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Flexible perovskite solar cells often experience constant or cyclic bending during their service life. Catastrophic failure of devices may occur due to the crack of polycrystalline perovskite films and delamination at the perovskite and the substrate interfaces, posing a significant stability concern. Here, a multiple dynamic hydrogen bonding polymer network is developed to enhance the mechanical strength of flexible perovskite solar cells in two ways. The main chain of poly(acrylic acid) decreases the mismatch of the coefficient of thermal expansion between the perovskite and the substrate by 16.7% through its flexibility and spatial occupation. The dopamine branch chains provide multiple dynamic hydrogen bonding sites, which contribute to increased energy dissipation upon stress deformation and reduce Young's modulus of perovskite by 54.3%. The inverted flexible perovskite solar cells achieve a champion power conversion efficiency of 23.02% and retain 81.3% of the initial PCE over 2000 h under continuous 1‐sun equivalent illumination. Moreover, devices show excellent mechanical stability by remaining 90.2% of the original value after 5000 bending cycles. [ABSTRACT FROM AUTHOR]

This article is concerned with the trajectory tracking control problem for the nonlinear systems in the sense of the predefined settling time and accuracy. In contrast with the existing works, we focus on the cases where the system dynamics, its bounding functions, the unmatched disturbances, and the time‐varying parameters are totally unknown; the derivatives of the desired trajectory are not required to be available. They significantly challenge the identification and/or approximation‐based control solutions. To overcome this obstacle, a novel robust prescribed performance control approach via state feedback is put forward in this article. It not only ensures the natural satisfaction of the specific initial condition but also realizes a full‐time performance specification for trajectory tracking. Furthermore, for the case of unmeasured state variables, an output‐feedback control approach is further derived by adopting an input‐driven filter and conducting trivial changes on the design procedure. Moreover, both approaches exhibit significant simplicity, without the needs for parameter identification, function approximation, disturbance estimation, derivative calculation, or command filtering. Three simulation studies are conducted to clarify and verify the above theoretical findings. [ABSTRACT FROM AUTHOR]

Urothelial damage and barrier dysfunction emerge as the foremost mechanisms in Hunner‐type interstitial cystitis/bladder pain syndrome (HIC). Although treatments aimed at urothelial regeneration and repair have been employed, their therapeutic effectiveness remains limited due to the inadequate understanding of specific cell types involved in damage and the lack of specific molecular targets within these mechanisms. Therefore, we harnessed single‐cell RNA sequencing to elucidate the heterogeneity and developmental trajectory of urothelial cells within HIC bladders. Through reclustering, we identified eight distinct clusters of urothelial cells. There was a significant reduction in UPK3A+ umbrella cells and a simultaneous increase in progenitor‐like pluripotent cells (PPCs) within the HIC bladder. Pseudotime analysis of the urothelial cells in the HIC bladder revealed that cells faced challenges in differentiating into UPK3A+ umbrella cells, while PPCs exhibited substantial proliferation to compensate for the loss of UPK3A+ umbrella cells. The urothelium in HIC remains unrepaired, despite the substantial proliferation of PPCs. Thus, we propose that inhibiting the pivotal signaling pathways responsible for the injury to UPK3A+ umbrella cells is paramount for restoring the urothelial barrier and alleviating lower urinary tract symptoms in HIC patients. Subsequently, we identified key molecular pathways (TLR3 and NR2F6) associated with the injury of UPK3A+ umbrella cells in HIC urothelium. Finally, we conducted in vitro and in vivo experiments to confirm the potential of the TLR3–NR2F6 axis as a promising therapeutic target for HIC. These findings hold the potential to inhibit urothelial injury, providing promising clues for early diagnosis and functional bladder self‐repair strategies for HIC patients. © 2024 The Pathological Society of Great Britain and Ireland. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) is a significant global health concern. The gut microbiota plays an essential role in the onset and development of IBD. Sanghuangporus (SH), a traditional Chinese medicinal mushroom, has excellent anti‐inflammatory effects and is effective at modulating the gut microbiota. Despite these attributes, the specific anticolitic effects of SH and the mechanisms through which the gut microbiota mediates its benefits remain unclear. Herein, we demonstrated that polyphenol‐rich extract from SH effectively alleviated the pathological symptoms of dextran sodium sulfate (DSS)‐induced colitis in mice by modulating the gut microbiota. Treatment with SH distinctly enriched Alistipes, especially Alistipes onderdonkii, and its metabolite 5‐hydroxyindole‐3‐acetic acid (5HIAA). Oral gavage of live A. onderdonkii or 5HIAA potently mitigated DSS‐induced colitis in mice. Moreover, both 5HIAA and SH significantly activated the aromatic hydrocarbon receptor (AhR), and the administration of an AhR antagonist abrogated their protective effects against colitis. These results underscore the potent efficacy of SH in diminishing DSS‐induced colitis through the promotion of A. onderdonkii and 5HIAA, ultimately activating AhR signaling. This study unveils potential avenues for developing therapeutic strategies for colitis based on the interplay between SH and the gut microbiota. Highlights: Sanghuangporus (SH) polyphenol extract potently alleviated symptoms of colon colitis in dextran sodium sulfate‐induced colitis mice.The gut microbiota especially Alistipes onderdonkii mediates the anticolitic effect of SH.The SH‐enriched microbial metabolite 5‐hydroxyindole‐3‐acetic acid exhibited an anticolitic effect via the activation of the aryl hydrocarbon receptor.The "gut microbiota‐metabolites‐signaling pathway" provides an effective perspective for the study of complex Chinese medicine systems. [ABSTRACT FROM AUTHOR]

Aims: Red blood cell distribution width‐to‐albumin ratio (RAR), an innovate biomarker of inflammation, can independently predict adverse cardiovascular outcomes. However, the association between RAR and prognosis in patients with non‐ischaemic heart failure (NIHF) remains unclear. Methods and results: A total of 2077 NIHF patients admitted to the Heart Failure Care Unit, Fuwai Hospital, were consecutively enrolled from December 2006 to October 2017 in this retrospective study. The primary endpoint was a composite outcome of all‐cause mortality and heart transplantation. The correlation between RAR and the composite outcome was assessed by the Kaplan–Meier survival analysis and the Cox regression analysis. Incremental predictive values and the clinical performance of RAR for all‐cause mortality or heart transplantation were also assessed based on a 12‐variable traditional risk model. The median follow‐up time in this study was 1433 (1341, 1525) days. As the gender no longer satisfied the Cox proportional risk assumption after 1150 days, we set 1095 days as the follow‐up time for analysis. A total of 500 patients reached the composite outcome. Multivariable Cox regression showed that per log2 increase of RAR was significantly associated with a 132.9% [hazard ratio 2.329, 95% confidence interval (CI) 1.677–3.237, P < 0.001] increased risk of all‐cause mortality or heart transplantation. Better model discrimination [concordance index: 0.766 (95% CI 0.754–0.778) vs. 0.758 (95% CI 0.746–0.770), P < 0.001], calibration (Akaike information criterion: 1487.3 vs. 1495.74; Bayesian information criterion: 1566.25 vs. 1569.43; Brier score: 1569.43 vs. 1569.43; likelihood ratio test P < 0.001), and reclassification (integrated discrimination improvement: 1.35%, 95% CI 0.63–2.07%, P < 0.001; net reclassification improvement: 13.73%, 95% CI 2.05–27.18%, P = 0.034) were improved after adding RAR to the traditional model (P < 0.001 for all). A higher overall net benefit was also obtained in the threshold risk probability of 20–55%. Conclusions: High level of RAR was an independent risk factor of poor outcome in NIHF. [ABSTRACT FROM AUTHOR]

