Bilayer graphene (BLG) comprises a 2D nanospace sandwiched by two parallel graphene sheets that can be used to intercalate molecules or ions for attaining novel functionalities. However, ...intercalation is mostly demonstrated with small, exfoliated graphene flakes. This study demonstrates intercalation of molybdenum chloride (MoCl5) into a large‐area, uniform BLG sheet, which is grown by chemical vapor deposition (CVD). This study reveals that the degree of MoCl5 intercalation strongly depends on the stacking order of the graphene; twist‐stacked graphene shows a much higher degree of intercalation than AB‐stacked. Density functional theory calculations suggest that weak interlayer coupling in the twist‐stacked graphene contributes to the effective intercalation. By selectively synthesizing twist‐rich BLG films through control of the CVD conditions, low sheet resistance (83 Ω ▫−1) is realized after MoCl5 intercalation, while maintaining high optical transmittance (≈95%). The low sheet resistance state is relatively stable in air for more than three months. Furthermore, the intercalated BLG film is applied to organic solar cells, realizing a high power conversion efficiency.
Intercalation of MoCl5 into large‐area bilayer graphene (BLG) grown by chemical vapor deposition is performed. Twist stacking gives a much higher degree of MoCl5 intercalation than AB stacking. A low sheet resistance with high optical transmittance is obtained by using twist‐rich BLG. A transparent electrode suitable for use in organic solar cells is developed from this intercalated bilayer.
Heatstroke is a serious heat-related illness that can even cause death. Heat alert systems play an important role in reducing the number of patients experiencing heat illness, as they encourage ...preventive actions such as the use of air conditioning, hydration, or other strategies. However, to date, the Japanese hazard classification has not considered seasonal and regional variations, despite clear differences in meteorological conditions across different regions in Japan. Moreover, several studies have reported a difference in thermoregulation between older and younger adults, implying that the hazard classification should also consider age differences. This study examined the relationship between the number of ambulance dispatches related to heat illness (ADRHI) and the Japanese heat hazard classification from 2010 to 2019, focusing on monthly and regional differences. Data from 47 prefectures during the 10-year period were collected and analyzed. ADRHI and wet bulb globe temperature (WBGT) data were collected from Japan's Ministry of Internal Affairs and Communications and the Ministry of the Environment Heat Illness Prevention Information website, respectively. The findings showed a significant relationship between ADRHI and WBGT.sub.max (p < 0.05, r = 0.74). ADRHI per 100,000 people showed significant differences across months. The post hoc test detected the first steep increase in ADRHI at a WBGT.sub.max of 23°C than at 22°C in June, and at a WBGT.sub.max of 26°C, 27°C, and 25°C in July, August, and September, respectively. Moreover, the first significant increase in ADRHI per 100,000 people at WBGT.sub.max differed across each region, at a WBGT.sub.max of 24°C in Hokkaido-Tohoku, 25°C in Kanto, Kansai, and Chugoku, 26°C in Chubu, 27°C in Shikoku, and 28°C in Kyushu-Okinawa. Further, Poisson regression analysis revealed that the relative risks differed across each region and month. These results imply that the hazard classification should be adjusted according to region and month in Japan.
Blood types are classified based on the specific antigenic characteristics they possess. Despite documented associations between antigens and inflammation, a scarcity of data exists concerning the ...impact of antigens on atrial fibrillation (AF).
OSHOH-rhythm study is a multi-center, prospective observational study of 601 patients who underwent catheter ablation for AF. We examined the correlation between blood type groups and both the incidence and recurrence of AF. Additionally, we analyzed the recurrence of AF across antigenic profiles.
