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It is well known that limited joint mobility of the ankle and foot, impaired muscular performance and reduced gait speed are risk factors for ulceration in diabetic foot. The aim of this study was to evaluate the effect of an experimental protocol of exercise therapy on joint mobility, muscular strength and gait speed in a group of longterm diabetic subjects. The protocol consisted of a 12-week supervised training program; both joint mobility and muscular strength at the ankle were measured before and after exercise therapy by an inclinometer and isometric dynamometers respectively, in 26 diabetic subjects and compared to 17 healthy controls. Ankle joint mobility in plantar flexion was reduced about 36% and dorsal flexion by about 23% in diabetic subjects compared to controls (p, Italian Journal of Anatomy and Embryology, Vol. 120, No. 1 (Supplement) 2015

In previous researches severe damages induced by Cadmium (an ubiquitary environmental pollutant whose intracellular oxidative effects are increasingly lethal) exposure in human have been demonstrated. Morphologic effects were observed in Central Nervous System, liver, kidney, placenta. Recently, the involvement of immune system in Cadmium intoxication was demonstrated in mammalians; we, therefore, tried to evidence such effect in a simple model as Apis Mellifera. In this animal the immune system is represented by “fat bodies” which produce proteins active in defense against pathogenic agents. It is important to stress out that a dangerous syndrome causing the collapse of Apis mellifera hives has intensified recently, in Europe and North America. Current research in this field is oriented towards identifying a synergy of contributing factors to the weakening of the hive. In this paper, we aim to determine whether contamination by cadmium may have an immunosuppressive effect on the insect. Preliminary results denote that the heavy metal causes a severe damage in fat bodies, leading to substantial immunodeficiency in exposed bees, suggesting that in polluted areas the hives may have difficulty in dealing with pests and pathogens that threaten them., Italian Journal of Anatomy and Embryology, Vol. 120, No. 1 (Supplement) 2015

Prolonged exposure to Cadmium may cause serious toxic effects due to its accu- mulation on both central and peripheral nervous systems. Cadmium could be uptak- en from the nasal mucosa via the olfactory pathways and gain direct access into the nervous system circumventing the blood-brain barrier. However, mechanisms under- lying the cadmium uptake and neurotoxicity remain not completely understood. Oxidative damage, interference with calcium-, copper- and zinc-dependent processes, dysregulation of cell repair mechanisms, estrogen-like effects, and epigenetic modifi- cations may be considered mechanisms for cadmium-induced neurotoxicity [1]. Our previous data demonstrated that zinc chloride counteracts the toxic effects of cadmium chloride (CdCl2) on human neurons in vitro [2]. Thus, in this study we evaluate the efficacy of Sodium Selenite (Na2SeO3) in preventing and/or counteracting the damages induced by exposure to cadmium chloride on a human neuronal cell line. In this study we treated SH-SY5Y human neurons with different sub-toxic concentrations of CdCl2 for 24 h with and without a 24 h pre-treatment with Na2SeO3. Cell viability, morphological modifications, and protein expression of specific neuronal plasticity and apoptosis (Gap43 and caspase 3) markers were evaluated. Our results suggest that toxic effects of CdCl2 can be prevented and reverted by Na2SeO3 suggesting a role for selenium compounds in protecting neuronal cells and rebuilding the complex network connections., Italian Journal of Anatomy and Embryology, Vol. 120, No. 1 (Supplement) 2015

Objective: It is well known that limited joint mobility of the ankle and foot level, impaired muscular performance and reduced gait speed are risk factors for ulceration in diabetic foot. The aim of this study was to evaluate the effect of an experimental protocol of exercise therapy on joint mobility, muscular strength and gait speed in a group of long-term diabetic subjects.Methods: The protocol consisted of a 12-week supervised training program; both joint mobility and muscular strength at the ankle were measured before and after exercise therapy respectively by an inclinometer and isometric dynamometers in 26 diabetic subjects and compared to 17 healthy controls.Results: Ankle joint mobility of plantar flexion was reduced about 36% and dorsal flexion by about 23% in diabetic subjects compared to controls (pConclusion: A 12-week supervised program of exercise therapy significantly improves joint mobility, muscular performance and walking speed in diabetic patients--thus limiting one of the pathogenic factors of diabetic foot and potentially preventing disability., Italian Journal of Anatomy and Embryology, Vol 120, No 1 (2015)

