Objective:To evalaute the role of hippocampal ubiquinol cytochrome C reductase core protein 1 (UQCRC1) in cognitive dysfunction after global cerebral ischemia (GCI) in mice.Methods:Forty SPF healthy male C57BL/6J mice, aged 12 weeks, weighing 22-26 g, were selected, and 20 of them were divided into 2 groups ( n=10 each) using a random number table method: sham operation group and GCI1 group. The other 20 mice were divided into 2 groups ( n=10 each) by the random number table method: GCI2 group and GCI+ UQCRC1 overexpression group (GCI+ UQCRC1 group). In Sham group, the skin was directly sutured after exposing both common carotid arteries. Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries for 20 min in GCI1, GCI2 and GCI+ UQCRC1 group, and lentivirus VSVG-Lentivirus-hSyn-EGFP-P2A-UQCRC1-WPRE-pA 500 nl was injected into the bilateral hippocampus at 2 weeks before developing the model in GCI+ UQCRC1 group. The novel object recognition task was carried out on the 2nd day following completion of model development, and the percentage of time spent exploring the novel object was calculated. The fear conditioning test was carried out on days 3-4 after completion of model development, and the freezing time was recorded. Morris water maze test was performed on days 5-10 after completion of model development, and the escape latency and time spent in the target quadrant were recorded. After the Morris water maze test, the expression of UQCRC1 in the hippocampal CA1 region was detected by immunofluorescence and Western blot. Results:Compared with Sham group, the percentage of time spent exploring the novel object was significantly decreased, the percentage of freezing time in training and test stages was decreased, the escape latency on days 6-9 was prolonged, the percentage of time spent in the target quadrant was decreased, and the expression of UQCRC1 in the hippocampal CA1 was down-regulated in GCI1 group ( P<0.05). Compared with GCI2 group, the percentage of time spent exploring the novel object was significantly increased, the percentage of freezing time in training and test stages was increased, the escape latency on days 6-9 was shortened, the percentage of time spent in the target quadrant was increased, and the expression of UQCRC1 in the hippocampal CA1 region was up-regulated in GCI+ UQCRC1 group ( P<0.05). Conclusions:Hippocampal UQCRC1 is involved in the process of cognitive dysfunction following GCI in mice.

Objective To investigate the intrinsic neural mechanism of aggressive behavior in CD 1 mice.Methods CD1 mice with aggressive behavior were screened out by resident intruder test.After the aggressive conditioned pair preference was further verified,the activated brain regions of the whole brain were labeled with c-Fos,and the types of neurons activated by the aggressive behavior were analyzed by double immunofluorescence labeling.Finally,the effects of activity of these neurons regulated by optogenetics on aggressive behavior were observed.Results The c-Fos screening revealed that about 82％of the CD1 mice showed aggressive behavior.After the occurrence of aggressive behavior,the main activation occured in the medial prefrontal cortex(mPFC),and the results of immunofluorescence double labeling showed that the c-Fos positive neurons in the mPFC were mainly glutamatergic neurons.Finally,glutamatergic neurons in the mPFC could be activated by optogenetics,and the activation inhibited the aggressive behavior of CD1 mice.In contrast,optogenetics could inhibit glutamatergic neurons in the mPFC and then promote the aggressive behavior of CD1 mice.Conclusion Glutamatergic neurons in the mPFC are an important component in the regulation of aggressive behavior in CD1 mice.

Objective:To evalaute the role of hippocampal ubiquinol cytochrome C reductase core protein 1 (UQCRC1) in cognitive dysfunction after global cerebral ischemia (GCI) in mice.Methods:Forty SPF healthy male C57BL/6J mice, aged 12 weeks, weighing 22-26 g, were selected, and 20 of them were divided into 2 groups ( n=10 each) using a random number table method: sham operation group and GCI1 group. The other 20 mice were divided into 2 groups ( n=10 each) by the random number table method: GCI2 group and GCI+ UQCRC1 overexpression group (GCI+ UQCRC1 group). In Sham group, the skin was directly sutured after exposing both common carotid arteries. Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries for 20 min in GCI1, GCI2 and GCI+ UQCRC1 group, and lentivirus VSVG-Lentivirus-hSyn-EGFP-P2A-UQCRC1-WPRE-pA 500 nl was injected into the bilateral hippocampus at 2 weeks before developing the model in GCI+ UQCRC1 group. The novel object recognition task was carried out on the 2nd day following completion of model development, and the percentage of time spent exploring the novel object was calculated. The fear conditioning test was carried out on days 3-4 after completion of model development, and the freezing time was recorded. Morris water maze test was performed on days 5-10 after completion of model development, and the escape latency and time spent in the target quadrant were recorded. After the Morris water maze test, the expression of UQCRC1 in the hippocampal CA1 region was detected by immunofluorescence and Western blot. Results:Compared with Sham group, the percentage of time spent exploring the novel object was significantly decreased, the percentage of freezing time in training and test stages was decreased, the escape latency on days 6-9 was prolonged, the percentage of time spent in the target quadrant was decreased, and the expression of UQCRC1 in the hippocampal CA1 was down-regulated in GCI1 group ( P<0.05). Compared with GCI2 group, the percentage of time spent exploring the novel object was significantly increased, the percentage of freezing time in training and test stages was increased, the escape latency on days 6-9 was shortened, the percentage of time spent in the target quadrant was increased, and the expression of UQCRC1 in the hippocampal CA1 region was up-regulated in GCI+ UQCRC1 group ( P<0.05). Conclusions:Hippocampal UQCRC1 is involved in the process of cognitive dysfunction following GCI in mice.

