Dalla Francia all'Italia: impegno politico, inchiesta e transfers culturali alle origini della sociologia del lavoro in Italia

Sociology of work in Italy revived at the end of WWII, after thirty years of forced oblivion. This thesis examines the history of discipline by considering three paths that it followed from its revival up to its institutionalization: the influence of the productivity drive, the role of trade unions and the activity of early young researchers. European Productivity Agency's Italian office Comitato Nazionale per la Produttività propagandised studies on management and on the effects of the industrialization on work and society. Academicians, technicians, psychologists who worked for CNP started rethinking sociology of work, but the managerial use of sociology was unacceptable for both trade unions and young researchers. So “free union” CISL created a School in Florence with an eager attention to social sciences as a medium to become a new model union, while Marxist CGIL, despite its ideological aversion to sociology, finally accepted the social sciences lexicon in order to explain the work changes and to resist against the employers' association offensive. On the other hand, political and social engagement led a first generation of sociologists to study social phenomenon in the recently industrialized Italy by using the sociological analysis. Finally, the thesis investigate the cultural transfers from France, whose industrial sociology (sociologie du travail) was considered as a reference in continental Europe. Nearby the wide importance of French sociologie, financially aided by planning institutions in order to employ it in the industrial reconstruction, other minor experiences such as the social surveys accomplished by worker-priests in the suburbs of industrial cities and the heterodox Marxism of the review “Socialisme ou Barbarie” influenced Italian sociology of work.

L'impiego del modello di Rash per la valutazione della soddisfazione del paziente nell'ambito delle strutture sanitarie di ricovero

Hospitals and health service providers are use to collect data about patient’s opinion to improve patient health status and communication with them and to upgrade the management and the organization of the health service provided. A lot of survey are carry out for this purpose and several questionnaire are built to measure patient satisfaction. In particular patient satisfaction is a way to describe and assess the level of hospital service from the patient’s point of view. It is a cognitive and an emotional response to the hospital experience. Methodologically patient satisfaction is defined as a multidimensional latent variable. To assess patient satisfaction Item Response Theory has greater advantages compared to Classical Test Theory. Rasch model is a one-parameter model which belongs to Item Response Theory. Rasch model yield objective measure of the construct that are independent of the set of people interviewed and of set of items used. Rasch estimates are continuous and can be useful to “calibrate” the scale of the latent trait. This research attempt to investigate the questionnaire currently adopted to measure patient satisfaction in an Italian hospital, completed by a large sample of 3390 patients. We verify the multidimensional nature of the variable, the properties of the instrument and the level of satisfaction in the hospital. Successively we used Rasch estimates to describe the most satisfied and the less satisfied patients.

Sonno e funzioni cognitive: ruolo della microstruttura del sonno NREM

STUDY OBJECTIVE: Cyclic Alternating Pattern (CAP) is a fluctuation of the arousal level during NREM sleep and consists of the alternation between two phases: phase A (divided into three subtypes A1, A2, and A3) and phase B. A1 is thought to be generated by the frontal cortex and is characterized by the presence of K complexes or delta bursts; additionally, CAP A1 seems to have a role in the involvement of sleep slow wave activity in cognitive processing. Our hypothesis was that an overall CAP rate would have a negative influence on cognitive performance due to excessive fluctuation of the arousal level during NREM sleep. However, we also predicted that CAP A1 would be positively correlated with cognitive functions, especially those related to frontal lobe functioning. For this reason, the objective of our study was to correlate objective sleep parameters with cognitive behavioral measures in normal healthy adults. METHODS: 8 subjects (4 males; 4 females; mean age 27.75 years, range 2334) were recruited for this study. Two nocturnal polysomnography (night 2 and 3 = N2 and N3) were carried out after a night of adaptation. A series of neuropsychological tests were performed by the subjects in the morning and afternoon of the second day (D2am; D2pm) and in the morning of the third day (D3am). Raw scores from the neuropsychological tests were used as dependent variables in the statistical analysis of the results. RESULTS: We computed a series of partial correlations between sleep microstructure parameters (CAP, A1, A2 and A3 rate) and a number of indices of cognitive functioning. CAP rate was positively correlated with visuospatial working memory (Corsi block test), Trial Making Test Part A (planning and motor sequencing) and the retention of words from the Hopkins Verbal Learning Test (HVLT). Conversely, CAP was negatively correlated with visuospatial fluency (Ruff Figure Fluency Test). CAP A1 were correlated with many of the tests of neuropsychological functioning, such as verbal fluency (as measured by the COWAT), working memory (as measured by the Digit Span – Backward test), and both delay recall and retention of the words from the HVLT. The same parameters were found to be negatively correlated with CAP A2 subtypes. CAP 3 were negatively correlated with the Trial Making Test Parts A and B. DISCUSSION: To our knowledge this is the first study indicating a role of CAP A1 and A2 on behavioral cognitive performance of healthy adults. The results suggest that high rate of CAP A1 might be related to an improvement whereas high rate of CAP A2 to a decline of cognitive functions. Further studies need to be done to better determine the role of the overall CAP rate and CAP A3 on cognitive behavioral performances.

