神舟家和1100C

虽然配置并不高,不过低廉的价格也降低了许多家庭购买电脑的门槛。

从CT图片到3D互动解剖教学模型的制作——以颅骨解剖结构教学模型制作为例

文章探讨了从CT图片到3D互动解剖教学模型的制作过程:通过一个真实人体的CT图片,进行3D解剖数字模型制作,并利用Unity3D制作成可在多个平台运行并互动的软件,以利于医学解剖教学。

Effect of NGF on c-fos mRNA Expression in Spinal Neuron after Spinal Cord Injury

Objective: To expound the mechanism of nerve growth factor (NGF) to protectspinal cord against injury. Methods: Forty-five rats with 10 g X 2. 5 cm impact T_8 spinal cordinjury (SCI) were divided into 3 groups. The experimental animals received 60 g NGF purified frombovine seminal plasma instantly, 1, 2, 4 h after in jury and an equal volume of normal saline wasgiven to the control group at the same time. The c-fos mRNA levels were detected by in situhybridization. Results: The results showed no evident c-fos expression in normal control group. Thec-fos expression increased markedly in damaged neurons. The peak value of c-fos mRNA arose at 1 h,and c-fos levels in NGF group reduced evidently. Conclusion: NGF could inhibit c-fos expression. Itmay serve as one of the action mechanisms of NGF to protect spinal cord against injury.

Central nervous system vasculitis and polyneuropathy as first manifestations of hepatitis C

Sensory or motor peripheral neuropathy may be observed in a significant proportion of hepatitis C virus (HCV)-infected patients.However,central nervous system (CNS) involvement is uncommon,especially in cryoglobulin-negative subjects.We describe a case of peripheral neuropathy combined with an ischemic CNS event as primary manifestations of chronic HCV infection without cryoglobulinemia.Significant improvement was observed after antiviral therapy.We discuss the spectrum of neurological manifestations of HCV infection and review the literature.

DOWN－REGULATION OF C－MYC ONCOGENE DURING NGF－INDUCED DIFFERENTIATION OF NEUROBLASTOMA CELL LINES

There may be a close relationship between myc oncogenes and carcinogenesis of human neuroblastoma. In previous studies, we were able to induce differentiation of certain neuroblastoma cell lines with NGF. In order to study gene regulation during differentiation, N-myc and c-myc cDNA probe were hybridized with RNA extracted from different cell lines before and after NGF treatment. It was found that cell lines which expressed N-myc did not express c-myc while those with c-myc did not express N-myc except for SHEP cell line which had neither c-myc nor N-myc expression. In NGF-induced differentiated neuroblastoma cells, c-myc oncogene was down-regulated in comparison with the control samples. The time course of c-myc down-regulation was concomitant with the appearance of morphological differentiation. In situ hybridization also showed remarkable reduction of c-myc oncogene expression in NGF-induced differentiated cells as compared with the untreated control cells. These results indicate that down-regulation of c-myc oncogene may be a key event during NGF-induced differentiation and overexpression of c-myc oncogene may, at least partially, be responsible for the genesis of neuroblastoma.

Myenteric neurons and intestinal mucosa of diabetic rats after ascorbic acid supplementation

AIM: To investigate the effect of ascorbic acid (AA) dietary supplementation on myenteric neurons and epithelial cell proliferation of the jejunum of adult rats with chronic diabetes mellitus. METHODS: Thirty rats at 90 d of age were divided into three groups: Non-diabetic, diabetic and diabetic treated with AA (DA) (1 g/L). After 120 d of treatment with AA the animals were killed. The myenteric neurons were stained for myosin-V and analyzed quantitatively in an area of 11.2 mm2/animal. We further measured the cellular area of 500 neurons per group. We also determined the metaphasic index (MI) of the jejunum mucosa layer of about 2500 cells in the intestinal crypts, as well as the dimensions of 30 villi and 30 crypts/animal. The data area was analyzed using the Olympus BX40 microscope. RESULTS: There was an increase of 14% in the neuronal density (792.6 ± 46.52 vs 680.6 ± 30.27) and 4.4% in the cellular area (303.4 ± 5.19 vs 291.1 ± 6.0) respectively of the diabetic group treated with AA when compared to control diabetic animals. There were no signifi cant differences in MI parameters, villi height or crypt depths among the groups.CONCLUSION: Supplementation with AA in the diabetic animal promoted moderate neuroprotection. There was no observation of alteration of the cellular proliferation of the jejunum mucosa layer of rats with chronic diabetes mellitus with or without supplementation with AA.

