ObjectiveTo explore the effect of brain derived neurotrophic factor(BDNF) on regeneration of distal axon in sciatic nerve after cfrush injury. MethodDistal axon was assessed by quantitavtive and qualitative analysis of pathology ResultLight microscope indicated thedensity of large diameter of peroneal-nerve was higher in study group compared with control group( P ＜0.01 ). No differences in density of littlediameter fiber were found between study and control group. EM showed the density of non-medullated fibers with diameter ＜0.5μm in studygroup was higher than that of control group. The numbers of layer in myelin was positively related to transverse axonal area( P ＜0.01 ) . The re-gression codfficient in study group wsa higher compared with control group( P = 0. 0023).ConclusionBDNF may promoted maturation ofsensoy nerve and formation of the myeline.

Periostin is a matri-cellular protein which was originally identified in MC3T3-E 1 osteoblast-like cell line,expressing in multiple tissues like bones,teeth,skin and cardiac valves.Periostin is also found in a large variety of cancers and injured tissues,involving in cancer cell invasion and metastasis as well as wound repair.Recent studies have suggested the role of Periostin in osteoblast adhesion and differentiation,fibrillogenesis,mineralization and bone fracture healing,and its expression is regulated by mechanical stress,various transcription factors,hormones and growth factors.In this article,we will discuss the expression,localization and general characteristics of Periostin,and provide a review on the study of it in bone biology.

BACKGROUND:Ola rats is a kind of rats with genovariation, who displays Wallerian degeneration after peripheral neuroaxonal damage that is slower than that normal 6J rats, thereby additional damage factor may help fully understand the property of Ola rats.OBJECTIVE: To observe the effect of acrylamide on the degeneration and regeneration of sciatic nerve medullated fibers following crush injury of C57BL/Ola (Ola) rat and C57BL/6J (6J) rat.DESIGN: Randomized controlled experiment.SETTING: Department of Neurology,Second People's hospital of Shenzhen; Department of Neurology of First hospital of Jilin University MATERIALS: This experiment was carried out in the neurological department in the University of Occupational and Environmental, Japan from January to June 1996. Twelve adult Ola rats and 6J rats were adopted and evenly randomly divided into experimental group and comparison group.METHODS: Rats were subjected to general anaesthesia, and then the proximal section of sciatic nerve was exposed and frustrated with hemostatic forceps for 10 s before suture. Rats in the experimental group were given intraperitoneal injection of acrylamide in a total dosage of 350 mg, which replaced by the same volume of physiological saline in comparison group.At 14 days after sciatic nerve torsion injury, all rats were anaesthetized again and the distal section of sciatic nerve was obtained and cut into slices, meanwhile the cross sectional area, the density and size frequency distribution of medullated fibers, as well as the number of medullated fibers in each nerve were determined.MAIN OUTCOME MEASURES: The density and size frequency distribution of sciatic nerve medullated fibers, as well as the number, the maximum diameter and the mean diameter of medullated fibers in two group of 0la rats and 6J rats.RESULTS: Totally 12 Ola rats and 6J rats entered the result analysis.① No Ola rat displayed Wallerian degeneration; But medullated fiber degeneration and following neonatal small diameter medullated fibers could be observed in 6J rats. ②In the experimental group, the total density of sciatic nerve medullated fibers in 6J rats was lower than that of Ola rat (P ＜ 0.05) ;with the total number of medullated fibers in 6J rats also less than that of Ola rat (P ＜ 0.01 ), which predominated by obviously reduced big diameter fibers (P ＜ 0.01); The mean diameter of medullated fiber in 6J rats was also obviously smaller than that of 0la rat (P ＜ 0.01 ).CONCLUSION: The Wallerian degeneration is extremely slow in Ola rat after torsion injury, which cannot be affected by acrylamide; while acrylamide has obvious inhibition on the axonal neogenesis in 6J rat after torsion injury.