Aim: Post‐stroke inflammation increases the risk of functional disability through enlarged cerebral infarct size directly and follow‐up stroke event indirectly. We aimed to use post‐stroke proinflammatory cytokine interleukin‐6 (IL‐6) as a marker of inflammatory burden and quantify post‐stroke inflammation's direct and indirect effect on functional disability. Methods: We analyzed patients with acute ischemic stroke admitted to 169 hospitals in the Third China National Stroke Registry. Blood samples were collected within 24 h of admission. Stroke recurrence and functional outcome measured by the modified Rankin scale (mRS) were assessed via face‐to‐face interviews at 3 months. Functional disability was defined as an mRS score ≥2. Mediation analyses under the counterfactual framework were performed to examine the potential causal chain in which stroke recurrence may mediate the relationship between IL‐6 and functional outcome. Results: Among the 7053 analyzed patients, the median (interquartile range [IQR]) NIHSS score was 3 (1–5), and the median (IQR) level of IL‐6 was 2.61 (1.60–4.73) pg/mL. Stroke recurrence was observed in 458 (6.5%) patients, and functional disability was seen in 1708 (24.2%) patients at the 90‐day follow‐up. Per stand deviation (4.26 pg/mL) increase in the concentration of IL‐6 was associated with an increased risk of stroke recurrence (adjusted odds ratio [aOR], 1.19; 95% CI, 1.09–1.29) and disability (aOR, 1.22; 95% CI, 1.15–1.30) within 90 days. Mediation analyses revealed that 18.72% (95% CI, 9.26%–28.18%) of the relationship between IL‐6 and functional disability was mediated by stroke recurrence. Conclusions: Stroke recurrence mediates less than 20% of the association between IL‐6 and functional outcome at 90 days among patients with acute ischemic stroke. In addition to typical secondary prevention strategies for preventing stroke recurrence, more attention should be paid to novel anti‐inflammatory therapy to improve functional outcomes directly. [ABSTRACT FROM AUTHOR]

Recently, all‐inorganic perovskite solar cells have attracted a large amount of attention, due to the much better water resistance compared to the organic counterparts. Unfortunately, the undesired phase transition remains a significant challenge, despite the many attempts. An important step forward is made here by numerical simulation, which discovers the significance of external strain to the stability of desired α‐CsPbI3, whose lifetime can be extended up to three times by nonhydrostatic tension, as is verified by both modeling and experimental results. In addition, such lifetime can be even enhanced further by hydrostatic tension, as indicated by the simulation. The unexpected observation provides not only an effective method to extend the lifetime of the perovskite devices, but also opens an unexpected path for the wide research community to utilize the straining engineering method that is extensively investigated in the perovskite research. [ABSTRACT FROM AUTHOR]

Previous work showed that FABP5 inhibitors suppressed the malignant progression of prostate cancer cells, and this suppression might be achieved partially by promoting apoptosis. But the mechanisms involved were not known. Here, we investigated the effect of inhibitors on apoptosis and studied the relevant mechanisms. WtrFABP5 significantly reduced apoptotic cells in 22Rv1 and PC3 by 18% and 42%, respectively. In contrast, the chemical inhibitor SB‐FI‐26 produced significant increases in percentages of apoptotic cells in 22Rv1 and PC3 by 18.8% (±4.1) and 4.6% (±1.1), respectively. The bio‐ inhibitor dmrFABP5 also did so by 23.1% (±2.4) and 15.8% (±3.0), respectively, in these cell lines. Both FABP5 inhibitors significantly reduced the levels of the phosphorylated nuclear fatty acid receptor PPARγ, indicating that these inhibitors promoted apoptosis‐induction sensitivity of the cancer cells by suppressing the biological activity of PPARγ. Thus, the phosphorylated PPARγ levels were reduced by FABP5 inhibitors, the levels of the phosphorylated AKT and activated nuclear factor kapper B (NFκB) were coordinately altered by additions of the inhibitors. These changes eventually led to the increased levels of cleaved caspase‐9 and cleaved caspase‐3; and thus, increase in the percentage of cells undergoing apoptosis. In untreated prostate cancer cells, increased FABP5 suppressed the apoptosis by increasing the biological activity of PPARγ, which, in turn, led to a reduced apoptosis by interfering with the AKT or NFκB signaling pathway. Our results suggested that the FABP5 inhibitors enhanced the apoptosis‐induction of prostate cancer cells by reversing the biological effect of FABP5 and its related pathway. [ABSTRACT FROM AUTHOR]

Invasive species can successfully and rapidly colonize new niches and expand ranges via founder effects and enhanced tolerance towards environmental stresses. However, the underpinning molecular mechanisms (i.e., gene expression changes) facilitating rapid adaptation to harsh environments are still poorly understood. The red seaweed Gracilaria vermiculophylla, which is native to the northwest Pacific but invaded North American and European coastal habitats over the last 100 years, provides an excellent model to examine whether enhanced tolerance at the level of gene expression contributed to its invasion success. We collected G. vermiculophylla from its native range in Japan and from two non‐native regions along the Delmarva Peninsula (Eastern United States) and in Germany. Thalli were reared in a common garden for 4 months at which time we performed comparative transcriptome (mRNA) and microRNA (miRNA) sequencing. MRNA‐expression profiling identified 59 genes that were differently expressed between native and non‐native thalli. Of these genes, most were involved in metabolic pathways, including photosynthesis, abiotic stress, and biosynthesis of products and hormones in all four non‐native sites. MiRNA‐based target‐gene correlation analysis in native/non‐native pairs revealed that some target genes are positively or negatively regulated via epigenetic mechanisms. Importantly, these genes are mostly associated with metabolism and defence capability (e.g., metal transporter Nramp5, senescence‐associated protein, cell wall‐associated hydrolase, ycf68 protein and cytochrome P450‐like TBP). Thus, our gene expression results indicate that resource reallocation to metabolic processes is most likely a predominant mechanism contributing to the range‐wide persistence and adaptation of G. vermiculophylla in the invaded range. This study, therefore, provides molecular insight into the speed and nature of invasion‐mediated rapid adaption. [ABSTRACT FROM AUTHOR]

