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CO 2 methanation is a promising technology to enable the use of CO 2 as a resource. Thermal control of CO 2 methanation, which is a highly active exothermic reaction, is important to avoid thermal runaway and subsequent degradation of the catalyst. Using the heat storage capacity of a phase change material (PCM) for thermal control of the reaction is a novel passive approach. In this study a novel structure was developed, wherein catalysts were directly loaded onto a micro-encapsulated PCM (MEPCM). The MEPCM was prepared in three steps consisting of a boehmite treatment, precipitation treatment, and heat oxidation treatment, and an impregnation process was adopted to prepare a Ni catalyst. The catalyst-loaded MEPCM did not show any breakage or deformation of the capsule or a decrease in the heat storage capacity after the impregnation treatment. MEPCM demonstrated a higher potential as an alternative catalyst support in CO 2 methanation than the commercially available α-Al 2 O 3 particle. In addition, the heat storage capacity of the catalyst-loaded MEPCM suppressed the temperature rise of the catalyst bed at a high heat absorption rate (2.5 MW m −3 ). In conclusion, the catalyst-loaded MEPCM is a high-speed, high-precision thermal control device because of its high-density energy storage and resolution of a spatial gap between the catalyst and cooling devices. This novel concept has the potential to overcome the technical challenges faced by efficiency enhancement of industrial chemical reactions.

Pancreatic ductal adenocarcinoma has a particularly poor prognosis as it is often detected at an advanced stage and acquires resistance to chemotherapy early during its course. Stress adaptations by mitochondria, such as metabolic plasticity and regulation of apoptosis, promote cancer cell survival; however, the relationship between mitochondrial dynamics and chemoresistance in pancreatic ductal adenocarcinoma remains unclear. We here established human pancreatic cancer cell lines resistant to gemcitabine from MIA PaCa‐2 and Panc1 cells. We compared the cells before and after the acquisition of gemcitabine resistance to investigate the mitochondrial dynamics and protein expression that contribute to this resistance. The mitochondrial number increased in gemcitabine‐resistant cells after resistance acquisition, accompanied by a decrease in mitochondrial fission 1 protein, which induces peripheral mitosis, leading to mitophagy. An increase in the number of mitochondria promoted oxidative phosphorylation and increased anti‐apoptotic protein expression. Additionally, enhanced oxidative phosphorylation decreased the AMP/ATP ratio and suppressed AMPK activity, resulting in the activation of the HSF1–heat shock protein pathway, which is required for environmental stress tolerance. Synergistic effects observed with BCL2 family or HSF1 inhibition in combination with gemcitabine suggested that the upregulated expression of apoptosis‐related proteins caused by the mitochondrial increase may contribute to gemcitabine resistance. The combination of gemcitabine with BCL2 or HSF1 inhibitors may represent a new therapeutic strategy for the treatment of acquired gemcitabine resistance in pancreatic ductal adenocarcinoma.

