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Long non-coding RNA steroid receptor RNA activator (lncRNA-SRA) has been proven to regulate vascular smooth muscle cell (VSMC) proliferation, indicating its possible involvement in cardiovascular disease. Diabetes is a major cause of cardiovascular disease. The aim of the present study was to investigate the involvement of lncRNA-SRA in type II diabetic cardiovascular disease. The plasma levels of lncRNA-SRA were identified to be significantly lower in patients with type II diabetic cardiovascular disease compared with those in type II diabetic patients without any obvious complications and in healthy controls. A 5-year follow-up study revealed that low vs. high expression levels of lncRNA-SRA were associated with an increased incidence of cardiovascular disease in type II diabetic patients. High-glucose treatment did not significantly affect the expression of lncRNA-SRA in human VSMCs in vitro. However, ectopic overexpression of lncRNA-SRA increased the viability of human VSMCs in a high-glucose environment. It was concluded that downregulation of lncRNA-SRA may participate in the development of cardiovascular disease in type II diabetic patients. [ABSTRACT FROM AUTHOR]

Castleman disease (CD) is clinically divided into unicentric CD (UCD) and multicentric CD (MCD). Hyaline-vascular variant (HV) is the most common pathological type of UCD, while the plasma cell type (PC) is the most common type of MCD and thus, hyaline-vascular variant multicentric CD (HV-MCD) is a rare type of CD. In addition, its etiology has remained elusive. The present study retrospectively analyzed the medical records of 3 patients diagnosed as HV-MCD admitted to The First Affiliated Hospital of Guangxi Medical University (Guangxi, China) between January 2007 and September 2020. A total of 2 males and 1 female were admitted. The areas involved varied considerably. Respiratory symptoms were seen in 3 cases, along with fever, weight loss and splenomegaly. Damage to the skin and mucous membranes resulted in oral ulcers when accompanied by paraneoplastic pemphigus (PNP). Dry and wet rales were found in all patients. All 3 cases were complicated with PNP and had hypoxemia and obstructive ventilation dysfunction. In accordance with PC-MCD, it manifested as lymph node enlargement and may involve several lymph nodes. Computed tomography mainly indicated bronchiectasis and mediastinal lymph node enlargement. In 1 case, chemotherapy failed after local mass excision, 1 case remitted after chemotherapy but the lung lesion was irreversible and 1 case was untreated and soon died of respiratory failure. The cases of HV-MCD with pulmonary involvement were induced by small airway lesions and associated with poor prognosis. Respiratory symptoms along with systemic symptoms were common. [ABSTRACT FROM AUTHOR]

Multidrug resistance (MDR) is a major challenge for the management of the majority of cancers. The precise molecular mechanisms of MDR remain elusive. In a previous study, a multidrug resistant osteosarcoma model [MG63/vincristine (VCR)] was established by intermittent exposure of MG63 cells to gradually increasing concentrations of VCR. These cells exhibited cross-resistance to multiple structurally and mechanistically unrelated chemotherapeutic agents. The development of MDR was associated with increased expression of LIM kinase 1 (LIMK1). Compared with that in normal human fetal osteoblasts (hFOB) 1.19, the messenger RNA and protein expression of LIMK1 was significantly elevated both in MG63 and U2OS osteosarcoma cells. To observe the expression pattern of LIMK1 in osteosarcoma, immunohistochemical analyses were performed on specimens derived from 6 patients. The results indicated that LIMK1 was expressed to a greater extent in the tumor parenchyma than in the mesenchyme. The role of LIMK1 in MDR was confirmed by transfecting plasmids coding LIMK1-small interfering RNA (siRNA), wild-type-LIMK1 or empty vector into MG63/VCR cells, and measuring the expression of LIMK1 and multidrug resistance protein 1 (MDR1), also known as P-gycoprotein (P-gp). The results demonstrated that the level of MDR1/P-gp was positively correlated with the level of LIMK1. This correlation was also shown with the doxorubicin efflux assay and by measuring apoptosis. Specifically, after 6 h of incubation with VCR, 25.6% of the cells transfected with the LIMK1-siRNA plasmid were apoptotic compared with 6.2% in the empty vector group and 1.3% in the group of cells transfected with the wild-type-LIMK1 plasmid. Thus, it was concluded that LIMK1 serves a key role in the MDR of osteosarcoma and functions through MDR1. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the expression levels and clinical significance of Toll-like receptor (TLR) 3 and 4 in peripheral blood mononuclear cells (PBMCs) collected from children with Henoch-Schönlein purpura (HSP) nephritis. The randomized controlled trial was conducted between August 2011 and March 2013, and 105 children with a clinical diagnosis of HSP were enrolled in the study. According to the 24-h urinary protein measurements and the presence of renal damage, the 105 cases were divided into groups A, B and C as follows: Group A, children with HSP but without renal damage; group B, children with HSP nephritis but without proteinuria; group C, children with HSP nephritis and proteinuria. A total of 30 healthy children were enrolled in the normal control group (group N). The primary endpoints were the detection of TLR3 and 4 mRNA and protein expression levels in PBMCs by flow cytometry and quantitative polymerase chain reaction. The mRNA and protein expression levels of TLR4 in the PBMCs were significantly higher in groups A, B and C when compared with group N. In addition, the mRNA and protein expression levels of TLR4 in group C were much higher when compared with groups A and B. A positive correlation was identified between TLR4 protein expression and 24-h urinary protein levels in group C. The expression levels of TLR3 did not significantly differ among the groups. Protein and mRNA expression levels of TLR4 in PBMCs significantly increased and exhibited a positive correlation with urinary protein excretion. These results indicate that aberrant activation of TLR4 may be relevant to the development of HSP nephritis. [ABSTRACT FROM AUTHOR]