Objective: Bioscaffolds are widely used for tissue engineering, but failed and inconsistent preclinical results have hampered the clinical use of bioscaffolds for tissue engineering. We aimed to construct a cellular remodelling landscape and to identify the key cell subpopulations and important genes driving bladder remodelling. Methods: Twenty‐four reconstructed mouse bladders using porcine small intestinal submucosa (PSIS) were harvested at 1, 3, and 6 weeks to perform single‐cell RNA sequencing. Cell types were identified and their differentially expressed genes (DEGs) at each stage were used for functional analysis. Immunofluorescence was used to validate the specific cell type. Results: The remodelling landscape included 13 cell types. Among them, fibroblasts, smooth muscle cells (SMCs), endothelial cells, and macrophages had the most communications with other cells. In the process of regeneration, DEGs of fibroblasts at 1, 3, and 6 weeks were mainly involved in wound healing, extracellular matrix organization, and regulation of development growth, respectively. Among these cells, Saa3+ fibroblasts might mediate tissue remodelling. The DEGs of SMCs at 1, 3, and 6 weeks were mainly involved in the inflammatory response, muscle cell proliferation, and mesenchyme development, respectively. Moreover, we found that Notch3+ SMCs potentially modulated contractility. From 1 to 6 weeks, synchronous development of endothelial cells was observed by trajectory analysis. Conclusions: A remoulding landscape was successfully constructed and findings might help surficial modifications of PSIS and find a better alternative. However, more in vivo and in vitro studies are needed to further validate these results. [ABSTRACT FROM AUTHOR]

BACKGROUND: The adverse effects of pesticides has led to a series of ecological, environmental and public health issues. Amide herbicides are an important agrochemical, yet many are prone to leach and pollute the environment, which limits their further application. In this study, metolachlor (METO) was selected as a model pesticide and a controlled released nanoparticle (NP) system was constructed employing a zeolitic imidazolate framework‐8 hybrid inorganic–organic porous material (METO@ZIF‐8). RESULTS: The synthesis parameters of METO@ZIF‐8 were optimized, and the loading content of METO@ZIF‐8 was maximized by a central composite design of response surface test. The NPs were regular dodecahedron with uniform size (mostly 54.3 nm diameter). METO@ZIF‐8 had high specific surface area and good dispersal in water. Moreover, it endowed the active ingredient with a pH‐responsive release property. The nanocarrier effectively improved the adsorption capacity of METO in soil and reduce the leaching by 10.3–21.7%. Pot experiments suggested that the control effect of METO@ZIF‐8 was 16.6 and 48.4% higher than that of METO emulsifiable concentrate (EC) and METO technical concentration (TC) at the recommended dose. Based on the excellent controlled release profiles, METO@ZIF‐8 did not affect corn plant growth and significantly reduced the risk of phytotoxicity induced by METO. METO@ZIF‐8 effectively reduced acute toxicity in zebrafish compared with METO EC. CONCLUSION: This study explored the fabrication of a nanocarrier for improving the efficacy and promoting the environmental safety of leachable amide herbicides. © 2022 Society of Chemical Industry. [ABSTRACT FROM AUTHOR]

Fibrosis is a chronic inflammation process with excess extracellular matrix (ECM) deposition that cannot be reversed. Patients suffer from bladder dysfunction caused by bladder fibrosis. Moreover, the interactive mechanisms between ECM and bladder fibrosis are still obscure. Hence, we assessed the pivotal effect of Yes‐associated protein (YAP) on the proliferation of bladder smooth muscle in fibrosis process. We identified that stiff ECM increased the expression and translocation of YAP in the nucleus of human bladder smooth muscle cell (hBdSMC). Sequencings and proteomics revealed that YAP bound to Smad3 and promoted the proliferation of hBdSMC via MAPK/ERK signaling pathway in stiff ECM. Moreover, CUT and TAG sequencing and dual‐luciferase assays demonstrated that Smad3 inhibited the transcription of JUN. The YAP inhibitor CA3 was used in a partial bladder outlet obstruction (pBOO) rat model. The results showed that CA3 attenuated bladder smooth muscle proliferation. Collectively, YAP binding with Smad3 in the nucleus inhibited the transcription of JUN, and promoted the proliferation of bladder smooth muscle through the MAPK/ERK signaling pathway. The current study identified a novel mechanism of mechanical force induced bladder fibrosis that provided insights in YAP‐associated organ fibrosis. [ABSTRACT FROM AUTHOR]

The causation between lipids and renal cancer remains inconclusive. Our purpose is to explore the causal relationships between the three primary lipid metabolism‐related substances, namely triglycerides (TG), low‐density lipoprotein (LDL) and high‐density lipoprotein (HDL) with the risk of renal cancer using Mendelian randomization (MR) methods. Genetic instruments for lipids were acquired from the UK Biobank. Outcome data were from the FinnGen study (1397 renal cancer cases and 204 070). Single‐variable MR (SVMR) and multi‐variable MR (MVMR) analyses were conducted with TwoSampleMR package based on R 4.0.3. The random‐effect inverse‐variance weighted (IVW), MR‐Egger, weighted‐median method, and weighted mode were the four main computing methods. We found that per 1 SD elevated LDL level was causally associated with renal cancer occurrence based on SVMR (OR, 1.31, 95% CI: 1.05‐1.64, P =.016). Similar significant associations were found in other methods. However, the results of SVMR did not support significant associations between TG, and HDL with renal cancer risk in all methods. The association between LDL and renal cancer was still significant in MVMR analysis (OR for IVW method: 1.22 per 1 SD higher trait (SD, 95% CI: 1.11‐1.34, P <.001; OR for MR‐Egger: 1.22 per 1 SD higher trait, 95% CI: 1.01‐1.47, P =.042) when taking TG and HDL into consideration. Our study supported that elevated serum LDL levels is causally associated with an increased risk of renal cancer independent of TG and HDL. [ABSTRACT FROM AUTHOR]

CD38 is a multifunctional receptor and enzyme present on the surface of B lymphocytes, which can induce B lymphocytes proliferation and apoptosis by crosslinking related cytokines to affect the function of B cells, thus affecting immune regulation in humans and promoting tumorigenesis. The level of CD38 expression in B cells has become an important factor in the clinical diagnosis, treatment, and prognosis of malignant tumors and other related diseases. Therefore, studying the relationship between CD38 expression on the surface of B cells and the occurrence of the disease is of great significance for elucidating its association with disease pathogenesis and the clinical targeted therapy. In this paper, we review the effects of CD38 on B‐cell activation, proliferation, and differentiation, and elaborate the functional role and mechanism of CD38 expression on B cells. We also summarize the relationship between the level of CD38 expression on the surface of B cells and the diagnosis, treatment, and prognosis of various diseases, as well as the potential use of targeted CD38 treatment for related diseases. This will provide an important theoretical basis for the scientific research and clinical diagnosis and treatment of B‐cell‐related diseases. [ABSTRACT FROM AUTHOR]

