Objective To study the inhibition of iron-dependent lipid peroxidation(IDLPO)by apigenin on rat cerebral homogenate in vitro and to evaluate the neuroprotective effects of apigenin on acute transient focal cerebral ischemia-reperfusion injury in rats.Methods In vitro IDLPO on rat cerebral homogenate was induced with ferrous sulfate,the incubation mixture was observed at three various concentration of apigenin and deferoxamine(DFX),and malondialdehyde(MDA)level was assayed by the 2-thiobarbituric acid(TBA)test.In vivo,the transient focal cerebral ischemia-reperfusion model in rats was established with insertion of thread embolish into middle cerebral artery.In experiment groups the neurological behavior scores,TTC stain of brain slices,and neurocyte morphology were observed.The homogenate of left hemisphere was collected for investigating the effect of apigenin on content of MDA and activity of superoxide dismutase(SOD)in 24,48,and 72 h.Results MDA was reduced in three various concentration of apigenin on rat cerebral homogenate(P0.05).In vivo,abnormal neurological behavior scores existed and typical cortical infarct lesions were found by TTC stain in both apigenin and model groups.An obvious intracellular and intercellular edema and vacuolization were found in the cerebral cortexes and hippocampuses in model group.There was karyopycnosis in glias and neurons.However lesion was alleviated in apigenin group.The MDA contents in both apigenin and model groups were increased greatly compared to ones of Sham-operated group,respectively(P

Objective To observe the effect of apigenin on the recovery of neurological function following cerebral ischemia-reperfusion and investigate its mechanism. Methods Ninety male Sprague-Dawley rats were randomized into a sham-operated group, a model group and an apigenin-treated group. A transient ( 1.5 h) focal cerebral ischemia-reperfu-sion model was established in the rats of the model and apigenin-treated groups. In the sham-operated rats the middle cere-bral artery was not occluded. The rats in the apigenin-treated group received an intra-abdominal injection of apigenin, and the rats in the other two groups received injections of normal saline solution. Neurological behavior scores were assessed in accordance with the Zea Longa method at the 24th, 48th and 72nd hour and the 7th day after reperfusion. Cellular and sub-cellular morphology were observed with an optical microscope and an electron microscope, and the levels of TNF-α and IL-1β were measured using ELISA. Results Neurological function improved by the 7th day after reperfusion in the model group, but improved significantly by the 72nd hour after reperfusion in the apigenin-treated group. Average TNF-α and IL-1β levels in the model group and the apigenin-treated group were significantly higher than in the sham-operated group. Av-erage TNF-α and IL-1β levels in the apigenin-treated group were significantly lower than in the model group at the 48th and 72nd hour after reperfusion. Neurological behavior scores had a positive correlation with the IL-1β and TNF-α levels. In the model group, obvious intracellular and intercellular edema and vacuolization were observed in the ischemic cortices and hippocampuses, with remarkable karyopycnosis and organelle broadening and dissolution and vacuolization in glial cells and neurons. In the apigenin-treated group, similar but significantly milder morphological changes were observed. Conclusion Apigenin can promote the recovery of neurological function in rats by downregulating the expression of TNF-α and IL-1βfollowing focal cerebral ischemia-reperfusion.

Objective To establish an early cognitive disorder model in rats and investigate the early cognitive functioning after ischemic hypoxic brain injury during the neonatal period. Methods Forty-six newborn Sprague-Dawley rats were randomized into a 21-d-old group and a 31-d-old group. These 2 groups were then subdivided into model and sham-operated subgroups (M21, n=12; SH21, n=11; M31, n=12; SH31, n=11). A model of neonatal early cognitive disorder was established in the rats of the M21 and M31 groups using a modification of Rice's method. Rats in the SH21 and SH31 groups received skin incisions and common carotid artery separation without ligation or hypoxia. Each group was tested with a Morris water maze. The rats were sacrificed after testing, and brain tissue was examined under the electron microscope. Nissl staining allowed Nissl body quantification and neurocyte acin the M21 group was significantly longer than in the SH21 group. The 31-d-old subgroups had shorter average escaping latencies than the corresponding 21-d-old subgroups. (b) Spatial memory: The average platform times, Ⅰ region times and Ⅰ region distances showed no significant differences among groups. ②Brain pathology (a) Gross appearance: Obvious ischemic hemisphere atrophy was observed in the M group, and no abnormality was observed in the SH group. (b) Electron microscopic observation: In the SH group cell ultrastructures in the ischemic hippocampus were normal. Karyopyknosis and dilated endoplasmic reticulums were found in the M group. More mitochondria were found in the presynaptic membranes of the ischemic hippocampus in the M group than that in the SH group. (c) Nissl body quantification and neurocyte activity analysis: Significantly less activity in the ischemic cortex was found in the M21 group compared to the SH21 group. More activity was observed in the 31-d-old subgroups than in the corresponding 21-d-old subgroups. Conclusions ①The neonatal rats with ischemic hypoxic brain injury had prolonged average escaping latency and depressed neuronal activity. ②The 31-d-old rats had better spatial localization learning ability than the 21-d-old rats.