Objective To investigate the effects of nicorandil on hypoxia-inducible factor (HIF)-1α mRNA and protein in lung tissue of one-lung ventilation.Methods Twenty-four clean New Zealand white rabbits were randomly divided into sham group (group S) (two-lung ventilation+thoracotomy),negative control group (group C) (one-lung ventilation + thoracotomy + saline),nicorandil group (group N) (one-lung ventilation+ thoracotomy+ nicorandil) and antagonist group (group J) (one-lung ventilation + thoracotomy + nicorandil + glibenclanide) equally.The implementation of mechanical ventilation depended on self-made double-lumen endotracheal tube after intravenous induction through ear marginal vein.Intravenous maintenance medicine was infused by trace injection pump after anesthesia induction.The implementation of thoracic surgery was simulated through one-lung and two-lung ventilation by auscultation,bubble test and direct observation.Group S was given anaesthesia only,no one-lung ventilation group S,the other three groups had single lung ventilation,and the drug was injected before the operation.Group N was infused nicorandil 100 ptg· kg-1 · h-1 before the implementation of single lung ventilation for 1 h.Group C was injected with the same amount of normal saline.Group J was intravenous infusion of glibenclamide 75 μg· kg-1 · h-1 and nieorandil 100μg · kg-1 · h-1 the implementation of single lung ventilation for 1 h.Then wet and dry weight ratio(W/D) and superoxide dismutase (SOD) activity were measured after non-ventilatory lung was processed and preserved.The expression of HIF-1α protein of non ventilatory lung tissue was detected by Western-blot in the four groups.The transcription of HIF-1α mRNA was detected by real-time quantitative real-time PCR (qRT-PCR) in all groups.Results W/D in groups C and J were significantly higher compared with that of groups S and N (P＜0.05).The activity of SOD in groups C and J was significantly lower compared with groups S and N (P＜0.05).The expression of HIF1α protein and transcription of HIF-1α mRNA in groups C,N and J were significantly higher than those in group S,and that of group N was significantly higher than those of groups C and J (P＜0.05).Conclsion Nicorandil has a protective effect on the collapse and inflation of non-ventilatory lung in rabbit with one-lung ventilation,reducing oxidative stress by SOD,acting on mito KATP and coming into play by up-regulation of HIF-1α.