Objective :To observate the axon changes in pathology of Ola mice,compared with those of 6Jmice. Methods:The peroneal nerve and sural nerve were studied by light-microscope and electronmi-croscope. Results :In light-microscope,the total transverse fascicular area was significantly large ;density ofmyelinated fibers was significantly less;the maximal diameter of myelinated fibers was significantly less;minimal diameter of myelinated fibers had no changens in 6J mice. The Ola mice were nomal. In electronmi-croscope observation, the neurofilament was accumulated within axons. Conclusion: In Ola mice treatedwith ACR,the like-Wallerian degeneration wes delayed. However,in 6J mice the neurofilament and mito-chondria accumulation was found within axons.

Objective To investigate the neonatal death causes and the relationship between the causes and the neonatal age,fetus age and the year in order to reduce neonatal mortality.Methods Data of neonatal autopsy and pathological records from 107 neonates in our hospital from January 1998 to May 2008 were collected,analyzed and summarized.Results 40.2%of the cases died within 24 hours and 72.9%died within 7 days after birth.The main death cause for those who died within 7 days was asphyxia(48.6%),and the main death causes ior those who died after 7 days were deformity(34.5%)and hemorrhage(34.5%).The most common death cause for premature bahies Was hyaline membrane disease(29.7%),and the most common one for term infants was congenital heart disease(23.3%).In the past 5 years.asphyxia Was still the most common death causein our country,those who died of infection were on the rise and the deformed babies increased too;on the contrary.those who died of obstetric causes and hemorrhage decreased.Conclusion Neonatal mortality could be reduced by prenatal management,prevention of premature delivery,improvement of the cooperation between pediatrics and obstetrics,and better management of NICU.

A total of 175 patients with type 2 diabetes mellitus (T2DM) were composed of 69 with normoalbuminuria,60 with microalbuminuria,and 46 with macroalbuminuria.The control group consisted of 64 healthy individuals.Serum YKL-40 levels were determined with ELISA method and related metabolic data were collected.Serum YKL-40 levels were significantly higher in T2DM group than in control group(P＜0.01).Significant correlations of YKL-40 were found with the ratio of microalbuminuria to uric creatinine(r=0.677,P＜0.01),HbA1C (r =0.562,P＜0.01),systolic blood pressure (r =0.372,P =0.001),HOMA-IR (r =0.460,P =0.001),low density lipoprotein-cholesterol (r=0.304,P=0.012),age(r=0.260,P=0.015),blood uric acid (r=0.329,P=0.018),and high density lipoprotein-cholesterol (r=-0.247,P=0.032).YKL-40 may play a role in the occurrence and development of diabetic nephropathy.

OBJECTIVETo explore the changes of brain energy metabolism following acrylamide (ACR) poisoning.

METHODSCreatie kinase (CK), adenosine triphosphate (ATP), adenosine diphosphate(ADP), adenosine 5'-monophosphate(AMP) and glucose contents in brain were observed in O1a mice and 6J mice following ACR intoxication by enzyme analytical method.

RESULTSATP, CK and glucose levels decreased transiently in O1a mice, while ATP level in 6J mice was significantly decreased (1.76 mumol/g, P < 0.01), as compared to the control (2.53 mumol/g) but ADP and AMP were increased, glucose was decreased. The activity of CK in poisoned group (1.13 mumol/g, P < 0.01) was lower than that of control (3.16 mumol/g and lasted for 5 weeks).

CONCLUSIONThe influence of ACR on O1a mice was slight and reversible but on 6J mice was severe and lasting. There was severe damage to the potential energy supply compensation, which might be the biochemical basis of neuron damage induced by acrylamide.

Acrylamide ; poisoning ; Adenosine Triphosphate ; analysis ; Animals ; Brain ; drug effects ; metabolism ; Creatine Kinase ; analysis ; Energy Metabolism ; drug effects ; Glucose ; analysis ; Mice

Objective To investigate the diagnostic value of the texture analysis in differentiating adult pilocytic astrocytomas (PA)from hemangioblastomas(HB).Methods 22 adult patients with PA and 20 patients with HB which were confirmed by postoperative pathological were retrospectively reviewed.The conventional MRI features and texture parameters were analyzed.Eight texture parameters were extracted using run-length matrix(RLM),and the differences of texture parameters of the two groups were analyzed by independent-samples t test.Results The short run emphasis(SRE),grey-level non-uniformity(GLNU),run-length non-uniformity(RLNU),high grey-level run emphasis(HGRE)and short run high grey-level emphasis(SRHGE)were higher in adult PA than in HB.The long run emphasis(LRE),low grey-level run emphasis(LGRE)and short run low grey-level emphasis(SRLGE)were lower in adult PA than in HB.The eight texture parameters had significant differences between the two groups(P<0.05).Conclusion Texture analysis can provide reliably objective basis for differentiating adult PA from HB.

