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ROS1) were the five most frequent alterations in STAS-positive ADC.

Poorly differentiated histological subtypes likely played a crucial role in promoting the invasiveness of STAS, especially in small tumor-size cases. Epidermal growth factor receptor (EGFR), TP53, KARS, anaplastic lymphoma kinase (ALK), and ROS proto-oncogene 1 (ROS1) were the five most frequent alterations in STAS-positive ADC.

Myocardial ischemia (MI) often causes angina, arrhythmia, and cardiac insufficiency, sometimes resulting in death. Crenolanib Ischemia-induced myocardial tissue damage is attributed to the hypoxic damage of myocardial cells producing apoptosis and decreased proliferation. Taurine has been shown to improve MI, but its mechanism is largely unknown.

In this study, the relationship between taurine and severity of MI in vivo was evaluated by quantifying myocardial infarct areas and metabolic indicators of myocardial damage and measuring taurine levels in cardiac muscle and plasma by high performance liquid chromatography (HPLC). To elucidate how taurine might suppress ischemic injury, we established an

ischemia model with isolated primary rat cardiomyocytes cultured without serum or glucose and under hypoxia. We evaluated the indicators of MI and damage, including lactic dehydrogenase (LDH), creatine kinase (CK), and cardiac troponin I (cTnI). We also examined the levels of taurine transporter (TauT), cysteine dioxygestrated that TauT is critical for the attenuation of myocardial ischemic damage by taurine, facilitating taurine absorption and synthesis. These findings provided new insights and a theoretical foundation for future studies examining taurine as a potential treatment for MI.

We demonstrated that TauT is critical for the attenuation of myocardial ischemic damage by taurine, facilitating taurine absorption and synthesis. These findings provided new insights and a theoretical foundation for future studies examining taurine as a potential treatment for MI.

Eosinophilic granulomatosis with polyangiitis (EGPA) is often misdiagnosed as severe asthma due to their similar clinical presentations. We compared the pulmonary radiologic features of EGPA to those of severe asthma by high-resolution computed tomography (HRCT) in order to early diagnose EGPA.

We retrospectively reviewed clinical records and HRCT findings of 96 patients with EGPA and 82 patients with severe asthma who were seen at our hospital from 2011 to 2017. We used a semi-quantitative grading system to evaluate radiological findings. A radiological only and a clinical-radiological model were used to differentiate EGPA from severe asthma.

Bronchial wall thickening, air trapping, tree-in-bud opacities, bronchial mucus plugging, bronchiectasis, diffuse ground-glass opacities (GGOs), consolidation, and increased small vascular markings were more common in EGPA patients than in severe asthmatics (P<0.05). The gradings of GGO (grade 2

grade 1) and tree-in-bud opacities (grade 2

grade 0) were higher in EGPA patients than in severe asthmatics. The total image score of EGPA patients was significantly higher than that of severe asthmatics (P<0.05). In the radiological only and the clinical-radiological model, the area under the receiver operating characteristic (ROC) curves (AUCs) for the identification of EGPA and severe asthma were 0.904 [95% confidence interval (CI) 0.860 to 0.948] and 0.974 (95% CI 0.955 to 0.993), respectively.

Lung HRCT scan is useful in differentiating EGPA from severe asthma. In patients with difficult-to-treat asthma, an HRCT scan of the thorax should be performed should there be features that raise the suspicion of EGPA.

Lung HRCT scan is useful in differentiating EGPA from severe asthma. In patients with difficult-to-treat asthma, an HRCT scan of the thorax should be performed should there be features that raise the suspicion of EGPA.

Among patients with lung cancer, metastatic and relapsed cases account for the largest proportion of disease-associated deaths. Tumor metastasis and relapse are believed to originate from cancer stem cells (CSCs), which have the capacity to be highly proliferative and invasive. In our previous studies, we established a conditional basement membrane extract-based (BME-based) 3-dimensional (3D) culture system to mimic the tumor growth environment

and further amplified lung cancer stem cells (LCSCs) in our system. However, the molecular mechanisms of LCSC amplification and development in our 3D culture system have not been fully uncovered.

We established the conditional 3D culture system to amplify LCSCs in other lung cancer cell lines, followed by examining the expression of Lin28A and let-7 microRNAs in them. We also explored the expression of Lin28A and let-7 microRNAs in LCSCs from clinical lung cancer tissue samples and even analyzed the correlation of Lin28A/let-7c and patients' survival outcomes. W signaling pathway in promoting the proliferation and cancer stemness of LCSCs, which might be a potential therapeutic target for reducing and even eliminating LCSCs in the future.

Our study uncovered the functions and mechanisms of the Lin28A/let-7c/MAPK signaling pathway in promoting the proliferation and cancer stemness of LCSCs, which might be a potential therapeutic target for reducing and even eliminating LCSCs in the future.

Preeclampsia (PE) is a complex pregnancy-related disease that endangers the safety of maternal and fetal. The purpose of this study is to reveal the pathogenesis of preeclampsia and discover new predictors from the perspective of peptidomics. The umbilical cord blood of PE and control group was analyzed by peptidomics. A peptide named Regulation of Proliferation Process in Preeclampsia (ROPPIP) was screened out to explore its role in the proliferation, migration and apoptosis of trophoblast cells in preeclampsia.

