Analysis of cases of reinfection of past SARS-CoV-2 patients in Pudong New Area of Shanghai / 上海预防医学

ObjectiveTo identify the rate， population characteristics， and vaccination history of repeat infections among previously infected people in the current epidemic based on the rate of repeat infection and population characteristics of different mutant strains at different times in Pudong New Area of Shanghai， and to provide reference for the prevention and control strategies of novel coronavirus repeat infections. MethodsA total of 9 250 investigated subjects were randomly selected from the new cases of asymptomatic infection and confirmed cases reported by Pudong New Area from March to May 2022. The investigation mainly focused on demographic characteristics， nucleic acid or antigen test results， and symptoms after infection. The repeat infection rates among different populations were compared， and logistic regression was used to analyze the impact of gender， age， and vaccination status on repeat infections. ResultsThe survey sample of 9 250 people had a response rate of 81.85%. There were 4 043 males （53.40%） and 3 528 females （46.60%）， with a median age of 34 years old （P25， P75： 7， 61）. The overall vaccine uptake rate was 59.44% （4 500/7 571）. In December of 2022， there were 563 cases of repeat infection， with an infection rate of 7.44%. The lowest rate of repeat infection was seen in the 3‒ year-old group （2.86%） and the highest rate in the 30‒ year-old group （12.42%）， with significant differences between different age groups. The repeated infection rate for those who had completed their vaccinations was significantly lower （6.57%） compared to those who had not （7.11%）. The age groups of 3‒ years， 70‒79 years， as well as individuals who completed full vaccination and received booster shots were protective factors against repeat infections. ConclusionThe overall rate of reinfection among the infected in Shanghai during the spring of 2022 was low in the outbreak of the Omicron variant， and the rate of reinfection in the 3‒ year-old group was significantly lower than in other age groups. Completing the full course of vaccination significantly reduces the risk of reinfection. Although the reinfection rate is high in individuals who received booster shots， it remains a mitigating factor compared to those who do not receive the vaccine. It is recommended to continue monitoring reinfections in key populations and further strengthen immunization efforts.

Hepatitis C virus infection and organ transplantation / 临床肝胆病杂志

In recent years， rapid progress has been made in strategies for the prevention and treatment of hepatitis C virus （HCV） in organ transplant candidates and recipients， and although HCV infections no longer threaten transplantation outcomes in liver or non-hepatic solid organ transplantation， they remain a focus of research. Since hepatitis C is still a leading cause of death worldwide due to decompensated cirrhosis， liver failure， and hepatocellular carcinoma， appropriate organ transplantation is needed to improve survival rate and quality of life. With the increase in HCV-positive solid organ donors in recent years and the fact that the demand for organs still greatly exceeds organ supply， as well as the development of direct-acting antiviral agents， transplantation of HCV-viraemic organs into HCV-naïve recipients will significantly increase transplantation rates and reduce waitlist mortality. The efficacy of current HCV therapies has created an important opportunity to improve the survival rate of patients with end-organ failure by enhancing access to organ transplantation and reducing waitlist mortality.

Role of SIRTl/Nrf2/HO-l pathway in attenuation of learning and memory impairment by sevoflurane postcondition in a mouse model of hemorrhagic shock and resuscitation / 中国药理学通报

Aim To explore the role of SIRT1/Nrf2 / HO-1 in alleviating the cognitive function impairment by sevoflurane treatment in a mouse model of postoperative cerebral reperfusion. Methods C57BL/6J mice were randomly divided into five groups: sham operation group, hemorrhagic shock reperfusion group, sevoflurane postconditioning group, sevoflurane postcondition-ing + SIRT1 inhibitor group and sevoflurane postconditioning + Nrf2 inhibitor group. Mice were subjected to Morris water maze test after cerebral ischemia reperfusion. The ATP, superoxide dismutase (SOD), ROS and MDA contents in tissue of mice were detected. SIRT1, Nrf2 and HO-1 proteins in tissue were detected by Western blot. Results After hemorrhagic shock, the learning and memory ability of mice was reduced.ATP and SOD concentration in hippocampus was reduced , MDA and ROS concentration increased, and the SIRT, Nrf2 and HO-1 concentration was reduced. Sevoflurane improved the cognitive dysfunction and oxi-dative damage in postoperative mice, and the neuro-protective effect of sevoflurane on hemorrhagic shock and resuscitation mice was weakened followed with SIRT1 and Nrf2 inhibitors. Conclusion Sevoflurane probably alleviates the oxidative reaction damage and cognitive impairment caused by cerebral reperfusion in mice through SIRT1/Nrf2/H0-1 pathway.

