10) on inflammatory reaction in mouse alveolar macrophages (AM). METHODS: AM from mice were stimulated by lipopolysaccharides (LPS) 10 mg.L-1 and nitric-oxide synthase inhibitor, S-methylisothiorea sulfate (SMT) or nitric-oxide donor, S-nitroso-N-acetyl-D, L-penicillamine (SNAP). The production of tumor necrosis factor alpha (TNF alpha), IL-1 beta, IL-6, and IL-10 by AM were measured by ELISA. RESULTS: After LPS-stimulation, TNF alpha, IL-1 beta, and IL-6 peaked at 6, 12, and 24 h, respectively by AM. SMT inhibited LPS-induced nitric oxide release and increased IL-1 beta and IL-6 secretions in AM, but the TNF alpha levels remained unchanged. SNAP had inhibitory effects on IL-1 beta and IL-6 secretions in a concentration-dependent manner, but exerted no effect on TNF alpha release. TNF alpha, IL-1 beta, and IL-6 secretions were inhibited by recombinant IL-10, but the cytokines release was upregulated by anti-IL-10 monoclonal antibody. CONCLUSION: Both endogenous and exogenous nitric oxide and IL-10 had inhibitory effects on the LPS-induced TNF alpha, IL-1 beta, and IL-6 secretions in mouse AM.

Animals↗

Effects of dexamethasone, ibuprofen, and ligustrazini on lipopolysaccharides-induced tumor necrosis factor alpha production.

AIM: To study the influence of dexamethasone (Dex), ibuprofen (Ibu), and ligustrazini (Lig) on lipopolysaccharides (LPS)-induced tumor necrosis factor alpha (TNF alpha) gene expression (both mRNA and protein). METHODS: TNF alpha in supernatants of human whole blood was measured by ELISA; The TNF alpha mRNA was assessed by slot blot analysis. RESULTS: LPS-induced TNF alpha production was in a dose-dependent manner. TNF alpha levels in the whole blood increased markedly at 3 h and peaked at 6 h. The induction of TNF alpha mRNA was very rapid, peaking at 2 h after LPS challenge. Dex exerted inhibitory effects on TNF alpha production in a dose-dependent manner. Ibu and Lig had 2-phase effects on TNF alpha release. CONCLUSION: Dex, Ibu, and Lig affected TNF alpha gene expression, so they may be new approaches of anti-TNF alpha for treatment of sepsis.

Anti-Inflammatory Agents↗

Effects of dexamethasone and ibuprofen on LPS-induced gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung.

AIM: To study the kinetics of tumor necrosis factor alpha (TNF alpha), interleukine-1 (IL-1 beta), and macrophage inflammatory protein-1 alpha (MIP-1 alpha) gene expression in rat lung after i.p. lipopolysaccharides (LPS) and the effect of dexamethasone (Dex) and ibuprofen (Ibu) on the cytokines gene expression. METHODS: The amount of Evans blue in lung was measured by fluorescence method. The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung were assessed by slot blot analysis. RESULTS: The mRNA levels of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung after i.p. LPS increased in a dose-dependent manner, and peaked at 2, 6, and 12 h, respectively. Both Dex 50 mg.kg-1 and Ibu 90 mg.kg-1 injected at 1 h before i.p. LPS markedly decreased the content of Evans blue in lung at 1 h after i.p. LPS. After Dex or Ibu pretreatment, the peak levels of TNF alpha, IL-1 beta, and MIP-1 alpha mRNA decreased markedly compared with LPS alone. CONCLUSION: The gene expression of TNF alpha, IL-1 beta, and MIP-1 alpha in rat lung increased after i.p. LPS. Dex and Ibu prevented LPS-induced lung injury through inhibiting the cytokines gene expression.

Animals↗

Anhydroicaritin 3-O-rhamnosyl(1-->2)rhamnoside from epimedium koreanum and a reappraisal of other rhamnosyl(1-->2, 1-->3 and 1-->4)rhamnoside structures.

An anhydroicaritin 3-O-rhamnosylrhamnoside from Epimedium koreanum is defined as the 3-O-alpha-L-[alpha-L-rhamnopyranosyl(1-->2)rhamnopyranoside] on the basis of 2D NMR evidence. Complete assignments of the 1H and 13C NMR spectra of this compound are presented for the first time. The NMR distinction of 1-->2, 1-->3 and 1-->4 linked rhamnopyranosylrhamnopyranosides are discussed and indicate that baohuosides III and V from E. davidii and baohuoside VI from E. davidii and E. pubescens, respectively, are (1-->2) linked.

Carbohydrate Conformation↗

Effects of propylene glycol mannate sulfate on thrombosis in abdominal aorta in rabbits.

