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To investigate the risk factors as well as their impact on patients' survival of central nervous system (CNS) complications following allogeneic hematopoietic stem cell transplantation (HSCT).

All relevant clinical data from a total of 323 patients, who underwent allogeneic HSCT in Xiangya Hospital of Central South University from September 2016 to September 2019, were retrospectively reviewed in this study. The complications' occurrence time, common symptoms and some other clinical data of the patients who developed CNS complications were analyzed descriptively. The risk factors for CNS complications following allogeneic HSCT were analyzed through univariate and multivariate analysis. And the survival analysis was conducted as well.

Among the 323 patients who underwent allogeneic HSCT, 32 patients developed CNS complications. These complications occurred in these patients at a median of 32 (range from -1 to 584) d after transplantation. Common symptoms were disturbance of consciousness (78.1%), convuls mortality (TRM) and 2-year TRM were significantly higher in patients who developed CNS complications than those in the non-CNS complication group (45%±9% vs 8%±2%, 58%±11% vs 11%±2%; both

<0.001).

The delay or the failure of PLT engraftment and combined with aGVHD are the risk factors for CNS complications. The facts indicate that we should prevent CNS complications when patients who underwent allogeneic HSCT with the delay or the failure of PLT engraftment or aGVHD. Compared with non-CNS complication group, patients who developed CNS complications usually have poor prognosis.

The delay or the failure of PLT engraftment and combined with aGVHD are the risk factors for CNS complications. The facts indicate that we should prevent CNS complications when patients who underwent allogeneic HSCT with the delay or the failure of PLT engraftment or aGVHD. Compared with non-CNS complication group, patients who developed CNS complications usually have poor prognosis.

To explore the influential factors and titer trend of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) specific IgG antibody in convalescent patients with coronavirus disease 2019 (COVID-19), and to provide theoretical basis for the feasibility of clinical treatment of convalescent plasma.

Colloidal gold immunochromatography assay was used to detect the SARS-CoV-2 specific IgG antibody and its titer in 113 convalescent patients with COVID-19 who were followed up from February 19, 2020 to April 6, 2020. The basic characteristics and treatment factors of patients in the high titer group (antibody titer≥1꞉160,

=22) and the low titer group (antibody titer <1꞉160,

=91) were analyzed. The IgG antibody titer in the high titer group was continuously monitored and the trend of titer was analyzed.

The difference in the clinical type of COVID-19, onset time, first admission C-reactive protein, absolute value of lymphocyte, absolute value of CD19

CD3

lymphocytes, and the treatment of glucocorticoid were not statistically significant between the patients in the high titer group and the low titer group (all

>0.05). The male patients in the high titer group were more than those in the low titer group (

<0.05). The titer of SARS-CoV-2 specific IgG antibody in the high titer group decreased to less than 1꞉160 28 d after discharge.

Male COVID-19 patients might be more likely to produce high titer SARS-CoV-2 specific IgG antibodies than female. The peak level of SARS-CoV-2 specific IgG antibody in convalescent patients is maintained for a short period. Using plasma from convalescent COVID-19 patients for treatment should be within 28 d after discharge.

Male COVID-19 patients might be more likely to produce high titer SARS-CoV-2 specific IgG antibodies than female. The peak level of SARS-CoV-2 specific IgG antibody in convalescent patients is maintained for a short period. Using plasma from convalescent COVID-19 patients for treatment should be within 28 d after discharge.

Primary carnitine deficiency (PCD) is a rare fatty acid metabolism disorder that can cause neonatal death. This study aims to analyze carnitine levels and detect SLC22A5 gene in newborns with carnitine deficiency, to provide a basis for early diagnosis of PCD, and to explore the relationship between carnitine in blood and SLC22A5 genotype.

A total of 40 neonates with low free carnitine (C0<10 μmol/L) in blood were the subjects of the study. SLC22A5 gene was detected by Sanger sequencing to analyze the value of carnitine, the results of gene test and their relationship.

A total of 15 variants of SLC22A5 gene were detected, including 11 pathogenic or likely pathogenic variants and 4 variants of uncertain significance. There were 5 new mutations c.288delG (p.G96fsX33), c.744_745insTCG (p.M258_L259insS), c.752A>G (p.Y251C), c.495 C>A (p.R165E), and c.1298T>C (p.M433T). We found 14 PCD patients including 2 homozygous mutations and 12 heterozygous mutations, 14 with 1 mutation, and 12 with no mutae 5 new mutations which enriched the mutation spectrum of SLC22A5 gene. C0 less then 5 μmol/L is highly correlated with SLC22A5 gene homozygous or compound heterozygous mutations. Children with truncated mutation may have lower C0 concentration than that with untruncated mutation in the initial screening.

Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α) controls mitochondrial biogenesis, but its role in cardiovascular diseases is unclear. The purpose of this study is to explore the effect of PGC1α on myocardial ischemia-reperfusion injury and the underlying mechanisms.

The transverse coronary artery of SD rat was ligated for 30 minutes followed by 2 hours of reperfusion. selleck compound Triphenyltetrazolium chloride (TTC) staining was performed to measure the area of myocardial infarction. Immunohistochemistry and Western blotting were used to detect the PGC1α expression in myocardium. The rat cardiomyocyte H9C2 was subjected to hypoxia/reoxygenation (H/R) with the knockdown of PGC1α or hypoxia- inducible factor 1α (HIF-1α), or with treatment of metformin. Western blotting was used to detect the expression of PGC1α, HIF-1α, p21, BAX, and caspase-3. CCK-8 was performed to detect cell viability, and flow cytometry was used to detect apoptosis and mitochondrial superoxide (mitoSOX) release. RT-qPCR was used to detect the mRNA expression of PGC1α and HIF-1α.