It is known that in the silkworm ( Bombyx mori ), males have two Z sex chromosomes whereas females have Z and W and the W chromosome has a dominant role in female determination; here a single female-specific W-chromosome-derived PIWI-interacting RNA is shown to be the feminizing factor in B. mori . The silkworm feminizing factor Susumu Katsuma and colleagues have answered a question that has perplexed insect geneticists for more than eight decades — how does the W chromosome determine femaleness in the silkworm Bombyx mori and many other Lepidoptera? In this system, males have two Z sex chromosomes and females have one Z and one W. The authors show that the feminizing factor is a single W chromosome-derived PIWI-interacting RNA (piRNA). The piRNA silences the product of a gene located on the Z chromosome (named Masc ) that encodes a CCCH-type zinc finger protein. This silencing is in turn important for the production of female-specific isoforms of the doublesex gene that acts at the downstream end of the sex differentiation cascade in the embryo. In male embryos Masc protein controls both dosage compensation and masculinization. The silkworm Bombyx mori uses a WZ sex determination system that is analogous to the one found in birds and some reptiles. In this system, males have two Z sex chromosomes, whereas females have Z and W sex chromosomes. The silkworm W chromosome has a dominant role in female determination 1 , 2 , suggesting the existence of a dominant feminizing gene in this chromosome. However, the W chromosome is almost fully occupied by transposable element sequences 3 , 4 , 5 , and no functional protein-coding gene has been identified so far. Female-enriched PIWI-interacting RNAs (piRNAs) are the only known transcripts that are produced from the sex-determining region of the W chromosome 6 , but the function(s) of these piRNAs are unknown. Here we show that a W-chromosome-derived, female-specific piRNA is the feminizing factor of B. mori . This piRNA is produced from a piRNA precursor which we named Fem . Fem sequences were arranged in tandem in the sex-determining region of the W chromosome. Inhibition of Fem -derived piRNA-mediated signalling in female embryos led to the production of the male-specific splice variants of B. mori doublesex ( Bmdsx ), a gene which acts at the downstream end of the sex differentiation cascade 7 , 8 . A target gene of Fem -derived piRNA was identified on the Z chromosome of B. mori . This gene, which we named Masc , encoded a CCCH-type zinc finger protein. We show that the silencing of Masc messenger RNA by Fem piRNA is required for the production of female-specific isoforms of Bmdsx in female embryos, and that Masc protein controls both dosage compensation and masculinization in male embryos. Our study characterizes a single small RNA that is responsible for primary sex determination in the WZ sex determination system.

Post-hepatectomy bile leakage (PHBL) is a potentially fatal complication that can arise after hepatectomy. Previous studies have identified obesity as a risk factor for PHBL. In this study, we investigated the impact of sarcopenic obesity on PHBL in hepatocellular carcinoma (HCC) patients. In total, we enrolled 409 patients who underwent hepatectomy without bilioenteric anastomosis for HCC between January 2010 and August 2021. Patients were grouped according to the presence or absence of PHBL. Patient characteristics, including body mass index and sarcopenic obesity, were then analyzed for predictive factors for PHBL. Among the 409 HCC patients included in the study, 39 developed PHBL. Male sex, hypertension, cardiac disease, white blood cell counts, the psoas muscle area, and visceral fat area, and intraoperative blood loss were significantly increased in the PHBL (+) group compared with the PHBL (-) group. Multivariate analysis showed that the independent risk factors for the occurrence of PHBL were intraoperative blood loss [greater than or equal to]370 mL and sarcopenic obesity. Our results show that it is important to understand whether a patient is at high risk for PHBL prior to surgery and to focus on reducing intraoperative blood loss during surgery for patients with risk factors for PHBL.

