Objective:To analyze the level of interleukin-36(IL-36) family cytokines in peripheral blood, and explore the regulatory role of recombinant human IL-36α in monocyte function in patients with diabetic kidney disease(DKD).Methods:A total of 41 type 2 diabetes mellitus(T2DM) patients, 36 DKD patients, and 20 controls were consecutively enrolled. Plasma and peripheral blood mononuclear cells(PBMCs) were isolated. Enzyme-linked immunosorbent assay(ELISA) was used to measure plasma levels of IL-36α, IL-36β, IL-36γ, and IL-36 receptor antagonist(IL-36Ra). PBMCs were sorted, and real-time quantitative PCR was performed to detect the mRNA expression of IL-36 receptor subunits in monocytes. Monocytes were stimulated with recombinant IL-36α, and levels of cytotoxic molecules and cytokines in the culture supernatant were measured. Flow cytometry was used to assess the expressions of programmed death receptor-1(PD-1) and cytotoxic T-lymphocyte-associated protein 4(CTLA-4). Co-culture of monocytes with Vero cells was performed to evaluate monocyte cytotoxicity.Results:Plasma levels of IL-36α and IL-36β in the T2DM and DKD groups were significantly higher than those in the control group. The DKD group also showed higher plasma levels of IL-36α compared to the T2DM group( P<0.05). There were no significant differences in IL-36γ and IL-36Ra levels among the three groups( P>0.05). The mRNA expression of IL-36 receptor subunits in monocytes was comparable among the three groups( P>0.05). The DKD group had higher level of tumor necrosis factor-alpha(TNF-α) compared to the control and T2DM groups( P<0.05). The levels of PD-1 and CTLA-4 were lower in the DKD group than those in the control and T2DM groups( P<0.05). The proportion of monocyte-induced Vero cell death was significantly higher in the DKD group compared to the control and T2DM groups( P<0.05). After stimulation with recombinant human IL-36α, monocytes from DKD patients showed a significant increase in the secretion of granzyme B and TNF-α( P<0.05), as well as an increased proportion of monocyte-induced Vero cell death( P=0.024). Conclusion:In DKD patients, elevated IL-36α and granzyme B levels in monocytes enhance monocyte function.

Objective: To analyze the epidemiological and molecular characteristics of norovirus outbreaks in schools in Xicheng District of Beijing from 2017 to 2022, so as to provide evidence for the prevention and control of norovirus outbreaks in schools. Methods: Data of norovirus outbreaks in schools in Xicheng District, Beijing during 2017 to 2022 were collected and analyzed by descriptive epidemiological methods. Realtime PCR was used to detect the nucleic acid of group GⅠand GⅡnorovirus, the positive norovirus nucleic acid samples were sent to Beijing Center for Disease Control and Prevention for molecular typing. Results: From 2017 to 2022, 185 norovirus outbreaks were reported in schools in Xicheng District, including 166 cluster outbreaks and 19 outbreaks. A total of 2 044 cases were reported, with a total attack rate of 13.92%. There were two peaks in the outbreak time, which were from March to June after the spring semester and from October to December after autumn semester. Primary schools were the most common place of occurrence (101 cases), followed by nursery institutions (68 cases) and secondary schools (16 cases). There were statistically significant differences in the incidence rates among different sites(12.37%, 22.78%, 8.47%, χ2=263.34, P<0.01). There were significant differences in the incidence of vomiting, diarrhea, nausea and stomachache among different students (χ2=263.33, 90.58, 20.42, 30.29, P<0.01). Vomiting was the main symptom in primary school and nursery school children (96.41%, 98.28%), and the diarrhea rate was higher in middle school students (68.22%). The outbreaks were mainly caused by type GⅡ norovirus. The genotype from 2017 to 2021 showed the characteristics of diversity, mainly GⅡ.2[P16], but there was no significant advantage for the GⅡ.2 [P16] during 2019 to 2021. Conclusions The norovirus outbreak in schools in Xicheng district of Beijing from 2017 to 2022 are mainly caused by GⅡ type genome. The main genotype is GⅡ.2[P16]. Norovirus infection mainly occurred in primary schools and kindergartens. For the vulnerable populations, it is necessary to improve the capacity to early identification, student infectious disease management, active infection control and prevention measures, and pathogen surveillance and sporadic case monitoring.

