Subarachnoid hemorrhage (SAH) is a serious intracranial hemorrhage characterized by acute bleeding into the subarachnoid space. The effects of shikonin, a natural compound from the roots of Lithospermum erythrorhizon, on oxidative stress and blood–brain barrier (BBB) injury in SAH was evaluated in this study. A rat model of SAH was established by endovascular perforation to mimic the rupture of intracranial aneurysms. Rats were then administered 25 mg/kg of shikonin or dimethylsulfoxide after surgery. Brain edema, SAH grade, and neurobehavioral scores were measured after 24 h of SAH to evaluate neurological impairment. Concentrations of the oxidative stress markers superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the brain cortex were determined using the corresponding commercially available assay kits. Evans blue staining was used to determine BBB permeability. Western blotting was used to quantify protein levels of tight junction proteins zonula occludens-1, Occludin, and Claudin-5. After modeling, the brain water content increased significantly whereas the neurobehavioral scores of rats with SAH decreased prominently. MDA levels increased and the levels of the antioxidant enzymes GSH and SOD decreased after SAH. These changes were reversed after shikonin administration. Shikonin treatment also inhibited Evans blue extravasation after SAH. Furthermore, reduction in the levels of tight junction proteins after SAH modeling was rescued after shikonin treatment. In conclusion, shikonin exerts a neuroprotective effect after SAH by mitigating BBB injury and inhibiting oxidative stress in the cerebral cortex.

Subarachnoid hemorrhage (SAH) is a serious intracranial hemorrhage characterized by acute bleeding into the subarachnoid space. The effects of shikonin, a natural compound from the roots of Lithospermum erythrorhizon, on oxidative stress and blood–brain barrier (BBB) injury in SAH was evaluated in this study. A rat model of SAH was established by endovascular perforation to mimic the rupture of intracranial aneurysms. Rats were then administered 25 mg/kg of shikonin or dimethylsulfoxide after surgery. Brain edema, SAH grade, and neurobehavioral scores were measured after 24 h of SAH to evaluate neurological impairment. Concentrations of the oxidative stress markers superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the brain cortex were determined using the corresponding commercially available assay kits. Evans blue staining was used to determine BBB permeability. Western blotting was used to quantify protein levels of tight junction proteins zonula occludens-1, Occludin, and Claudin-5. After modeling, the brain water content increased significantly whereas the neurobehavioral scores of rats with SAH decreased prominently. MDA levels increased and the levels of the antioxidant enzymes GSH and SOD decreased after SAH. These changes were reversed after shikonin administration. Shikonin treatment also inhibited Evans blue extravasation after SAH. Furthermore, reduction in the levels of tight junction proteins after SAH modeling was rescued after shikonin treatment. In conclusion, shikonin exerts a neuroprotective effect after SAH by mitigating BBB injury and inhibiting oxidative stress in the cerebral cortex.

Subarachnoid hemorrhage (SAH) is a serious intracranial hemorrhage characterized by acute bleeding into the subarachnoid space. The effects of shikonin, a natural compound from the roots of Lithospermum erythrorhizon, on oxidative stress and blood–brain barrier (BBB) injury in SAH was evaluated in this study. A rat model of SAH was established by endovascular perforation to mimic the rupture of intracranial aneurysms. Rats were then administered 25 mg/kg of shikonin or dimethylsulfoxide after surgery. Brain edema, SAH grade, and neurobehavioral scores were measured after 24 h of SAH to evaluate neurological impairment. Concentrations of the oxidative stress markers superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the brain cortex were determined using the corresponding commercially available assay kits. Evans blue staining was used to determine BBB permeability. Western blotting was used to quantify protein levels of tight junction proteins zonula occludens-1, Occludin, and Claudin-5. After modeling, the brain water content increased significantly whereas the neurobehavioral scores of rats with SAH decreased prominently. MDA levels increased and the levels of the antioxidant enzymes GSH and SOD decreased after SAH. These changes were reversed after shikonin administration. Shikonin treatment also inhibited Evans blue extravasation after SAH. Furthermore, reduction in the levels of tight junction proteins after SAH modeling was rescued after shikonin treatment. In conclusion, shikonin exerts a neuroprotective effect after SAH by mitigating BBB injury and inhibiting oxidative stress in the cerebral cortex.

