シュッセイリツ ノ チョウキテキ ナ ケッテイ ヨウイン セイベツ ネンレイ カイソウベツ ニヨル キョウイク ノ ヤクワリ

本稿は、出生率の長期的な決定要因を考察した論文である。長期的なデータを活用することで、人口転換における出生率の低下の要因を明らかにした。実証分析における内生性の問題を、システムGMM推計を用いることで解消し、出生率における因果関係の特定化を行った。主な結論は、男性の教育水準は出生率には影響を与えない一方で、女性の教育水準の上昇が出生率の低下をもたらすというものである。特に、若年世代の女性の教育水準が出生率の決定には重要であるという帰結を得た

Up-regulation of Na+,K+-ATPase α3-isoform and down-regulation of the α1-isoform in human colorectal cancer

AbstractWe investigated expression levels of Na+,K+-ATPase α-isoforms and their ATPase activities in human colorectal cancer tissue and the accompanying normal mucosa. A decrease in expression of the α1-isoform protein was observed in all sampled cancer tissues compared with the normal mucosae. The level of ouabain (5 μM)-sensitive Na+,K+-ATPase activity in carcinomas was 81±5% that of in the normal mucosae. The mRNA expression of α2- and α4-isoforms was decreased in almost all the carcinoma samples. Interestingly, the expression level of the α3-isoform protein in the cancer tissue was higher than that of the normal mucosa. These results indicate that a decrease in the α1-isoform expression and an increase in the α3-isoform expression may be associated with colorectal cancer

Exogenous IFN-γ ex vivo shapes the alloreactive T-cell repertoire by inhibition of Th17 responses and generation of functional Foxp3+ regulatory T cells

Interferon (IFN)-γ was originally characterized as a pro-inflammatory cytokine with T helper type 1-inducing activity, but subsequent work has demonstrated that mice deficient in IFN-γ or IFN-γ receptor show exacerbated inflammatory responses and accelerated allograft rejection, suggesting that IFN-γ also has important immunoregulatory functions. Here, we demonstrate that ex vivo IFN-γ conditioning of CD4 T cells driven by allogeneic immature dendritic cells (DC) results in the emergence of a Foxp3+ regulatory T-cell (Treg)- dominant population that can prevent allograft rejection. The development of this population involves conversion of non-Treg precursors, preferential induction of activation-induced cell death within the non-Treg population and suppression of Th2 and Th17 responses. The suppressive activity of IFN-γ is dependent on the transcription factor signal transducer and activator of transcription 1 and is mediated by induced nitric oxide. These data indicate not only how IFN-γ could be used to shape beneficial immune responses ex vivo for possible cell therapy but also provide some mechanistic insights that may be relevant to exacerbated inflammatory responses noted in several autoimmune and transplant models with IFN-γ deficiency

糖尿病とがんを併せ持つ患者のがん治療中のセルフマネジメントの実際

Objective: To describe the state of self-management during cancer treatment in patients with diabetes and cancer.Methods: Patients with diabetes and cancer who visited the diabetes outpatient clinic of general hospitals in Japan were recruited as participants. Data were collected in interviews using a semi-structured questionnaire and were analyzed qualitatively and inductively using content analysis.Results: Two categories and six subcategories of self-management for cancer treatment were revealed. The categories included “adhering to blood glucose management for cancer treatment” and “getting into shape for cancer treatment” and the subcategories included “remembering to measure blood glucose,” “thorough glycemic control through drug therapy,” “ensuring glycemic control through exercise therapy,” “addressing adverse events of anticancer drugs,” “reconsidering tobacco and alcohol consumption in the wake of cancer,” and “performing indicated rehabilitation.”Two categories and three subcategories of self-management for diabetes treatment were revealed. The categories included “continuing a diabetes treatment lifestyle true to oneself” and “judging the state of diabetes,” and the subcategories included “eating a diet that does not aggravate diabetes,” “continuing self-management without overdoing it,” and “estimating whether blood sugar levels are high or low.”Discussion: It was revealed that patients were self-managing both cancer and diabetes, suggesting the need for information sharing and collaboration between cancer and diabetic nurses.論

Regulatory T cells and their role in rheumatic diseases: a potential target for novel therapeutic development

Regulatory T cells have an important role in limiting immune reactions and are essential regulators of self-tolerance. Among them, CD4+CD25high regulatory T cells are the best-described subset. In this article, we summarize current knowledge on the phenotype, function, and development of CD4+CD25high regulatory T cells. We also review the literature on the role of these T cells in rheumatic diseases and discuss the potential for their use in immunotherapy

The therapeutic potential of regulatory T cells for the treatment of autoimmune disease

IntroductionImmune tolerance remains the holy grail of therapeutic immunology in the fields of organ and tissue transplant rejection, autoimmune diseases, and allergy and asthma. We have learned that FoxP3(+)CD4(+) regulatory T cells play a vital role in both the induction and maintenance of self-tolerance.Areas coveredIn this opinion piece, we highlight regulatory T cells (Treg) cell biology and novel immune treatments to take advantage of these cells as potent therapeutics. We discuss the potential to utilize Treg and Treg-friendly therapies to replace current general immunosuppressives and induce tolerance as a path towards a drug-free existence without associated toxicities.Expert opinionFinally, we opine on the fact that biomedicine sits on the cusp of a new revolution: the use of human cells as versatile therapeutic engines. We highlight the challenges and opportunities associated with the development of a foundational cellular engineering science that provides a systematic framework for safely and predictably regulating cellular behaviors. Although Treg therapy has become a legitimate clinical treatment, development of the therapy will require a better understanding of the underlying Treg biology, manufacturing advances to promote cost effectiveness and combinations with other drugs to alter the pathogenicity/regulatory balance