ObjectiveTo investigate the neuroprotective mechanism of edaravone for cerebral ischemia-reperfusion injury in rats.MethodsThirty-six healthy adult male SD rats were randomly divided into three groups: a sham operation group, an ischemic model group, and an edaravone group (n=12 in each group).A focal cerebral ischemia model was induced by the suture method.Reperfusion was resumed after 2 h of ischemia;then the animals were sacrificed at 24 h after reperfusion.Edaravone 3 mg/kg was injected intraperitoneally immediately after cerebral ischemia-reperfusion in the edaravone group.The rats in the model group were injected equal volume normal saline.HE staining was used to observe the pathological changes.TUNEL staining was used to detect apoptotic cells in the ischemic cortex.Western blot and immunofluorescent staining were used to detect the expression levels of LIM domain protein 4 (LMO4) and LMO4 positive cells.Results HE staining showed that cellular morphology was basically normal in the sham operation group;both the model group and edaravone group had cell necrosis, but the latter was less severe.The number of morphologically normal cells in the edaravone group was significantly more than that in the model group (P<0.01).TUNEL staining showed that no TUNEL positive cells in the sham operation group were observed.The TUNEL positive cells in the edaravone group was significantly less that in the model group (P<0.01).Immunofluorescence staining showed that the expression level of LMO4 in the ischemic cortex in the edaravone group was significantly higher than that in the model group (P<0.01).ConclusionsEdaravone can alleviate the cerebral ischemia-reperfusion injury and inhibit neuronal apoptosis.Its mechanism may be associated with the upregulation of LMO4 expression.

Objective To investigate perfusion imaging and parameters of normal pancreas by dual-source CT and to evaluate the appropriate perfusion imaging scan.Methods Sixty-six subjects with normal pancreas underwent low-dose pancreatic perfusion and plain scan.CT images were sent to a separate workstation via a network.The blood flow (BF)and blood volume (BV)of pancreas head,body and tail were measured using the VPCT Body software and analyzed by one-way ANOVA.Then the time-density curve of pancreas was drawn,and the enhancement peak time and the corresponding CT value were also measured.Results The average BF values of pancreas head,body and tail were (1 1 6.09 ± 31.83)mL·100 g-1 ·min-1 ,(1 1 9.72±32.50)mL·100 g-1 ·min-1 , (1 14.65±31.42)mL·100 g-1 ·min-1 ,and the mean BV values were (29.83 ±1 9.07)mL/100 g,(30.39 ± 1 9.38)mL/100 g, (28.82±1 9.22)mL/100 g,respectively.The perfusion parameters in different pancreatic parts were not statistically different.The mean enhancement peak time was (27.92 s±4.52)s,(28.02±5.34)s in pancreas head,(27.40±4.36)s in pancreas body,(27.34±4.57)s in pancreas tail.On plain image,the average CT value of pancreas was (41.43±5.88)HU.However,on enhanced image,the mean CT value was (95.96±18.44)HU in normal pancreas [(96.73±19.71)HU in pancreas head,(98.45±17.52)HU in body,(92.69±18.1 7)HU in tail].Conclusion The perfusion parameters including blood flow and blood volume in pancreatic head,body and tail are identical. The mean enhancement peak time is (27.92±4.52)s,and the corresponding enhancement CT value is (95.96±18.44)HU.

Objective To understand the current situation and characteristics of occupational exposure(OE)among health care workers(HCWs),and provide basis for making preventive measures.Methods Self-designed question-naire about OE was adopted,OE among all HCWs in a hospital in January-December 2015 were surveyed and statis-tically analyzed.Results A total of 1888 HCWs were surveyed,there were 304 cases of OE,the mean OE rate in the whole hospital was 16.10%;OE occurred 370 times(19.60%).Doctors,trainees,and HCWs who worked for≤1 year had relatively higher OE rates,which were 23.18%(102/440),17.88%(49/274),and 18.34%(95/518) respectively.Sharp injury is the main OE mode,accounting for 83.24%(n=308),sharp injuries mainly occurred before disposing the used devices and during the process of use,accounting for 37.99%(n=117)and 36.69%(n=113)respectively.Among 370 times of OE,315 could be traced to the sources of exposure.Among the known ex-posure sources,OE of bloodborne pathogens accounted for 24.13% (n=76).59 of 370 times of OE implemented complete local treatment and reporting procedures,reporting rate of OE was 15.95%.Conclusion Hospital should take comprehensive measures to promote occupational safety precaution,and reduce the incidence of OE.

