In recent years, the situation of climate change has intensified, posing a threat to public health. There is an urgent need to promote public health adaptation actions to climate change. In January 2025, the National Disease Control and Prevention Administration issued the "Guidelines for Public Health Adaptation Actions to Climate Change" (hereinafter referred to as the "Guidelines"). The Guidelines put forward 20 items of guidance on six categories of public health adaptation actions, including understanding basic concepts, comprehending important policies, learning core knowledge, paying attention to key populations, practicing a low-carbon lifestyle, and mastering protection skills. It elaborates on the key concepts and the latest policies that the public needs to understand, and also provides the behavioral concepts and protection skills that should be mastered to adapt to climate change. This article provides a systematic interpretation of the Guidelines, introducing the background, ideas, connotations, and applications of their compilation, with the aim of enhancing society′s cognitive understanding of the Guidelines.

In recent years, the situation of climate change has intensified, posing a threat to public health. There is an urgent need to promote public health adaptation actions to climate change. In January 2025, the National Disease Control and Prevention Administration issued the "Guidelines for Public Health Adaptation Actions to Climate Change" (hereinafter referred to as the "Guidelines"). The Guidelines put forward 20 items of guidance on six categories of public health adaptation actions, including understanding basic concepts, comprehending important policies, learning core knowledge, paying attention to key populations, practicing a low-carbon lifestyle, and mastering protection skills. It elaborates on the key concepts and the latest policies that the public needs to understand, and also provides the behavioral concepts and protection skills that should be mastered to adapt to climate change. This article provides a systematic interpretation of the Guidelines, introducing the background, ideas, connotations, and applications of their compilation, with the aim of enhancing society′s cognitive understanding of the Guidelines.

BACKGROUND: Benvitimod cream, a novel synthetic small molecule, was effective in treating mild-to-moderate plaque psoriasis. We conducted a phase III clinical trial to assess the efficacy and safety of benvitimod cream in patients with mild-to-moderate plaque psoriasis. METHODS: We randomly assigned 686 patients (2:1:1) to receive 1% benvitimod cream, 0.005% calcipotriol ointment or placebo twice a day for 12 weeks. The primary efficacy end points were the percentage of patients with a 75% or greater reduction from baseline in the psoriasis area and severity index (PASI 75) score and with a score of 0 or 1 in static physician's global assessment (sPGA) at week 12. RESULTS: The results showed that 50.4% of patients in the benvitimod group achieved PASI 75, which was significantly higher than that in the calcipotriol (38.5%, P < 0.05) and placebo (13.9%, P < 0.05) groups. The proportion of patients achieving an sPGA score 0 or 1 was 66.3% in the benvitimod group and 63.9% in the calcipotriol group, which were both significantly higher than that in the placebo group (34%, P < 0.05). In the long-term follow-up study, 50.8% of patients experienced recurrence. After retreatment with 1% benvitimod, 73.3% of patients achieved an sPGA score of 0 or 1 again at week 52. Adverse events included application site irritation, follicular papules, and contact dermatitis. No systemic adverse reactions were reported. CONCLUSION: During this 12-week study, benvitimod cream was demonstrated with high effectiveness and safety in patients with mild-to-moderate plaque psoriasis. TRIAL REGISTRATION Chinese Clinical Trial Registry (ChiCTR), ChiCTR-TRC-13003259; http://www.chictr.org.cn/showprojen.aspx?proj=6300.
Double-Blind Method ; Follow-Up Studies ; Humans ; Ointments ; Psoriasis/drug therapy* ; Resorcinols ; Severity of Illness Index ; Stilbenes ; Treatment Outcome

Objectives To explore the calcium signaling mechanism of STIM1 in breast cancer cells. Meth-ods After SiRNA interruption, Western blot and Transwell were used to measure protein expression of STIM1 and cell migration in MDA-MB-231 cells respectively. The relationship between STIM1 and SOCE calcium signaling were analysed by Laser confocal microscopy. Western blots were used to measure protein expression of FAK after si-lence STIM1. Results The numbers of cells without STIM1 were significantly lower than those cells with STIM1 by Transwell assay. STIM1 mediated SOCE in MDA-MB-231. Blocking SOCE might inhibite cells migration. Si-lence STIM1 did not affect the expression or activation of FAK in MDA-MB-231 cells. Conclusion STIM1 influ-ences cell migration through SOCE pathway in breast cancer cells, which is independent on the expression or activa-tion of FAK.

AIM: JS-38 (mitothiolore), a synthetic version of a metabolite isolated from Xenorhabdus sp., was evaluated for its anti-tumor and white blood cell (WBC) elevating activities. METHOD: These anti-proliferative activities were assessed in vitro using a panel of ten cell lines. The anti-tumor activities were tested in vivo using B16 allograft mouse models and xenograft models of A549 human lung carcinoma and QGY human hepatoma in nude mice. The anti-tumor interactions of JS-38 and cyclophosphamide (CTX) or 5-fluorouracil (5-Fu) were studied in a S180 sarcoma model in ICR mice. Specific stimulatory effects were determined on peripheral neutrophils in normal and CTX- and 5-Fu-induced neutropenic mice. RESULTS: The IC50 values ranged from 0.1 to 2.0 μmol·L(-1). JS-38 (1 μmol·L(-1)) caused an increase in A549 tumor cell apoptosis. Multi-daily gavage of JS-38 (15, 30, and 60 mg·kg(-1)·d(-1)) inhibited in vivo tumor progression without a significant effect on body weight. JS-38 additively enhanced the in vivo anti-tumor effects of CTX or 5-Fu. JS-38 increased peripheral neutrophil counts and neutrophil rates in normal BALB/c mice almost as effectively as granulocyte colony-stimulating factor (G-CSF). In mice with neutropenia induced by CTX or 5-Fu, JS-38 rapidly restored neutrophil counts. CONCLUSION These results suggest that JS-38 has anti-tumor activity, and also has the ability to increase peripheral blood neutrophils.
Animals ; Antineoplastic Agents ; administration & dosage ; metabolism ; Cell Count ; Female ; Humans ; Hydrocarbons, Fluorinated ; administration & dosage ; metabolism ; Lung Neoplasms ; drug therapy ; physiopathology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred ICR ; Neutrophils ; cytology ; drug effects ; Xenorhabdus ; chemistry ; metabolism