To analyze the factors affecting the cost of hospitalization for patients and provide insights using the intrauterine lesion surgery group (DRG code NE19) as an example.

Background::Whether the dynamic weight change is an independent risk factor for mortality remains controversial. This study aimed to examine the association between weight change and risk of all-cause and cause-specific mortality based on the Linxian Nutrition Intervention Trial (NIT) cohort.Methods::Body weight of 21,028 healthy residents of Linxian, Henan province, aged 40-69 years was measured two times from 1986 to 1991. Outcome events were prospectively collected up to 2016. Weight maintenance group (weight change <2 kg) or stable normal weight group was treated as the reference. Cox proportional hazard model was performed to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs) to estimate the risk of mortality.Results::A total of 21,028 subjects were included in the final analysis. Compared with the weight maintenance group, subjects with weight loss ≥2 kg had an increased risk of death from all-cause (HR All-cause = 1.14, 95% CI: 1.09-1.19, P <0.001), cancer (HR Cancer = 1.12, 95% CI: 1.03-1.21, P = 0.009), and heart disease (HR Heart diseases = 1.21, 95% CI: 1.11-1.31, P <0.001), whereas subjects with weight gain ≥5 kg had 11% (HR Cancer = 0.89, 95% CI: 0.79-0.99, P = 0.033) lower risk of cancer mortality and 23% higher risk of stroke mortality (HR Stroke = 1.23,95% CI: 1.12-1.34, P <0.001). For the change of weight status, both going from overweight to normal weight and becoming underweight within 5 years could increase the risk of total death (HR Overweight to normal = 1.18, 95% CI: 1.09-1.27; HR Becoming underweight = 1.35, 95% CI: 1.25-1.46) and cancer death (HR Overweight to normal = 1.20, 95% CI: 1.04-1.39; HR Becoming underweight = 1.44, 95% CI: 1.24-1.67), while stable overweight could increase the risk of total death (HR Stable overweight = 1.11, 95% CI: 1.05-1.17) and death from stroke (HR Stable overweight = 1.44, 95% CI: 1.33-1.56). Interaction effects were observed between age and weight change on cancer mortality, as well as between baseline BMI and weight change on all-cause, heart disease, and stroke mortality (all Pinteraction <0.01). Conclusions::Weight loss was associated with an increased risk of all-cause, cancer, and heart disease mortality, whereas excessive weight gain and stable overweight were associated with a higher risk of stroke mortality. Efforts of weight management should be taken to improve health status.Trial registration::https://classic.clinicaltrials.gov/, NCT00342654.

Currently the main treatment of acute myeloid leukemia (AML) is chemotherapy combining hematopoietic stem cell transplantation. However, the unbearable side effect of chemotherapy and the high risk of life-threatening infections and disease relapse following hematopoietic stem cell transplantation restrict its application in clinical practice. Thus, there is an urgent need to develop alternative therapeutic tactics with significant efficacy and attenuated adverse effects. Here, we revealed that umbilical cord-derived mesenchymal stem cells (UC-MSC) efficiently induced AML cell differentiation by shuttling the neutrophil elastase (NE)-packaged extracellular vesicles (EVs) into AML cells. Interestingly, the generation and release of NE-packaged EVs could be dramatically increased by vitamin D receptor (VDR) activation in UC-MSC. Chemical activation of VDR by using its agonist 1α,25-dihydroxyvitamin D3 efficiently enhanced the pro-differentiation capacity of UC-MSC and then alleviated malignant burden in AML mouse model. Based on these discoveries, to evade the risk of hypercalcemia, we synthetized and identified sw-22, a novel non-steroidal VDR agonist, which exerted a synergistic pro-differentiation function with UC-MSC on mitigating the progress of AML. Collectively, our findings provided a non-gene editing MSC-based therapeutic regimen to overcome the differentiation blockade in AML.

