Objective To assess the methodology of papers on systematic reviews and meta-analysis of interventions published in Journal of Evidence-Based Medicine .Methods Basic data were extracted from 70 papers on systematic reviews and meta-analysis of interventions published in Journal of Evidence-Based Medicinefrom 2001 to 2011 .Methodology used in these papers was assessed according to the AMSTAR Scale.The data were input into the Excelland analyzed using the SPSS7.0 and Meta-Analyst software.Results The methodology used in 34 papers (48.6%) was assessed using the Cochrane bias risk assessment tools.Fund support, number of authors and their affiliated institutions did not sig-nificantly affect the total score of methodology used in the 70 papers .Conclusion The methodology used in papers on systematic reviews and meta-analysis of interventions published in Journal of Evidence-Based Medicine is not quite valid as its early design program and retrieval strategies are imperfect , and it does not provide the excluded literature list and the interest conflict.

Objective To assess the effect of PRISMA statement on intervention-related systematic reviews and meta-analyses published in Evidence-based medicine .Methods Intervention-related systematic reviews and meta-analyses published in Evidence-based medicine from 2001 to 2011 were assessed according to the PRISMA scale and analyzed by Meta Analysist software.Results Seventy intervention-related systematic reviews and meta-analyses involving 14-disease spectra were included in this study.PRISMA statement and systematic reviews and meta-analysespublished by au-thors in colleges and universities could improve their academic level (P<0.05), fund support and the number of authors showed no significant effect on their academic level.Conclusion Literature retrieval methods,literature screening methods,bias assessment methods, and other analyzing methods used systematic reviews and meta-analyses published in Evidence-based medicine and their academic level can be improved by PRISMA statement.

Objective To investigate the diagnostic value of MRI in reversible splenial lesion syndrome (RESLES) in children.Methods The clinical and MRI imaging data of 14 cases of RESLES in children were retrospectively reviewed.There were 4 males and 10 females,aging 11 to 35 months.Average age was (20±3) months.MRI studies were conducted in all the cases.Two experienced doctors analyzed independently the images and reached consensus.Results Fourteen cases showed the single abnormal signal in the splenial of corpus callosum on the initial cerebral MRI.Lesions in 10 of 14 cases appeared as isointensity on T1WI,hypo-intensity in 4 cases.Lesions in 14 cases were appeared as hyper-intensity on T2WI,hyper-/slightly hyper-intensity on FLAIR T2WI.The lesions were round,oval or irregular,with fuzzy boundary.DWI showed round or oval high signal with clear boundary.No edema around the lesion and no occupying effect were detected.After treatment,8 of 14 cases were reviewed after 7-14 d,and the abnormal signal in the corpus callosum disappeared in 5 cases,while the range was significantly reduced in 3 cases.MRI were reexamined after 1-2 months in 5 cases,and the lesions disappeared in the corpus callosum.One case didn't have MRI examination again after treatment and the clinical symptoms disappeared.Conclusions The clinical manifestations of RESLES in children are lack of specificity.And the cerebral MRI imaging is characterized by the reversible solitary lesion of the splenium,which can provide a reliable basis for clinical diagnosis and prognosis.