In order to investigate the sleep quality and influencing factors in patients with Parkinson's disease (PD),201 PD patients were enrolled and underwent extensive clinical evaluations.Subjective sleep evaluation was assessed using the Pittsburgh Sleep Quality Index (PSQI),and the Epworth Sleepiness Scale (ESS).It was found that poor sleep quality (77.11％) and excessive daytime sleepiness (32.34％) were commonly seen in PD patients and positively correlated with disease severity.Then 70 out of the 201 PD patients and 70 age-and sex-matched controls underwent a polysomnographic recording.The parameters were compared between PD group and control group and the influencing factors of sleep in PD patients were analyzed.The results showed that sleep efficiency (SE) was significantly decreased (P＜0.01),and sleep latency (SL) and the arousal index (AI) were increased (P＜0.05) in the PD group as compared with those in the control group.SE and total sleep time (TST) were positively correlated with the Hoehn and Yahr (H&Y) stage.There was significant difference in the extent of hypopnea and hypoxemia between the PD group and the control group (P＜0.05).Our results indicate that PD patients have an overall poor sleep quality and a high prevalence of sleep disorder,which may be correlated with the disease severity.Respiratory function and oxygen supply are also affected to a certain degree in PD patients.

The purpose of this study was to find the rare individual JK(a-b-) phenotype of proband family and explore its molecular mechanism and the genetic background, in order to provide base for searching compatible donor to blood transfusion of the individuals with rare JK(a-b-) phenotype. Urea lysis test was used to screen the JK(a-b-) phenotype and results were confirmed with serological method. The genotypes were detected with PCR-SSP. The 4-11 exons and their flanking intron regions of JK gene were amplified and sequenced. The results showed that her elder brother has a same phenotype JK(a-b-) and genotypes JK(a)/JK(b) with proband. The phenotype and genotypes of their parent is JK (a+b-) and JK(a)/JK(b), respectively; and the younger sister's is JK (a+b-) and JK(a)/JK(a). Acceptor site of intron 5 3' g > a mutation was detected in proband and her elder brother, which may cause the JK(a-b-) phenotype of proband and her elder brother. There is g/a and a at this site in their parent and younger sister, respectively. Additionally, the SNP (ncbi:rs8090908) a > g at nt-99 in intron 3 was found in proband and her elder brother, it needs to be explored whether the SNP is related to JK(a-b-) phenotype. This SNP was not found in their parent and younger sister. This JK(a-b-) phenotype abides by the rule of dominant inheritance in the family, suggesting that there is higher probability to find homology phenotype and genotype by investigating in their family, especially in their siblings.
Adult ; Alleles ; Exons ; Female ; Genotype ; Humans ; Introns ; Kidd Blood-Group System ; genetics ; Male ; Pedigree ; Phenotype

Since Nei Jing, through the development and supplement of ancient physicians, syndrome differentiation of TCM ophthalmology has been gradually improved. To the Jin and Yuan Dynasties, LI Dong-yuan's Pi Wei Lun paid attention to spleen and stomach,which made raising yang therapy has been accepted and widely used in medical subjects. After 40 years of clinical practice and inheritance and innovation of LI Dong-yuan's raising yang therapy, Professor LV Hai-jiang gradually formed his own experience features of using raising yang therapy to treat ophthalmic diseases. Combined with the clinical medical records, this article reviewed diagnosis and treatment experience of Professor LV in using raising yang therapy to treat ophthalmic diseases from the aspects of raising yang and removing obstruction in collaterals, raising yang and dissipating heat, activating blood circulation and expelling stasis, and eliminating dampness and phlegm.

OBJECTIVETo explore the possibilities of bone marrow stromal cells (MSCs) to adopt Schwann cell phenotype in vitro and in vivo in SD rats.

METHODSMSCs were obtained from tibia and femur bone marrow and cultured in culture flasks. Beta-mercaptoethanol followed by retinoic acid, forskolin, basic-FGF, PDGF and heregulin were added to induce differentiation of MSCs'. Schwann cell markers, p75, S-100 and GFAP were used to discriminate induced properties of MSCs' by immunofluorescent staining. PKH-67-labelled MSCs were transplanted into the mechanically injured rat sciatic nerve, and laser confocal microscopy was performed to localize the PKH67 labelled MSCs in the injured sciatic nerve two weeks after the operation. Fluorescence PKH67 attenuation rule was evaluated by flow cytometry in vitro.

RESULTSMSCs changed morphologically into cells resembling primary cultured Schwann cells after their induction in vitro. In vivo, a large number of MSCs were cumulated within the layer of epineurium around the injured nerve and expressed Schwann cell markers, p75, S-100, and GFAP.

CONCLUSIONMSCs are able to support nerve fiber regeneration and re-myelination by taking on Schwann cell function, and can be potentially used as possible substitutable cells for artificial nerve conduits to promote nerve regeneration.

Animals ; Biomarkers ; analysis ; Bone Marrow Cells ; cytology ; Cell Differentiation ; Cells, Cultured ; Flow Cytometry ; Fluorescent Antibody Technique, Indirect ; Fluorescent Dyes ; Glial Fibrillary Acidic Protein ; analysis ; Morphogenesis ; Organic Chemicals ; analysis ; Phenotype ; Rats ; Receptor, Nerve Growth Factor ; analysis ; S100 Proteins ; analysis ; Schwann Cells ; cytology ; metabolism ; Sciatic Nerve ; cytology ; injuries ; Stromal Cells ; cytology ; metabolism ; transplantation