Noradrenaline as a putative neurotransmitter mediating hypotension-induced Fos-like immunoreactivity inthe supraoptic nucleus of the rat

Hemorrhage or hypotension induces extensive Foslike immunoreactivity in the magnocellular neurosecretory cells in the supraoptic nucleus of the hypothalamus in rat, especially in the vasopressin neurons. The present study was to explore the neurotransmitter mediating this effect. Microinfusion of the alpha-adrenergic blocker into the supraoptic nucleus reduced the hypotension-induced Fos, whereas beta-antagonist did not affect it significantly. Alpha1- and alpha2-antagonist, prazosin and yohimbine,both reduced the Fos-positive cell counts. However, the effective dosage of yohimbine was much larger. Alpha1-agonist, methoxamine, induced abundant Fos-like immnnoreactivity in the vasopressin cells in this nucleus,while beta-and alpha2-agonist did not elicit such effect.Administration of the noradrenergic re-uptake inhibitor,desipramine, to this nucleus to locally accumulate the spontaneously released noradrenaline from the nerve terminals also induced Fos expression, mostly in the vasopressin cells.

Val 70, Phe 72 and the last seven amino acid residues of C-terminal are essential to the function of norepinephrine transporter

The norepinephrine transporter(NET) is a member of the Na+/Cl- dependent neurotransmitter transporter family and constitutes the target of several clinically important antidepressants. To delineate the critical amino acid residues and the function of C-terminal in regulating transport activity of NET, here we constructed two site mutants (V70F, F72V; V70I, F72V) and one C-terminal truncated mutant (△611-617). The wild type and mutants of NET were expressed in Xenopus oocytes by injection of their cRNA. We found that all of these mutants lost their transport activity. These results indicate that the amino acid residues of V70 and F72 3 and the last seven amino acids of C-terminal are essential to the transport activity of NET.

THE RELATIONSHIP BETWEEN EXPRESSIONS OF N-myc AND c-myc ONCOGENES IN NEUROBLASTOMA:AN IN SITU HYBRIDIZATION AND IMMUNOCYTOCHEMICAL STUDY

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BEHAVIOR AND ACTIVITIES IN THE CENTRAL NERVOUS SYSTEM AFTER ACTIVATION OF L-TYPE CALCIUM CHANNELS IN MICE

The distribution of the immediate early gene c-fos expression in the mouse central nervous system after subcutaneous injection of Bay K 8644 was observed immunohistochemically. Half an hour after injection, cfos protein (FOS) was expressed in the piriform cortex, sensorimotor cortex, caudate putamen, thalamic paraventricular nucleus and striate cortex,etc. Intense FOS immunoreactive (FOS-ir) cells were seen during 2 ～ 4 h after injection. The restllts suggested that the distribution of FOS-ir ce1ls after subcutaneous injection of Bay K 8644 was coincldent with that of L-type calcium channels in the different areas of the CNS. After Bay K 8644 injection, mice appeared seizure-like behavior. The percentage of cells double-labelled by FOS and CaBP immunoreactivities in the observed regions was about 60. 2～72. 8% in CaBP-ir cells. It suggested that most CaBP-lr cells may have L-type calcium channels.

C-peptide and Diabetic Encephalopathy

With the changes of life style, diabetes and its complications have become a major cause of morbidity and mortality. It is reasonable to anticipate a continued rise in the incidence of diabetes and its complications along with the aging of the population, increase in adult obesity rate, and other risk factors. Diabetic en- cephalopathy is one of the severe microvascular complications of diabetes, characterized by impaired cogni- tive functions, and electrophysiological, neurochemical, and structural abnormalities. It may involve direct neuronal damage caused by intracellular glucose. However, the pathogenesis of this disease is complex and its diagnosis is not very clear. Previous researches have suggested that chronic metabolic alterations, vascular changes, and neuronal apoptosis may play important roles in neuronai loss and damaged cognitive functions. Multiple factors are responsible for neuronal apoptosis, such as disturbed insulin growth factor （IGF） system, hyperglycemia, and the aging process. Recent data suggest that insulin/C-peptide deficiency may exert a primary and key effect in diabetic encephalopathy. Administration of C-peptide partially improves the condition of the IGF system in the brain and prevents neuronal apoptosis in the hippocampus of diabetic patients. Those findings provide a basis for application of C-peptide as a potentially effective therapy for diabetes and diabetic encephalopathy.

