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すでに「ディアコニー研究」にとって基本テキストとなっているE.バイロイター著「ディアコニーと近代における内国伝道の歴史」の第3章の翻訳である。ヨーロッパを目覚めさせた敬度主義の信仰覚醒運動は啓蒙主義との緊張関係の中でディアコニーの分野を様々に展開した。聖書協会の聖書頒布運動は,監獄に囚人を訪問し,監獄改善を要求し,さらに社会改善へと運動を展開した。また貧困だったスイスで時計や計量器などの精密機械産業を育成した。そして,幼児教育が全ヨーロッパに広がった

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すでに「ディアコニー研究」にとって基本テキストとなっているE.バイロイター著「ディアコニーと近代における内国伝道の歴史」の第2章の翻訳である。宗教改革後の中世ヨーロッパをおそった困窮と,それにたいするキリスト教の救護活動をのべている。政治や経済の行き届かなかった負い目をぬぐっていくという消極的な思考ではなく,救護活動が人材を育成し,新しい産業を生み出した

Teens, Tweets, and Tanning Beds: Rethinking the Use of Social Media for Skin Cancer Prevention

The incidence of skin cancer is rising in the U.S., and melanoma, the deadliest form, is increasing disproportionately among young white women. Indoor tanning is a modifiable risk factor for all skin cancers and continues to be used at the highest rates in young white women. Adolescents and young adults report personal appearance-based reasons for using indoor tanning. Previous research has explored the influences on tanning bed use, including individual factors as well as relationships with peers, family, schools, media influences, legislation, and societal beauty norms. Adolescents and young adults also have high rates of social media usage, and research is emerging on how best to utilize these platforms for prevention. Social media has the potential to be a cost-effective way to reach large numbers of young people and target messages at characteristics of specific audiences. Recent prevention efforts have shown that comprehensive prevention campaigns that include technology and social media are promising in reducing rates of indoor tanning among young adults. This review examines the literature on psychosocial influences on indoor tanning among adolescents and young adults, and highlights ways in which technology and social media can be used for prevention efforts

Perioperative Laboratory Abnormalities in Gynecologic Oncology Surgical Patients

Background: Laboratory blood testing incurs financial costs and the blood draws can increase discomfort, yet minimal data exists regarding routine testing in gynecologic oncology surgical patients. Additionally, an increasing number of gynecologic oncology surgeries are performed via a laparoscopic approach. Thus, further investigation into perioperative laboratory testing for gynecologic oncology patients is warranted. An increasing number of gynecologic oncology surgeries are performed via a laparoscopic approach. Thus, further investigation into perioperative laboratory testing for gynecologic oncology patients is warranted. Objective: The aims of this study were (1) to evaluate the frequency and etiology of perioperative laboratory test abnormalities in patients undergoing laparoscopic and laparotomy surgery in a gynecologic oncology service, and (2) to establish an evidence-based algorithm to reduce unnecessary laboratory testing. Materials and Methods: A single-institution retrospective study was completed, investigating laparoscopic and laparotomic surgeries over 4 years. Information on preoperative and postoperative laboratory data, surgical parameters, perioperative interventions, and patient demographics was collected. Quality-assurance data were reviewed. Data were tabulated and analyzed using Statistical Product and Service Solutions (SPSS) version 22. A Student's t-test was used to test for group differences for continuous variables with equal variance, the Mann-Whitney?U test for continuous variables when unequal variance was detected, and Pearson's ?2 was used to investigate categorical variables of interest. p-Values 98% of patients underwent at least one preoperative and postoperative laboratory test, totaling 8060 preoperative and 5784 postoperative results. The laparoscopy group was significantly less likely to have postoperative metabolic abnormalities or to undergo perioperative blood transfusion. Patients taking an angiotensin-converting-enzyme inhibitor, angiotensin-II?receptor blocker, or diuretic were significantly more likely to have elevated creatinine preoperatively (odds ratio [OR]: 5.0; p?Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140101/1/gyn.2015.0106.pd

Bacterial species associated with interdigital phlegmon outbreaks in Finnish dairy herds

