Nitinol stenting improves primary patency of the superficial femoral artery after percutaneous transluminal angioplasty in hemodialysis patients: A propensity-matched analysis

BackgroundAlthough percutaneous transluminal angioplasty (PTA) has become a common therapeutic standard for peripheral artery disease (PAD), high restenosis rates in the superficial femoral artery (SFA) remain a major problem. Nitinol stent implantation is reported to reduce restenosis in SFA after PTA in the general population; however, little is known about whether the nitinol stent improves primary patency after PTA in hemodialysis patients who are at higher risk of revascularization failure. The aim of this study was to clarify the effects of nitinol stent implantation for primary patency in SFA after PTA in hemodialysis patients with PAD.MethodsEighty consecutive hemodialysis patients (167 SFA lesions) who underwent PTA with nitinol stents from January 2006 to January 2008 were compared with 64 hemodialysis patients (128 SFA lesions) who received stainless steel stents in the preceding 2 years. In the follow-up study to 2 years, incidence of restenosis, amputation, and all-cause mortality were analyzed. End points between the groups were examined with the Kaplan-Meier and log-rank methods. Prognostic values for end points were calculated by a Cox univariate analysis and Cox multivariable regression models. To statistically minimize the differences in each stent group, a propensity-matched analysis was also performed using the model including male gender, age, diabetes, hypertension, hyperlipidemia, smoking, incidence of ulcer/gangrene, and TransAtlantic Inter-Society Consensus (TASC) type C+D.ResultsThe 2-year primary patency rate was 58% in the nitinol group vs 42% in the stainless steel group (hazard ratio [HR], 0.58; 95% confidence interval [CI], 0.39-0.84; P = .0045), despite a higher prevalence of TASC C+D lesion in the nitinol group (68% vs 49%, P = .0014). In 108 lesions matched after propensity score analysis, the primary patency for 2 years was 64% in the nitinol group vs 42% in the stainless steel group (HR, 0.39; 95% CI, 0.24-0.65; P = .0003). Cox multivariate models showed nitinol stent (HR, 0.42; 95% CI, 0.25-0.73; P = .002), age (HR, 1.04; 95% CI, 1.01-1.08; P = .031), and incidence of ulcer/gangrene (HR, 2.35; 95% CI, 1.17-4.75; P = .017) were independent predictors of restenosis.ConclusionThese data suggest that nitinol stent implantation improves primary patency in SFA after PTA compared with the stainless steel stent, even in hemodialysis patients with PAD

Double strand break repair by capture of retrotransposon sequences and reverse-transcribed spliced mRNA sequences in mouse zygotes

Ono, R., Ishii, M., Fujihara, Y. et al. Double strand break repair by capture of retrotransposon sequences and reverse-transcribed spliced mRNA sequences in mouse zygotes. Sci Rep 5, 12281 (2015). https://doi.org/10.1038/srep1228

Induction of DNA Methylation by Artificial piRNA Production in Male Germ Cells

SummaryGlobal DNA demethylation and subsequent de novo DNA methylation take place in mammalian male embryonic germ cells [1–3]. P-element-induced wimpy testis (PIWI)-interacting RNAs (piRNAs), which are germline-specific small RNAs, have been postulated to be critically important for de novo DNA methylation of retrotransposon genes, and many proteins, including PIWI family proteins, play pivotal roles in this process [4–6]. In the embryonic mouse testis, two mouse PIWI proteins, mouse PIWI-like (MILI) and mouse PIWI2 (MIWI2), are involved in the biogenesis of piRNAs through the so-called ping-pong amplification cycle [7–10], and long single-stranded RNAs transcribed from the gene regions of piRNA clusters have been proposed to be the initial material [11–16]. However, it remains unclear whether transcription from the piRNA clusters is required for the biogenesis of piRNAs. To answer this question, we developed a novel artificial piRNA production system by simple expression of sense and antisense EGFP mRNAs in embryonic male germ cells in the piRNA biogenesis phase. EGFP expression was silenced by piRNA-dependent DNA methylation, indicating that concomitant expression of sense and antisense RNA transcripts is necessary and sufficient for piRNA production and subsequent piRNA-dependent gene silencing. In addition, we demonstrated that this artificial piRNA induction paradigm could be applied to an endogenous gene essential for spermatogenesis, DNMT3L [3, 17, 18]. This study not only provides novel insights into the molecular mechanisms of piRNA production, but also presents an innovative strategy for inducing epigenetic modification in germ cells

