By scanning the serosal side of the digestive organ during the laparoscopic surgical procedure, the detector senses the modified clip and thus pinpoints to the location of the tumor. Additional engineering of the standard endoscopic hemostatic clips by coating them with various combinations of metallic alloys of Cu and Zn was necessary to improve the detection range and sensitivity without compromising on their functionality. The clips were also covered with nanometric layers of Au to ensure their biocompatibility. The ex-vivo dry-lab experiments showed a satisfactory detection distance which was later confirmed in ex-vivo wet-lab experiments on animal organs and human surgical specimens.In 2016, the World Health Organization recommended that isocitrate dehydrogenase (IDH) mutation status be included in the classification of diffuse astrocytic gliomas. IDH mutations are part of the current definition of oligodendrogliomas and are predictive of a better outcome in diffuse astrocytic gliomas. A few studies, examining the role of routine IDH testing in older patients, came to differing conclusions and made differing recommendations regarding a routine IDH testing algorithm with respect to patient age. The purpose of this study was to examine IDH mutations in a series of diffuse astrocytic gliomas [N = 381; 53 diffuse astrocytomas (WHO grade II), 66 anaplastic astrocytomas (WHO grade III) and 262 glioblastomas (WHO grade IV)], paying particular attention to age of patient and any relationship between age and IDH status. IDH status was evaluated by immunohistochemistry with IDH-1 (R132H) antibody and if negative staining was noted, followup polymerase chain reaction (PCR) testing assessing for IDH-1 and IDH-2 mutations was performed. Overall, IDH mutations were discovered in 50.1% of grade II tumors, 54.4% of grade III tumors and 15.1% of grade IV tumors. Of tumors studied, 224 tumors (58.8%) arose in patients 55 years or older. Higher rates of IDH mutations were observed in the patient group less than 55 years of age versus those 55 years or older. By PCR testing in patients 55 years or older, non IDH-1 (R132H) mutations were noted in 0/4 grade II tumors, 3/11 grade III tumors and 26/37 grade IV tumors. The results of this study suggest that although IDH mutations in diffuse astrocytic gliomas are more frequently encountered in patients less than 55 years of age, a significant subset of older patients have mutations that would not be discovered on routine immunohistochemistry and therefore, followup PCR testing is recommended for all patients whose tumors are negative by immunohistochemistry.There is growing evidence that mechanical factors affect brain functioning. However, brain components responsible for regulating the physiological mechanical environment are not completely understood. To determine the relationship between structure and stiffness of brain tissue, we performed high-resolution viscoelastic mapping by dynamic indentation of the hippocampus and the cerebellum of juvenile mice brains, and quantified relative area covered by neurons (NeuN-staining), axons (neurofilament NN18-staining), astrocytes (GFAP-staining), myelin (MBP-staining) and nuclei (Hoechst-staining) of juvenile and adult mouse brain slices. Results show that brain subregions have distinct viscoelastic parameters. In gray matter (GM) regions, the storage modulus correlates negatively with the relative area of nuclei and neurons, and positively with astrocytes. The storage modulus also correlates negatively with the relative area of myelin and axons (high cell density regions are excluded). Furthermore, adult brain regions are ∼ 20%-150% stiffer than the comparable juvenile regions which coincide with increase in astrocyte GFAP-staining. Several linear regression models are examined to predict the mechanical properties of the brain tissue based on (immuno)histochemical stainings.Lipid disorders are relatively common in dogs. Hyperlipidemia can be primary or secondary to other diseases. In humans, fenofibrate is used to control hypertriglyceridemia. In dogs, there are no studies evaluating fenofibrate in hypertriglyceridemia. The aim of the study was to evaluate the safety and efficacy of fenofibrate to control severe hypertriglyceridemia in dogs. Bezafibrate A total of 124 dogs (n = 124) with severe hypertriglyceridemia (>300 mg/dL, 3.39 mmol/L) were randomly distributed in the fenofibrate group (n = 64) and the diet group (n = 60). Dogs of the fenofibrate group were treated with fenofibrate (10 mg/Kg) once daily. Dogs of the diet group were treated with low-fat diet (10%). Serum triglycerides (TGs), total cholesterol (TC), liver enzymes, and creatine kinase concentrations were evaluated, before and after 1 mo of medical or dietary treatment. Triglyceride concentrations were reduced with fenofibrate (P less then 0.001), and 85.93% of the dogs normalized their levels. Triglyceride concentrations also decreased with low-fat diet (P less then 0.001), but only 26.6% of the dogs normalized their levels. Triglyceride concentrations were reduced with fenofibrate (P less then 0.01) and with low-fat diet (P less then 0.01). Of the cases with hypercholesterolemia, 53.7% and 50% of the dogs normalized their TC concentrations, with fenofibrate and diet, respectively. No significant adverse effects were observed (3% showed diarrhea). Fenofibrate was safe and effective in reducing and normalizing TG concentrations in dogs with severe hypertriglyceridemia, regardless of the cause of hyperlipidemia. The low-fat diet was effective in reducing, but not normalizing, TG concentrations. Fenofibrate and low-fat diet were effective in reducing TC concentrations. This is the first study evaluating fibrates in dogs with severe hypertriglyceridemia and comparing results with a low-fat diet.A major question remaining in the field of evolutionary biology is how prokaryotic organisms made the leap to complex eukaryotic life. The prevailing theory depicts the origin of eukaryotic cell complexity as emerging from the symbiosis between an α-proteobacterium, the ancestor of present-day mitochondria, and an archaeal host (endosymbiont theory). A primary contribution of mitochondria to eukaryogenesis has been attributed to the mitochondrial genome, which enabled the successful internalisation of bioenergetic membranes and facilitated remarkable genome expansion. It has also been postulated that a key contribution of the archaeal host during eukaryogenesis was in providing 'archaeal histones' that would enable compaction and regulation of an expanded genome. Yet, how the communication between the host and the symbiont evolved is unclear. Here, we propose an evolutionary concept in which mitochondrial TCA cycle signalling was also a crucial player during eukaryogenesis enabling the dynamic control of an expanded genome via regulation of DNA and histone modifications.