High-throughput screening of novel TFEB agonists in protecting against acetaminophen-induced liver injury in mice

Macroautophagy (referred to as autophagy hereafter) is a major intracellular lysosomal degradation pathway that is responsible for the degradation of misfolded/damaged proteins and organelles. Previous studies showed that autophagy protects against acetaminophen (APAP)-induced injury (AILI) via selective removal of damaged mitochondria and APAP protein adducts. The lysosome is a critical organelle sitting at the end stage of autophagy for autophagic degradation via fusion with autophagosomes. In the present study, we showed that transcription factor EB (TFEB), a master transcription factor for lysosomal biogenesis, was impaired by APAP resulting in decreased lysosomal biogenesis in mouse livers. Genetic loss-of and gain-of function of hepatic TFEB exacerbated or protected against AILI, respectively. Mechanistically, overexpression of TFEB increased clearance of APAP protein adducts and mitochondria biogenesis as well as SQSTM1/p62-dependent non-canonical nuclear factor erythroid 2-related factor 2 (NRF2) activation to protect against AILI. We also performed an unbiased cell-based imaging high-throughput chemical screening on TFEB and identified a group of TFEB agonists. Among these agonists, salinomycin, an anticoccidial and antibacterial agent, activated TFEB and protected against AILI in mice. In conclusion, genetic and pharmacological activating TFEB may be a promising approach for protecting against AILI.

Temporal-spatial Generation of Astrocytes in the Developing Diencephalon / 神经科学通报·英文版

Astrocytes are the largest glial population in the mammalian brain. However, we have a minimal understanding of astrocyte development, especially fate specification in different regions of the brain. Through lineage tracing of the progenitors of the third ventricle (3V) wall via in-utero electroporation in the embryonic mouse brain, we show the fate specification and migration pattern of astrocytes derived from radial glia along the 3V wall. Unexpectedly, radial glia located in different regions along the 3V wall of the diencephalon produce distinct cell types: radial glia in the upper region produce astrocytes and those in the lower region produce neurons in the diencephalon. With genetic fate mapping analysis, we reveal that the first population of astrocytes appears along the zona incerta in the diencephalon. Astrogenesis occurs at an early time point in the dorsal region relative to that in the ventral region of the developing diencephalon. With transcriptomic analysis of the region-specific 3V wall and lateral ventricle (LV) wall, we identified cohorts of differentially-expressed genes in the dorsal 3V wall compared to the ventral 3V wall and LV wall that may regulate astrogenesis in the dorsal diencephalon. Together, these results demonstrate that the generation of astrocytes shows a spatiotemporal pattern in the developing mouse diencephalon.

Reduced expression of semaphorin 3A in osteoclasts causes lymphatic expansion in a Gorham-Stout disease (GSD) mouse model / 浙江大学学报（英文版）（B辑：生物医学和生物技术）

