Objective To explore the effect of miR-582-5p on Mycobacterium tuberculosis (Mtb)-infected macrophages by regulating dual specificity phosphatase 1 (DUSP1). Methods THP-1 macrophages were divided into six groups: control group, Mtb group, inhibitor-NC group, miR-582-5p inhibitor group, miR-582-5p inhibitor+si-NC group, and miR-582-5p inhibitor+si-DUSP1 group. QRT-PCR was applied to detect the gene expression of miR-582-5p and DUSP1 in cells. ELISA kit was used to detect the levels of interferon γ (IFN-γ), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and interleukin 1β (IL-1β). CCK-8 method was applied to detect cell proliferation. Flow cytometry was applied to detect cell apoptosis rate. Western blot analysis was used to measure the protein expression levels of B-cell lymphoma 2 (Bcl2), Bcl2-associated X (BAX), and cleaved-caspase 3 (c-caspase-3) in cells. In addition, the target relationship between miR-582-5p and DUSP1 was verified. Results Compared with the control group, the expression of miR-582-5p, levels of IFN-γ, IL-6, TNF-α, IL-1β, bacterial load and OD450 values (24 h, 48 h), and the protein expression of Bcl2 in macrophages were higher in the Mtb group, while the mRNA expression of DUSP1, apoptosis rate, and the protein expression levels of c-caspase-3, BAX and DUSP1 were lower. Compared with the Mtb group and the inhibitor-NC group, the above-mentioned indicators in the miR-582-5p inhibitor group were partially reversed. Down-regulation of DUSP1 expression partially reversed the inhibitory effect of down-regulation of miR-582-5p expression on Mtb-infected macrophages. Conclusion Inhibiting the expression of miR-582-5p can up-regulate DUSP1, thereby inhibiting the proliferation and inflammatory response of Mtb-infected macrophages and promoting cell apoptosis.
Humans ; Macrophages/metabolism* ; Dual Specificity Phosphatase 1/metabolism* ; MicroRNAs/metabolism* ; Mycobacterium tuberculosis/physiology* ; Tuberculosis/microbiology* ; Apoptosis/genetics* ; THP-1 Cells ; Cell Proliferation/genetics* ; Interferon-gamma/genetics* ; Tumor Necrosis Factor-alpha/genetics* ; Interleukin-1beta/genetics*

Background Asthma poses a serious threat to children's growth, development, and mental health, thus there has been an increasing focus on the control of asthma morbidity in children and the assessment of its risk factors. A growing body of research has found that exposure to ambient air pollutants an significatly increase the risk of childhood asthma. Objective To understand the changes of ambient air pollutant concentrations in Nanjing and asthma outpatient visits to Nanjing Children's Hospital, and to quantitatively analyze the effects of exposure to different ambient air pollutants on children's asthma outpatient visits. Methods Daily data of ambient air pollutants fine particulate matter (PM_2.5), inhalable particle (PM₁₀), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), carbon monoxide (CO), ozone (O₃), meteorological factors (air temperature & relative humidity), and outpatient visits due to asthma in the hospital from January 1, 2019 to December 31, 2023 were collected, and a generalized additive model based on quasi poisson distributions was used to quantitatively analyze the short-term effects of ambient air pollutant exposure on outpatient visits due to asthma in the hospital. Results The annual average concentrations of PM_2.5, PM₁₀, SO₂, and NO₂ in Nanjing from 2019 to 2023 did not exceed the national limits. For single-day lagged effects, the single-pollutant model showed that the effects of PM_2.5, PM₁₀, NO₂, and CO on children's asthma outpatient visits were greatest for every 10 units increase at lag0, with excess risk (ER) of 1.39% (95%CI: 0.65%, 2.14%), 1.46% (95%CI: 0.97%, 1.95%), 5.46% (95%CI: 4.36%, 6.57%), and 0.18% (95%CI: 0.11%, 0.26%), respectively, and SO₂ reached the maximum effect at lag1, with an ER of 23.15% (95%CI: 13.57%, 33.53%) for each 10 units increase in concentration. Different pollutants reached their maximum cumulative lag effects at different time. The PM₁₀, PM_2.5, SO₂, NO₂, and CO showed the largest cumulative lag effects at lag01, lag01, lag02, lag02, and lag03, respectively, with ERs of 1.35% (95%CI: 0.77%, 1.92%), 0.96% (95%CI: 0.10%, 1.83%), 28.50% (95%CI: 15.49%, 42.98%), 6.92% (95%CI: 5.53%, 8.33%), and 0.31% (95%CI: 0.20%, 0.42%), respectively. The influences of PM_2.5 and PM₁₀ on outpatient visits due to asthma in the hospital became more pronounced with advancing age, while the associations with NO₂, SO₂, and CO were weakened as children grew older. Conclusion Ambient air pollutants (PM_2.5, PM₁₀, SO₂, NO₂, CO) can increase childhood asthma visits, and different pollutants have varied effects on the number of asthmatic children's visits at different ages.

