Objective To explore histopathological features in the nigrostriatal tissues of Parkinson’s disease (PD)and Parkisonism plus syndrome. Methods The substantia nigra and the striatum of 5 PD cases, 3 progressive supralnuclear palsy (PSP) cases and 3 multiple system atrophy (MSA) cases, and 5 normal aging control cases were examined by routine neuropathological methods and Gallyas-Braak staining and tau, ubiquitin and ?-synuclein immunohistochemistry. Pigmented neurons in the substantia nigra of PD, PSP, MSA cases and normal aging control cases were counted. The neuronal and glial cytoplasmic inclusions in the nigrostriatal tissues were observed. Components of the abnormal proteins were identified. Results Nerve cells in the substantia nigra of PD,PSP and MSA groups showed severe loss in number,especially the ventrolateral zone and the ventromedial zone. Compared with those in the normal aging control group,numbers of nerve cells in the ventrolateral zone of PD, PSP and MSA groups decreased to 37.5%, 24.2%, 33.8% in the right side, and 48.0%, 25.8%, 33.9% in the left side respectively. There were ?-synuclein and ubiquitin-positive Lewy bodies in the substantia nigra of PD. A lot of tau-positive, argyrophilic globous neurofibrinary tangles, tuft-shaped astrocytes and coiled bodies in the substantia nigra and the striatum of PSP were observed.Severe loss of neurons and gliosis in the caudate nucleus and putamen of MSA were found. In addition, ?-synuclein and ubiquitin-positive glial cytoplasmic inclusions were found in the substantia nigra and striatal region of MSA. Conclusions Lewy bodies in PD and glial cytoplasmic inclusions in MSA are related to abnormal depositions of ?-synuclein and ubiquitin.Neuronal and glial cytoplasmic inclusions in PSP are related to abnormal aggregation of tau.

Objective To analyze the morbidity of the old people with hypertension and metabolic syndrome (MS),the characteristics of MS components distribution,and correlation hypertension and MS.Methods 438 old patients over 60 with hypertension were selected randomly from cheek-up crowd in the physical examination center of Affiliated Zhongshan Hospital of Dalian University in 2013.Abdominal girth,height,body mass were measured,and then calculated BMI.The indicators such as FPG,TC,TG,HDL-C,LDL-C were detected and analyzed.Results The total morbidity of MS in the old people with hypertension was 37.7％,39.0％ from male people,36.7％ from female people,and there was no difference between genders(x2 =0.46,P ＞ 0.05).The level of BMI,abdominal girth,FPG,and TG in the old people with MS were higher than the people without MS(t =4.83,8.53,5.08,7.29,all P ＜0.05),and HDL-C was lower than the people without MS(t =-9.67,P ＜ 0.05).The level of FPG in women was higher than that in men apparently(x2 =5.82,P ＜ 0.05),and the level of HDL-C was lower than that in men apparently (x2 =8.73,P ＜ 0.01).The risk factors to MS include BMI,abdominal girth,FPG,TG (OR =2.139,1.106,2.156,2.315,all P ＜0.05),and HDL-C is protective factor to MS(OR =0.039,P ＜0.05).Conclusion Hypertension might increase MS morbidity of old patients.Hypertension related with MS closely.The risk factors include BMI,abdominal girth,FPG,TG,on the other hand HDL-C is protective factor to MS.