Gorham-Stout disease (GSD) is a sporadic chronic disease characterized by progressive bone dissolution, absorption, and disappearance along with lymphatic vessel infiltration in bone-marrow cavities. Although the osteolytic mechanism of GSD has been widely studied, the cause of lymphatic hyperplasia in GSD is rarely investigated. In this study, by comparing the RNA expression profile of osteoclasts (OCs) with that of OC precursors (OCPs) by RNA sequencing, we identified a new factor, semaphorin 3A (Sema3A), which is an osteoprotective factor involved in the lymphatic expansion of GSD. Compared to OCPs, OCs enhanced the growth, migration, and tube formation of lymphatic endothelial cells (LECs), in which the expression of Sema3A is low compared to that in OCPs. In the presence of recombinant Sema3A, the growth, migration, and tube formation of LECs were inhibited, further confirming the inhibitory effect of Sema3A on LECs in vitro. Using an LEC-induced GSD mouse model, the effect of Sema3A was examined by injecting lentivirus-expressing Sema3A into the tibiae in vivo. We found that the overexpression of Sema3A in tibiae suppressed the expansion of LECs and alleviated bone loss, whereas the injection of lentivirus expressing Sema3A short hairpin RNA (shRNA) into the tibiae caused GSD-like phenotypes. Histological staining further demonstrated that OCs decreased and osteocalcin increased after Sema3A lentiviral treatment, compared with the control. Based on the above results, we propose that reduced Sema3A in OCs is one of the mechanisms contributing to the pathogeneses of GSD and that expressing Sema3A represents a new approach for the treatment of GSD.

Risk Assessment of the Onset of Sleep-related Painful Erection / 中山大学学报(医学科学版)

ObjectiveSleep-related painful erections （SRPE） is a rare sleep disorder characterized by repeated awakening due to painful interruptions of penile erections during nighttime sleep， and its etiology is currently unclear. The purpose of this study is to explore the impact of potential risk factors on the incidence of SRPE. MethodsInformation was collected through questionnaires administered to patients who presented at the urology department and suffered from SRPE or did not suffer from SRPE. A total of 290 participants completed the study， including 145 controls and 145 cases. Logistic regression analysis was used to assess the impact of age， occupation， sleep initiation time per night， frequency of sexual intercourse per week， psychological status， erectile dysfunction， chronic prostatitis， prostate enlargement， lumbar spine disease， central nervous system disease， hypertension， diabetes and family history on the onset of SRPE. ResultsSingle-factor logistic regression analysis found that a history of chronic prostatitis， intellectual labor occupation， central nervous system disease， late sleep onset， frequency of sexual activity， and anxiety status might be related to the onset of SRPE. After incorporating these factors into a multivariate regression analysis model， it was found that having sexual activity ≥2 times/week （OR 95%CI = 0.326（0.179，0.592） and late sleep onset （after 24：00） （OR 95%CI = 0.494（0.265，0.918）might be protective factors for SRPE， while a history of chronic prostatitis（OR 95%CI = 3.779（2.082，6.859） might be a risk factor for SRPE. However， there was no significant statistical difference in the impact of central nervous system diseases and occupation on multivariate analysis. ConclusionChronic prostatitis and anxiety status may be independent risk factors for SRPE； having sexual activity ≥2 times/week and delaying sleep time appropriately may be independent protective factors.

Association between temperature and mortality: a multi-city time series study in Sichuan Basin, southwest China

BACKGROUND@#There are few multi-city studies on the association between temperature and mortality in basin climates. This study was based on the Sichuan Basin in southwest China to assess the association of basin temperature with non-accidental mortality in the population and with the temperature-related mortality burden.@*METHODS@#Daily mortality data, meteorological and air pollution data were collected for four cities in the Sichuan Basin of southwest China. We used a two-stage time-series analysis to quantify the association between temperature and non-accidental mortality in each city, and a multivariate meta-analysis was performed to obtain the overall cumulative risk. The attributable fractions (AFs) were calculated to access the mortality burden attributable to non-optimal temperature. Additionally, we performed a stratified analyses by gender, age group, education level, and marital status.@*RESULTS@#A total of 751,930 non-accidental deaths were collected in our study. Overall, 10.16% of non-accidental deaths could be attributed to non-optimal temperatures. A majority of temperature-related non-accidental deaths were caused by low temperature, accounting for 9.10% (95% eCI: 5.50%, 12.19%), and heat effects accounted for only 1.06% (95% eCI: 0.76%, 1.33%). The mortality burden attributable to non-optimal temperatures was higher among those under 65 years old, females, those with a low education level, and those with an alternative marriage status.@*CONCLUSIONS@#Our study suggested that a significant association between non-optimal temperature and non-accidental mortality. Those under 65 years old, females, and those with a low educational level or alternative marriage status had the highest attributable burden.