Objective:To explore the anti-aging effects of berberine hydrochloride and underlying mechanism.Methods:Twelve 4-week-old C57BL6/J mice were divided into aging group (fed with normal chaw), aging+ BBR intervention group(fed with normal chaw containing 1 g/kg berberine hydrochloride). At the age of 64 weeks, all the experimental mice were executed. The liver tissues were made into paraffin sections for HE staining to observe the morphological and structural integrity of liver parenchymal cells for pathological evaluation. Immunofluorescence was used to detect p16 protein expression levels in liver. The expression levels of malondialdehyde(MDA), superoxide dismutase(SOD), and glutathione peroxidase(GSH-Px) were detected by colorimetry. The expression levels of interleukin(IL)-1β, IL-6, and tumor necrosis factor-α(TNF-α) in liver tissues and IL-8 in serum were detected by enzyme linked immunosorbent assay(ELISA) technique. The p16, p21, nuclear factor erythroid-2 related factor 2(Nrf2), nuclear factor-κB(NF-κB), phospho(p-)NF-κB, inhibitory κB(IκB)α, p-IκBα, and p38 mitogen-activated protein kinase(MAPK) protein expression levels in liver were detected by Western blotting. The same indices were tested in the 16-week-old mice as the young control group.Results:Compared with the young control group, the liver tissue in the aging control group exhibited morphological aging and antioxidant capacity were reduced( P<0.01), and inflammatory factors were increased( P<0.05 or P<0.01). Compared with the aging group, the liver tissues in the aging+ BBR intervention group were still maintain regular arrangement of hepatocytes, the p16 and p21 protein expression levels were significantly increased( P<0.05 or P<0.01), the antioxidant capacity were increased( P<0.05 or P<0.01), the level of inflammatory factors were decresed( P<0.05 or P<0.01), and the p38 MAPK/NF-κB pathway and Nrf2 pathway were inhibited( P<0.001). Conclusion:Berberine hydrochloride improves the aging morphology of the liver, potentially by suppressing the p38 MAPK/NF-κB pathway to reduce inflammation levels and inhibiting the Nrf2 pathway to ameliorate oxidative stress.

Objective:To evaluate the effect of Parkinson′s disease factor on the sedative efficacy of dexmedetomidine.Methods:The patients of either sex, aged 45-64 yr, of American Society of Anesthesiologists Physical Status classification Ⅱor Ⅲ, with body mass index of 18.5-30.0 kg/m 2, undergoing non-intracranial space-occupying lesions in neurosurgery, were selected.Patients were divided into control group (group C) and Parkinson′s disease group (group P) according to whether they had Parkinson′s disease or not.The ED 50 of dexmedetomidine was determined by using the Dixon′s up-and-down method.The initial dose of dexmedetomidine was 0.5 μg/kg in both groups, and each time the concentration increased/decreased by 0.05 μg/kg in the next patient, which was repeated until 7th independent crossover pair (loss of consciousness) appeared, and then the test was ended.The ED 50 and 95% confidence interval of dexmedetomidine inducing loss of consciousness were calculated using the probit test in a Logistic regression model.Hypertension, hypotension, bradycardia and nausea and vomiting were recorded. Results:Compared with group C, the ED 50 of dexmedetomidine inducing loss of consciousness was significantly increased in group P ( P<0.05), and no significant change was found in the incidence of adverse reactions in group P ( P>0.05). Conclusions:Parkinson′s disease factor can decrease the sedative efficacy of dexmedetomidine.