https://digitalcommons.wustl.edu/cgi/viewcontent.cgi?article=10660&context=open_access_pubs

American Society of Hematology 2020 guidelines for management of venous thromboembolism: treatment of deep vein thrombosis and pulmonary embolism.

// Hua-Chuan Zheng 1 1 Department of Experimental Oncology and Animal Center, Shengjing Hospital of China Medical University, Shenyang 110004, China Correspondence to: Hua-Chuan Zheng, email: zheng_huachuan@hotmail.com Keywords: cancer, chemoresistance, molecular mechanisms, chemotherapy Received: March 31, 2017      Accepted: June 24, 2017      Published: July 06, 2017 ABSTRACT Overcoming intrinsic and acquired drug resistance is a major challenge in treating cancer patients because chemoresistance causes recurrence, cancer dissemination and death. This review summarizes numerous molecular aspects of multi-resistance, including transporter pumps, oncogenes (EGFR, PI3K/Akt, Erk and NF-κB), tumor suppressor gene (p53), mitochondrial alteration, DNA repair, autophagy, epithelial-mesenchymal transition (EMT), cancer stemness, and exosome. The chemoresistance-related proteins are localized to extracellular ligand, membrane receptor, cytosolic signal messenger, and nuclear transcription factors for various events, including proliferation, apoptosis, EMT, autophagy and exosome. Their cross-talk frequently appears, such as the regulatory effects of EGFR-Akt-NF-κB signal pathway on the transcription of Bcl-2, Bcl-xL and survivin or EMT-related stemness. It is essential for the realization of the target, individualized and combine therapy to clarify these molecular mechanisms, explore the therapy target, screen chemosensitive population, and determine the efficacy of chemoreagents by cell culture and orthotopic model.

/pdf/the-molecular-mechanisms-of-chemoresistance-in-cancers-2mj89ke3i8.pdf

The molecular mechanisms of chemoresistance in cancers.

MicroRNA in lung cancer: role, mechanisms, pathways and therapeutic relevance

In the current SARS-CoV-2 pandemic, there has been worldwide debate on the use of corticosteroids in COVID-19. In the recent RECOVERY trial, evaluating the effect of dexamethasone, a reduced 28-day mortality in patients requiring oxygen therapy or mechanical ventilation was shown. Their results have led to considering amendments in guidelines or actually already recommending corticosteroids in COVID-19. However, the effectiveness and safety of corticosteroids still remain uncertain, and reliable data to further shed light on the benefit and harm are needed. The aim of this systematic review and meta-analysis was to evaluate the effectiveness and safety of corticosteroids in COVID-19. A systematic literature search of RCTS and observational studies on adult patients was performed across Medline/PubMed, Embase and Web of Science from December 1, 2019, until October 1, 2020, according to the PRISMA guidelines. Primary outcomes were short-term mortality and viral clearance (based on RT-PCR in respiratory specimens). Secondary outcomes were: need for mechanical ventilation, need for other oxygen therapy, length of hospital stay and secondary infections. Forty-four studies were included, covering 20.197 patients. In twenty-two studies, the effect of corticosteroid use on mortality was quantified. The overall pooled estimate (observational studies and RCTs) showed a significant reduced mortality in the corticosteroid group (OR 0.72 (95%CI 0.57–0.87). Furthermore, viral clearance time ranged from 10 to 29 days in the corticosteroid group and from 8 to 24 days in the standard of care group. Fourteen studies reported a positive effect of corticosteroids on need for and duration of mechanical ventilation. A trend toward more infections and antibiotic use was present. Our findings from both observational studies and RCTs confirm a beneficial effect of corticosteroids on short-term mortality and a reduction in need for mechanical ventilation. And although data in the studies were too sparse to draw any firm conclusions, there might be a signal of delayed viral clearance and an increase in secondary infections.

/pdf/corticosteroid-use-in-covid-19-patients-a-systematic-review-3cp59vynvi.pdf

Corticosteroid use in COVID-19 patients: a systematic review and meta-analysis on clinical outcomes.

The acute respiratory distress syndrome (ARDS) secondary to viral pneumonitis is one of the main causes of high mortality in patients with COVID-19 (novel coronavirus disease 2019). We systematical...

https://www.tandfonline.com/doi/pdf/10.1080/17476348.2020.1804365

Mortality in COVID-19 patients with acute respiratory distress syndrome and corticosteroids use: a systematic review and meta-analysis.

OBJECTIVE Down-regulation of miR-138 is observed in a variety of cancers, which suggests that miR-138 may be involved in cancer pathogenesis. Our current work aimed to evaluate the effects of miR-138 in adriamycin (ADM)-resistant human NSCLC cells. MATERIALS AND METHODS Cell proliferation was determined by MTT assay. Real-time PCR and western blot were performed to detect the mRNA and protein expression levels. The target of miR-138 was validated by luciferase activity assay. RESULTS Compared with the chemosensitive parental cells, miR-138 was remarkably decreased in A549/ADM and NCI-H23/ADM cells. Ectopic expression of miR-138 sensitized chemoresistant tumor cells to ADM administration. In addition, the epithelial-mesenchymal transition (EMT) related markers E-cadherin or vimentin was up-regulated or down-regulated upon the overexpression of miR-138 in NSCLC cells. Further studies identified zinc finger E-box-binding homeobox 2 (ZEB2) as the target of miR-138 and up-regulation of miR-138 suppressed the mRNA and protein expression of ZEB2. Notably, luciferase reporter assay confirmed that ZEB2 was a direct target of miR-138. CONCLUSIONS Our study demonstrates that miR-138 sensitizes NSCLC cells to ADM via EMT, suggesting that miR-138 might be a potential therapeutic target for drug-resistant NSCLC patients.

