Objective To explore the effect of different position replacement orders on single side effect of blue light treatment of neonatal jaundice.Methods 100 cases newborns requiring phototherapy were randomly divided into the control group and the observation group.The control group adopted conventional phototherapy position change sequence (horizontal position-lateral position-prone position),the observation group used the new position replacement order (prone position-lateral position-horizontal position).The resistance reaction of babies and treatment effect of phototherapy were observed in two groups.Results Significant difference existed in resistance reaction (cry loudly,milk refusal)and phototherapy effects between the observation group and the control group.Conclusions The position change order such as prone position-lateral position-horizontal position by neonates during phototherapy,can reduce resistance reaction and improve treatment effect.

AIM: To investigate the relationships between antiproliferative mechanisms of probucol and protein expressions of signaling molecules ERK1/2, MKP-1, HO-1 and Trx-1 in rat aortic smooth muscle cells (RASMCs) stimulated with ox-LDL. METHODS: The effects of probucol on cell cycle, cell proliferation and the expressions of ERK1/2, MKP-1, HO-1 and Trx-1 in the presence of ox-LDL were observed by means of MTT test, FCM and Western blotting. RESULTS: (1) Probucol significantly inhibited the proliferation of RASMCs stimulated with ox-LDL. A value in 100 μmol/L probucol+35 mg/L ox-LDL group was reduced by 34.9% as compared to ox-LDL group (P<0.01). (2) Probucol protected against ox-LDL-induced RASMCs proliferation through inducing cell growth arrest at G_0/G_1 phase and cell apoptosis. (3) ox-LDL increased the expression of p-ERK1/2 by 34.7% (P<0.01) and decreased MKP-1 by 60.0% (P<0.01), respectively, as compared to control. Probucol attenuated the increase in ox-LDL-stimulated p-ERK1/2 level by 15.7%, but increased MKP-1 expression by 2 times (P<0.01). (4)ox-LDL at concentration of 35 mg/L decreased the intracellular Trx-1 expression by 28.9% (P<0.05), and slightly increased the level of HO-1 expression as compared to control (P<0.05). Probucol enhanced the expression of Trx-1 by 91.6% (P<0.01) and HO-1 by 31.9% (P<0.01), respectively as compared to ox-LDL group. CONCLUSION: Probucol inhibits ox-LDL-stimulated the proliferation of RASMCs through increases in MKP-1/HO-1 expression, suppression of cell cycle progression and induction of cell apoptosis.

Objective To evaluate the protective effect and underlying mechanism of ulinastatin on hepatic ischemia-reperfusion injury. Methods Twenty-four male SD rats were divided into three groups: sham operation group (Sham group), hepatic ischemia-reperfusion injury group (HIRI group) and hepatic ischemia-reperfusion injury + ulinastatin pretreatment group (HIRI+UTI group), with 8 rats in each group. The HIRI rat models were established by occluding hepatic portal vein and hepatic artery for 1 h. In the HIRI+UTI group, the rats were intraperitoneally injected with ulinastatin at 30 min before model establishment, and an equivalent amount of normal saline was given in the Sham and HIRI groups. The rats were sacrificed at 6 h after model establishment. Serum samples were collected to detect alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Pathological changes of liver tissues were observed by hematoxylin-eosin (HE) staining. Ultrastructural changes of mitochondria in liver tissues were observed by transmission electron microscopy. The expression of glutathione peroxidase 4 (GPX4) was determined by immunofluorescent staining. The contents of malondialdehyde (MDA), glutathione (GSH), Fe, reactive oxygen species (ROS) and GPX4 were detected. The expression levels of GPX4 and acyl-CoA synthetase long-chain family 4 (ACSL4) messenger RNA (mRNA) and proteins in liver tissue were measured. Results Compared with the Sham group, serum ALT and AST levels were up-regulated, pathological changes such as congestion, hepatocyte necrosis and abnormal hepatic lobule structure were observed, pathological score was increased, the mitochondria shrank, the membrane density was increased, the mitochondrial crest was damaged or even absent, the contents of ROS, MDA and Fe were elevated, the GSH content was decreased, the fluorescent intensity of GPX4 was weakened, the relative expression levels of ACSL4 mRNA and protein were up-regulated, and the relative expression levels of GPX4 mRNA and protein were down-regulated in the HIRI group (all P<0.05). Compared with the HIRI group, serum ALT and AST levels were down-regulated, liver tissue injury was alleviated, pathological score was decreased, mitochondrial shrinkage and crest breakage were mitigated, the contents of ROS, MDA and Fe were down-regulated, the GSH content was up-regulated, the fluorescent intensity of GPX4 was enhanced, the relative expression levels of ACSL4 mRNA and protein were down-regulated, and the relative expression levels of GPX4 mRNA and protein were up-regulated in the HIRI+UTI group (all P<0.05). Conclusions Ulinastatin may alleviate hepatic ischemia-reperfusion injury in rats probably through inhibiting ferroptosis.

The Omicron family of SARS-CoV-2 variants are currently driving the COVID-19 pandemic. Here we analyzed the clinical laboratory test results of 9911 Omicron BA.2.2 sublineages-infected symptomatic patients without earlier infection histories during a SARS-CoV-2 outbreak in Shanghai in spring 2022. Compared to an earlier patient cohort infected by SARS-CoV-2 prototype strains in 2020, BA.2.2 infection led to distinct fluctuations of pathophysiological markers in the peripheral blood. In particular, severe/critical cases of COVID-19 post BA.2.2 infection were associated with less pro-inflammatory macrophage activation and stronger interferon alpha response in the bronchoalveolar microenvironment. Importantly, the abnormal biomarkers were significantly subdued in individuals who had been immunized by 2 or 3 doses of SARS-CoV-2 prototype-inactivated vaccines, supporting the estimation of an overall 96.02% of protection rate against severe/critical disease in the 4854 cases in our BA.2.2 patient cohort with traceable vaccination records. Furthermore, even though age was a critical risk factor of the severity of COVID-19 post BA.2.2 infection, vaccination-elicited protection against severe/critical COVID-19 reached 90.15% in patients aged ≽ 60 years old. Together, our study delineates the pathophysiological features of Omicron BA.2.2 sublineages and demonstrates significant protection conferred by prior prototype-based inactivated vaccines.
Humans ; Aged ; Middle Aged ; COVID-19/prevention & control* ; SARS-CoV-2 ; Pandemics/prevention & control* ; China/epidemiology* ; Disease Outbreaks/prevention & control* ; Vaccination