Objective To study the change of metabolism of serum lipids in patients with mild cognitive impairment(MCI). Methods The serum levels of total cholesterol(TC),triglyceride(TG),low density lipoprotein(LDL) and high density lipoprotein(HDL) were measured in 60 patients with MCI and 100 age-matched normal controls. ResultsThe serum levels of TC,TG and LDL were significantly higher and HDL significantly lower in patients with MCI than in normal controls(P

Objective To assess the value of detecting sympathetic skin response (SSR) in the diagnosis of autonomic dysfunction in patients with Parkinson disease (PD). Methods SSR measurement was performed in 47 PD patients and 20 healthy control subjects and the results were compared. The SSR was also comparatively analyzed between patients with and those without autonomic dysfimction. Results Compared with the healthy controls, the PD patients showed significantly lowered mean amplitude (2.56±1.47 vs 1.87±0.26, P<0.05) and prolonged latency (1.42±0.29 vs 1.55± 0.18, P<0.05) of the SSR in the upper limbs, with also lowered mean amplitude (0.76±0.39 vs 0.49±0.21, P<0.05) and prolonged latency (2.04±0.27 vs 2.13±0.16, P<0.05) in the lower limbs. Compared with the PD patients without autonomic dysfunction, those having autonomic dysfunction showed significantly lowered mean amplitude (1.89±0.33 vs 1.75±0.21, P<0.05) and prolonged latency (1.53±0.15 vs 1.56±0.17, P<0.05) of SSR in the upper limbs and lowered mean amplitude (0.51±0.17 vs 0.46±0.20,P<0.05) and prolonged latency (2.08±0.24 vs 2.17±0.18, P<0.05) in the lower limbs. Conclusion The results of SSR measurements are consistent with the clinical manifestations of the PD patients. SSR can be of value in the diagnosis of autonomic nerve dysfunction in PD.

OBJECTIVETo observe the distribution of toll-like receptor 4 (TLR4) in rats' respiratory tract. To study the influence of LPS and Eucalyptus globulus oil on the distribution of TMR4.

METHODThe Sprague-Dawley rats were intratracheally instilled with lipopolysaccharide (LPS,2 mg x kg(-1) per day) for two days to induce acute lung injury. The rats were sacrificed at 72 hours after LPS instillation. Lung morphology was studied. Leukocytes in Bronchoalveolar lavage fluid (BALF) were measured and TLR4 were detected by immunohistochemistry.

RESULTThe result of immunohistochemistry showed that TLR4 distributed widely in common rats' respiratory tract. In the group of acute lung injury, the number of leucocyte in BALF was increased apparently, the inflammation in bronchus and bronchioles was more apparently than that of the control group in morphology. And the expression of TLR4 was reinforced in main bronchus and bronchioles. In the group of E. globules oil (300 mg x kg(-1)), the leucocyte number was decreased apparently in BALF, the inflammation was lightened and the expression of TLR4 decreased as compared with the group of models.

CONCLUSIONThe expression of TLR4 distributes widely in rats' respiratory tract. The stimulation of LPS can reinforce the expression of TLR4. The E. globules oil can reduce the increase of TLR4 induced by LPS in bronchioles.

Animals ; Anti-Inflammatory Agents, Non-Steroidal ; isolation & purification ; pharmacology ; Bronchi ; metabolism ; Bronchoalveolar Lavage Fluid ; cytology ; Eucalyptus ; chemistry ; Leukocyte Count ; Lipopolysaccharides ; Lung ; pathology ; Male ; Oils, Volatile ; isolation & purification ; pharmacology ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Respiratory Distress Syndrome, Adult ; chemically induced ; metabolism ; pathology ; Toll-Like Receptor 4 ; metabolism

OBJECTIVESTo investigate the relationship between the epithelial growth factor receptor (EGFR) mutation status and clinicopathological factors, and to analyze the mutation on the effect in non-small cell lung cancer (NSCLC) after surgery.

METHODSThe NSCLC patients who were resected and detected EGFR gene from March 2009 to March 2011 were retrospectively reviewed. The relationship between EGFR mutation status and clinicopathological factors, tumor markers, prognostic was analyzed.

