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Aim: The aim of this qualitative meta‐synthesis was to discover the factors impacting on missed nursing care of nurses through systematic thinking. Background: Although nurses are responsible for high‐quality care, missed nursing care is common, endangering patient safety. Understanding of the causes related to missed nursing care could help nursing managers improve the quality of nursing care. Design: A qualitative meta‐synthesis guided by the Preferred Reporting Items for Systematic Reviews and Meta‐analyses (PRISMA). Methods: As a method designed to contribute to knowledge development, meta‐synthesis allows for integration of qualitative study findings using thematic synthesis. Six databases were searched up to October 2021; nine studies met the inclusion and quality assessment criteria and meta‐synthesis were conducted. Results: Three themes related to the causes why nurses missed nursing care were found. The themes included intrinsic resources (professional and ethical values, ambiguous nurse role, prioritization, education system, and knowledge), system structure (staff and resources shortage, heavy workload but limited time, and organizational management failure), and social environment (communication, working relationship and skill mix, and inappropriate ward layout). Conclusion: The phenomenon of missed nursing care is a global tissue, with variations in its elements but also notable similarities. Meta‐synthesis provides evidence of intrinsic and extrinsic factors that contribute to missed nursing care. Relevance to Clinical Practice: Recognizing and understanding the causes of missed nursing care is essential for nursing managers to ensure patient safety and the provision of high‐quality care. [ABSTRACT FROM AUTHOR]

Surgical site infections (SSIs) after thyroid surgery are rare complications, with incidence rates of 0.3%–1.6%. Using a Japanese database, we conducted exploratory analyses on the incidence of SSIs, investigated the incidence of SSIs by the National Nosocomial Infections Surveillance risk index, and identified the causative bacteria of SSIs. SSIs occurred in 50 (0.7%) of 7388 thyroid surgery cases. Risk index‐0 patients had the lowest incidence rate of SSIs (0.41%). The incidence of SSIs in risk index‐1 patients was 3.05 times the incidence of SSIs in risk index‐0 patients. The rate of SSI occurrence for risk index‐2 patients was 4.22 times the rate of SSI occurrence for risk index‐0 patients. Thirty‐one bacterial species were identified as the cause of SSIs in thyroid surgery cases, of which 12 (38.7%) SSIs were caused by Staphylococcus aureus and Staphylococcus epidermidis. Of the nine SSIs caused by Staphylococcus aureus, 55.6% (five cases) were attributed to methicillin‐resistant Staphylococcus aureus. Therefore, routine prophylactic antibiotic administration should be avoided, while the target for administration should be narrowed, according to the SSI risk. Administration of prophylactic antibiotics, such as 2 g piperacillin or 1 g cefazolin, is considered appropriate. [ABSTRACT FROM AUTHOR]

Aims Immunohistochemistry for mismatch repair ( MMR) proteins is being increasingly used to examine MMR status in tumours. The aim of the present article was to report the case of a colon cancer patient with Lynch syndrome who showed unusual cytoplasmic MMR protein localization. Methods and results Histologically, the colon cancer was diagnosed as medullary carcinoma associated with prominent tumour-infiltrating lymphocytes and a Crohn's-like reaction. Immunohistochemistry revealed cytoplasmic and nuclear expression of MSH2 in non-neoplastic cells, and exclusively cytoplasmic expression in tumour cells. MSH6 expression was nuclear in non-neoplastic cells, but was lost in tumour cells. Nuclear expression of MLH1 and PMS2 was retained in both non-neoplastic and tumour cells. The tumour was microsatellite instability-high, which is indicative of defective MMR function. A subsequent germline mutation analysis identified a genomic deletion spanning the 3′ region of EPCAM and the 5′ region of MSH2, resulting in an in-frame fusion of EPCAM and MSH2. Conclusions The unusual cytoplasmic immunoreactivity of MSH2 was considered to be attributable to the non-functional EPCAM-MSH2 fusion product. The present case illustrates that not only loss of expression, but also abnormal localization, of MMR proteins is indicative of a defective MMR system. [ABSTRACT FROM AUTHOR]