Background: The causal effects of individual risk factors of metabolic syndrome on erectile dysfunction (ED) are still unclear. Objectives: To evaluate the causal effect of risk factors of metabolic syndrome on ED through Mendelian randomization (MR). Materials and methods: Data for risk factors were obtained from multiple databases with 173,082–757,601 individuals, and that for ED were collected from a genome‐wide association study including 223,805 Europeans. We performed univariate MR analysis using inverse‐variance weighted, MR‐Egger, weighted‐median, weighted mode methods and multivariable MR analysis to evaluate the total and direct causal effects. Results: The univariable MR supported that type 2 diabetes mellitus (odds ratios [OR] = 1.14, 95% confidence intervals [CI]: 1.08–1.21, p < 0.001) and body mass index (BMI) (OR = 1.27, 95% CI: 1.12–1.44, p < 0.001) were associated with ED. After excluding the SNPs associated with BMI and other risk factors, the results of multivariable MR for T2D (OR = 1.15, 95% CI: 1.05–1.25, p = 0.001) remained consistent. However, the results of multivariable MR provided limited evidence for the causality between BMI and ED (OR = 1.06, 95% CI: 0.88–1.29, p = 0.532). For systolic blood pressure and lipid components (low‐density lipoprotein, high‐density lipoprotein and triglycerides), both univariable and multivariable MR failed to offer sufficient evidence to confirm their causal effect on ED. Conclusion: T2D showed a direct causal effect on ED independent of obesity and dyslipidemia. [ABSTRACT FROM AUTHOR]

In China, the prevalence of undernutrition among children under 5 years of age has declined significantly during recent decades. However, noticeable gaps exist between rural and urban areas. Since 2012, a government‐funded nutrition programme, Ying Yang Bao (YYB; soybean powder‐based iron‐rich supplement) programme, has been implemented in poor rural areas to decrease the risk of developing anaemia among children aged 6–23 months, but there are still inadequate health care awareness, feeding knowledge and skills among caregivers. From June 2018 to December 2020, a child health counselling intervention was delivered through a home visit based on the YYB programme in Liangshan. Child health messages were given by trained village child health assistants while distributing YYB. Surveys were conducted before and after the intervention to analyse changes in child health check‐up frequency, complementary feeding practice and prevalence of undernutrition. After the intervention, the proportion of children who had regular health check‐ups, who were vaccinated and who met the minimum YYB consumption significantly increased from 26.0%, 81.6%, and 67.8% to 59.7%, 95.0%, and 79.2%. Increased rates of IYCF indicators (introduction of solid, semisolid, or soft foods, minimum dietary diversity and consumption of iron‐rich or iron‐fortified foods) were observed after the intervention. The prevalence of stunting, underweight, wasting, and anaemia significantly decreased from 26.3% to 10.8%, 13.4% to 8.7%, 14.0% to 10.5%, and 52.1% to 43.9%. This intervention can be well integrated into the YYB programme with less additional resources. Children in resource‐limited areas will benefit more from a comprehensive nutritional package, including food supplements and child health education. Key messages: Current evidence suggests there is a decrease in the prevalence of undernutrition among children under 5 years of age in China during recent decades. However, imbalanced development exists between rural and urban areas.Government‐funded Ying Yang Bao (YYB) programme has been implemented in poor rural areas across China covering over 800 counties, to decrease the risk of developing anaemia among children aged 6–23 months.After a child health counselling intervention jointly implemented with YYB programme, the prevalence of stunting, underweight, wasting, and anaemia among children decreased significantly.Child health counselling intervention could be well integrated into the ongoing YYB programme to reach resource‐limited areas on a large scale. [ABSTRACT FROM AUTHOR]

BACKGROUND Soil fumigants—the most effective agrochemicals for managing soil‐borne diseases—have been used extensively. However, high volatility, moderate toxicity and insufficient effective duration considerably limit their application. In the present study, interface polymerization was used to combine modified biochar (BC) and polyurea microcapsules (MCs) to co‐encapsulate allyl isothiocyanate (AITC), developing a model fumigant for controlled release (AITC@BC‐MCs). RESULTS: The physical characteristics of BC modified by sand‐milling were significantly improved. In addition, chemical properties and morphological features of AITC@BC‐MCs characterized by integrated methods revealed successful preparation of BC‐MCs. Compared with monolayer MCs, BC‐MCs could significantly delay AITC release owing to the composite obstruction effect. Moreover, modifying BC endowed the cargo molecules with a pH‐responsive release property. Additionally, this composite showed a longer persistent duration by prolonging AITC degradation half‐life, which was 3.2–3.5‐fold greater than that of the AITC technical concentrate under different soil conditions. Finally, the control efficacy of the AITC@BC‐MC against pathogens, including nematodes and fungi, as well as against weeds was significantly enhanced at the same dose, but the composite did not inhibit seed germination and growth after 10 days when fumigated soil was aerated. CONCLUSION: Construction of a composite encapsulation system enhanced pesticide efficacy, reduced dose via controlled release and delayed fumigant degradation in soil, indicating the great potential of this strategy for developing an effective and environmentally friendly fumigant formulation. © 2021 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

Purpose: To investigate the frailty status in Chinese cancer patients through establishing a novel prediction algorithm. Methods: The percentage of frailty in various age groups, locations, and tumor types in Chinese cancer patients was investigated. The prediction capacity of frailty on mortality of Chinese cancer patients was analysed by the frailty index composing of routine laboratory data (FI‐LAB) accessible from a blood test and calculated as the ratio of abnormal factors to 22 total variables. The establishment of a novel algorithm, MCP (mortality of cancer patients), to predict the 5‐year mortality in Chinese cancer patients was accomplished and the algorithm's prediction capacity was tested in the training and validation sets using receiver operating characteristic (ROC) analysis. Results: We found that the risk of death in cancer patients can be successfully identified through FI‐LAB. The univariable and multivariable Cox regression were used to evaluate the effect of frailty on death. In the 5‐year follow‐up, 20.6% of the 2959 participants (age = 55.8 ± 11.7 years; 43.5% female) died, while the mean FI‐LAB score in baseline was 0.23 (standard deviation = 0.13; range = 0–0.73). Frailty (after adjusting for gender, age, and other confounders) directly correlated with an increased risk of death, hazard ratio of 12.67 (95% confidence interval [CI]: 7.19, 22.31), compared to those without frailty. In addition, the MCP algorithm (MCP) = 3.678 × FI‐LAB + 1.575 × sex + 1.779 × first tumor node metastasis staging, presented an area under the ROC (AUC) of 0.691 (95% CI: 0.656–0.726) and 0.648 (95% CI: 0.613–0.684) in the training and validation sets, respectively. Conclusion: Frailty as defined by FI‐LAB was common and indicated a significant death risk in cancer patients. Our novel developed algorithm MCP had a passable prediction capacity on 5‐year MCP. [ABSTRACT FROM AUTHOR]

Memristive logic‐in‐memory (LIM) is an attractive candidate for in‐memory computing and thus would overcome some of the issues concerning the von Neumann bottleneck, which has been intensively investigated. Here, a multi‐bit and functionally complete LIM strategy is designed to efficiently perform multi logical functions in parallel. This strategy is experimentally demonstrated by a multi‐bit ferroelectric tunnel junction (FTJ) memristor with a sub‐nanosecond operation speed which is nearly two orders of magnitude faster than the previous memristive LIM. Using the four resistance states (2‐bit) of only a single FTJ memristor cell, two logical computations are successfully performed in parallel, and the 16 complete Boolean logic functions are implemented within only two steps. In addition, the multi‐encoding schemes are proposed to further improve the efficiency and flexibility of parallel logical computations. Accordingly, the 1‐bit binary full adder can be implemented using as less as three parallel memristors by only performing five steps, and on this basis the N‐bit full adder can also be realized. These results provide a highly efficient LIM approach, which could be a promising candidate for future computing architecture. [ABSTRACT FROM AUTHOR]

