In Situ Confocal Raman Mapping Study of a Single Ti-Assisted ZnO Nanowire

In this work, we succeeded in preparing in-plane zinc oxide nanowires using a Ti-grid assisted by the chemical vapor deposition method. Optical spatial mapping of the Confocal Raman spectra was used to investigate the phonon and geometric properties of a single ZnO nanowire. The local optical results reveal a red shift in the non-polar E2 high frequency mode and width broadening along the growth direction, reflecting quantum-confinement in the radial direction

Effect of intramuscular adipose tissue in the skeletal muscle of thigh on glucose metabolism in male patients with obesity

Objective·To investigate the correlation between intramuscular adipose tissue (IMAT) content and glucose metabolism in male patients with obesity.Methods·Eighty male patients with obesity were recruited from the Endocrinology Department of Renji Hospital, Shanghai Jiao Tong University School of Medicine from December 2019 to December 2020. According to the results of oral glucose tolerance test (OGTT), they were divided into normal glucose tolerance (NGT) group and impaired glucose regulation (IGR) group. General data and laboratory test indicators of the two groups were collected and compared. mDixon-Quant technique was used to measure the IMAT content in each skeletal muscle of the thigh in the two groups, and the proton density fat fractions (PDFF) of skeletal muscle in the two groups were compared. The multivariate Logistic regression model was used to analyze the independent influencing factors of IGR occurrence.Results·Compared with the NGT group, patients in the IGR group had a larger waist circumference (P=0.017), higher glutamic-pyruvic transaminase level, glutamic-oxaloacetic transaminase level, γ-glutamyl transferase (GGT) level, triacylglycerol (TAG) level, nonestesterified fatty acid (NEFA) level and sartorius PDFF (all P<0.05). After adjusting for confounding factors such as age, body mass index, GGT, TAG and NEFA, the results of multivariate Logistic regression analysis showed that PDFF of vastus lateralis, semitendinosus and sartorius were the risk factors for IGR (all P<0.05).Conclusion·Higher levels of IMAT content in vastus lateralis, semitendinosus and sartorius will increase the risk of IGR in male patients with obesity

Baseline of Pollution of Heavy Metals and Physico-chemical Parameters in Surface Sediments from Quanzhou Bay, China, in 2006-2007

According to the monitoring results of the near-shore sediments of Quanzhou Bay in 2006-2007, we analyzed the near-shore depositional environmental quality of Quanzhou Bay and assessed it by the single-factor evaluation on the basis of corresponding standards of local marine functional areas. The results showed that the sediments from the inner part of Quanzhou Bay were polluted more seriously than that of the open part, which might be due to the increasing human activities in coastal areas. The main exceeding standard items are petroleum, Cu, Zn and Pb. In additions, the pollutions caused by sulfide and Cr are different in different regions. The contents of Hg and As are basically in according with the sedimentary quality standards of the corresponding marine functional areas. According the evaluating results, we also provided the corresponding measures to control the pollutions in sedimentary environment of Quanzhou Bay. (C) 2011 Published by Elsevier B.V. Selection and/or peer-review under responsibility of National University of Singapore

Could the wild population of Large Yellow Croaker Larimichthys crocea (Richardson) in China be restored? A case study in Guanjingyang, Fujian, China

Over 90% of the world's fisheries have been fully exploited or over-fished. Included is the large yellow croaker (Larimichthys crocea), an important commercial fish species in China whose population was nearly depleted prior to the 1980s. Although overfishing and natural resources collapse present a daunting issue, some studies indicate that improved management strategies could aid in natural stock restoration to prevent depletion. We developed an integrated assessment method grounded on an ecosystem-based approach and deigned an integrated index with three key aspects of habitat suitability, natural population status and government & social interventions, to evaluate the potential restoration capacity of the species in a designated “national aquatic germplasm resource protected area” in Guanjinyang based on a data set spanning 1987 to 2015. The results show that although restoration efforts on research and rehabilitation have increased greatly since late 1990s, the effectiveness stays moderate and the natural population remains near depletion

The long non-coding RNA MALAT1 regulates intestine host-microbe interactions and polyposis

