Hypoxia Strongly Affects Mitochondrial Ribosomal Proteins and Translocases, as Shown by Quantitative Proteomics of HeLa Cells.

Hypoxia is an important and common characteristic of many human tumors. It is a challenge clinically due to the correlation with poor prognosis and resistance to radiation and chemotherapy. Understanding the biochemical response to hypoxia would facilitate the development of novel therapeutics for cancer treatment.

Cell inactivation by combined low dose-rate irradiation and intermittent hypoxia.

Purpose: To investigate in detail the earlier observed combined effect of low dose-rate β-irradiation delivered at a dose-rate of 15 mGy/h and continued intermittent hypoxia that leads to extensive cell death after approximately 3-6 weeks.

Material And Methods: Continuous low dose-rate β-irradiation at a dose rate of 15, 1.5 or 0.

Alterations of monocarboxylate transporter densities during hypoxia in brain and breast tumour cells.

Background: Tumour cells are characterized by aerobic glycolysis, which provides biomass for tumour proliferation and leads to extracellular acidification through efflux of lactate via monocarboxylate transporters (MCTs). Deficient and spasm-prone tumour vasculature causes variable hypoxia, which favours tumour cell survival and metastases. Brain metastases frequently occur in patients with advanced breast cancer.

[Congenital hyperinsulinism--new causes and clinical variations].

Congenital hyperinsulinism (CHI) is a heterogeneous disease with variable onset, non- or hypoketotic hypoglycaemia, onset from birth to adulthood and a persistent, intermittent, or transient course with possible later conversion to non-autoimmune diabetes. Giving insights to beta cell function, CHI mutations are now known in eight genes (ABCC8, KCNJ11, GLUD1, GCK, HADH, SLC16A1, HNF4A and UCP2). However, 40-50% of the patients are still genetically unexplained.

[Congenital hyperinsulinism--diagnosis and treatment].

Congenital hyperinsulinism (CHI) is a rare and heterogeneous disease with a challenging diagnostic process and a need of individualised treatment of each patient. In severe, neonatal or infant CHI, differentiation between the focal and diffuse form by rapid genetics, 18F-fluoro-L-dihydroxyphenylalanine positron emission tomography/computed tomography and peroperative microscopy of frozen section allows surgeons to resect the focal lesion instead of performing subtotal pancreatectomy. Milder CHI, sometimes difficult to diagnose, is treated conservatively.