Explore the vast range of titles available.

ObjectiveThis study aimed to investigate the work engagement of clinical nursing teachers and examine whether psychological capital and perceived supervisor social support mediates the association between role stress and work engagement among clinical nursing teachers.DesignA cross-sectional study design was used.SettingThis study was conducted in five tertiary hospitals affiliated with medical universities in Shandong Province, China.ParticipantsA total of 412 clinical nursing teachers were recruited out of which 406 completed the questionnaires effectively.MethodsQuestionnaires were administered offline and the items consisted of social demographic characteristics, scale related to role stress, psychological capital, perceived supervisor social support and work engagement. T-tests, one-way analysis of variance and Pearson’s correlation analysis were conducted using SPSS, and mediation analysis was performed using structural equation modelling.ResultsThe work engagement scores of clinical nursing teachers were high, with an average score of 4.76±0.69. Structural equation modelling showed a good fit of the data to the hypothesised model. Role stress did not directly affect work engagement (β=0.057, p>0.001). However, a strong indirect effect of role stress on work engagement (β=−0.373, p<0.001) mediated by psychological capital and perceived supervisor social support was observed, with path coefficient of −0.319 (p<0.01) and −0.054 (p<0.01), respectively. The model explains 57% of the variance in work engagement.ConclusionPsychological capital and perceived supervisor social support fully mediated the relationship between role stress and work engagement among clinical nursing teachers. Thus, to promote the work engagement of clinical nursing teachers, their psychological capital needs to be improved. Furthermore, superiors should provide more support, particularly to clinical nursing teachers experiencing high role stress.

Ocular inoculation of a clade 2.3.4.4b highly pathogenic avian influenza A(H5N1) virus caused severe and fatal infection in ferrets. Virus was transmitted to ferrets in direct contact. The results highlight the potential capacity of these viruses to cause human disease after either respiratory or ocular exposure.

Since 2020, there has been unprecedented global spread of highly pathogenic avian influenza A(H5N1) in wild bird populations with spillover into a variety of mammalian species and sporadically humans 1 . In March 2024, clade 2.3.4.4b A(H5N1) virus was first detected in dairy cattle in the USA, with subsequent detection in numerous states 2 , leading to more than a dozen confirmed human cases 3 , 4 . In this study, we used the ferret, a well-characterized animal model that permits concurrent investigation of viral pathogenicity and transmissibility 5 , in the evaluation of A/Texas/37/2024 (TX/37) A(H5N1) virus isolated from a dairy farm worker in Texas 6 . Here we show that the virus has a remarkable ability for robust systemic infection in ferrets, leading to high levels of virus shedding and spread to naive contacts. Ferrets inoculated with TX/37 rapidly exhibited a severe and fatal infection, characterized by viraemia and extrapulmonary spread. The virus efficiently transmitted in a direct contact setting and was capable of indirect transmission through fomites. Airborne transmission was corroborated by the detection of infectious virus shed into the air by infected animals, albeit at lower levels compared to those of the highly transmissible human seasonal and swine-origin H1 subtype strains. Our results show that despite maintaining an avian - like receptor-binding specificity, TX/37 exhibits heightened virulence, transmissibility and airborne shedding relative to other clade 2.3.4.4b virus isolated before the 2024 cattle outbreaks 7 , underscoring the need for continued public health vigilance. Analysis of a human isolate of the A/Texas/37/2024 strain of highly pathogenic avian influenza A(H5N1) virus in the ferret model demonstrates its pathogenicity and transmission in both direct and indirect contact settings, including airborne transmission.