Research progress on anhepatic phase in rat liver transplantation / 器官移植

With persistent advancement of surgical instruments, methods and techniques, clinical efficacy of liver transplantation has been steadily enhanced. However, the length of anhepatic phase is still an important factor affecting the efficacy of liver transplantation. Rat is one of the major animal models for liver transplantation-related basic research. In this article, multiple approaches for prolonging the anhepatic phase and shortening the operation time during anhepatic phase in rat liver transplantation were reviewed, which consisted of sevoflurane inhalation anesthesia, intravenous infusion via jugular vein indwelling needle, clamping of the abdominal aorta before anhepatic phase, injection of normal saline into portal vein before anhepatic phase, subcutaneous transposition of the spleen, electrocoagulation of hepatic esophageal artery, magnetic ring anastomosis of the superior and inferior hepatic vena cava, cannula anastomosis of the superior and inferior hepatic vena cava, stent anastomosis of the superior and inferior hepatic vena cava, rapid connection device and cannula of portal vein, and ring-shaped cannula of hepatic tissue-preserving inferior hepatic vena cava, aiming to add evidence for prolonging the duration of anhepatic phase, improving the operation efficiency during anhepatic phase and elevating the success rate of rat liver transplantation.

Study on improvement effect mechanism of Xibining prescription on knee osteoarthritis model rats based on AMPK/mTOR signaling pathway / 中国药房

OBJECTIVE To investigate the improvement effect mechanism of Xibining prescription （XBN） on knee osteoarthritis （KOA） model rats based on AMP-activated protein kinase（AMPK）/mammalian target of rapamycin （mTOR） signaling pathway. METHODS Totally 36 rats were randomly divided into blank group， model group， XBN group （12.56 g/kg）， XBN+metformin （AMPK agonist） group （12.56 g/kg XBN+100 mg/kg metformin）， with 9 rats in each group. Except for blank group， KOA model was induced by anterior cruciate ligament transection in other groups. After modeling， each group was given relevant medicine/normal saline， XBN and normal saline intragastrically， once a day， and metformin intraperitoneally， every other day， for 4 consecutive weeks. The pathomorphological changes of cartilage tissue in rats were observed and Mankin scoring was conducted. The expression level of Aggrecan in rat cartilage， mRNA and protein expressions of platelet reactive protein disintegrin and metalloproteinase with thrombospondin motifs 4 （ADAMTS-4）， ADAMTS-5， matrix metalloproteinase 3 （MMP-3） and MMP- 13， and the phosphorylation level of AMPK and mTOR proteins were detected. RESULTS Compared with blank group， the structure of cartilage tissue in the model group was disordered， the matrix of cartilage layer was lightly stained，the tide line was distorted or interrupted， and Mankin score was significantly increased （P＜0.05）. The protein expression of Aggrecan in cartilage tissue and the phosphorylation level of AMPK protein were all decreased significantly （P＜0.05）； mRNA and protein expressions of ADAMTS-4， ADAMTS-5， MMP-3 and MMP-13 and the phosphorylation levels of mTOR protein were significantly increased in cartilage tissues （P＜0.05）. Compared with model group， the pathological morphology of cartilage was improved significantly in each administration group， and above score or indexes were reversed significantly （P＜0.05）. Compared with XBN group， the degree of cartilage lesions in rats was further alleviated in XBN+ metformin group， and the levels of above score or indicators were further improved （P＜0.05）. CONCLUSIONS XBN can ameliorate cartilage injury in KOA model rats， promote cartilage synthesis and reduce cartilage degradation， the mechanism of which may be associated with activating AMPK/mTOR signaling pathway.

