女性がんサバイバーの心理的適応

The purpose of this study is to explore the psychological adjustments female cancer survivors undergo with respect to their femininity. Semi-structured interviews were performed with ２９ female cancer（breast or gynecologic cancer）survivors in their２０s to５０s. Qualitative descriptive study data was interpreted according to Krippendorff’s content analysis method. As a result, six categories were generated as psychological adjustments utilized by female cancer survivors from the viewpoint of femininity : “I like the way I am” ; “I am charming as a woman” ; “I live independently as a woman” ; “I am expanding my life as a woman” ; “I can feel connected with someone” ; and “I have graduated from pessimism.” These could be interpreted as psychological adaptations that reflect feminine emotions and reflect the strength and resilience of female cancer survivors. In order for female cancer survivors to adjust to living with cancer in a psychologically healthy way, it was suggested that nursing support was important to restore the feelings of the survivors from the perspective of these feminine characteristics

Impact of adverse events on patient outcomes in a Japanese intensive care unit: a retrospective observational study

AimWe investigated adverse events (AEs) in a Japanese intensive care unit (ICU) and evaluated the impact of cause-specific AEs on mortality and length of stay.DesignA retrospective observational study in the ICU of an academic hospital.MethodsWe reviewed medical records with the Global Trigger Tool.ResultsOf the 246 patients, 126 (51%) experienced one or more AEs with an incidence of 201 per 1000 patient-days and 115 per 100 admissions. A total of 294 AEs were detected with 119 (42%) adverse drug events, 67 (24%) procedural complications, 63 (22%) surgical complications, 26 (9%) nosocomial infections, 5 (2%) therapeutic errors and 4 (1%) diagnostic errors. Adverse event (AE) presence was associated with length of ICU stay (β = 2.85, 95% confidence interval [CI]: 1.09–4.61). Adverse drug events, procedural complications and nosocomial infections were strongly associated with length of ICU stay (β = 2.38, 95% CI: 0.77–3.98; β = 3.75, 95% CI: 2.03–5.48; β = 6.52, 95% CI: 4.07–8.97 respectively)

Development of the Japanese version of the Intensive Care Unit Trigger Tool to detect adverse events in critically ill patients

AimThe Intensive Care Unit Trigger Tool (ICUTT) was developed to detect adverse events (AEs) in intensive care unit (ICU) patients. The purpose of this study was to determine the validity and reliability of the Japanese version of the ICUTT (ICUTT-J).MethodsThe translation of ICUTT was carried out based on the guideline for translation of instruments. Subsequently, two review teams independently reviewed 50 patients\u27 medical records using the ICUTT-J, and agreement regarding the presence and number of AEs was evaluated to ensure reliability.ResultsThe ICUTT-J was submitted to the authors of the original ICUTT, who confirmed it as being equivalent to the original version. The item-content validity index and scale-content validity index were 1.00 and 1.00, respectively. Interrater reliability showed moderate agreement of κ = 0.52 in terms of the presence of AEs and linear weighting of κ = 0.49 (95% confidence interval, 0.28, 0.71) in terms of the number of AEs.ConclusionThis study\u27s findings suggest that the ICUTT-J is valid and moderately reliable for use in ICUs

Enhanced resistance to herpes simplex virus type 1 infection in transgenic mice expressing a soluble form of herpesvirus entry mediator

AbstractHerpesvirus entry mediator (HVEM) is a member of the tumor necrosis factor (TNF) receptor family used as a cellular receptor by virion glycoprotein D (gD) of herpes simplex virus (HSV). Both human and mouse forms of HVEM can mediate entry of HSV-1 but have no entry activity for pseudorabies virus (PRV). To assess the antiviral potential of HVEM in vivo, three transgenic mouse lines expressing a soluble form of HVEM (HVEMIg) consisting of an extracellular domain of murine HVEM and the Fc portion of human IgG1 were generated. All of the transgenic mouse lines showed marked resistance to HSV-1 infection when the mice were challenged intraperitoneally with HSV-1, but not to PRV infection. The present results demonstrate that HVEMIg is able to exert a significant antiviral effect against HSV-1 infection in vivo

