Background: Carbapenem-resistant Acinetobacter baumannii (CRAB) tops the list of threats to human health. Studies exploring predictors of mortality in patients with CRAB infection produced conflicting results. Methods: A systematic search of the PubMed, Embase, and the Cochrane Library databases was performed from inception to June 2018 to identify studies reporting mortality predictors in patients infected with CRAB. Two authors independently assessed trials for inclusion and data extraction. Results: A total of 19 observational studies were enrolled in this study. Factors associated with mortality of patients infected with CRAB were inappropriate empirical antimicrobial treatment (odds ratio [OR]

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This paper analyzed the results of a modified and simpler technique for distinguishing the intersegmental border during lung segmentectomy surgery. From January 2013 to December 2015, 539 patients with screening‐detected lung nodules <2 cm in maximum diameter underwent anatomic segmentectomy. With the guidance of preoperative three‐dimensional computed tomography bronchography and angiography, the bronchus, artery, and intrasegmental vein of the targeted segment could be precisely dissected under unilateral differential ventilation, and then intersegmental demarcation was confirmed by the modified inflation‐deflation method. The demarcation presented by this method was highly coincident with the real intersegmental border. Dissection along the border between the collapsed and inflated segments using either electrocautery or staples was safe, with almost no air leak or bleeding. This technique is a simple and effective alternative to previously described intersegmental border marking methods.

BackgroundExtended or combined segmentectomies are usually adapted for intersegmental pulmonary nodules. This study explored precise combined subsegmentectomy (CSS) under the guidance of three‐dimensional computed tomography bronchography and angiography (3D‐CTBA).MethodsThe definition of a pulmonary intersegmental nodule was based on a minimum distance between the nodule and the involved intersegmental veins in the preoperative 3D‐CTBA being less than the size of the nodule. Centering on the involved intersegmental vein, two adjacent subsegments belonging to the different segments were combined as a resected unit.ResultsWe retrospectively reviewed the records of 47 patients (mean age 53.6 ± 12.3, range: 26–81 years) who underwent CSS. Thirty‐nine (83.0%) nodules were involved in most intersegmental locations of the upper lobes; the remainder in the lower lobes. The mean nodule size was 0.86 ± 0.32 cm; the mean margin width was 2.20 ± 0.38 cm. Pathological stages included: Tis (8 cases), T1mi (16), IA1 (T1aN0M0, 13), and IA2 (T1bN0M0, 5). Pathological diagnoses included: invasive adenocarcinoma (18 cases), minimally invasive adenocarcinoma (16), adenocarcinoma in situ (8), atypical adenomatous hyperplasia (3), and benign (2). The average operative duration was 190.8 ± 54.9 minutes; operative hemorrhage was 42.7 ± 23.0 mL; 5.8 ± 2.8 lymph nodes dissected had not metastasized; the duration of postoperative chest tube drainage was 3.0 ± 1.8 days; and the postoperative hospital stay was 5.3 ± 2.4 days.ConclusionsUnder 3D navigation, thoracoscopic CSS is a safe technique for intersegmental nodules, sparing more pulmonary parenchyma and ensuring safe margins to achieve anatomical resection.

Non-small cell lung cancer (NSCLC) is one of the most common aggressive malignancies. miRNAs have been identified as important biomarkers and regulators of NSCLC. However, the functional contributions of miR-1260b to NSCLC cell proliferation and apoptosis have not been studied. In this study, miR-1260b was upregulated in NSCLC plasma, tissues, and cell lines, and its high expression was correlated with tumor size and progression. Functionally, miR-1260b overexpression promoted cell proliferation and cell cycle, conversely inhibited cell apoptosis and senescence. Mechanically, miR-1260b negatively regulated SOCS6 by directly binding to its 3′-UTR. Furthermore, miR-1260b-mediated suppression of SOCS6 activated KIT signaling. Moreover, YY1 was an upstream regulator of miR-1260b. This study is the first to illustrate that miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate NSCLC cell proliferation and apoptosis, and is a potential biomarker and therapeutic target for NSCLC. In sum, our work provides new insights into the molecular mechanisms of NSCLC involved in cell proliferation and apoptosis.

SARS‐CoV‐2 caused the emerging epidemic of coronavirus disease in 2019 (COVID‐19). To date, there are more than 82.9 million confirmed cases worldwide, there is no clinically effective drug against SARS‐CoV‐2 infection. The conserved properties of the membrane fusion domain of the spike (S) protein across SARS‐CoV‐2 make it a promising target to develop pan‐CoV therapeutics. Herein, two clinically approved drugs, Itraconazole (ITZ) and Estradiol benzoate (EB), are found to inhibit viral entry by targeting the six‐helix (6‐HB) fusion core of SARS‐CoV‐2 S protein. Further studies shed light on the mechanism that ITZ and EB can interact with the heptad repeat 1 (HR1) region of the spike protein, to present anti‐SARS‐CoV‐2 infections in vitro, indicating they are novel potential therapeutic remedies for COVID‐19 treatment. Furthermore, ITZ shows broad‐spectrum activity targeting 6‐HB in the S2 subunit of SARS‐CoV and MERS‐CoV S protein, inspiring that ITZ have the potential for development as a pan‐coronavirus fusion inhibitor.

The prolonged duration of the severe acute respiratory syndrome coronavirus−2 (SARS−CoV−2) pandemic has resulted in the continuous emergence of variants of concern (VOC, e.g., Omicron) and variants of interest (VOI, e.g., Lambda). These variants have challenged the protective efficacy of current COVID−19 vaccines, thus calling for the development of novel therapeutics against SARS−CoV−2 and its VOCs. Here, we constructed a novel fusion inhibitor−based recombinant protein, denoted as 5−Helix, consisting of three heptad repeat 1 (HR1) and two heptad repeat 2 (HR2) fragments. The 5−Helix interacted with the HR2 domain of the viral S2 subunit, the most conserved region in spike (S) protein, to block homologous six−helix bundle (6−HB) formation between viral HR1 and HR2 domains and, hence, viral S−mediated cell–cell fusion. The 5−Helix potently inhibited infection by pseudotyped SARS−CoV−2 and its VOCs, including Delta and Omicron variants. The 5−Helix also inhibited infection by authentic SARS−CoV−2 wild−type (nCoV−SH01) strain and its Delta variant. Collectively, our findings suggest that 5−Helix can be further developed as either a therapeutic or prophylactic to treat and prevent infection by SARS−CoV−2 and its variants.