The Deubiquitinating Enzyme USP14 Promotes the Proliferation and Migration Ability of Pancreatic Cancer Cells / 中国生物化学与分子生物学报

Pancreatic cancer remains one of the deadliest cancer types with few effective treatment options. While the overexpression of ubiquitin-specific protease 14 (USP14) has been observed in many tumor cells, including pancreatic cancer cells, its precise role in pancreatic cancer is not well defined. Here, we investigated the biological function of USP14 in pancreatic cancer and its molecular mechanisms. Our analysis of the Cancer Genome Atlas database revealed that USP14 was highly expressed in pancreatic cancer tissues,and further investigation revealed that its expression level was negatively correlated with the prognosis of patients. In SW1990 and MIAPaCa2 pancreatic cancer cells,we established stable USP14-knockdown cell lines using the shRNA-USP14 lentivirus and found that USP14 knockdown inhibited the proliferation and migration ability of pancreatic cancer cells by CCK8, colony formation assay, wound-healing and Transwell assays. Western blotting analysis showed that downregulation of USP14 expression resulted in a decrease in CyclinD3 protein levels, while overexpression of USP14 increased the protein levels in SW1990 and MIAPaCa2 pancreatic cancer cells. Furthermore, co-immunoprecipitation demonstrated that USP14 interacts with CyclinD3 and ubiquitination assays show that overexpression of USP14 reduces the ubiquitination level of CyclinD3. Moreover, CRISPR / Cas9-mediated USP14 knockout in SW1990 pancreatic cancer cells resulted in decreased CyclinD3 protein levels. These findings suggest that USP14 promotes the proliferation and migration ability of pancreatic cancer cells by interacting with CyclinD3, highlighting USP14 as a potential therapeutic target for pancreatic cancer.

Autophagy and Inflammation in Fish / 中国生物化学与分子生物学报

Autophagy and inflammation are the important physiological reactions, especially in innate immunity. Autophagy, as a conservative metabolic process, can degrade its own disorder components through lysosomes to maintain cell homeostasis. Autophagy plays a pivotal role in degrading damaged organelles, resisting pathogenic infection and regulating inflammatory response. In the past decades, the study of autophagy in yeast and mammals has greatly increased our understanding for autophagy and its relationship with the diseases. In human, the regulation on autophagy levels can be used to prevent or treat neurodegenerative diseases, inflammatory diseases, tumors and various pathogenic microbial infections. However, in fish, the researches on autophagy and application are limited. Inflammation is a highly complex biological process, which is a natural defense response under the stimulation of ultraviolet, pathogen infection, oxidative stress and mechanical damage. Fish, as a lower vertebrate, has an incomplete acquired immune system. Innate immunity plays an important role in defensing against pathogen infection. Compared with higher vertebrate animals, although the researches on autophagy in fish cells were carried out lately, the great progress has been made in recent years on autophagy phenomenon, expression regulation of autophagy-related genes, and mechanism caused by pathogenic infection. As an important part of innate immunity, autophagy is involved in a variety of fish pathogenic infections, and fish diseases are usually accompanied by inflammatory reaction. In this review, we summarized the update findings in recent references on the autophagy and inflammatory response caused by pathogenic infection in fish, and the correlation between them, in order to deeply understand the correlation relationship between autophagy and inflammatory response in fish. This review could provide the guidance for understanding the immune mechanism of fish, and supply the foundation for developing new strategy to prevent and control fish disease.