Nonsense and Frameshift Mutations in ZFHX1B, Encoding Smad-Interacting Protein 1, Cause a Complex Developmental Disorder with a Great Variety of Clinical Features

Mutations in ZFHX1B, encoding Smad-interacting protein 1 (SIP1), have been recently reported to cause a form of Hirschsprung disease (HSCR). Patients with ZFHX1B deficiency typically show mental retardation, delayed motor development, epilepsy, microcephaly, distinct facial features, and/or congenital heart disease, in addition to the cardinal form of HSCR. To investigate the breadth of clinical variation, we studied DNA samples from six patients with clinical profiles quite similar to those described elsewhere for ZFHX1B deficiency, except that they did not have HSCR. The results showed the previously reported R695X mutation to be present in three cases, with three novel mutations—a 2-bp insertion (760insCA resulting in 254fs262X), a single-base deletion (270delG resulting in 91fs107X), and a 2-bp deletion (2178delTT resulting in 727fs754X)—newly identified in the other three. All mutations occurred in one allele and were de novo events. These results demonstrate that ZFHX1B deficiency is an autosomal dominant complex developmental disorder and that individuals with functional null mutations present with mental retardation, delayed motor development, epilepsy, and a wide spectrum of clinically heterogeneous features suggestive of neurocristopathies at the cephalic, cardiac, and vagal levels

Cathepsin E is a marker of gastric differentiation and signet-ring cell carcinoma of stomach: a novel suggestion on gastric tumorigenesis.

Gastric cancer (GC) presents various histological features, though the mechanism underlying its diversity is seldom elucidated. It is mainly classified into well differentiated tubular adenocarcinoma (tub1), moderately differentiated tubular adenocarcinoma (tub2), poorly differentiated adenocarcinoma (por), signet-ring cell carcinoma (sig), mucinous adenocarcinoma (muc), and papillary adenocarcinoma (pap). By screening, we found cathepsin E (CTSE) expresses universally in sig-type, occasionally in por-type, and rarely in tub1/tub2-type GC cell lines. In surgically-resected specimens, CTSE was immunostained in 50/51 sig-type (98.0%), 3/10 tub1-type (30.0%), 7/18 tub2-type (38.9%), 15/26 por-type (57.7%), 4/10 pap-type (40.0%), and 0/3 muc-type (0.0%) GC. In endoscopically-resected specimens, 6/7 sig-type (85.7%), 7/52 tub1-type (13.7%), 5/12 tub2-type (41.7%), 2/7 pap-type (28.6%) GC and 0/6 adenoma (0.0%) expressed CTSE. For non-malignant tissues, CTSE is universally expressed in normal fundic, pyloric, and cardiac glands of stomach, but hardly in other digestive organs. In the precancerous intestinal metaplasia of stomach, CTSE is mostly observed in mixed gastric-and-intestinal type and deficient in solely-intestinal type. CTSE expression is positively correlated with gastric marker MUC5AC (p<0.0001) and negatively correlated with intestinal marker MUC2 (p = 0.0019). For sig-type GC, in both tumors and background mucosa, expression of MUC5AC and CTSE is high whereas that of MUC2 is low, indicating that sig-type GC reflects the features of background mucosa. For gastric adenoma and tub1/tub2-type GC, more undifferentiated tumors tend to show higher expression of CTSE with MUC5AC and lower expression of MUC2 in tumors, but they tend to present lower expression of CTSE, MUC5AC and MUC2 in background mucosa. These suggest that more malignant gastric adenocarcinoma with stronger gastric and weaker intestinal properties tend to arise from background mucosa with decreased both gastric and intestinal features. In conclusion, CTSE is a marker of both gastric differentiation and signet-ring cell carcinoma, which should shed light on the mechanism of gastric tumorigenesis