Objective:To analyze the characteristics of drug resistance genes in a Klebsiella pneumoniae strain coproducing carbapenemases KPC-2 and NDM-5. Methods:Klebsiella pneumoniae KPN-hnqyy was separated from the stool specimen of a patient in the Hematology Department of Affiliated Cancer Hospital of Zhengzhou University. The strain was identified with a BD Phenix-M50 automated microbiology system and the minimum inhibitory concentration against the strain was measured as well. The genotypes of the carbapenemases were tested by enzyme immunochromatographic assay and PCR method. The transferability of related plasmids was analyzed by conjugation test. Whole-genome sequencing of the strain was conducted using PacBio and Illumina platforms. The MLST type, resistance gene and plasmid type of the strain were retrieved in BacWGSTdb. The genome and open reading frame sequence of the strain were compared using Easyfig_2.2.3. Visual cycle graphs were generated using BRIG v0.95. Results:Klebsiella pneumoniae KPN-hnqyy was resistant to carbapenem antibiotics. It belonged to ST11 and carried two carbapenemase genes of blaKPC-2 and blaNDM-5. The conjugant only harbored the blaKPC-2 gene. Whole-genome sequencing revealed that the strain contained one chromosome and three plasmids. Its chromosome genome shared more than 99.9% similarity with that of Klebsiella pneumonia KP69 and KP19-2029. Moreover, a similar IncR and IncFⅠ resistance gene fusion region was contained in different types of plasmids carried by them: the blaKPC-2 gene was located in a structure—which evolved from the Tn3-△Tn4401-Tn1721/Tn1722 sequence—inside this fusion region with its ends inserted into the transposase IS26 gene; the blaNDM-5 gene was located on a transposon containing the special plasmids of the insertion fragment in phages, with its ends inserted into the transposase IS26 gene too. Conclusions:The IncR and IncFⅡ resistance gene fusion region of blaKPC-2 carried by Klebsiella pneumoniae ST11 might be widely coexistent with the chromosomal genome. The blaNDM-5 gene carried by special plasmids might be accidentally obtained through gene recombination mediated by transposable element IS26. The wide transmission of Klebsiella pneumoniae ST11 carrying the blaKPC-2 gene in China and its ability to obtain other carbapenemase genes through transposable element IS26 were well worth attention.

Esophageal cancer (EC) is one of the most fatal cancers worldwide. According to GLOBOCAN 2020, it was estimated that there were 600, 000 new EC cases and 540 000 EC deaths, while nearly half of all newly diagnosed cases of EC and associated deaths worldwide occurred in China. The annual incidence and mortality of EC have been reduced in the last 20 years in China. However, the early symptoms and signs of EC are not easily distinguished and the disease tends to be within the middle and late stage of pathogenesis when identified, leading to its low 5-year survival rate. Therefore, it could help effectively reduce the burden of EC by clarifying its etiology and risk factors, as well as taking preventive and early diagnosis measures. This article reviews the epidemiology, etiology, screening and early diagnosis of EC in China, to provide systematic references for EC prevention and control.

Objective:To establish the method for detecting lower respiratory infections (LRIs) bacterialpathogens using nanopore sequencing, and evaluate the feasibility of this method.Methods:Bronchoalveolar lavage fluid (BALF) samples from 33 patients with LRIs who visited the Department of Respiratory and Critical Care Medicine of Beijing Hospital from July 2019 to September 2020 were collected.Nanopore 16S amplicon sequencing were performed on these samples. In order to evaluate the clinical value of the nanopore sequencing, χ 2 test was used to analyze the pathogen differences between the detection rate and pathogen types results found with using the nanopore 16S sequencing and the results found with bacterial culture. Results:The process and method of nanopore sequencing used in the detection of the LRIs pathogens were established. The pathogen detection rate of the 16S sequencing was higher than that of the traditional bacterial culture (75.8% [25/33], 45.5% [15/33], χ2=5.140, P<0.05). From the 25 positive samples found with nanopore 16S sequencing, 16 pathogens were detected, including Haemophilus parainfluenzae, Haemophilus influenzae, Streptococcus pneumoniae, Streptomonas maltophilia, Acinetobacter baumannii, and Acinetobacter junii, Staphylococcus aureus, Klebsiella pneumoniae, Enterococcus faecalis, Enterococcus gallinarum, Corynebacterium striatum, Mycobacterium paraintracellulare, Serratia marcescens, Achromobacter insuavis, Citrobacter murliniae and Mycoplasma pneumoniae. More than 6 pathogens were tested in clinical culture, including Haemophilus parainfluenzae, Acinetobacter baumannii, Pseudomonas aeruginosa, Staphylococcus aureus, Klebsiella pneumoniae and Streptomonas maltophilia (χ2=7.949, P<0.05). 16S sequencing aligned to species level sequences accounted for 80.0 (60.0, 86.0)% of the genus level. The results obtained by using16S sequencing and bacterial culture were consistent in 11 (33.3%) samples. Conclusions:Nanopore 16S amplicon sequencing can quickly identify pathogenic bacteria from BALF in LRIs patients. Nanopore 16S amplicon sequencing has a high detection rate, it can detect more pathogens than traditional bacterial culture, and it can also identify most bacteria to the species level. This technology is a very promising platform with broad application prospects.