Debio0932 is a promising lead compound in phase I clinical trials targeting the N‐terminal ATP‐binding pocket of the molecular chaperone heat‐shock protein 90 (Hsp90N). The absence of a crystal structure of the Hsp90N–Debio0932 complex, however, has impeded further structural optimization of Debio0932 and understanding of the molecular‐interaction mechanism. Here, a high‐resolution crystal structure of the Hsp90N–Debio0932 complex was successfully determined (resolution limit 2.20 Å; PDB entry 6lr9) by X‐ray diffraction and the molecular‐interaction mechanism was analysed in detail, which suggested that Debio0932 suppresses cancer cells by accommodating itself in the ATP‐binding pocket of Hsp90N, disabling its molecular‐chaperone capability. The results of a thermal shift assay (ΔTm = 8.83 ± 0.90°C) and isothermal titration calorimetry (Kd = 15.50 ± 1.30 nM) indicated strong binding and favourable thermodynamic changes in the binding of Hsp90N and Debio0932. Based on the crystal structure of the complex and on molecular‐interaction analysis, 30 new Debio0932 derivatives were designed and nine new derivatives exhibited increased binding to Hsp90N, as determined by molecular‐docking evaluation. Additionally, Debio0932 suppressed cell proliferation (IC50 values of 3.26 ± 2.82 µM for A549, 20.33 ± 5.39 µM for H1299 and 3.16 ± 1.04 µM for H1975), induced cell‐cycle arrest and promoted apoptosis in three non‐small‐cell lung cancer (NSCLC) cell lines. These results provide novel perspectives and guidance for the development of new anti‐NSCLC drugs based on the lead compound Debio0932. [ABSTRACT FROM AUTHOR]

Aims: Abnormal intravesical pressure created by partial bladder outlet obstruction (PBOO) triggered the progression from chronic inflammation to fibrosis, initiating structural and functional alterations of bladder. To elucidate the underlying mechanisms of contraction and inflammatory response, we investigated the isolated human bladder smooth muscle cells (hBSMC) under pathological hydrostatic pressure (HP) mimicking the in vivo PBOO condition. Methods: hBSMCs were subjected to HP of 200 cm H2O to explore the contraction and inflammatory cytokine expression of hBSMC treated with β‐adrenoceptors (ADRBs) and/or autophagy signaling pathway agonists and/or antagonists. Results: We showed that pathological HP induced the release of the proinflammatory cytokines, including monocyte chemotactic protein‐1, regulated upon activation normal T cell expressed and secreted factor, and interleukin‐6. HP downregulated ADRB2 and ADRB3 expression, which was consistent with the results of the PBOO rat model. ADRB2 or autophagy activation repressed pathological HP‐induced proinflammatory cytokine production. ADRB2, ADRB3 or autophagy activation ameliorated the HP‐enhanced contraction. The increased contraction and autophagy activity by ADRB2 agonist under HP conditions were reversed by pretreatment with antagonists of adenosine monophosphate‐activated protein kinase (AMPK). Conclusion: The present study provides evidence that the ADRB3 agonist suppresses hBSMC contraction under pathological HP conditions. Moreover, the ADRB2 agonist negatively regulates the contraction and inflammatory response of hBSMCs through AMPK/mTOR‐mediated autophagy under pathological HP. These findings provide a theoretical basis for potential therapeutic strategies for patients with PBOO. [ABSTRACT FROM AUTHOR]

Background: The severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) and the associated coronavirus disease (COVID‐19) have spread throughout China. Previous studies predominantly focused on its place of origin, Wuhan, causing over estimation of the disease severity due to selection bias. We analyzed 465 confirmed cases in Zhejiang province to determine the epidemiological, clinical, and virological characteristics of COVID‐19. Methods: Epidemiological, demographic, clinical, laboratory, and management data from qRT‐PCR confirmed COVID‐19 patients from January 17, 2020, to January 31, 2020, were collected, followed by multivariate logistic regression analysis for independent predictors of severe/critical‐type COVID‐19 and bioinformatic analysis for features of SARS‐CoV‐2 from Zhejiang province. Results: Among 465 COVID‐19 patients, median age was 45 years, while hypertension, diabetes, and chronic liver disease were the most common comorbidities. History of exposure to the epidemic area was present in 170 (36.56%) and 185 (39.78%) patients were clustered in 77 families. Severe/critical‐type of COVID‐19 developed in 49 (10.54%) patients. Fever and cough were the most common symptoms, while diarrhea/vomiting was reported in 58 (12.47%) patients. Multivariate analysis revealed eight risk factors for severe/critical COVID‐19. Glucocorticoids and antibiotics were administered to 60 (12.90%) and 218(46.88%) patients, respectively. Bioinformatics showed four single amino acid mutations and one amino acid position loss in SARS‐CoV‐2 from Zhejiang province, with more similarity to humans than to viruses. Conclusions: SARS‐CoV‐2 showed virological mutations and more human transmission in Zhejiang province, indicating considerable epidemiological and clinical changes. Caution in glucocorticoid and antibiotics use is advisable. [ABSTRACT FROM AUTHOR]

The relationship of gut microbiota and calcium oxalate stone has been limited investigated, especially with no study of gut microbiota and short chain fatty acids (SCFAs) in nephrolithiasis. We provided Sprague Dawley rats of renal calcium oxalate stones with antibiotics and examined the renal crystals deposition. We also performed a case‐control study by analyzing 16S rRNA microbial profiling, shotgun metagenomics and SCFAs in 153 fecal samples from non‐kidney stone (NS) controls, patients with occasional renal calcium oxalate stones (OS) and patients with recurrent stones (RS). Antibiotics reduced bacterial load in feces and could promote the formation of renal calcium crystals in model rats. In addition, both OS and RS patients exhibited higher fecal microbial diversity than NS controls. Several SCFAs‐producing gut bacteria, as well as metabolic pathways associated with SCFAs production, were considerably lower in the gut microbiota among the kidney stone patients compared with the NS controls. Representation of genes involved in oxalate degradation showed no significance difference among groups. However, fecal acetic acid concentration was the highest in RS patients with high level of urinary oxalate, which was positively correlated with genes involvement in oxalate synthesis. Administration of SCFAs reduced renal crystals. These results shed new light on bacteria and SCFAs, which may promote the development of treatment strategy in nephrolithiasis. [ABSTRACT FROM AUTHOR]

