SIDE: Self-supervised Intermediate Domain Exploration for Source-free Domain Adaptation

Domain adaptation aims to alleviate the domain shift when transferring the knowledge learned from the source domain to the target domain. Due to privacy issues, source-free domain adaptation (SFDA), where source data is unavailable during adaptation, has recently become very demanding yet challenging. Existing SFDA methods focus on either self-supervised learning of target samples or reconstruction of virtual source data. The former overlooks the transferable knowledge in the source model, whilst the latter introduces even more uncertainty. To address the above issues, this paper proposes self-supervised intermediate domain exploration (SIDE) that effectively bridges the domain gap with an intermediate domain, where samples are cyclically filtered out in a self-supervised fashion. First, we propose cycle intermediate domain filtering (CIDF) to cyclically select intermediate samples with similar distributions over source and target domains. Second, with the aid of those intermediate samples, an inter-domain gap transition (IDGT) module is developed to mitigate possible distribution mismatches between the source and target data. Finally, we introduce cross-view consistency learning (CVCL) to maintain the intrinsic class discriminability whilst adapting the model to the target domain. Extensive experiments on three popular benchmarks, i.e. Office-31, Office-Home and VisDA-C, show that our proposed SIDE achieves competitive performance against state-of-the-art methods.Comment: code at https://github.com/se111/SID

A novel frame-shift mutation in FRMD7 causes X-linked idiopathic congenital nystagmus in a Chinese family

Purpose: To screen mutations in the FERM domain-containing 7 (FRMD7) gene in a Chinese family with X-linked idiopathic congenital nystagmus (ICN). Methods: It has been reported that FRMD7 mutations account for approximately 47% of X-linked nystagmus in Chinese patients. We collected 5 ml of blood samples from members of a family with X-linked ICN and 100 normal controls. Mutations in FRMD7 were determined by sequencing PCR products. Results: We identified a previously unreported 4 bp deletion in FRMD7 (c.1486-1489 del TTTT) in a Chinese family. The mutation co-segregated with the disease phenotype in patients and female carriers, while it was not detected in other relatives or in the 100 normal controls. Conclusions: Our results expand the spectrum of FRMD7 mutations causing ICN, and further confirm the role of FRMD7 in the pathogenesis of ICN. Direct sequencing of FRMD7 could be used as a diagnostic testing of idiopathic congenital nystagmus.Biochemistry & Molecular BiologyOphthalmologySCI(E)PubMed4ARTICLE297-992765-27681

A new novel mutation in FBN1 causes autosomal dominant Marfan syndrome in a Chinese family

Purpose: Screening of mutations in the fibrillin-1 (FBN1) gene in a Chinese family with autosomal dominant Marfan syndrome (MFS). Methods: It has been reported that FBN1 mutations account for approximately 90% of Autosomal Dominant MFS. FBN1 mutations were analyzed in a Chinese family of 36 members including 13 MFS patients. The genomic DNAs from blood leukocytes of the patients and their relatives were isolated and the entire coding region of FBN1 was amplified by PCR. The sequence of FBN1 was dertermined with an ABI 3100 Genetic Analyzer. Results: A previously unreported the missense mutation G214S (caused by a 640 A -> G heterozygous change) in FBN1 was identified in the Chinese family. The mutation was associated with the disease phenotype in patients, but not detected in their relatives or in the 100 normal controls. Conclusions: This is the first report of molecular characterization of FBN1 in the MFS family of Chinese origin. Our results expand the spectrum of FBN1 mutations causing MFS and further confirm the role of FBN1 in the pathogenesis of MFS. Direct sequencing of the mutation in FBN1 may be used for diagnosis of MFS.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000301238300001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyOphthalmologySCI(E)PubMed10ARTICLE10-1181-861

GWAS Identifies Novel Susceptibility Loci on 6p21.32 and 21q21.3 for Hepatocellular Carcinoma in Chronic Hepatitis B Virus Carriers

