Ricerc@Sapienza

Hydrogen sulfide (H2S) plays key roles in human (patho)physiology. Synthesized endogenously by known enzymatic systems, H2S is mainly metabolized through a mitochondrial sulfide-oxidizing pathway that comprises sulfide:quinone oxidoreductase (SQR) and a few other enzymes. H2S degradation through this pathway is coupled to electron injection into the respiratory chain and, thus, to stimulation of ATP synthesis. In cancer cells, H2S was reported to be synthesized at high levels and to stimulate energy metabolism and cell proliferation.

Hydrogen sulfide (H2S), a known inhibitor of cytochrome c oxidase (CcOX), plays a key signaling role in human (patho)physiology.
H2S is synthesized endogenously and mainly metabolized by a mitochondrial sulfide-oxidizing pathway including sulfide:quinone
oxidoreductase (SQR), whereby H2S-derived electrons are injected into the respiratory chain stimulating O2 consumption and ATP
synthesis. Under hypoxic conditions, H2S has higher stability and is synthesized at higher levels with protective effects for the cell.

Glioblastoma (GBM) cells express large-conductance, calcium-activated potassium (BK) channels, whose activity is important for several critical aspects of the tumor, such as migration/invasion and cell death. GBMs are also characterized by a heavy hypoxic microenvironment that exacerbates tumor aggressiveness. Since hypoxia modulates the activity of BK channels in many tissues, we hypothesized that a hypoxia-induced modulation of these channels may contribute to the hypoxia-induced GBM aggressiveness.

Hypoxia is a condition commonly observed in the core of solid tumors. The hypoxia-inducible factors (HIF) act as hypoxia sensors that orchestrate a coordinated response increasing the pro-survival and pro-invasive phenotype of cancer cells, and determine a broad metabolic rewiring. These events favor tumor progression and chemoresistance.

Solid tumors often grow in a micro-environment characterized by < 2% O2 tension. This condition, together with the aberrant activation of specific oncogenic patwhays, increases the amount and activity of the hypoxia-inducible factor-1α (HIF-1α), a transcription factor that controls up to 200 genes involved in neoangiogenesis, metabolic rewiring, invasion and drug resistance. Hypoxia also induces endoplasmic reticulum (ER) stress, a condition that triggers cell death, if cells are irreversibly damaged, or cell survival, if the stress is mild.

Background: One-lung ventilation (OLV) in thoracic anesthesia is required to provide good surgical exposure. OLV is commonly achieved through a double lumen tube (DLT) or a bronchial blocker (BB). Malposition is a relevant issue related to these devices use. No prospective studies with adequately large sample size have been performed to evaluate the malposition rate of DLTS and BBs.Methods: A total of 2,127 patients requiring OLV during thoracic surgery were enrolled.

The recently renewed focus on the human exploration of outer space has boosted the
interest toward a variety of questions regarding health of astronauts and cosmonauts.
Among the others, sleep has traditionally been considered a central issue. To extend
the research chances, human sleep alterations have been investigated in several
analog environments, called ICEs (Isolated, Confined, and Extreme). ICEs share different
features with the spaceflight itself and have been implemented in natural facilities and

Glioblastoma multiforme (GBM) is the most malignant brain tumor. Hypoxic condition
is a predominant feature of the GBM contributing to tumor growth and resistance to conventional
therapies. Hence, the identification of drugs able to impair GBM malignancy and aggressiveness
is considered of great clinical relevance. Previously, we demonstrated that the activation of M2
muscarinic receptors, through the agonist arecaidine propargyl ester (Ape), arrests cell proliferation