Germline PMS2 gene mutations were detected by RT- PCR/direct sequencing of total RNA extracted from puromycin-treated peripheral blood lymphocytes ( PBL) and multiplex ligation-dependent probe amplification ( MLPA) analyses of Japanese patients with colorectal cancer ( CRC) fulfilling either the revised Bethesda Guidelines or being an age at disease onset of younger than 70 years, and screened by mismatch repair protein immunohistochemistry of formalin-fixed paraffin embedded sections. Of the 501 subjects examined, 7 (1.40%) showed the downregulated expression of the PMS2 protein alone and were referred to the genetic counseling clinic. Germline PMS2 mutations were detected in 6 (85.7%), including 3 nonsense and 1 frameshift mutations by RT- PCR/direct sequencing and 2 genomic deletions by MLPA. No mutations were identified in the other MMR genes (i.e. MSH2, MLH1 and MSH6). The prevalence of the downregulated expression of the PMS2 protein alone was 1.40% among the subjects examined and IHC results predicted the presence of PMS2 germline mutations. RT- PCR from puromycin-treated PBL and MLPA may be employed as the first screening step to detect PMS2 mutations without pseudogene interference, followed by the long-range PCR/nested PCR validation using genomic DNA. [ABSTRACT FROM AUTHOR]

SUMMARY The main subject of this investigation is to perform research and development and verification experiments on underwater communications (underwater visible light communications; VLCs) under the assumption that VLC can be used for tourism and environmental protection under the ocean conditions of the Okinawa region (Zamami village), which is one of the most popular diving spots, with the most transparent water and abundant coral and fish. Radio is rarely used as a communications tool underwater because the attenuation rate of radio signals is high. The only communications tool now available under water is sonic (ultrasonic) communications, although it has not spread among divers because it is subject to noise from reflections of the water surface or the sea floor, and its use is not simple. Another disadvantage of this mode of communication is that it is very difficult to identify the speaker when several divers are present in the same area. With the underwater VLC device, most of the underwater communications problems are already solved, for the following reasons: (1) the device is easy to move and does not involve cables; (2) it is much easier to capture another person's words because communication does not diverge as sonic communication does; (3) conversation is much easier since the other party can recognize the speaker visually. [ABSTRACT FROM AUTHOR]

β-Secretase β-site APP cleaving enzyme 1 (BACE1), is a membrane-bound aspartyl protease necessary for the generation of amyloid β-protein (Aβ), which accumulates in the brains of individuals with Alzheimer's disease (AD). To gain insight into the mechanisms by which BACE1 activity is regulated, we used proteomic methods to search for BACE1-interacting proteins in human neuroblastoma SH-SY5Y cells, which overexpress BACE1. We identified reticulon 4-B (RTN4-B; Nogo-B) as a BACE1-associated membrane protein. Co-immunoprecipitation experiments confirmed a physical association between BACE1 and RTN4-B, RTN4-C (the shortest isoform of RTN-4), and their homologue reticulon 3 (RTN3), both in SH-SY5Y cells and in transfected human embryonic kidney (HEK) 293 cells. Overexpression of these reticulons (RTNs) resulted in a 30–50% reduction in the secretion of both Aβ40 and Aβ42 from HEK293 cells expressing the AD-associated Swedish mutant amyloid precursor protein (APP), but did not affect Aβ secretion from cells expressing the APP β-C-terminal fragment (β-CTF), indicating that these RTNs can inhibit BACE1 activity. Furthermore, a BACE1 mutant lacking most of the N-terminal ectodomain also interacted with these RTNs, suggesting that the transmembrane region of BACE1 is critical for the interaction. We also observed a similar interaction between these RTNs and the BACE1 homologue BACE2. Because RTN3 and RTN4-B/C are substantially expressed in neural tissues, our findings suggest that they play important roles in the regulation of BACE1 function and Aβ production in the brain. [ABSTRACT FROM AUTHOR]