Over past decades, nitric oxide (NO) has emerged as a molecule of interest in cancer treatment because of its tumouricidal properties (Choudhari et al., 2013). Gcprotein- derived Macrophage Activating Factor (GcMAF) induces the synthesis and release of NO by activated macrophages. It was previously demonstrated that molecular complexes of oleic acid (OA) and GcMAF (OA-GcMAF) stimulate macrophage activation in cancer patients (Ward et al., 2014). Here we demonstrate that intratumoural injection of OA-GcMAF leads NO synthesis and release inside the tumour. Under ultrasound guidance, OA-GcMAF was injected into patients harbouring different types of solid tumours; a metastasis from a melanoma, and a metastasis from breast cancer. Intra-tumoural NO synthesis and release was monitored in real-time by power-doppler ultrasonography. One to two minutes after injection, we observed a significant increase in blood flow and in blood vessels diameter, a clear indication of vasodilation due to NO synthesis and release. These observations substantiate the dramatic clinical results previously observed by Ward et al. (2014), and open the way to further investigation in the role of GcMAF as a powerful anticancer agent., Italian Journal of Anatomy and Embryology, Vol 119, No 1 (Supplement) 2014

HER2/Neu/ERBB2 is a receptor tyrosine kinase overexpressed in a high percentage of human breast cancers. Gc-protein-derived Macrophage Activating Factor (GcMAF) is a powerful stimulant of the immune system endowed with intrinsic anticancer properties (Pacini et al., 2012). We recently demonstrated that molecular complexes of oleic acid (OA) and GcMAF (OA-GcMAF) show significant therapeutic activity in a variety of tumours (Ward et al., 2014). Here we demonstrate that OAGcMAF eradicates ERBB2 expression in human breast cancer. A biopsy taken before OA-GcMAF treatment showed strong positivity to ERBB2. The patient was then treated with OA-GcMAF administered through subcutaneous injections and with food naturally rich in OA-GcMAF for 3 weeks prior to mastectomy. The subsequent surgery specimen was negative for ERBB2. These results lead to hypothesize: 1. OAGcMAF completely reversed the neoplastic phenotype. 2. OA-GcMAF induced the apoptosis of all ERBB2-positive cancer cells., Italian Journal of Anatomy and Embryology, Vol 119, No 1 (Supplement) 2014

Oxaliplatin-based regimens are effective in metastasised advanced cancers. However, a major limitation to their use is represented by neurotoxicity leading to peripheral neurophaty (Wolf et al., 2008). In this study we evaluate the effects of an immunotherapeutic agent (Gc protein-derived macrophage activating factor, GcMAF) in preventing oxaliplatin-induced neuronal damage and in restoring microglial activation. The effects of oxaliplatin was studied in human neurons (SH-SY5Y) and microglial cells (c13-nj). Cell density, morphology and viability as well as production of cAMP and expression of vascular endothelial growth factor (VEGF), markers of neuron regeneration and markers of microglia activation were determined. GcMAF reverted the damage inflicted by oxaliplatin on human neurons and preserved their viability; it also increased cAMP production, VEGF and neuromodulin expression. GcMAF did not revert the effects of oxaliplatin on microglial cell viability. However, it induced microglial activation resulting in an increased expression of a specific marker without any increase in cell number. Our results demonstrate that GcMAF may significantly contribute to neutralize the neurotoxicity induced by oxaliplatin, at the same time concurring to an integrated anti-cancer effect., Italian Journal of Anatomy and Embryology, Vol 119, No 1 (Supplement) 2014