We aimed to detect the functions of miR‐375/SLC7A11 axis on oral squamous cell carcinoma (OSCC) cell proliferation and invasion. Expression levels of miR‐375 and SLC7A11 in OSCC tissues and cells were measured with RT‐qPCR and western blot. Targeting site was predicted by TargetScan and confirmed by dual luciferase reporting assay. By way of manipulating the expression level of miR‐375 and SLC7A11 in CAL‐27 and Tca8113 cell lines, the cell biological abilities were evaluated. MTT, colony formation, Transwell, wound healing assays and flow cytometry were used to detect OSCC cell viability, proliferation, invasion, migration and apoptosis, respectively. MiR‐375 was significantly downregulated in OSCC tissues and cells compared to adjacent tissue and normal oral cell line respectively while SLC7A11 was upregulated. Targeting relationship was verified by luciferase reporting assay, and miR‐375 could effectively suppress SLC7A11 level in OSCC cells. Replenishing of miR‐375 significantly repressed OSCC cell viability, proliferation, invasion and migration and induced cell apoptosis and G1/G0 arrest. Overexpression of SLC7A11 recovered those biological abilities in miR‐375 upregulated cells. Collective data suggested that miR‐375 served as a tumor suppressor via regulating SLC7A11. Replenishing of miR‐375 or knockout of SLC7A11 could be therapeutically exploited. MTT, colony formation, Transwell, wound healing assays and flow cytometry were used to detect oral squamous cell carcinoma (OSCC) cell viability, proliferation, invasion, migration and apoptosis, respectively. Collective data suggested that miR‐375 served as a tumor suppressor via regulating SLC7A11. Replenishing of miR‐375 or knockout of SLC7A11 could be therapeutically exploited.

As the number of human infections with avian and swine influenza viruses continues to rise, the pandemic risk posed by zoonotic influenza viruses cannot be underestimated. Implementation of global pandemic preparedness efforts has largely focused on H5 and H7 avian influenza viruses; however, the pandemic threat posed by other subtypes of avian influenza viruses, especially the H9 subtype, should not be overlooked. In this review, we summarize the literature pertaining to the emergence, prevalence and risk assessment of H9N2 viruses, and add new molecular analyses of key mammalian adaptation markers in the hemagglutinin and polymerase proteins. Available evidence has demonstrated that H9N2 viruses within the Eurasian lineage continue to evolve, leading to the emergence of viruses with an enhanced receptor binding preference for human-like receptors and heightened polymerase activity in mammalian cells. Furthermore, the increased prevalence of certain mammalian adaptation markers and the enhanced transmissibility of selected viruses in mammalian animal models add to the pandemic risk posed by this virus subtype. Continued surveillance of zoonotic H9N2 influenza viruses, inclusive of close genetic monitoring and phenotypic characterization in animal models, should be included in our pandemic preparedness efforts.

Pure invasive apocrine carcinoma is a rare type of primary breast cancer, constituting ~1% of all breast cancers. Since most pure invasive apocrine carcinomas are triple negative, the lack of targeted therapies for triple-negative breast cancer has fostered efforts to discover actionable molecular targets in these tumors. In this study, we analyzed the clinicopathologic characteristics and comprehensive genomic profiling of 18 patients with pure triple-negative apocrine carcinomas (TNACs) using a 324-gene panel assay (FoundationOne CDx). The median age of these patients was 55.5 years, and the postmenopausal status rate was 77.8%. In total, 83.3% of patients were diagnosed with histological grade II, and 16.7% were diagnosed with grade III. The majority of patients presented at an early tumor-node-metastasis (TNM) stage (I: 38.9%; II: 50.0%; and III: 11.1%). The mean Ki-67 index was 9.7%, and the percent of PD-L1 positivity was 11.7%. With a median follow-up period of 76.5 months, one patient died, and two experienced distant metastases. There were 61 clinically relevant genomic alterations among all 18 pure TNACs, and the mean tumor mutation burden (TMB) was 3 Mut/Mb. The top ranked altered genes were PIK3CA (72.2%), PTEN (33.3%) and TP53 (27.8%). There were four novel mutations found in PTEN and an actionable rearrangement involving FGFR2-TACC2 that has not been reported in breast cancer before. In total, 88.9%, 50%, 44.4%, and 16.7% of TNACs had at least one clinically relevant genomic alteration in genes involved in the PI3K/mTOR, cell cycle, RAS/RAF/MEK and growth factor receptor-related pathways, respectively. All patients had at least one clinically relevant genomic alteration, and 94.4% had at least one actionable alteration. To the best of our knowledge, this study is the largest genomic sequencing cohort of pure TNACs. Incorporation of comprehensive genomic profiling into TNACs might shed light on potential therapeutic opportunities for both targeted drugs and immune checkpoint inhibitors.

