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The creation of treatment strategies in clinical settings follows criteria, such as patterns of metastases, complexity of the resection and biological factors (metachronous/synchronous metastases, prognostic factors). CONCLUSION Neoadjuvant treatment in the context of conversion therapy is the standard procedure for metastasized colorectal cancer. The biological selection of favorable tumors as the basis for neoadjuvant treatment of resectable lesions is not a consistently used standard for colorectal cancer. Non-colorectal liver metastases are resected only as part of individual concepts.Recent advances in chronic toxoplasmosis understanding became the focus of discussion about behavioral abnormalities, which could be explained by cyst location and neuronal impairment in specific brain areas. Perineuronal nets (PNNs) are specialized extracellular matrices that surround the neuronal body and proximal dendrites and play key roles in neuronal circuitry maintenance and stabilization. Capsazepine molecular weight Its impairment can lead to abnormal synaptic functioning with behavioral repercussions. In this context, we analyzed the impact of Toxoplasma gondii infection on neuronal integrity in the Corpus striatum of chronically infected mice. C57BL/6 and Balb/c female mice were infected with T. gondii ME49 cysts. Brain sections were submitted to immunohistochemistry with Wisteria floribunda agglutinin (WFA) for PNN labeling followed by quantification of tissue cyst and labeled neuronal cells 30 days after infection. Our results revealed that C57BL/6 exhibited a significant decrease in PNN-positive (WFA+) labeled neurons and an expressively higher number of tissue cysts than Balb/c mice. It was also possible to observe that the number of T. gondii tissue cysts and the number of WFA+ neurons were inversely correlated for C57BL/6-infected mice. However, no correlation was observed for Balb/c mice. These data suggest how the impact of parasite dissemination in the brain and host characteristics can influence neuronal integrity impairment during infection by decreasing WFA+ neurons. This might be a plausible pathway in which the presence of T. gondii contributes to behavioral changes in the infected host.PURPOSE Surgery is recommended for most patients with gastro-entero-pancreatic neuroendocrine neoplasias (GEP-NENs). Rates of complications and perioperative mortality have been reported in few mostly retrospective single-center series, but there has been no detailed analysis on risk factors for perioperative complications and mortality to date. METHODS Data of patients with GEP-NENs operated between January 2015 and September 2018 were retrieved from EUROCRINE©, a European online endocrine surgical quality registry, and analyzed regarding rate and risk factors of surgical complications. Risk factors were assessed by logistic regression. RESULTS Some 376 patients (211 female, 167 male; age median 63, range 15-89 years) were included. Most NENs were located in the small intestine (SI) (n = 132) or pancreas (n = 111), the rest in the stomach (n = 34), duodenum (n = 30), appendix (n = 30), colon, and rectum (n = 22), or with unknown primary (n = 15). Of the tumors, 320 (85.1%) were well or moderately differentiated, and 147 (39.1%) of the patients had distant metastases at the time of operation. Severe complications (Dindo-Clavien ≥ 3) occurred in 56 (14.9%) patients, and 4 (1.1%) patients died perioperatively. Severe complications were more frequent in surgery for duodenopancreatic NENs (n = 31; 22.0%) compared with SI-NENs (n = 15; 11.4%) (p = 0.014), in patients with lymph node metastases operated with curative aim of surgery (n = 24; 21.4%) versus non-metastasized tumors or palliative surgery (n = 32; 12.1%) (p = 0.020), and in functioning tumors (n = 20; 23.0%) versus non-functioning tumors (n = 30; 13.5%) (p = 0.042). Complication rates were not significantly associated with tumor stage or grade. CONCLUSIONS Severe complications are frequent in GEP-NEN surgery. Besides duodenopancreatic tumor location, curative resection of nodal metastases and functioning tumors are risk factors for complications.We evaluated the effects of glucocorticoids on bone mineral density (BMD), and prevalence of osteoporosis and fracture in rheumatoid arthritis (RA) by meta-analysis. Until June 26, 2019, we conducted a systematic literature search in EMBASE, Web of science, PubMed, and Cochrane Library to obtain BMD and the prevalence of osteoporosis and fracture in glucocorticoid-treated subjects with RA. The BMD of the treatment and control groups were analyzed by meta-analysis (Stata. version 15), and the 95% confidence interval (CI) was calculated. We identified 15 observational studies, including 46,711 RA subjects and 857 healthy controls. The BMD of the lumbar spine (- 0.038 g/cm2; CI, - 0.052, - 0.024) and femoral neck (- 0.017 g/cm2; - 0.030, - 0.003) in RA treated with glucocorticoids were significantly lower than those in RA controls. Compared with healthy control group, the BMD of the lumbar spine (- 0.094 g/cm2; - 0.126, - 0.061) and femoral neck (- 0.097 g/cm2, - 0.109, - 0.085) of RA treated with glucocorticoids decreased more significantly. The prevalence of osteoporosis in whole body, spine, and femur was 38.6% (0.305, 0.466), 32.9% (0.277, 0.381), and 21.7% (0.106, 0.328), respectively. And the prevalence of vertebral fracture was 13.0% (0.058, 0.203). Glucocorticoids may lead to a decline in skeletal health in subjects with RA, especially in vertebral and femoral BMD, compared with normal people or RA without glucocorticoid therapy. Meanwhile, osteoporosis and fractures were also common. Therapeutic measures should be targeted at individuals, which needs further study. Through meta-analysis, we found that glucocorticoids have some negative effects on the bone health of subjects with rheumatoid arthritis. Therefore, when using glucocorticoids to treat rheumatoid arthritis, we should take strategic measures to prevent the decline of bone quality.AIMS/HYPOTHESIS We aimed to investigate whether the impact of obesity and unfavourable lifestyle on type 2 diabetes risk is accentuated by genetic predisposition. METHODS We examined the joint association of genetic predisposition, obesity and unfavourable lifestyle with incident type 2 diabetes using a case-cohort study nested within the Diet, Cancer and Health cohort in Denmark. The study sample included 4729 individuals who developed type 2 diabetes during a median 14.7 years of follow-up, and a randomly selected cohort sample of 5402 individuals. Genetic predisposition was quantified using a genetic risk score (GRS) comprising 193 known type 2 diabetes-associated loci (excluding known BMI loci) and stratified into low (quintile 1), intermediate and high (quintile 5) genetic risk groups. Lifestyle was assessed by a lifestyle score composed of smoking, alcohol consumption, physical activity and diet. We used Prentice-weighted Cox proportional-hazards models to test the associations of the GRS, obesity and lifestyle score with incident type 2 diabetes, as well as the interactions of the GRS with obesity and unfavourable lifestyle in relation to incident type 2 diabetes.
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