[Spatial and temporal responses of habitat quality to urbanization: A case study of Changchun City, Jilin Province, China]. / 生境质量对城镇化的时空响应­­ä»¥é•¿æ˜¥å¸‚为例.

Habitat quality is an important index to evaluate regional ecological security. Revealing its spatial and temporal responses to urbanization is conducive to the in-depth implementation of new urbanization. Based on land use data, we analyzed the spatio-temporal characteristics of Changchun's landscape pattern, habitat quality and its sample zone from the grid scale with comprehensive utilization of spatial analysis and ecological model analysis. We further discussed the responses of habitat quality during urbanization. The results showed that the low values of patch density (PD), edge density (ED) and Shannon diversity index (SHDI) were distributed in the western plains, while the high aggregation index (AI) showed a patchy distribution in eastern and southern of the city. During 2000-2015, the habitat quality of Changchun showed a trend of degradation and significant spatial heterogeneity, showing a distribution of "high in the east, and low in the west". The expansion of construction land and the transportation infrastructure played a leading role in the degradation of regional habitat quality. The changes of habitat quality differed significantly in different zones. The overall variation of water belt was relatively small, while the variation frequency and amplitude of mountain, urban expansion, and traffic belt were relatively high. Natural factors including slope and elevation basically shaped the overall distribution pattern of habitat quality in Changchun, while urbanization factors including population density, GDP and night light index showed significant negative correlation with habitat quality. To alleviate the ecological pressure of urbanization and promote habitat quality, we proposed differentiated development strategies, such as preventing deforestation in the Dahei Mountains, using ecological strategies to restore habitat degradation areas, improving land use efficiency in built-up urban areas, promoting "smart growth" in urban areas, setting red line of farmland in hilly areas, and strengthening ecological infrastructure construction.

[Effect of electroacupuncture intervention on autophagy pathway in APP 695 V 717 I transgenic mice].

OBJECTIVE: To observe the effect of electroacupuncture (EA) therapy on the intraneuronal Abeta1-42 and dysfunction of autophagy pathway, so as to reveal its mechanism underlying improvement of Alzheimer's disease (AD). METHODS: APP 695 V 717 I transgenic female mice were randomly divided into model group (n = 6) and EA group (n = 6); and C 57 BL/6 mice were used as the control group (n = 6). After 3 months' treatment by EA therapy at "Baihui" (GV 20) and "Yongquan" (KI 1) (15 min, once every other day, 2 Hz/100 Hz, 1-2 mA), the expression level of Abeta1-42 of the striate cortex was detected by immunohistochemistry. TUNEL staining was used to detect the degree of apoptosis of the striate cortex, and ultrastructural changes of autophagosome in the cortex were observed using electron microscope. RESULTS: In comparison with the control group, Abeta1-42 expression level and the apoptotic neurons in the striate cortex were significantly up-regulated in the model group (P < 0.01). Following EA intervention for 3 months, the Abeta1-42 expression level and the number of apoptotic neurons were significantly decreased in the EA group (P < 0.01, P < 0.05). Accordingly, transgenic induced dark degenerated neurons exhibiting irregular body deformation, analosis, and abundant secondary lysosomes and autophagosomes were reduced in the EA group. CONCLUSION: EA intervention can effectively down-regulate Abeta1-42 expression and number of the apoptotic neurons in the striate cortex in APP transgenic model mice, which may contribute to its effect in improving pathological changes of ultrastructure of neurons.

[Effect of electroacupuncture on learning-memory ability, and Abeta and LRP1 immunoactivity in hippocampal sulcus microvessels in APP transgenic mice].