Rapporti tra tettonica e clima durante l'esumazione nelle Alpi Centrali. Evidenze dalla termocronologia e dall'analisi strutturale lungo il traforo ferroviario del Sempione

(U-Th)/He and fission-track analyses of apatite along deep-seated tunnels crossing high-relief mountain ranges offer the opportunity to investigate climate and tectonic forcing on the topographic evolution. In this study, the thermochronologic analysis of a large set of samples collected in the Simplon railway tunnel (western-central Alps; Italy and Switzerland) and along its surface trace, coupled with kinematic and structural analysis of major fault zones intersecting the tunnel, constrains the phenomena controlling the topographic and structural evolution, during the latest stage of exhumation of the Simplon Massif, and the timing in which they operated. The study area is located at the western margin of the Lepontine metamorphic dome where a complex nappe-stack pertaining to the Penninic and Ultrahelvetic domains experienced a fast exhumation from the latest Oligocene onward. The exhumation was mainly accommodated by a west-dipping low-angle detachment (the Simplon Fault Zone) which is located just 8 km to the west of the tunnel. However, along the section itself several faults related to two principal phases both with important dip-slip kinematics have been detected. Cooling rates derived from our thermocronological data vary from about 10 °C/Ma at about 10 Ma to about 35 °C/Ma in the last 5 Ma. Such increase in the cooling rate corresponds to the most important climatic change recorded in the northern hemisphere in the last 10 Ma, i.e. the shift to wetter conditions at the end of the Messinian salinity crisis and the inception of glacial cycles in the northern hemisphere. In addition, (U-Th)/He and fission-track age patterns lack of important correlation with the topography suggesting that the present-day relief morphology is the result of recent erosional dynamics. More in details, the (U-Th)/He tunnel ages show an impressive uniformity at 2 Ma, whereas cooling rates calculated at 1 Ma increase towards the two major valleys. This indicates a focusing of erosive processes in the valleys which led to the shaping of present-day topography. Structural analysis documents the presence of two phases of brittle deformation postdating the metamorphic phases in the area. The first one is directly related to the last phase of activity along the Simplon Fault Zone and is characterized by extension towards SO and vertical shortening. The young one is characterized by extension towards NO and horizontal shortening in a along the NE-SO direction. Structures related to the first phase of brittle deformation generate important variations in the older ages' dataset, until 3 Ma, suggesting that tectonics controlled rocks exhumation up to that age. Structures related to the second phase generate some variations also in the younger age dataset, highlighting the activity of faults bordering the massif and suggesting a continuous activity also after 2 Ma. However, most of (U-Th)/He tunnel ages, varying slightly around 2 Ma, document that the Simplon area has experienced primarily erosional exhumation in this time span. In conclusion, all our data suggest that in the central Italian Alps the climatic signal gradually overrode the tectonic effects after about 5 Ma, as a consequence of the climatic instability started at end of Messinian salinity crisis and improved by the onset of glaciations in the northern hemisphere.