AIM: To study the effects of propylene glycol mannate sulfate (PGMS) on platelet adhesion, aggregation and thrombosis in abdominal aorta in rabbits. METHODS: Platelet adhesion assay was performed with a platelet-adhesion-meter. The platelet concentration was determined with an electronic particle counter, and the total radio-activity was determined with Clinigamma-1272. RESULTS: PGMS inhibited washed platelet aggregation induced by thrombin in vitro. The value of IC50 was 0.9 mg.L(-1). (95% confidence limit = 4.1-13.7 mg.L(-1). At 10, 30, and 60 min after i.v. PGMS 75 mg.kg(-1), the inhibition rates of platelet adhesion were 90.4%, 41.8%, and 26.3% and the inhibition rates of platelet aggregation induced by thrombin were 99%, 122%, and 110%, respectively. It did not exhibit any noticeable effect on platelet aggregation induced by ADP and collagen at this dosage. After 1.5 h of i.v. PGMS 75 mg.kg-1 and total autologous 111In-platelets 3.3 x 10(9) the radioactivity and dry weight of the injured and uninjured segments were determined. The PGMS group showed a significantly lower radioactivity (1.1 +/- 0.6 MBq), 111In-platelets (8.3 +/- s 3.3 x 10(8)) as well as the radioactivity deposited.g(-1) out of the total radioactivity infused % (0.24 +/- 0.21) compared with the control group (3.7 +/- 0.5 MBq, 24.6 +/- 3.5 x 10(8), and 0.86 +/- 0.25, respectively). CONCLUSION: PGMS prevented the platelet adhesion and aggregation at the injured arterial wall.

Animals↗

Effects of artesunate on immune function in mice.

AIM: To study the effects of artesunate (dihydroartemisinine-12-alpha-succinate, Art) on immune function in mice. METHODS: Hemolysin concentration was determined by colorimetric method. Serum IgG and C3 contents were measured by single immunodiffusion method. Percentage of lymphocyte transformation, phagocytosis percentage and phagocytic index were counted under microscope. RESULTS: Art im 75 mg kg-1 bid x 7 d decreased the humolysin-forming capacity and levels of serum IgG of mice sensitized with sheep red blood cell. The serum complement 3 level rose remarkably, when Art was given im to Plasmodium berghei-infected mice. Art enhanced the PHA-induced lymphocyte transformation rate (in vivo) in mice and increased the weight of spleen but reduced that of thymus in mice. Art elevated the DNFB-induced delayed-type hypersensitivity. Art im 75 mg kg-1 bid x 5 d reduced the percentage of phagocytosis of peritoneal macrophages and the phagocytic index. CONCLUSION: Art suppressed the humoral immune responses but enhanced the cell-mediated immunity.

Adjuvants, Immunologic↗

[Antiphospholipid antibodies: clinical significance in systemic lupus erythematosus].

A radioimmunoassay using cardiolipin as antigen and labelled SPA, anti-human IgG, anti-human IgM, anti-human IgA as second antibodies in detecting anti-cardiolipin antibody with the sera from 308 patients and 70 normal controls. Among them, 126 patients were of SLE, 27 systemic sclerosis, 40 rheumatoid arthritis, 40 Sjögren syndrome, 26 other connective tissue diseases, 7 syphilis and 32 with obstetric complications. The positive rate of anticardiolipin antibody were 42.9% (SLE), 29.7% (PSS), 20% (RA), 15% (SS), 26.9% (CTD), 85.7% (syphilis), 3.1% (obstetric complication), 0% (NC). In SLE the anticardiolipin antibody were well correlated with thrombocytopenia, cerebral lupus, thrombosis of vein and spontaneous recurrent abortion. Lupus anticoagulant (APTT) was found in 21.3% of SLE and biological false positive of VDRL test in 4.8%. Both of them correlated with the anticardiolipin antibody detected by the radioimmunoassay. The authors concluded that antiphospholipid antibodies is a group of commonly seen antibodies, which may play a rule in the pathogenesis of SLE. Further study is progressing.

Adolescent↗

[Pharmacological deaggregation of platelet aggregation].

Antagonists of increasing concentrations were added to PRP which had exhibited irreversible aggregation and the extent of deaggregation was determined. Several classes of platelet antagonists with different mechanisms have been undertaken to reverse platelet aggregation induced by ADP, collagen, arachidonic acid, U46619 and PAF. The results indicate that maintenance of platelet aggregation is a complex phenomenon involving multiple mechanisms which depend on agonists. Maintenance of ADP induced aggregation requires exogenous calcium and active intracellular calcium mobilization. Active intracellular calcium mobilization appears to be essential for maintaining aggregation by PAF, U46619 and arachidonic acid. But additional pathway may be operative in maintaining collagen-induced aggregation. Calmodulin inhibitors with multiple actions are effective deaggregators. Calmodulin plays a role in maintaining platelet aggregation. The present study indicates that the ability of various antagonists to reverse platelet aggregation is closely related to three factors: 1) agonists used to stimulate platelet, 2) the time period following the initiation of platelet aggregation and 3) the kinds of antagonists used.

Calcium↗