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Background Transplant kidney function is thought to be affected by sex differences, such as physical conditions including muscle volume, sex hormones, immune responses, and so forth. We examined the effect of sex differences on transplant kidney function. Methods The subjects were selected from kidney transplant recipients, who received kidney transplantation on our hospital between January 2000 and August 2015. Cadaveric donors and parent-child pairs with an age difference were excluded, then we included 47 recipients whose sex was different from the sex of the donor. We compared transplant kidney function between male donors and female recipients group (M→F, n = 20) and female donors and male recipients group (F→M, n = 27). Results Nadir creatinine value was higher in the F→M group than in the M→F group (1.09 mg/dL vs 0.76 mg/dL, P < .0001). The estimated glomerular filtration rate (eGFR) was significantly higher in the M→F group than in the F→M group (66.6 mL/min/1.73 m 2 vs 50.1 mL/min/1.73 m 2 , P = .002), and eGFR ratio (recipient to donor) was significantly higher in the M→F group than in the F→M group (1.13 vs 0.57, P < .0001). Multiple linear regression analysis showed that the only the sex of the recipient was significant prognostic factor of eGFR after renal transplantation ( P = .037). Conclusions The short-term kidney function of the graft from male to female was better than that of the graft from female to male. [ABSTRACT FROM AUTHOR]

Abstract: Background: Advanced glycation end products (AGEs) accumulate in lesions of arteriosclerosis, Alzheimer’s disease, rheumatoid arthritis, diabetic retinopathy, and diabetic nephropathy. Among AGEs, chemical quantification and immunohistologic methods for pentosidine have been established. Free pentosidine—eliminated by renal excretion— is mainly affected by renal function. In this study, we measured concentrations of plasma free and total pentosidine and immunohistologically investigated kidney graft biopsy specimens in patients after renal transplantation to investigate the renal function, plasma free and total pentosidine, and its relationship with deposition in the renal tissue. Patients and methods: In 28 patients who underwent renal transplantation from 1996 to 2003, we measured the time course of plasma concentrations of free pentosidine, total pentosidine, and serum creatinine starting right after renal transplantation. Thirty-four graft biopsy specimens were immunohistologically investigated using anti-pentosidine antibody. Plasma free and total pentosidine, and serum creatinine were measured at the same time. Results: Plasma free and total pentosidine were positively correlated with serum creatinine. Plasma free pentosidine and serum creatinine reached nadir values on day 34.2 ± 14.2, when the blood concentrations were 5.1 ± 1.6 pmol/mL and 1.7 ± 0.7 mg/dL, respectively. Plasma total pentosidine reached a nadir on day 116.5 ± 39.7 when the plasma concentration was 4.0 ± 1.5 pmol/mg. We correlated the time required to reach the nadir of plasma free and total pentosidine concentrations. However, neither the concentration of plasma free nor plasma total pentosidine at nadir correlated with serum creatinine. The intensity of immunostaining with anti-pentosidine antibody in proximal tubular cells was graded as weakly positive, positive, or strongly positive. Significant differences were obtained among plasma free pentosidine values between the weakly positive and strongly positive groups. Conclusions: Renal transplantation improves renal function and decreases renal excretion of free pentosidine. Accordingly, total pentosidine also decreases. However, the concentrations of plasma free and total pentosidine at nadir varied among individuals; the blood concentrations were not determined by renal function alone. It was suggested that deposition of pentosidine in proximal tubular cells was more severe among patients with higher plasma free pentosidine and serum creatinine values. [Copyright &y& Elsevier]

Abstract: A 50-year-old man, who had received an ABO-incompatible living related preemptive renal transplantation 1 year before, presented with painful lesions on both lower extremities and fever. At first, bacterial cellulitis was suspected and antibiotic therapy was initiated, but it was not effective. The serum cryptococcal antigen titer was 1:4,098, and pathologic examination of debrided tissue and wound pus culture revealed cryptococcal necrotizing fasciitis. Liposomal amphotericin B and fluconazole were started, and repeated debridement and skin grafting were performed. Because his graft function deteriorated because of antibody-mediated rejection and polyoma viral nephropathy, hemodialysis was induced on day 9 of hospitalization. During the treatment, he suffered repeated urinary tract infections, which were treated with antibiotics, and cytomegalovirus retinopathy, which was treated with ganciclovir. His cryptococcal necrotizing fasciitis was successfully cured by the combination of antimicrobial treatment and surgical procedures. He could walk with a cane and was discharged on day 298 of hospitalization. Cryptococcal necrotizing fasciitis in renal transplant recipients is so rare that only 14 cases have been reported. The mortality is not very high, but the prognosis of the patient is complicated by worsening of the cryptococcal infection of the central nervous system (CNS). Early detection and treatment to prevent spreading to other sites, especially the CNS or disseminated disease, is very important in cases of cryptococcal necrotizing fasciitis. [Copyright &y& Elsevier]