Objective To analyze the predictive value of serum levels of procalcitonin(PCT)and cytokines on the prognosis of patients with COVID-19 at admission.Methods From November 2022 to February 2023,patients diagnosed with COVID-19 who were admitted to Beijing Chest Hospital were enrolled.Chemiluminescence was used to detect serum PCT levels,and flow microsphere array was used to detect serum cytokines IL-1β,IL-2,IL-4,IL-5,IL-6,IL-8,IL-10,IL-12p70,IL-17A,IL-17F,IL-22,TNF-α,TNF-β,IFN-γ level.ICU admission,mechanical ventilation and in-hospital death were defined as poor prognosis.After excluding patients with bacterial infection,the relationship between serum PCT and cytokine levels at admission and the prognosis of COVID-19 patients was analyzed.After excluding patients with bacterial infection,the relationship between serum PCT and cytokine levels at admission and the prognosis of COVID-19 patients was analyzed.Results A total of 176 patients with complete data were included,including 134 in the PCT-normal group and 42 in the PCT-elevated group,with a median age of 71.50 years and 71.59%males.Patients in the PCT elevated-group had significantly higher rates of ICU admission(38.41%vs.13.11%,P<0.05),mechanical ventilation(76.92%vs.24.59%,P<0.001)and in-hospital mortality(38.46%vs.6.56%,P<0.001)were significantly higher than those in the PCT-normal group.Serum levels of cytokines IL-6(7.40 pg/mL vs.4.78 pg/mL,P = 0.033 4)and IL-8(10.97 pg/mL vs.5.92 pg/mL,P<0.001)were significantly higher in patients with poor prognosis than in those with good prognosis.The area under the curve for PCT,IL-6,and IL-8 to predict poor prognosis in COVID-19 patients was 0.687,0.660,and 0.746,respectively;sensitivity was 52.78%,55.17%,and 72.41%,respectively;and specificity was 81.58%,74.19%,and 74.19%,respectively,as calculated from the ROC curve.When PCT,IL-6 and IL-8 jointly predict the prognosis of COVID-19 patients,the area under the curve is 0.764,the sensitivity is 70.00%,and the specificity is 80.00%.Conclusion Serum PCT and cytokines IL-6 and IL-8 could be used as predictive markers for poor prognosis in patients with COVID-19.

The aim of this study was to investigate the role of selenoprotein M (SelM) in endoplasmic reticulum stress and apoptosis in nickel-exposed mouse hearts and to explore the detoxifying effects of melatonin. At 21 d after intraperitoneal injection of nickel chloride (NiCl₂) and/or melatonin into male wild-type (WT) and SelM knockout (KO) C57BL/6J mice, NiCl₂ was found to induce changes in the microstructure and ultrastructure of the hearts of both WT and SelM KO mice, which were caused by oxidative stress, endoplasmic reticulum stress, and apoptosis, as evidenced by decreases in malondialdehyde (MDA) content and total antioxidant capacity (T-AOC) activity. Changes in the messenger RNA (mRNA) and protein expression of genes related to endoplasmic reticulum stress (activating transcription factor 4 (ATF4), inositol-requiring protein 1 (IRE1), c-Jun N-terminal kinase (JNK), and C/EBP homologous protein (CHOP)) and apoptosis (B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, Caspase-9, and Caspase-12) were also observed. Notably, the observed damage was worse in SelM KO mice. Furthermore, melatonin alleviated the heart injury caused by NiCl₂ in WT mice but could not exert a good protective effect in the heart of SelM KO mice. Overall, the findings suggested that the antioxidant capacity of SelM, as well as its modulation of endoplasmic reticulum stress and apoptosis, plays important roles in nickel-induced heart injury.
Animals ; Male ; Mice ; Antioxidants/pharmacology* ; Apoptosis ; Endoplasmic Reticulum Stress ; Melatonin/pharmacology* ; Mice, Inbred C57BL ; Nickel/adverse effects* ; Selenoproteins/genetics* ; Heart/drug effects*

Using chemoproteomic techniques, we first identified EIF2AK2, eEF1A1, PRDX3 and VPS4B as direct targets of berberine (BBR) for its synergistically anti-inflammatory effects. Of them, BBR has the strongest affinity with EIF2AK2 via two ionic bonds, and regulates several key inflammatory pathways through EIF2AK2, indicating the dominant role of EIF2AK2. Also, BBR could subtly inhibit the dimerization of EIF2AK2, rather than its enzyme activity, to selectively modulate its downstream pathways including JNK, NF-κB, AKT and NLRP3, with an advantage of good safety profile. In EIF2AK2 gene knockdown mice, the inhibitory IL-1β, IL-6, IL-18 and TNF-α secretion of BBR was obviously attenuated, confirming an EIF2AK2-dependent anti-inflammatory efficacy. The results highlight the BBR's network mechanism on anti-inflammatory effects in which EIF2AK2 is a key target, and inhibition of EIF2AK2 dimerization has a potential to be a therapeutic strategy against inflammation-related disorders.