MicroRNA-138 regulates chemoresistance in human non-small cell lung cancer via epithelial mesenchymal transition.

Circular RNAs (circRNAs) are non-coding RNAs molecules consisting of a covalently closed continuous loop which have no 5'-3' polarity and contain no polyA tail. Accumulating evidence demonstrates that circRNAs are involved in the initiation and progression of human malignancies. In this study, we explored the expression profile and regulatory role of circ-baculoviral IAP repeat-containing 6 (circ-BIRC6), a circular RNA, in malignant behaviors in non-small cell lung cancer (NSCLC). Expression levels of circ-BIRC6 and miR-4491 were examined in NSCLC patient samples and cell lines using quantitative real time PCR (qRT-PCR). In vitro roles of circ-BIRC6 knockdown on cell viability, colony formation, and apoptosis were assessed using the CCK-8, colony formation assay, and flow cytometry, respectively. The interactions between circ-BIRC6 and miR-449 were assessed using luciferase reporter and qRT-PCR assays. The in vivo role of circ-BIRC6 knockdown on tumor growth and apoptosis was evaluated in a xenograft mouse model of NSCLC. We found that expression levels of circ-BIRC6 in NSCLC patient samples and cell lines were elevated. Small interfering RNA (siRNA)-mediated circ-BIRC6 knockdown suppressed cell proliferation, colony formation, migration and invasion, and promoted apoptosis in NCI-H460 and A549 cells. In addition, miR-4491 was identified as a tumor-suppressor miRNA in NSCLC and circ-BIRC6 functions as a molecular sponge for miR-4491. Furthermore, circ-BIRC6 knockdown suppressed Wnt2B/β-catenin pathway. In vivo assay showed that depletion of circ-BIRC6 suppressed tumor growth, enhanced apoptosis, and decreased miR-4491 levels in a mouse xenograft model. These findings demonstrate that circ-BIRC6 functions as a critical regulator of proliferation and apoptosis via binding to and negatively regulating miR-4491, suggesting that circ-BIRC6 might be a potential target for treatment of NSCLC.

Depletion of circ-BIRC6, a circular RNA, suppresses non-small cell lung cancer progression by targeting miR-4491.

Objectives: To investigate the efficacy and safety of initial thrombolysis by recombinant tissue-type plasminogen activator (rt-PA) in compared with anticoagulant therapy in patients with acute intermediate-risk pulmonary embolism (PE). Methods : Sixty-six patients with acute intermediate-risk PE were randomly assigned to receive rt-PA or LMWH between June 2014 and June 2017 in our department. We obtained information regarding the difference in the right ventricle/left ventricle (RV/LV) ratio, pulmonary artery systolic pressure (PASP), clinical symptoms improvement, PE-related mortality, hemodynamic decompensation, recurrent PE, and major and minor bleeding. Results : In the rt-PA group, the mean PASP was reduced from 52.0±12.2 at baseline to 34.8±9.4 ( p less than  0.001) and the mean RV/LV ratio was reduced from 1.26±0.22 at baseline to 0.96±0.18 ( p less than  0.001) at 24 hours. In the LMWH group, the mean PASP was 53.4±12.8 at baseline and 48.5±11.9 at 24 hours ( p =0.11), and the mean RV/LV ratio was 1.22±0.19 at baseline and 1.17±0.21 at 24 hours ( p =0.31). In comparison with the LMWH group, there was a significant reduction in PASP and an improvement in the symptom severity in the rt-PA group. At 90 days, there was no difference in mortality, recurrent venous thromboembolism and major bleeding as a safety outcome, but increased minor bleeding and decreased hemodynamic decompensation occurred in the rt-PA group. Conclusions : In patients with acute intermediate-risk PE, low dose thrombolytic therapy is considered safe and effective, it can be recommended as an alternative option in clinical treatment.

https://smj.org.sa/content/smj/39/11/1090.full.pdf

Clinical efficacy of low dose recombinant tissue-type plasminogen activator for the treatment of acute intermediate-risk pulmonary embolism.

Radiation resistance of the lung adenocarcinoma is related to the AKT-Onzin-POU5F1 axis.

The use of corticosteroids has been controversial in viral pneumonia. In most cases, application of methylprednisolone in severe and critical viral pneumonia patients can quickly alleviate the symptoms of dyspnea and prevent disease progression. However, some scholars have confirmed that corticosteroids delayed the body's clearance of the virus. In our retrospective non-randomised study, 34 patients under 50 years old and diagnosed with coronavirus disease 2019 (COVID-19) were included, according to given methylprednisolone treatment (n = 18) or not (n = 16), they were separated into 2 groups. By comparing the clinical data we concluded that corticosteroids therapy can effectively release COVID-19 symptoms such as persistent fever and difficult breathing, improve oxygenation and prevent disease progression. However, it can prolong the negative conversion of nucleic acids. This article is protected by copyright. All rights reserved.

Effects of methylprednisolone use on viral genomic nucleic acid negative conversion and CT imaging lesion absorption in COVID-19 patients under 50 years old.

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