OBJECTIVE: To study the mechanism of tumor necrosis factor( TNF)-α and its receptor( TNFR) signal transduction pathways in regulating cell apoptosis of alveolar macrophage( AM) in coal workers' pneumoconiosis( CWP).METHODS: Twenty-four coal workers with pneumoconiosis at stage Ⅰ were selected as CWP group and four observation subjects exposed to coal were chosen as observation group by using simple random sampling method. The bronchoalveolar lavage fluids of whole-lung lavage of two groups were collected. AMs were separated and purified. Then they were divided into 6 groups: a control group,a superoxide dismutase( SOD) group,a TNF/TNFR group,an anti-TNF-α antibody group,a Caspase-8 suppression group and a nuclear factor-κB( NF-κB) suppression group. The AMs of 6 groups with corresponding treatment were cultivated. After 24 hours,the cells were harvested and proteins extracted. The relative expression of TNF-α,TNFR1,TNFR2,Caspase-8,Caspase-3,NF-κB P50 and NF-κB P65 protein was detected by Western blotting. RESULTS: The protein relative expression of TNF-α,TNFR2,Caspase-8,Caspase-3,NF-κB P50 and NF-κB P65 in CWP group was significantly higher than those in the observation group( P < 0. 05). The protein relative expression of TNF-α,TNFR1,Caspase-8,Caspase-3 and NF-κB P50 in the TNF/TNFR group and the anti-TNF-αantibody group was lower than that of the control group( P < 0. 05). The above indexes in the anti-TNF-α antibody group were lower than that of the NF-κB suppression group( P < 0. 05). The protein relative expression of TNFR1,Caspase-8and Caspase-3 in the TNF/TNFR group was higher than that of the SOD group and the Caspase-8 suppression group( P <0. 05). The protein relative expression of TNFR1,Caspase-8 and NF-κB P50 in the TNF/TNFR group was lower than that of the NF-κB suppression group( P < 0. 05). Among the CWP patients,the relative expression of TNFR2 and NF-κB P65 in the TNF/TNFR group was lower than that of the control group( P < 0. 05),and higher than that of the SOD group( P <0. 05). CONCLUSION: AM apoptosis mediated by TNF-α/TNFR/NF-κB signal transduction pathway plays an important role in the occurrence and development of CWP. The TNF-α/TNFR/NF-κB signal transduction pathways inhibited or blocked at different stages can affect the expression of proteins related to AM apoptosis.

Alzheimer’s disease (AD) remains to be a grand challenge for the international commu-nity despite over a century of exploration. A key factor likely accounting for such a situation is the vast heterogeneity in the disease etiology, which involves very complex and divergent pathways. Therefore, intervention strategies shall be tailored for subgroups of AD patients. Both demographic and in-depth information is needed for patient stratification. The demographic information includes primarily APOE genotype, age, gender, education, environmental exposure, life style, and medical history, whereas in-depth information stems from genome sequencing, brain imaging, peripheral biomarkers, and even functional assays on neurons derived from patient-specific induced pluripo-tent cells (iPSCs). Comprehensive information collection, better understanding of the disease mech-anisms, and diversified strategies of drug development would help with more effective intervention in the foreseeable future.

In this short review, we have presented a brief overview on major web resources relevant to stem cell research. To facilitate more efficient use of these resources, we have provided a pre-liminary rating based on our own user experience of the overall quality for each resource. We plan to update the information on an annual basis.

OBJECTIVETo investigate psychological stress and influence factors on the mine emergency rescue personnel.

METHOD564 mine emergency rescue personnel from a rescue group were select as subjects, and 60 designers from a steel design institute were as controls. Self-made questionnaire and general job stress questionnaire were used to investigate the basic information, rescue history, psychosomatic symptoms, depression symptoms, daily job stress and negative emotions of emergency rescue personnel. SPSS17.0 software was used to analysis the psychological stress on the mine rescue personnel and its influence factors.

RESULTSThe detection rate (41.94%) of depression symptoms in rescue team was higher than that of controls (24.90%). The score of daily job stress was higher than that of logistical support. The older age group with higher negative emotional and daily job stress than the younger. The highest negative emotion was in age group of more than 40 years old. The highest score of daily job stress was in ≤30 years old. The score of depression and psychosomatic symptoms were higher than those of the college and the above. The scores of depression in group of duration of rescue <10 years was higher than that of duration≥10 years. The score of daily job stress is the lowest in rescue for 1 to 2 times per year and the highest in group of simulation training once a week. The score of daily job stress and depressive symptoms were getting higher with the extension of combat duty time. Age, hours of combat duty, training times a week, education and life events were the main affecting fectors on mental health of mine rescuers.

CONCLUSIONSMine rescuers have more psychological stress than generic population. The psychological stress of the mine crew is related to age, education, life events, training and combat readiness duty time.

Adult ; Cross-Sectional Studies ; Depression ; Disasters ; Emergency Responders ; psychology ; Humans ; Mental Health ; Mining ; Rescue Work ; Stress, Psychological ; Surveys and Questionnaires

Neurological disorders comprise a variety of complex diseases in the central nervous system, which can be roughly classified as neurodegenerative diseases and psychiatric disorders. The basic and translational research of neurological disorders has been hindered by the difficulty in accessing the pathological center (i.e., the brain) in live patients. The rapid advancement of sequencing and array technologies has made it possible to investigate the disease mechanism and biomarkers from a systems perspective. In this review, recent progresses in the discovery of novel risk genes, treatment targets and peripheral biomarkers employing genomic technologies will be dis-cussed. Our major focus will be on two of the most heavily investigated neurological disorders, namely Alzheimer’s disease and autism spectrum disorder.