The frequencies of individual blood types were 239 (39.8 %), 190 (31.6 %), 122 (20.3 %), and 50 (8.3 %) for A, O, B, and AB, respectively, aligning closely with the prevalent blood type distribution among the Japanese populace. During follow-up period (18.8 months, median), AF recurrence occurred in 96 patients (22.4 %) lacking the B antigen (A and O), and 26 patients (15.1 %) possessing B antigen (B and AB), respectively (Log-rank test: P = 0.034). A multivariate analysis demonstrated that blood types lacking the B antigen (hazard ratio HR, 1.55; 95 % CI, 1.01 to 2.42; P = 0.037), hypertension (HR, 1.51; 95 % CI, 1.05 to 2.17; P = 0.026) and non-paroxysmal AF (HR, 1.70; 95 % CI, 1.17 to 2.47; P = 0.005) were independently associated with the recurrence of AF.
This study elucidates that, despite the absence of direct correlation between blood types and the occurrence of AF, blood types devoid of the B antigen exhibit an enhanced predisposition to AF recurrence. Nonetheless, the intricate mechanism linking blood type to recurrence remains elusive, warranting further comprehensive foundational research on blood types.
•The distribution of atrial fibrillation patients according to blood type was in concordance with the proportions of blood types observed within the Japanese populace.•Notably, there was no clear difference in incidence of atrial fibrillation between the different blood types.•Non-B antigen blood types (A and O) emerged as independent risk factors for the recurrence of atrial fibrillation after catheter ablation.•This study constituted a research endeavor that elucidated variations in the recurrence rates of atrial fibrillation across different blood groups, thereby implying a novel clinical approach.
Metformin has been widely used as a first-line agent to treat type 2 diabetes mellitus. Lactic acidosis is a rare but serious adverse effect in patients treated with metformin. Recent studies noted a ...correlation between metformin accumulation and lactic acidosis. Continuous renal replacement therapy for the treatment of metformin-associated lactic acidosis has been documented in some case reports; however, there is currently no specific treatment for metformin-associated lactic acidosis.
A 70-year-old Japanese woman with type 2 diabetes mellitus presented to an emergency room with metformin-associated lactic acidosis. She was found to be hypotensive and laboratory examinations revealed severe lactic acidosis: pH 6.618, partial pressure of carbon dioxide in arterial blood 17.3 mmHg, bicarbonate 1.7 mmol/L, and lactate 18 mmol/L. Severe acidemia persisted despite supportive care including intravenously administered fluids, sodium bicarbonate, antibiotics, and vasopressors. Continuous renal replacement therapy was initiated in our intensive care unit. After dialysis for 3 days, her lactate level and pH value completely normalized. The concentration of metformin detected was 77.5 mg/L, which is one of the highest in metformin-associated lactic acidosis successfully treated without overdose.
The present case had one of the highest metformin concentrations in metformin-associated lactic acidosis successfully treated with continuous renal replacement therapy, and serum metformin concentrations may be useful for the diagnosis of metformin-associated lactic acidosis. Metformin-associated lactic acidosis is a rare but important etiology of lactic acidosis. Continuous renal replacement therapy is advantageous for the treatment of hemodynamically unstable patients with metformin-associated lactic acidosis.