RESULTSThe mutation and the wild group had 169 and 214 patients respectively. EGFR mutation in female, non-smoking, adenocarcinoma and less than 60 years old accounted for 63.91%, 61.54%, 88.76% and 62.13% with statistical significance compared with male (χ(2) = 53.490, P = 0.000), smoking (χ(2) = 48.568, P = 0.000), non-adenocarcinoma (χ(2) = 105.560, P = 0.000) and more than 60 years old (χ(2) = 6.057, P = 0.017). Disease free survival (DFS) of the wild group was better than mutation group (χ(2) = 11.329, P = 0.001). In addition, there were some relations between mutation status and excision repair cross complementing (ERCC1) protein, carcinoembryonic antigen (CEA), squamous cell carcinoma (SCC) and Cyfra21-1. ERCC1(+) (χ(2) = 6.739, P = 0.012), SCC(χ(2) = 16.839, P = 0.000) and Cyfra21-1(χ(2) = 6.638, P = 0.013) more than normal value was common in wild group. Increased CEA was common in mutation group (χ(2) = 5.436, P = 0.023).

CONCLUSIONSEGFR mutation is commonly found in female, non-smoking, adenocarcinoma and less than 60 years old NSCLC patients. The wild group obtains better DFS than mutation group. Tumor markers may predict the mutation status, which need further research.

Carcinoma, Non-Small-Cell Lung ; genetics ; mortality ; pathology ; Disease-Free Survival ; Female ; Humans ; Lung Neoplasms ; genetics ; pathology ; surgery ; Male ; Middle Aged ; Mutation ; Prognosis ; Receptor, Epidermal Growth Factor ; genetics ; Retrospective Studies

OBJECTIVETo investigate the cell proliferation and differentiation in the developing brain of mouse.

METHODSC57/BL6 mice were divided into 3 groups at random. Bromodeoxyuridine (BrdU) was injected into the brains in different development periods once a day for 7 d. The brains were retrieved 4 weeks after the last BrdU injection. Immunohistochemical and immunofluorescent studies were carried out for detecting cell proliferation (BrdU) and cell differentiation (NeuN, APC, Iba1, and S100beta), respectively.

RESULTSThe number of BrdU labeled cells decreased significantly with the development of the brain. Cell proliferation was prominent in the cortex and striatum. A small portion of BrdU and NeuN double labeled cells could be detected in the cortex at the early stage of development, and in the striatum and CA of the hippocampus in all groups. The majority of BrdU labeled cells were neuroglia, and the number of neuroglia cells decreased dramatically with brain maturation. Neurogenesis is the major cytogenesis in the dentate gyrus.

CONCLUSIONThese results demonstrated that cell proliferation, differentiation and survival were age and brain region related.

Animals ; Animals, Newborn ; Brain ; cytology ; growth & development ; Bromodeoxyuridine ; Cell Count ; Cell Differentiation ; physiology ; Cell Proliferation ; Cerebral Cortex ; cytology ; growth & development ; Corpus Striatum ; cytology ; growth & development ; Fluorescent Antibody Technique ; Hippocampus ; cytology ; growth & development ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Tissue Proteins ; metabolism ; Neuroglia ; cytology ; physiology ; Neurons ; cytology ; physiology ; Nuclear Proteins ; metabolism

Objective To study the dynamic changes of cytokines including tumor necrosis factor-alpha (TNF-?),interleukin-6 (IL-6),IL-8 in serum and cerebrospinal fluid (CSF) of asphyxia neonates,and to analyze the relationship between cytokines levels and severity of brain damage and neurological outcome. Methods The concentrations of TNF-?,IL-6,IL-8 in serum and CSF were measured by radioimmunoassay in 63 asphyxia neonates. Neurological development was evaluated at 12 months by children′s developmental scale of china.Results The serum concentrations of TNF-?, IL-6,IL-8 were significantly higher in asphyxiated neonates than those in the controls,and they were correlated with the degree of encephalopathy. The level of serum TNF-? was hig-(hest) at the first day and IL-6 was highest at the third day. There was no marked dynamic changes within 5 days in serum IL-8 level. The concentrations of TNF-?,IL-8 in CSF were higher at the first and the third day.The dynamic changes of IL-6 in CSF were similar in serum and they were positively correlated. The serum concentration of IL-6 in severe brain injury group was much higher than those of normal and mild group.The CSF concentration of IL-6 in severe brain injury group was much higher than that of normal group. The CSF concentration of IL-8 in severe brain injury group was much higher than those of the normal and mild group. Conclusions The concentrations of TNF-?,IL-6 and IL-8 are increased both in serum and CSF in asphyxiated neonates which are correlated with severity of hypoxic-ischemic encephalopathy. Cytokine-mediated inflammatory reactions may participate in the mechanism of hypoxic-ischemic brain injury after asphyxiaion.The concentration of IL-6 in serum and IL-6, IL-8 in CSF are correlated with the neurological outcome.

