Giuseppe Attisani

Human gut microbiota physiologically and actively participates as a symbiont to a wide number of fundamental biological processes, such as absorption and metabolism of nutrients, regulation of immune response and inflammation; gut microbiota plays also an antitumor role. However, dysbiosis, resulting from a number of different situations—dysmicrobism, infections, drug intake, age, diet—as well as from their multiple combinations, may lead to tumorigenesis and is associated with approximately 20% of all cancers. In a diagnostic, prognostic, therapeutic, and epidemiological perspective, it is clear that the bifaceted role of microbiota needs to be thoroughly studied and better understood. Here, we discuss the anti- and pro-tumorigenic potential of gut and other microbiota districts along with the causes that may change commensal bacteria from friend to foes.

Cancer affects more than 19 million people and is the second leading cause of death in the world. One of the principal strategies used in cancer therapy is the inhibition of topoisomerase II, involved in the survival of cells. Side effects and adverse reactions limit the use of topoisomerase II inhibitors; hence, research is focused on discovering novel compounds that can inhibit topoisomerase II and have a safer toxicological profile. Marine organisms are a source of secondary metabolites with different pharmacological properties including anticancer activity. The objective of this review is to present and discuss the pharmacological potential of marine-derived compounds whose antitumor activity is mediated by topoisomerase II inhibition. Several compounds derived from sponges, fungi, bacteria, ascidians, and other marine sources have been demonstrated to inhibit topoisomerase II. However, some studies only report docking interactions, whereas others do not fully explain the mechanisms of topoisomerase II inhibition. Further in vitro and in vivo studies are needed, as well as a careful toxicological profile evaluation with a focus on cancer cell selectivity.

Introduction: Aging is associated with a large increase in the prevalence of hypovitaminosis D. 25- Hydroxyvitamin D, 25(OH)D, is the best indicator for vitamin D status. Its possible role in the pathogenesis of Alzheimer’s disease (AD), the leading cause of dementia in the elderly, is particularly important. The aim of the present study was to examine the association between 25-hydroxyvitamin D (25(OH)D) and cognitive functions in a group of Italian elderly patients affected with AD. Methods: We studied the relationship between 25(OH)D and cognitive functions assessed by MMSE (Mini Mental State Examination) in 150 consecutive elderly patients (F 76 %, age 78,66+ 6,05 years old) attending our Geriatric ambulatory for cognitive disorders with diagnosis of AD. Results: In our sample hypovitaminosis D was present in 100% of the screened patients; 111 patients (74%) had 25(OH)D serum levels inferior to 20 ng/ml; 39 (26%) patients had serum levels included between 20 and 30 ng/ml. After adjustment for age, gender, systolic blood pressure, education, cardiovascular diseases and antihypertensive treatment, a significant relationship was observed between 25(OH)D and cognitive status. MMSE appeared significantly higher in subjects with 25(OH)D serum levels ≥ 20 ng/ml than in those with 25(OH)D < 20 ng/ml (18,42+4,33 vs 12,22+4,44; p=0,000). Conclusion: Our results showed a relationship between 25(OH)D and cognitive impairment in patients with AD, suggesting that 25(OH)D could be involved in the onset of dementia.

We tested whether cutaneous afferents from the skin field close to an upper limb muscular region would carry information to spinal neurons at the onset or at the offset of a voluntary elbow extension movement lasting 1 s. We detected a depression of EMG activity both at onset and at the offset of the reaching movement but in the latter case depression was significantly larger and immediate. The marked depression of EMG activity suggests an inhibition, via spinal neurons, of the descending excitation to the motoneurones supplying the triceps brachii. This spinal control might be a very efficient mechanism for the termination of voluntary movement.

Movement control in hypoxia might be affected by several factors such as depression of propioceptive and vestibular afferents and changes in physical properties of ambient air at altitude (2,3). These factors may cause disturbance in coordination of aimed voluntary movements with a reduction of accuracy and altered kinematics variables. These changes may occur particularly in conditions as acute or chronic mountain sickness, where symptoms such as headache, dizziness, nausea, dimness of vision and generalized weakness are present.