Abstract This paper introduces CMOS/magnetic tunnel junction (MTJ)-based asynchronous circuits for re-initialization free computing against power failures. The use of MTJ devices can realize continuous operations upon frequent power failures as data being processed are stored with nonvolatility. As asynchronous circuits exploit local control signals instead of a global clock signal, the MTJ-based asynchronous circuits can immediately restart operations after the power supply is recovered without waiting for the calibration time of phase-locked loops used in synchronous circuits. For the safe restore operations, the proposed circuits address issues of metastable states that might occur in the backup phase because of different timings of local control signals. In addition, write-reliable nonvolatile keepers (latches) are introduced in order to reduce write-error rates of MTJ devices for the safe backup operations. To evaluate the performance overheads due to the nonvolatile operations, the proposed asynchronous circuits are designed using TSMC 65 nm CMOS technology and a three-terminal MTJ model and are compared with conventional volatile asynchronous circuits in several benchmarks. [ABSTRACT FROM AUTHOR]

Background: Giant cell tumor of bone (GCTB) is a rare primary bone tumor, characterized by osteoclast-like giant cells that express receptor activator of nuclear factor-kappa B (RANK), and stromal cells that express RANK ligand (RANKL), a key mediator of osteoclast activation. A RANKL-specific inhibitor, denosumab, was predicted to reduce osteolysis and control disease progression in patients with GCTB. Patients and methods: Seventeen patients with GCTB were enrolled. Patients were treated with denosumab at 120 mg every 4 weeks, with a loading dose of 120 mg on days 8 and 15. To evaluate efficacy, objective tumor response was evaluated prospectively by an independent imaging facility on the basis of prespecified criteria. Results: The proportion of patients with an objective tumor response was 88% based on best response using any tumor response criteria. The proportion of patients with an objective tumor response using individual response criteria was 35% based on the modified Response Evaluation Criteria in Solid Tumors (RECIST) criteria, 82% based on the modified European Organization for Research and Treatment of Cancer (EORTC) criteria, and 71% based on inverse Choi criteria. The median time of study treatment was 13.1 months. Conclusion: The findings demonstrate that denosumab has robust clinical efficacy in the treatment of GCTB. [ABSTRACT FROM AUTHOR]

Abstract: The release of toxic anions during the chemical weathering of alkaline wastes such as blast furnace slag and coal fly ash presents a serious problem to public health and the environment. This study investigated arsenate sorption behavior onto Mg-bearing minerals formed in the Mg–Si–Al system at alkaline pH conditions in order to understand the safe removal and encapsulation of arsenate by Mg-bearing minerals under such conditions. Sorption experiments were performed during and after mineral formation and leaching tests using phosphate bearing solution were conducted to understand arsenic association with the minerals. The results revealed that brucite (Mg(OH)2), hydrotalcite (Mg6Al2(CO3)(OH)16·4(H2O)) and serpentine (MgSi2O5(OH)4) have high uptake capacity for arsenate. However, arsenic incorporation was only observed during the formation of high Al content hydrotalcite and serpentine minerals and was greatly enhanced at higher temperature. This implies that by controlling pore water chemistry of alkaline wastes with high reactivity, the irreversible fixation of arsenic by Mg-bearing minerals in alkaline conditions can be expected. [Copyright &y& Elsevier]

Abstract: Background: PRKAR1A gene encodes the type 1A regulatory subunit of protein kinase A. The mutation of this gene causes Carney complex which is an autosomal dominant multiple neoplasia syndrome characterized by spotty pigmentations, endocrine overactivity and cardiac myxoma. We hypothesized that cardiac myxoma may be associated with PRKAR1A gene mutation and determined whether mutation in the PRKAR1A gene is the cause of familial and sporadic cardiac myxoma. Methods: We studied seven patients (three males and four females) with cardiac myxoma. Two of them had familial cardiac myxoma complicated with Carney complex. The other five patients were characterized as sporadic cardiac myxomas. We analyzed the PRKAR1A gene of all patients by the polymerase chain reaction (PCR)–single-strand conformation method, followed with direct sequence analysis. Results: We identified a novel mutation (494delTG) in exon 4A of the PRKAR1A gene in the patients with Carney complex. A 16-year-old proband had a left atrial myxoma, pituitary adenoma and skin pigmentation. His father also had left atrial myxoma and skin pigmentation. In contrast, no mutations in the PRKAR1A gene were identified in the other five patients with sporadic cardiac myxomas. Conclusions: These results suggest that mutation of the PRKAR1A gene may be associated with familial cardiac myxoma in Carney complex but may not be associated with sporadic cardiac myxoma. [Copyright &y& Elsevier]