Background: Severe outbreaks of bovine interdigital phlegmon (IP) have occurred recently in several free stall dairy herds in Finland. We studied the aetiology of IP in such herds, and the association of bacterial species with the various stages of IP and herds of various morbidity of IP. Nineteen free stall dairy herds with IP outbreaks and three control herds were visited and bacteriological samples collected from cows suffering from IP (n = 106), other hoof diseases (n = 58), and control cows (n = 64). The herds were divided into high morbidity (morbidity ≥50%) and moderate morbidity groups (9–33%) based on morbidity during the first two months of the outbreak. Results: F. necrophorum subspecies necrophorum was clearly associated with IP in general, and T. pyogenes was associated with the healing stage of IP. Six other major hoof pathogens were detected; Dichelobacter nodosus, Porphyromonas levii, Prevotella melaninogenica, Treponema spp. and Trueperella pyogenes. Most of the samples of acute IP (66.7%) harboured both F. necrophorum and D. nodosus. We found differences between moderate morbidity and high morbidity herds. D. nodosus was more common in IP lesion in high than in moderate morbidity herds. Conclusions: Our result confirms that F. necrophorum subspecies necrophorum is the main pathogen in IP, but also T. pyogenes is associated with the healing stage of IP. Our results suggest that D. nodosus may play a role in the severity of the outbreak of IP, but further research is needed to establish other bacteriological factors behind these severe outbreaks

Hyperglycemia regulates thioredoxin-ROS activity through induction of thioredoxin-interacting protein (TXNIP) in metastatic breast cancer-derived cells MDA-MB-231

<p>Abstract</p> <p>Background</p> <p>We studied the RNA expression of the genes in response to glucose from 5 mM (condition of normoglycemia) to 20 mM (condition of hyperglycemia/diabetes) by microarray analysis in breast cancer derived cell line MDA-MB-231. We identified the thioredoxin-interacting protein (TXNIP), whose RNA level increased as a gene product particularly sensitive to the variation of the level of glucose in culture media. We investigated the kinesis of the TXNIP RNA and protein in response to glucose and the relationship between this protein and the related thioredoxin (TRX) in regulating the level of reactive oxygen species (ROS) in MDA-MB-231 cells.</p> <p>Methods</p> <p>MDA-MB-231 cells were grown either in 5 or 20 mM glucose chronically prior to plating. For glucose shift (5/20), cells were plated in 5 mM glucose and shifted to 20 mM at time 0. Cells were analyzed with Affymetrix Human U133A microarray chip and gene expression profile was obtained. Semi-quantitative RT-PCR and Western blot was used to validate the expression of TXNIP RNA and protein in response to glucose, respectively. ROS were detected by CM-H2DCFDA (5–6-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate) and measured for mean fluorescence intensity with flow cytometry. TRX activity was assayed by the insulin disulfide reducing assay.</p> <p>Results</p> <p>We found that the regulation of TXNIP gene expression by glucose in MDA-MB-231 cells occurs rapidly within 6 h of its increased level (20 mM glucose) and persists through the duration of the conditions of hyperglycemia. The increased level of TXNIP RNA is followed by increased level of protein that is associated with increasing levels of ROS and reduced TRX activity. The inhibition of the glucose transporter GLUT1 by phloretin notably reduces TXNIP RNA level and the inhibition of the p38 MAP kinase activity by SB203580 reverses the effects of TXNIP on ROS-TRX activity.</p> <p>Conclusion</p> <p>In this study we show that TXNIP is an oxidative stress responsive gene and its expression is exquisitely regulated by glucose level in highly metastatic MDA-MB-231 cells.</p

CSF from Parkinson disease Patients Differentially Affects Cultured Microglia and Astrocytes

<p>Abstract</p> <p>Background</p> <p>Excessive and abnormal accumulation of alpha-synuclein (α-synuclein) is a factor contributing to pathogenic cell death in Parkinson's disease. The purpose of this study, based on earlier observations of Parkinson's disease cerebrospinal fluid (PD-CSF) initiated cell death, was to determine the effects of CSF from PD patients on the functionally different microglia and astrocyte glial cell lines. Microglia cells from human glioblastoma and astrocytes from fetal brain tissue were cultured, grown to confluence, treated with fixed concentrations of PD-CSF, non-PD disease control CSF, or control no-CSF medium, then photographed and fluorescently probed for α-synuclein content by deconvolution fluorescence microscopy. Outcome measures included manually counted cell growth patterns from day 1-8; α-synuclein density and distribution by antibody tagged 3D model stacked deconvoluted fluorescent imaging.</p> <p>Results</p> <p>After PD-CSF treatment, microglia growth was reduced extensively, and a non-confluent pattern with morphological changes developed, that was not evident in disease control CSF and no-CSF treated cultures. Astrocyte growth rates were similarly reduced by exposure to PD-CSF, but morphological changes were not consistently noted. PD-CSF treated microglia showed a significant increase in α-synuclein content by day 4 compared to other treatments (p ≤ 0.02). In microglia only, α-synuclein aggregated and redistributed to peri-nuclear locations.</p> <p>Conclusions</p> <p>Cultured microglia and astrocytes are differentially affected by PD-CSF exposure compared to non-PD-CSF controls. PD-CSF dramatically impacts microglia cell growth, morphology, and α-synuclein deposition compared to astrocytes, supporting the hypothesis of cell specific susceptibility to PD-CSF toxicity.</p

