Objective? To establish a digital protection system for incontinence-associated dermatitis based on earlier prevention to reduce the incidence of incontinence-associated dermatitis. Methods? Based on the informationization of nursing platform, we run the digital protection system module of incontinence-related dermatitis based on the forward moving of the prevention gateway in Zhejiang Provincial People＇s Hospital. Through comparative study, 108 patients with incontinence and incontinence-related dermatitis from January to March 2018 were randomly selected as the pre-operation data, and 108 patients with incontinence and incontinence-related dermatitis from January to March 2019 as the post-operation data. The nurses of the two groups were observed and compared in terms of their assessment accuracy in patients＇ incontinence risk, position and Incontinence Associated Dermatitis Severity(IADS), clinical staging, and implementation of prevention strategies. Meanwhile, the incidence of incontinence-related dermatitis among all inpatients in the hospital from January to March in 2018 was compared with the same period of 2019. Results? After the operation of the digital protection system for incontinence-related dermatitis based on earlier prevention, the nursing staff's accuracy rate in the risk assessment of incontinence (χ2=38.095,P＜0.01), IADS (χ2=64.901,P＜0.01), clinical staging accuracy (χ2=42.424,P＜0.01) and the implementation of protective measures (χ2=50.000, P＜0.01) had significant statistical differences. The incidence of incontinence-related dermatitis in hospitalized patients decreased from 0.35% before operation to 0.06% after operation with statistical significance(χ2=41.031, P＜0.01). Conclusions? The operation of the digital protection system for incontinence-associated dermatitis based on earlier prevention can reduce the incidence of incontinence-associated dermatitis and improve the prevention and management competence of nursing staff.

Calcific aortic valve disease(CAVD)is the most common disease affecting the heart valves,character-ized by thickening,fibrosis,and mineralization of the aortic valve leaflets.Currently,there is no effective pharmacologi-cal treatment.Aortic valve calcification is a complex and multifactorial process involving valve inflammation,fibrosis,calcification,valve thickening and outflow tract obstruction.The exact pathophysiological mechanisms of CAVD are not fully understood,but many studies have suggested that innate immune cells play a key role in the development of aortic valve calcification.This review focuses on the current role of innate immune cells in the development of CAVD.

Congenital hydrocephalus is a major neurological disorder with high rates of morbidity and mortality; however, the underlying cellular and molecular mechanisms remain largely unknown. Reproducible animal models mirroring both embryonic and postnatal hydrocephalus are also limited. Here, we describe a new mouse model of congenital hydrocephalus through knockout of β-catenin in Nkx2.1-expressing regional neural progenitors. Progressive ventriculomegaly and an enlarged brain were consistently observed in knockout mice from embryonic day 12.5 through to adulthood. Transcriptome profiling revealed severe dysfunctions in progenitor maintenance in the ventricular zone and therefore in cilium biogenesis after β-catenin knockout. Histological analyses also revealed an aberrant neuronal layout in both the ventral and dorsal telencephalon in hydrocephalic mice at both embryonic and postnatal stages. Thus, knockout of β-catenin in regional neural progenitors leads to congenital hydrocephalus and provides a reproducible animal model for studying pathological changes and developing therapeutic interventions for this devastating disease.
Animals ; Disease Models, Animal ; Hydrocephalus/genetics* ; Mice ; Mice, Knockout ; Neurons ; beta Catenin/genetics*

Abivertinib, a third-generation tyrosine kinase inhibitor, is originally designed to target epidermal growth factor receptor (EGFR)-activating mutations. Previous studies have shown that abivertinib has promising antitumor activity and a well-tolerated safety profile in patients with non-small-cell lung cancer. However, abivertinib also exhibited high inhibitory activity against Bruton's tyrosine kinase and Janus kinase 3. Given that these kinases play some roles in the progression of megakaryopoiesis, we speculate that abivertinib can affect megakaryocyte (MK) differentiation and platelet biogenesis. We treated cord blood CD34⁺ hematopoietic stem cells, Meg-01 cells, and C57BL/6 mice with abivertinib and observed megakaryopoiesis to determine the biological effect of abivertinib on MK differentiation and platelet biogenesis. Our in vitro results showed that abivertinib impaired the CFU-MK formation, proliferation of CD34⁺ HSC-derived MK progenitor cells, and differentiation and functions of MKs and inhibited Meg-01-derived MK differentiation. These results suggested that megakaryopoiesis was inhibited by abivertinib. We also demonstrated in vivo that abivertinib decreased the number of MKs in bone marrow and platelet counts in mice, which suggested that thrombopoiesis was also inhibited. Thus, these preclinical data collectively suggested that abivertinib could inhibit MK differentiation and platelet biogenesis and might be an agent for thrombocythemia.
Acrylamides/pharmacology* ; Animals ; Blood Platelets/drug effects* ; Cell Differentiation ; Megakaryocytes/drug effects* ; Mice ; Mice, Inbred C57BL ; Piperazines/pharmacology* ; Pyrimidines/pharmacology*