OBJECTIVEThe study was to investigate the effect of different temperatures during hypoxia on brain injury in mice of different ages.

METHODSNewborn C57/BL6 mice at 7 days or 21 days of life were subjected to left carotid artery ligation followed by exposure with 10% oxygen. The mice were kept in a incubator with a predetermined, constant temperature, either 34 degrees centigrade (Hypothermia group) or 36 degrees centigrade (Normothermia group). Brain injury was evaluated 7 days after hypoxia-ischemia (HI). Active caspase-3 and apoptosis-inducing factor (AIF) expressions in the brain tissue were detected by immunohistochemistry and Western Blot was used to evaluate the phosphor-Akt (P-Akt) expression in the brain tissue at 24 hrs post-HI.

RESULTSBrain injuries, including the cortex, hippocampus, striatum and thalamus injuries, occurred in the Normothermia group at 7 days post-HI. The brain cortex showed cystic cavitation in the postnatal day (P)7 pups mice and laminar infarct of the brain cortex was observed in P21 mice. In the Hypothermia group, the P7 mice did not present with laminar infarct of the cortex and had lower scores of neuropathological lesions in cortex, hippocampus, striatum and thalamus than P7 mice from the Normothermia group (P < 0.01); the cortex injuries were significantly relieved but the injuries of hippocampus, striatum and thalamus in P21 mice were similar to those from the Normothermia group. Active caspase-3 (7.0 +/- 5.6) and AIF positive cells (3.7 +/- 6.2) in the cortex of P7 mice from the Hypothermia group were significantly lower than those of the Normothermia group (51.5 +/- 23.2 and 31.8 +/- 22.4) at 24 hrs post-HI (P < 0.01). Wetstern Blot showed the P-Akt expression was obviously decreased in the ipsilateral hemisphere to the occlusion compared with that of the contralateral hemisphere after HI in the Normothermia group (P < 0.05), while in the Hypothermia group the P-Akt expression was not significantly different between the two hemispheres.

CONCLUSIONSHypothermia has protective effects against HI insults. The protection was more pronounced for the immature brain than the mature brain.

Active Transport, Cell Nucleus ; Age Factors ; Animals ; Apoptosis Inducing Factor ; metabolism ; Brain ; pathology ; Caspase 3 ; Caspases ; metabolism ; Hypothermia, Induced ; Hypoxia-Ischemia, Brain ; metabolism ; pathology ; therapy ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-akt ; metabolism

OBJECTIVEp53-induced apoptosis is crucial in the development of hypoxic-ischemia (HI) brain damage and neurodegenerative disorders. Some experimental research has shown that a synthetic inhibitor of p53 can protect neurons against apoptosis. This study aimed to explore the expression of p53 in neonatal mice following HI brain damage and the effect of p53 inhibitor (pifithrin-alpha, PFT-alpha) on brain damage.

METHODSHI was induced in 9-day-old mice pups by ligation of left carotid artery and 10% oxygen exposure for 55 minutes. The pups were sacrificed and the brains were taken out at 3, 8, 24, and 72 hrs post-HI. The brains were sectioned and stained with antibody against p53 and microtubule-associated protein 2 (MAP-2). PFT-alpha was injected intraperitoneally: in experiment 1, immediately after HI with different dosages (1, 2 and 8 mg/kg); in experiment 2, 2 mg/kg at different HI times (1 hr before HI, and immediately and 1 hr after HI). Control animals without HI received injections of 0.5% dimethyl sulfoxide. Brain damage was evaluated by gross morphology scoring at 72 hrs after HI.

