Objective To study the relationship between velocities of ductus venosus(DV),inferior vena cava(IVC) and right hepatic vein(RHV) of fetus,and abnormal perinatal outcome in high-risk pregnancy so as to find out which venous velocity can predict abnormal perinatal outcome and which velocity is the best for predicting abnormal perinatal outcome. Methods Velocities of DV,IVC and RHV in 67 cases of high-risk pregnancy were examined through color Doppler and their relationship with perinatal outcome was analyzed respectively. Results RHV-pulsatility index(PI) ,DV-pre-load index(PLl) ,DV-S/A and IVC-peak velocity index(PVI) could all predict abnormal perinatal outcome in high-risk pregnancy. But RHV-PI had the best prediction, and when its positive cutoff value was taken as 2. 89,the sensitivity for abnormal outcome was 75. 0% ,the specificity was 76. 7% ,and the correct index (Youden index) was 0. 52. Conclusions RHV-PI can best predict abnormal perinatal outcome in high-risk pregnancy,which can help a lot for prompt clinical treatment.

Objective To study changes of phosphorylated cyclic adenosine monophosphate(c-AMP) response element binding protein in hippocampus(CA1) of neonatal rats after cerebral hypoxic-ischemia(HI)and effects of gangliosides (GM1)on the p-CREB.Methods An animal model of neonatal hypoxic-ischemia brain damage was established. Changes of p-CREB in hippocampal CA1 was detected with immunohistochemical methods.Results The p-CREB levels in the CA1 of HI and GM1 groups increased transiently and then decreased quickly, but there was no significant difference between HI and GM1 group.Conclusion The p-CREB levels in the CA1 of HI group increase transiently and then decrease quickly after HI ;GM1 has little effect on p-CREB in the CA1 after HI.

Objective To study the effect of exogenous prostaglandin E 1 (PGE 1) on the superoxide dismutase(SOD) and nitric oxide(NO) levels in brain tissue of neonatal rats with hypoxic-ischemic brain damage(HIBD).Methods Sixty 7-day old newborn Wistar rats to establish HIBD models,intraperitoneally and subcutaneous injected PGE 1 and TMP,then the rats were killed after hypo- xia and ischemia for 48 hours.Take cerebral cortex of arteria carotis ligation side and made them into homogenate to detect SOD and NO levels in brain tissue.Results SOD level in HIBD group was lower,and NO level was higher than those of normal group(P

Objective To investigate the role of ?7nAChR in the pathogenesis of Alzheimer's disease(AD)through exploring the relationship between ?7nAChR and A?_(1-42) in AD brains.Methods The accumulation of ?7nAChR and the possible relationship between ?7nAChR and A?_(1-42) were observed in 3 clinically and pathologically confirmed AD brains by immunohistochemistry. 3 normal brains were set as controls.Results Respective staining of anti-?7nAChR and anti-A?_(1-42) showed that the abnormal accumulation of ?7nAChR existed in AD brains. The main location was at hippocampus and temporal cortex which was just in accordance with senile plaque consisted mainly of A?_(1-42). The major part of ?7nAChR was located extra-cellular and within senile plaque from the view of morphology. No accumulation of ?7nAChR existed in normal brains. Co-staining of anti-?7nAChR and anti-A?_(1-42) further showed that ?7nAChR and A?_(1-42) could accumulate together in senile plaque of AD brain. The average rate of positive co-staining in hippocampus, temporal lobe and frontal lobe is 57.8%, 51.0% and 21.8% respectively. The accumulation of ?7nAChR in hippocampus and temporal lobe seems much than that in the frontal lobe. Conclusion ?7nAChR may combine with A?_(1-42) in AD brains. It is suggested that the combination should destroy the ?7nAChR receptor, block the receptor or mediate the injury of cholinergic neurons with the result of recognition and memory impairment and that ?7nAChR might play an important role in the pathogenesis of Alzheimer's disease.

BACKGROUNDL-glutamate (L-GLU) is a major neurotransmitter in the nucleus ambiguus (NA), which can modulate respiration, arterial pressure, heart rate, etc. This study investigated the effects and mechanisms of L-GLU microinjected into NA on gastric motility in rats.

METHODSA latex balloon connected with a pressure transducer was inserted into the pylorus through the forestomach for continuous recording of the gastric motility. The total amplitude, total duration, and motility index of gastric contraction waves within 5 minutes before microinjection and after microinjection were measured.

RESULTSL-GLU (5 nmol, 10 nmol and 20 nmol in 50 nl normal saline (PS) respectively) microinjected into the right NA significantly inhibited gastric motility, while microinjection of physiological saline at the same position and the same volume did not change the gastric motility. The inhibitory effect was blocked by D-2-amino-5-phophonovalerate (D-AP5, 5 nmol, in 50 nl PS), the specific N-methyl-D-aspartic acid (NMDA) receptor antagonist, but was not influenced by 6-cyaon-7-nitroquinoxaline-2,3-(1H,4H)-dione (CNQX) (5 nmol, in 50 nl PS), the non-NMDA ionotropic receptor antagonist. Bilateral subdiaphragmatic vagotomy abolished the inhibitory effect by microinjection of L-GLU into NA.

