Osteoporosis is a bone disorder defined by a decrease in bone mineral density (BMD) which can lead to an increased risk of fractures. Patients with epilepsy are more prone to having fractures. When accounting for seizure-related fractures, the epilepsy patient population still suffers from an increased risk of fractures. This can be attributed to adverse effects of antiepileptic drugs (AEDs). The aim of this study was to investigate the association between the use of AEDs and decreased BMD in a large unselected population of Danish patients with epilepsy. The study was a cross-sectional study based on data retrieved from 835 patients visiting an outpatient Epilepsy Clinic in Glostrup, Denmark, from January 1st 2006 - January 31st 2018. The data included results from DXA-scans and demographic information. Logistic regression models and other statistical analyses were performed. The results showed that the odds for having osteoporosis when taking EIAEDs were 2.2 (95 % CI 1.2-3.8, P = 0.007) times higher than those taking NEIAEDs. Furthermore, the odds for having osteoporosis increased with duration of epilepsy (OR = 1.0, 95 % CI 1.0 - 1.0, P = 0.001) and when the patients consume two AEDs compared to one AED (OR = 2.3, 95 % CI 1.3-4.1, P < 0.001). Additionally, consuming three AEDs compared to one lead to a 2.3 times higher risk of having osteoporosis (95 % CI 1.2-4.4, P = 0.01). When accounted for many riskfactors, EIAEDs, polytherapy with AEDs and duration of epilepsy are correlated with osteoporosis. There is a need for using these known riskfactors as guidelines in indentifying patients at increased risk of developing osteoporosis. When accounted for many riskfactors, EIAEDs, polytherapy with AEDs and duration of epilepsy are correlated with osteoporosis. https://www.selleckchem.com/products/2-deoxy-d-glucose.html There is a need for using these known riskfactors as guidelines in indentifying patients at increased risk of developing osteoporosis. Report of the contribution of invasive EEG (iEEG) and epileptogenicity mappings (EM) in a pediatric cohort of patients with epilepsy associated with focal polymicrogyria (PMG) and candidates for resective surgery. Retrospective pediatric case series of patients presenting focal PMG-related refractory epilepsy undergoing an invasive exploration (iEEG) at Fondation Rothschild Hospital. We reviewed clinical data, structural MRI, and visual analysis of iEEG recordings. Moreover, time-frequency analysis of SEEG signals with a neuroimaging approach (epileptogenicity maps) was used to support visual analysis. Between 2012 and 2019, eight patients were selected. Five patients were explored with stereoelectroencephalography (SEEG) only, one patient with subdural exploration (SDE) only and two patients first underwent SEEG and then SDE. The mean age at seizure onset was 40.3 months (range 3-120), and the mean age for the iEEG 10.8 years (range 7-15). The epileptogenic zone (EZ) appeared concordant to the PMG lesion in only one case, was larger in three cases, smaller in two cases and different in one case. Four cases were selected for tailored resective surgery and one for total callosotomy. Two patients remained seizure-free at their last follow-up (mean 32.6 months, range 7-98). Epileptogenicity mapping (EM) refined the qualitative analysis, showing in four patients an EZ larger than visually defined. This study is the first pediatric study to analyze the value of iEEG and EM as well as operability in focal PMG-related refractory epilepsy. The results illustrate the complexity of this pathology with variable concordance between the EZ and the lesion and mixed response to surgery. This study is the first pediatric study to analyze the value of iEEG and EM as well as operability in focal PMG-related refractory epilepsy. The results illustrate the complexity of this pathology with variable concordance between the EZ and the lesion and mixed response to surgery. Osteosarcoma is a common bone malignancy in patients of all ages. Surgical and chemotherapy interventions fail to shrink tumor growth and metastasis. The development of efficient patient-specific therapeutic strategies for osteosarcoma is of great interest in tissue engineering and personalized medicine. The present manuscript aimed to review the advancements in tissue engineering and personalized medicine strategies to overcome osteosarcoma and the relevant biological aspects as well as the current tumor models in vitro and in vivo. Tissue engineering and personalized medicine contribute to gene/cell engineering and cell-based therapies specific to genomic and proteomic profiles of individual patients to improve the current treatment options. Also, tissue engineering scaffolds provide physical support to missing bones, could trap cancer cells and deliver immune cells. Taken together, these strategies suppress tumor growth, angiogenic potential, and the subsequent metastasis as well as elicit desirable imnt coupled with pre-clinical results give new intelligence into the translation of strategies into the clinic.There is a growing body of evidence related to the importance of body composition in cancer survivorship. Current evidence exclusive to the metastatic prostate cancer setting is limited, yet sheds light on the importance of body composition to reduce risk of mortality and disease progression in this patient population. In our commentary we present the current state of evidence related to body composition and metastatic prostate cancer survival among metastatic castration-resistant and castration-sensitive prostate cancer patients among varying treatment modalities. Additionally, we discuss the proposed biological mechanisms that may underpin how favorable changes in body composition may be helpful for survivorship, and review promising lifestyle strategies that can be implemented as part of survivorship care to improve body composition in this patient population. ACE2 a key molecule of the Renin-Angiotensin system has been identified as the receptor for SARS-CoV-2 entry into human cells. In the context of human cancers, there is evidence that ACE2 might function as a tumor suppressor. The expression levels of ACE2 among the different subtypes of breast cancer has not been investigated. We have examined the differential expression of ACE2 and its correlation with prognosis in breast cancer subtypes using the METABRIC (n=1898) and TCGA (n=832) cohorts. Correlations were evaluated by Pearsons's correlation co-efficient and Kaplan-Meier analysis was used to estimate differences in disease-free survival between the ACE2 high and ACE2 low groups. There is minimal expression of ACE2 in the luminal classes, but significantly higher levels in the Basal-like and HER2-enriched subclasses. Metastatic biopsies of these tumor types also show enhanced expression of ACE2. High levels of ACE2 correlated with decreased disease-free survival in the HER2-enriched subtype, and it was positively correlated with EGFR expression.