Background:The epidemiological data of pulmonary hypertension (PH) due to left heart disease (LHD) are limited. This study investigated hemodynamic and clinical factors associated with mortality in ...patients with PH due to LHD.Methods and Results:We conducted a retrospective review in 243 patients with PH due to LHD, defined as mean pulmonary arterial pressure ≥25 mmHg and pulmonary wedge pressure >15 mmHg at rest in right heart catheterization. Kaplan-Meier and Cox proportional hazard regression analyses were performed. Seventy-five patients died during an average follow-up of 52 months (range, 20–73 months). On multivariate analysis, only diastolic pulmonary vascular pressure gradient (DPG) ≥7 mmHg among hemodynamic measurements was a predictor of mortality. Elevated N-terminal pro-brain natriuretic peptide (NT-pro BNP), more severe New York Heart Association (NYHA) class, anemia, and renal dysfunction were more strongly associated with mortality. Mean right atrial pressure (RAP) and currently available markers of pulmonary vascular remodeling including transpulmonary pressure gradient (TPG) and pulmonary vascular resistance (PVR) had no effect on survival.Conclusions:DPG is weakly associated with mortality in PH due to LHD. Clinical factors such as NT-pro BNP, NYHA class, anemia and renal dysfunction are superior predictors. The prognostic ability of hemodynamic factors such as mean RAP, TPG, PVR and DPG is limited. (Circ J 2016; 80: 243–249)
Focal atrial tachycardia (AT) originating from the left atrial appendage (LAA) is one of the rare supraventricular tachycardias and is likely to cause arrhythmia-induced heart failure. Surgical ...treatment could be an alternative therapy because antiarrhythmic drugs and catheter ablation therapy to focal AT originating from the distal portion of the LAA is still challenging. We report a case of successful operation of minimally invasive thoracoscopic appendectomy in a patient with poor left ventricular (LV) function due to drug-resistant AT originating from the LAA for the first time. A 51-year-old female who had AT with a poor LV function suffered from congestive heart failure. We diagnosed the ongoing AT as focal AT that originated from the distal portion of LAA by electrophysiological examination. Total thoracoscopic stand-alone appendectomy was performed safely. AT was terminated and restored to sinus rhythm immediately after appendectomy.
<Learning objective: Although catheter ablation has become a first-line treatment for almost all cardiac arrhythmias, it is difficult to achieve complete cure of atrial tachycardia (AT) originating from the distal portion of left atrial appendage (LAA) because there is AT recurrence and risk of cardiac perforation and ischemic stroke. Minimally invasive thoracoscopic appendectomy is curative and can be applied safely even in patients who have poor left ventricular function due to focal AT originating from the LAA.>
Gastritis cystica polyposa (GCP) is a recently recognized entity histologically characterized by hyperplasia and cystic dilatation of the gastric glands spreading through the submucosal layer. Its ...symptoms include those affecting the upper gastrointestinal tract, such as upper abdominal pain, nausea, and anorexia, although some patients might be asymptomatic. GCP rarely causes severe hemorrhage. Recently, we encountered a GCP case that exhibited severe hemorrhage.
A 53 year-old man visited the emergency department complaining of hematemesis. He underwent distal gastrectomy and Billroth II reconstruction for duodenal ulcers 32 years ago. Upper gastrointestinal endoscopy detected bleeding from the reddened mucosa at the anastomosis; thus, tentative endoscopic hemostasis was conducted. Despite medical treatment with transfusion, melena with significant hemodynamic impairment persisted. He was treated again with endoscopic hemostasis and interventional radiology (IVR) but remained unresponsive to these procedures. He eventually underwent partial resection of the anastomosis site with Roux-en-Y reconstruction and finally achieved excellent postoperative recovery. Histopathological examination of the resected specimen suggested a GCP bleeding.
GCP can indeed cause severe hemorrhage. Hemorrhage caused by GCP may not respond to endoscopic hemostasis or IVR; therefore, surgical treatment should be decided without delay.
Regulatory T cells (Tregs) have been reported to play a pivotal role in the vascular remodeling of pulmonary arterial hypertension (PAH). Recent studies have revealed that Tregs are heterogeneous and ...can be characterized by three phenotypically and functionally different subsets. In this study, we investigated the roles of Treg subsets in the pathogenesis of PAH in eight patients with PAH and 14 healthy controls. Tregs and their subsets in peripheral blood samples were analyzed by flow cytometry. Treg subsets were defined as CD4
+
CD45RA
+
FoxP3
low
resting Tregs (rTregs), CD4
+
CD45RA
−
FoxP3
high
activated Tregs (aTregs), and CD4
+
CD45RA
−
FoxP3
low
non-suppressive Tregs (non-Tregs). The proportion of Tregs among CD4
+
T cells was significantly higher in PAH patients than in controls (6.54 ± 1.10 vs. 3.81 ± 0.28 %,
p
< 0.05). Of the three subsets, the proportion of non-Tregs was significantly elevated in PAH patients compared with controls (4.06 ± 0.40 vs. 2.79 ± 0.14 %,
p
< 0.01), whereas those of rTregs and aTregs were not different between the two groups. Moreover, the expression levels of cytotoxic T lymphocyte antigen 4, a functional cell surface molecule, in aTregs (
p
< 0.05) and non-Tregs (
p
< 0.05) were significantly higher in PAH patients compared with controls. These results suggested the non-Treg subset was expanded and functionally activated in peripheral lymphocytes obtained from IPAH patients. We hypothesize that immunoreactions involving the specific activation of the non-Treg subset might play a role in the vascular remodeling of PAH.