We compared and analyzed the umbilical cord blood of patients with PE and normal pregnant women using liquid chromatography-tandem mass spectrometry (LC-MS). hTR-8/Svneo cells cultured

were divided into ROPPIP group and a disordered peptide group as control. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, Transwell chamber assays and western blot analysis were performed to detect cell proliferation, invasion, migration and apoptosis, in addition to the expression of Matrix metalloproteinaseomotes HTR-8/Svneo cells migration and proliferation, and inhibits apoptosis, by regulating the activation of the PI3K/AKT/mTOR signaling pathway.

Defecation delay (greater than or equal to 3 days post-surgery) is a common symptom in patients after lung tumor surgery. This study investigated the incidence and relevant risk factors of defecation delay in patients after lung tumor surgery.

Between October 2019 and March 2020, a prospective nested case-control study was conducted in 80 patients who received lung tumor surgery in the Department of Thoracic Surgery at the Sun Yat-sen University Cancer Center. According to the Rome III criteria for functional constipation and the accepted definitions in the literature, patients with defecation delay time greater than or equal to 3 days post-surgery were classified as the defecation delay group, and the remaining patients were considered the control group. A questionnaire survey was conducted to explore the trait of the stool, defecation time, postoperative activity, diet, and perioperative pain score. Statistical analyses were performed to compare the risk factors affecting defecation time in the two grou and is related to operation method, pain score, and changes in stool characteristics. This study identified that minimally invasive surgery, postoperative pain relief treatment, and health education may play an important role in preventing delayed defecation.

The renal artery plays a central role in renal perfusion and is critical for proper renal function. Ageing is an independent risk factor for both impaired renal function and vascular disorders, and associated with an increase in the expression of the vasoconstrictor endothelin-1 (ET-1), and caloric restriction (CR) without malnutrition has been shown to be an effective inhibitor of renal dysfunction induced by ageing. The objective of this study was to determine whether CR-mediated alleviation of renal dysfunction is mediated by ET-1 expression.

The young (2 months, 2 M) and old (12 months, 12 M) Sprague-Dawley male rats were used and fed ad libitum. The 12-month-old rats were further divided into 12 M and 12 M-caloric restriction (CR) (30% calorie restriction). After 8 weeks, the renal tissues were showed by PAS staining, and age-related metabolic parameters and renal functions were detected in each group of rats. The inflammatory cytokines of interleukin (IL)-6, IL-1β, tumor necrosis factor alpha (TNF-αexpression. CR might be used as an alternative to prevent the ageing induced renal artery dysfunction.

Moderate CR can reverse the ageing related kidney dysfunction by reducing the ET-1 expression. CR might be used as an alternative to prevent the ageing induced renal artery dysfunction.

Keratinocyte is a key component of the skin barrier and maintains skin homeostasis. As an environmental pathogenic factor, PM2.5 can cause epidermal cell damage, but the mechanism remains to be elucidated. The present study aimed to evaluate the effect caused by PM2.5 in HaCaT cells and investigate the underlying mechanisms.

HaCaT cells were treated with PM2.5 for 12 h or 24 h, either alone or combined with UVB irradiation. A Cell Counting Kit (CCK-8) assay was carried out to detect the effect of PM2.5 on HaCaT cell viability. Flow cytometry, Western Blot, and AO staining were employed to detect the changes of apoptosis and autophagy. The changes of cytotoxicity and apoptosis in HaCaT cells were analyzed by CCK-8 and flow cytometry after pretreatment with autophagy inhibitor 3-MA.

The results showed that PM2.5 induced cytotoxicity by increasing cell apoptosis and activating autophagy. Apoptosis was determined to be increased significantly after autophagy inhibition. Moreover, solar radiation intensified PM2.5-induced damage in HaCaT cells, which further enhanced the autophagy. However, there was no significant difference in apoptosis after inhibition of autophagy in combined treatment.

Our data reveals that PM2.5 induces damage in HaCaT cells, and autophagy plays a protective role to promote cell survival.

Our data reveals that PM2.5 induces damage in HaCaT cells, and autophagy plays a protective role to promote cell survival.

The aim of the present study was to evaluate the curative effect and safety of thoracic full-endoscopic unilateral laminotomy with bilateral decompression (TE-ULBD) for treating ossification of the ligamentum flavum (OLF) with myelopathy.

Between January 2015 and December 2018, 23 consecutive patients with symptomatic thoracic OLF were treated with TE-ULBD. Of these, 21 (13 women and 8 men, aged 49-75 years) were included in the study and followed up for a minimum of 1 year. The mean blood loss was 15.48 mL (10-30 mL), operative duration was 78.86 min (55-115 min), and hospitalization was 5.05 days (3-15 days). The Japanese Orthopaedic Association (JOA) was used to evaluate spinal cord function, and the curative effect was defined by the JOA improvement rate. The area of OLF (AOLF), the maximum spinal cord compression (MSCC), and the area of spinal cord (ASC) were used to evaluate OLF clearance and spinal cord decompression status.

At the final follow up,the JOA score was 8.33 points (5-11 points), which was a significant improvement from the preoperative 5.