Trasduzione del segnale e poliamine nell'apoptosi di cellule cardiache

Introduction: Apoptotic cell death of cardiomyocytes is involved in several cardiovascular diseases including ischemia, hypertrophy and heart failure, thus representing a potential therapeutic target. Apoptosis of cardiac cells can be induced experimentally by several stimuli including hypoxia, serum withdrawal or combination of both. Several lines of research suggest that neurohormonal mechanisms play a central role in the progression of heart failure. In particular, excessive activation of the sympathetic nervous system or the renin-angiotensin-aldosterone system is known to have deleterious effects on the heart. Recent studies report that norepinephrine (NE), the primary transmitter of sympathetic nervous system, and aldosterone (ALD), which is actively produced in failing human heart, are able to induce apoptosis of rat cardiomyocytes. Polyamines are biogenic amines involved in many cellular processes, including apoptosis. Actually it appears that these molecules can act as promoting, modulating or protective agents in apoptosis depending on apoptotic stimulus and cellular model. We have studied the involvement of polyamines in the apoptosis of cardiac cells induced in a model of simulated ischemia and following treatment with NE or ALD. Methods: H9c2 cardiomyoblasts were exposed to a condition of simulated ischemia, consisting of hypoxia plus serum deprivation. Cardiomyocyte cultures were prepared from 1-3 day-old neonatal Wistar rat hearts. Polyamine depletion was obtained by culturing the cells in the presence of α-difluoromethylornithine (DFMO). Polyamines were separated and quantified in acidic cellular extracts by HPLC after derivatization with dansyl chloride. Caspase activity was measured by the cleavage of the fluorogenic peptide substrate. Ornithine decarboxylase (ODC) activity was measured by estimation of the release of 14C-CO2 from 14C-ornithine. DNA fragmentation was visualized by the method of terminal transferase-mediated dUTP nick end-labeling (TUNEL), and DNA laddering on agarose gel electophoresis. Cytochrome c was detected by immunoflorescent staining. Activation of signal transduction pathways was investigated by western blotting. Results: The results indicate that simulated ischemia, NE and ALD cause an early induction of the activity of ornithine decarboxylase (ODC), the first enzyme in polyamine biosynthesis, followed by a later increase of caspase activity, a family of proteases that execute the death program and induce cell death. This effect was prevented in the presence of DFMO, an irreversible inhibitor of ODC, thus suggesting that polyamines are involved in the execution of the death program activated by these stimuli. In H9c2 cells DFMO inhibits several molecular events related to apoptosis that follow simulated ischemia, such as the release of cytochrome c from mitochondria, down-regulation of Bcl-xL, and DNA fragmentation. The anti-apoptotic protein survivin is down-regulated after ALD or NE treatement and polyamine depletion obtained by DFMO partially opposes survivin decrease. Moreover, a study of key signal transduction pathways governing cell death and survival, revealed an involvement of AMP activated protein kinase (AMPK) and AKT kinase, in the modulation by polyamines of the response of cardiomyocytes to NE. In fact polyamine depleted cells show an altered pattern of AMPK and AKT activation that may contrast apoptosis and appears to result from a differential effect on the specific phosphatases that dephosphorylate and switch off these signaling proteins. Conclusions: These results indicate that polyamines are involved in the execution of the death program activated in cardiac cells by heart failure-related stimuli, like ischemia, ALD and NE, and suggest that their apoptosis facilitating action is mediated by a network of specific phosphatases and kinases.

Studio del pathway della Displasia Ectodermica Anidrotica (EDA)