Research progress in the reprogramming of retinal Müller glia cells / 解剖学报

[Abstract] Blinding eye diseases caused by retinal degeneration have a detrimental effect on human health. Mammalian retina exhibits very limited capacity for self-repair after degenerative disease or injury. In contrast, zebrafish retina possesses a robust regenerative response that regenerates all types of retinal neurons and restores vision. Retina regeneration in zebrafish depends on a type of glia cells called Müller glia. Following retinal injury, zebrafish Müller glia undergo a reprogramming process and proliferate into multipotent progenitor cells that further differentiate into newborn retinal neurons. In recent years, significant progress has been made in the field of Müller glia-based retina regeneration. Here we summarize the mechanisms governing zebrafish retina regeneration and the recent advances in mammalian Müller glia reprogramming.

Progress on the pathological mechanism and treatment of frostbite / 中国临床药理学与治疗学

Frostbite is a tissue injury that occurs when the body is exposed to extreme cold. Its pathological mechanism is complex and has not been fully elucidated. In high cold and high altitude areas, outdoor sports people have a high risk of injury, and severe frostbite has high disability and mortality. Exploring the pathological mechanism of frostbite is helpful to determine the treatment methods and timing. At present, the clinical treatment of frostbite is mainly symptomatic treatment, such as drug treatment and surgical treatment, but the curative effect can not meet the clinical needs. Therefore, it is of great significance to seek more efficient drugs or treatment methods. This article reviews the relevant research progress in pathophysiological mechanism, clinical treatment, cellular and molecular pathways of frostbite in recent years, in order to provide new ideas for future research and clinical treatment.

Lactate dehydrogenase inhibitor alleviates LPS/D-Gal-induced acute liver injury in mice / 中国药理学通报

Aim To investigate the effect of lactate dehydrogenase inhibitor on LPS/D-Gal-induced acute liver injury in mice. Methods BALB/ C mice were divided into four groups:solvent control group, lactate dehydrogenase inhibitor NHI-2 group, lipopolysaccharide(LPS)/ D-galactosamine(D-Gal)group and LPS/D-Gal+NHI-2 group. To induce acute liver injury, mice were injected intraperitoneally with LPS(10 μg·kg-1)and D-Gal(700 mg·kg-1), NHI-2 was intraperitoneally injected 30 min before LPS/D-Gal exposure. Liver tissue and serum were harvested 1.5 or 6 h after LPS/D-Gal exposure, serum lactate, serum aspartate aminotransferase(ALT), serum alanine aminotransferase(AST), serum tumor necrosis factor alpha(TNF-α)liver malondialdehyde(MDA)and liver caspase-3/8/9 levels were determined. HE staining was used to evaluate the degree of liver injury. TUNEL staining was used to evaluate hepatocyte apoptosis. Survival curve was used to record survival situation of tested mice. Results Serum lactate level of model mice was significantly reduced after treatment with NHI-2. Compared with LPS/D-Gal group, level of serum TNF-α showed no significant difference, but serum ALT and AST level of LPS/D-Gal+NHI-2 group significantly decreased, injury of liver structure was remarkably attenuated, level of MDA and activity of caspase-3/8/9 in liver were significantly down-regulated, and the number of TUNEL-positive cells was significantly reduced. Treatment with NHI-2 also significantly improved the survival rate of LPS/D-Gal-insulted mice. Conclusion Lactate dehydrogenase inhibitor alleviates LPS/D-Gal-induced acute liver injury in mice.

Effects of Zishen Huoxue Prescription on OGD/R-induced mitophagy in hippocampal neurons / 中国药理学通报

Aim To explore the protective effect of Zishen Huoxue Prescription on OGD/R-induced primary hippocampal neuron damage in rats and the possible mechanism. Methods After the isolated primary hippocampal neurons were identified by immunofluorescence, OGD/R induced neuronal damage, and the changes of autophagic flux at different re-oxygenation time were observed by confocal laser scanning microscopy. After OGD/R-induced primary hippocampal neurons were intervened with serum containing Zishen Huoxue Prescription, cell viability was detected by CCK-8, cell apoptosis was detected by flow cytometry, autophagosomes were detected by transmission electron microscopy, and autophagy-related protein expressions were detected by Western blot. Results 10% Zishen Huoxue Prescription-containing serum could significantly improve cell viability and reduce the proportion of cell apoptosis, increase the number of autophagosomes in neurons, and up-regulate the expression of autophagy-related protein PINK1, Parkin, and pATG16L1. Conclusions Zishen Huoxue Prescription can effectively resist OGD/R-induced apoptosis of primary hippocampal neurons in rats, and its effect may be related to the regulation of PINK1-Parkin pathway to promote mitophagy.