Subarachnoid hemorrhage (SAH) is a serious intracranial hemorrhage characterized by acute bleeding into the subarachnoid space. The effects of shikonin, a natural compound from the roots of Lithospermum erythrorhizon, on oxidative stress and blood–brain barrier (BBB) injury in SAH was evaluated in this study. A rat model of SAH was established by endovascular perforation to mimic the rupture of intracranial aneurysms. Rats were then administered 25 mg/kg of shikonin or dimethylsulfoxide after surgery. Brain edema, SAH grade, and neurobehavioral scores were measured after 24 h of SAH to evaluate neurological impairment. Concentrations of the oxidative stress markers superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the brain cortex were determined using the corresponding commercially available assay kits. Evans blue staining was used to determine BBB permeability. Western blotting was used to quantify protein levels of tight junction proteins zonula occludens-1, Occludin, and Claudin-5. After modeling, the brain water content increased significantly whereas the neurobehavioral scores of rats with SAH decreased prominently. MDA levels increased and the levels of the antioxidant enzymes GSH and SOD decreased after SAH. These changes were reversed after shikonin administration. Shikonin treatment also inhibited Evans blue extravasation after SAH. Furthermore, reduction in the levels of tight junction proteins after SAH modeling was rescued after shikonin treatment. In conclusion, shikonin exerts a neuroprotective effect after SAH by mitigating BBB injury and inhibiting oxidative stress in the cerebral cortex.

Subarachnoid hemorrhage (SAH) is a serious intracranial hemorrhage characterized by acute bleeding into the subarachnoid space. The effects of shikonin, a natural compound from the roots of Lithospermum erythrorhizon, on oxidative stress and blood–brain barrier (BBB) injury in SAH was evaluated in this study. A rat model of SAH was established by endovascular perforation to mimic the rupture of intracranial aneurysms. Rats were then administered 25 mg/kg of shikonin or dimethylsulfoxide after surgery. Brain edema, SAH grade, and neurobehavioral scores were measured after 24 h of SAH to evaluate neurological impairment. Concentrations of the oxidative stress markers superoxide dismutase (SOD), glutathione (GSH), and malondialdehyde (MDA) in the brain cortex were determined using the corresponding commercially available assay kits. Evans blue staining was used to determine BBB permeability. Western blotting was used to quantify protein levels of tight junction proteins zonula occludens-1, Occludin, and Claudin-5. After modeling, the brain water content increased significantly whereas the neurobehavioral scores of rats with SAH decreased prominently. MDA levels increased and the levels of the antioxidant enzymes GSH and SOD decreased after SAH. These changes were reversed after shikonin administration. Shikonin treatment also inhibited Evans blue extravasation after SAH. Furthermore, reduction in the levels of tight junction proteins after SAH modeling was rescued after shikonin treatment. In conclusion, shikonin exerts a neuroprotective effect after SAH by mitigating BBB injury and inhibiting oxidative stress in the cerebral cortex.

