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The stagnation of autophagic flux accompanied by these phenomena was also observed with the addition of a GAK inhibitor. Furthermore, the addition of Rho‑associated protein kinase (ROCK) inhibitor or ROCK1 knockdown mitigated GAK KO‑mediated effects. The results suggested a vital role of GAK in controlling lysosomal dynamics via maintaining lysosomal homeostasis during autophagy.The selection of effective therapeutic agents is critical for improving the survival of patients with renal cell carcinoma (RCC). The aim of the present study was to develop an ex vivo drug testing assay using patient‑derived tumor organoid (TO) cultures. For this purpose, surgical tumor specimens were obtained from 20 patients with RCC. TOs were developed ex vivo from freshly resected RCC tumors, and their histopathological and molecular characteristics were evaluated using histological staining and whole‑exome sequencing (WES). Using a cell viability assay, the therapeutic efficacy of standard of care tyrosine kinase inhibitors in RCC TOs was determined. It was found that TOs recapitulated the histological features of primary RCC tumors. Using WES, a strong concordance was identified at the genetic level between the primary tumors and their corresponding TOs. Using patient‑derived TO models, a prototype of an ex vivo drug testing assay was developed, and it was found that RCC TOs exhibited differential responses to sunitinib, pazopanib, cabozantinib, axitinib and sorafenib treatment. On the whole, although the predictive value of the current assay has to be tested and validated in future clinical studies, the findings of the present study demonstrate a novel approach for ex vivo drug testing in patient‑derived TO models, which may have potential for use in the personalized treatment of cancer patients.Cervical cancer is a serious gynecological cancer and one of the primary causes of mortality in female patients with cancer. Despite advances in cancer research, the molecular mechanism underlying cancer remains poorly understood. High levels of MIR9‑3 host gene (HG) are associated with the occurrence and development of cervical cancer. However, the specific role of MIR9‑3HG during the development of cervical cancer is unclear. In the present study, the expression of MIR9‑3HG was silenced in C33A and SiHa cervical cancer cell lines. Proliferation and apoptosis were measured in these cells using 5‑ethynyl‑2’‑deoxyuridine assay and flow cytometry, respectively. In addition, targeting microRNAs (miRs) of MIR9‑3HG and mRNAs of miR‑498 were predicted using public databases. The predicted interactions between these molecules were validated using RNA immunoprecipitation, RNA pull‑down and luciferase reporter assays. Lastly, C33A cells transfected with short hairpin MIR‑3HG alone or in combination with miR‑498 inhibid new insight into the pathogenesis of cervical cancer.Following the publication of this paper, the authors contacted the Editorial Office to request that the article be retracted on account of an inability to obtain consistent results after having repeated the experiments portrayed in Figs. CQ31 1B and 3B. Independently, it was drawn to the Editor’s attention that certain of the western blotting data shown in these figures were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that these other articles were under consideration for publication at the same time as the above article was submitted for publication to Molecular Medicine Reports, the Editor has agreed to the authors’ request that this article should be retracted from the Journal. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 12 753‑759, 2015; DOI 10.3892/mmr.2015.3425].Following the publication of this paper, the Journal was alerted by an investigation committee of Niigata University to the fact that the paper had been identified as a duplicate publication, which had already been published. Therefore, in accordance with the rules of Niigata University Fraud Investigation committee, a request was made that the paper be retracted. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 38 1227-1236, 2011; DOI 10.3892/ijo.2011.959].Circular RNA (circRNA) is a type of endogenous, high‑stability, noncoding RNA. circRNAs exhibit various biological functions, and are involved in physiological and pathological processes occurring in various diseases, including cancers. They can not only act as microRNA and protein sponges, but also interact with proteins, translated peptides, and transcriptional and translational regulators, and compete with pre‑mRNA splicing. Chemotherapy is one of the most important types of cancer treatment. However, the resistance of cancer cells to chemotherapy is a leading reason for the failure of chemotherapy. It has been reported that circRNAs play important roles in cancer resistance via a number of mechanisms. The functions of the circRNAs provide insight into their roles in chemoresistance pathways. In addition, some circRNAs may serve as novel biomarkers for the diagnosis and prognosis of cancer resistance. Obtaining improved understanding of the molecular regulatory networks featuring circRNAs in tumors and searching for markers for the diagnosis and treatment of cancer resistance are leading issues in circRNA research. The present review introduced the functions of circRNAs, illustrated the mechanisms underlying drug resistance in cancer, described the contributions of circRNAs to this resistance and discussed the potential application of circRNAs in the treatment of drug‑resistant cancer. In particular, the review aimed to reveal the main mechanisms of circRNAs in cancer drug resistance, including mechanisms involving drug transport and metabolism, alterations of drug targets, DNA damage repair, downstream resistance mechanisms, adaptive responses and the tumor microenvironment. The findings may provide novel therapeutic targets for clinical treatment of cancer chemoresistance.The aim of the present study was to investigate the effect of penehyclidine hydrochloride (PHC) pretreatment on mice with lipopolysaccharide (LPS)‑induced acute lung injury (ALI) and its possible underlying mechanisms. Mice were randomly separated into six groups i) Sham group; ii) LPS group; iii) LPS + PHC group; iv) tumor necrosis factor a‑induced protein 8‑like protein 2 (TIPE2) group; v) LPS + TIPE2 group; and vi) LPS + TIPE2 + PHC group. The ALI model was induced using LPS through intratracheal injection. The mice received adenovirus gene to induce the overexpression of TIPE2. After mice were sacrificed, lung injury indices were assessed, and arterial blood, bronchoalveolar lavage fluid and lung tissues were collected for subsequent assays. Expression levels of related proteins were detected by using western blotting. It was found that compared with the sham group, the mice treated with LPS showed increased lung injury and dysfunctions of gas exchange. However, these trends were significantly ameliorated in the LPS + PHC group. Evaluation of protein expression in lung tissues showed that the increased expression of nuclear NF‑κB p65 and p‑c‑Jun N‑terminal kinase (JNK) induced by LPS were suppressed in the LPS + PHC group and the expression of TIPE2 was increased. The mice that received adenovirus gene to induce TIPE2 overexpression could also showed protective effects compared with the mice in the LPS group. However, the expression of TIPE2 decreased rather than increased in LPS group. In the mice pretreated with PHC, the expression of TIPE2 increased in mice with LPS‑induced ALI. To conclude, PHC pretreatment could inhibit the occurrence of inflammation and apoptosis in LPS‑induced ALI. This process may be related to the activation of TIPE2 and the inhibition of NF‑κB and JNK signaling pathway in the lungs of mice.