Background: Age at the time of breast cancer diagnosis not only predicts clinical outcome but also indicates distinct molecular characteristics that provide the rationale for appropriate treatment strategies. However, to the authors' knowledge, little is known regarding the molecular profile and biological basis of triple-negative breast cancers (TNBCs) occurring in young and elderly patients.Methods: Using the study institution's largest, single-center, multiomics TNBC data set, the authors analyzed the clinical and genomic features of young (aged ≤39 years) and elderly (aged ≥65 years) patients with TNBC.Results: In the current study, a total of 50 patients, 354 patients, and 69 patients, respectively, were grouped as young, intermediate, and elderly patients with TNBC. Young patients with TNBC had worse short-term survival, upregulation of DNA repair, cell cycle and RNA metabolism gene sets, frequent pathogenic germline variants, and predominant homologous recombination deficiency-related mutational signatures. Several copy number alterations also were found to be enriched in young patients with TNBC. Nearly one-half of the TNBC cases in elderly patients were of the luminal androgen receptor subtype. TNBC in elderly patients was identified as being associated with severe fibrosis; a lower Ki-67 index; and somatic mutations in PIK3CA, KMT2D, ERBB2, ERBB3, and their corresponding pathways. Elderly patients with TNBC also were more likely to harbor targetable mutations.Conclusions: The findings of the current study indicated that young patients with TNBC had an enhanced cell cycle, which may have helped to explain their inferior short-term survival, whereas the homologous recombination deficiency and enriched pathogenic germline variants observed among young patients with TNBC suggested the need for genetic counseling and testing, as well as the potential use of DNA damage agents and poly(adenosine diphosphate ribose) polymerase (PARP) inhibitors. Molecular characteristics of elderly patients with TNBC, although suggesting less response to chemotherapy, provided a rationale for the routine detection of actionable somatic mutations. [ABSTRACT FROM AUTHOR]

The bladder wall is constantly subjected to intravesical pressure during the filling and voiding cycles. An imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) under elevated intravesical pressure contributes to pathological changes in the bladder. To investigate the changes in human urothelial cells (HUCs) under elevated intravesical pressure, this study analyzed the effect of β‐adrenoceptor signaling on the expression of MMPs and TIMPs in HUCs exposed to pathological hydrostatic pressure (HP) (70 cm H2O) for 6 hours. Quantitative polymerase chain reaction, Western blot analysis, and cell fluorescence staining were used to explore the effect of β‐adrenoceptor signaling on the expression of MMPs and TIMPs in HUCs after agonist and/or antagonist treatment. The expression levels of β2‐ and β3‐adrenoceptor, MMP1, and MMP2 were greatly downregulated, while the expression of TIMP1 was greatly upregulated. Formoterol and BRL 37344, which are agonists of β2‐ and β3‐adrenoceptor, respectively, significantly increased MMP1 and MMP2 expression under 70 cm H2O. As a classic downstream pathway of β2‐ and β3‐adrenoceptor, protein kinase A (PKA) signaling inhibited MMP1 and MMP2 expression by regulating cAMP response element binding protein (CREB) activity. MMP1 and MMP2 expression in HUCs under 70 cm H2O was modified by β2‐ and β3‐adrenoceptor via the PKA/CREB pathway. This outcome suggests that MMPs likely participate in the pathological effects of elevated intravesical pressure. The underlying mechanism of β2‐ and β3‐adrenoceptor in elevated intravesical pressure was also revealed; this mechanism constitutes a new potential therapeutic target for partial bladder outlet obstruction. [ABSTRACT FROM AUTHOR]

Benign prostatic hyperplasia (BPH) occurs most commonly among older men, often accompanied by chronic tissue inflammation. Although its aetiology remains unclear, autoimmune dysregulation may contribute to BPH. Regulatory T cells (Tregs) prevent autoimmune responses and maintain immune homeostasis. In this study, we aimed to investigate Tregs frequency, phenotype, and function in BPH patients and to evaluate adoptive transfer Tregs for immunotherapy in mice with BPH via CD39. Prostate specimens and peripheral blood from BPH patients were used to investigate Treg subsets, phenotype and Treg‐associated cytokine production. Sorted CD39+/− Tregs from healthy mice were adoptively transferred into mice before or after testosterone propionate administration. The Tregs percentage in peripheral blood from BPH patients was attenuated, exhibiting low Foxp3 and CD39 expression with low levels of serum IL‐10, IL‐35 and TGF‐β. Immunohistochemistry revealed Foxp3+ cells were significantly diminished in BPH prostate with severe inflammatory. Although the Tregs subset was comprised of more effector/memory Tregs, CD39 was still down‐regulated on effector/memory Tregs in BPH patients. Before or after testosterone propionate administration, no alterations of BPH symptoms were observed due to CD39‐ Tregs in mice, however, CD39+Tregs existed more potency than Tregs to regulate prostatic hyperplasia and inhibit inflammation by decreasing IL‐1β and PSA secretion, and increasing IL‐10 and TGF‐β secretion. Furthermore, adoptive transfer with functional Tregs not only improved prostate hyperplasia but also regulated muscle cell proliferation in bladder. Adoptive transfer with Tregs may provide a novel method for the prevention and treatment of BPH clinically. [ABSTRACT FROM AUTHOR]

The quantity of soil fumigants has increased globally that has focused attention on their environmental behavior. However, simultaneous analysis of traces of fumigant residues is often unreported because analysis methods are not readily available to measure them at low concentrations. In this study, typical solvent extraction methods were compared with headspace solid‐phase microextraction methods. Both methods can be used for simultaneously measuring the concentrations of five commonly used soil fumigants in soil or water. The solvent extraction method showed acceptable recovery (76–103%) and intraday relative standard deviations (0.8–11%) for the five soil fumigants. The headspace solid‐phase microextraction method also showed acceptable recovery (72–104%) and precision rates (1.3–17%) for the five soil fumigants. The solvent extraction method was more precise and more suitable for analyzing relatively high fumigant residue levels (0.05–5 μg/g) contained in multiple soil samples. The headspace solid‐phase microextraction method, however, had a much lower limits of detection (0.09–2.52 μg/kg or μg/L) than the solvent extraction method (5.8–29.2 μg/kg), making headspace solid‐phase microextraction most suitable for trace analysis of these fumigants. The results confirmed that the headspace solid‐phase microextraction method was more convenient and sensitive for the determination of fumigants to real soil samples. [ABSTRACT FROM AUTHOR]

Summary: This article studies the fault‐tolerant control problem for unknown nonlinear strict‐feedback systems subject to actuator failures yet with dynamic redundancies. The prescribed performance control methodology is newly combined with a modification‐based supervisory switching strategy to solve the problem. To implement failure detection, the performance function is properly modified to synthesize a monitoring function to supervise the behavior of an error variable. Once a failure is detected, the current actuator is shut down and the backup actuator is switched in to execute the reconfigured control command. Compared with the existing results, (1) the postfailure and postswitching tracking performance is improved, other than uniform ultimate boundedness and (2) the dependence on extra robust control schemes (eg, adaptive or approximating structures) to deal with model uncertainties or the need to compute analytic derivatives of virtual control signals in the backstepping design is eliminated. [ABSTRACT FROM AUTHOR]