CONCLUSIONSMicroinjection of L-GLU into NA inhibits the gastric motility through specific NMDA receptor activity, not non-NMDA receptor activity, and the efferent pathway is the vagal nerves.

2-Amino-5-phosphonovalerate ; pharmacology ; 6-Cyano-7-nitroquinoxaline-2,3-dione ; pharmacology ; Animals ; Gastrointestinal Motility ; drug effects ; Glutamic Acid ; administration & dosage ; pharmacology ; Male ; Medulla Oblongata ; drug effects ; metabolism ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate ; antagonists & inhibitors ; Vagotomy

OBJECTIVETo observe the effects of Salvia miltiorrhiza (SM) on levels of neuropeptide Y1-36 and calcitonin gene-related peptide immune reactive substances (ir-NPY, ir-CGRP) in blood plasma and pons-oblongata after hypoxia-ischemic brain injury (HIBI) in neonatal rats.

METHODSSeven-day old rats were randomized into HIBI group (A), HIBI + SM group (B) and sham operation group(C). And each group was subdivided into 4 subgroups according to the different time after operation. 0.5 ml SM was injected intraperitoneally immediately and every 12 hrs afterwards. Changes of ir-NPY and ir-CGRP levels in plasma and pons-oblongata were observed immediately and 12, 24 and 48 hrs after HIBI by radioimmunoassay.

RESULTSPlasma levels of ir-NPY and ir-CGRP in different times after HIBI were all significantly raised but those in pons-oblongata were either raised or lowered to a certain degree. Part of the elevated ir-NPY could be reversed by SM injection.

CONCLUSIONCentral and peripheral neuropeptide Y1-36 and calcitonin gene-related peptide take part in the pathophysiological process of HIBI, SM could partially reverse the abnormal post-HIBI elevation of ir-NPY, which may be one of the pathways of SM in promoting recovery of damaged brain function.

Animals ; Animals, Newborn ; Brain Ischemia ; blood ; Calcitonin Gene-Related Peptide ; blood ; Drugs, Chinese Herbal ; pharmacology ; Female ; Male ; Neuropeptide Y ; blood ; Peptide Fragments ; blood ; Phytotherapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; blood ; Salvia miltiorrhiza ; chemistry

Objective: To observe the effects of electroacupuncture (EA) on the protein and gene expressions of Bax, Caspase-3 and Bcl-2 in cerebral cortex of type 2 diabetic rats with cognitive impairment (CI), and to explore the mechanism of EA in improving the learning and memory abilities. Methods: A total of 100 Sprague-Dawley (SD) rats were divided into a normal group (n=10) and a model group (n=90) by random number table method. Rats in the model group were intraperitoneally injected with a small dose of streptozotocin (STZ) to establish the type 2 diabetic models, after being fed with high-fat and high-sugar diet for 1 month. Twenty CI rats were selected from the 50 successful model rats by the Morris water maze (MWM) test and randomly divided into a model group and an EA group according to the blood glucose level and MWM data (n=10). Rats in the EA group received acupuncture at Zusanli (ST 36), Neiting (ST 44) and Yishu (Extra), of which Zusanli (ST 36) and Neiting (ST 44) were stimulated by EA apparatus, 20 min/time, once a day for 6 d a week and 4 consecutive weeks. The rats in the model and the normal groups were fixed without treatment. After 4-week treatment, the random blood glucose level of the rats was measured; the learning and memory abilities of rats were measured by MWM; terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was used to detect apoptotic cells; Western blot (WB) and real-time quantitative polymerase chain reaction (RT-qPCR) were used to detect the protein and gene expressions of Bax, Caspase-3 and Bcl-2 in cerebral cortex. Results: After modeling, the random blood glucose level and the escape latency tested by MWM were significantly increased, and the number of crossing the platform tested by the MWM was decreased in the EA and model groups, and were significantly different from those in the normal group (P<0.05 or P<0.01), while the differences between the model group and the EA group were not statistically significant (all P>0.05). After 4-week treatment, the random glucose level and the escape latency tested by MWM were significantly increased (both P<0.05), and the number of crossing the original platform tested by the MWM was significantly reduced (P<0.01), the protein and gene expressions of Bax and Caspase-3 were significantly increased (all P<0.001), the protein and gene expressions of Bcl-2 were significantly reduced (both P<0.001), and the number of neuron apoptosis was significantly increased (P<0.001) in the model group than in the normal group; the random blood glucose level was significantly reduced (P<0.05), the escape latency tested by MWM was significantly shortened (P<0.05), and the number of crossing the original platform tested by MWM was significantly increased (P<0.05), the protein and gene expressions of Bax and Caspase-3 were significantly reduced (all P<0.001), the protein and gene expressions of Bcl-2 were significantly increased (both P<0.001), and the number of neuron apoptosis was significantly reduced (P<0.001) in the EA group than in the model group. Conclusion: EA can improve the learning and memory damages induced by type 2 diabetic model rats with CI; the action mechanism may be achieved via anti-apoptosis.