Following the principles of evidence-based medicine,in accordance with the structure and drafting rules of standardized documents,based on literature research,according to the characteristics of chronic cough in children and issues that need to form a consensus,the TCM Guidelines for Diagnosis and Treatment of Chronic Cough in Children was formulated based on the Delphi method,expert discussion meetings,and public solicitation of opinions.The guideline includes scope of application,terms and definitions,eti-ology and diagnosis,auxiliary examination,treatment,prevention and care.The aim is to clarify the optimal treatment plan of Chinese medicine in the diagnosis and treatment of this disease,and to provide guidance for improving the clinical diagnosis and treatment of chronic cough in children with Chinese medicine.

Objective:To evaluate the diagnostic efficacy and practicality of the Jaundice color card (JCard) as a screening tool for neonatal jaundice.Methods:Following the standards for reporting of diagnostic accuracy studies (STARD) statement, a multicenter prospective study was conducted in 9 hospitals in China from October 2019 to September 2021. A total of 845 newborns who were admitted to the hospital or outpatient department for liver function testing due to their own diseases. The inclusion criteria were a gestational age of ≥35 weeks, a birth weight of ≥2 000 g, and an age of ≤28 days. The neonate′s parents used the JCard to measure jaundice at the neonate′s cheek. Within 2 hours of the JCard measurement, transcutaneous bilirubin (TcB) was measured with a JH20-1B device and total serum bilirubin (TSB) was detected. The Pearson′s correlation analysis, Bland-Altman plots and the receiver operating characteristic (ROC) curve were used for statistic analysis.Results:Out of the 854 newborns, 445 were male and 409 were female; 46 were born at 35-36 weeks of gestational age and 808 were born at ≥37 weeks of gestational age. Additionally, 432 cases were aged 0-3 days, 236 cases were aged 4-7 days, and 186 cases were aged 8-28 days. The TSB level was (227.4±89.6) μmol/L, with a range of 23.7-717.0 μmol/L. The JCard level was (221.4±77.0) μmol/L and the TcB level was (252.5±76.0) μmol/L. Both the JCard and TcB values showed good correlation ( r=0.77 and 0.80, respectively) and agreements (96.0% (820/854) and 95.2% (813/854) of samples fell within the 95% limits of agreement, respectively) with TSB. The JCard value of 12 had a sensitivity of 0.93 and specificity of 0.75 for identifying a TSB ≥205.2?μmol/L, and a sensitivity of 1.00 and specificity of 0.35 for identifying a TSB ≥342.0?μmol/L. The TcB value of 205.2?μmol/L had a sensitivity of 0.97 and specificity of 0.60 for identifying TSB levels of 205.2 μmol/L, and a sensitivity of 1.00 and specificity of 0.26 for identifying TSB levels of 342.0 μmol/L. The areas under the ROC curve (AUC) of JCard for identifying TSB levels of 153.9, 205.2, 256.5, and 342.0 μmol/L were 0.96, 0.92, 0.83, and 0.83, respectively. The AUC of TcB were 0.94, 0.91, 0.86, and 0.87, respectively. There were both no significant differences between the AUC of JCard and TcB in identifying TSB levels of 153.9 and 205.2 μmol/L (both P>0.05). However, the AUC of JCard were both lower than those of TcB in identifying TSB levels of 256.5 and 342.0 μmol/L (both P<0.05). Conclusions:JCard can be used to classify different levels of bilirubin, but its diagnostic efficacy decreases with increasing bilirubin levels. When TSB level are ≤205.2 μmol/L, its diagnostic efficacy is equivalent to that of the JH20-1B. To prevent the misdiagnosis of severe jaundice, it is recommended that parents use a low JCard score, such as 12, to identify severe hyperbilirubinemia (TSB ≥342.0 μmol/L).

ObjectiveTo determine the risk factors associated with colorectal adenoma among the residents in Nanchang city， and provide scientific evidence for primary preventive measures against colorectal cancer. MethodsA matched case-control study was conducted. A total of 155 patients newly diagnosed with colorectal adenomas during 2018‒2019 were selected as cases， and 155 healthy persons attending the screening as controls. Both the case group and control group completed the questionnaires on the risk factors. Conditional logistic regression analysis was performed using SPSS 25.0. ResultsAge， gender， and educational level were used for match between case group and control group. Conditional multivariate logistic regression analysis showed that salted and dried food intake（OR=5.634， 95%CI：1.308‒24.256）， smoking（OR=3.266， 95%CI：1.419‒7.518）， passive smoking（OR=3.125，95%CI：1.415‒6.898）， and hyperlipidemia（OR=3.975， 95%CI：1.643‒9.618）were associated with higher risk of colorectal adenoma. In contrast， coarse grain intake ≥500 g/week（OR=0.377， 95%CI：0.177‒0.805） was a protective factor. ConclusionColorectal adenoma may be caused by multiple risk factors， particularly salted and dried food intake， smoking， passive smoking and hyperlipidemia. It warrants specific intervention to reduce the risk of colorectal adenoma.