Core-binding factor α1 (Cbfa1) is an essential transcription factor for osteoblastic differentiation and osteogenesis. Bone morphogenetic protein (BMP) is also a powerful inducer of differentiation of pluripotent mesenchymal cells to osteoblast lineage and bone formation. Recent studies suggest that Cbfa1 plays a critical role during BMP-induced osteoblastic differentiation through association with cytoplasmic BMP signaling molecules, Smads. However, other studies have suggested that Cbfa1 may exhibit its osteogenic function without interaction with Smads. Therefore, it remains unclear whether association with Smad is essential for Cbfa1 function. In this study we examine the effects of Cbfa1 on osteoblastic differentiation in the presence or absence of interactions with Smad1 or Smad5 using C2C12 undifferentiated mesenchymal cells. Cbfa1 expression was induced upon stimulation with BMP-2 in C2C12 cells. Introduction of Cbfa1 into C2C12 cells induced osteoblastic differentiation and promoted transactivation of osteocalcin gene promoter without forming the complex with Smad1 or Smad5. Furthermore, in C2C12 cells in which the association of Cbfa1 with Smad1/Smad5 was prevented by the overexpression of the natural antagonist, Smad6, Cbfa1 still induced osteoblastic differentiation and transactivated osteocalcin gene promoter, regardless of BMP-2 stimulation. These results suggest that the interactions with Smad1 or Smad5 are not essential for Cbfa1 to demonstrate its osteogenic actions. However, interactions with Smad1/Smad5 enhance these osteogenic actions of Cbfa1. Of note, BMP-2-induced or Smad-induced osteoblastic differentiation was inhibited by dominant-negative Cbfa1, suggesting that the function of Cbfa1 is critical for BMP-2-induced osteoblastic differentiation. Our results suggest that Cbfa1 is essential and also sufficient to induce osteoblastic differentiation in undifferentiated mesenchymal cells, and establishment of an association with Smad1/Smad5 enhances the osteogenic actions of Cbfa1. On the other hand, Cbfa1 expression requires the activation of Smad1/Smad5 by BMP-2. [ABSTRACT FROM AUTHOR]

Purpose The perioperative survival of lung transplantation (LTx) for patients with idiopathic pulmonary arterial hypertension is known to be worse than for those with other underlying diseases because of difficulties in managing perioperative haemodynamic instability. High dose epoprostenol (PGI 2) is frequently used for patients with end-stage pulmonary hypertension (PH) before transplantation, however, it is generally discontinued at the time of transplantation. We hypothesized that tapering epoprostenol rather than abrupt discontinuation after reperfusion would improve perioperative outcomes. Methods We performed 193 LTxs since 2008 and 16 PH patients were on high dose epoprostenol (10-200 ng/kg/min) therapy. Epoprostenol was discontinued at the time of lung transplantation in 6 patients and it was tapered after reperfusion in ten patients. In the Discontinued group, epoprostenol was discontinued intraoperatively during extracorporeal membrane oxygenation (ECMO) or cardiopulmonary bypass and was not resumed postoperatively. In the Tapered group, epoprostenol was discontinued during extracorporeal support and was resumed at the quarter of preoperative dose after reperfusion. It was then gradually tapered typically over the following two weeks according to the heart function on echocardiography. Results One patient in the Discontinued group died on day 125 due to multiple organ failure, in contrast, no operative death was encountered in the Tapered group. Delayed chest closure and postoperative ECMO were more frequently required in the Discontinued group than the Tapered group (p = 0.0076, respectively). Primary graft dysfunction score was significantly lower in the Tapered group than the Discontinued group (0.6 ± 1.3 vs 2.2 ± 1.3 at 0h, p = 0.031; 0.4 ± 0.8 vs 2.0 ± 1.5 at 24h, p = 0.028; 0.3 ± 0.7 and 1.8 ± 1.5 at 48h, p = 0.033). Furthermore, the Tapered group required significantly shorter duration of postoperative mechanical ventilation (15.1 ± 6.8 vs 41.5 ± 41.9 days, p = 0.039). Conclusion Tapering epoprostenol administration after reperfusion for PH may be a valuable new strategy which is associated with better perioperative outcomes. [ABSTRACT FROM AUTHOR]