The long non-coding RNA (lncRNA) Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) maintains the integrity of the intestinal epithelial barrier and regulates local inflammation. However, its influences on intestinal microbial communities and tissue susceptibility to cancer development remain unexplored. Here, we report that MALAT1 regulates host anti-microbial response gene expression and the composition of mucosal-associated microbial communities in a region-specific manner. In the APC mutant mouse model of intestine tumorigenesis, knocking out MALAT1 results in higher polyp counts in the small intestine and colon. Interestingly, intestine polyps that developed in the absence of MALAT1 were smaller in size. These findings highlight the unexpected bivalent role of MALAT1 in restricting and promoting cancer progression at different disease stages. Among the 30 MALAT1-targets shared by both the small intestine and colon, ZNF638 and SENP8 levels are predictive of colon adenoma patient overall survival and disease-free survival. Genomic assays further revealed that MALAT1 modulates intestinal target expression and splicing through both direct and indirect mechanisms. This study expands the role of lncRNAs in regulating intestine homeostasis, microbial communities, and cancer pathogenesis

Ubiquilin and p97/VCP bind erasin, forming a complex involved in ERAD

Loss of ubiquilin or erasin activates ER stress, increases accumulation of polyubiquitinated proteins, and shortens lifespan in worms

Sirt6-dependent gene regulation of oncofetal gene loci in hepatocytes

Hepatocellular carcinoma (HCC), the primary malignant tumor of liver, represents the third leading cause of cancer-related deaths globally due to the lack of effective treatment options. Accumulating studies have revealed that SIRT6, a NAD+-dependent histone deacetylase, plays pivotal roles in liver-related disease and liver tumor formation. Genetic deletion of Sirt6 in mice develops a pro-oncogenic phenotype in the liver with dramatic elevation of oncofetal genes typical for HCC, such as Igf2, H19 and α-Fetoprotein (Afp). However, the underlying mechanisms regulating these genes remain unknown. For delineating the role of Sirt6 in the tumor-related phenotype, Sirt6 knockout mice model together with primary human hepatocytes and human hepatoma cells (Hep3B) were used in this study. The present study shows that Sirt6 suppresses the expression of these oncofetal genes. Functional analysis of the Igf2/H19 gene locus as a model showed that loss of Sirt6 causes nucleosome remodeling, altered chromatin loop, enhancer switch from the poised (enriched with H3K27me3 and H3K4me1) to active (enriched with H3K27ac and H3K4me1) by recruiting pioneer factors Foxa1 and Foxa2. Interestingly, these alterations establish a super-enhancer to drive H19 and Igf2 transcription. Moreover, Sirt6 deletion causes cytoplasmic translocation of Suz12, a core component of the Polycomb repressive complex 2 (PRC2), and weakens PRC2-mediated repression at the Igf2/H19 gene locus. Further analysis of Hep3B cells in relation to primary human hepatocytes indicated that this regulatory mechanism is relevant for human cancer development. Besides, this study also suggests the role of Sirt6 in hepatic differentiation. Sirt6 knockout leads to the increased expression of embryonic hepatoblast markers and the reduced transcription of adult hepatocytes markers. Correspondingly, this trend reversed when SIRT6 was overexpressed in Hep3B cells. Functional analysis of this regulatory mechanism at the Alb/Afp gene locus as a model showed that Sirt6 deletion causes epigenetic and genetic alterations, which induces Foxa2 switch from enhancer of Alb (hepatocytes marker) to Afp (hepatoblast marker). However, PRC2-mediated repression is not evident at these temporal enhancers. Altogether, in hepatocytes, loss of Sirt6 induces disruption of enhancer activity through genetic and epigenetic alterations, resulting in activation