Application of different packing media for the biofiltration of gaseous effluents from waste composting.

A pilot-scale experiment was implemented in a waste bioreactor with an inner capacity of 1 m in order to simulate a real-scale composting process. The waste underwent composting conditions that are typical of the initial bio-oxidation phase, characterised by a high production of volatile organic compounds (VOCs), hydrogen sulphide (HS) and odorants. The waste bioreactor was fed with an intermittent airflow rate of 6 Nm/h.

The VMP1-Beclin 1 interaction regulates autophagy induction.

The Vacuole Membrane Protein 1 -VMP1- is a pancreatitis-associated transmembrane protein whose expression triggers autophagy in several human diseases. In the current study, we unveil the mechanism through which this protein induces autophagosome formation in mammalian cells. We show that VMP1 autophagy-related function requires its 20-aminoacid C-terminus hydrophilic domain (VMP1-AtgD).

Novel AKT1-GLI3-VMP1 pathway mediates KRAS oncogene-induced autophagy in cancer cells.

Autophagy is an evolutionarily conserved degradation process of cytoplasmic cellular constituents. It has been suggested that autophagy plays a role in tumor promotion and progression downstream oncogenic pathways; however, the molecular mechanisms underlying this phenomenon have not been elucidated. Here, we provide both in vitro and in vivo evidence of a novel signaling pathway whereby the oncogene KRAS induces the expression of VMP1, a molecule needed for the formation of the authophagosome and capable of inducing autophagy, even under nutrient-replete conditions.

Chemotherapy and autophagy-mediated cell death in pancreatic cancer cells.

Autophagy is an evolutionarily preserved degradation process of cytoplasmic cellular constituents and plays important physiological roles in human health and disease. It has been proposed that autophagy plays an important role both in tumor progression and in promotion of cancer cell death, although the molecular mechanisms responsible for this dual action of autophagy in cancer have not been elucidated. Pancreatic ductal adenocarcinoma is one of the most aggressive human malignancies with 2-3% five-year survival rate.

Long-term effects of a multidisciplinary treatment of uncomplicated obesity on carotid intima-media thickness.

Obesity is associated with well-known cardiovascular risk factors and a lower life expectancy. This study investigated whether nonoperative nutritional treatment of obesity without comorbidities influenced the carotid intima-media thickness (c-IMT) in the long run. Fifty-four subjects of an original cohort of 251 subjects were re-evaluated 10 years after a medical nutritional treatment (MNT) with cognitive-behavioral approach for uncomplicated obesity.

Zymophagy, a novel selective autophagy pathway mediated by VMP1-USP9x-p62, prevents pancreatic cell death.

Autophagy has recently elicited significant attention as a mechanism that either protects or promotes cell death, although different autophagy pathways, and the cellular context in which they occur, remain to be elucidated. We report a thorough cellular and biochemical characterization of a novel selective autophagy that works as a protective cell response. This new selective autophagy is activated in pancreatic acinar cells during pancreatitis-induced vesicular transport alteration to sequester and degrade potentially deleterious activated zymogen granules.

Gemcitabine induces the VMP1-mediated autophagy pathway to promote apoptotic death in human pancreatic cancer cells.

Background/aim: Autophagy is a degradation process of cytoplasmic cellular constituents. We have described the vacuole membrane protein-1 (VMP1) whose expression triggers autophagy in mammalian cells. The aim of this study was to analyze the role of autophagy in human pancreatic cancer cell death.

Intra-renal hemodynamics and carotid intima-media thickness in the metabolic syndrome.

Aims: Metabolic syndrome (MetS) is associated with increased cardiovascular risk. We hypothesize that early vascular changes are already present at the time of diagnosis of MetS. The relationship of different measures of early vascular impairment with body fat distribution and the natural progression of MetS was examined in newly diagnosed subjects non-pharmacologically treated.

[Serum sialic acid, cellular anionic charge and erythrocyte aggregation in diabetic and hypertensive patients].

The aim of this work was to study the relationship between serum sialic acid (SSA) and erythrocyte anionic charge (EAC) with erythrocyte aggregation in two groups: diabetic (DBT, n=20) and hypertensive (HT, n=21) patients, compared to a control group (n=20). We worked with anticoagulated blood with EDTA and serum. The erythrocyte aggregation was studied by microscopically observing and quantifying aggregates using an ASP (Aggregate Shape Parameter).

Autophagy and VMP1 expression are early cellular events in experimental diabetes.

Background/aims: We have described VMP1 as a new protein which expression triggers autophagy in mammalian cells. Here we show that experimental diabetes activates VMP1 expression and autophagy in pancreas beta cells as a direct response to streptozotocin (STZ).

Methods: Male Wistar rats were treated with 65 mg/kg STZ and pancreas islets from untreated rats were incubated with 1 mM STZ.

The pancreatitis-induced vacuole membrane protein 1 triggers autophagy in mammalian cells.

Autophagy is a degradation process of cytoplasmic cellular constituents, which serves as a survival mechanism in starving cells, and it is characterized by sequestration of bulk cytoplasm and organelles in double-membrane vesicles called autophagosomes. Autophagy has been linked to a variety of pathological processes such as neurodegenerative diseases and tumorigenesis, which highlights its biological and medical importance. We have previously characterized the vacuole membrane protein 1 (VMP1) gene, which is highly activated in acute pancreatitis, a disease associated with morphological changes resembling autophagy.