Objective To investigate the operative methods and their efficacy of the modified decompressive craniectomy in combination with indirect revascularization for the treatment of massive cerebral infarction. Methods The clinical data of 15 patients with massive cerebral infarction who underwent modified decompressive craniectomy in combination with encephaloduroarteriomyosynangiosis were analyzed retrospectively. The clinical efficacy was assessed according to the mortality, Barthel Index and modified Rankin scale. Results All the patients were followed up, and 12 patients survived 3 months after operation, of those, 4 had a good functional outcome; 11 patients survived 6 month after operation, of those, 7 had a good functional outcome. Conclusions The modified decompressive craniectomy in combination with indirect revascularization for the treatment of massive cerebral infarction could effectively treat massive cerebral infarction and increase the survival rate and life quality of patients, however, the surgical timing, surgical indications and surgical skills are needed to master accurately.

Background Di(2-ethylhexyl)phthalate (DEHP) and dibutyl phthalate (DBP) are representative environmental endocrine disruptors of phthalate esters (PAEs). Some studies have shown that PAEs exposure may have an impact on lipid metabolism. Objective To investigate the effects of DEHP and/or DBP on lipid metabolism in rats and their possible mechanisms of action. Methods Thirty-six weaned healthy SD male rats, 3 weeks old, weighing 50-70 g, were divided into four groups, i.e., a corn oil control group, a DEHP (750 mg·kg⁻¹) group, a DBP (500 mg·kg⁻¹) group, and a DEHP+DBP (750 mg·kg⁻¹+500 mg·kg⁻¹) group. The rats were exposed to DEHP and/or DBP by oral gavage for 8 weeks, and weighed once a week. The rats were anesthetized 24 h after the last dose, and blood was taken from the apical part of the heart. Serum high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), total cholesterol (TC), and triglyceride (TG) were detected. Liver tissues and perigenital adipose tissues were collected, weighed, and one portion of the tissues was fixed in 10% neutral formalin for pathomorphological observation, and another portion was used for mRNA detection of lipid metabolism-related genes such as Janus kinase 3 (JAK3), signal transducer and activator of transcription 5b (STAT5b), and peroxisome proliferator-activated receptor γ (PPARγ). Results During the DEHP and/or DBP exposure period, the rats in all groups were free to eat and drink without death or injury observed. Compared with the control group: The body weight gain in the DEHP+DBP group was lower at all time points from the 2nd week onwards (P<0.05); the liver organ coefficients of the DEHP and the DEHP+DBP groups were higher (P<0.05); the serum LDL-C levels in the DEHP and the DBP groups were higher (P<0.05). Compared with the DEHP+DBP group: The body weight gains in the DEHP group at the 2nd, 4th, 5th, and 8th weeks were higher (P<0.05), and the body weight gains in the DBP group were higher at all time points except the 1st week (P<0.05); the liver organ coefficients in the DEHP group and the DBP group were lower (P<0.05); the serum TG level in the DEHP group was higher(P<0.05), and the serum LDL-C levels in the DEHP and the DBP groups were higher (P<0.05). The pathomorphological results of liver tissues showed that the hepatocytes in the DEHP, DBP, and DEHP+DBP groups were disordered with loss of cord-like arrangement, swelling (suggesting change of cell proliferation), and presented bilirubin pigmentation. The pathomorphological results of rat perigenital adipose tissues showed had irregular alignment, sizes, and arrangement of adipocyte in the DEHP, DBP, and DEHP+DBP groups. The results of rat liver lipid metabolism-related gene mRNA levels showed that the liver JAK3, STAT5b, and PPARγ mRNA levels in the DEHP, DBP, and DEHP+DBP groups were lower than those in the control group (P<0.05); the rat liver PPARγ mRNA levels in the DEHP and DBP groups were lower than those in the DEHP+DBP group (P<0.05). Conclusion DEHP and/or DBP can inhibit the increase of body weight to varying degrees, induce inflammatory damage to liver tissues, and cause abnormal lipid metabolism in rats, and the associated mechanism may be related to inhibiting the activation of JAK3/STAT5b/PPARγ signaling pathway in rat liver tissues.