Genome-wide association studies (GWAS) have recently identified KIF1B as susceptibility locus for hepatitis B virus (HBV)–related hepatocellular carcinoma (HCC). To further identify novel susceptibility loci associated with HBV–related HCC and replicate the previously reported association, we performed a large three-stage GWAS in the Han Chinese population. 523,663 autosomal SNPs in 1,538 HBV–positive HCC patients and 1,465 chronic HBV carriers were genotyped for the discovery stage. Top candidate SNPs were genotyped in the initial validation samples of 2,112 HBV–positive HCC cases and 2,208 HBV carriers and then in the second validation samples of 1,021 cases and 1,491 HBV carriers. We discovered two novel associations at rs9272105 (HLA-DQA1/DRB1) on 6p21.32 (OR = 1.30, P = 1.13×$10^{−19}$) and rs455804 (GRIK1) on 21q21.3 (OR = 0.84, P = 1.86×$10^{−8}$), which were further replicated in the fourth independent sample of 1,298 cases and 1,026 controls (rs9272105: OR = 1.25, P = 1.71×$10^{−4}$; rs455804: OR = 0.84, P = 6.92×$10^{−3}$). We also revealed the associations of HLA-DRB1*0405 and 0901*0602, which could partially account for the association at rs9272105. The association at rs455804 implicates GRIK1 as a novel susceptibility gene for HBV–related HCC, suggesting the involvement of glutamate signaling in the development of HBV–related HCC

Optimal Designs of Phononic Crystal Microstructures Considering Point and Line Defects

In this paper, a two-stage optimization strategy for designing defective unit cells of phononic crystal (PnC) to explore the localization and waveguide states for target frequencies is proposed. In the optimization model, the PnC microstructures are parametrically described by a series of hyperelliptic curves, and the optimal designs can be obtained by systematically changing the designable parameters of hyperellipse. The optimization contains two individual processes. We obtain the configurations of a perfect unit cell for different orders of band gap maximization. Subsequently, by taking advantage of the supercell technique, the defective unit cells are designed based on the unit cell configuration for different orders of band gap maximization. The finite element models show the localization and waveguide phenomenon for target frequencies and validate the effectiveness of the optimal designs numerically

Effect of rock fragment cover on nutrient loss under varied rainfall intensities : A laboratory study

Surface rock fragments retard overland flow discharge, reduce the runoff generation rate and soil erosion as well as nutrients loss. In Northwest China, a common method for minimizing water, soil, and nutrient losses is the use of rock fragment cover. We used lab stimulation testing to evaluate rock fragment cover efficacy for nutrient conservation. Nutrient losses were determined in both the runoff and sediments under three rain intensities (30, 60 and 90 mm·h1), four rock fragment covers (0, 10, 20 and 30%) and a slope of 10. The results showed that rock fragment cover significantly reduced the nutrient losses. Compared with the bare soil control, the rock fragment cover reduced the runoff volume and sediments by 18-38 and 11-69%, respectively, and reduced N and P losses by 9-43 and 16-70%, respectively. These results indicate that rock fragment cover is an effective method for reducing land degradation and improving local environmental conditions

Adoptive immunotherapy in postoperative hepatocellular carcinoma: a systemic review.

PURPOSE: The effectiveness of immunotherapy for postoperative hepatocellular carcinoma patients is still controversial. To address this issue, we did a systemic review of the literatures and analyzed the data with emphasis on the recurrence and survival. METHODS: We searched six randomized controlled trials that included adoptive immunotherapy in the postoperative management of hepatocellular carcinoma and compared with non-immunotherapy postoperation. A meta-analysis was carried out to examine one- and 3-year recurrence and survival. RESULTS: The overall analysis revealed significantly reduced risk of 1-year recurrence in patients receiving adoptive immunotherapy (OR=0.35; 95% CI, 0.17 to 0.71; p=0.003), in that the risk of 3-year recurrence with a pooled OR estimated at 0.31 (95% CI 0.16 to 0.61; p=0.001). However, no statistically significant difference was observed for 3-year survival between groups with adoptive immunotherapy and without adjuvant treatment (OR=0.91; 95% CI, 0.45 to 1.84; P=0.792). CONCLUSIONS: Adjuvant immunotherapy with cytokine induced killer cells or lymphokine activated killer cells may reduce recurrence in postoperative hepatocellular carcinoma patients, but may not improve survival

Angelicin impedes the progression of glioblastoma via inactivation of YAP signaling pathway