Purpose The primary purpose of this study was to evaluate the second-look arthroscopic findings 1 year postoperatively and magnetic resonance imaging (MRI) findings 2 years after anterior cruciate ligament reconstruction (ACLR) using bone-patellar tendon–bone autograft (BTB) or hamstring tendon autograft (HT). Secondary purpose included clinical results from physical examination, including range of motion, Lachman test, pivot shift test, and knee anterior laxity evaluation, and the clinical score for subjective evaluations at 2 years after surgery. Methods Between 2015 and 2018, 75 patients with primary ACL injuries were divided into either the BTB group ( n  = 30) or HT group ( n  = 45). When using HT, an anatomical double-bundle ACLR was performed. BTB was indicated for athletes with sufficient motivation to return to sporting activity. Graft maturation on second-look arthroscopy was scored in terms of synovial coverage and revascularization. All participants underwent postoperative MRI evaluation 2 years postoperatively. The signal intensity (SI) characteristics of the reconstructed graft were evaluated using oblique axial proton density-weighted MR imaging (PDWI) perpendicular to the grafts. The signal/noise quotient (SNQ) was calculated to quantitatively determine the normalized SI. For clinical evaluation, the Lachman test, pivot shift test, KT-2000 evaluation, Lysholm score, and Knee injury and Osteoarthritis Outcome Score (KOOS) were used. Results Arthroscopic findings showed that the graft maturation score in the BTB group (3.6 ± 0.7) was significantly greater than that in the anteromedial bundle (AMB; 2.9 ± 0.2, p  = 0.02) and posterolateral bundle (PLB; 2.0 ± 0.9, p  = 0.001) in the HT group. The mean MRI-SNQs were as follows: BTB, 2.3 ± 0.5; AMB, 2.9 ± 0.9; and PLB, 4.1 ± 1.1. There were significant differences between BTB, AMB, and PLB (BTB and AMB: p  = 0.04, BTB and PLB: p  = 0.003, AMB and PLB: p  = 0.03). Second-look arthroscopic maturation score and MRI-SNQ value significantly correlated for BTB, AMB, and PLB. No significant differences were detected in clinical scores. There was a significant difference ( p  = 0.02) in the knee laxity evaluation (BTB: 0.9 ± 1.1 mm; HT: 2.0 ± 1.9 mm). Conclusion BTB maturation is superior to that of double-bundle HT based on morphological and MRI evaluations following anatomical ACLR, although no significant differences were found in clinical scores. Regarding clinical relevance, the advantages of BTB may help clinicians decide on using the autograft option for athletes with higher motivation to return to sporting activity because significant differences were observed in morphological evaluation, MRI assessment, and knee anterior laxity evaluation between BTB and double-bundle HT. Level of evidence Level IV.

No therapeutic targets have been identified for lung squamous cell cancer (SqCC) which is the second most prevalent lung cancer because its molecular profiles remain unclear. This study aimed to unveil disease-related protein networks by proteomic and bioinformatic assessment of laser-microdissected cancerous cells from seven SqCCs compared with eight representative lung adenocarcinomas. We identified three network modules significant to lung SqCC using weighted gene co-expression network analysis. One module was intrinsically annotated to keratinization and cell proliferation of SqCC, accompanied by hypoxia-induced aerobic glycolysis, in which key regulators were activated ( HIF1A , ROCK2 , EFNA1-5 ) and highly suppressed ( KMT2D ). The other two modules were significant for translational initiation, nonsense-mediated mRNA decay, inhibited cell death, and interestingly, eIF2 signaling, in which key regulators, MYC and MLXIPL , were highly activated. Another key regulator LARP1 , the master regulator in cap-dependent translation, was highly suppressed although upregulations were observed for hub proteins including EIF3F and LARP1 targeted ribosomal proteins, among which PS25 is the key ribosomal protein in IRES-dependent translation. Our results suggest an underlying progression mechanism largely caused by switching to the cap-independent, IRES-dependent translation of mRNA subsets encoding oncogenic proteins. Our findings may help to develop therapeutic strategies to improve patient outcomes.

Janus kinase (JAK) is a tyrosine kinase that binds to cytokine receptors and regulates transcription through signal transducer and activator of transcription (STAT) phosphorylation. Oclacitinib is a JAK1 inhibitor that is approved for the treatment of canine atopic dermatitis because it inhibits IL-31 signaling. Recent studies suggest clinical remission in dogs with cutaneous lymphoma treated with oclacitinib; however, the underlying mechanisms remain unclear. Its effects on high-grade canine lymphomas beyond cutaneous lymphoma are unknown. In this study, we examined the antitumor mechanism of oclacitinib in canine cutaneous lymphoma and determined its effects on high-grade canine lymphoma cell lines in vitro. EO-1 (cutaneous lymphoma) and eight high-grade lymphoma cell lines were treated with oclacitinib. Growth inhibition, cell death, G0/G1 phase cell cycle arrest, and apoptosis based on caspase-3 activation were observed in five sensitive cell lines. JAK1 and STAT5 phosphorylation was detected in these cells and decreased upon treatment, suggesting a dependence on JAK1/STAT5 signaling. In canine cutaneous lymphoma tissues, JAK1/STAT5 phosphorylation correlated with clinical sensitivity to oclacitinib. Similar phosphorylation profiles were observed in some multicentric and gastrointestinal lymphomas, suggesting broader applicability. Taken together, the results indicate that oclacitinib exerts antitumor effects by inhibiting JAK1/STAT5 signaling. The phosphorylation of these proteins may serve as a biomarker for predicting response to this inhibitor in canine lymphoma.

