The relationship between anti epidemic mentality and post traumatic stress disorder in medical college students during the COVID-19 pandemic / 中国学校卫生

Objective@#To explore the relationship between an anti epidemic mentality and post traumatic stress disorder (PTSD) among college students during the corona virus disease 2019 (COVID-19) pandemic, and to provide a scientific basis for the prevention of PTSD when college students experience sudden crisis events in the future.@*Methods@#An online questionnaire survey was conducted among 9 399 undergraduates from Shanxi Medical University using the Posttraumatic Stress Disorder Checklist Civilian Version (PCL-C) and the public anti epidemic psychology self examination scale.@*Results@#During the COVID-19 pandemic, the total PCL-C scores of college students were (22.74±7.78), and the positive rate of PTSD symptoms was 5.3%. The detection rates of symptom recurrence, avoidance/numbness symptoms and increased alertness symptoms were 27.0%, 16.6% and 8.6 %, respectively. The average score of avoidance/numbness symptoms in the three symptom groups was (9.21±3.39), the two items with the highest scores were repeated recall of traumatic events (1.57±0.71) and impaired concentration (1.47±0.71). Females scored higher than males on the increased alertness dimension(6.82±2.61，6.67±2.72) ( t = -6.49 ， P <0.05). In respect to PCL-C total scores and the scores of each dimension, rural areas were associated with higher scores than urban areas, and non medical students scored higher than medical students, while the scores of those who grew up with siblings were higher than only children ( P <0.05). There was a significant positive correlation between an anti epidemic mentality and total PTSD scores ( r =0.51, P <0.01). Multiple regression analysis showed that the place of origin, choice of college major, and antiepidemic mentality were predictors of PTSD symptoms ( P <0.01).@*Conclusion@#Anti epidemic mentality is associated with the occurrence of PTSD among college students.

Isoflurane provides neuroprotection in neonatal hypoxic ischemic brain injury by suppressing apoptosis / Isoflurano fornece neuroproteção em lesão cerebral hipóxico-isquêmica neonatal por inibição da apoptose

Abstract Background and objectives: Isoflurane is halogenated volatile ether used for inhalational anesthesia. It is widely used in clinics as an inhalational anesthetic. Neonatal hypoxic ischemia injury ensues in the immature brain that results in delayed cell death via excitotoxicity and oxidative stress. Isoflurane has shown neuroprotective properties that make a beneficial basis of using isoflurane in both cell culture and animal models, including various models of brain injury. We aimed to determine the neuroprotective effect of isoflurane on hypoxic brain injury and elucidated the underlying mechanism. Methods: A hippocampal slice, in artificial cerebrospinal fluid with glucose and oxygen deprivation, was used as an in vitro model for brain hypoxia. The orthodromic population spike and hypoxic injury potential were recorded in the CA1 and CA3 regions. Amino acid neurotransmitters concentration in perfusion solution of hippocampal slices was measured. Results: Isoflurane treatment caused delayed elimination of population spike and improved the recovery of population spike; decreased frequency of hypoxic injury potential, postponed the onset of hypoxic injury potential and increased the duration of hypoxic injury potential. Isoflurane treatment also decreased the hypoxia-induced release of amino acid neurotransmitters such as aspartate, glutamate and glycine induced by hypoxia, but the levels of γ-aminobutyric acid were elevated. Morphological studies showed that isoflurane treatment attenuated edema of pyramid neurons in the CA1 region. It also reduced apoptosis as evident by lowered expression of caspase-3 and PARP genes. Conclusions: Isoflurane showed a neuro-protective effect on hippocampal neuron injury induced by hypoxia through suppression of apoptosis.

Resumo Justificativa e objetivos: Isoflurano é um éter volátil halogenado usado para anestesia por via inalatória. É amplamente usado na clínica como um anestésico para inalação. A lesão hipóxico-isquêmica neonatal ocorre no cérebro imaturo e resulta em morte celular tardia via excitotoxicidade e estresse oxidativo. Isoflurano mostrou ter propriedades neuroprotetoras que formam uma base benéfica para o seu uso tanto em cultura de células quanto em modelos animais, incluindo vários modelos de lesão cerebral. Nosso objetivo foi determinar o efeito neuroprotetor de isoflurano em hipóxia cerebral e elucidar o mecanismo subjacente. Métodos: Fatias de hipocampo, em fluido cerebrospinal artificial (CSFA) com glicose e privação de oxigênio, foram usadas como um modelo in vitro de hipóxia cerebral. O pico de população ortodrômica (PPO) e o potencial de lesão hipóxica (PLH) foram registrados nas regiões CA1 e CA3. A concentração de neurotransmissores de aminoácidos na solução de perfusão das fatias de hipocampo foi medida. Resultados: O tratamento com isoflurano retardou a eliminação do PPO e melhorou a recuperação do PPO; diminuiu a frequência do PLH, retardou o início do PLH e aumentou a duração do PLH. O tratamento com isoflurano também diminuiu a liberação de neurotransmissores de aminoácidos induzida pela hipóxia, como aspartato, glutamato e glicina, mas os níveis de ácido γ-aminobutírico (GABA) estavam elevados. Estudos morfológicos mostram que o tratamento de edema com isoflurano atenuou o edema de neurônios piramidais na região CA1. Também reduziu a apoptose, como mostrado pela expressão reduzida da caspase-3 e genes PARP. Conclusões: Isoflurano mostrou um efeito neuroprotetor na lesão neuronal no hipocampo induzida por hipóxia através da supressão de apoptose.

Telmisartan but not Valsartan Inhibits TGF-β-mediated Accumulation of Extracelluar Matrix via Activation of PPARγ / 华中科技大学学报（医学）（英德文版）

Summary: Glomerulosclerosis, defined as phenotype transition of mesangial cell and deposition of extracelluar matrix, remains a chronic disease with excessive morbidity and mortality. The molecular mechanism underlying the suppression of mesangial cell activation is not fully understood. Since activation of peroxisome proliferators-activated receptor γ (PPAR1,) has been proposed to decrease the effects of transforming growth factor-β (TGF-β) on glomerulosclerosis, we examined here whether and how telmisartan, an angiotensin Ⅱ type Ⅰ receptor blocker with PPARγ-modulating activity, inhibited TGF-β-induced giomerulosclerosis in rat glomerular mesangial cells. Protein levels of PPARγ were detected by Western blot. Activation of PPARγ response element (PPRE) was analyzed by luciferase assays. Deposition of extracelluar matrix was tested by confocol laser scanning. The results showed that telmisartan, but not valsartan, another angiotensin Ⅱ type Ⅰ receptor blocker,up-regulated PPARγ protein levels in a dose-dependent manner (P<0.05). Activation of PPRE, represented by luciferase activity, was also increased with higher concentration of telmisartan in a dose-dependent manner (P<0.05). Furthermore, telmisartan inhibited TGF-β-induced α-smooth muscle actin expression and collagen IV secretion in mesangial cells. GW9662, an inhibitor of PPAR-γ,blocked the inhibitory effects of telmisartan on TGF-β-induced glomerulosclerosis in mesangial cells. Our study indicates a benefit of telmisartan as a PPARγ agonist against TGF-β-induced mesangial cells activation in renal glomerulus. It may provide possibility that telmisartan works as a potential agent against diabetic nephropathy and hypertensive renal disease.