Objective To explore the relationship between serum homocysteine (Hcy) level before coronary angiography(CAG) and contrast induced nephropathy (CIN) after CAG.Methods We included 2264 cases of suspected coronary heart disease from May 2013 to May 2016 and all patients received CAG examination.According to whether CIN has developed or not after CAG, the patients were divided into the non-CIN group (n=2162) and the CIN group (n=102).We analyzed and compared the clinical baseline data, serum Hcy and creatinine (Cr) levels and the estimated glomerular filtration rate between the 2 groups eGFR.Results Patients in the non-CIN group were younger and with less comorbidities of diabetes and chronic kidney disease (all P<0.05).The volume of contrast media consumed in the non-CIN group was less than the CIN group [(122±21)ml vs.(147±24)ml, P=0.012).Hcy level in the non-CIN group (12.81±6.71) μmol/L was lower than that in the CIN group (21.74±11.9)μmol/L before CAG (P<0.05).No significant differences in serum Cr level and eGFR before CAG (P>0.05).At 72 hours after CAG, Cr level of the non-CIN group (69.34±19.54 μmol/L) was lower than that of the CIN group (87.34±21.38) μmol/L (P<0.05).eGFR was higher in the non-CIN group (79.34±19.54)ml/min than that in the CIN group (67.34±21.38)ml/min (P<0.05).Linear regression analysis showed that Hcy level before CAG were positively correlated with Cr level after CAG (r=0.547,P<0.01) and negatively correlated with eGFR after CAG (r=-0.271,P<0.01).Conclusions Hcy level before CAG can be used as one of an effective parameter to predict CIN.

Aim To study the mechanism of the anti-aging effect of total extract of astragalus(TEA) in mice. Methods MDA content, the activities of Mn-SOD and GSHpx and the reduced to oxidized glutathione (GSH/GSSG) ratio in mitochondria of D-galactose(D-gal) treated mice and 17-month-old mice were measured. Results Treatment with TEA(40 mg?kg-1?d-1 ig) for 10 wk would lower the content of MDA and restore activities of Mn-SOD,GSHpx and GSH/GSSG ratio in mitochondria of D-gal treated mice.Treatment with TEA (40 mg?kg-1 ?d-1 ig) for 3 mon had the same effect on 17-month-old mice.Conclusion TEA has anti-aging effect on D-gal treated mice and 17-month-old mice significantly, probably being related to its anti-oxidative effect.

AIM: To explore the role of NO in the induction of brain ischemic tolerance (BIT) by observing changes of NOS activity and NO_2-/NO_3- content following a transient cerebral ischemia. METHODS: The rat 4-vessel occluding brain ischemic model was used. 140 male Wistar rats were divided into sham, cerebral ischemic preconditioning (CIP), ischemic insult and CIP+ischemic insult groups. An occlusion of the 4 vessels for 3 min was normally used as CIP, and a relative long one for 10 min was used as ischemic insult. When CIP was followed by ischemic insult, the interval between them was 3 d. The CA1 region of the hippocampus of rats was dissected out at 0 h, 2 h, 16 h, 24 h, 36 h, 72 h and 7 d after the last time of ischemia to assay its NOS activity and NO_2-/NO_3- content. RESULTS: The NOS activity and NO_2-/NO_3- content began to increase at 16 h, peaked at 24 h and decreased to basal level at 36 h of reperfusion after CIP. The duration of the up-regulation of NOS activity and NO_2-/NO_3- content was much shorter than that of BIT, which usually takes place 1-7 d after CIP. The pattern of upregulation of the NOS activity and NO_2-/NO_3- content was similar to the CIP group, but the maximum (24 h) was much more than that in CIP group (P