Background Clinical nursing practice has a significant meaning and role in nursing education. Efficient clinical nursing practices under the guidance of clinical nursing teachers can promote patient safety and healthcare quality. This study aimed to investigate the profiles of clinical nursing teachers’ role stress, determine whether sociodemographic factors and psychological capital correlate with different role stress profiles. It also examined the relationship between different role stress profiles and work engagement. Design Cross-sectional study. Methods A total of 412 clinical nursing teachers were enrolled in China through convenience sampling. The Role Stress Scale, Psychological Capital Questionnaire, Work Engagement Scale, and sociodemographic questionnaire were used. Latent profile analysis (LPA) was conducted by using Mplus version 8.0 to identify the different role stress profiles of clinical nursing teachers. Univariate and multivariate unordered logistic regression analyses were used to identify the factors associated with the profiles. Results Four hundred and six valid questionnaires were returned. The findings of latent profile analysis showed three profiles: low role stress-high lack of teaching resources profile (34.3%), moderate role stress profile (57.0%), and high role stress-low lack of teaching resources profile (11.7%). Multivariate unordered logistic regression showed that clinical nursing teachers with lower education levels, contract employment, regular qualification audits, and lower psychological capital scores were more likely to belong to Profiles 2 and 3 when Profile 1 was used as a reference. The analysis of variance revealed that the work engagement scores of Profile 3 were significantly lower than those of Profiles 1 and 2. Conclusions Clinical nursing teachers reported heterogeneous sociodemographic and psychological capital, with significant differences in the degree of role stress between the identified profiles. Targeted interventions should be provided according to the role stress profiles to improve work engagement.

The new H7N9 influenza virus, recently emerged in China, can replicate in human airway cells and in the respiratory tract of ferrets to a higher level than can seasonal H3N2 virus and shows higher lethality in mice than genetically related H7N9 and H9N2 viruses, but shows limited transmission in ferrets by respiratory droplets. Transmission of emerging H7N9 virus By 20 July 2013, there had been 134 laboratory-confirmed human cases of infection with avian influenza A H7N9 virus infection, including 43 deaths. Yoshihiro Kawaoka and colleagues characterize the biology of two recent isolates of the virus. They provide a wealth of data from infections in mice, pigs, macaques and ferrets. H7N9 virus is shown to be less sensitive to neuraminidase inhibitors than pandemic H1N1 virus, but equally susceptible to an experimental polymerase inhibitor. Terrence Tumpey and colleagues determine the capacity of two clinical H7N9 isolates to cause disease and transmit between mammals. They show that the virus can replicate in human airway cells and in the respiratory tract of ferrets to a higher level than can seasonal H3N2 virus, and show higher lethality in mice than genetically related H7N9 and H9N2 viruses. In transmission studies, the H7N9 virus showed limited transmission in ferrets by respiratory droplets. Ron Fouchier and colleagues investigate the transmissibility of H7N9 virus between ferrets. They show that airborne transmission can occur, but inefficiently. They also show that on passage in ferrets, virus variants that have higher avian receptor binding, higher pH of fusion and lower thermostability are selected, and they suggest that these characteristics may result in reduced transmissibility. On 29 March 2013, the Chinese Center for Disease Control and Prevention confirmed the first reported case of human infection with an avian influenza A(H7N9) virus 1 . The recent human infections with H7N9 virus, totalling over 130 cases with 39 fatalities to date, have been characterized by severe pulmonary disease and acute respiratory distress syndrome (ARDS) 2 . This is concerning because H7 viruses have typically been associated with ocular disease in humans, rather than severe respiratory disease 3 . This recent outbreak underscores the need to better understand the pathogenesis and transmission of these viruses in mammals. Here we assess the ability of A/Anhui/1/2013 and A/Shanghai/1/2013 (H7N9) viruses, isolated from fatal human cases, to cause disease in mice and ferrets and to transmit to naive animals. Both H7N9 viruses replicated to higher titre in human airway epithelial cells and in the respiratory tract of ferrets compared to a seasonal H3N2 virus. Moreover, the H7N9 viruses showed greater infectivity and lethality in mice compared to genetically related H7N9 and H9N2 viruses. The H7N9 viruses were readily transmitted to naive ferrets through direct contact but, unlike the seasonal H3N2 virus, did not transmit readily by respiratory droplets. The lack of efficient respiratory droplet transmission was corroborated by low receptor-binding specificity for human-like α2,6-linked sialosides. Our results indicate that H7N9 viruses have the capacity for efficient replication in mammals and human airway cells and highlight the need for continued public health surveillance of this emerging virus.