OBJECTIVE: To explore biomarkers for early auxiliary diagnosis of pneumoconiosis in coal workers(CWP) and its clinical significance. METHODS: Sixty-nine male coal miners exposed to dust were selected as control group, and sixty-seven CWP male patients were chosen as CWP group by purposive sampling method. Serum samples were collected from subjects of the two groups. The levels of malonaldehyde(MDA) and superoxide dismutase(SOD) were determined by colorimetric method. The enzyme-linked immunosorbent assay was used to measure the level of interleukin-6(IL-6) and tumor necrosis factor alpha(TNF-α). The acetylcholinesterase(AChE) activity was determined by modified Ellman method. The logistic regression model was used to analyze the risk factors of CWP. The receiver operating characteristic(ROC) curve was established to analyze the sensitive indicators in the pathogenesis of CWP. RESULTS: The serum SOD activity decreased(median: 65.1 vs 59.2 kU/L, P<0.05), and the MDA, IL-6 and TNF-α levels increased in the CWP group(median: 4.92 vs 6.68 μmol/L, 129.82 vs 163.18 ng/L, 63.90 vs 70.93 ng/L, P<0.05) compared with the control group. The logistic regression analysis results showed that AChE was the protective factor of CWP, while age, chronic respiratory symptoms, IL-6 and MDA were the risk factors of CWP(P<0.05). The ROC curve showed that IL-6 and MDA can be used as early indicators for the diagnosis of CWP in dust-exposed workers. CONCLUSION: The serum IL-6 and MDA levels can be used as biomarkers for early auxiliary diagnosis of CWP.

Background Di(2-ethylhexyl) phthalate (DEHP) is the highest consumed and the most widely used phthalic acid ester, their effects on lipid metabolism have attracted the attention of many scholars. However, the associated mechanism is still unclear. Objective To observe the effect of DEHP on lipid metabolism in rats, probe its possible mechanism, and provide a research basis for the effect of DEHP on human lipid metabolism. Methods Forty healthy male SD rats were randomly divided into 4 groups: solvent control (0 mg·kg⁻¹ DEHP), low DEHP (187 mg·kg⁻¹), medium DEHP (375 mg·kg⁻¹), and high DEHP (750 mg·kg⁻¹) groups. DEHP was administered by oral gavage for 6 d per week, consecutively 8 weeks. The rats were weighed once a week during the exposure period. At 24 h after the last exposure, the rats were anesthetized with 20% urethane and sacrificed by apical puncture. Rat livers were harvested and weighed before hematoxylin-eosin (HE) histopathological observation. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA levels of lipid metabolism-related genes Janus kinase 3 (JAK3), signal transducer and activator of transcription 5b (STAT5b), and peroxisome proliferator-activated receptor γ (PPARγ) in liver, and Western blot was used to detect the expression levels of lipid metabolism-related proteins JAK3, STAT5b, and PPARγ in liver. Results Compared with the control group, there was no significant difference in the body weight gain of the rats in each group (P>0.05). The liver organ coefficients of the DEHP exposure groups were higher than that of the control group (P<0.001), and increased with higher DEHP dosages. The level of high-density lipoprotein cholesterol (HDL-C) in serum decreased in all DEHP exposure groups (P<0.05), and the level of low-density lipoprotein cholesterol (LDL-C) in serum increased in the high DEHP group (P<0.05). The results of liver histopathological morphology showed that the hepatocytes of each DEHP group were enlarged and edematous in varying degrees, with loose stroma and irregular arrangement of cells, which were manifested as inflammatory cell infiltration and fatty degeneration of liver cells. Compared to the control group, the mRNA levels of JAK3, STAT5b, and PPARγ in liver tissues of rats in each DEHP group decreased (P<0.001). Compared to the control group, the relative expression levels of JAK3 in each DEHP group decreased (P<0.05), and the relative expression levels of STAT5b and PPARγ in the medium and high DEHP groups decreased (P<0.05). Conclusion DEHP exposure can induce abnormal lipid metabolism in rats, and the mechanism may be related to DEHP inhibiting the activation of JAK3/STAT5b/PPARγ signaling pathway.

Developmental exposure to bisphenol A (BPA), an endocrine-disrupting contaminant, impairs cognitive function in both animals and humans. However, whether BPA affects the development of primary sensory systems, which are the first to mature in the cortex, remains largely unclear. Using the rat as a model, we aimed to record the physiological and structural changes in the primary auditory cortex (A1) following lactational BPA exposure and their possible effects on behavioral outcomes. We found that BPA-exposed rats showed significant behavioral impairments when performing a sound temporal rate discrimination test. A significant alteration in spectral and temporal processing was also recorded in their A1, manifested as degraded frequency selectivity and diminished stimulus rate-following by neurons. These post-exposure effects were accompanied by changes in the density and maturity of dendritic spines in A1. Our findings demonstrated developmental impacts of BPA on auditory cortical processing and auditory-related discrimination, particularly in the temporal domain. Thus, the health implications for humans associated with early exposure to endocrine disruptors such as BPA merit more careful examination.
Humans ; Rats ; Animals ; Benzhydryl Compounds/toxicity* ; Phenols/toxicity* ; Auditory Perception/physiology* ; Neurons/physiology*