AlM: To investigate the relationship between the anterior ischemic optic neuropathy ( AlON ) and the carotid artery change using doppler ultrasound.METHODS:Fifty-four cases of AlON patients and 54 cases of healthy control were observed, atherosclerotic spots were detected by the application of color ultrasound.RESULTS:ln AlON group of 54 patients, 38 cases appeared carotid atherosclerosis, accounting for 70%. The number of cases with hard plaque, soft plaque and mixed plaques were 18, 13, and 7 respectively, accounting for 33%, 24% and 13%. ln the control group, 20 cases were detected atherosclerotic change, accounting for 37%. And the number of cases with hard plaque, soft plaque and mixed plaques were 12, 5 and 3 respectively, accounting for 22%, 9%, 6%. Significant stenosis and velocity change were showed in neither AlON group nor control group. Compared with the control group, AlON group had more cases of atherosclerotic plaque, the difference was statistically significant (χ2=12. 836, P=0. 005)CONCLUSlON: The incidence of AlON is correlated with carotid atherosclerosis, and carotid ultrasonography is significantly valuable for AlON etiology and diagnosis.

Administration, Oral ; Adult ; Atrial Flutter ; drug therapy ; physiopathology ; Digoxin ; therapeutic use ; Echocardiography ; Female ; Fetal Diseases ; drug therapy ; physiopathology ; Humans ; Hydrops Fetalis ; drug therapy ; physiopathology ; Infant, Newborn ; Male ; Pregnancy

OBJECTIVETo prepare monoclonal antibody (mAb) against prM epitope.

METHODSThe gene encoding prM was isolated using RT-PCR from brain of JEV infected mouse and cloned into prokaryotic expression vector pET-32a. Recombinant plasmid was transformed into E.coli BL21/DE3/LysS, then the transformed cells were expressed with the induction of IPTG. The expression and purification of the prM protein was analyzed by SDS-PAGE. The BALB/c mice were immunized with purified prM protein. Hybridoma cell lines secreting monoclonal antibodies against prM were established after cell fusion of mouse splenic cell and P3-X63-Ag8.653 cells. The specificity of mAb was identified by ELISA, Western Blot and Immunohistochemistry assay.

RESULTSmAb against prM epitope of JEV was prepared successfully.

CONCLUSIONThe obtained prM specific mAb was valuable for the prevention and dignosis of Japanese encephalitis.

Animals ; Antibodies, Monoclonal ; analysis ; immunology ; isolation & purification ; Antibody Specificity ; BALB 3T3 Cells ; Cell Line ; Cloning, Molecular ; Electrophoresis, Polyacrylamide Gel ; Encephalitis Virus, Japanese ; genetics ; immunology ; Epitopes ; immunology ; Escherichia coli ; genetics ; Mice ; Plasmids ; genetics ; metabolism ; Prokaryotic Cells ; metabolism ; Sequence Analysis, DNA ; Viral Proteins ; biosynthesis ; genetics ; immunology ; isolation & purification

AIMTo investigate the effects of the duration of cerebral ischemic preconditioning(CIP) and interval between CIP and the subsequent ischemic insult on the protection of CIP against delayed neuronal death (DND) in the CA1 hippocampus normally induced by brain ischemic insult.

METHODSFour-vessel occlusion cerebral ischemic model of rats (54) was used. The brain of the rats was sectioned and stained with thionin to show DND in the CA1 hippocampus.

RESULTSNo DND was found in the hippocampus of the rats subjected to sham operation and CIP, in which 3 min cerebral ischemic preconditioning was performed. Obvious destruction of the CA1 hippocampus was found in brain ischemic insult group, in which histological (HG) was 2-3 in 6 min and 10 min ischemia subgroups and grade 3 in 15 min ischemia subgroup. In CIP + brain ischemic insult group, no obvious neuronal damage was found in 3 min-3d-6 min (CIP for 3 min was followed by a brain ischemic insult for 6 min at an interval of 3 d, the same as the following) and 3 min-3 d-10 min groups, indicating that CIP effectively protected neurons of the CA1 hippocampus against DND normally induced by ischemic insult for 6 or 10 min. However, in 3 min-1 d-10 min and 3 min-3 d-15 min groups, the protective effect of CIP was lower than that in the 3 min-3 d-10 min group. The quantitative analysis of the protective effect of CIP on the CA1 hippocampal neurons showed that there was no significant difference in protecting number and protecting index between 3 min-3 d-6 min and 3 min-3 d-10 min groups (P > 0.05). However, the growth index in 3 min-3 d-10 min group was obvious larger than that in 3 min-3 d-6 min (P < 0.05).