The addition of graphic health warnings to cigarette packets can facilitate smoking cessation, primarily through their ability to elicit a negative affective response. Smoking has been linked to COVID-19 mortality, thus making it likely to elicit a strong affective response in smokers. COVID-19-related health warnings (C19HW) may therefore enhance graphic health warnings, when compared to traditional health warnings (THW). Further, because impulsivity influences smoking behaviours, we also examined whether these affective responses were associated with delay discounting.

In a between-subjects design, 240 smokers rated the valence and arousal elicited by tobacco packaging that contained either a C19HW or THW (both referring to death). Participants also completed questionnaires to quantify delay discounting and attitudes towards COVID-19 and smoking (eg, health risks, motivation to quit).

There were no differences between the two health warning types on either valence or arousal, nor any secondary outcomeng efficacy, which may explain poorer cessation success in this population.The COVID-19 pandemic requires military nurse leaders in various patient care settings to engage in disaster response. Evidence supports essential leadership attributes for nurses that include skilled communication, organizational influence, and personnel management. Yet, nursing expertise that shapes nurse leader responsibilities during disaster management remains unclear. A description of how military nurse leaders contributed their nursing expertise during the COVID-19 pandemic response at one U.S. Military health care facility is provided to begin to delineate disaster management responsibilities.Military nurses have been placed in the forefront of clinical and leadership roles during the COVID-19 pandemic. Serving in critical roles, military nurses have spearheaded innovations in clinical practice, conducted research, and implemented evidence-based practice projects that have advanced the capabilities of the Armed Forces Nurse Corps. This collection captures and highlights many of these military nursing contributions combating the COVID-19 pandemic.Initial DoD support of Federal Emergency Management Agency (FEMA) operations for New York City (NYC) coronavirus disease 2019 (COVID-19) relief included the deployment of military medics to the Javits New York Medical Station and USNS Comfort. When Air Force (AF) Reservists arrived in NYC, 64th Air Expeditionary Group leaders worked with FEMA, Task Force New York/New Jersey, and NYC chains of command to send Airmen to NYC hospitals, including Lincoln Medical Center (LMC). Within 72 hours of arrival, 60 AF Reservists, including 30 registered nurses and 3 medical technicians, integrated into LMC to provide support during April and May 2020. This assistance began during the peak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections. Air Force nurses provided over 6,000 hours of care to over 800 patients in the emergency department and ad hoc intensive care and medical-surgical units. As infections declined, AF nurses shifted to providing care in established units. In these units, AF nurses provided patient care and worked directly with LMC nurses to provide directed teaching experiences to improve their comfort and competency with caring for acutely ill COVID-19 patients.