IgSF11 regulates osteoclast differentiation through association with the scaffold protein PSD-95

Kim, H., Takegahara, N., Walsh, M.C. et al. IgSF11 regulates osteoclast differentiation through association with the scaffold protein PSD-95. Bone Res 8, 5 (2020). https://doi.org/10.1038/s41413-019-0080-

QUALITY OF LIFE IN PATIENTS WITH DIABETES MELLITUS

We evaluated the quality of life (QOL) in 268 patients with diabetes mellitus (NIDDM, 250 cases; IDDM, 10 cases; and other type of diabetes, 8 cases) to determine which aspects were adversely affected by the disease. Information concerning life satisfaction, social activities, ability to work, sexual problems and physical symptoms was obtained from a 30-item questionnaire. Clinical characteristics including duration of diabetes, glycemic control, current treatment, obesity, hypertension, hyperlipidemia, macro- and microvascular complications were obtained from medical records. Diminished QOL was most pronounced in patients who had had a long duration of disease, required insulin therapy, and whose health was disturbed by cerebrovascular disease, end-stage renal disease, mono- and autonomic neuropathy. A significant difference in the subdimensional QOL score was noted in life satisfaction, social activities, ability to work, sexual problems and physical symptoms under these circumstances

A facile approach to synthesize an oxo-functionalized graphene/polymer composite for low-voltage operating memory devices

Memory devices are a key technology of our era and one of the constant challenges is the reduction of their power consumption. Herein, we demonstrate that graphene oxide with very few defects, that is, about 1 nm thin oxo-functionalized graphene derivative, can be used in memory devices operating at 3 V. A memory device stores charges in the material of the active channel. Thereby, writing and erasing information can be performed at low voltage, facilitating low power consumption. To enable operation at low voltage, a novel synthetic approach is necessary. We find that the selective non-covalent electrostatic functionalization of mainly organosulfate ions is possible with dodecylammonium. This functionalization allows the non-covalent coating of flakes with a polystyrene-derivative as nm-thin dielectric medium. The resulting polymer-wrapped composite has a height of about 5 nm. We find that the thin coating of a few nm is mandatory to make the memory device work at low voltage. Furthermore, a self-assembled monolayer of an imidazolium derivative further enhances the function of the memory device. The prepared composite materials are characterized by state-of-the-art analysis including solid state nuclear magnetic resonance spectroscopy and thermogravimetric analysis coupled with gas chromatography, mass spectroscopy or infrared spectroscopy. Reference experiments prove the importance of the controlled synthesis to enable the function of the memory device

Disease-specific autoantibody production in the lungs and salivary glands of anti-synthetase syndrome

Interstitial lung disease is a common complication of anti-synthetase syndrome (ASS), and lymphocytic infiltration is often observed in the lesion. We have recently reported that disease-specific autoantibodies are produced by infiltrating lymphocytes in some autoimmune diseases. Here, we investigate the antigen specificity of B cells in the lung lesions of ASS patients. A total of 177 antibodies were produced from antibody-secreting cells in bronchoalveolar fluid (BALF) of three each of serum anti-Jo-1 and serum anti-EJ antibody–positive patients. Twelve to 30% and 50 to 62% of these antibodies were disease-specific autoantibodies, respectively. These autoantibodies recognized conformational epitopes of the whole self-antigen and had affinity maturations, indicating that self-antigens themselves are the target of humoral immunity. In addition, 100 antibodies were produced from two salivary gland tissues, obtained by chance, of ASS patients. Salivary glands are not generally recognized as lesions of ASS, but unexpectedly, ASS-related autoantibody production was also observed similar to that of BALF. Immunostaining confirmed the presence of ASS-related autoantibody-producing cells in salivary glands. Our results suggest that disease-specific autoantibody production at lesion sites is a common pathogenesis of autoimmune diseases, and that tissue-specific production of autoantibodies can provide insights regarding the distribution of organ manifestations in autoimmune diseases