Objective To investigate the expression of hypoxia-inducible factor-1α (HIF-1α) in patients with traumatic brain injury (TBI) and their clinical significance. Methods Peripheral blood and brain tissue samples were obtained from 60 TBI patients. According to the GCS score, 60 TBI patients were divided into the moderate damage group, the severe damage group and the especially severe damage group. According to the different time points after the injury, the patients were divided into <6 hours group, 6-24 hours group, 24-72 hours group and >72 hours group. The 60 control brain tissue samples were obtained from patients with cerebral aneurysms and undergoing craniotomy at the same time; and control peripheral blood were collected from 60 healthy people. The levels of HIF-1α were measured with RT-PCR and Western blot . One-way ANOVA and t-test were used to analyze the results with SPSS 18.0. Results The expression of HIF-1α in the control group [peripheral blood: HIF-1α mRNA (0.35±0.12), HIF-1α protein (0.28±0.06) ;brain tissue: HIF-1α mRNA (0.65±0.08),HIF-1α protein (0.78±0.08)] was obviously lower than those in the TBI groups, and the differences were statistically significant (P<0.05). Along with the damage degree aggravating, the expression of HIF-1α was increased. The expression of HIF-1α in the especially severe damage group was statistically higher than those of the severe damage group and the moderate damage group (P<0.05). The expression of HIF-1α was increased along with the extension of time after the injury. The expression of HIF-1α in the 24-72 h group was significantly higher than those of the >72 h group, 6-24 h group and <6 h group (P<0.05). Conclusions The expression of HIF-1α is closely related to the severity of TBI and may play an important role in the progress of TBI.

ViewRay magnetic resonance (MR) guided radiotherapy system not only solves the problem of imaging dose,but also can set up accurately,online adaptive radiotherapy and gated irradiation according to magnetic resonance imaging (MRI).The development of this system provides a new technical means of accurate radiotherapy.This review describes the main structure of the ViewRay system,and summarizes quality assurance (QA),dosimetric comparison,respiratory motion management,online adaptive radiotherapy,and preliminary treatment effect.

Objective To explore the mechanism underlying the poor prognosis in cerebral infarction (CI) patients with low T3 syndrome by comparing the NIHSS scores in these patients with or without low T3 syndrome.Methods One hundred and sixty-two patients with CI,admitted to our hospital from January 2010 to December 2012,were chosen in our study; the levels of thyroid hormones,including triiodothyronine (T3),four iodine thyronine (T4),thyroid stimulating hormone (TSH),free Triiodothyronine (iT3) and free four iodine thyronine (fT4),were measured by radioimmunoassay.CI lesions and TOAST distribution were determined by cranial MRI,magnetic resonance angiography (MRA) or CT angiography (CTA),and carotid ultrasonography.NIHSS scores at the worst in cerebral infarction inpatients were detected.Results In the 162 patients with CI,29 patients (17.90％) were combined with low T3 symptom and 20 had fT3 level lower than the lowest normal level (2.63 pmol/L); and T4,fT4 and TSH levels were within normal limits.T3,fr3 and TSH levels in patients with low T3 symptom were significantly lower than those of patients without low T3 symptom (P＜0.05).The distribution of TOAST showed no significant difference between patients with low T3 symptom and patients without low T3 symptom (P＞0.05).In patients with large artery atherosclerosis-internal carotid artery,the NIHSS scores at the worst in patients with low T3 level were significantly higher as compared with those in patients with normal T3 levels (P＜0.05).Conclusion The neurologic impairment is more severe in large artery atherosclerosis-intemal carotid artery patients with low T3 level than those without low T3 level,which might be responsible for the poor prognosis of the illness with low T3 syndrome.

Objective: To investigate the expression of macrophage migration inhibitory factor (MIF) in pulmonary tissues from patients with chronic obstructive pulmonary disease (COPD) and the relationship with its clinical features. Methods: One hundred and eighty patients who underwent pulmonary bullectomy lobectomy due to pneumatocele from January 2015 to September 2018 in Longgang Central Hospital were enrolled and classified into patients without COPD (control group)and patients with COPD (COPD group), with 90 patients each group. According to the lung function parameters, 90 patients with COPD were divided into the mild COPD group, the moderate COPD group, and the severe COPD group. The levels of mRNA and protein of MIF were measured with RT-PCR, ELISA and Western blot. One-way ANOVA, Pearson correlation analysis and SNK-q test were used to analyze the results with SPSS 18.0, and P<0.05 was considered statistically significant. Results: The level of MIF in pulmonary tissues from the control group was obviously lower than those in the COPD group (P<0.05). The level of MIF in pulmonary tissues in the severe COPD group was obviously higher than those in pulmonary tissues in the mild COPD, moderate COPD and control groups (P<0.05). MIF was positively correlated with the lung function parameters (P<0.05). Conclusion The high expression of MIF in pulmonary tissues is closely related to the severity of COPD.

Ischemic stroke is a severe disorder resulting from acute cerebral thrombosis. Here we demonstrated that post-ischemic treatment with ciclopirox olamine (CPX), a potent antifungal clinical drug, alleviated brain infarction, neurological deficits and brain edema in a classic rat model of ischemic stroke. Single dose post-ischemic administration of CPX provided a long-lasting neuroprotective effect, which can be further enhanced by multiple doses administration of CPX. CPX also effectively reversed ischemia-induced neuronal loss, glial activation as well as blood-brain barrier (BBB) damage. Employing quantitative phosphoproteomic analysis, 130 phosphosites in 122 proteins were identified to be significantly regulated by CPX treatment in oxygen glucose deprivation (OGD)-exposed SH-SY5Y cells, which revealed that phosphokinases and cell cycle-related phosphoproteins were largely influenced. Subsequently, we demonstrated that CPX markedly enhanced the AKT (protein kinase B, PKB/AKT) and GSK3 (glycogen synthase kinase 3) phosphorylation in OGD-exposed SH-SY5Y cells, and regulated the cell cycle progression and nitric oxide (NO) release in lipopolysaccharide (LPS)-induced BV-2 cells, which may contribute to its ameliorative effects against ischemia-associated neuronal death and microglial inflammation. Our study suggests that CPX could be a promising compound to reduce multiple ischemic injuries; however, further studies will be needed to clarify the molecular mechanisms involved.