The effect of 1-deoxynojirimycin(DNJ)on the proliferation of rat mesangial cells was observed and its mechanism was explored.The results showed that DNJ significantly inhibited the proliferation of rat mesangial cells induced by high glucose in time-and dose-dependent manners.DNJ significantly decreased expressions of?-smooth muscle action(?-SMA),integrin?1 mRNA and protein and focal adhesion kinase (FAK)protein stimulated by high glucose in rat mesangial cells(P

This study is to assess the efficacy of BPCBG on the decorporation of uranium (VI) and protecting human renal proximal tubular epithelial cells (HK-2) against uranium-induced damage. BPCBG at different doses was injected intramuscularly to male SD rats immediately after a single intraperitoneal injection of UO2(CH3COO)2. Twenty-four hours later uranium contents in urine, kidneys and femurs were measured by ICP-MS. After HK-2 cells were exposed to UO2(CH3COO)2 immediately or for 24 h followed by BPCBG treatment at different doses for another 24 or 48 h, the uranium contents in HK-2 cells were measured by ICP-MS, the cell survival was assayed by cell counting kit-8 assay, formation of micronuclei was determined by the cytokinesis-block (CB) micronucleus assay and the production of intracellular reactive oxygen species (ROS) was detected by 2',7'-dichlorofluorescin diacetate (DCFH-DA) oxidation. DTPA-CaNa3 was used as control. It was found that BPCBG at dosages of 60, 120, and 600 micromol kg(-1) resulted in 37%-61% increase in 24 h-urinary uranium excretion, and significantly decreased the amount of uranium retention in kidney and bone to 41%-31% and 86%-42% of uranium-treated group, respectively. After HK-2 cells that had been pre-treated with UO2(CH3COO)2 for 24 h were treated with the chelators for another 24 h, 55%-60% of the intracellular uranium was removed by 10-250 micromol L(-1) of BPCBG. Treatment of uranium-treated HK-2 cells with BPCBG significantly enhanced the cell survival, decreased the formation of micronuclei and inhibited the production of intracellular ROS. Although DTPA-CaNa3 markedly reduced the uranium retention in kidney of rats and HK-2 cells, its efficacy of uranium removal from body was significantly lower than that of BPCBG and it could not protect uranium-induced cell damage. It can be concluded that BPCBG effectively decorporated the uranium from UO2(CH3COO)2-treated rats and HK-2 cells, which was better than DTPA-CaNa3. It could also scavenge the uranium-induced intracellular ROS and protect against the uranium-induced cell damage. BPCBG is worth further investigation.
Animals ; Cell Line ; Cell Survival ; drug effects ; Chelating Agents ; administration & dosage ; chemistry ; pharmacology ; Dose-Response Relationship, Drug ; Epithelial Cells ; cytology ; metabolism ; Humans ; Kidney ; metabolism ; Kidney Tubules, Proximal ; cytology ; Male ; Micronucleus Tests ; Molecular Structure ; Organometallic Compounds ; toxicity ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; metabolism ; Uranium ; metabolism ; urine

Objective To unveil the changes of endemic fluorosis in order to provide the scientific basis for making countermeasure. Methods Seven villages was selected as monitoring points in Qianan County of Jilin Province where drinking water was improved or was going tobe improved. Dental fluorosis was surveyed with Dean method and for urine fluoride content was tested using fluoride ion-selective electrode analysis in 8 - 12 years old children. Clinical skeletal fluorosis was detected in all residents of aged 16 and over in the beginning of the monitor and every 3 years. X-ray films were taken in those over 16 years old at the beginning of the monitor and every 5 years. Results Detectable rate of dental fluorosis was decreased compared with before(Weizi: 11.3% to 2.2%, Danzi: 16.3% to 12.1%, Houqi: 53.7% to 37.5%, Houju: 38.6% to 33.3%), and severity was declining, for example, in Dongnanjing, rate of being moderate was dropping from 11.3% to 7.8%, severe rate from 2.8% to 0;in Houqi: moderate rate from 16.7% to 0, severe rate from 1.9% to 0;in Houju, moderate rate from 1.4% to 0,severe rate from 1.4% to 0. However, detectable rate of dental fluorosis rose in Dabin from 61.7% to 70.0% and in Dongbin-donju from 52.7% to 71.1% due to increased fluorides in drinking water. Urine fluorides content in 8 - 12 years old children was decreased to normal level(1.5 mg/L) in most of monitoring spots, but in Dabin it still remained at a high level, being 4.03 and 4.57 mg/L before and after respectively. Detectable rate clinical skeletal fluorosis was between 11.1% - 25.7% among those aged 16 and over in 7 monitoring point in 1991 - 2006, however it increased year after year in Dabin (15.9%, 21.6% and 25.7% in 1991, 1993 and 1995). Positive X-ray rate for skeletal fluorosis was decreased from 54.9% to 24.0% in Dabin, from 40.7% to 23.5% in Dongbin-donju and from 28.6% to 20.4% in Dangnanjing. Conclusions Endemic fluorosis has been controlled attributed to improved drinking water and decreased fluorides content in drinking water. Combined methods are needed to decrease to the intake of fluorides to control the diseases.