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Seed composition, including the protein, lipid and sucrose contents of 334 accessions of wild soybean (Glycine soja) collected in Japan, was evaluated using near-infrared reflectance spectroscopy (NIRS) technology. The distribution of protein, lipid and sucrose contents and correlations among these three classes of seed components were determined. Protein, lipid and sucrose levels ranged in accessions from 48.6 to 57.0, 9.0 to 14.3 and 1.24 to 3.53%, respectively. Average levels of protein, lipid and sucrose in the accessions were 54, 11 and 2.5%, respectively. High negative correlations were observed between the protein and lipid contents, and the protein and sucrose contents. Mean levels of the three constituents were compared among collection sites classified by climatic conditions. The total protein content of accessions from regions with a high annual mean temperature was high. The protein content of accessions from the II-1 region was higher than those from the III-3 region, and the sucrose content from the II-1 region was lower than those from regions III-2 and IV-3. The lipid content of plants from the II-1 region was lower than those from other regions, and the accessions in region II had a higher protein content and lower sucrose and lipid contents than the other regions. These results provide diverse and wide-ranged protein, lipid and sucrose contents information of Japanese wild soybean resources according to climatic region; thus, providing a foundation for the future development and selection of new soybean varieties with desired traits in global environmental changes.

Renal congestion is an issue of cardiorenal syndrome in patients with heart failure. Recent clinical and basic studies suggest a renoprotective potential of sodium–glucose cotransporter (SGLT) 2 inhibitors. However, the effect on renal congestion and its mechanism is not fully understood. Thus, we aimed to clarify the effect of SGLT inhibition in a renal congestion model. Renal congestion was induced in the left kidney of male Sprague-Dawley rats by ligation of the inferior vena cava between the renal veins. The SGLT2 inhibitor tofogliflozin or vehicle was orally administered daily from the day before IVC ligation until two days after surgery. On the third postoperative day, both the right control kidney and the left congested kidney were harvested and analyzed. Kidney weight and water content was increased, and renal injury and fibrosis were observed in the left congested kidney. Kidney weight gain and hydration were improved with tofogliflozin treatment. Additionally, this treatment effectively reduced renal injury and fibrosis, particularly in the renal cortex. SGLT2 expression was observed in the congested kidney, but suppressed in the damaged tubular cells. Molecules associated with inflammation were increased in the congested kidney and reversed by tofogliflozin treatment. Mitochondrial dysfunction provoked by renal congestion was also improved by tofogliflozin treatment. Tofogliflozin protects against renal damage induced by renal congestion. SGLT2 inhibitors could be a candidate strategy for renal impairment associated with heart failure.

Congestive heart failure produces fluid volume overload, central and renal venous pressure elevation, and consequently renal congestion, which results in worsening renal function. Pericyte detachment and pericyte-myofibroblast transition (PMT) were linked to renal interstitial fibrosis. Dahl salt-sensitive hypertensive (DahlS) rats are a non-surgical renal congestion model. The relation, however, between renal interstitial damage, pericyte morphology, and PMT in the renal congestion of DahlS rats has not been reported. DahlS rats (8-week-old) were fed normal salt (NS, 0.4% NaCl) or high salt (HS, 4% NaCl), and the left kidney was decapsulated to reduce renal interstitial hydrostatic pressure (RIHP) at 9 weeks old. One week after capsulotomy, both kidneys were analyzed by molecular and histological techniques. Renal pericyte structure was assessed in the body donors with/without venous stasis. Markers of tubulointerstitial damage, interstitial fibrosis, and PMT were upregulated in the right non-decapsulated kidney of DahlS rats fed HS. Renal tubular injury and fibrosis were detected in the HS diet groups in histological analysis. Pericyte detachment was observed in the right non-decapsulated kidney of DahlS rats fed HS by low vacuum-scanning electron microscopy. Decapsulation in DahlS rats fed HS attenuated these findings. Also, renal pericytes detached from the vascular wall in patients with heart failure. These results suggest that pericyte detachment and PMT induced by increased RIHP are responsible for tubulointerstitial injury and fibrosis in DahlS rats and humans with renal congestion. Renal venous congestion and subsequent physiological changes could be therapeutic targets for renal damage in cardiorenal syndrome.

BackgroundTolvaptan is an effective treatment for polycystic kidney disease (PKD), but also causes unfortunate polyuria. Hydrochlorothiazide (HCTZ) has been shown to reduce urine volume in nephrogenic diabetes insipidus, raising the possibility that HCTZ could also be effective in reducing tolvaptan-induced polyuria. In this study, we examined the combined administration of HCTZ and tolvaptan.MethodsMale PCK rats were divided into four groups of normal chow (Cont), normal chow plus tolvaptan, gavage HCTZ treatment, and tolvaptan + HCTZ. Biochemical examinations of the plasma and urine were performed as well as histological and molecular (mRNA and protein expression) analyses.ResultsGroups treated with tolvaptan had significantly higher 24 h urine excretion, which was significantly reduced in the tolvaptan + HCTZ group after 2 weeks. Cyst size, pERK protein expression, and Cyclin D1 mRNA expression were all significantly reduced in both the tolvaptan and tolvaptan + HCTZ groups, indicating that HCTZ did not affect the beneficial functions of tolvaptan. Notably, aquaporin 2 redistribution from the apical to intracellular domains was observed in tolvaptan-treated rats and was partially reversed in the tolvaptan + HCTZ group. The renal glomerular filtration rate was reduced in the tolvaptan + HCTZ group. Significantly lowered mRNA expression of neuronal nitric oxide synthase, prostaglandin E synthase 2 and renin were also found in the medulla, but not in the cortex.ConclusionHCTZ reduces tolvaptan-induced polyuria without altering its beneficial effects on PKD. This novel therapeutic combination could potentially lead to better PKD treatments and improved quality of life for the affected patients.