Accumulation of Endogenous LITAF in Aggresomes

LITAF is a 161 amino acid cellular protein which includes a proline rich N-terminus and a conserved C-terminal domain known as the simple-like domain. Mutations in LITAF have been identified in Charcot-Marie tooth disease, a disease characterized by protein aggregates. Cells transfected with cellular LITAF reveal that LITAF is localized to late endosomes/lysosomes. Here we investigated the intracellular localization of endogenous LITAF. We demonstrated that endogenous LITAF accumulates at a discrete cytoplasmic site in BGMK cells that we identify as the aggresome. To determine the domain within LITAF that is responsible for the localization of LITAF to aggresomes, we created a construct that contained the C-terminal simple-like domain of LITAF and found that this construct also localizes to aggresomes. These data suggest the simple-like domain is responsible for targeting endogenous LITAF to the aggresome

Apoptosis Signal-Regulating Kinase 1 Mediates MPTP Toxicity and Regulates Glial Activation

Apoptosis signal-regulating kinase 1 (ASK1), a member of the mitogen-activated protein kinase 3 family, is activated by oxidative stress. The death-signaling pathway mediated by ASK1 is inhibited by DJ-1, which is linked to recessively inherited Parkinson's disease (PD). Considering that DJ-1 deficiency exacerbates the toxicity of the mitochondrial complex I inhibitor 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we sought to investigate the direct role and mechanism of ASK1 in MPTP-induced dopamine neuron toxicity. In the present study, we found that MPTP administration to wild-type mice activates ASK1 in the midbrain. In ASK1 null mice, MPTP-induced motor impairment was less profound, and striatal dopamine content and nigral dopamine neuron counts were relatively preserved compared to wild-type littermates. Further, microglia and astrocyte activation seen in wild-type mice challenged with MPTP was markedly attenuated in ASK1−/− mice. These data suggest that ASK1 is a key player in MPTP-induced glial activation linking oxidative stress with neuroinflammation, two well recognized pathogenetic factors in PD. These findings demonstrate that ASK1 is an important effector of MPTP-induced toxicity and suggest that inhibiting this kinase is a plausible therapeutic strategy for protecting dopamine neurons in PD

Molecular chaperone-mediated rescue of mitophagy by a Parkin RING1 domain mutant

Mitochondrial dysfunction is characteristic of many neurodegenerative diseases. The Parkinson's disease-associated ubiquitin–protein ligase, Parkin, is important in the elimination of damaged mitochondria by autophagy (mitophagy) in a multistep process. Here, we show that a Parkin RING domain mutant (C289G) fails to redistribute to damaged mitochondria and cannot induce mitophagy after treatment with the mitochondrial uncoupler carbonyl cyanide m-methylhydrazone, because of protein misfolding and aggregation. Parkin(C289G) aggregation and inclusion formation were suppressed by the neuronal DnaJ/Hsp40 chaperone HSJ1a(DNAJB2a). Importantly, HSJ1a and DNAJB6 also restored mitophagy by promoting the relocation of Parkin(C289G) and the autophagy marker LC3 to depolarized mitochondria. The rescue of Parkin activity and suppression of aggregation were J domain dependent for HSJ1a, suggesting the involvement of Hsp70 in these processes, but were not dependent on the HSJ1a ubiquitin interaction motif. HSJ1a expression did not enhance mitophagy mediated by wild-type Parkin. These data show the potential of molecular chaperones to mediate the functional recovery of Parkin misfolding mutants and to combat deficits associated with Parkin aggregation in Parkinson's disease