Glioblastoma (GBM) is a human malignant tumor with low survival and high recurrence rate. Angelicin, an active furanocoumarin compound, has been reported to possess potential antitumor activity towards various malignancies. However, the effect of angelicin on GBM cells and its mechanism are still unclear. In this study, we found that angelicin inhibited the proliferation of GBM by inducing the cell cycle arrested in G1 phase and suppressed the migration of GBM cells in vitro. Mechanically, we found that angelicin downregulated the expression of YAP and decreased the nuclear localization of YAP, and suppressed the expression of β-catenin. Furthermore, overexpression of YAP partially restored the inhibitory effect of angelicin on GBM cells in vitro. Finally, we found that angelicin could inhibit the growth of tumor and reduce the expression of YAP in the subcutaneous xenograft model of GBM in nude mice and the syngeneic intracranial orthotopic model of GBM in C57BL/6 mice. Taken together, our results suggest that the natural product angelicin exerts its anticancer effects on GBM via YAP signaling pathway, and is expected to be a promising compound for the treatment of GBM

Acute gastroenteritis outbreaks caused by human astrovirus, 1978–2021: A systematic review

Human astrovirus (HAstV) is one of the main pathogens that cause sporadic cases of acute gastroenteritis, sometimes leading to outbreaks. This study aimed to elucidate the epidemiological and etiological characteristics of HAstV outbreaks worldwide. Literature on HAstV outbreaks published before January 2022 was retrieved from the China National Knowledge Infrastructure, WanFang, WeiPu, PubMed, and Web of Science databases. Date, region, population, settings, transmission modes, clinical symptoms, and etiological characteristics of the outbreaks were collected and analyzed. Thirty-one articles on 32 HAstV outbreaks reported between November 1978 and October 2018 were included. The outbreaks mainly occurred in autumn (14/32, 43.75%), and more of them were reported in 1996, 2004, and 2017. Outbreaks were primarily distributed in the Northern Hemisphere and mainly occurred in nursery centers and kindergartens (9/29, 31.03%), hospitals (5/29, 17.24%), and schools (4/29, 13.79%). Viral genotypes were identified during 19 outbreaks, and HAstV-1 was predominant (8/19, 42.10%). Eleven outbreaks were caused by mixed infection, and norovirus (9/11, 81.82%) and rotavirus (5/11, 45.45%) were the most common mixed pathogens. The transmission routes were reported in 9 outbreaks of mixed infection, and most (7/9) were related to waterborne and foodborne transmission. Although HAstV outbreaks are infrequently reported, it is necessary to consider HAstV in norovirus-negative gastroenteritis outbreaks. In addition, local Centers for Disease Control and Prevention should have the capacity to handle HAstV outbreaks and identify pathogens

Rosiglitazone Inhibits Angiotensin II-Induced Proliferation of Glomerular Mesangial Cells via the Gαq/Plcβ4/TRPC Signaling Pathway

Background/Aims: Mesangial cell proliferation and extracellular matrix accumulation (ECM) deposition play an important role in the pathogenesis of glomerulosclerosis. TRPC and PPAR-γ can regulate cell proliferation. Angiotensin II (AngII) can induce mesangial cell proliferation and affect TRPC expression. However, the mechanism has not been fully elucidated. This study was designed to investigate the role of TRPC and the effect of rosiglitazone (RSG) in the proliferation of rat glomerular mesangial cells (HBZY-1) that were stimulated by AngII and the underlying mechanisms. Methods: Immunofluorescence staining and qRT-PCR were performed to examine the expression levels of TRPCs in HBZY-1. Gene expression levels of TRPC, PPAR-γ, RGS4 (regulators of G protein signaling), the GPCR/Gαq/PLCβ4/TRPC signaling pathway and major downstream molecules (PCNA, SKP2, P21 and P27) were detected by qRT-PCR and western blotting. Additionally, changes in intracellular Ca2+ levels were determined through Fluo-4 Ca2+ imaging, and the cell cycle was analyzed by flow cytometry. Results: Our results found that TRPC1 and 6 were at higher expression levels in HBZY-1 cells. Following AngII stimulation, there were increased levels of TRPC1 and 6, Ca2+ entry, PCNA and SKP2, decreased expression levels of P21 and P27 and a reduced G0/G1 percentage. Silencing TRPC1 and 6 by siRNAs led to decrease in Ca2+ influx, G0/G1 cell cycle arrest and cell proliferation. Notably, PPAR-γ activation by RSG upregulated RGS4 expression, which can interact with the Gαq family to inhibit the Gαq-mediated signaling cascade. The results were similar to silencing TRPC1 and 6 by siRNAs. Conclusion: All these results indicate that RSG could inhibit HBZY-1 cell proliferation via the Gαq/PLCβ4/TRPC signaling pathway