BackgroundNarrow-band imaging (NBI) classifications for Barrett’s esophagus have been proposed for the detection of early esophageal adenocarcinoma. We developed a simplified classification system with demonstrated high diagnostic accuracy and reproducibility among experienced endoscopists, but the feasibility of this system among novice endoscopists was unclear.MethodsIn the present study, eight novice endoscopists with no experience of magnification endoscopy were asked to review 248 images of Barrett’s esophagus (72 dysplastic, 176 non-dysplastic) obtained using high-definition magnification endoscopy with NBI 6 weeks before (1st test), immediately after (2nd test), and 6 weeks after (3rd test) being taught the simplified classification system. The primary outcomes were differences in diagnostic accuracy for dysplasia among the three tests.ResultsThe specificity and overall accuracy improved significantly in the 2nd vs. 1st test [97% vs. 80% (p < 0.001) and 94% vs. 82% (p < 0.001), respectively], but sensitivity was comparable (87% in both tests; p = 0.42). In the 3rd test, the sensitivity and overall accuracy decreased significantly compared with the 2nd test [82% vs. 87% (p < 0.001) and 93% vs. 94% (p < 0.05), respectively], but there was no significant difference in specificity (97% in both tests; p = 0.16). The kappa values for interobserver agreement for the mucosal pattern, vascular pattern, and predicted histology were substantial, and improved significantly in the 2nd vs. 1st test (0.78 vs. 0.59, 0.70 vs. 0.53, and 0.79 vs. 0.66, respectively; p < 0.001 for all).ConclusionsThe simplified NBI classification system may be appropriate for novice endoscopists to use in providing high accuracy and reproducibility.

Abstract Background Severe burn injuries create large skin defects that render the host susceptible to bacterial infections. Burn wound infection often causes systemic sepsis and severe septicemia, resulting in an increase in the mortality of patients with severe burn injuries. Therefore, appropriate wound care is important to prevent infection and improve patient outcomes. However, it is difficult to heal a third-degree burn injury. The aim of this study was to investigate whether hyperdry human amniotic membrane (HD-AM) could promote early granulation tissue formation after full-thickness skin excision in third-degree burn injury sites in mice. Methods After the development of HD-AM and creation of a third-degree burn injury model, the HD-AM was either placed or not placed on the wound area in the HD-AM group or HD-AM group, respectively. The groups were prepared for evaluation on postoperative days 1, 4 and 7. Azan staining was used for granulation tissue evaluation, and estimation of CD163, transforming growth factor beta-1 (TGF-β1), vascular endothelial growth factor (VEGF), CD31, alpha-smooth muscle actin (α-SMA) and Iba1 expression was performed by immunohistochemical staining. Quantitative reverse-transcription polymerase chain reaction (PCR) was used to investigate gene expression of growth factors, cell migration chemokines and angiogenic and inflammatory markers. Results The HD-AM group showed significant early and qualitatively good growth of granulation tissue on the full-thickness skin excision site. HD-AM promoted early-phase inflammatory cell infiltration, fibroblast migration and angiogenesis in the granulation tissue. Additionally, the early infiltration of cells of the immune system was observed. Conclusions HD-AM may be useful as a new wound dressing material for full-thickness skin excision sites after third-degree burn injuries, and may be a new therapeutic technique for improving the survival rate of patients with severe burn injuries.

ObjectiveFew data regarding the incidence of cancer-associated thromboembolism (TE) are available for Asian populations. We investigated the incidence of TE (TEi) and its risk factors among gastric and colorectal cancer (GCC) patients received chemotherapy in a daily practice setting.DesignA retrospective cohort study.SettingA single-institutional study that used data from Sapporo City General Hospital, Japan, on patients treated between January 2008 and May 2015.ParticipantsFive hundred Japanese GCC patients who started chemotherapy from January 2008 to May 2015.Primary and secondary outcome measuresTE was diagnosed by reviewing all the reports of contrast-enhanced CT performed during the follow-up period. All types of thrombosis detected by CT or additional imaging tests, such as venous TE, arterial TE and cerebral infarction, were defined as TE. Medical records of all identified patients were reviewed and potential risk factors for TE, including clinicopathological backgrounds, were collected. We defined the following patients as ‘active cancer’; patients with unresectable advanced GCC, cancer recurrence during or after completing adjuvant chemotherapy and/or presence of other malignant tumours.ResultsOf the 500 patients, 70 patients (14.0%) developed TE during the follow-up period. TEi was 9.2% and 17.3% in GCC patients, 18.1% and 3.5% in active and non-active cancer patients, and 24.0% and 12.9% in multiple and single primary, respectively. Multivariate logistic regression analysis showed that colorectal cancer (CRC) (OR 2.371; 95% CI 1.328 to 4.233), active cancer (OR 7.593; 95% CI 2.950 to 19.543) and multiple primary (OR 2.527; 95% CI 1.189 to 5.370) were independently associated with TEi.ConclusionTEi was 14.0% among Japanese GCC patients received chemotherapy, and was significantly higher among patients with CRC, active cancer and multiple primary than among those with gastric cancer, non-active cancer and single primary, respectively.Trial registration numberUMIN000018912.