Objective To study the neuropathological characteristics of late-onset Alzheimer' s disease (LOAD) in Chinese people, to ensure correct diagnosis of LOAD.Methods Choosing cerebral cortex of temporal layer of 8 cases of LOAD and 5 cases of age-matched normal control group by autopsy.Histopathologlc diagnosis was established in all these 13 cases.Cerebral cortex were taken from temporal layer in 13-101 hours after death and were fixed with 40 g/L paraformaldehyde, followed by paraffin-embedding and serial sectioning with 6 μm thickness.Brain tissue was analyzed neuropatholically by using immunohistochemical staining for β-amyloid (Aβ) and AT8 on these cases.Positive distribution of temporal layer was observed under light microscope.Results The results of immunohistochemical stainings of Aβ and AT8 were positive in all of LOAD.Aβ immunoreactant located in the cerebral cortex.The diffuse plaques, primitive plaques and burn-out plaques of senile plaques were displayed clearly by immunohistochcmical stainings of Aβ.AT8 immunoreactants showed neurofibrillary tangles, neuropil thread and senile plaques in nerve cell of cerebral cortex in different degree respectively.The positive rate Aβ and AT8 were both 8/8 by semiquantitative analysis in AD group.As the normal aging control group, which was 0 and 1/5 respectively.There was significant difference of the positive rate Aβ and AT8 in two groups(χ2 = 13.000,P=0.001; χ2=9.244,P=0.007).Conclusions Sensitive immunnhistochemical technique was significant to display senile plaques and neurofibrillary tangles.The findings demonstrate that immunohistochemistry staining of Aβ and AT8 can display senile plaques and neurofibrillary tangles clearly.The connection of the 2 different methods might improve diagnose accordance rate of AD.

This study is to investigate the effect of baicalin (BL) against oxidative injury stress of SH-SY5Y cells induced by H2O2 and the possible mechanism. SH-SY5Y cells were pre-incubated with baicalin (25, 50, and 100 micromol x L(-1)) for 12 h prior to exposure to H2O2 (150 micromol x L(-1)) for 24 h. The viability of SH-SY5Y cells was measured by MTT assay. The contents of LDH and NO were determined. The percentage of apoptotic cells was assessed by flow cytometry (FCM). The content of Caspase-3 was tested by immunofluorescence histochemical method. BL at 50 and 100 micromol x L(-1) separately increased the cell viability and up-regulated SIRT1, reduced the contents of LDH, NO, Caspase-3 and the apoptotic percentage of SH-SY5Y cells. This study results suggest that baicalin could inhibit the H2O2-induced neuronal apoptosis. The further mechanism studies show that baicalin inhibit apoptosis via reducing Caspase-3 expression and up-regulating SIRT1.

Purpose To study the differences of shear wave elasticity and the content of collagen fiber between benign breast lesions and malignant breast lesions, and to analyze the correlation between shear wave elasticity and the content of collagen fiber. Materials and Methods 106 patients with 116 breast lesions who were referred to PLA General Hospital for ultrasound-guided biopsy or surgery underwent shear wave elasticity examination, the biopsy specimen underwent Van Gieson (VG) dye and Image-Pro Plus 5.1 software was used to quantitatively analyze the content of collagen fiber. Results Malignant lesions exhibited signiifcantly higher max elasticity, mean elasticity, and elasticity ratio between lesions and surrounding parenchyma (140.43±70.16) kPa, (63.11±33.68) kPa, 3.49±1.95 than benign lesions (54.64±48.53) kPa, (34.52±25.23) kPa, 2.25±1.48 (t=5.329, 4.382 and 4.487, P<0.01). The content of collagen fiber of malignant lesions was signiifcantly higher than that of benign lesions (t=8.437, P<0.01). There was a positive correlation between max elasticity and the content of ifber collagen (r=0.746, P<0.05). Conclusion The elasticity of breast lesions has a close correlation with the content of collagen ifber, and collagen ifber might play an important role in the development of breast carcinoma.

Objective To investigate the effect of brain derived neurotrophin factor (BDNF) transfected with cationic liposome in protecting nerve tissue and promoting regeneration of the myelin sheath. Methods Wistar rat Schwanns cells (SWCs) were cultured in vitro. The recombinant cationic liposomes mediated PCDNA 3 BDNF was transplanted into SWCs and then into electrical reticular lesion of the brain stem (Group Ⅰ). At the same time, pure cell transplantation group (Group Ⅱ), empty transfected vector cell transplantation (Group Ⅲ) and normal saline injection group (Group Ⅳ) were set. The concentration of BDNF in the brain stem was measured by ELISA, the survival of myelinated basic protein (MBP) and SWCs in the brain stem by immunohistochemistry and the regeneration of the myelin sheath by the transmission electron microscope (TEM). Results One week after transplantation, the concentration of BDNF in the brain stem in the Group Ⅰ was much higher than that in other three groups ( P

OBJECTIVETo determine cell proliferation and nestin expression in the ependyma of adult rat spinal cord after injury.