Anhidrotic Ectodermal Dysplasia (EDA), is the most frequent form among Ectodermal Dysplasias, hereditary genetic disorders causing ectodermal appendages defective development. Indeed, EDA is characterized by defective formation of hair follicles, sweat glands and teeth both in human patients and animals. EDA, the gene mutated in Anhidrotic Ectodermal Dysplasia, encodes Ectodysplasin, a TNF family member that activates NF-kB mediated transcription. This disease can occur with mutations in other EDA-NF-kB pathway members, as EDA receptor, EDAR and its adapter, EDARADD. Moreover, mutations in TRAF6, NEMO, IKB and NF-kBs genes are responsible for Immunodeficiency associated EDA (EDA-ID). Several molecules, as SHH, WNT/DKK, BMP and LTβ, have already been reported to be EDA pathway regulators or effectors although the knowledge of the full spectrum of EDA targets remains incomplete. During the first part of the research project a gene expression analysis was performed in primary keratinocytes from Wild-type and Tabby (EDA model mouse) mice to identify novel EDA target genes. Earlier expression profiling at various developmental time points in Tabby and Wild-type mouse skin reported genes differentially expressed in the two samples and, to increase the resolution to find genes whose expression may be restricted to epidermal cells, the study was extended to primary keratinocyte cultures established from E19 Wild-type and Tabby skin. Using microarrays bearing 44,000 gene probes, we found 385 “preliminary candidate” genes whose expression was significantly affected by Eda defect. By comparing expression profiles to those from Eda-A1 (where Eda-A1 is highly expressed) transgenic skin, we restricted the list to 38 “candidate EDA targets”, 14 of which were already known to be expressed in hair follicles or epidermis. This work confirmed expression changes for 3 selected genes, Tbx1, Bmp7, and Jag1, both in primary keratinocytes and in Wild-type and Tabby whole skin, by Q-PCR and Western blotting analyses. Thus, this study detected novel candidate pathways downstream of EDA. In the second part of the research project, plasmid constructs were produced and analyzed to create a transgenic mouse model for Immunodeficiency associated EDA disease (XL-EDA-ID). In particular, plasmids containing mouse Wild-type and mutated Nemo cDNA under K-17 epidermis-specific promoter control and a Flag tag, were prepared, on the way to confine transgene expression to mice epidermis and to determine EDA phenotype without immunodeficiency for a comparison to Tabby model phenotype. EDA-ID mutations reported in patients and selected for this study are: C417R (C409R in mouse), causing Zinc Finger protein domain destabilization and A288G (A282G in mouse) affecting oligomerization of the protein. Moreover, the ex-novo mutation, ZnF, C-terminal Zinc Finger domain deletion, was tested. Thus, the constructs were analyzed by transient transfection, Western blotting and luciferase assays techniques, detecting Nemo Wild-type and mutant protein products and residue NF-kB activity in presence of mutants, after TNF stimulation. In particular, MEF_Nemo-/- cell line was used to monitor NF-kB activity without endogenous Nemo gene. Results show reduced NF-kB activity in presence of mutated Nemo forms compared to Wild-type: 81% for A282G (A288G in human); 24% for C409R (C417R in human); 15% for ZnF. C409R mutation (C417R in human), reported in 6 EDA-ID human patients, was selected to prepare transgenic model mouse. Mice (white, FVP) born following K17-promoter-Flag-Nemo_C409R plasmid region pronuclear injection, were analyzed for the transgene presence in the genotype and a preliminar examination of their phenotype was performed. In particular, one mouse showed considerable coat defects if compared to Wild-type mice. This preliminar analysis suggests a possible influence of Nemo mutant over-expression in epidermis without immunodeficiency. Still, more microscopic studies to analyze hair subtypes, Guard, Awl and Zigzag (usually alterated inTabby mouse model), Immunohistochemistry experiments to detect epidermis restricted Nemo expression and sweat glands analysis, will follow. This and other transgene positive mice will be crossed with black mice C57BL6 to obtain at least two indipendent agouti lines to analyze. Theses mice will be used in EDA target genes detection through microarrays. Following, plasmid constructs containing other Nemo mutant forms (A282G and ZnF) might be studied by the same experimental approaches to prepare more transgenic model mice to compare to Nemo_C409R and Tabby mouse models.

Controllo dell'atto di prensione: coinvolgimento dell'area V6A nell'orientamento del polso

