ASRS Questionnaire and Tobacco Use: Not Just a Cigarette. A Screening Study in an Italian Young Adult Sample

Young adults exhibit greater sensitivity than adults to nicotine reinforcement, and Attention Deficit Hyperactivity Disorder (ADHD) increases the risk for early-onset smoking. We investigated the correlation between ADHD Self-Report Scale (ASRS) scores and smoking, evaluated the prevalence of ADHD symptomatology (not diagnoses) in smokers and non-smokers and its comorbidity with benzodiazepine and gambling addictions. A total of 389 young adults from 14 schools in Northern Italy fill out a survey and the Adult ADHD Self-Report Scale (ASRS). A total of 15.2% of subjects tested positive at the ASRS, which correlated with smoking; moreover, smokers had twice the probability of testing positive at the ASRS. ADHD symptomatology, especially when comorbid with tobacco abuse, is an important condition to monitor because early nicotine exposure could be a gateway for other addictive behaviors

Undercover Toxic Ménage à Trois of Amylin, Copper (II) and Metformin in Human Embryonic Kidney Cells

In recent decades, type 2 diabetes complications have been correlated with amylin aggregation, copper homeostasis and metformin side effects. However, each factor was analyzed separately, and only in some rare cases copper/amylin or copper/metformin complexes were considered. We demonstrate for the first time that binary metformin/amylin and tertiary copper (II)/amylin/metformin complexes of high cellular toxicity are formed and lead to the formation of aggregated multi-level lamellar structures on the cell membrane. Considering the increased concentration of amylin, copper (II) and metformin in kidneys of T2DM patients, our findings on the toxicity of amylin and its adducts may be correlated with diabetic nephropathy development

Living with the enemy: from protein-misfolding pathologies we know, to those we want to know

Conformational diseases are caused by the aggregation of misfolded proteins. The risk for such pathologies develops years before clinical symptoms appear, and is higher in people with alpha-1 antitrypsin (AAT) polymorphisms. Thousands of people with alpha-1 antitrypsin deficiency (AATD) are underdiagnosed. Enemyaggregating proteins may reside in these underdiagnosed AATD patients for many years before a pathology for AATD fully develops. In this perspective review, we hypothesize that the AAT protein could exert a new and previously unconsidered biological effect as an endogenous metal ion chelator that plays a significant role in essential metal ion homeostasis. In this respect, AAT polymorphism may cause an imbalance of metal ions, which could be correlated with the aggregation of amylin, tau, amyloid beta, and alpha synuclein proteins in type 2 diabetes mellitus (T2DM), Alzheimer’s and Parkinson’s diseases, respectively

“Physiological” renal regenerating medicine in VLBW preterm infants: could a dream come true?

An emerging hypothesis from the recent literature explain how specific adverse factors related with growth retardation as well as of low birth weight (LBW) might influence renal development during fetal life and then the insurgence of hypertension and renal disease in adulthood. In this article, after introducing a brief overview of human nephrogenesis, the most important factors influencing nephron number at birth will be reviewed, focusing on the "in utero" experiences that lead to an increased risk of developing hypertension and/or kidney disease in adult. Since nephrogenesis in preterm human newborns does not stop at birth, but it continues for 4-6 weeks postnatally, a better knowledge of the mechanisms able to accelerate nephrogenesis in the perinatal period, could represent a powerful tool in the hands of neonatologists. We suggest to define this approach to a possible therapy of a deficient nephrogenesis at birth "physiological renal regenerating medicine". Our goal in preterm infants, especially VLBW, could be to prolong the nephrogenesis not only for 6 weeks after birth but until 36 weeks of post conceptual age, allowing newborn kidneys to restore their nephron endowment, escaping susceptibility to hypertension and to renal disease later in life

Thymosin β4 Is an Endogenous Iron Chelator and Molecular Switcher of Ferroptosis

Thymosin β4 (Tβ4) was extracted forty years agofrom calf thymus. Since then, it has been identified as a G-actin binding protein involved in blood clotting, tissue regeneration, angiogenesis, and anti-inflammatory processes. Tβ4 has also been implicated in tumor metastasis and neurodegeneration. However, the precise roles and mechanism(s) of action of Tβ4 in these processes remain largely unknown, with the binding of the G-actin protein being insufficient to explain these multi-actions. Here we identify for the first time the important role of Tβ4 mechanism in ferroptosis, an iron-dependent form of cell death, which leads to neurodegeneration and somehow protects cancer cells against cell death. Specifically, we demonstrate four iron2+ and iron3+ binding regions along the peptide and show that the presence of Tβ4 in cell growing medium inhibits erastin and glutamate-induced ferroptosis in the macrophage cell line. Moreover, Tβ4 increases the expression of oxidative stress-related genes, namely BAX, hem oxygenase-1, heat shock protein 70 and thioredoxin reductase 1, which are downregulated during ferroptosis. We state the hypothesis that Tβ4 is an endogenous iron chelator and take part in iron homeostasis in the ferroptosis process. We discuss the literature data of parallel involvement of Tβ4 and ferroptosis in different human pathologies, mainly cancer and neurodegeneration. Our findings confronted with literature data show that controlled Tβ4 release could command on/off switching of ferroptosis and may provide novel therapeutic opportunities in cancer and tissue degeneration pathologies.Financial support from FIR 2019 and from Regione Autonoma della Sardegna (grant RASSR79857) is gratefully acknowledged

The design and validation of the R1 personal humanoid

In recent years the robotics field has witnessed an interesting new trend. Several companies started the production of service robots whose aim is to cooperate with humans. The robots developed so far are either rather expensive or unsuitable for manipulation tasks. This article presents the result of a project which wishes to demonstrate the feasibility of an affordable humanoid robot. R1 is able to navigate, and interact with the environment (grasping and carrying objects, operating switches, opening doors etc). The robot is also equipped with a speaker, microphones and it mounts a display in the head to support interaction using natural channels like speech or (simulated) eye movements. The final cost of the robot is expected to range around that of a family car, possibly, when produced in large quantities, even significantly lower. This goal was tackled along three synergistic directions: use of polymeric materials, light-weight design and implementation of novel actuation solutions. These lines, as well as the robot with its main features, are described hereafter

Kojic Acid derivate as a selective inhibitor of mitosis in colorectal and glioblastoma cancer cells

The invention relates to the production of kojic acid derivatives which are able to selectively block the cell cycle of cancer cells and in particular colorectal and glioblastoma cancer cells. The invention also relates to the various pharmaceutical combinations to be used in the treatment of human clinical cases and in the veterinary fiel

An electron microscopic study of apoptosis induced by cycloheximide in rat liver

A histological and ultrastructural study, coupled with transmission and scanning electron microscopy of the early changes in the liver following a single administration of cycloheximide (CHX), was carried out in male Wistar rats. At the histological level, apoptosis was already present in the liver 2 h after treatment. By scanning electron microscopy, the following sequential changes were observed: brightness and progressive detachment of hepatocytes from neighbouring cells, formation of surface infolds with multiple blebs and, finally, release of several membrane-bounded apoptotic bodies (ABs) in the extracellular space and into the sinusoidal lumen. Three hours after CHX administration, the apoptotic cycle was completed, as shown by the presence of phagocytosed ABs inside the cytoplasm of intact Liver cells. Light microscopic examination of the liver 6 h after CHX administration showed ABs mainly located in the cytoplasm of intact hepatocytes and inside activated Kupffer cells. By transmission electron microscopy, it was possible to demonstrate that cells undergoing apoptosis were hepatocytes. At 24 h, the livers of treated animals appeared normal, with no evidence of apoptosis