The relationship between nNOS and Cyt-c in mitochondria of glioma

Objective： The aim of this study was to investigate the association between neuronal nitric oxide synthase （nNOS） and the expression level of Cytochrome C （Cyt-c） in mitochondria. Methods： The pathological diagnosis of glioma and tumor classification was by HE staining, and we use immunohistochemistry method to analyse the level of nNOS in different pathological grade glioma and the expression level of Cyt-c in mitochondria meanwhile. Results： The levels of nNOS were highest in grade Ⅲ tumors, moderate in grade Ⅱ tumors, and lowest different in grade I tumors. There was significant difference of the nNOS levels among different pathological grade tumors （P 〈 0.05）. Furthermore, the similar phenomenon was observed in the expression level of Cyt-c in mitochondria （P 〈 0.05）. Conclusion： The expression level of nNOS and Cyt-c in mitochondria was significantly related to the pathological grade of glioma.

8000元以下笔记本电脑导购

笔记本电脑有外形小巧、便于携带等特点，因此很多消费者把目光转向了笔记本电脑。一直以来笔记本电脑给人的印象都是高高在上，价格成为很多消费者的一道门槛，由于消费能力的限制，很多消费者不可能购买国际知名品牌。

Protein kinase C regulates neurite outgrowth in spinal cord neurons

Objective The functional roles of protein kinase C （PKC） in the neurite outgrowth and nerve regeneration remain controversial. The present study was aimed to investigate the role of PKC in neurite outgrowth, by studying their regulatory effects on neurite elongation in spinal cord neurons in vitro. Methods The anterior-horn neurons of spinal cord from embryonic day 14 （E14） Sprague-Dawley （SD） rats were dissociated, purified and cultured in the serum-containing medium. The ratio of membrane-PKC （mPKC） activity to cytoplasm-PKC （cPKC） activity （m/c-PKC） was studied at different time points during culture. Results Between 3-11 d of culture, the change of m/c-PKC activity ratio and PKC-βⅡ expression in the neurite were both significantly correlated with neurite outgrowth （r=0.95, P 〈 0.01; r=0.73, P 〈 0.01, respectively）. Moreover, PMA, an activator of PKC, induced a dramatic elevation in the m/c-PKC activity ratio, accompanied with the increase in neurite length （r=-0.99, P 〈 0.01）. In contrast, GF 109203X, an inhibitor of PKC, significantly inhibited neurite elongation, which could not be reversed by PMA. Conclusion PKC activity may be important in regulating neurite outgrowth in spinal cord neurons, and βⅡ isoform of PKC probably plays a major role in this process.

Effects of SKF-96365, a TRPC inhibitor, on melittin-induced inward current and intracellular Ca^2+ rise in primary sensory cells

Objective Melittin （MEL） is a major component of bee venom and can produce both persistent spontaneous nociception and pain hypersensitivity when injected subcutaneously in the periphery. The present study aimed to examine the roles of transient receptor potential canonical （TRPC） channels in mediation of MEL-indueed activation of primary nociceptive cells. Methods Whole-cell patch-clamp and laser scanning confocal calcium detection were used to evalu- ate the effects of SKF-96365, a TRPC inhibitor, applied on the acutely isolated dorsal root ganglion （DRG） cells of rat, on MEL-induced increase in intracellular calcium concentration （[Ca2＋]i） and inward current. Results Under voltage- clamp mode, 43.9% （40/91） DRG cells were evoked to give rise to the inward current by 2 pmol/L MEL, which could be significantly suppressed by 3 doses of SKF-96365 （1, 5 and 10μmol/L） in a dose-dependent manner. Of the other 210 cells, 67.6% responded to MEL with an intracellular Ca2＋ rise, as revealed by confocal calcium imaging. Of these MEL- sensitive cells, 46.5% （66/142） were suppressed by the highest dose of SKF-96365. Conclusion MEL-induced activation of small to medium-sized DRG cells can be suppressed by SKF-96365, suggesting the involvement of TRPC channels in the mediation of MEL-induced activation of primary nociceptive cells.

Fabrication and characterization of implantable silicon neural probe with microfluidic channels

In this paper, a silicon-based neural probe with microfluidic channels was developed and evaluated. The probe can deliver chemicals or drugs to the target neurons while simultaneously recording the electrical action of these neurons extracellularly. The probe was fabricated by double-sided deep reactive ion etching （DRIE） from a silicon-on-insulator （SO1） wafer. The flu- idic channels were formed with V-shape groove etching on the silicon probe and sealed with silicon nitride and parylene-C. The shank of the probe is 4 mm long and 120 ~tm wide. The thickness of the probe is 100 ~tm. The probe has two fluidic chan- nels and two recording sites. The microfluidic channels can withstand a pressure drop as much as 30 kPa and the flow resisti ity of the microfluidic channel is 0.13 μL min-1 kPa-1, The typical impedance of the neural electrode is 32.3 kΩ at 1 kHz at room temperature.