To investigate whether the laboratory specimens preserved in Beijing Hospital Biobank during a specific period had been contaminated by SARS-Cov-2 through a cross-sectional study, and to establish a retrospective biobank safety screening system. Laboratory specimens were collected from the Department of Respiratory and Critical Care Medicine and the Fever Clinic of Beijing Hospital from November 1, 2019 to January 22, 2020, nucleic acid and serological antibody testing were performed for SARS-CoV-2 in these specimens (including 79 serum, 20 urine, 42 feces and 21 bronchoalveolar lavage fluid specimens). The safety of the stored samples during this period was defined by negative and positive results. Both the nucleic acid test and serological antibody test showed negative for SARS-CoV-2, indicating that these specimens were safely stored in the biobank. High-risk specimens collected in our hospital during the early stage of the COVID-19 outbreak are free of SARS-CoV-2, and a safety screening strategy for the clinical biobank is established to ensure the biosafety of these samples.
Biological Specimen Banks ; COVID-19 ; Cross-Sectional Studies ; Hospitals ; Humans ; Retrospective Studies ; SARS-CoV-2

COVID-19 is an emerging infectious disease caused by SARS-CoV-2. After the infection of the virus, the host immune system is stimulated to produce multifarious specific antibodies to decrease or eliminate effects of the pathogen. Study of the specific antibodies dynamic characteristics in patients with COVID-19 is very important for the understanding and diagnosis of the disease, research and development of vaccine, and planning of prevention and control strategy. This paper reviews and summarizes the domestic and oversea research on dynamic characteristics of specific antibodies of COVID-19 patients, including the antibody producing, duration and level, and its possible influencing factors in order to improve the understanding of the immunological characteristics of COVID-19.

As the progress of population aging in China, the proportion of elderly population is increasing. Both chronic diseases and infectious diseases can threaten the health of the elderly. There are many kinds of infectious diseases, including vaccine preventable infectious diseases affecting the health of adults, such as influenza, pneumococcal diseases and herpes zoster. In addition, the newly emerged COVID-19 has caused a pandemic in the world, resulting the highest proportion of deaths occurred in the elderly and posing a serious threat to the health of the elderly. This paper mainly summarizes the prevention and control of vaccine preventable diseases and COVID-19 to which the elderly are susceptible, analyzes the infectious disease problems affecting the health of elderly population, and recommends countermeasures for the prevention and control of these diseases in elderly population.

Objective:To observe the effect and underlying mechanism of down-regulation of VEGFA on the radiosensitivity of esophageal cancer ECA-109 cells.Methods:Esophageal cancer cells were divided into four groups: sh-VEGFA group, vector control group, X-ray plussh-VEGFA group and X-ray plus vector group. The expressions of VEGFA gene and protein were detected by qPCR and Western blot, respectively. Cell proliferation and survival was measured by CCK8 assay and cloning formation, respectively. Cell apoptosis was detected by flow cytometry, and γ-H2AX foci were detected by immune-fluorescence assay.Results:Compared with the vector group, the expression of VEGFA gene was decreased in sh-VEGFA group ( t=11.98, P<0.05), and the expression of VEGFA protein was also reduced( t=12.38, P<0.05). After VEGFA being down-regulated, the cell proliferation( A450)was obviously inhibited( t=2.78, 7.25, 21.93, 13.21, P<0.05), and the cell clone formation of the sh-VEGFA group was significantly decreased so that D0, Dqand SF2 of sh-VEGFA group were decreased( t=5.83, 8.56, 7.68, P<0.05), and SERD0and SERDqwere increased. Compared with the vector group, the apoptosis rate in the sh-VEGFA group and the X-ray group was significantly increased and further increased in the sh-VEGFA plus X-ray group( t=17.63, 22.48, 33.87, P<0.05), and the number of γ-H2AX foci in both sh-VEGFA and vector groups were significantly increased within 2 h after X-ray irradiation. At 24 h after irradiation, the number of γ-H2AX foci returned to normal level in the vector group but remained at a higher level in the sh-VEGFA group ( t=7.00, P<0.05). Conclusions:Down-regulation of VEGFA inhibits the proliferation and colony formation, promotes apoptosis and hence increases the radiosensitivity of esophageal carcinoma cells via a pathway related to DNA damage repair.