A Sub-Aperture Overlapping Imaging Method for Circular Synthetic Aperture Radar Carried by a Small Rotor Unmanned Aerial Vehicle.

Circular synthetic aperture radar (CSAR) can obtain higher image resolution and more target information using 360° observation of the target. Due to the anisotropy of target scattering characteristics in the actual scene, the sub-aperture imaging method is usually used for CSAR imaging. However, the uniformly divided overlapping sub-aperture CSAR imaging algorithm only considers phase compensation, ignoring the effect of target scattering characteristics on echo amplitude.

Surufatinib-induced renal thrombotic microangiopathy: first case report and review of literature.

Angiogenesis inhibitors such as tyrosine kinase inhibitors (TKIs) are common therapeutics currently used to treat oncologic disease. Surufatinib is a novel, small-molecule multiple receptor TKI approved by the National Medical Products Administration (NMPA) for the treatment of progressive, advanced, and well-differentiated pancreatic and extrapancreatic neuroendocrine tumours (NETs). Thrombotic microangiopathy (TMA) is a well-documented complication of TKIs targeting the VEGF-A/VEGFR2 signalling pathway.

In-frame deletion of SMC5 related with the phenotype of primordial dwarfism, chromosomal instability and insulin resistance.

Background: SMC5/6 complex plays a vital role in maintaining genome stability, yet the relationship with human diseases has not been described.

Methods: SMC5 variation was identified through whole-exome sequencing (WES) and verified by Sanger sequencing. Immunoprecipitation, cytogenetic analysis, fluorescence activated cell sorting (FACS) and electron microscopy were used to elucidate the cellular consequences of patient's cells.

ELK1-mediated YTHDF1 drives prostate cancer progression by facilitating the translation of Polo-like kinase 1 in an m6A dependent manner.

: N6-methyladenosine (m6A) is one of the most prevalent mRNA modifications in mammals, and it regulates the fate of modified RNA transcripts. In the current study, we aimed to elucidate the role of YTH m6A RNA-binding protein 1 (YTHDF1), a "reader" of m6A modification, in prostate cancer tumorigenesis. : We employed a multi-omics approach to detect the direct target of YTHDF1 upon manipulation of YTHDF1 expression in prostate cancer cells.

Association Between Single Nucleotide Polymorphisms of miRNAs and Gastric Cancer: A Scoping Review.

Gastric cancer (GC) is the third leading cause of cancer-related mortality worldwide, and single nucleotide polymorphisms (SNPs) in microRNAs (miRNAs) are believed to affect the occurrence and progression of cancer by altering the expression and biological functions of miRNAs. The present scoping review was designed to evaluate and discuss microRNA SNPs (miR-SNPs) that have been found to be associated with GC in the following two contexts: (1) the biological effects on GC based on SNP localization; and (2) the associations between miRNA-SNPs and clinical factors (susceptibility, tumor size, metastasis, overall survival, and prognosis) of GC. Information on miRNAs was collected, including the SNPs, their proven target genes, and the possible impact of the SNPs on GC outcome.

Lessons from 17β-HSD3 deficiency: Clinical spectrum and complex molecular basis in Chinese patients.

17β-Hydroxysteroid dehydrogenase type 3 (17β-HSD3) deficiency is rarely reported in Chinese patients with 46, XY disorders of sexual development (DSD). Seven subjects with 17β-HSD3 deficiency were identified from 206 Chinese 46, XY DSD patients using targeted next-generation sequencing (NGS). Serum AD and T levels were measured by liquid chromatography-tandem mass spectrometry (LC-MS/MS).

MAFG-AS1 is a prognostic biomarker and facilitates prostate cancer progression.

Long Noncoding RNAs (LncRNAs) have recently been identified as key regulator in tumor progression. The LncRNA MAFG-AS1 has been reported to facilitate the progression of multiple cancers, however, its role in prostate cancer is still unknown. Here, we reported that MAFG-AS1 was upregulated in prostate cancer.