Background In the context of China's rapid economic growth and social acceleration, long working hours are emerging as a key factor affecting well-being and contributing to depression. Objective To examine the longitudinal interaction between working hours and depressive symptoms, and evaluate potential mediating role of internet use in the relationship between working hours and depressive symptoms. Method This study utilized two waves of panel data from the China Family Panel Studies (CFPS) collected between 2016 and 2018. It constructed a longitudinal sample of 4900 individuals aged 18-70 years who were employed with known working hours across various occupations. Based on survey data and the Center for Epidemiologic Studies Depression Scale (CES-D), we measured and compared working hours, internet use, and depressive symptoms. Pearson correlation analysis was employed to examine the associations among key variables. Through cross-lagged panel models and a semi-longitudinal mediation model, we examined the bidirectional interactive mechanisms between working hours and depressive symptoms, with a particular focus on revealing the mediating pathways of internet use and any group heterogeneity. Result The study sample comprised 4900 participants, aged 18 to 70 years. Of these, 43.8% were male, and 77.35% were married. In 2016, the average working hours were (48.55 ± 22.17) h, and over half of the participants used the internet (59.84%). The average score on the depressive symptoms scale was (5.11 ± 3.78). The cross-lagged panel models revealed a dynamic interplay between working hours, internet use, and depressive symptoms. Specifically, working hours, internet use, and depressive symptoms in 2016 all positively predicted their respective counterparts in 2018. Furthermore, working hours in 2016 positively predicted internet use in 2018 (β=0.045, P < 0.001) and depressive symptoms in 2018 (β=0.027, P < 0.05), indicating that longer working hours were associated with an increased likelihood of internet use and worsened depressive symptoms. The half-longitudinal mediation models demonstrated a significant mediating effect of internet use in the relationship between working hours and depressive symptoms (effect size=−0.0013, P < 0.05), suggesting that internet use may buffer the adverse effects of long working hours on depressive symptoms. The subgroup analyses of the half-longitudinal mediation model revealed significant mediation effects of internet use within the female and married female subgroups, as well as significant mediating pathways within the older adult and employment stability subgroups. The Panel Logit regression results indicated that internet use (high or low) was associated with a lower risk of depressive symptoms compared to non-internet use, positioning internet use as a protective factor against depressive symptoms symptoms among younger adults, those with stable employment, and married women. Conclusion This study confirms that prolonged working hours are detrimental to psychological health. Internet use mediates the relationship between working hours and depressive symptoms, effectively mitigating the psychological harm of long working hours. This mediating effect is particularly pronounced for women, especially married women.

Background In the context of China's rapid economic growth and social acceleration, long working hours are emerging as a key factor affecting well-being and contributing to depression. Objective To examine the longitudinal interaction between working hours and depressive symptoms, and evaluate potential mediating role of internet use in the relationship between working hours and depressive symptoms. Method This study utilized two waves of panel data from the China Family Panel Studies (CFPS) collected between 2016 and 2018. It constructed a longitudinal sample of 4900 individuals aged 18-70 years who were employed with known working hours across various occupations. Based on survey data and the Center for Epidemiologic Studies Depression Scale (CES-D), we measured and compared working hours, internet use, and depressive symptoms. Pearson correlation analysis was employed to examine the associations among key variables. Through cross-lagged panel models and a semi-longitudinal mediation model, we examined the bidirectional interactive mechanisms between working hours and depressive symptoms, with a particular focus on revealing the mediating pathways of internet use and any group heterogeneity. Result The study sample comprised 4900 participants, aged 18 to 70 years. Of these, 43.8% were male, and 77.35% were married. In 2016, the average working hours were (48.55 ± 22.17) h, and over half of the participants used the internet (59.84%). The average score on the depressive symptoms scale was (5.11 ± 3.78). The cross-lagged panel models revealed a dynamic interplay between working hours, internet use, and depressive symptoms. Specifically, working hours, internet use, and depressive symptoms in 2016 all positively predicted their respective counterparts in 2018. Furthermore, working hours in 2016 positively predicted internet use in 2018 (β=0.045, P < 0.001) and depressive symptoms in 2018 (β=0.027, P < 0.05), indicating that longer working hours were associated with an increased likelihood of internet use and worsened depressive symptoms. The half-longitudinal mediation models demonstrated a significant mediating effect of internet use in the relationship between working hours and depressive symptoms (effect size=−0.0013, P < 0.05), suggesting that internet use may buffer the adverse effects of long working hours on depressive symptoms. The subgroup analyses of the half-longitudinal mediation model revealed significant mediation effects of internet use within the female and married female subgroups, as well as significant mediating pathways within the older adult and employment stability subgroups. The Panel Logit regression results indicated that internet use (high or low) was associated with a lower risk of depressive symptoms compared to non-internet use, positioning internet use as a protective factor against depressive symptoms symptoms among younger adults, those with stable employment, and married women. Conclusion This study confirms that prolonged working hours are detrimental to psychological health. Internet use mediates the relationship between working hours and depressive symptoms, effectively mitigating the psychological harm of long working hours. This mediating effect is particularly pronounced for women, especially married women.