Luminal breast cancer (BC) has a sustained risk of late disease recurrence and death. Considerable numbers of patients suffer from antiendocrine therapy resistance. Here, we identified a novel lncRNA whose expression is high in breast cancer and especially higher in luminal breast cancer, dubbed LOL (lncRNA of luminal), that acts as a natural sponge for let‐7 microRNAs to regulate tumor growth and tamoxifen resistance. LOL overexpression in parental MCF‐7 cells exhibited a proliferative advantage in the addition of tamoxifen than negative control. Knocking down LOL in TamR MCF‐7 cells, recovered the sensitivity of cells to tamoxifen. Strikingly, we demonstrated that LOL is transcribed from a genomic locus of an enhancer to maintain its high expression in luminal BC and that it is extremely sensitive to enhancer‐regulating factors, such as ZMYND8 and BRD4. Estrogen deprivation or ERα signaling pathway blockage can further stimulate LOL expression, which can promote tumor progression. Clinical analysis of 374 luminal breast cancer samples indicated that LOL is an independent prognostic factor for poor survival in luminal BC. In conclusion, targeting LOL using preclinical/clinical drugs, such as BRD4 inhibitors, may represent a promising approach to inhibit luminal breast cancer progression and tamoxifen resistance. What's new? Luminal breast cancer makes up two‐thirds of all breast cancers, and carries an increased risk of relapse after 5 years. These authors identified a novel lncRNA associated with luminal breast cancer, which they dubbed LOL (lncRNA of luminal). Overexpression of LOL, they found, allows cells to resist tamoxifen; knocking down LOL restores tamoxifen sensitivity. They also showed that reducing estrogen receptor alpha (ERα) expression upregulated LOL, and ERα overexpression caused no change in LOL. Inhibiting LOL, they suggest, could help stop tamoxifen resistance and cancer recurrence. [ABSTRACT FROM AUTHOR]

Background: Type 1 diabetes (T1D) is an autoimmune disease resulting from an attack by autoreactive T lymphocytes against pancreatic islet β‐ cells. In recent studies, regulatory T cells (Tregs) have been implicated in the process of T1D. Furthermore, cluster of differentiation 39 (CD39), which is involved in the suppression of inflammation, has been shown to be expressed on Tregs. However, the pathological importance of CD39 to the memory Treg population remains unclear. Methods: This study investigated Treg subsets, focusing on resting, effector, and memory Tregs, and determined CD39 expression on Tregs. In addition, changes in Treg subsets and Treg‐associated cytokine secretion after CD3/CD28 stimulation of peripheral blood mononuclear cells were evaluated in diabetic patients and healthy controls. The suppressive function of Tregs was measured using the mixed lymphocyte reaction (MLR) test. Results: There was a higher percentage of memory Tregs in T1D patients than healthy controls. However, Tregs in T1D patients showed impaired suppression, with low forkhead box P3 (Foxp3) expression and low serum interleukin (IL)‐10 levels. Furthermore, CD39 expression on Tregs, and on memory Tregs in particular, was lower in T1D patients than healthy controls. After stimulation, the percentage of resting Tregs was decreased and that of effector/memory Tregs was increased in both healthy controls and T1D patients, but CD39 expression on effector/memory Tregs was still lower and there was no increase in IL‐10 secretion in T1D patients. Conclusions: The defective suppressive function of Tregs in T1D patients is due to lower expression of CD39 on memory Tregs. [ABSTRACT FROM AUTHOR]

Summary: This paper is concerned with the tracking control problem for a class of multiple‐input–multiple‐output systems with unmatched disturbances and the unknown additive and multiplicative nonlinearities. The objective is to provide a low‐complexity control solution in the sense that (i) approximating structures are not involved, despite unknown nonlinearities and (ii) iterative calculations of command derivatives are avoided in the backstepping design. A robust adaptive control strategy is proposed to fulfill the task. In the control design, a new‐type adaptive law is first developed to update Nussbaum gains to handle control direction uncertainties, while ensuring Nussbaum gains bounded. Then, the potential robustness of error constraint techniques is exploited to counteract the effects of unknown nonlinearities and disturbances and achieve predefined transient and steady‐state tracking performance. Finally, simulation results are given to illustrate the above theoretical findings. [ABSTRACT FROM AUTHOR]

Summary: This paper focuses on the asymptotic stabilization problem for a class of multivariable nonlinear systems with relative degree one, practical examples of which incorporate the liquid level control of water tanks, and the speed control of interconnected carts. The presence of the unknown (other than uncertain) additive and multiplicative nonlinearities renders asymptotic stability difficult to be achieved by the existing robust control methods. To conquer this obstacle, a novel adaptive control strategy is proposed. In the control design, the state constraint technique is newly introduced to the adaptive design to generate a proper control gain to compensate for unknown nonlinearities, instead of the use of extra approximating structures. By this means, both the prescribed transient performance regarding the convergence rate and the expected asymptotic stability are preserved. Finally, simulation results are given to illustrate the established theoretical findings. [ABSTRACT FROM AUTHOR]

Background: Pretreatment controlling nutritional status (CONUT) score is a novel index which was used to predict outcomes in cancer patients. We aim to explore the prognostic significance of CONUT score in patients with upper tract urothelial carcinoma (UTUC) after radical nephroureterectomy (RNU). Patients and methods: A total of 662 UTUC patients between 2004 and 2016 were retrospectively analyzed. Patients were categorized into three groups based on CONUT score (Normal: 0‐1; Light: 2‐4; Moderate/severe: 5‐12). Associations of CONUT score with oncological outcomes were analyzed using Logistic and Cox regression analysis. Harrell concordance index was used to assess the predictive accuracy of the multivariate models. Subgroup analyses were conducted according to tumor grade and stage. Results: The median follow‐up duration was 41 months. Multivariate Logistic analysis showed that high CONUT score was independently associated with high‐grade disease, high pT stage, lymphovascular invasion, sessile carcinoma, variant histology, and positive surgical margins (each P < 0.05). Multivariate analysis demonstrated that CONUT score 5‐12 was an independent factor for worse cancer‐specific survival (CSS, hazard ratio [HR]:2.39, 95% confidence interval [CI] 1.55‐3.68, P < 0.0001), disease recurrence‐free‐survival (RFS, HR: 1.80, 95% CI 1.24‐2.60, P = 0.002), and overall survival (OS, HR: 2.26, 95% CI 1.53‐3.34, P < 0.0001). The estimated c‐index of the multivariate models for CSS, RFS, and OS increased from 0.755, 0.715 and 0.745 to 0.772, 0.723, and 0.756 when CONUT score supplemented. Subgroup analyses showed that especially in patients with high‐grade carcinoma and advanced stage (≥pT3), higher CONUT score predicts decreased CSS, RFS, and OS (all P < 0.05). Conclusion: Preoperative CONUT score is a negative independent prognostic indicator for both pathologic and survival outcomes in UTUC, especially in those with high‐grade carcinoma and advanced stage. Adding this parameter into our clinical prediction model is appropriate so as to improve its predictive accuracy. CONUT score independently predicted worse survival in UTUC patients, especially in patients with high‐grade disease and advanced stage. The addition of CONUT score would improve the predictive accuracy of the multivariate models for survival outcomes. We therefore suggest adding the CONUT score to the traditional predictive model and to the risk stratifications of patients with UTUC. [ABSTRACT FROM AUTHOR]