Objective:To investigate the expression and biological function of AHNAK nucleoprotein 2(AHNAK2)in thyroid cancer.Methods:The expression of AHNAK2 in thyroid cancer tissues was analyzed using The Cancer Genome Atlas(TCGA),Gene Expression Omnibus(GEO),and Human Protein Atlas(HPA)databases.The correlation between AHNAK2 expression and patients'prognosis,clinicopathological characteristics,immune cell infiltration,and subcellular localization was evaluated.AHNAK2 mRNA expression in thyroid cancer cells was detected by RT-qPCR.A stable AHNAK2 knockdown TPC-1 cell line was established via lentiviral transfection,and the transfection efficiency was validated using RT-qPCR and Western blot.TPC-1 cells were divided into the sh-NC and sh-AHNAK2 groups.The impact of AHNAK2 knockdown on TPC-1 cell proliferation,migration,and invasion was assessed using colony formation assay,CCK-8 assay,wound healing assay,and Transwell assay.Results:AHNAK2 was up-regulated in thyroid cancer tissues and was associated with poor prognosis.It was primarily localized in the cytoplasm and cytoplasmic membrane.GO analysis revealed that AHNAK2 was mainly enriched in biological processes such as organelle disassembly,cellular components such as the spindle,and molecular functions such as microtubule binding.KEGG pathway analysis indicated that AHNAK2 was primarily enriched in the cell cycle pathway.Immune infiltration analysis suggested that AHNAK2 expression was positively correlated with macrophage infiltration and negatively correlated with plasmacytoid dendritic cell infiltration in thyroid cancer.AHNAK2 was overexpressed in multiple thyroid cancer cell lines.In vitro experiments demonstrated that AHNAK2 knockdown inhibited the proliferation,migration,and invasion of TPC-1 cells.Conclusion:AHNAK2 may serve as an important prognostic biomarker and immunotherapy target for thyroid cancer,as it can promote the proliferation,migration and invasion of thyroid cancer cells.

OBJECTIVE To standardize the strategies for prevention and control of Chikungunya(CHIK)in healthcare in-stitutions so as to reduce the risk of transmission in the institutions.METHODS A working group comprising the ex-perts in hospital infection control,infectious diseases,and microbiology systematically reviewed domestic and international evidence and current guidelines,integrated China's vector ecology and healthcare realities,conducted two rounds of Delphi to achieve expert consensus,and graded the evidence and recommendation strength using the Oxford Centre for Evidence Based Medicine system.RESULTS The consensus issues 18 actionable recommendations on triage,patient mosquito-proof isolation,integrated vector control,protection of susceptible populations,environmental cleaning and disinfection,specimen management,medical textile handling,and outbreak emergency response,with each statement assigned an evi-dence level and recommendation strength.CONCLUSION This consensus is for the first time in China to provide evidence-graded strategies for control of CHIK in healthcare institutions,offering work flow-oriented,implementable guidance for clinicians,laboratorians,and infection-control personnel under different risk scenarios and enhancing the comprehensive coping capacity of the healthcare institutions.

Objective:To investigate the expression and biological function of AHNAK nucleoprotein 2(AHNAK2)in thyroid cancer.Methods:The expression of AHNAK2 in thyroid cancer tissues was analyzed using The Cancer Genome Atlas(TCGA),Gene Expression Omnibus(GEO),and Human Protein Atlas(HPA)databases.The correlation between AHNAK2 expression and patients'prognosis,clinicopathological characteristics,immune cell infiltration,and subcellular localization was evaluated.AHNAK2 mRNA expression in thyroid cancer cells was detected by RT-qPCR.A stable AHNAK2 knockdown TPC-1 cell line was established via lentiviral transfection,and the transfection efficiency was validated using RT-qPCR and Western blot.TPC-1 cells were divided into the sh-NC and sh-AHNAK2 groups.The impact of AHNAK2 knockdown on TPC-1 cell proliferation,migration,and invasion was assessed using colony formation assay,CCK-8 assay,wound healing assay,and Transwell assay.Results:AHNAK2 was up-regulated in thyroid cancer tissues and was associated with poor prognosis.It was primarily localized in the cytoplasm and cytoplasmic membrane.GO analysis revealed that AHNAK2 was mainly enriched in biological processes such as organelle disassembly,cellular components such as the spindle,and molecular functions such as microtubule binding.KEGG pathway analysis indicated that AHNAK2 was primarily enriched in the cell cycle pathway.Immune infiltration analysis suggested that AHNAK2 expression was positively correlated with macrophage infiltration and negatively correlated with plasmacytoid dendritic cell infiltration in thyroid cancer.AHNAK2 was overexpressed in multiple thyroid cancer cell lines.In vitro experiments demonstrated that AHNAK2 knockdown inhibited the proliferation,migration,and invasion of TPC-1 cells.Conclusion:AHNAK2 may serve as an important prognostic biomarker and immunotherapy target for thyroid cancer,as it can promote the proliferation,migration and invasion of thyroid cancer cells.

