Developing and validating the Chinese nursing core competence scale for tertiary hospital nurses based on evolving health care needs in China.

Background: Evolving healthcare paradigms and shifting population health needs necessitate the advancement of nurses' core competencies. Under China's new-era health development strategy, there is an urgent demand to establish a culturally adapted, contemporary competency assessment framework.

Methods: This three-phase study involved: (1) Constructing a preliminary competency framework through systematic literature review and semi-structured interviews; (2) Refining dimensions via two-round Delphi consultations; (3) Validating the Chinese Nursing Core Competence Scale (CNCCS) with data from 1,415 nurses across seven geographical regions (Nov 2022-May 2023), assessing validity through content/structure/criterion-related validation and reliability via internal consistency/test-retest analysis.

Ameliorating macrophage pyroptosis via ANXA1/NLRP3/Caspase-1/GSDMD pathway: Ac2-26/OGP-loaded intelligent hydrogel enhances bone healing in diabetic periodontitis.

Craniofacial bone defect healing in periodontitis patients with diabetes background has long been difficult due to increased blood glucose levels which cause overproduction of reactive oxygen species (ROS) and a low pH environment. These conditions negatively affect the function of macrophages, worsen inflammation and oxidative stress, and ultimately, hinder osteoblasts' bone repair potential. In this study, we for the first time found that annexin A1 (ANXA1) expression in macrophages was reduced in a diabetic periodontitis (DP) environment, with the activation of the NLRP3/Caspase-1/GSDMD signaling pathway, and, eventually, increased macrophage pyroptosis.

Exploring the core competencies of clinical nurses in chinese tertiary hospitals: a qualitative content analysis.

Background: With the changes in social and medical environments and people's health needs, the nursing core competency should be updated and developed promptly. This study aimed to explore the core competencies of nurses in Chinese tertiary hospitals under the new health development strategy.

Methods: Descriptive qualitative research was conducted using qualitative content analysis.

Dehydration Accelerates Cytogenesis and Cyst Growth in Pkd1 Mice by Regulating Macrophage M2 Polarization.

Adult autosomal dominant polycystic kidney disease (ADPKD) has been shown to be related as a "third hit" to the occurrence of acute or chronic kidney injury. Here, we examined whether dehydration, as a common kidney risk factor, could cause cystogenesis in chronic-onset Pkd1 mice by regulating macrophage activation. First, we confirmed that dehydration accelerated cytogenesis in Pkd1 mice and that macrophages infiltrated the kidney tissues even earlier than macroscopic cyst formation.

Association between serum uric acid levels and simple renal cyst risk in a nondiabetic population: A nested case-control study.

Background: Previous studies have found a relationship between hypertension or cardiovascular disease and simple renal cysts (SRCs) in health check-up population, but SRCs incidence is still controversially associated with serum uric acid (SUA) concentration in the nondiabetic participants. In this single-centre nest case-control study, serum uric acid levels were examined in relation to the incidence of SRCs in nondiabetic individuals.

Method: Participants who underwent at least two renal ultrasound examinations with an interval of more than 12 months were enrolled.

Macrophages promote heat stress nephropathy in mice via the C3a-C3aR-TNF pathway.

Heat-stress nephropathy (HSN) is associated with recurrent dehydration. However, the mechanisms underlying HSN remain largely unknown. In this study, we evaluated the role of dehydration in HSN and kidney injury in mice.

Anoctamin 1 Inhibition Suppresses Cystogenesis by Enhancing Ciliogenesis and the Ciliary Dosage of Polycystins.

Background: Autosomal dominant polycystic kidney disease (ADPKD) is a ciliopathy characterized by abnormal tubular epithelial proliferation and fluid secretion. Anoctamin 1 (ANO1) is a calcium-dependent chloride channel. However, how ANO1 contributes to ADPKD is largely unexplored.

Matrix metalloproteinase-7 in platelet-activated macrophages accounts for cardiac remodeling in uremic mice.

Heart failure is the leading cause of mortality in patients with end-stage renal disease, and progressive cardiac remodeling is the key pathological basis of heart failure. However, the mechanism by which uremia-induced cardiac remodeling occurs is not well understood. Here, we showed that platelets were significantly activated in 5/6 nephrectomy-operated mice, and cardiac remodeling in the uremic mice was significantly improved when platelets were effectively depleted.

The role of the complement factor B-arginase-polyamine molecular axis in uremia-induced cardiac remodeling in mice.

The role of complement system in heart diseases is controversial. Besides, the mechanisms by which complement components participate in cardiac remodeling (CR) and heart failure during uremia are unclear. In this study, 5/6 nephrectomy was performed to adult mice to establish the uremic model and CR deteriorated over the course of uremia.

Interactions between Macrophages and Cyst-Lining Epithelial Cells Promote Kidney Cyst Growth in -Deficient Mice.

Background: Autosomal-dominant polycystic kidney disease (ADPKD) is the leading inherited renal disease worldwide. The proproliferative function of macrophages is associated with late-stage cyst enlargement in mice with PKD; however, the way in which macrophages act on cyst-lining epithelial cells (CLECs) has not been well elucidated.

Methods: We generated a rapid-onset PKD mouse model by inactivating on postnatal day 10 (P10) and compared cell proliferation and differential gene expression in kidney tissues of the PKD mice and wild-type (WT) littermates.

Saikosaponin-d inhibits proliferation by up-regulating autophagy via the CaMKKβ-AMPK-mTOR pathway in ADPKD cells.

Autosomal dominant polycystic kidney disease (ADPKD) is a common heritable human disease. Recently, the role of repressed autophagy in ADPKD has drawn increasing attention. Here, we investigate the mechanism underlying the effect of Saikosaponin-d (SSd), a sarcoplasmic/endoplasmic reticulum Ca ATPase pump (SERCA) inhibitor.

Olmesartan Prevents Microalbuminuria in db/db Diabetic Mice Through Inhibition of Angiotensin II/p38/SIRT1-Induced Podocyte Apoptosis.

Background/aims: Blockage of the renin-angiotensin II system (RAS) prevents or delays albuminuria in diabetic patients. The aim of this study was to investigate the inhibitory mechanism of the angiotensin receptor blocker olmesartan on albuminuria in a murine model of diabetic nephropathy.

Methods: Male db/db diabetic mice were fed with placebo or 20 mg/kg olmesartan by daily gavage for 12 weeks.

Resveratrol delays polycystic kidney disease progression through attenuation of nuclear factor κB-induced inflammation.

Background: Inflammation plays an important role in polycystic kidney disease (PKD). The current study aimed to examine the efficacy of the anti-inflammatory compound resveratrol in PKD and to investigate its underlying mechanism of action.

Methods: Male Han:SPRD (Cy/+) rats with PKD were treated with 200 mg/kg/day resveratrol or vehicle by gavage for 5 weeks.

The C-terminal tail of polycystin-1 regulates complement factor B expression by signal transducer and activator of transcription 1.

Inhibition of the overactivated alternative complement pathway in autosomal dominant polycystic kidney disease (ADPKD) retards disease progression in animal models; however, it remains unknown how complement factor B (CFB) is upregulated in ADPKD. Here, we showed that the overexpression of CFB in cystic kidneys is associated with increased JAK2/STAT1 activity and enhanced expression of the polycystin-1 C-terminal tail (PC1-CTT). Overexpression or blockage of STAT1 increased or decreased CFB expression and CFB promoter activity.