Prehension in an act of coordinated reaching and grasping. The reaching component is concerned with bringing the hand to object to be grasped (transport phase); the grasping component refers to the shaping of the hand according to the object features (grasping phase) (Jeannerod, 1981). Reaching and grasping involve different muscles, proximal and distal muscles respectively, and are controlled by different parietofrontal circuit (Jeannerod et al., 1995): a medial circuit, involving area of superior parietal lobule and dorsal premotor area 6 (PMd) (dorsomedial visual stream), is mainly concerned with reaching; a lateral circuit, involving the inferior parietal lobule and ventral premotor area 6 (PMv) (dorsolateral visual stream), with grasping. Area V6A is located in the caudalmost part of the superior parietal lobule, so it belongs to the dorsomedial visual stream; it contains neurons sensitive to visual stimuli (Galletti et al. 1993, 1996, 1999) as well as cells sensitive to the direction of gaze (Galletti et al. 1995) and cells showing saccade-related activity (Nakamura et al. 1999; Kutz et al. 2003). Area V6A contains also arm-reaching neurons likely involved in the control of the direction of the arm during movements towards objects in the peripersonal space (Galletti et al. 1997; Fattori et al. 2001). The present results confirm this finding and demonstrate that during the reach-to-grasp the V6A neurons are also modulated by the orientation of the wrist. Experiments were approved by the Bioethical Committee of the University of Bologna and were performed in accordance with National laws on care and use of laboratory animals and with the European Communities Council Directive of 24th November 1986 (86/609/EEC), recently revised by the Council of Europe guidelines (Appendix A of Convention ETS 123). Experiments were performed in two awake Macaca fascicularis. Each monkey was trained to sit in a primate chair with the head restrained to perform reaching and grasping arm movements in complete darkness while gazing a small fixation point. The object to be grasped was a handle that could have different orientation. We recorded neural activity from 163 neurons of the anterior parietal sulcus; 116/163 (71%) neurons were modulated by the reach-to-grasp task during the execution of the forward movements toward the target (epoch MOV), 111/163 (68%) during the pulling of the handle (epoch HOLD) and 102/163 during the execution of backward movements (epoch M2) (t_test, p ≤ 0.05). About the 45% of the tested cells turned out to be sensitive to the orientation of the handle (one way ANOVA, p ≤ 0.05). To study how the distal components of the movement, such as the hand preshaping during the reaching of the handle, could influence the neuronal discharge, we compared the neuronal activity during the reaching movements towards the same spatial location in reach-to-point and reach-to-grasp tasks. Both tasks required proximal arm movements; only the reach-to-grasp task required distal movements to orient the wrist and to shape the hand to grasp the handle. The 56% of V6A cells showed significant differences in the neural discharge (one way ANOVA, p ≤ 0.05) between the reach-to-point and the reach-to-grasp tasks during MOV, 54% during HOLD and 52% during M2. These data show that reaching and grasping are processed by the same population of neurons, providing evidence that the coordination of reaching and grasping takes place much earlier than previously thought, i.e., in the parieto-occipital cortex. The data here reported are in agreement with results of lesions to the medial posterior parietal cortex in both monkeys and humans, and with recent imaging data in humans, all of them indicating a functional coupling in the control of reaching and grasping by the medial parietofrontal circuit.

Interazioni tra Glicoproteine che mediano la penetrazione del Virus Herpes Simplex nella cellula e disegno razionale di Peptidi Inibitori

Herpes simplex virus entry into cells requires a multipartite fusion apparatus made of gD, gB and heterodimer gH/gL. gD serves as receptor-binding glycoprotein and trigger of fusion; its ectodomain is organized in a N-terminal domain carrying the receptor-binding sites, and a C-terminal domain carrying the profusion domain, required for fusion but not receptor-binding. gB and gH/gL execute fusion. To understand how the four glycoproteins cross-talk to each other we searched for biochemical defined complexes in infected and transfected cells, and in virions. We report that gD formed complexes with gB in absence of gH/gL, and with gH/gL in absence of gB. Complexes with similar composition were formed in infected and transfected cells. They were also present in virions prior to entry, and did not increase at virus fusion with cell. A panel of gD mutants enabled the preliminary location of part of the binding site in gD to gB to the aa 240-260 portion and downstream, with T306P307 as critical residues, and of the binding site to gH/gL at aa 260-310 portion, with P291P292 as critical residues. The results indicate that gD carries composite independent binding sites for gB and gH/gL, both of which partly located in the profusion domain. The second part of the project dealt with rational design of peptides inhibiting virus entry has been performed. Considering gB and gD, the crystal structure is known, so we designed peptides that dock in the structure or prevent the adoption of the final conformation of target molecule. Considering the other glycoproteins, of which the structure is not known, peptide libraries were analyzed. Among several peptides, some were identified as active, designed on glycoprotein B. Two of them were further analyzed. We identified peptide residues fundamental for the inhibiting activity, suggesting a possible mechanism of action. Furthermore, changing the flexibility of peptides, an increased activity was observed,with an EC50 under 10μM. New approaches will try to demonstrate the direct interaction between these peptides and the target glycoprotein B.