Regulation of platelet function by cantharidin via PI3K/Akt/PKC pathway / 中国药理学通报

To investigate the effect of cantharidin ( CTD) on platelet function and the mechanism of anti-platelet aggregation. Methods Washed platelets were collected from the venous blood of healthy volunteers. The effect of CTD on platelet aggregation and release was determined by aggregometer. The CTD concentration was 2.5 ,5 ,10 μmol • L

Role of CypD-mediated mPTP in melatonin improving cognitive impairment induced by repeated exposure to sevoflurane / 中国药理学通报

Aim To investigate the involvement of cy-clophilin D ( CypD ) -mediated mitochondrial permeability transition pore ( mPTP) in the neuroprotective effects of melatonin on cognitive impairment induced by repeated exposure to sevoflurane in newborn animals. Methods Mice were randomly assigned into control group, sevoflurane ( Sevo) group, and melatonin pre-treatment + sevoflurane ( Sevo + Mel) group. JC-1 kit was used to assess the mitochondrial membrane potential ( MMP) ; Western blot analysis was used to evaluate the protein expressions of CypD, postsynaptic density protein 95 ( PSD95 ), and Synapsin-1; and behavioral test were employed to measure cognitive function. Results The MMP level in the Sevo group was significantly reduced compared to the control group (P < 0. 01 ), the expression of CypD increased (P <0. 05), whereas the expression of PSD95 and Synapsin-1 decreased ( P < 0. 01) . Furthermore, the new object recognition index and spatial memory ability both exhibited a significant decline (P < 0. 01, P < 0. 05). However, when compared to the Sevo group, Sevo + Mel group could raise the MMP level (P <0. 01), increase the expression of synaptic proteins ( P < 0. 05 ), decrease the expression of CypD (P <0. 01) and elevate the new object recognition index and the spatial memory capacity ( P < 0. 01 ). Conclusions Melatonin could ameliorate cognitive impairment induced by repeated exposure to sevoflurane in newborn mice, and the underlying mechanism may be attributed to the inhibition of mPTP mediated by CypD and the promotion of synaptic protein synthesis.

Efficacy and safety of intermediate-dose cytarabine in the treatment of children with refractory high risk Langerhans cell histiocytosis / 中华儿科杂志

Objective: To analyze the efficacy, safety, and long-term prognosis of intermediate-dose cytarabine (Ara-c) regimen in the treatment of children with refractory risk organ involvement Langerhans cell histiocytosis (LCH). Methods: Clinical data of 17 children with multisystem and risk organ involvement LCH who failed the first-line therapy and were treated with intermediate-dose Ara-c (250 mg/m2, twice daily) regimen in the Hematology Center, Beijing Children's Hospital from January 2013 to December 2016 were analyzed retrospectively. In addition to the basic treatment of vindesine and dexamethasone, the patients received two regimens: regimen A: the intermediate-dose Ara-c combined with cladribine and regimen B: the intermediate-dose Ara-c alone. The efficacy, safety and prognosis of the two regimens were analyzed. Results: Among all 17 patients, there were 11 males and 6 females, with the diagnosis age of 2.1 (1.6, 2.7) years. Ten children received regimen A, all of them achieved active disease-better (AD-B) after 8 courses of induction therapy. The disease activity scores (DAS) decreased from 5.5 (3.0, 9.0) to 1.0 (0, 2.3). Seven children received regimen B, and 6 of them achieved AD-B after 8 courses of induction therapy. The DAS decreased from 4.0 (2.0, 4.0) to 1.0 (0, 2.0). The follow-up time was 6.2 (4.9,7.2) and 5.2 (3.7,5.8) years in group A and B. The 5-year overall survival rate was 100.0% in both groups, and the 5-year event free survival rate was (88.9±10.5)% and (85.7±13.2)% in group A and B. Grade 3 or 4 myelosuppression was observed in 8 patients in group A and 2 patients in group B. Conclusions: The intermediate-dose Ara-c regimen (with or without cladribine) is effective and safe for patients with refractory high-risk LCH, with a good long-term prognosis.