0bjective To investigate the relationships between the peripheral lung cancer and pulmonary vessels or bronchi by 16-row muhislice computed tomography(MSCT)and analyze the related factors.Methods Fifty-four patients with peripheral lung cancer confirmed pathologically underwent contrast-erdaanced MSC TI Multiplanar reformation(MPR)and maximum intensity projection(MIP)in all patients were used to demonstrate the relationships between the peripheral lung cancer and pulmonary vessels,bronchi.The relationships were categorized five types:Type 1,erupted at the edge of nodule. Type 2,erupted at the center of nodule.Type 3,penetrated through the nodule.Type 4,contacting the nodule but stretched or encased.Type 5,contacting the nodule but smoothly compressed.The pathology type,stage,size,density and location of the peripheral lung cancer were recorded and the relationships with five types were evaluated by using Chi-square test and correlation analysis.Results (1)Tumor-bronchi relationship:type 1(33,61.1%)was more often seen in≥2.0 cm and solid lesions with stage Ⅱ-Ⅳ.while Type 2(14,25.9%)was often seen in<2.0 am and part-solid or non-solid lesions with stage Ⅰ.(2)Tumor-PA relationship:Type 1 was more often seen in≥2.0 am and solid lesions with stage Ⅱ-Ⅳ.while Type 2 was often seen in part-solid or non-solid lesions with stage Ⅰ.(3)Tumor-PV relationship:type 4 was the most common type(29,53.7%).Type 2(13,24.1%)was more often seen in part-solid or non-solid lesions.(4)Tumor-bronchi relationship and tumor-PA relationship had a positive correlation(r=0.5265,P<0.01).Conclusions MSCT can demonstrate the relations between the peripheral lung cancer and bronchi.PA and PV.It is useful for the differential diagnosis and prognosis evaluation of the lung csncer.

Objective:To analyze the MRI features of medulloblastoma (MB) in children, and screen out the key signs that can predict the risk of MB before surgery.Methods:Clinical and radiological data of 62 children with MB confirmed by pathology in Shenzhen Children′s Hospital from December 2012 to December 2021 were retrospectively analyzed. According to the diagnosis and treatment guidelines for children with MB (2021 edition), the patients were divided into standard risk group (43 cases) and high risk group (19 cases). MRI features of MB were observed and recorded, including tumor site, location of tumor center, tumor morphology, signal intensity of T 1WI, T 2WI and diffusion weighted imaging (DWI), enhancement pattern, cystic lesion size, location and number, peritumoral edema and hydrocephalus, and the maximum diameter of tumor was measured. The χ 2 test or Fisher exact probability method was used to compare the differences in age, gender and MRI signs between the two groups. The t test of two independent samples was used to compare the differences in the maximum diameter of tumors between the two groups. The indicators with statistically significant differences were included in binary logistic regression analysis to obtain independent influencing factors associated with the risk groups. The receiver operation characteristic curve was used to evaluate the diagnostic efficacy. Results:There were significant differences in age ( P=0.026), enhancement pattern ( P=0.018), cystic lesion size ( P=0.005), location ( P=0.011) and number ( P=0.003) between standard risk group and high risk group. There were no significant differences in gender, tumor site, location of tumor center, tumor morphology, signal intensity of T 1WI, T 2WI and DWI, peritumoral edema, hydrocephalus and maximum diameter of tumor between the two groups ( P>0.05). Binary logistic regression results showed the age (OR=0.207, 95%CI 0.040-0.983, P=0.042) and the number of cystic lesions (OR=0.215, 95%CI 0.073-0.630, P=0.005) were the protective factors for MB in high risk group, the enhancement pattern Ⅲ (OR=5.226, 95%CI 1.516-52.920, P=0.048) was the dangerous factor for MB in high risk group. The area under the curve of the combined diagnosis of high risk MB was 0.845 (95%CI 0.741-0.949). Conclusions:The age and MRI signs the pattern of tumor enhancement Ⅲ and the number of cystic lesion can be used to predict the risk grouping of MB preoperatively. When the child is younger and MB enhancement pattern is mainly peripheral enhancement without obvious cystic change, it may indicate high risk MB.

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.