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The bloodstream infections (BSI) caused by
pose a serious threat to human health. To explore molecular characteristics of
causing BSI, we collected
isolates causing BSI in Huashan Hospital, Shanghai, China during 2010-2015.

In all
isolates causing BSI collected from this study, polymerase chain reaction (PCR) was used to detect ESBLs and carbapenemase genes, and minimum inhibitory concentrations (MICs) were determined with agar dilution method. Outer membrane proteins were examined by SDS-PAGE in carbapenem-resistant strains. The genetic background of

gene was investigated by combining next-generation sequencing with a PCR mapping approach. Conjugation and transformation experiments were performed to verify the mobilization of

. The transcription levels of the

gene were measured by RT-PCR.

During 2010-2015, a total of 207
BSI strains were isolated. The positive rates of β-lactamase resistant genes were 0.48% (

), 57% (

), 23.67% (

), 18.84% (

), and 1.93% low expression of bla KPC may be the reason for the low resistance to carbapenems.
Multidrug-resistant tuberculosis threatens global tuberculosis care and prevention and remains a major public health concern in many countries. In 2016, there were an estimated 490,000 cases of MDR and 110,000 more cases resistant to rifampicin (RR TB). Ethiopia is among the highest MDR TB burden countries according to the WHO. This study aims to describe the magnitude, trends, and geographical distribution of the drug-resistant TB in Bale Zone during study period.

A descriptive study was conducted. We reviewed secondary data of MDR and RR TB cases from July 2014 to June 2018. Data were extracted from the Bale zone health management information system database, checked for completeness, and then analyzed for trends over time.

A total of 43 cases (67.4% female) of drug-resistant TB were reviewed, with 30.2% MDR and 69.8% RR TB. The prevalence of drug-resistant tuberculosis cases declined from 0.81% to 0.62% (trend

=2.18; P=0.14) during study period. Among drug-resistant TB cases, RR TB increased from 52.6% to 81% (trend

=6.5; P=0.01).

Drug-resistant TB decreased over the period studied, although the trend did not reach statistical significance. These trends may reflect the efficacy of TB control programs to reduce drug-resistant TB transmission, as well as improved RR TB detection due to increased use of molecular diagnostic platforms like GeneXpert MTB/RIF.
Drug-resistant TB decreased over the period studied, although the trend did not reach statistical significance. These trends may reflect the efficacy of TB control programs to reduce drug-resistant TB transmission, as well as improved RR TB detection due to increased use of molecular diagnostic platforms like GeneXpert MTB/RIF.
Sporotrichosis is an increasing threat for humans, affecting mainly skin and subcutaneous tissues but that can cause disseminated infection in immunocompromised patients.
, and
are the main etiological agents of this mycosis, and each species show different virulence levels. The gold standard to assess fungal virulence is the mouse model that is expensive and time-consuming. Thus, invertebrate models have been reported as an alternative for the evaluation of fungal virulence. Here, we assessed whether
larvae could be a new alternative to study
spp. virulence.

larvae were inoculated with different doses of
, and
, and animal mortality, cytotoxicity, and immunological parameters were analyzed, including the ability to stimulate immunological priming.

Mortality curves demonstrated that yeast-like cells were the best fungal morphology to kill larvae and showed a similar ranking in virulence than that reported in other animal models, ie, being
and
the species with the highest and lowest. brasiliensis, and S. globosa. Additionally, hemocyte levels, phenoloxidase activity, cytotoxicity, uptake by hemocytes, and immunological priming are biological parameters that can be used to study the Sporothrix-T. molitor interaction.
In Japan, biologic therapy was initiated for patients with severe asthma in 2009. In recent years, four biologics with different mechanisms of action have become available in the clinical setting. However, the efficacy of switching between biologics remains uncertain.

To elucidate the efficacy of switching between biologics, 97 patients were enrolled who had received any biologic therapy for severe asthma at Jikei University Hospital, Tokyo, Japan, from July 2009 to December 2020. We retrospectively examined the patient characteristics, biomarkers, pulmonary function test results, selected biologics, and efficacy.

Thirty-one males and 66 females received any biologics. The mean age was 53.3 years at the initiation of biologic therapy. Initially, 33, 41, 15 and eight patients received omalizumab, mepolizumab, benralizumab, and dupilumab, respectively. Among three representative indicators for biologics administration, the peripheral blood eosinophil count, serum IgE levels and fractional exhaled nitric oxide, 64% of the patients had two indicators, and 28% had three indicators. Thirty-four patients (35%) switched from the initial biologic to another, and the reasons for switching included persistent asthmatic symptoms (n=22), schedule of hospital visits (n=5), and other reasons. Thus, the treatment was effective in 11 patients after switching. In addition, two patients received combination therapy with different biologics. Eighteen patients (19%) interrupted treatment for various reasons. Regardless of whether the biologic was the initial therapy, the overall efficacy of the four biologics was 60% based on the global evaluation of treatment effectiveness.

Switching between biologics can be a promising option for severe asthma patients in whom treatment with an initial biologic is ineffective.
Switching between biologics can be a promising option for severe asthma patients in whom treatment with an initial biologic is ineffective.
The mortality and morbidity of hepatocellular carcinoma (HCC) are still unacceptably high, despite decades of extensive studies. Aerobic glycolysis is a hallmark of cancer metabolism, closely relating to invasion and metastasis of HCC. MicroRNAs (miRNAs) are involved in the regulation of aerobic glycolysis.
, an oncogenic miRNA, is highly expressed in HCC, but the regulatory mechanism of
in migration, invasion and aerobic glycolysis in HCC remains unclear.