IF1 (ATPIF1) is a nuclear DNA-encoded mitochondrial protein whose activity is inhibition of the F

Objective:To investigate the effects of T-2 toxin on expression of inflammatory cytokines, human leukocyte differentiation antigen (CD) 44 and integrin in chondrocytes cultured in vitro. Methods:Primary chondrocytes from SPF Wistar rats aged 1 to 2 days were isolated and cultured in vitro, and the chondrocytes were identified by toluidine blue staining. The effects of different dose of T-2 toxin (0, 2, 4, 6, 10, 12, 20 ng/ml) on proliferation of chondrocytes for 24, 48 and 72 h were detected via the cell counting kit-8 (CCK-8) method. According to the cell survival rate, T-2 toxin concentrations of 0 (control), 2, 4, 6 and 8 ng/ml were selected for subsequent experiments, and the exposure time was 48 h. The contents of interleukin (IL)-6, IL-1β, tumor necrosis factors (TNF)-α and CD44 in cell supernatant were detected via the enzyme linked immunosorbent assay (ELISA). The protein expression levels of integrin α5 and integrin β1 in chondrocytes were detected by Western blotting. Results:At the same exposure time, there were significant differences of the survival rate of chondrocytes between different dose groups ( F = 130.759, 258.250, 123.337, P < 0.01). At 48 h after exposure, there were statistically significant differences in IL-6, IL-1β, TNF-α and CD44 contents in the culture supernatant of chondrocytes between different dose of T-2 toxin groups ( F = 10.613, 4.805, 2.943, 12.395, P < 0.01 or < 0.05); among them, the IL-6 levels of 2, 4, 6 and 8 ng/ml groups were higher than that of control group ( P < 0.05); the IL-1β levels of 6, 8 ng/ml groups were higher than that of control and 2 ng/ml groups, and the 6 ng/ml group was higher than that of 4 ng/ml group ( P < 0.05); the TNF-α levels of 6, 8 ng/ml groups were lower than that of control group ( P < 0.05); the CD44 levels of 2, 4, 6 and 8 ng/ml groups were lower than that of control group ( P < 0.05). At 48 h after exposure, there were statistically significant differences in integrin α5 and integrin β1 protein expression levels between different dose of T-2 toxin groups ( F = 4.635, 4.376, P < 0.05). Among them, the protein expression levels of integrin α5 in 6, 8 ng/ml groups were significantly lower than that of control group ( P < 0.05); the protein expression levels of integrin β1 in 6, 8 ng/ml groups were significantly higher than that of control group ( P < 0.05). Conclusion:T-2 toxin may up-regulate the expressions of IL-6, IL-1β and integrin β1, while down-regulate the expressions of TNF-α, CD44 and integrin α5, then disrupt the balance between chondrocytes and extracellular matrix, and cause chondrocytes damage.

Background: Cardiopulmonary resuscitation (CPR) strategies in COVID-19 patients differ from those in patients suffering from cardiogenic cardiac arrest. During CPR, both healthcare and non-healthcare workers who provide resuscitation are at risk of infection. The Working Group for Expert Consensus on Prevention and Cardiopulmonary Resuscitation for Cardiac Arrest in COVID-19 has developed this Chinese Expert Consensus to guide clinical practice of CPR in COVID-19 patients. Main recommendations: 1) A medical team should be assigned to evaluate severe and critical COVID-19 for early monitoring of cardiac-arrest warning signs. 2) Psychological counseling and treatment are highly recommended, since sympathetic and vagal abnormalities induced by psychological stress from the COVID-19 pandemic can induce cardiac arrest. 3) Healthcare workers should wear personal protective equipment (PPE). 4) Mouth-to-mouth ventilation should be avoided on patients suspected of having or diagnosed with COVID-19. 5) Hands-only chest compression and mechanical chest compression are recommended. 6) Tracheal-intubation procedures should be optimized and tracheal-intubation strategies should be implemented early. 7) CPR should be provided for 20-30 min. 8) Various factors should be taken into consideration such as the interests of patients and family members, ethics, transmission risks, and laws and regulations governing infectious disease control. Changes in management: The following changes or modifications to CPR strategy in COVID-19 patients are proposed: 1) Healthcare workers should wear PPE. 2) Hands-only chest compression and mechanical chest compression can be implemented to reduce or avoid the spread of viruses by aerosols. 3) Both the benefits to patients and the risk of infection should be considered. 4) Hhealthcare workers should be fully aware of and trained in CPR strategies and procedures specifically for patients with COVID-19.

