HIG2A promotes cell survival under hypoxia and mediates the assembly of complex III and complex IV into respiratory chain supercomplexes. In the present study, we show that human HIGD2A and mouse Higd2a gene expressions are regulated by hypoxia, glucose, and the cell cycle‐related transcription factor E2F1. The latter was found to bind the promoter region of HIGD2A. Differential expression of the HIGD2A gene was found in C57BL/6 mice in relation to tissue and age. Besides, the silencing of HIGD2A evidenced the modulation of mitochondrial dynamics proteins namely, OPA1 as a fusion protein increases, while FIS1, a fission protein, decreases. Besides, the mitochondrial membrane potential (ΔΨm) increased. The protein HIG2A is localized in the mitochondria and nucleus. Moreover, we observed that the HIG2A protein interacts with OPA1. Changes in oxygen concentration, glucose availability, and cell cycle regulate HIGD2A expression. Alterations in HIGD2A expression are associated with changes in mitochondrial physiology.

Purpose Recent advancements of 3D printing technology have brought forward the interest for this technique in many engineering fields. This study aims to focus on mechanical properties of the polylactic acid (PLA) feeding material under different thermal conditions for a typical fusion deposition of 3D printer system. Design/methodology/approach Specimens were tested under static loading within the range 20ºC to 60ºC considering different infill orientations. The combined effect of temperature and filament orientation is investigated in terms of constitutive material parameters and final failure mechanisms. The difference between feeding system before and post-3D printing was also assessed by mechanical test on feeding filament to verify the thermal profile during the deposition phase. Findings The results in terms of Young’s modulus, ultimate tensile strength (UTS), strain at failure (εf) and stress at failure (σf) are presented and discussed to study the influence of process settings over the final deposited material. Fracture surfaces have been investigated using an optical microscope to link the phenomenological interpretation of the failure with the micro-mechanical behaviour. Experimental results show a strong correlation between stiffness and strength with the infill orientation and the temperature values. Moreover, a relevant effect is related to deformed geometry of the filament approaching glass transition region of the polymer according to the deposition orientation. Research limitations/implications The developed method can be applied to optimise the stiffness and strength of any 3D-printed composite according to the infill orientation. Practical implications To avoid the failure of specimens outside the gauge length, a previously proposed modification to the geometry was adopted. The geometry has a parabolic profile with a curvature of 1,000 mm tangent to the middle part of the specimen. Originality/value Several authors have reported the stiffness and strength of 3D-printed parts under static and ambient temperature for different build parameters. However, there is a lack of literature on the combination of the latter with the temperature effects on the mechanical properties which this paper covers.

PARKIN (E3 ubiquitin ligase PARK2), PINK1 (PTEN induced kinase 1) and DJ-1 (PARK7) are proteins involved in autosomal recessive parkinsonism, and carcinogenic processes. In damaged mitochondria, PINK1’s importing into the inner mitochondrial membrane is prevented, PARKIN presents a partial mitochondrial localization at the outer mitochondrial membrane and DJ-1 relocates to mitochondria when oxidative stress increases. Depletion of these proteins result in abnormal mitochondrial morphology. PINK1, PARKIN, and DJ-1 participate in mitochondrial remodeling and actively regulate mitochondrial quality control. In this review, we highlight that PARKIN, PINK1, and DJ-1 should be regarded as having an important role in Cancer Biology. The STRING database and Gene Ontology (GO) enrichment analysis were performed to consolidate knowledge of well-known protein interactions for PINK1, PARKIN, and DJ-1 and envisage new ones. The enrichment analysis of KEGG pathways showed that the PINK1/PARKIN/DJ-1 network resulted in Parkinson disease as the main feature, while the protein DJ-1 showed enrichment in prostate cancer and p53 signaling pathway. Some predicted transcription factors regulating PINK1, PARK2 (PARKIN) and PARK7 (DJ-1) gene expression are related to cell cycle control. We can therefore suggest that the interplay among PINK1/PARKIN/DJ-1 network during mitochondrial quality control in cancer biology may occur at the transcriptional level. Further analysis, like a systems biology approach, will be helpful in the understanding of PINK1/PARKIN/DJ-1 network.