Role of DTL in Hepatocellular Carcinoma and Its Impact on the Tumor Microenvironment.

Background: The crucial role of has been previously implicated in genomic stability; however, its prognostic value and its relation with tumor immunity in hepatocellular carcinoma (HCC) remain to be further explored.

Methods: Transcriptional and mutational datasets as well as clinical information were retrieved from the GEO, ICGC, and TCGA databases. Differentially expressed genes (DEGs) were obtained from the comparison of DTL and DTL expression groups of the TCGA-HCC cohort.

E2F transcription factor 2-activated DLEU2 contributes to prostate tumorigenesis by upregulating serum and glucocorticoid-induced protein kinase 1.

Long noncoding RNAs (lncRNAs) participate in biological processes in multiple types of tumors. However, the regulatory patterns of lncRNAs in prostate cancer remain largely unclear. Here, we evaluated the expression and roles of the lncRNA DLEU2 in prostate cancer.

Mutation Screening and Functional Study of in Chinese Patients with Congenital Hypothyroidism.

Objective: Defects in the human solute carrier family 26 member 4 () gene are reported to be one of the causes of congenital hypothyroidism (CH). We aimed to identify mutations in Chinese patients with CH and analyze the function of the mutations.

Methods: Patients with primary CH were screened for 21 CH candidate genes mutations by targeted next-generation sequencing.

Phenotypic and biochemical characteristics and molecular basis in 36 Chinese patients with androgen receptor variants.

Background: Androgen insensitive syndrome (AIS) is a rare genetic disease resulting from androgen receptor (AR) mutations and one of the causes of 46, XY disorder of sexual development (DSD). This study aimed to describe the clinical features and molecular defects of 36 Chinese patients with AR variants and investigate the functional alterations of novel variants in vitro.

Material And Methods: Subjects with AR variants were identified from 150 Chinese 46, XY DSD patients using targeted next-generation sequencing.

Comprehensive lipidomics in apoM mice reveals an overall state of metabolic distress and attenuated hepatic lipid secretion into the circulation.

Apolipoprotein M (apoM) participates in both high-density lipoprotein and cholesterol metabolism. Little is known about how apoM affects lipid composition of the liver and serum. In this study, we systemically investigated the effects of apoM on liver and plasma lipidomes and how apoM participates in lipid cycling, via apoM knockout in mice and the human SMMC-7721 cell line.

Increased expression levels of inflammatory cytokines and adhesion molecules in lipopolysaccharide‑induced acute inflammatory apoM‑/‑ mice.

Apolipoprotein M (apoM) may serve a protective role in the development of inflammation. Nuclear factor‑κB (NF‑κB) and its downstream factors (including a number of inflammatory cytokines and adhesion molecules) are essential for the regulation of inflammatory processes. In the present study, the importance of apoM in lipopolysaccharide (LPS)‑induced acute inflammation and its potential underlying mechanisms, were investigated using an apoM‑knockout mouse model.

Non-negligible factors in studying the ApoM-S1P axis using EA.hy926 cells.

Background: The apolipoprotein M (ApoM)-sphingosine-1-phosphate (S1P) axis was recently identified, and research into its function has received increasing attention. However, there are some factors which might influence the results of studies into the function of the ApoM-S1P axis using the EA.hy926 cells.

Influence of the type of carrier on ferromagnetism in a Si semiconductor implanted with Cu ions.

Silicon semiconductor samples implanted with Cu ions and samples co-implanted with Cu- and N-ions were prepared by MEVVA and the Kaufman technique. None of the samples showed evidence of secondary phases. The initially n-type Si matrix, when implanted with Cu ions, changed to a p-type semiconductor, and the Cu ions existed as local Cu2+ cations in the p-type environment.

Insulin Resistance in Apolipoprotein M Knockout Mice is Mediated by the Protein Kinase Akt Signaling Pathway.

Background: Previous clinical studies have suggested that apolipoprotein M (apoM) is involved in glucose metabolism and plays a causative role in insulin sensitivity.

