Ludehn6031

Besides, DLX6-AS1 was regarded as an oncogene in ESCC. MTX-211 clinical trial Furthermore, DLX6-AS1 acted as a competing endogenous RNA via sponging miR-577 in ESCC. CONCLUSIONS In summary, DLX6-AS1 promotes development and metastasis of ESCC by sponging miR-577 and could be a potential therapeutic target.OBJECTIVE To investigate the effect of GREM1 on the sensitivity of cervical squamous carcinoma cells to radiotherapy and chemotherapy. PATIENTS AND METHODS The resected cancer tissues and paracancerous tissues of patients with cervical carcinoma were collected. The expressions of GREM1 protein and mRNA in SiHa cell line of cervical squamous carcinoma were tested by Western blot and reverse transcription-polymerase chain reaction (qRT-PCR). The effect of GREM1 on chemotherapy sensitivity of SiHa cells was tested by MTT assay. SiHa cells were irradiated with different doses of X-ray, and the changing trend of GREM1 in cell lines was observed. RESULTS Compared with paracancerous tissues, the expression level of GREM1 in cervical squamous carcinoma was significantly higher than that in paracancerous tissues (p less then 0.05). After adding different concentrations of chemotherapeutic drugs, the relative survival rate of SiHa cells overexpressing GREM1 group was significantly increased. After high-energy X-ray irradiation with different radiation doses of SiHa cells, the expression levels of GREM1mRNA and protein in SiHa cell lines showed a significant downward trend. GREM1 was highly expressed in cervical squamous carcinoma. CONCLUSIONS Down-regulating GREM1 expression can increase the chemotherapy sensitivity of SiHa cells. GREM1 may be related to the radiotherapy sensitivity of cervical squamous carcinoma.OBJECTIVE To study the effect of strontium ranelate (SR) on steroid-induced osteonecrosis of the femoral head (SIONFH) in rabbits and its regulatory mechanism. MATERIALS AND METHODS The ONFH model was established in 30 rabbits using steroid and they were randomly divided into Control group, Model group, and SR group. After SR intervention, the rabbits were sacrificed and sampled. The pathological injury of the femoral head in each group was detected via hematoxylin-eosin (HE) staining, the level of vascular endothelial growth factor (VEGF) in the femoral head in each group was detected via enzyme-linked immunosorbent assay (ELISA). The messenger ribonucleic acid (mRNA) and protein expression levels of transforming growth factor-β1 (TGF-β1), as well as the bone morphogenetic protein 2 (BMP2) in the femoral head in each group, were determined using Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting. RESULTS The rabbit model of SIONFH was successfully established. Compared with Control group, the Model group had a severer pathological injury of the femoral head, a lower level of VEGF in the femoral head, significantly decreased mRNA and protein levels of TGF-β1 and BMP2. Compared with Model group, the SR group had markedly improved pathological injury of the femoral head, a higher level of VEGF in the femoral head, significantly increased mRNA and protein levels of TGF-β1, as well as BMP2. CONCLUSIONS SR can remarkably improve the pathological injury of the femoral head and increase the expression of VEGF in SIONFH rabbits, whose potential mechanism may be related to the activation of the TGF-β1/BMP2 signaling pathway.OBJECTIVE Protein-energetic malnutrition (PEM) affects prognosis and mortality in elderly patients as an inadequate nutritional status is a risk factor for the development and worsening of pressure sores (PS). We aimed to evaluate the incidence of PEM in outpatients with PS and to study the impact of nutritional support on the stage of PS. PATIENTS AND METHODS   PS patients, divided in a group treated with artificial nutrition (group A) and those fed orally (group B) at home, were consecutively enrolled in the Integrated Home Care program of Ascoli Piceno between June and September 2015. At T0 the patients underwent medical history, nutritional, anthropometric/biochemical parameters assessment, and the staging of the PS. The same assessments and staging of the pressure lesions were performed three months later (T1). RESULTS Group A (n=25) started from a better nutritional status vs. group B (n=25) at T0, according to MNA assessment. Group A showed a significant improvement of nutritional status correlating with detailed control of nutrients intake and improvement of PS stage (T0 vs. T1, p less then 0.05). On the other hand, group B showed a significant difference between nutrients intake and nutritional needs that correlated with both malnutrition state increase and worsening of the PS staging (T0 vs. T1, p less then 0.05). CONCLUSIONS The present study shows that PEM has a significant prevalence in the elder, in general, and in older people with PS, in particular. A targeted nutritional intake can prevent and help the healing of PS.OBJECTIVE This review inspects the relations between the microbiota and the intestinal immune system in the advancement of metabolic illnesses, such as obesity and diabetes mellitus. The role of the microbiota in intestinal immune defense and the control of metabolism are subject to examination. MATERIALS AND METHODS In type 1 diabetes, the adhesion proteins prompt inside the intestinal epithelium prompt a more significant immune response that may result in the destruction of pancreatic β cells by CD8+ T-lymphocytes, as well as increased articulation of interleukin-17, which is associated with autoimmunity. Studies suggest that the beginning of metabolic ailments and certain co-morbidities can be viewed in light of the protection between the gut microbiota and the intestinal immune system. The gut microbiota is analyzed as a key regulator of metabolic ailments. Research demonstrates that obese patients with type 2 diabetes have a certain gut microbiota and that the microbiota is translocated from the gut to the tissues in conjunction with the illness, which instigates inflammation. RESULTS Research in animals and people suggests that a probiotic supplement may regulate the gut microbiota, thereby improving the prognosis for diabetes. CONCLUSIONS The mechanism underlying this phenomenon relates to a decrease in the inflammatory reaction and oxidative stress, as well as a decrease in leaky gut. Such reactions increase insulin sensitivity and reduce autoimmune responses.