OBJECTIVE: To investigate the effect of electroacupuncture (EA) of "Baihui" (GV 20) and "Yongquan" (KI 1) on the expression of amyloid beta protein (Abeta) and low density lipoprotein (LDL) receptor-related protein 1 (LRP 1) in the hippocampal sulcus microvessels in amyloid precursor protein (APP) 695 V717 I transgenic mice, so as to study its mechanism underlying relief of Alzheimer Disease (AD). METHODS: Twelve APP 695 V717 I transgenic mice were randomly divided into model group and EA group. Six C 57 BL/6 mice were used as the control group. EA (2 Hz/100 Hz, 3-5 mA) was applied to "Baihui" (GV 20) and "Yongquan" (KI 1) for 15 min, once every other day for three months. The learning-memory ability of mice was detected by using Lashley III water maze system. The expression level of Abeta(1-42), and LRP 1 in the hippocampal sulcus microvessels were measured by immunohistochemistry. RESULTS: Water maze test showed that the swimming duration from the start to the goal box (terminal) in the Lashley III water maze was significantly longer in the model group than in the control group (P < 0.05), suggesting a markedly lower learning-memory capacity of APP 695 V717 I transgenic mice. Compared with the model group, the swimming duration in the EA group was decreased considerably (P < 0.05). The integrated optical density (IOD) value of hippocampal Abeta(1-42) immunoreaction (IR) positive products in the model group was significantly higher than that in the control group (P < 0.01) and the IOD value of hippocampal LRP 1 IR-positive products in the model group was apparently lower than that in the control group (P < 0.01). In comparison with the model group, the IOD value of Abeta(1-42) IR-positive products in the EA group was obviously lower than that in the model group (P < 0.05), while that of LRP 1 IR-positive products in the EA group was significantly higher than that in the model group (P < 0.05), suggesting down-regulation of hippocampal Abeta(1-42) expression and up-regulation of LRP 1 expression after EA, and reduction of deposition of Abeta in the cerebral microvessels after EA. CONCLUSION: EA can improve the learning-memory capacity of APP transgenic mice, which is closely related to its effects in up-regulating hippocampal LRP 1 expression and down-regulating hippocampal Abeta(1-42) expression.

[Effect of Ginkgo biloba Pingchan Recipe on neuronal nitric oxide synthase mRNA expression in the brain of mouse models of Parkinson disease].

OBJECTIVE: To study the effect of the Chinese compound prescription Ginkgo biloba Pingchan Recipe (GBPR) on experimental Parkinson disease (PD) in mice and explore the possible mechanism. METHODS: Male C57/BL6J mice were divided into normal control, PD model and treatment groups. PD model was established by intraperitoneal injection with 1-methl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP) in the mice, and in the treatment group, GBPR was administered intragastrically after the injection. The mice were sacrificed 14 and 28 days later, and using in situ hybridization with Digoxin-labeled nNOS cDNA oligonucleotide probe, neuronal nitric oxide synthase (nNOS) mRNA was detected in the striatum and substantia nigra in the brain of mice. RESULTS: nNOS mRNA expression was detected in the striatum and substantia nigra of the PD model mice, and GBPR treatment significantly reduced its expressions. CONCLUSION: GBPR has obvious inhibitory effect against the neurotoxicity of NO probably by producing an anti-oxiditive effect through decreasing nNOS synthesis in the brain.

[Effect of electroacupuncture on the behavior and the expression of amyloid beta-protein, amyloid precursor protein and ChAT in APP 695 V 717 I transgenic mice].