TGF-β1, which can cause renal tubular injury through a vacuolar-type H + -ATPase (V-ATPase)-mediated pathway, is induced by the glucose degradation product methylglyoxal to yield peritoneal injury and fibrosis. The present study investigated the roles of V-ATPase and its accessory protein, the (pro)renin receptor, in peritoneal fibrosis during peritoneal dialysis. Rats daily administered 20 mM methylglyoxal intraperitoneally developed significant peritoneal fibrosis after 7 days with increased expression of TGF-β and V-ATPase, which was reduced by the inhibition of V-ATPase with co-administration of 100 mM bafilomycin A1. The (pro)renin receptor and V-ATPase were expressed in acidic organelles and cell membranes of human peritoneal mesothelial cells. TGF-β1 upregulated the expression of collagens, α-SMA, and EDA-fibronectin, together with ERK1/2 phosphorylation, which was reduced by inhibition of V-ATPase, (pro)renin receptor, or the MAPK pathway. Fibronectin and the soluble (pro)renin receptor were excreted from cells by acidic organelle trafficking in response to TGF-β1; this excretion was also suppressed by inhibition of V-ATPase. Soluble (pro)renin receptor concentrations in effluents of patients undergoing peritoneal dialysis were associated with the dialysate-to-plasma ratio of creatinine. Together, these results demonstrate a novel fibrosis mechanism through the (pro)renin receptor and V-ATPase in the acidic organelles of peritoneal mesothelial cells.

Rituximab maintains remission of complicated frequently relapsing or steroid-dependent nephrotic syndrome (FRNS/SDNS) by depleting peripheral B cells, but most patients eventually experience relapses after B cell recovery. We performed a multicenter, double-blind, randomized, placebo-controlled trial to assess rituximab’s efficacy and safety for childhood-onset uncomplicated FRNS/SDNS (without prior treatment with glucocorticoid-sparing immunosuppressive agents) with a follow-up study to assess rituximab’s long-term effect after B cell recovery. Patients were randomly assigned to receive either rituximab (375 mg/m 2 , maximum 500 mg, once weekly for 2 weeks) or placebo. The primary endpoint was the relapse-free period. Of 43 randomized patients, 40 received the intervention (18 rituximab, 22 placebo). The relapse-free period during the 1-year trial was significantly longer in the rituximab vs. placebo groups (median: 285 vs. 81 days; p  < 0.001). Infusion reactions were more frequent in the rituximab group ( p  < 0.001), with no difference in adverse events incidence between the groups. Interestingly, the follow-up study demonstrated markedly higher 3-year cumulative relapse-free survival probability without further treatments in the rituximab vs. placebo groups (38% vs. 9%). A mini-systematic review with meta-analyses supported the findings. Rituximab is effective and well-tolerated, potentially leading to long-term remission with substantially high rates after B cell recovery for childhood-onset uncomplicated FRNS/SDNS. Trial registration JSKDC10, Clinical Trials Registry ID: jRCT1091220380; JSKDC10 follow-up study, Clinical Trials Registry ID: jRCT1050230024

In recent years, the study of resting state neural activity has received much attention. To better understand the roles of different brain regions in the regulation of behavioral activity in an arousing or a resting period, we developed a novel behavioral paradigm (8-arm food-foraging task; 8-arm FFT) using the radial 8-arm maze and examined how AcbC lesions affect behavioral execution and learning. Repetitive training on the 8-arm FFT facilitated motivation of normal rats to run quickly to the arm tips and to the center platform before the last-reward collection. Importantly, just after this point and before confirmation of no reward at the next arm traverse, locomotor activity decreased. This indicates that well-trained rats can predict the absence of the reward at the end of food seeking and then start another behavior, namely planned resting. Lesions of the AcbC after training selectively impaired this reduction of locomotor activity after the last-reward collection without changing activity levels before the last-reward collection. Analysis of arm-selection patterns in the lesioned animals suggests little influence of the lesion in the ability to predict the reward absence. AcbC lesions did not change exploratory locomotor activity in an open-field test in which there were no rewards. This suggests that the AcbC controls the activity level of planned resting behavior shaped by the 8-arm FFT. Rats receiving training after AcbC lesioning showed a reduction in motivation for reward seeking. Thus, the AcbC also plays important roles not only in controlling the activity level after the last-reward collection but also in motivational learning for setting the activity level of reward-seeking behavior.