Excessive training and inadequate recovery can lead to states of overtraining and performance decrements. The anabolic-catabolic balance by testosterone, cortisol and DHEA-S resulted a useful endogenous indicator to evaluate and monitor the athlete’s training state and the effectiveness of the training program [1]. In this study sixteen professional rugby players provided saliva samples during the official preseason training period. Hormone saliva levels were determined by immunoenzymatic assay (Grifols, Italy). The results showed that both cortisol levels and DHEA-S to cortisol ratio levels significantly decreased during the initial reduced training sub-period according to the goal of the training program. Furthermore the testosterone to cortisol ratio levels significantly increased during the initial sub-period as weel as during the organic muscle conditioning period and after a 2-day recovery time following the conditioning period. Testosterone levels were positively correlated with the Gacon physical test and the maximum cardiac frequence during the initial reduced training sub-period. No correlation was observed between hormone levels and genotype. However ACE genotypes (I/D polymorphism) statistically correlated with the different morphotype related to the rugby player position. Our data shows that cortisol and testosterone to cortisol ratio levels can be considered useful tools to evaluate the athlete’s physical stress during the training program. According to data available in literature the morphotype related to the rugby player position is deeply affected by the ACE gene polymorphism., Italian Journal of Anatomy and Embryology, Vol 118, No 2 (Supplement) 2013

The genetic architecture that underlies complex traits, such as speech and language in humans, makes it extremely unlikely that one single gene has been selected in the evolution of our language capabilities. Hence the purpose of this research was to compare the sequences of NAGPA, GNPTAB and GNPTG, genes whose mutations are linked to stuttering in humans [1], among species for which the nucleotide sequences of the entire genome are known, and are relevant to human evolution, that is: Homo sapiens, Pan troglodytes, Pongo abelii, Macaca mulatta, Mus musculus, Equus caballus, Gallus domesticus, Taeniopygia guttata and Danio rerio. In this way, through the study of homologies and divergences at the level of the encoded proteins, we aim to achieve greater knowledge about the genetic control of the organization of brain areas that are involved in the function and evolution of human language. With an extensive bioinformatics analysis regarding expression of GNPTAB, GNPTG, and NAGPA genes, we have found one amino-acid substitution between Homo sapiens and Pan troglodytes in each of these three genes. All substitutions have a high functional value. Therefore, it is reasonable to infer that NAGPA, GNPTAB and GNPTG genes have had a crucial role in the evolution of human language. Acknowledgements: PRIN 2009LFSNAN, Italian Journal of Anatomy and Embryology, Vol 118, No 2 (Supplement) 2013

We previously demonstrated that chronic exposure of the human breast cancer cell line MCF-7 to non-cytotoxic concentrations of Cadmium reduced viability and angiogenic potential of this cell line. In order to better understand these effects, cells, after Cadmium exposure, were treated with vitamin D binding protein-derived macrophage activating factor (DBP-MAF). DBP-MAF is a potent macrophage-activating factor derived from vitamin D binding protein, a polymorphic serum glycoprotein with multiple functions also known as a group specific component or Gc protein. Besides stimulating macrophages, DBP-MAF has anti-tumour properties. Our data demonstrate that the decrease of MCF-7 cell viability following Cadmium treatment was completely reversed when DBP-MAF was present in the cell medium. Following this observation, we further investigated the role of DBP-MAF in modulating angiogenesis, morphology and cytoskeleton structure of MCF-7 cell line. As shown by chorioallantoic membrane assay, DBP-MAF inhibited MCF-7 cancer cell-stimulated angiogenesis. Concerning cell morphology (studied by contrast phase light microscopy and after Papanicolaou staining), following DBP-MAF treatment, cell shape and growth pattern were significantly modified. Vimentin expression (studied by immunohistochemistry and Western blot analysis), considered a hallmark of human breast cancer progression, after DBP-MAF treatment, significantly varied. Intermediate filament status changes, consisting in a shift from a keratin-rich to a vimentin-rich network (epithelial-mesenchymal transition), were observed. In conclusion, we demonstrate that the anti-cancer effects of DBP-MAF can be attributed to multiple actions independent of macrophage stimulation such as reversal of Cadmium effects on cell viability, reversal of morphological malignant phenotype and inhibition of cancer cell-stimulated angiogenesis. For these reasons, DBP-MAF might represent an useful tool to control progression and differentiation of human breast cancer., Italian Journal of Anatomy and Embryology, Vol 116, No 1 (Supplement) 2011