To elucidate whether
affects aerobic glycolysis to regulate the migration and invasion of HCC, and to explore its regulatory mechanism.

We attempted to observe the effects of
on the migration and invasion of HepG2 cells by a wound-healing assay and Transwell assays. The effect of
on glycolysis was determined by glucose uptake and lactate generation. Western blot and qPCR were used to detect the relevant proteins and miRNA expression.

Our results show that
promoted migration and invasion, enhanced glycolysis via increasing glucose uptake and lactate generation, and up-regulated glycolysis-related gene (
,
,
,
) expression in HepG2 cells. Further experiments indicated that
could decrease PTEN expression, but increased Akt, p-Akt and mTOR expression in HepG2 cells.

These findings suggest that
may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/mTOR signaling.
These findings suggest that miR-183-5p may promote HCC migration and invasion via increasing aerobic glycolysis through targeting PTEN and then activating Akt/mTOR signaling.
MicroRNAs (miRNAs) function as important regulators of gene expression involved in tumor pathogenesis, including retinoblastoma. However, the expression profiles and potential roles in retinoblastoma are still largely unclear.

Differentially expressed miRNAs (DEmiRs) and genes (DEGs) in retinoblastoma were extracted from Gene Expression Omnibus (GEO) repository. Expression levels of miR-340 and WIF1 were detected in retinoblastoma tissues and cell lines by qRT-PCR. Both gain-of-function and loss-of-function experiments were performed to explore the effects of miR-340 on cell proliferation, migration and invasion. Bioinformatics analysis and luciferase reporter assay were used to explore the interaction between miR-340 and WIF1.

A total of 11 DEmiRs were identified in retinoblastoma tissue and blood samples. Among them, we validated that miR-340 was the most highly expressed miRNA and correlated with tumor size, ICRB stage and optic nerve invasion. miR-340 was observed to enhance the proliferation, migration and invasion capacity of retinoblastoma cells. We then identified 26 DEGs from 3 retinoblastoma GEO datasets and subsequently constructed a miRNA-mRNA regulatory network. Further analysis revealed that WIF1 was a direct target of miR-340. Moreover, overexpression of WIF1 could repress retinoblastoma progression induced by miR-340 in vitro and in vivo.

Collectively, miR-340 functioned as an oncomiRNA to promote retinoblastoma cell proliferation, migration and invasion via regulating WIF1. Our data also provided multiple miRNAs and genes that may contribute to a better understanding of retinoblastoma pathogenesis.
Collectively, miR-340 functioned as an oncomiRNA to promote retinoblastoma cell proliferation, migration and invasion via regulating WIF1. SSR128129E FGFR inhibitor Our data also provided multiple miRNAs and genes that may contribute to a better understanding of retinoblastoma pathogenesis.
Chronic obstructive pulmonary disease (COPD) and lung adenocarcinoma (LUAD) are common disorders and usually co-exists. However, genetic mechanisms between COPD and LUAD are rarely reported. This study aims to identify susceptible genes of COPD with LUAD.

Using the published data of GSE106899, co-expression modules were constructed by weighted gene co-expression network analysis (WGCNA). Subsequently, top 50 genes in the most tumor-related module were identified, among which hub genes were selected and validated.

Twenty co-expression modules were constructed on 13,865 genes from 62 lung tissues of COPD patients with or without LUAD, in which one module (blue) was most related to tumorigenesis. Functional enrichment analyses showed that the genes in the blue module were mainly enriched in cell cycle, DNA transcription/replication and cancer pathways, etc. Combined with protein-protein interaction network, MTA1, PKMYT1 and FZR1 genes had the most intramodular connectivity, which were regarded as the hub genes. However, only FZR1 was validated to be overexpressed in lung tissues of COPD with LUAD and cigarette smoke extract-stimulated A549 cells, a human LUAD cell line.

This study suggests overexpression of FZR1 may play a key role in the tumorigenesis of LUAD in patients with COPD.
This study suggests overexpression of FZR1 may play a key role in the tumorigenesis of LUAD in patients with COPD.
Endocrine therapy is the backbone therapy in estrogen receptor α (ER)-positive breast cancer, and tamoxifen resistance is a great challenge for endocrine therapy. Tamoxifen-resistant and sensitive samples from the international public repository, the Gene Expression Omnibus (GEO) database, were used to identify therapeutic biomarkers associated with tamoxifen resistance.

In this study, integrated analysis was used to identify tamoxifen resistance-associated genes. Differentially expressed genes (DEGs) were identified. Gene ontology and pathway analysis were then analyzed. Weighted correlation network analysis (WGCNA) was performed to find modules correlated with tamoxifen resistance. Protein-protein interaction (PPI) network was used to find hub genes. Genes of prognostic significance were further validated in another GEO dataset and cohort from Shanghai Ruijin Hospital using RT-PCR.

A total of 441 genes were down-regulated and 123 genes were up-regulated in tamoxifen-resistant samples. Those up-regulated genes were mostly enriched in the cell cycle pathway.
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