CONCLUSIONAlthough the protective effects of CIP in 3 min-3 d-6 min and 3 min-3 d-10 min groups were similar, the protective effect of CIP in 3 min-3 d-10 min group was sensitively found. Maximal protective potential of CIP could be induced when using the time parameters of 3 min-3 d-10 min to establish the model of global cerebral ischemic tolerance.

Animals ; Brain Injuries ; pathology ; prevention & control ; Brain Ischemia ; pathology ; prevention & control ; Cell Death ; Hippocampus ; pathology ; Ischemic Preconditioning ; Male ; Neurons ; pathology ; Rats ; Rats, Wistar ; Time Factors

AIMTo explore the effects of limb ischemic preconditioning (LIP) on cerebral ischemia/reperfusion injuries.

METHODSThirty six wistar rats, of which bilateral vertebral arteries were occluded permanently, were randomly divided into the following 6 groups: control group, cerebral ischemic group, limb ischemic group, LIP 0 d group (cerebral ischemia was given immediately after LIP), LIP 1 d group (cerebral ischemia was given 1 d after LIP) and LIP 2 d group (cerebral ischemia was given 2 d after LIP). Global cerebral ischemia was performed by four vessels occlusion in rats. LIP was performed by occluding the bilateral femoral arteries for 10 min 3 times in a interval of 10 min. The histological grade and pyramidal neuronal density in the CA1 hippocampus were measured to quantitate the degree of hippocampal injury under thionin staining.

RESULTSThe histological grade was increased and the pyramidal neuronal density was decreased in the CA1 hippocampus of the cerebral ischemic group (P < 0.01). The damage of the CA1 hippocampus in LIP 0 d group was significantly diminished, which represented by decreased histological grade and increased neuronal density compared with the cerebral ischemic group (P < 0.01). But the CA1 hippocampus still showed obvious injuries in the LIP 1 d and LIP 2 d group.

CONCLUSIONLIP performed immediately prior to cerebral ischemia could confer obvious protective effects on CA1 hippocampus against cerebral ischemia/reperfusion injuries. But LIP performed 1 d and 2 d prior to cerebral ischemia could not afford the protection against injuries induced by cerebral ischemia/reperfusion.

Animals ; Brain Ischemia ; prevention & control ; Extremities ; blood supply ; Hippocampus ; blood supply ; Ischemic Preconditioning ; methods ; Rats ; Rats, Wistar ; Reperfusion Injury ; prevention & control

To explore the role of NO in the induction of brain ischemic tolerance (BIT) in vivo, the effect of nitric oxide synthase (NOS) inhibitor L-NAME on the induction of BIT induced by cerebral ischemic preconditioning (CIP) was investigated in the hippocampal CA1 subfield in CIP and ischemic insult models established by rat four-vessel occlusion using brain tissue section and thionine staining methods. Fifty-four male Wistar rats were divided into 6 groups: (1) sham-operated group (n=6): bilateral common arteries were separated without occluding the cerebral blood flow; (2) ischemia group (n=6): an ischemic insult for 10 min was given; (3) CIP+ischemia group (n=6): 3-min CIP was preformed 72 h prior to 10-min ischemic insult; (4) L-NAME group (total n=24, n=6 for each subgroup): L-NAME (5 mg/kg, i.p.) was administered 1 h prior to CIP and 1, 12 and 36 h after CIP, respectively. Other procedures were the same as those for the CIP+ischemia group; (5) L-NAME+L-Arg group (n=6): L-NAME (5 mg/kg, i.p.) and L-Arg (300 mg/kg, i.p.) were administered 1 h prior to CIP, other procedures were the same as those for the L-NAME group; (6) L-NAME+ischemia group (n=6): L-NAME (5 mg/kg, i.p.) was administered 72 h before the 10-min ischemic insult. The results showed that (1)10-min ischemic insult resulted in an increase in the histological grade (indicating a more serious tissue injury) and a decrease in pyramidal neuronal density (P<0.01); (2) the histological grade and neuronal density in hippocampal CA1 in the CIP+ischemia group were similar to those in the sham-operated group (P>0.05); (3) in the L-NAME group, administration of L-NAME brought about an increase in the histological grade and a decrease in neuronal density (P<0.01), suggesting that L-NAME blocked the protection of CIP; (4) the neuronal damage in L-NAME+L-Arg group was slighter than that in the L-NAME group, but still more serious than that in the CIP+ischemia group, suggesting that L-Arg partly reversed the blocking effect of L-NAME; (5) the morphological representations in L-NAME+ischemia group were basically similar to those in the ischemia group. The results mentioned above indicate that NO is involved in the induction of BIT in vivo. The blocking effect of L-NAME administered at 36 h after CIP was obviously weaker than the effects of L-NAME administered 1 h prior to CIP, and 1 or 12 h after CIP. It is suggested that NO is involved in the induction of BIT at an early stage and that the involvement might take place via activating cascades of the events.
Animals ; Brain Ischemia ; physiopathology ; prevention & control ; Enzyme Inhibitors ; pharmacology ; Hippocampus ; physiology ; Ischemic Preconditioning ; methods ; Male ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide ; physiology ; Nitric Oxide Synthase ; antagonists & inhibitors ; Rats ; Rats, Wistar