Objective: The potential mechanism of apoM on modulating glucose homeostasis is explored and differentially expressed genes are analyzed by employing ApoM deficient (ApoM-/- ) and wild type (WT) mice.

Methods: The metabolism of glucose in the hepatic tissues of high-fat diet ApoM-/- and WT mice was measured by a glycomics approach.

17β-estradiol regulates the expression of apolipoprotein M through estrogen receptor α-specific binding motif in its promoter.

Background: We have previously demonstrated that estrogen could significantly enhance expression of apolipoprotein M (apoM), whereas the molecular basis of its mechanism is not fully elucidated yet. To further investigate the mechanism behind the estrogen induced up-regulation of apoM expression.

Results: Our results demonstrated either free 17β-estradiol (E2) or membrane-impermeable bovine serum albumin-conjugated E2 (E2-BSA) could modulate human apoM gene expression via the estrogen receptor alpha (ER-α) pathway in the HepG2 cells.

Hyperglycemia-induced downregulation of apolipoprotein M expression is not via the hexosamine pathway.

Background: We previously demonstrated that hyperglycemia could suppress apolipoprotein M (apoM) synthesis both in vivo and in vitro; however, the mechanism of hyperglycemia-induced downregulation of apoM expression is unknown yet.

Methods: In the present study we further examined if hexosamine pathway, one of the most important pathways of glucose turnover, being involved in modulating apoM expression in the hyperglycemia condition. We examined the effect of glucosamine, a prominent component of hexosamine pathway and intracellular mediator of insulin resistance, on apoM expression in HepG2 cells and in rat's models.

Increased mRNA levels of apolipoprotein M and apolipoprotein AI in the placental tissues with fetal macrosomia.

Purpose: The present study examined mRNA levels of apolipoprotein M (apoM) and apolipoprotein AI (apoAI) in the term placental tissues obtained from 37 women with normal birth weight neonates and from 37 women with macrosomic neonates (birth body weight ≥4,000 g), and further discussed possible clinical significance of these observations.

Methods: The mRNA levels of apoM and apoAI in the placental tissues were determined by the real time RT-PCR, which demonstrated that both apoM and apoAI mRNA levels were significantly higher in the placentas from macrosomia than those from normal birth. Moreover, we analyzed the overexpressions of apoM and apoAI with the clinical data.

Intralipid decreases apolipoprotein M levels and insulin sensitivity in rats.

Background: Apolipoprotein M (ApoM) is a constituent of high-density lipoproteins (HDL). It plays a crucial role in HDL-mediated reverse cholesterol transport. Insulin resistance is associated with decreased ApoM levels.

Rosiglitazone enhances apolipoprotein M (Apom) expression in rat's liver.

Apolipoprotein M (APOM) has been suggested as a vasculoprotective constituent of high density lipoprotein (HDL), which plays a crucial role behind the mechanism of HDL-mediated anti-atherosclerosis. Previous studies demonstrated that insulin resistance could associate with decreased APOM expressions. In agreement with our previous reports, here, we further confirmed that the insulin sensitivity was also reduced in rats treated with high concentrations of glucose; such effect could be reversed by administration of rosiglitazone, a peroxisome proliferator-activated receptor-γ (PPARγ).

Decreased activities of apolipoprotein m promoter are associated with the susceptibility to coronary artery diseases.

The present study investigated the correlation among genetic polymorphisms of the proximal promoter region of apolipoprotein M (apoM) gene, the polymorphisms in relation to apoM expressions and the susceptibility to coronary artery diseases (CAD) in a Han Chinese population. Four common polymorphic sites, i.e.

Palmitic acid suppresses apolipoprotein M gene expression via the pathway of PPARβ/δ in HepG2 cells.

It has been demonstrated that apolipoprotein M (APOM) is a vasculoprotective constituent of high density lipoprotein (HDL), which could be related to the anti-atherosclerotic property of HDL. Investigation of regulation of APOM expression is of important for further exploring its pathophysiological function in vivo. Our previous studies indicated that expression of APOM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF), leptin, hyperglycemia and etc.