ObjectiveTo investigate the effects of maternal rat with marginal iodine deficiency on the nerve and intelligence development in its offspring and the related mechanisms.MethodsThe rat model of marginal iodine deficiency was established on the basis of epidemiological characteristics and iodine metabolism characteristics of rats reported in literatures.Marginal iodine deficiency rats were given 3 μg iodine a day ; normal control rats were given 4 μg iodine daily ; iodine deficiency rats were given 1.2 μg iodine daily,respectively.Western blot was used to detect the protein levels of brain derived neurophic factor (BDNF) and early growth response factor 1 ( EGR1 ) in the hippocampus of 7 days newborn rats.Immunohistochemistry was used to measure c-jun and c-fos expressions in the hippocampal CA1 region of 40 days rats.Water maze method was used to measure the ability of learning and spatial memory.Results FT4 level in rats of marginal iodine deficiency group during pregnancy decreased by about 30％.Seven days after birth,the contents of EGR1 and BDNF proteins in the hippocampus of the offspring from marginal iodine deficiency group were significantly decreased compared with normal control group (both P ＜ 0.05 ).Forty-day-old newborn rats in marginal iodine deficiency group also showed significantly decreased c-jun and c-fos expressions in the hippocampal CA1 region ( both P＜0.05 ),along with a decreased trend of spatial learning and memory ability.Conclusions FT4 level will significantly decrease after pregnancy if rats have marginal iodine deficiency,affecting the expression of related proteins in the brain of newborn rats and having a negative impact on offspring brain development.

AIM:To investigate the protective effects of sodium ferulate(SF)on apoptosis in cultured hippocampal neurons induced by sodium nitroprusside(SNP),and the effect of SF on expression of bcl-2 and bax.METHODS:The primary cultured hippocampal neurons were exposed to 50 ?mol SNP,a nitric oxide-donor,for 24 h after pretreatment with different concentrations of SF(10-160 ?mol/mL)for 6 h.Then neuronal viability was tested by MTT assay.Fluorescent staining with Hoechst 33258 and agarose gel electrophoresis was used to analyze apoptosis.The expressions of bcl-2,bax mRNA and protein were tested by RT-PCR and Western blotting.RESULTS:Pretreatment with SF(10-160 ?mol/L)for 6 h increased the survival rate of neurons.SF prevented the neuronal nuclei from shrinkage,condensation and cleavage and blocked neuronal nuclear DNA fragmentation induced by SNP.SF also increased the expressions of bcl-2 mRNA and Bcl-2 protein and decreased the expressions of bax mRNA and Bax protein.CONCLUSION:SF prevents the cultured hippocampal neurons against SNP neurotoxicity.The mechanism of protection is related to the increase in Bcl-2 level and the decrease in Bax level.As a result,the ratio of Bcl-2/Bax is changed.

This article discussed how to separate examination from teaching but at the same time prevent the content of examination being out of joint with teaching when developing the warehouse and review course wares of the examination of emergency medical science,as well as how to make use of a computer to manage the warehouse and review course wares of emergency call medical science examination.

BACKGROUND: Acidic peptide is the tripeptide composed of 3 glutamic acids, which cannot bring excitatory nerve signal transmission into playlike single glutamic acid through presynaptic release and integration withpostsynaptic NMDA receptor directly as excitable neurotransmitter. It is quite possible that acidic peptide plays its actions by integrating with multiple metabolic glutamic acidic receptors so as to promote neuron proliferation or release nerve growth factor (NGF). OBJECTIVE: To probe into whether acidic peptide induces changes in learning and memory of model rats with Alzheimer disease (AD).DESIGN: Randomized controlled single experiment was designed.SETTING: Teaching-Research Room of Biochemistry and Molecular Biology of Basic Medical College of Zhengzhou University.MATERIALS: The experiment was performed in 2nd Research Room and Experimental Animal Room of Teaching-Research Room of Biochemistry and Molecular Biology of Basic Medical College of Zhengzhou University.Totally 100 SD male rats were selected and some of them were excluded due to retarded response in step down test. Totally 84 rats were included in the experiment and randomized into 7 groups, named normal control,model group, physiological saline group (PS group), piracetam group, acidic peptide groups of 60, 30 and 15 mg/kg, 12 rats in each group. Acidic peptide is a new small molecular peptide separated from bovine brain in this research team and is tripeptide composed of three glutamic acids.METHODS: Except normal control, in the rest groups, after 1 week routine breeding, cerebral stereotactic microinjection was used to inject 5 μg ibotenic acid in hippocampus of rats to destroy bilateral Meynert's basal ganglia to establish AD model. In normal control and model group, no medication was applied. In PS group, physiological saline was used for gastric perfusion. In piracetam group, piracetam of 0.3 g/kg was used for gastric perfusion and in acidic peptide groups of 15, 30 and 60 mg/kg,acidic peptide of 60, 30 and 15 mg/kg was applied for gastric perfusion successively, continuously for 20 days, once per day, 2 mL/time. On the expiration of gastric perfusion, learning and memory of rats were examined with step down test in every group. The animal was placed on the safe table on step down platform to adapt to the environment for 3 minutes, afterwards, 36 V electric current was given. Error response was recorded if the animal jumped to the copper railings after electric shock and correct response was recorded if the animal jumped back the safe area. Step-up latent phase and frequency of correct response were recorded in 3 minutes.MAIN OUTCOME MEASURES: Comparison of learning and memory of rats in every group. RESULTS: Totally 84 rats were all included in the result analysis. ①Comparison of learning in every group: Compared with model group, stepup latent phase was shortened remarkably in every acidic peptide group[(102.03±5.33), (71.77±4.38), (68.28±9.53), (69.13±8.79) s, P ＜ 0.01] and the frequency of correct response was improved remarkably [(12.92±2.91),(16.17±2.79), (15.83±3.27), (16.33±2.53) times, P ＜ 0.01]. ② Comparison of memory in every group: Compared with model group, step-up latent phase was shortened remarkably in every acidic peptide group [(43.17±4.66),(29.78±4.48), (26.20±3.28), (22.09±4.43) s, P ＜ 0.01] and the frequency of correct response was improved remarkably [(15.67±2.15), (20.92±2.68),(20.83±2.29), (20.25±2.05) times, P ＜ 0.01].CONCLUSION: Acidic peptide can shorten remarkably the step-up latent phase of AD rats in step down test and improve the frequency of correct response. It is indicated that acidic peptide provides good intervention on learning and memory of rat model of Alzheimer disease.