OBJECTIVE: To observe the effect of electroacupuncture (EA) on the expression of amyloid precursor protein (APP) and amyloid beta-protein (Abeta) in hippocampal CA 1 area and cerebral cortex in APP 695 V717 I transgenic mice, so as to investigate its underlying mechanism in improving Alzheimer's disease (AD). METHODS: APP 695 V 717 I transgenic mice were randomly divided into model and EA groups, with 6 cases in each. The other 6 negatively-transgenic mice (C 57 BL/6 J) were used as the normal control group. EA (2 Hz/100 Hz, 3 mA) was applied to "Baihui" (GV 20) and "Yongquan" (KI 1) for 15 min, once every other day for 3 months. The learning-memory ability of mice was measured by Y-type maze test and the expression levels of APP, Abeta, and choline acetyltransferase (ChAT) in the cerebral cotex and hippocampal CA 1 area were detected by immunohistochemistry. RESULTS: In comparison with control group, the times of training for gaining correct reaction and the expression levels of Abeta and APP in both cerebral cortex and hippocampal CA 1 area in model group increased significantly (P < 0.05, P < 0.01), while the expression level of ChAT of cerebral cortex in model group decreased considerably (P < 0.05). Compared to model group, +he times of training for gaining correct reaction and the expression levels of APP in both cerebral cortex and hippocampal CA 1 area, and Abeta in CA 1 area of EA group lowered remarkably (P < 0.05), while those of ChAT in cerebral cortex and hippocampal CA 1 area of EA group increased evidently (P < 0.05, P < 0.01). CONCLUSION: Electroacupuncture can improve the learning-memory capacity of the APP transgenic mice, which may be related to its effects in increasing the production of acetylcholine and lowering the levels of APP and Abeta in the brain.

[Effect of electroacupuncture on the behavior and hippocampal ultrastructure in APP 695 V 717 I transgenic mice].

OBJECTIVE: To investigate the ultrastructural basis underlying electroacupuncture (EA) induced improvement of Alzheimer disease (AD) in transgenic mice. METHODS: Twelve APP 695 V 717 I transgenic mice were randomly divided into model group and EA group; and other 6 negative transgenic mice (C 57 BL/6 J) were made up of normal control group. After 3 months treatment by EA (15 min per other day, 2 Hz/100 Hz, 3-4 mA) applied to "Baihui" (GV 20) and "Yongquan" (KI 1), the learning and memory ability of mice was measured by Lashley III water maze test, and the ultrastructural changes of hippocampal CA 1 region was observed by electronic microscopy. RESULTS: The swimming escape latency and the number of navigating errors (dead-end forward swimming) in model group were significantly longer and more than those in normal control group (P < 0.05); and those in EA group were considerably shorter and fewer than those in model group (P < 0.05), suggesting an improvement of learning-memory ability after EA. Comparison of the ultrastructure of the neurons in the hippocampal CA 1 region showed swelling of the mitochondria, broken or disappearance of the mitochondrial cristae, degeneration of the synapses, breakage and vague outline of the basement membrane of the blood capillaries in mice of model group; and basically distinct outline of the mitochondrial cristae and microvessels, and more synaptic vesicles in EA group. CONCLUSION: EA may effectively improve the learning-memory capacity of the APP transgenic AD mice and alleviate the pathological changes of neurons of the hippocampal CA 1 region, which may be one of the mechanisms underlying the improvement of AD by EA.

Morphological and functional characterization of predifferentiation of myelinating glia-like cells from human bone marrow stromal cells through activation of F3/Notch signaling in mouse retina.

Recently, we have demonstrated that F3/contactin and NB-3 are trans-acting extracellular ligands of Notch that promote differentiation of neural stem cells and oligodendrocyte precursor cells into mature oligodendrocytes (OLs). Here, we demonstrate that human bone marrow stromal cells (hBMSCs) can be induced to differentiate into cells with myelinating glial cell characteristics in mouse retina after predifferentiation in vitro. Isolated CD90(+) hBMSCs treated with beta-mercaptoethanol for 1 day and retinoic acid for 3 days in culture changed into myelinating glia-like cells (MGLCs). More cells expressed NG2, an early OL marker, after treatment, but expression of O4, a mature OL marker, was negligible. Subsequently, the population of O4(+) cells was significantly increased after the MGLCs were predifferentiated in culture in the presence of either F3/contactin or multiple factors, including forskolin, basic fibroblast growth factor, platelet-derived growth factor, and heregulin, in vitro for another 3 days. Notably, 2 months after transplantation into mouse retina, the predifferentiated cells changed morphologically into cells resembling mature MGLCs and expressing O4 and myelin basic protein, two mature myelinating glial cell markers. The cells sent out processes to contact and wrap axons, an event that normally occurs during early stages of myelination, in the retina. The results suggest that CD90(+) hBMSCs are capable of morphological and functional differentiation into MGLCs in vivo through predifferentiation by triggering F3/Notch signaling in vitro.