OBJECTIVE To standardize the strategies for prevention and control of Chikungunya(CHIK)in healthcare in-stitutions so as to reduce the risk of transmission in the institutions.METHODS A working group comprising the ex-perts in hospital infection control,infectious diseases,and microbiology systematically reviewed domestic and international evidence and current guidelines,integrated China's vector ecology and healthcare realities,conducted two rounds of Delphi to achieve expert consensus,and graded the evidence and recommendation strength using the Oxford Centre for Evidence Based Medicine system.RESULTS The consensus issues 18 actionable recommendations on triage,patient mosquito-proof isolation,integrated vector control,protection of susceptible populations,environmental cleaning and disinfection,specimen management,medical textile handling,and outbreak emergency response,with each statement assigned an evi-dence level and recommendation strength.CONCLUSION This consensus is for the first time in China to provide evidence-graded strategies for control of CHIK in healthcare institutions,offering work flow-oriented,implementable guidance for clinicians,laboratorians,and infection-control personnel under different risk scenarios and enhancing the comprehensive coping capacity of the healthcare institutions.

Late-onset cobalamin C (cblC) deficiency is an inherited organic acid metabolic disorder characterized by clinical heterogeneity, which often presents challenges in accurate diagnosis. This article presents a case study of a young female patient who initially experienced epileptic-like seizures. Over a span of 9 years, she subsequently developed psychotic symptoms. Her condition has been steadily deteriorating over a period of 16 years, leading to mutism, loss of ambulation, dysphagia, and urinary and fecal incontinence. Although electroencephalography and cranial computed tomography did not show significant findings during the course of the illness, cranial magnetic resonance imaging showed evidence of cerebral atrophy. Biochemical analysis revealed elevated levels of blood homocysteine and urinary methylmalonic acid-2. Genetic testing identified two pathogenic mutations in the MMACHC gene, confirming the diagnosis of late-onset cobalamin C (cblC) deficiency. Despite receiving interventions such as antiepileptic and antipsychotic medications during the diagnostic and therapeutic phases, the patient′s clinical progress remained limited.Following the definitive diagnosis, targeted metabolic therapy was initiated, leading to significant clinical improvement. This article provides a comprehensive review of the patient′s clinical data, along with a synthesis of relevant literature, in order to enhance the awareness of psychiatric practitioners regarding this rare disorder. The primary objective is to promote early identification, prompt diagnosis, and timely intervention.

Late-onset cobalamin C (cblC) deficiency is an inherited organic acid metabolic disorder characterized by clinical heterogeneity, which often presents challenges in accurate diagnosis. This article presents a case study of a young female patient who initially experienced epileptic-like seizures. Over a span of 9 years, she subsequently developed psychotic symptoms. Her condition has been steadily deteriorating over a period of 16 years, leading to mutism, loss of ambulation, dysphagia, and urinary and fecal incontinence. Although electroencephalography and cranial computed tomography did not show significant findings during the course of the illness, cranial magnetic resonance imaging showed evidence of cerebral atrophy. Biochemical analysis revealed elevated levels of blood homocysteine and urinary methylmalonic acid-2. Genetic testing identified two pathogenic mutations in the MMACHC gene, confirming the diagnosis of late-onset cobalamin C (cblC) deficiency. Despite receiving interventions such as antiepileptic and antipsychotic medications during the diagnostic and therapeutic phases, the patient′s clinical progress remained limited.Following the definitive diagnosis, targeted metabolic therapy was initiated, leading to significant clinical improvement. This article provides a comprehensive review of the patient′s clinical data, along with a synthesis of relevant literature, in order to enhance the awareness of psychiatric practitioners regarding this rare disorder. The primary objective is to promote early identification, prompt diagnosis, and timely intervention.

Myosteatosis is the main manifestation of malnutrition and is a common complication of chronic liver diseases, with a negative impact on the progression and prognosis of liver diseases. There is no gold standard for the diagnosis of myosteatosis, and CT is a commonly used diagnostic method. Myosteatosis in chronic liver diseases has diverse mechanisms, and hyperammonemia, increased cathepsin D level in circulation, insulin resistance, mitochondrial dysfunction, and chronic systemic microinflammation play an important role in myosteatosis. Early intervention of these factors can improve prognosis. With reference to related studies in China and globally, this article reviews the features, diagnostic methods, pathogenesis, treatment, and intervention of myosteatosis.

Antipsychotic medications are commonly used to treat schizophrenia,but they can have negative effects on lipid metabolism,leading to an increased risk of cardiovascular diseases,reduced life expectancy,and difficulties with treatment adherence.The specific mechanisms by which antipsychotics disrupt lipid metabolism are not well understood.Sterol regulatory element-binding proteins(SREBPs)are important transcriptional factors that regulate lipid metabolism.Proprotein convertase subtilisin/kexin type 9(PCSK9),a gene regulated by SREBPs,plays a critical role in controlling levels of low-density lipoprotein cholesterol(LDL-C)and has become a focus of research on lipid-lowering drugs.Recent studies have shown that antipsychotic drugs can affect lipid metabolism through the SREBP/PCSK9 pathway.A deep understanding of the mechanism for this pathway in antipsychotic drug-related metabolic abnormalities will promote the prevention of lipid metabolism disorders in patients with schizophrenia and the development and application of new drugs.