Although most cancer deaths are caused by metastasis, there are no effective therapeutic approaches. This study describes the efficacy of a short synthetic mRNA (s-mRNA) designed by the sequence of non-vesicular extracellular IL1β-mRNA found in the pre-metastatic lung of tumor-bearing mice. The administration of s-mRNA inhibits murine lung metastasis by inducing the innate and adaptive immune systems. s-mRNA binds to ZC3H12D, an RNA-binding protein on natural killer cells and cytotoxic T lymphocytes. The ZC3H12D-s-mRNA complex translocated to the nucleus without being involved in translation. This process induces cytolytic activity and cell death in cancer cells without inducing a cytokine storm, and immune cells retain their antitumor activity. Although the antitumor activity of cytotoxic lymphocytes declines as the disease progresses in cancer patients, s-mRNA induces sustained high killing capacities of natural killer cells and cytotoxic T lymphocytes from colon cancer patients. Therefore, s-mRNA could be a breakthrough solution to prevent metastasis. Extracellular mRNAs are found to play an important role in premetastatic organs. Here this group reports the non-vesicular extracellular IL1β-mRNA complexes binding to ZC3H12D followed by the translocation into nucleus without being translated, thereby killing NK cells/CTLs and inhibiting lung metastasis in a preclinical colon cancer model.

Bovine endometritis is a common postpartum disease that significantly impairs reproductive performance and reduces economic sustainability in dairy and beef cattle. It is primarily caused by gram-negative and -positive bacteria, triggering strong inflammatory responses in the endometrium. Serum amyloid A (SAA) is an acute-phase protein and precursor of amyloid A (AA) in AA amyloidosis. In cattle, multiple SAA isoforms have been identified; however, the biological functions of SAA3 remain unclear. Hence, this study investigated the role of SAA3 in bovine endometrial epithelial cells (BEnEpCs) following stimulation with gram-negative or -positive bacterial antigens. BEnEpCs were treated with lipopolysaccharide (LPS) and lipoteichoic acid (LTA) and, subsequently, the expression levels of SAA3 and SAA1 mRNA were compared by real-time PCR. To further investigate protein-level changes, immunocytochemistry (ICC) was performed to assess the expressions of SAA3 and SAA1. These analyses revealed that SAA3 mRNA expression was significantly enhanced by LPS and LTA, whereas SAA1 mRNA remained undetectable or showed only minimal responsiveness. Notably, only SAA3 protein expression increased in response to stimulation. These results indicate that SAA3 plays a crucial role in the innate immune response of BEnEpCs against gram-negative bacteria. Our in vitro findings may facilitate understanding of the innate immune activity in bovine uterus.

Popliteal venous aneurysms (PVAs) are rare vascular anomalies that can result in serious thromboembolic complications. We present a case of a 77-year-old woman with a thrombosed right PVAs complicated by pulmonary embolism. Following initial anticoagulation, surgical resection of the aneurysm was performed, and individualized venous reconstruction was achieved using an autologous great saphenous vein (GSV) roll graft. This technique was selected over conventional panel or spiral grafts due to its simplicity, adaptability to size discrepancy, and reduced suture lines. To our knowledge, the use of a GSV roll graft, specifically tailored for popliteal vein reconstruction in thrombosed PVAs, has not been previously reported. Postoperative anticoagulation was continued with direct oral anticoagulants. Graft patency was confirmed by duplex ultrasonography and contrast-enhanced CT venography at regular intervals. At 1.5 years post-surgery, graft patency was maintained, and the patient remained symptom-free. This case highlights the effectiveness of individualized venous reconstruction using a GSV roll interposition graft in managing complex thrombosed PVAs.