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According to the movement characteristics of the surrounding rock of the gob-side entry retaining by roof cutting (GERRC), the structural evolution mechanism and stability control countermeasures are studied in this paper. Taking the roof cutting and bulking as the core point, the movement process of the surrounding rock of GERRC is divided into five stages: roof cutting, dynamic pressure support, gangue bulking, double arch roadway support, and roadway formation. Combined with mechanical analysis, the roof pressure of the mechanical model of the short-arm beam formed by roof cutting is calculated, and the roof breaking criterion is obtained, which provides a basis for roof control design and reasonable support strength calculation. A structural model of double-arch roadway protection under the action of hydrostatic roof cutting and gangue bulking was established, and the mechanism of roadway formation stability was studied. The gob-side bulking gangue and short-arm beam are formed by roof cutting, and the solid coal seam forms the immediate balance arch, the bulking gangue in goaf, articulated transfer rock beam, and solid coal seam forms the main balance arch. The two together are called double balance arch. With the support of the double-balanced arch on the overlying rock strata, the roadway below is located in the low-stress zone, which ensures the stability of the roadway surrounding rock. Through mechanical analysis and field observation, the law of bulking and deformation and mechanical characteristics of gob-side gangue in the above structural model are analyzed, and the reasonableness of the structural model of the double-arch guard lane is verified through numerical simulation of the cut top into lanes. and the reasonableness of the structural model of double-arch protection in GERRC is verified by using numerical simulation. In this paper, a mechanical double-arch model has been developed that allows us to understand the mechanism of stress transfer of roof cutting roadway from the perspective of a dynamic balance of roadway surrounding rock and overlying rock strata, helping us to specify efficient support countermeasures.

It has been demonstrated that hypoxic preconditioning (HP) enhances the survival ability of the organism against the subsequent acute anoxia (AA). However, it is not yet clear whether necrosis induced by AA can be prevented by HP, and what are the underlying mechanisms. In this study, we examined the effect of HP (10% O(2), 48 h) on necrosis induced by AA (0% O(2), 24 h) in PC12 cells. We found that HP delayed the regulatory volume decrease and reduced cell swelling after 24 h of exposure to AA. Since aldose reductase (AR) is involved in cell volume regulation, we detected AR mRNA expression with reverse transcription-polymerase chain reaction (RT-PCR) techniques. The AR mRNA level was dramatically elevated by HP. Furthermore, an HP-induced decrease in cell injury was reversed by berberine chloride (BB), the inhibitor of AR. In addition, sorbitol synthesized from glucose catalyzed by AR is directly related to cell volume regulation. Subsequently, we tested sorbitol content in the cytoplasm. HP clearly elevated sorbitol content, while BB inhibited the elevation induced by HP. Further study showed that a strong inhibitor of sorbitol permease, quinidine, completely reversed the protection induced by HP after AA. These data provide evidence that HP prevents necrosis induced by AA and is mediated by AR and sorbitol pathway.

It is known that hypoxic preconditioning (HP, a brief period of sublethal hypoxia) provides neuroprotection against subsequent severe anoxia, but the mechanisms of this increased tolerance have not been fully elucidated. A hypoxic preconditioning model was established by exposing a 4-day hippocampal culture to 1% O(2) for 20 min/day for 8 days. The preconditioning significantly decreased the number of apoptotic neurons at reoxygenation 24 h after 4 h of severe anoxia (0% O(2)). Further study demonstrated that the degradation of mitochondrial membrane potential (MMP) was greatly inhibited and the expression of B-cell lymphoma protein-2 (Bcl-2) was increased considerably after severe anoxia in the HP groups. These results indicate that the increased anoxic tolerance, which is induced by HP in cultured hippocampal cells, may be correlated with Bcl-2 overexpression and enhanced stability of MMP, which ultimately reduces apoptosis 24 h after reoxygenation.

To establish the model of oxygen-glucose deprivation in vitro rat hippocampal neurons.The hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5-4 h and then cultured with original medium in normoxia for 24 h. Auto-biochemical analyzer determined LDH activity. The change of neuronal morphology and neuron survival were observed by converted contrast microscope and assessed by photography analysis system. Neuron apoptosis was detected by using the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL) method.The neurons swelled, LDH release increased and neuron survival decreased after gradually oxygen-glucose deprivation. The percentage of apoptosis increased obviously 24 h after recovering the supply of oxygen and glucose.The model of oxygen-glucose deprivation in vitro rat hippocampal neurons is established successfully by using the modified ACSF (artificial cerebral spinal fluid) with serum and glucose free.

To investigate the effects of oxygen-glucose deprivation on cultured rat hippocampal neurons.The hippocampal neurons cultured for 12 d were exposed to combined oxygen-glucose deprivation for 0.5 - 4 h and then cultured with original medium in normoxia for 28 h. Necrotic neurons were identified by 0.4% trypan blue staining and apoptotic neurons were detected by a TUNEL technique. Meanwhile, the area, perimeter and circle diameter of cell bodies were measured respectively by a photography analysis system.The percentage of necrotic cells in cultured hippocampal neurons increased significantly during oxygen-glucose deprivation, but the percentage of apoptotic cells increased significantly after 28 h oxygen-glucose recovery. Photography analysis showed that area, perimeter and circle diameter of the necrotic cell bodies were larger than those of the apoptotic ones.Oxygen-glucose deprivation can lead to severe damage of cultured hippocampal neurons. The necrosis is major during acute oxygen-glucose deprivation, while the apoptosis is major 28 h after oxygen-glucose recovery.

The effects of hypoxic preconditioning (HP) on changes in mitochondrial membrane potential (MMP) and Bcl-2 expression in cultured hypothalamic neurons after severe anoxia were investigated. In the HP group, hypothalamic neurons, after a 4-day culture, were preconditioned daily under a hypoxic condition (1% O2, 10 min) for 8 days; subsequently, the HP neurons and those in the control group (similarly cultured, but without HP) were exposed to 6 h of severe anoxia (0% O2). The preconditioned neurons had a higher survival rate and a lower lactate dehydrogenase leakage, compared with the control group. Although HP did not prevent the degradation of MMP during severe hypoxia, preconditioned neurons exhibited a higher level of MMP than that of the control group. Increased expression of Bcl-2 was also observed in the preconditioned hypothalamic neurons. These results suggest that HP enhances the hypoxic tolerance of hypothalamic neurons, and the underlying mechanisms may be related to the increased stability of MMP and the overexpression of Bcl-2 induced by HP.