To explore the role of metabotropic glutamate receptor 2/3 mGluR 2/3 in the induction of brain ischemic tolerance (BIT), the influences of mGluR2/3 antagonist alpha-methyl-(4-tetrazolyl-phenyl) glycine (MTPG) on the induction of BIT and expression of glial fibrillary acidic protein (GFAP) in the hippocampus were observed using thionin staining and GFAP immunohistochemical staining in a rat brain ischemic model with four-vessel occlusion (4VO). Fifty-four rats, of which bilateral vertebral arteries were occluded permanently by electrocautery, were divided into 5 groups: (1) sham operated group (n=8): the bilateral carotid common arteries (BCCA) were separated, but the blood flow was not blocked; (2) ischemia group (n=8): the blood flow of BCCA was blocked for 8 min; (3) ischemic preconditioning (IP) group (n=8): the blood flow of BCCA was occluded for 3 min as a cerebral ischemic preconditioning (CIP), and then the rats were exposed to an 8-min brain ischemic insult 24 h after the CIP; (4) MTPG+IP group (n=22): MTPG was administered 20 min before the CIP, then the rats were exposed to an 8-min brain ischemia insult 24 h after the CIP. In order to examine dosage dependency in the effect of MTPG, 4 dosages of MTPG (0.4, 0.2, 0.04 and 0.008 mg) were administered; (5) MTPG+ischemia group (n=8): an ischemic insult for 8 min was given 24 h after the administration of MTPG (0.2 mg). MTPG was injected into the right lateral cerebral ventricle. The results obtained are as follows. (1) Ischemic insult for 8 min increased the histological grade (HG) and reduced the neuronal density (ND) significantly, and also increased the expression of GFAP significantly (P<0.05 vs sham-operated group). (2) In the IP group, the above changes were not observed, indicating that CIP could protect pyramidal neurons against the ischemic insult. (3) The protective effects of CIP were blocked by MTPG, as manifested by the significant increase in HG and decrease in ND in the MTPG+IP group (P<0.05 vs sham-operated group). The changes were dose-dependent. (4) No obvious difference in the HG, ND and expression of GFAP was detected between the groups of MTPG+ischemia and ischemia. The above results indicate that MTPG blocks the induction of BIT induced by CIP, suggesting that mGluR2/3 participates in the induction of BIT.
Alanine ; analogs & derivatives ; pharmacology ; Animals ; Brain Ischemia ; physiopathology ; Hippocampus ; blood supply ; drug effects ; physiopathology ; Ischemic Preconditioning ; methods ; Male ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate ; antagonists & inhibitors ; Reperfusion Injury ; physiopathology ; prevention & control ; Tetrazoles ; pharmacology