We sought to identify a secreted biomarker for β-catenin activation commonly seen in hepatocellular carcinoma (HCC). By examination of our previously published genearray of hepatocyte-specific ...β-catenin knockout (KO) livers, we identified secreted factors whose expression may be β-catenin-dependent. We verified expression and secretion of the leading factor in HCC cells transfected with mutated (Hep3BS33Y)-β-catenin. Serum levels of biomarker were next investigated in a mouse model of HCC with β-catenin gene (Ctnnb1) mutations and eventually in HCC patients. Leukocyte cell-derived chemotaxin-2 (LECT2) expression was decreased in KO livers. Hep3BS33Y expressed and secreted more LECT2 in media as compared to Hep3BWT. Mice developing HCC with Ctnnb1 mutations showed significantly higher serum LECT2 levels. However patients with CTNNB1 mutations showed LECT2 levels of 54.28 ± 22.32 ng/mL (Mean ± SD; n = 8) that were insignificantly different from patients with non-neoplastic chronic liver disease (32.8 ± 21.1 ng/mL; n = 15) or healthy volunteers (33.2 ± 7.2 ng/mL; n = 11). Intriguingly, patients without β-catenin mutations showed significantly higher serum LECT2 levels (54.26 ± 22.25 ng/mL; n = 46). While β-catenin activation was evident in a subset of non-mutant β-catenin HCC group with high LECT2 expression, serum LECT2 was unequivocally similar between β-catenin-active and -normal group. Further analysis showed that LECT2 levels greater than 50 ng/ml diagnosed HCC in patients irrespective of β-catenin mutations with specificity of 96.1% and positive predictive value of 97.0%. Thus, LECT2 is regulated by β-catenin in HCC in both mice and men, but serum LECT2 reflects β-catenin activity only in mice. Serum LECT2 could be a potential biomarker of HCC in patients.
β-catenin signaling is a major oncogenic pathway in hepatocellular carcinoma (HCC). Since β-catenin phosphorylation by glycogen synthase kinase 3β (GSK3β) and casein kinase 1ε (CK1ε) results in its ...degradation, mutations affecting these phosphorylation sites cause β-catenin stabilization. However, the relevance of missense mutations in non-phosphorylation sites in exon 3 remains unclear. The current study explores significance of such mutations in addition to addressing the clinical and biological implications of β-catenin activation in human HCC.
Gene alteration in exon3 of CTNNB1, gene expression of β-catenin targets such as glutamate synthetase (GS), axin2, lect2 and regucalcin (RGN), and protein expression of β-catenin were examined in 125 human HCC tissues.
Sixteen patients (12.8%) showed conventional missense mutations affecting codons 33, 37, 41, and 45. Fifteen additional patients (12.0%) had other missense mutations in codon 32, 34, and 35. Induction of exon3 mutation caused described β-catenin target gene upregulation in HCC cell line. Interestingly, conventional and non-phosphorylation site mutations were equally associated with upregulation of β-catenin target genes. Nuclear localization of β-catenin was associated with poor overall survival (p = 0.0461). Of these patients with nuclear β-catenin localization, loss of described β-catenin target gene upregulation showed significant poorer overall survival than others (p = 0.0001).
This study suggests that both conventional and other missense mutations in exon 3 of CTNNB1 lead to β-catenin activation in human HCC. Additionally, the mechanism of nuclear β-catenin localization without upregulation of described β-catenin target genes might be of clinical importance depending on distinct mechanism.
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