Ti–Pd Alloys as Heterogeneous Catalysts for Hydrogen Autotransfer Reaction and Catalytic Improvement by Hydrogenation Effects

Ti−Pd alloys were investigated as heterogeneous catalysts for hydrogen autotransfer reactions. This is the first reported study of alloys as catalysts for hydrogen‐borrowing reactions using alcohols. We improved the catalytic activities of alloys by increasing their specific surface areas via a hydrogenation−powdering process. The reactivities and selectivities of hydrogenated Ti−Pd alloys [Ti−Pd (Hy) ] were higher than those of non‐hydrogenated alloy catalysts in N‐alkylation by hydrogen autotransfer using alcohols. A plausible catalytic cycle is proposed based on control studies and deuterium labelling experiments

A Case of Nephrotic Syndrome with Nephrotoxicity Induced by Low-Dose Cyclosporin Treatment

We report a 3-year-old girl with steroid resistant nephrotic syndrome (NS) who developed nephrotoxicity by low-dose cyclosporin (CsA) treatment. Initial prednisolone (PSL) treatment and subsequent additional cyclophosphamide treatment were not successful in leading her into remission. The first renal biopsy finding revealed neither a glomerular nor interstitial change. CsA therapy was initiated in addition to ongoing glucocorticoid therapy at 6 months from the time of onset. Proteinuria disappeared 3 weeks later and the patient went into complete remission. After experiencing the first relapse, the patient was gradually weaned from CsA, and treatment continued with 30 to 50 ng/mL of trough concentration. No elevations of the serum creatinine, serum urea, serum potassium, excretion of urinary β2-microglobulin, or urinary N-acetyl-β-D-glucosaminidase were demonstrated in the follow-up. A second renal biopsy specimen obtained 1 year later showed a tubulo-interstitial change, containing tubular atrophy and interstitial fibrosis, both of which are consistent with the morphological change associated with CsA nephrotoxicity. A follow-up biopsy should be done in order to evaluate the CsA nephrotoxicity, regardless of the treatment dosage

糖尿病患者の在宅ケア向上をめざしたTCDS育成の試み

The Tokushima City Medical Association has cultivated the talented persons of nursing care profession by both the education of diabetes and the instruction of medical treatments to secure the quality of home care for increasing diabetic patients. They are certified to be the Tokushima City Certified Diabetes Supporter（TCDS）. In Tokushima Prefecture, the rate of aging and the certification rate of care need are ranked high in Japan, and the medical measures should be provided for the aged diabetic patients utilizing team nursing care as well as team medical care, because many of these patients are obliged to receive home medical care owing to the introduction of community-based integrated care systems. Tokushima Prefecture kept the worst of age-adjusted diabetes mortality and also the worst of crude diabetes mortality in recent years. Therefore, the program for the TCDS was arranged by the staffs composed of board certified fellows of the Japan Diabetes Society, certified diabetes physicians of Tokushima, and Tokushima local certified diabetes educators （Tokushima LCDEs）. The program includes the lectures of diabetes and medical treatments, the practical training, and the group work by the World Café system collaborated with the medical staffs across many different fields, using the dramatic skit presented by the medical doctors and the LCDE staffs after narrating the scenario for the blood glucose control of diabetic patients to be treated. The persons who have completed the training course are certified as the TCDS by The Tokushima City Medical Association. The workshop is held twice a year and the certification is renewed every three years without examination. In conclusion, it is suggested that the development of TCDS leads to the improvement of the ability of nursing care staffs to support diabetic treatments and the advancement of the quality of home medical care for the aged diabetic patients

Integrated genetic and clinical prognostic factors for aggressive adult T-cell leukemia/lymphoma