METHODSRat spinal cord injury models were established by aneurysm clip compression, and nestin expression and proliferation of ependymal cells at different times were shown with pathological and immuno-histochemical staining.

RESULTSEpendymal cells adjacent to the injured site demonstrated a dramatic increase in nestin expression 24 hours after compression. Proliferating cell nuclear antigen was positive, and significant proliferation was observed after 7 days. Nestin expression was down regulated as time went by.

CONCLUSIONNormally quiescent mature ependymal cells appear to revert to an embryonic state in response to spinal cord injury.

Animals ; Cell Division ; Ependyma ; cytology ; metabolism ; Immunohistochemistry ; Intermediate Filament Proteins ; biosynthesis ; Male ; Nerve Tissue Proteins ; Nestin ; Rats ; Rats, Wistar ; Spinal Cord Injuries ; metabolism ; pathology

Midbrain gliomas are relatively rare neoplasms with a generally benign prognosis, with dissemination or metastasis not previously reported. We describe here a woman, in whom magnetic resonance imaging scans showed hydrocephalus and a tegmental lesion in the upper aqueduct. Endoscopic third ventriculostomy and biopsy were performed; during surgery, a second small lesion was observed in the infundibular recess. Histologically, the two lesions had the characteristics of low grade astrocytoma, suggesting that the midbrain astrocytoma may have been disseminated via the cerebral spinal fluid to the infundibular recess. Postoperatively this patient received radiotherapy for nearly one month. Although patients with these tumors are not usually administered adjunctive therapy, radiation and, combined modality therapy, including surgery, radiotherapy, and chemotherapy, may be beneficial in patients with midbrain gliomas with dissemination.
Adult* ; Astrocytoma* ; Biopsy ; Cerebrospinal Fluid* ; Combined Modality Therapy ; Drug Therapy ; Female ; Glioma ; Humans ; Hydrocephalus ; Magnetic Resonance Imaging ; Mesencephalon ; Neoplasm Metastasis ; Neuroendoscopes ; Prognosis ; Radiotherapy ; Ventriculostomy

BACKGROUND: As unspecific antagonist of opiate receptor, naloxone is widely used for multiple diseases which are related with abnormal release of endogenous opium. At present, researches suggest that large dosage of naloxone is used at early period can decrease death rate of patients with acute craniocerebral injury and promote neural functional recovery.OBJECTIVE: To investigate the effect of naloxone on improving the nervous function of rats with acute craniocerebral injury and to analyze effectively.DESIGN: Randomized grouping design based on the experimental animal.SETTING: Beijing Neurosurgical Institute.MATERIALS: Totally 250 SD rats were divided randomly into 0.3, 1.0,3.0, 9.0 mg/kg naloxone group, positive control group and negative control group.METHODS: Craniocerebral injured model was established with Feenly free fall struck, and the medicine was given 30 minutes after injury. The rats of the first four experimental group were injected transpeniponeally with naloxone hydrochloride by 0.3 mg/kg, 1.0 mg/kg, 3.0 mg/kg and 9.0 mg/kg respectively once a day; meanwhile, the control groups were given 2 mg citicoline sodium for injection and 0.5 mL normal saline per rat respectively. The longest time was 14 days.MAIN OUTCOME MEASURES: MNSS neural functional score was used every day. The brain edemas of 8 rats in each group were measured with wet-dry weight methods on the second and the fourth day after head trauma.RESULTS: Among 250 rats, 172 entered the final analysis. The nervous function of rats in naloxone groups was better than the two control groups (P ＜ 0.01), and that in 1, 3 and 9 mg/kg naloxone group were better than 0.3 mg/kg group (P ＜ 0.05), but there were no significant differences a mong the three naloxone groups (P ＞ 0.05). The brain edemas of rats in naloxone groups were lighter than that in the control groups (P ＜ 0.05), and that of 1, 3 and 9 mg/kg groups were lighter than 0.3 mg/kg (P ＜ 0.05), but there were no significant differences among these three groups (P ＞ 0.05).CONCLUSION: Naloxone can decrease the brain edemas of rats with traumatic brain injury, promote the nervous function recovery, and the treatment effect changes with the dosage during some range.Therefore, the experiment illustrates that naloxone can decrease the brain edemas of experimental brain injury in SD rats and improve the nervous function, but the effect of naloxone is associated with the dosages in some range.