[Effect of Bnxia Xexin Decoction and its disassembled recipes on somatostatin in rats with stress gastric ulcer].

OBJECTIVE: To explore the acting mechanism of Banxia Xiexin Decoction (BXD) and its disassembled recipes on stress gastric ulcer, for providing references to the scientific researches on the assembling rule of BXD. METHODS: The rat model of acute gastric ulcer was established by water immersion-restraint stress. The experimental rats were divided into the normal group, the model group and the treated groups treated with BXD and its disassembled recipes respectively to observe the therapeutic efficacy and the changes of somatostatin (SS) expression in brain and gastric tissues. RESULTS: In the model group, the SS expression was 0.0237 +/- 0.0056 in brain and 0.0171 +/- 0.0053 in gastric tissue respectively, which was significantly lower than those in the normal group (0.0305 +/- 0.0024 and 0.0282 +/- 0.0037) respectively. Compared to the model group, the two indexes in rats treated with full BXD were 0.0294 +/- 0.0050 and 0.0288 +/- 0.0027, treated with sweet flavor portion were 0.0314 +/- 0.0027 and 0.0219 +/- 0.0059, all showed increase of SS expression, and the increment was more significant in the former. CONCLUSION: BXD can increase the expression of SS to realize its therapeutic efficacy, and the recipe was assembled rationally.

Pathogenesis of Parkinson's disease: oxidative stress, environmental impact factors and inflammatory processes.

Current hypothesis of neuronal degeneration in Parkinson's disease (PD) have been proposed, including formation of free radicals and oxidative stress, mitochondrial dysfunction, excitotoxicity, trophic factor deficiency, inflammatory processes, genetic factors, environmental impact factors, toxic action of nitric oxide, apoptosis, and so on. This review mainly discussed oxidative stress, environmental impact factors, and inflammatory processes in PD.

[Effects of yinxing pingchan recipe and its components on activity of mitochondrial enzyme complex in brain of mice with Parkinson's disease].

OBJECTIVE: To investigate the mechanisms of Yinxing Pingchan recipe (YXPC) and its components, i.e. the components for detoxicating (A), for calming liver (B) and for dissolving blood stasis(C), in preventing and treating Parkinson's disease, and the path of its inhibition on nigrostriatal dopaminergic neuron (DAn) apoptosis in model mice of Parkinson's disease. METHODS: Male C57BL/6J mice were divided into the normal group, the model group and four Chinese medicinal groups, that is, the YXPC group, and Group A, B and C, treated with YXPC and its components A, B and C respectively. Mouse model of Parkinson's disease was established by intraperitoneal injection with 1-methl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP). All mice were sacrificed in 2 batches at the 14th and the 28th day respectively. The activity of mitochondrial enzyme complex I, II and IV (MEC I, II and IV) in the brain of mice were measured, respectively. RESULTS: As compared with the normal group, the activity of MEC I and IV in brain was significantly lower (P < 0.05 or P < 0.01), and that of MEC II had no obvious change in the model group. As compared with the model group, the activity of MEC I was significantly higher in YXPC group and Group C at the 14th day (P < 0.05), while the activity of MECII in Group A at the 14th day, Group B at the 28th day and Group C at both 14th and 28th day was significantly lower (P<0.05 or P<0.01). Activity of MEC IV in the four Chinese medicinal groups at the 14th day all significantly increased (P<0.05 or P<0.01), and retained at high level in Group B and Group C at the 28th day (P<0.05). CONCLUSION: YXPC and its components can maintain the mitochondrial function by partial inhibiting the activity of its enzyme complex, preventing DAn apoptosis to slow down the progress of Parkinson's disease.