ObjectiveTo explore the possible mechanism of Jianpi Huazhuo Tiaozhi Granule （健脾化浊调脂颗粒， JHTG） in treating atherosclerosis （AS） based on the regulation of perivascular adipose tissue （PVAT） browning via the phosphoinositide 3-kinase/protein kinase B （PI3K/AKT） signaling pathway. MethodsFifteen SPF male C57BL/6J mice served as control group， while 76 ApoE^-/- mice were first fed a high-fat diet for 16 weeks to establish AS model. After successful modeling， they were randomly divided into model group （n=16）， as well as the browning group， the low-， medium- and high-dose JHTG group， with 15 mice in each group. The browning group was intraperitoneally injected with β3-adrenergic receptor agonist CL 316243 at 1 mg/（kg·d） once daily. The low-， medium- and high-dose JHTG groups were treated with 4.3 g/（kg·d）， 8.6 g/（kg·d）， and 17.2 g/（kg·d） of JHTG by gavage， respectively， while the control group and the model group were given normal saline at 10 ml/（kg·d） by intragastric administration， once daily. All groups received continuous intervention for 4 weeks. The aorta was collected to assess the plaque ratio by gross oil red O staining. HE staining was used to measure the plaque area in cross-sections. Masson staining was employed to detect the proportion of collagen fibers in plaque. Transmission electron microscopy was used to observe the quantity and morphological changes of mitochondria and lipid droplets in adipocytes. The levels of serum triglycerides （TG）， total cholesterol （TC）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C） were detected， as well as tumor necrosis factor α （TNF-α） and interleukin 6 （IL-6） levels in the PVAT and aorta. The protein levels of adiponectin and leptin in PVAT， and protein expression levels of phosphoinositide 3-kinase （PI3K）， phosphorylated phosphoinositide 3-kinase （p-PI3K）， protein kinase B （AKT）， phosphorylated protein kinase B （p-AKT）， uncoupling protein 1 （UCP1）， peroxisome proliferator-activated receptor γ coactivator 1α （PGC-1α）， and PR domain containing 16 （PRDM16） were measured. The mRNA expression levels of UCP1， PGC-1α and PRDM16 in PVAT were detected. ResultsCompared to the control group， the model group showed increased serum TG， TC， and LDL-C levels and decreased HDL-C level， elevated TNF-α and IL-6 levels in PVAT and aorta， decreased average fluorescence intensity of adiponectin， increased average fluorescence intensity of leptin， reduced p-PI3K/PI3K and p-AKT/AKT values as well as protein levels and mRNA expression levels of UCP1， PGC-1α and PRDM16 （P＜0.01）. The pathological results showed that no significant plaque formation was observed in the aortas of mice in the control group. In the model group， multiple plaques were observed in the aortas， with large numbers of foam cells， cholesterol crystals， and inflammatory cell aggregation in the plaques. Compared to the model group， the browning group and the high-dose JHTG group significantly improved the above indicators and aortic pathological changes （P＜0.05 or P＜0.01）. Three JHTG groups showed a dose-dependent effect in reducing LDL-C level and plaque ratio by gross oil red O staining， elevating the average fluorescence intensity of adiponectin， the p-AKT/AKT value， the protein level of PGC-1α， and the mRNA expression levels of UCP1 and PRDM16 （P＜0.05）. The high-dose JHTG group and the browning group showed similar efficacy in improving the pathology of the aorta. ConclusionJHTG may promote PVAT browning in AS model mice through the PI3K/AKT pathway， improve the endocrine function of PVAT， inhibit aortic inflammation， and thereby ameliorate the formation of AS plaques.

Diffuse pediatric-type high-grade glioma (pHGG), H3- and isocitrate dehydrogenase (IDH)-wild-type, is a World Health Organization (WHO) grade 4 diffuse glioma with malignant histological features, which typically affects in children and adolescents. This multidisciplinary treatment case involves a 24-year-old young female patient initially diagnosed via biopsy. After concurrent chemoradiotherapy reduced the tumor size, complete resection was achieved, followed by adjuvant therapy with temozolomide and regorafenib. After recurrence, the tumor was resected again, and a second course of radiotherapy was administered, but the disease ultimately progressed rapidly, with an overall survival exceeding 32 months. pHGGs are highly malignant, aggressive, and associated with poor prognosis. Accurate diagnosis and targeted intervention require close collaboration among a multidisciplinary team, which highlights the critical value of multidisciplinary manage-ment in clinical practice.