BACKGROUND: Synaptic density, a key index of structure and function of brain tissues, is related to cognitive function. Synaptic loss occurs during human brain aging and in Alzheimer disease (AD), inducing the changes of synaptic density.OBJECTIVE: To observe quantitative synaptic alterations in human brain and changes of synaptic density in different parts during normal aging so as to compare them with those of AD patients.DESIGN: Sampling survey.SETTING: Senile Neurological Department of General Hospital of Chinese PLA.PARTICIPANTS: Pathological data were selected from General Hospital of Chinese PLA from June 1996 to December 2002. Inclusion criteria: had no major nervous system diseases and neuropathological changes. Brain tissues of 28 corpses in normal aging group, 23 males and 5 females aged 23-100 years with an average of (65±22.8) years, were obtained at autopsy.All corpses were divided into three groups according to their age, namely,adult group (23-55 years old, n=9), senile group (64-72 years old, n=7),and ＞75 group (76-100 years old, n=12). Cerebral hippocampal samples of other six corpses diagnosed with AD were selected from clinic. The corpses included 5 men and 1 woman aged 76-94 years with an average of (83±7.7) years.METHODS: Response intensity of synaptophysin immunochemistry remained stable after 4-8 hours of death, so brains were obtained at autopsy after 8-72 hours of death and fixed with 4% formalin for at least 6 weeks.In normal aging group, tissues were taken from left superior frontal gyrus,striatal area of left occipital lobe, left putamen (striatum section, including head of caudate nucleus), and left hippocampus (from lateral geniculate body section to medial occipitotemporal gyrus). In AD cases, tissues were taken from left hippocampus of 4 corpses and right hippocampus of other 2. All sections were stained with hematoxylin eosin (HE), toluidine blue and synaptophysin immunostaining (rabbit anti-human synaptophysin polyclonal antibody from Beijing Zhongshan Biotechnology Co., Ltd.). Morphology and distribution of positive objects in synapse immunologic reaction were observed under the light microscope. Relation between absorbance in each region and age was determined with Pearson's coefficient. Differences among groups were analyzed with nonparametric test, and the differences in hippocampal CA3 area between ＞ 75 group and AD group were analyzed with the same test.MAIN OUTCOME MEASURES:① Absorbency of synaptophysin at various sites of normal aging group and correlation with age; ② absorbance value in CA3 area between AD patients and advanced aged normal subjects (＞75 years) was compared.RESULTS:All the 34 cerebral samples entered the final analysis.①Synaptophysin-positive granules of various size were scattered through neocortex, putamen and hippocampus, neuronal somata, neuroglia, vessels and white matter. Density was particularly strong over layers Ⅱ and Ⅲ in frontal lobe, and layer ⅣV in occipital lobe. ② Synaptophysin density was negatively correlated with age, which was -0.688 in frontal lobe, -0.592 in occipital lobe, -0.458 in putamen and -0.619 in hippocampal CA2 area,respectively (P = 0.000, 0.001, 0.014, and 0.000). ③ Significant difference in synaptic density in CA3 area was found between AD patients (0.031 3±0.003 0)and normal subjects over the age of 75 (0.040 7±0.005 3) (Z=-2.997, P=0.001)in nonparametric test.CONCLUSION:① Synaptic density was found to decrease in frontal lobe, occipital lobe, CA3 area of hippocampus and putamen with age; the changes had significant correlation with age.② Synaptic density of AD patients was lower than that of normal subjects, and their cognitive hypofunction was related to synaptic loss. ③ All tissues were obtained after 8-72 hours of death and fixed over 6 weeks, which to the greatest extent reduced the effects of tissue autolysis and formalin fixation on the results.