Objective To investigate the value of CT guided 125 I seed implantation combined with chemotherapy in the treat-ment of unresectable non-small cell lung cancer .Methods The related data of 42 cases of middle and advanced non-small cell lung cancer treated in this hospital from January 2012 to December 2016 were retrospectively analyzed .The group A (23 cases) received the 125I seed implantation combined with chemotherapy ,while the group B(19 cases) adopted the simple chemotherapy .All cases conducted the chest CT re-examination at 1 ,2 ,6 months after treatment .The curative effects and complications were compared be-tween the two groups .Results The total effect rate (RR) at 1 ,2 ,6 months had statistical difference between the two groups (P<0 .05) .The adverse reactions in the group A were small ,large amounts of pneumothorax (26 .1% ,6/23) ,bone marrow suppression (26 .1% ,6/23) ,nausea and vomiting(30 .4% ,7/23) ,which in the group B were d 5 .3% (1/19) in the group B were bone marrow suppression (36 .8% ,7/19) ,nausea and vomiting (26 .3% ,5/19) .No severe complications were observed .The occurrence rate of adverse reactions had no statistical difference between the two groups (P>0 .05) .The adverse reactions were improved after symp-tomatic treatment .Conclusion CT guided 125 I seed implantation combined with chemotherapy has higher effective rate and more significant effect in treating unresectable non-small cell lung cancer .

A method was developed for simultaneous determination of Clozapine, Quetiapine and Risperidone in human serum by fully automated online solid phase extraction ( SPE )-high performance liquid chromatography. With Capcell MF Ph-1 column as SPE cartridge and Acclaim C18 as analytical column, high
selectivity could be achieved by this method according to the selective complementarity of the two columns. In the experiment, ACN-H2 O was used as the SPE mobile phase with a flow rate of 1 mL/min and ACN-10 mmol/L NH4 Ac was used as the analytical mobile phase with a flow rate of 1 mL/min. Serum samples were injected directly into the SPE column and the biological matrix was washed out with the loading solvent. By rotation of the switching valve, Clozapine, Quetiapine and Risperidone were eluted from the SPE cartridge in the back-flush mode and transferred to the analytical column by the chromatographic mobile phase. The whole time of the online SPE purification and chromatographic separation of the analytes was 18 min. Calibration curve of Clozapine with good linearity ( r=0 . 9996 ) was obtained in the range of 10-1800 μg/L in human serum, and the recoveries at low, medium and high concentration levels were 118. 4%, 105. 0% and 105 . 4%. Calibration curve of Quetiapine with good linearity ( r=0 . 9997 ) was obtained in the range of 3 . 6-640 μg/L in human serum, and the recoveries at low, medium and high concentration levels were 112. 8%, 101 . 1% and 101 . 5%. Calibration curve of Risperidone with good linearity ( r=0 . 9995 ) was obtained in the range of 0. 71-128 μg/L in human serum, and the recoveries at low, medium and high concentration levels were 100. 7%, 97. 2% and 98. 8%. In conclusion, the established automated online SPE-HPLC-UV method demonstrated good performance in terms of linearity, specificity, limits of quantification, and was successfully utilized to quantify Clozapine, Quetiapine and Risperidone in human serum.

A total of 60 hemiplegic patients after stroke were divided randomly into 2 groups.The control group received conventional rehabilitation training while the treatment group isokinetic training based on conventional rehabilitation training.Both groups were trained for 8 weeks.Results showed the differences of peak torque of knee flexors and extensors were significant between two groups (P ＜ 0.01).The ratio of flexion and extension showed significant difference (P ＜ 0.01).The treatment group was superior to control group in walking ability (P ＜ 0.01).Therefore isokinetic training provides significant improvement in stability of knees and walking ability in hemiplegic patients after stroke.