Cell death­related molecules and targets in the progression of urolithiasis (Review).

Urolithiasis is a high­incidence disease caused by calcium oxalate (mainly), uric acid, calcium phosphate, struvite, apatite, cystine and other stones. The development of kidney stones is closely related to renal tubule cell damage and crystal adhesion and aggregation. Cell death, comprising the core steps of cell damage, can be classified into various types (i.e., apoptosis, ferroptosis, necroptosis and pyroptosis). Different crystal types, concentrations, morphologies and sizes cause tubular cell damage via the regulation of different forms of cell death. Oxidative stress caused by high oxalate or crystal concentrations is considered to be a precursor to a variety of types of cell death. In addition, complex crosstalk exists among numerous signaling pathways and their key molecules in various types of cell death. Urolithiasis is considered a metabolic disorder, and tricarboxylic acid cycle­related molecules, such as citrate and succinate, are closely related to cell death and the inhibition of stone development. However, a literature review of the associations between kidney stone development, metabolism and various types of cell death is currently lacking, at least to the best of our knowledge. Thus, the present review summarizes the major advances in the understanding of regulated cell death and urolithiasis progression.

Using a multidisciplinary team for the staged management and optimally minimally invasive treatment of severe acute pancreatitis.

Severe acute pancreatitis (SAP) is a common critical disease with a high mortality rate that involves a complex, rapid change in condition and multiple organ systems. Therefore, a multidisciplinary team (MDT), including staff from the emergency department, intensive care unit, pancreatic surgery, gastroenterology , and imaging, is necessary for the early diagnosis, evaluation, and treatment of patients with SAP. This involves managing the systemic inflammatory response and maintaining organ function in the early stage and managing systemic infection and treatment of peripancreatic complications in the middle-to-late stages. The MDT should be led by departments corresponding to the clinical characteristics of each stage, and those departments should be responsible for the coordination and implementation of treatment by other relevant departments. In the late stage, pancreatic surgery and gastroenterology are the main departments that should manage peripancreatic complications. In line with the principle of minimally invasive treatment, the timely and reasonable selection of endoscopic or minimally invasive surgical debridement can achieve good therapeutic outcomes. Open surgery is also an effective method for treating an intractable massive hemorrhage in the abdominal cavity or necrotic cavity, intractable abdominal compartment syndrome, visceral perforation, and fistulae.

Effects of long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) on proliferation, metastasis and drug resistance of non-small cell lung cancer (NSCLC) cells through ERK1/2 and ß-catenin signaling pathways.

OBJECTIVES: This study was aimed to investigate the effects of long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) on the proliferation, metastasis and drug resistance of non-small cell lung cancer (NSCLC) cells. METHODS: The expression of CASC2c in NSCLC tissues and cell lines was detected by real-time fluorescence quantitative PCR (RT-qPCR). MTT and Transwell assay were used to determine the proliferation and migration of NSCLC cells in the experimental group and the control group respectively. The drug sensitivity test was used to confirm whether increasing the CASC2c expression level could reverse the resistance of NSCLC cells to the chemotherapy drug cisplatin. The effects of CASC2c on the expression levels of p-ERK1/2 and ß-catenin were detected by western blot. RESULTS: The results of RT-qPCR showed that CASC2c was under-expressed in NSCLC tissues and cells compared with normal adjacent lung tissues cells (p < 0.05). In addition, the CASC2c expression was remarkably correlated with TNM staging, tumor cell differentiation, lymph node metastasis, smoking and other pathological indicators of patients with NSCLC (p < 0.05). MTT and Transwell assay showed that the high-expression of CASC2c significantly reduced the proliferation and migration of NSCLC cells compared to that of the control group (p < 0.05). Western blot assay showed that the high-expressed CASC2c can decrease the expression of phosphorylated-ERK1/2 (p-ERK1/2) and ß-catenin. CONCLUSIONS: CASC2c was low expressed in NSCLC tissues and cells. What's more, it inhibited the proliferation and migration of NSCLC cells by inhibiting the expression of p-ERK1/2 and ß-catenin and reversed NSCLC cells' resistance to the chemotherapy drug cisplatin. Therefore, CASC2c may serve as a new biomarker and therapeutic target in the diagnosis and treatment of NSCLC.