Clade 2.3.4.4b highly pathogenic avian influenza A(H5N1) viruses have caused large outbreaks within avian populations on five continents, with concurrent spillover into a variety of mammalian species. Mutations associated with mammalian adaptation have been sporadically identified in avian isolates, and more frequently among mammalian isolates following infection. Reports of human infection with A(H5N1) viruses following contact with infected wildlife have been reported on multiple continents, highlighting the need for pandemic risk assessment of these viruses. In this study, the pathogenicity and transmissibility of A/Chile/25945/2023 HPAI A(H5N1) virus, a novel reassortant with four gene segments (PB1, PB2, NP, MP) from North American lineage, isolated from a severe human case in Chile, was evaluated in vitro and using the ferret model. This virus possessed a high capacity to cause fatal disease, characterized by high morbidity and extrapulmonary spread in virus-inoculated ferrets. The virus was capable of transmission to naïve contacts in a direct contact setting, with contact animals similarly exhibiting severe disease, but did not exhibit productive transmission in respiratory droplet or fomite transmission models. Our results indicate that the virus would need to acquire an airborne transmissible phenotype in mammals to potentially cause a pandemic. Nonetheless, this work warrants continuous monitoring of mammalian adaptations in avian viruses, especially in strains isolated from humans, to aid pandemic preparedness efforts.

Collection of systemic tissues from influenza A virus (IAV)-infected ferrets at a fixed timepoint post-inoculation represents a frequent component of risk assessment activities to assess the capacity of IAV to replicate systemically. However, few studies have evaluated how the frequency and magnitude of IAV replication at discrete tissues contribute to within-host phenotypic outcomes, limiting our ability to fully contextualize results from scheduled necropsy into risk assessment settings. Employing aggregated data from ferrets inoculated with > 100 unique IAV (both human- and avian-origin viruses, spanning H1, H2, H3, H5, H7, and H9 subtypes), we examined relationships between infectious virus detection in four discrete tissue types (nasal turbinate, lung, brain, and olfactory bulb [BnOB]) to clinical outcomes of IAV-inoculated ferrets, and the utility of including these discrete tissue data as features in machine learning (ML) models. We found that addition of viral tissue titer data maintained high performance metrics of a predictive lethality classification ML model with or without inclusion of serially-collected virological and clinical data. Interestingly, infectious virus in BnOB was detected at higher frequency and magnitude among IAV associated with high pathogenicity phenotypes in ferrets, more so than tissues from the respiratory tract; in agreement, BnOB was the highest relative ranked individual tissue specimen in predictive classification models. This study highlights the potential role of BnOB viral titers in assessing IAV pathogenicity in ferrets, and highlights the role ML approaches can contribute towards understanding the predictive benefit of in vivo-generated data in the context of pandemic risk assessment.