of a tumorigenic phenotype.Das Hepatozelluläre Karzinom (Hepatocellular carcinoma, HCC), der häufigste bösartige Tumor der Leber, ist aufgrund eines Mangels an effektiven Behandlungsoptionen die weltweit dritthäufigste krebsbedingte Todesursache. Aktuelle Untersuchungen zeigen, dass SIRT6, eine NAD+-abhängige Histon-Deacetylase, eine zentrale Rolle bei Lebererkrankungen und der Entstehung von Lebertumoren spielt. Mäuse mit einer genetischen Deletion von Sirt6 entwickeln in der Leber einen pro-onkogenen Phänotyp mit einer drastischen Erhöhung onkofetaler Gene wie Igf2, H19 and α-Fetoprotein (AFP), welche für das HCC kennzeichnend ist. Dennoch verbleiben die zugrunde liegenden Mechanismen, wie diese Gene reguliert werden, unbekannt. Um die Rolle von Sirt6 im tumor-assoziierten Phänotyp zu charakterisieren, wurden in dieser Arbeit Hepatozyten aus Sirt6-defizienten Mäusen, primäre humane Hepatozyten und humane Hepatomzellen (Hep3B) verwendet. Die vorliegende Arbeit zeigt, dass Sirt6 die Expression onkofetaler Gene supprimiert. Die funktionellen Untersuchungen des Igf2/H19 Genlokus zeigen, dass der Verlust von Sirt6 durch die Rekrutierung der Pionierfaktoren Foxa1 und Foxa2 zu einer Umordnung von Nukleosomen mit veränderten Chromatinschleifen und einem „Enhancer switch“ einer H3K27me3 und H3K4me1 Anreicherung zur Akkumulation der Aktivierungsmarker (H3K27ac und H3K4me1) führt. Diese Veränderungen führen interessanterweise zur Etablierung eines Super-Enhancers, welcher die Transkription von H19 und Igf2 vorantreibt. Die Sirt6-Deletion führt darüber hinaus zu einer zytoplasmatischen Translokation von Suz12, einer Kernkomponente des PRC2-Komplexes (Polycomb repressive complex 2), und schwächt damit die PRC2-vermittelte Repression am Igf2/H19 Genlokus. Weitere Untersuchungen von Hep3B Zellen im Vergleich zu primären humanen Hepatozyten deuten darauf hin, dass dieser regulatorische Mechanismus für die humane Krebsentwicklung von Bedeutung ist. Zudem legt diese Arbeit auch eine Rolle von Sirt6 bei der hepatischen Differenzierung nahe. Der Sirt6-knockout führt zu einer erhöhten Expression embryonaler Hepatoblasten-Marker und einer reduzierten Transkription von Markern adulter Hepatozyten. Übereinstimmend damit zeigt sich ein umgekehrter Trend bei der Überexpression von SIRT6 in Hep3B Zellen. Funktionelle Untersuchungen dieses regulatorischen Mechanismus am Albumin/α-Fetoprotein Genlokus als Modell zeigen, dass die Sirt6-Deletion hier in epigenetischen und genetischen Veränderungen resultieren, welche Foxa2 dazu veranlassen vom Albumin- (Hepatozyten Marker) zum α-Fetoprotein-Enhancer (Hepatoblasten Marker) zu wechseln. Allerdings ist eine PRC2-vermittelte Repression an diesen temporalen Enhancern nicht erkennbar. Insgesamt führt der Verlust von Sirt6 in Hepatozyten durch genetische und epigenetische Veränderungen zu einer gestörten Enhanceraktivität, was in einem tumorigenen Phänotyp resultiert

Estimation in Semi-Varying Coefficient Heteroscedastic Instrumental Variable Models with Missing Responses

This paper studies the estimation problem for semi-varying coefficient heteroscedastic instrumental variable models with missing responses. First, we propose the adjusted estimators for unknown parameters and smooth functional coefficients utilizing the ordinary profile least square method and instrumental variable adjustment technique with complete data. Second, we present an adjusted estimator of the stochastic error variance by employing the Nadaraya–Watson kernel estimation technique. Third, we apply the inverse probability-weighted method and instrumental variable adjustment technique to construct the adaptive-weighted adjusted estimators for unknown parameters and smooth functional coefficients. The asymptotic properties of our proposed estimators are established under some regularity conditions. Finally, numerous simulation studies and a real data analysis are conducted to examine the finite sample performance of the proposed estimators