DSCAM‐AS1 is one of the few intensively studied lncRNAs with high specific expression in luminal breast cancer. It is directly regulated by estrogen receptor α (ERα) and plays vital roles in tumor proliferation, invasion, and tamoxifen resistance. However, the detailed function of DSCAM‐AS1 in tumor progression and its clinical significance remain unclear. We reveal that DSCAM‐AS1 regulates cell proliferation and colony formation by inducing the G1/S transition. RNA‐seq analysis demonstrated that DSCAM‐AS1 participates in crucial biological processes, including DNA replication, the G1/S phase transition, sister chromatid cohesion, chromosome segregation, protein localization to the chromosome and DNA recombination. Most importantly, in the retrospectively registered clinical analysis, high expression of DSCAM‐AS1 is a poor prognostic factor in patients with luminal breast cancer treated with endocrine therapy. In conclusion, DSCAM‐AS1 is a promising clinical therapeutic target that may prolong survival of luminal breast cancer patients treated with endocrine therapy. We reveal that DSCAM‐AS1 regulates cell proliferation and colony formation by inducing the G1/S transition. RNA‐seq analysis demonstrated that DSCAM‐AS1 participates in crucial biological processes, including DNA replication, the G1/S phase transition, sister chromatid cohesion, chromosome segregation, protein localization to the chromosome and DNA recombination. Most importantly, in the retrospectively registered clinical analysis, high expression of DSCAM‐AS1 is a poor prognostic factor in patients with luminal breast cancer treated with endocrine therapy. [ABSTRACT FROM AUTHOR]

Summary: This paper focuses on the output stabilization problem for a class of strict‐feedback systems with unknown nonlinear dynamics and unknown measurement sensitivity. The imprecise sensor measurements render the existing robust control approaches such as neuro or fuzzy control infeasible. A solution is provided in this paper by a feat of the concept of tuning functions and barrier Lyapunov functions (BLFs). Utilizing the modification capability of tuning functions, global stability is preserved. Exploiting the potential robustness of BLFs, the effect of unmodeled dynamics is counteracted under sensitivity errors. The combination of tuning functions with BLFs further leads to a distinct property that the real system output converges to an adjustable region in finite time. Compared with the existing results, the need for prior knowledge of system nonlinearities and measurement sensitivity is removed in this paper. Finally, simulation results illustrate the established theoretical findings. [ABSTRACT FROM AUTHOR]

Summary: This paper focuses on the output‐feedback tracking control problem for a class of nonlinear systems with both unknown nonlinearities and unknown control directions. An adaptive prescribed performance controller combined with a Nussbaum gain and a dividing line is proposed to solve the problem. Compared with the existing results, (i) both the convergence rate and the ultimate bound of the tracking error can be prescribed; (ii) no approximating structures such as neuro/fuzzy systems are used, regardless of unknown nonlinear functions; and (iii) the computational burden is alleviated in the sense that the iterative calculation of command derivatives is avoided and the number of online learning parameters is largely reduced. Simulation results are given to further illustrate the established theoretical findings. [ABSTRACT FROM AUTHOR]

Abstract: Resolving atomic site‐specific electronic properties and correlated substrate–molecule interactions is challenging in real space. Now, mapping of sub‐10 nm sized Pt nanoislands on a Au(111) surface was achieved by tip‐enhanced Raman spectroscopy, using the distinct Raman fingerprints of adsorbed 4‐chlorophenyl isocyanide molecules. A spatial resolution better than 2.5 nm allows the electronic properties of the terrace, step edge, kink, and corner sites with varying coordination environments to be resolved in real space in one Pt nanoisland. Calculations suggest that low‐coordinate atomic sites have a higher d‐band electronic profile and thus stronger metal–molecule interactions, leading to the observed blue‐shift of Raman frequency of the N≡C bond of adsorbed molecules. An experimental and theoretical study on Pt(111) and mono‐ and bi‐atomic layer Pt nanoislands on a Au(111) surface reveals the bimetallic effect that weakens with the increasing number of deposited Pt adlayer. [ABSTRACT FROM AUTHOR]

Summary: This paper concentrates on the leader‐follower formation control problem for marine surface vessels with unknown nonlinear dynamics and actuator faults. The unknown inertia matrix and multiplicative fault render the existing methods infeasible. To solve this problem, a low‐complexity prescribed performance controller is first proposed without the help of auxiliary neural/fuzzy systems or adaptive mechanisms. A modification technique is further adopted to relax the initial condition, such that global closed‐loop stability is guaranteed. Finally, simulation results illustrate the above theoretical results. [ABSTRACT FROM AUTHOR]

Excess weight and obesity are severe public health threats worldwide. Recent evidence demonstrates that gut microbiota dysbiosis contributes to obesity and its comorbidities. The body weight-reducing and energy balancing effects of melatonin have been reported in several studies, but to date, no investigations toward examining whether the beneficial effects of melatonin are associated with gut microbiota have been carried out. In this study, we show that melatonin reduces body weight, liver steatosis, and low-grade inflammation as well as improving insulin resistance in high fat diet ( HFD)-fed mice. High-throughput pyrosequencing of the 16S rRNA demonstrated that melatonin treatment significantly changed the composition of the gut microbiota in mice fed an HFD. The richness and diversity of gut microbiota were notably decreased by melatonin. HFD feeding altered 69 operational taxonomic units ( OTUs) compare with a normal chow diet ( NCD) group, and melatonin supplementation reversed 14 OTUs to the same configuration than those present in the NCD group, thereby impacting various functions, in particular through its ability to decrease the Firmicutes-to- Bacteroidetes ratio and increase the abundance of mucin-degrading bacteria Akkermansia, which is associated with healthy mucosa. Taken together, our results suggest that melatonin may be used as a probiotic agent to reverse HFD-induced gut microbiota dysbiosis and help us to gain a better understanding of the mechanisms governing the various melatonin beneficial effects. [ABSTRACT FROM AUTHOR]

The first catalytic asymmetric [3+2] cycloaddition of 2-indolylmethanols with 3-vinylindoles has been established, which makes use of C-3 unsubstituted 2-indolylmethanol as a C3 building block in the presence of a chiral phosphoric acid. By using this strategy, biologically important cyclopenta[ b]indole frameworks were efficiently constructed with regiospecificity in high yields (up to 99%), excellent diastereo- and enantioselectivities (up to >95:5 dr, 96:4 er). This reaction not only represents the first catalytic asymmetric [3+2] cycloaddition of C-3 unsubstituted 2-indolylmethanols, but also has confronted the great challenges in 2-indolylmethanol-involved enantioselective transformations. [ABSTRACT FROM AUTHOR]

In this article, the crystal structure of solid hydrazine under pressure has been extensively investigated using ab initio evolutionary simulation methods. Calculations indicate that hydrazine remains both insulating and stable up to at least 300 GPa at low temperatures. A structure with P21 symmetry is found for the first time through theoretical prediction in the pressure range 0-99 GPa and it is consistent with previous experimental results. Two novel structures are also proposed, in the space groups Cc and C2/ c, postulated to be stable in the range 99-235 GPa and above 235 GPa, respectively. Below 3.5 GPa, C2 symmetry is found originally, but it becomes unstable after adding the van der Waals interactions. The P21→ Cc transition is first order, with a volume discontinuity of 2.4%, while the Cc→ C2/ c transition is second order with a continuous volume change. Pressure-induced hydrogen-bond symmetrization occurs at 235 GPa during the Cc→ C2/ c transition. The underlying mechanism of hydrogen-bond symmetrization has also been investigated by analysis of electron localization functions and vibrational Raman/IR spectra. [ABSTRACT FROM AUTHOR]