Objective:To observe the effects of deoxynivalenol (DON) on the expression of chondrocyte inflammatory cytokines, cluster of differentiation (CD) 44, matrix metalloproteinase (MMP)-13 and integrin in vitro. Methods:Primary chondrocytes from Wistar rats aged 1 to 2 days were isolated, and the chondrocytes were identified by toluidine blue staining. The effects of DON (dose groups of 0.0, 0.1, 0.2, 0.4, 0.8 μg/ml) on proliferation of chondrocytes were detected by CCK-8 method for 24, 48 and 72 h. According to the cell survival rate, the DON concentrations [0.00 (control), 0.05, 0.10, 0.15, 0.20 μg/ml] were selected for subsequent experiments, and the exposure time was 48 h. The contents of interleukin (IL)-6, IL-1β, tumor necrosis factors (TNF)-α, CD44 and MMP-13 in the cell culture supernatant were detected by enzyme linked immunosorbent assay (ELISA) kit. The expression levels of CD44 and integrin subunits α2, α5, and β1 protein in chondrocytes were detected by Western blotting.Results:The survival rate of chondrocytes decreased with the increase of DON concentrations and time ( P < 0.01). There were statistically significant differences in IL-6 content between different groups ( H = 13.425, P < 0.01), and 0.10 μg/ml group [256.89 (191.02, 477.58) pg/ml] was significantly higher than that of the control group [10.37 (0.00, 119.13) pg/ml, P < 0.05]. There were no statistically significant differences in IL-1β and TNF-α contents between the groups ( F = 0.881, 1.317, P > 0.05). The CD44 contents in 0.10, 0.15, and 0.20 μg/ml groups [(0.87 ± 0.21), (0.85 ± 0.24), (0.77 ± 0.17) pg/ml] were lower than that in the control group [(1.06 ± 0.19) pg/ml, P < 0.05]. There were statistically significant differences in MMP-13 expression between the groups ( F = 7.947, P < 0.01). There were statistically significant differences in protein expression of CD44, integrin subunits α2, α5 and β1 between the groups ( F = 5.737, 6.562, 6.074, 4.476, P < 0.05 or < 0.01). Conclusion:DON may disrupt the balance between cells and extracellular matrix by increasing the expression of IL-6, MMP-13, integrin subunits α2 and β1, and inhibiting the expression of CD44 and integrin subunit α5, thus causing cartilage injury.

Objective:To evaluate the effect of imatinib on growth impairment in children with chronic myeloid leukemia (CML-CP) in the chronic phase.Methods:From July 2018 to July 2019, questionnaires were distributed to CML children aged <18 years at the time of diagnosis who were receiving imatinib for at least 3 months or to their parents in China. The height-for-age standard deviation score (HtSDS) and the difference of standard deviation integral (△HtSDS) were used to explore the change in height with imatinib therapy.Results:The data of 238 respondents were included; 138 (58.0% ) respondents were men. The median age at the first diagnosis of CML was 11.0 years (range, 1.4-17.9 years) , and 93 (39.0% ) respondents were at the prepuberty stage. At the time of completing the questionnaires, the median age was 15.0 years (range, 2.0-34.0 years) . The median duration of imatinib therapy was 28 months (range, 3-213 months) . Among all the respondents, the mean HtSDS when completing the questionnaires (-0.063±1.361) was significantly lower than that at the time of starting imatinib treatment (0.391±1.244) ( P<0.001) . Total 71.0% respondents showed growth impairment that was more common in those starting imatinib therapy at prepubertal age than in those starting at pubertal age. Multivariate analysis showed that younger at the start of imatinib therapy ( P<0.001) and longer duration of imatinib therapy ( P<0.001) were significantly associated with severe growth impairment on imatinib therapy. Conclusions:Imatinib induced growth impairment in children with CML-CP. Younger the age of initiation and longer the duration of imatinib therapy, more obvious the effect of imatinib on growth impairment.