成人T細胞白血病リンパ腫（ATL）におけるゲノム情報と臨床情報を統合したリスクモデルを確立 --ATLの個別化医療を推進--. 京都大学プレスリリース. 2023-04-10.The prognosis of aggressive adult T-cell leukemia/lymphoma (ATL) is poor, and allogeneic hematopoietic stem-cell transplantation (allo-HSCT) is a curative treatment. To identify favorable prognostic patients after intensive chemotherapy, and who therefore might not require upfront allo-HSCT, we aimed to improve risk stratification of aggressive ATL patients aged <70 years. The clinical risk factors and genetic mutations were incorporated into risk modeling for overall survival (OS). We generated the m7-ATLPI, a clinicogenetic risk model for OS, that included the ATL prognostic index (PI) (ATL-PI) risk category, and non-silent mutations in seven genes, namely TP53, IRF4, RHOA, PRKCB, CARD11, CCR7, and GATA3. In the training cohort of 99 patients, the m7-ATLPI identified a low-, intermediate-, and high-risk group with 2-year OS of 100%, 43%, and 19%, respectively (hazard ratio [HR] 5.46, p < 0.0001). The m7-ATLPI achieved superior risk stratification compared to the current ATL-PI (C-index 0.92 vs. 0.85, respectively). In the validation cohort of 84 patients, the m7-ATLPI defined low-, intermediate-, and high-risk groups with a 2-year OS of 81%, 30%, and 0%, respectively (HR 2.33, p = 0.0094), and the model again outperformed the ATL-PI (C-index 0.72 vs. 0.70, respectively). The simplified m7-ATLPI, which is easier to use in clinical practice, achieved superior risk stratification compared to the ATL-PI, as did the original m7-ATLPI; the simplified version was calculated by summing the following: high-risk ATL-PI category (+10), low-risk ATL-PI category (−4), and non-silent mutations in TP53 (+4), IRF4 (+3), RHOA (+1), PRKCB (+1), CARD11 (+0.5), CCR7 (−2), and GATA3 (−3)

Accumulation of Pericardial Fat Correlates with Left Ventricular Diastolic Dysfunction in Patients with Normal Ejection Fraction

Background Left ventricular diastolic dysfunction (LVDD) plays an important role inheart failure with normal left ventricular ejection fraction (LVEF). Obesity is one ofthe major comorbid conditions of LVDD. Pericardial fat (PF) is an ectopic fat depotwith possible paracrine or mechanical effects on the coronary circulation and35 myocardial function.Methods We measured PF volume on 64 slice computed tomography and analyzedechocardiographic parameters to confirm LVDD in 229 consecutive patients suspectedof coronary artery disease with LVEF of more than 50% and no symptomatic heartfailure (59% men, 67±12 years). LVDD was defined as the ratio of transmitral40 Doppler early filling velocity to tissue Doppler early diastolic mitral annular velocity(E/e’) >10.Results PF volume correlated significantly with E/e’ (r=0.21, p<0.01), left ventricularmass index (r=0.23, p<0.001), and left atrial diameter (r=0.32, p<0.001). The mean PFvolume was significantly greater in patients with LVDD (184±61 cm3, n=141) than in45 those without LVDD (154±58, n=88, p<0.001). Multivariate logistic regressionanalysis indicated that PF volume correlated significantly with the presence of LVDD(odds ratio: 2.00 per 100 cm3 increase in PF volume, p=0.02) independent of age,gender, abdominal obesity, hypertension, and diabetes.Conclusions PF volumes are significantly associated with LVDD, independent of50 other factors such as hypertension or diabetes. PF may be implicated in the pathogenesis of LVDD in patients with normal LVEF

Aberrant overexpression of membrane-associated mucin contributes to tumor progression in adult T-cell leukemia/lymphoma cells.

Aberrant overexpression of membrane-associated mucin (MUC1) is implicated in the pathogenesis of cancer, particularly of adenocarcinomas. Adult T-cell leukemia/lymphoma (ATL), an aggressive neoplasm etiologically associated with human T-lymphotropic virus type-1 (HTLV-1), exhibits invasive tropism into various organs, resulting in disease progression and resistance to treatment. In the present study, we showed that MUC1 is overexpressed exclusively in cells of ATL among hematological malignancies. Furthermore, increased expression of MUC1 correlated with a poor prognosis, suggesting MUC1 to be a prognostic marker in ATL. Various functional analyses with knockdown experiments using a specific siRNA for MUC1 revealed that MUC1 is involved in cell growth, cell aggregation, and resistance to apoptosis. Although it has been shown that the anti-adhesive properties of MUC1 facilitate migration and metastasis of tumor cells, our findings indicated that MUC1 contributes to cell-cell adhesion. Mucins thus seem to play a role in the pathogenesis and/or progression of ATL