BACKGROUND: It is pointed in some experiment that acidic peptide improves learning and memory of model rat with Alzheimer disease (AD) by inhibiting the synthesis of toxic compounds of nitric oxide (NO).OBJECTIVE: Animal model with Alzheimer disease was established to observe the changes in the levels of NO, nitric oxide synthase (NOS) and acetylcholinesterase (AChE) treated with acidic peptide of various dose concentration.DESIGN: Randomized control and single experiment.SETTING: Teaching-Research Room of Biochemistry and Molecular Biology of Basic Medical College of Zhengzhou University.MATERIALS: The experiment was performed in 2nd Research Room and Experimental Animal Room of Teaching-Research Room of Biochemistry and Molecular Biology of Basic Medical College of Zhengzhou University.Totally 100 SD male rats were selected and some of them were excluded due to retarded response in step down test. Totally 84 rats were included in the experiment and randomized into 7 groups, named normal control,model group, physiological saline group (PS group), Piracetam group, acidic peptide groups of 15, 30 and 60 mg/kg, 12 rats in each group. Acidic peptide was a new small molecular peptide separated from bovine brain and is tripeptide composed of three glutamic acids.METHODS: Except normal control, in the rest groups, after 1 week routine breeding, cerebral stereotactic microinjection was used to inject 5 μg ibotenic acid in hippocampus of rats to destroy bilateral Meynert's nucleus basalis to establish AD model. In normal control and model group, no medication was applied. In PS group, physiological saline was used for gastric perfusion. In piracetam group, piracetam of 0.3 g/kg was used for gastric perfusion and in acidic peptide groupsof 15, 30 and 60 mg/kg,acidic peptide of 15, 30 and 60 mg/kg was applied for gastric perfusion successively, continuously for 20 days, once per day, 2 mL/time. On the expiration of gastric perfusion, the rats were sacrificed after anesthetized and the brain was collected on ice plate to prepare tissue homogenate. After centrifugated at 1 000 r/minute, 4℃ for 10 minutes, the supernatant was collected to assay the levels of NO, NOS and AChE with NO, NOS and AChE kits successively.MAIN OUTCOME MEASURES: Levels of NO, NOS and AChE in brain of rat in each groupRESULTS: Totally 84 rats were employed in the experiment and all entered result analysis. Comparison of levels of NO, NOS and AChE in rat brain of each group: compared with model group, NO levels in acidic peptide groups of 15, 30 and 60 mg/kg were reduced remarkably[(1.95±0.20), (1.39±0.10), (1.25±0.07), (1.00±0.04) mmoL/kg, P ＜ 0.05],NOS levels were reduced remarkably [(4.53±0.18), (3.39±0.09), (3.10±0.06),(2.97±0.06) μmol/kg, P ＜ 0.05] and AChE did not change remarkably[(0.67±0.12), (0.71±0.11), (0.72±0.08), (0.72±0.07) mmol/L, P ＞ 0.05].CONCLUSION: Acidic peptide reduces significantly the synthesis of NO and NOS in brain of AD rat, but it dose not affect AChE activity remarkably. It is suggested that acidic peptide improves learning and memory of rat with Alzheimer disease probably by inhibiting the synthesis of toxic compound of NO or its toxicity.

OBJECTIVETo observe the soft tissue regeneration after implantation of two novel citric acid-based biodegradable materials in the skull defects in rats.

METHODSTwo novel citric acid-based biodegradable materials were implanted in the muscular tissues in the thigh and harvested 2 weeks later. Another 40 rats with surgically induced cranial defect were randomized into control group, autograft group, CUPE-HA group, and POC-HA group (n=10), and 3 months after implantation, the materials were harvested for histological and morphometric analyses.

RESULTSSoft tissue regeneration was stimulated by the two biodegradable materials in the muscular tissues. The implants also stimulated angiogenesis and soft tissue regeneration in the cranial defect and accelerated of intramembranous ossification.

CONCLUSIONThe 2 novel citric acid-based biodegradable materials can induce angiogenesis and soft tissue regeneration and accelerate intramembranous ossification in rats with cranial defects.

Absorbable Implants ; Animals ; Citric Acid ; Neovascularization, Physiologic ; Osteogenesis ; Rats ; Regeneration ; Skull ; Soft Tissue Injuries ; therapy ; Wound Healing