Objective:To investigate the role of serum hepatitis B virus RNA (HBV RNA) in predicting HBeAg serological conversion in children with chronic hepatitis B.Methods:175 children aged 1~17 years with chronic hepatitis B who received interferon α (IFNα) for 48 weeks were selected. Patients were divided into HBeAg seroconversion and non-conversion based on whether HBeAg seroconversion occurred at 48 weeks of treatment.T-test and Mann-Whitney U test were used to compare between groups; chisquare test or Fisher exact probability method was used to compare the frequency between groups of classified variables; and Pearson correlation was used to analyze the correlation between indicators. Univariate and multivariate logistic regression analyses were used to identify influencing factors associated with HBeAg serological conversion. The predictive effect of HBV RNA, HBV DNA, and HBsAg on HBeAg serological conversion was compared and analyzed by the receiver operating characteristic curve (ROC).Results:The seroconversion rate of HBeAg at 48 weeks was 36.0% (63/175). The reduction in HBVRNA levels from baseline to the 12th, 24th, 36th, and 48th weeks of antiviral therapy was significantly greater in the HBeAg serological conversion group than that in the non-conversion group, and the difference was statistically significant between the two groups (P < 0.05). Univariate and multivariate regression analyses showed that age and a decline in HBV RNA levels at week 12 were independent predictors of HBeAg serological conversion. The area under the ROC curve (AUROC) of HBV RNA decline at week 12 was 0.677(95% CI∶0.549-0.806, P = 0.012), which was significantly better than the same period of AUROC of HBV DNA (0.657, 95% CI∶0.527-0.788, P = 0.025) and HBsAg (0.660, 95% CI∶0.526-0.795, P = 0.023) decline. HBV RNA levels decreased (>1.385 log10 copies/ml) at week 12, with a positive predictive value of 53.2%, a negative predictive value of 72.2%, a sensitivity of 77.4%, and a specificity of 57.9% for HBeAg seroconversion. Conclusion:HBV RNA level lowering during the 12th week of antiviral therapy can serve as an early predictor marker for HBeAg serological conversion in children with chronic hepatitis B.

OBJECTIVE: To explore the characteristics of peripheral nerve injury caused by occupational acute trimethyltin chloride(TMT) poisoning. METHODS: The clinical manifestations and test data of neurotic electrophysiology, pure tone hearing threshold and acoustic immittance in 16 patients with occupational acute TMT poisoning were retrospectively analyzed. The patients were followed up after 6 months of discharge. RESULTS: Among the 16 cases of occupational acute TMT poisoning, 6, 4 and 6 cases were with mild, moderate and severe poisoning, respectively. For the firstly appeared symptoms, 7 cases had abnormal mental behavior and memory loss, 5 cases had tinnitus and hearing loss, 5 cases had decreased visual acuity, 2 cases had diplopia and 2 cases had binocular pain. The main clinical manifestations included 8 cases of disturbance of consciousness, and 6 cases of abnormal orientation and aggressive behavior. After correction of hypokalemia, 7 cases of patients had limb muscle weakness, hypomyotonia and weakened tendinous reflect, 9 cases had decreased tactile sensation below the groin in the lower limbs, and 6 cases had instability of walking. The main manifestations of neuroelectrophysiological detection were: 9 patients(accounting for 56.3%) showed abnormal neuroelectromyography, 4 cases of severe poisoning had damaged motor nerve, sensory nerve axon and myelin sheath, and the proximal nerve was also partially damaged. There were 2 cases of moderate poisoning showing abnormal symptoms, the axon and myelin sheath of sensory nerve were damaged, one common peroneal nerve was demyelinated. Three cases of mild poisoning had one common peroneal nerve axon damaged, one proximal tibial nerve damaged, and the axon and myelin sheath of sensory nerve were damaged. Brainstem auditory evoked potential I wave and visual evoked potential P100 latency prolonged and amplitude decreased in some of the patients with mild, moderate and severe poisoning. The sensorineural hearing loss occurred in 81.3% of patients. CONCLUSION: Occupational acute TMT poisoning can cause damage to motor nerve, sensory nerve axon and myelin sheath of extremities. Both distal and proximal nerves might be involved. It can also damage cochlear hair cells and optic nerve. Attention should be paid to the early treatment of peripheral nerve damage, cochlear hair cell and optic nerve damage caused by TMT.

This article analyzes the clinical manifestations and magnetic resonance imaging (MRI) data of 2 patients with hypoxic encephalopathy after simple asphyxia gas poisoning. Both patients were in a moderate coma after being poisoned, and the arterial blood lactic acid level and carbon dioxide partial pressure were higher than the normal range within 1 week after poisoning. Two patients were cured and discharged after being treated with oxygen therapy and glucocorticoids. The prognosis was good.

This article analyzes the clinical manifestations and magnetic resonance imaging (MRI) data of 2 patients with hypoxic encephalopathy after simple asphyxia gas poisoning. Both patients were in a moderate coma after being poisoned, and the arterial blood lactic acid level and carbon dioxide partial pressure were higher than the normal range within 1 week after poisoning. Two patients were cured and discharged after being treated with oxygen therapy and glucocorticoids. The prognosis was good.