Clinical analysis of 86 cases of acute fatty liver of pregnancy / 中华妇产科杂志

Objective: To investigate the clinical characteristics and maternal and fetal prognosis of pregnant women with acute fatty liver of pregnancy (AFLP). Methods: The clinical data of 86 AFLP pregnant women admitted to the Third Affiliated Hospital of Guangzhou Medical University from September 2017 to August 2022 were collected, and their general data, clinical characteristics, laboratory tests and maternal and fetal outcomes were retrospectively analyzed. Results: (1) General information: the age of the 86 pregnant women with AFLP was (30.8±5.4) years, and the body mass index was (21.0±2.5) kg/m2. There were 50 primiparas (58.1%, 50/86) and 36 multiparas (41.9%, 36/86). There were 64 singleton pregnancies (74.4%, 64/86) and 22 twin pregnancies (25.6%, 22/86). (2) Clinical characteristics: the main complaints of AFLP pregnant women were gastrointestinal symptoms, including epigastric pain (68.6%, 59/86), nausea (47.7%, 41/86), anorexia (46.5%, 40/86), vomiting (39.5%, 34/86). The main non-gastrointestinal symptoms were jaundice of skin and/or scleral (54.7%, 47/86), edema (38.4%, 33/86), fatigue (19.8%, 17/86), bleeding tendency (16.3%, 14/86), polydipsia or polyuria (14.0%, 12/86), skin itching (8.1%, 7/86), and 17.4% (15/86) AFLP pregnant women had no obvious symptoms. (3) Laboratory tests: the incidence of liver and kidney dysfunction and abnormal coagulation function in AFLP pregnant women was high, and the levels of blood ammonia, lactate dehydrogenase and lactic acid were increased, and the levels of hemoglobin, platelet and albumin decreased. However, only 24 cases (27.9%, 24/86) of AFLP pregnant women showed fatty liver by imageology examination. (4) Pregnancy outcomes: ① AFLP pregnant women had a high incidence of pregnancy complications, mainly including renal insufficiency (95.3%, 82/86), preterm birth (46.5%, 40/86), hypertensive disorders in pregnancy (30.2%, 26/86), gestational diabetes mellitus (36.0%, 31/86), fetal distress (24.4%, 21/86), pulmonary infection (23.3%, 20/86), disseminated intravascular coagulation (16.3%, 14/86), multiple organ dysfunction syndrome (16.3%, 14/86), hepatic encephalopathy (9.3%, 8/86), and intrauterine fetal death (2.3%, 2/86). ② Treatment and outcome of AFLP pregnant women: the intensive care unit transfer rate of AFLP pregnant women was 66.3% (57/86). 82 cases were improved and discharged after treatment, 2 cases were transferred to other hospitals for follow-up treatment, and 2 cases (2.3%, 2/86) died. ③ Neonatal outcomes: except for 2 cases of intrauterine death, a total of 106 neonates were delivered, including 39 cases (36.8%, 39/106) of neonatal asphyxia, 63 cases (59.4%, 63/106) of neonatal intensive care unit admission, and 3 cases (2.8%, 3/106) of neonatal death. Conclusions: AFLP is a severe obstetric complication, which is harmful to mother and fetus. In the process of clinical diagnosis and treatment, attention should be paid to the clinical manifestations and laboratory tests of pregnant women, early diagnosis and active treatment, so as to improve maternal and fetal outcomes.