RESULTSThe number of p53 positive cells in the cortex, hippocampus and striatum of the ipsilateral hemisphere increased significantly and peaked at 3-8 hrs post-HI when compared with those of contralateral hemisphere as well as normal controls. The positive cells distributed mainly in the MAP-2 negative area. Both different dosages and different injection time PFT-alpha treatment did not reduce the extent of brain damage.

CONCLUSIONSThe immunoactivity of p53 increased significantly as early as 3 hrs post-HI. The distribution area of p53 expression was consistent with that of brain damage. The p53 inhibitor PFT-alpha has no protective effects against HI brain damage in neonatal mice.

Animals ; Animals, Newborn ; Benzothiazoles ; Brain ; drug effects ; pathology ; Dose-Response Relationship, Drug ; Female ; Hypoxia-Ischemia, Brain ; metabolism ; Immunohistochemistry ; Male ; Mice ; Mice, Inbred C57BL ; Thiazoles ; pharmacology ; Toluene ; analogs & derivatives ; pharmacology ; Tumor Suppressor Protein p53 ; analysis ; antagonists & inhibitors

OBJECTIVERecent studies suggest that hypothermia may be a potential treatment for perinatal hypoxic-ischemic (HI) brain damage. But the mechanisms of this effect are not well known. In the present study, the protective effect of systemic hypothermia as well as effect on apoptosis and associated biochemical events were investigated on neonatal rats with HI brain damage.

METHODSSeven-day-old Wistar rats were subjected to left carotid artery ligation and hypoxia was persisted for 60 min. Immediately at the end of hypoxia, the animals were maintained either at 36 degrees C or 30 degrees C for 10 h at random. Caspase-2, 3 activity in brain homogenate was detected with Western blotting at 24 h post-HI (n = 8 for each group). Immunoactivity of microtubule-associated protein-2 (MAP-2), active caspase-3, apoptosis inducing factor (AIF) and oligonucleotide hairpin probe staining were detected at 72 h post-HI. The infarct volume, neuronal loss in CA(1) sector of hippocampus as well as brain injury scoring were calculated according to MAP-2 staining and hematoxylin and eosin staining.

RESULTSCaspase-2, 3 activities were much higher in the normothermia group [(27.7 +/- 14.7), (94.9 +/- 53.1) pmol/(min.mg protein)] at 24 h post-HI than those of hypothermia [(7.9 +/- 3.4), (21.1 +/- 18.7) pmol/(min.mg protein)] and normal control groups [(7.6 +/- 0.7), (12.9 +/- 0.5) pmol/(min x mg protein)] (P < 0.01). The activities were not significantly different between hypothermia group and normal control group. Western blotting showed that caspase-3 activation process was blocked by hypothermia. The number of active caspase-3 and AIF positive cells in the cortex of ipsilateral hemisphere was much higher in the normothermia group (median: 148.5; 22/field) than that of hypothermia group (median: 48.5; 9/field) (P < 0.05). The number of apoptotic cells as judged by oligonucleotide hairpin probe labeling was much higher in normothermia group (median: 144/field) than that of hypothermia group (median: 133/field) (P < 0.05). The brain injury scoring, infarct volume and neuronal loss in CA(1) area of hippocampus were much less in the hypothermia group [10.4 +/- 2.9; 40.5 +/- 34.8)mm(3); 25.7 +/- 11.5] than that of normothermia group [14.2 +/- 3.5; (73.9 +/- 22.4) mm(3); 37.4 +/- 10.6, P < 0.05].

CONCLUSIONSSystemic hypothermia for 10 h after hypoxia-ischemia seemed to be effective in reducing brain damage and the mechanism is associated with alteration of apoptotic pathway.

Animals ; Animals, Newborn ; Apoptosis Inducing Factor ; Blotting, Western ; Brain ; blood supply ; physiopathology ; Caspase 3 ; Caspases ; analysis ; Female ; Flavoproteins ; analysis ; Hypothermia, Induced ; Hypoxia-Ischemia, Brain ; enzymology ; metabolism ; prevention & control ; Immunohistochemistry ; Male ; Membrane Proteins ; analysis ; Rats ; Rats, Wistar ; Time Factors