Objective: Characteristics of clinical, MRI and electroencephalogram after trimethyltin chloride (TMT) poisoning. Methods: The clinical manifestations, MRI, EEG, treatment and prognosis of 16 patients with TMT poisoning were analyzed retrospectively. Results: Among the 16 cases of TMT poisoning, 6 cases were severe poisoning, 4 cases were moderate poisoning, and 6 cases were mild poisoning. All patients had dizziness, headache, general fatigue, loss of appetite, nausea, vomiting and other general clinical symptoms. Six patients with severe poisoning had psychobehavioral abnormalities, including 4 patients with mania, delirium, ataxia, epileptic seizures. Glasgow was 15 points in mild and moderate poisoning. Of the 6 cases of severe poisoning, 4 cases of Glasgow were 9~11 points, and 2 cases of Glasgow were 13 points. 2 patients with severe poisoning had abnormal MRI in head, and the total abnormal rate was 12.50%. Toxic encephalopathy was considered in 1 case with abnormal signal of corpus callosum pressure, and patchy ischemic foci of left cerebral foot and mild cerebral atrophy in 1 case. The total abnormal rate of EEG was 56.25%. The abnormal rate of electroencephalogram in severe poisoning was 83.33%. There were 2 cases of severe abnormal electroencephalogram, 2 cases of moderate abnormal electroencephalogram and 1 case of slight abnormal electroencephalogram. Twelve patients were recovered and discharged from hospital. 4 cases of severe poisoning are still getting better, and there are still cerebellar ataxia symptoms such as dizziness and unstable walking. Conclusion In clinical work, attention should be paid to the identification of patients with mild and moderate TMT poisoning, and attention should be paid to the patients with severe TMT poisoning manifested by disturbance of consciousness. The positive rate of MRI test in TMT poisoning is low, and the lesion is nonspecific. Electroencephalogram test has a high positive rate in TMT poisoning, which can well reflect the degree of illness. Attention should be paid to the prevention and treatment of neurodegeneration caused by TMT poisoning.

Objective: Clinical analysis of sequelae of 16 patients with trimethyltin chloride (TMT) poisoning after 2 years. Methods: Sixteen patients with TMT poisoning from a waste recycling company in Ganzhou City in August 2016 were enrolled. They were investigated by questionnaires and assessed by various scales after two years. 6 cases of severe poisoning were examined by head MRI. The scale includes Hamilton Anxiety Scale (HAMA) , Depression Scale (HAMD) , Simple Mental State Examination Scale (MMSE) , Activity of Daily Living (ADL) , International Cooperative Ataxia Rating Scale (ICARS) . Results: 16 cases of TMT poisoning still have headache, dizziness and other symptoms. Instability of walking in 4 patients with severe poisoning, and the brain MRI manifestations included obvious atrophy of temporal lobe, hippocampus, insula lobe, cerebellum and ventricle enlargement. Two patients were rated as severe mixed anxiety and depression, one as moderate mixed anxiety and depression, and one as mild anxiety. 3 cases were diagnosed as dementia and 1 case as mild cognitive impairment. Two cases were totally dependent on living ability. ICARS scores were 66 points and 63 points respectively. Two cases were mildly dependent on living ability. ICARS scores were 28 points and 6 points respectively. There were 2 cases of mild mixed anxiety and depression in mild and moderate poisoning patients, and 1 case of mild cognitive impairment in each patient. They could live independently. ICARS scores were 0. Conclusion After 2 years of TMT poisoning, some patients still have general clinical symptoms such as dizziness, headache and so on. There are also mental and intellectual symptoms such as anxiety, depression and cognitive impairment. Some of patients with severe poisoning presented with dementia and cerebellar ataxia, and even lost independent living ability.

OBJECTIVE: To investigate the clinical characteristics of acute toxic encephalopathy caused by trimethyltin chloride(TMT). METHODS: Literatures related to TMT acute poisoning accidents occurred in China from 1998 to 2018 were collected and analyzed using the CNKI, WEIPU Database and WANFANG Database. The clinical manifestations, neuroimaging images, electroencephalography(EEG), treatment and other data were collected and analyzed. RESULTS: A total of 15 literatures were included in the study. These studies involved 15 incidents with 1 339 patients with TMT acute poisoning. Among them, 325 patients(24.3%) presented toxic encephalopathy. They were moderate to severe poisoning.The clinical manifestations were headache, dizziness, limb weakness, abnormal mental behavior and memory loss. Magnetic resonance imaging(MRI) and computed tomography(CT) were performed in 105 and 86 patients, respectively, with 29.5% and 26.7% of abnormal rate. There was no significant difference in the abnormal rate between the above two methods(P>0.05). 294 cases were examined by electroencephalogram. The abnormal rate was 93.9%, which was higher than that of the MRI and CT examination(P<0.05). Patients with toxic encephalopathy were treated with glucocorticoid. Some patients were treated with hyperbaric oxygen, nerve cell nutritional drugs and rehabilitation exercise after the conditions were stable. CONCLUSION: The patients with TMT toxic encephalopathy were moderately and severely poisoned by TMT. EEG examination is helpful for the diagnosis and treatment of TMT toxic encephalopathy.