Riparazione del danno ischemico ostruttivo del miocardio mediante cellule staminali mesenchimali sottoposte a stimolazione elettromeccanica in bioreattore

Nell’ambito dell’ingegneria dei tessuti, la possibilità di rigenerazione del miocardio post-infartuale è un argomento “caldo”, che suscita grandi speranze ma solleva altrettanto grandi interrogativi - sostenuti dal sussistere di dubbi di base sulle scelte operative praticabili. Esiste tuttavia concordanza nel considerare fondamentale l’utilizzo di un “supporto” che possa mantenere nella sede peri-infartuale le cellule competenti. Infatti, la semplice iniezione di cellule staminali per via endovenosa o direttamente nell’area infartuata non si è dimostrata particolarmente efficace, soprattutto a causa della cospicua perdita cellulare che si verifica rapidamente dopo il trapianto. Ci si orienta quindi verso la strategia di seminare cellule in grado di transdifferenziare in senso muscolare cardiaco su un materiale biocompatibile in vitro e di impiantare successivamente il costrutto ottenuto in vivo dove ci si attende il riassorbimento del biomateriale e l’integrazione delle cellule. Tuttavia, mentre in altri settori della medicina - quali ortopedia e dermatologia - l’impiego di pseudotessuti ingegnerizzati ha già permesso di conseguire ottimi risultati nella rigenerazione di tessuti danneggiati, allo stato attuale, i progressi ottenuti nell’ambito della rigenerazione del miocardio infartuato appaiono ancora aneddotici e distanti dall’ottenere protocolli condivisi per l’impiego in clinica. Il lavoro presentato in questa ricerca, condotto grazie alla sinergia di competenze interdisciplinari negli ambiti chimico, biologico e dell’ingegneria biomedica meccanica ed elettronica, è uno studio di fattibilità di una metodica standardizzata in grado di indirizzare cellule staminali mesenchimali (MSCs) indifferenziate verso l’acquisizione in vitro di caratteri fenotipici confrontabili con quelli delle cellule muscolari cardiache attraverso il paradigma della coltura dinamica in bioreattore. Il prototipo di bioreattore impiegato, in quanto sviluppato originalmente nel corso di questa attività di ricerca, presenta rispetto ad altri strumenti descritti l’innovazione e il vantaggio di non richiedere l’utilizzo di un incubatore, in quanto esso stesso permette di coltivare cellule al suo interno in condizioni controllate di temperatura, pH e concentrazione di CO2. La sua flessibilità operativa consente di impostare e controllare da personal computer leggi di moto di qualsiasi forma anche con cicliche molto veloci. Infine, la presenza di estensimetri in grado di misurare finemente la variazione di tensione esercitata sulla matrice polimerica utilizzata, posta in trazione tra due afferraggi, permette di applicare nel tempo una forza di stiramento costante, ottenendo deformazioni controllate e risultati riproducibili in termini di modificazioni cellulari. Il superamento delle problematiche sorte durante la fase di messa a punto del sistema, che deve essere ritenuto parte integrante del lavoro di sviluppo condotto, ha permesso di studiare l’adattamento di MSCs allo stiramento ciclico, mostrando che questo effettivamente determina alcune differenze fenotipiche rispetto al controllo statico. Inoltre le cellule hanno acquistato una disposizione orientata lungo l’asse longitudinale delle fibre, dato questo particolarmente importante se si considera la disposizione ordinata delle cellule del miocardio, le quali costituiscono un vero e proprio sincizio, indispensabile per una diffusione sincrona dell’impulso elettrico di contrazione. La creazione di uno pseudotessuto cardiaco ottimale richiederà ovviamente ulteriore lavoro, ma la metodica qui presentata si propone al tempo stesso come uno strumento di studio e come una strategia operativa per un approccio innovativo e standardizzabile alla medicina rigenerativa del miocardio.

Diabete ed ischemia critica degli arti inferiori. Studio del danno della parete arteriosa e del ruolo dell'endotelio circolante nella riparazione tessutale e nella neoangiogenesi

Objectives In diabetic and non diabetic patients with peripheral artery obstructive disease (PAOD), we sought to establish whether the vascular wall damage, the mature circulating endothelium and the "in situ" neoangiogenesis are related with each other. Design In the peripheral blood of diabetic patients suffering critical ischaemia associated with peripheral artery disease, low levels and poor function of circulating endothelial progenitor cells (EPCs) were observed. Moreover, circulating endothelial cells (CECs) have been described in different conditions of vascular injury. In this type of disorders, which are all characterized by endothelial damage, neoangiogenesis plays a key role. Materials In the study we recruited 22 diabetic and 16 non diabetic patients, all of them suffering PAOD and critical ischaemia; healthy subjects and multiorgan donors have also been considered like controls. Methods Histopathologic characterization was performed on arterial tissue samples under a light microscope. Flow cytofluorimetric analysis was used to quantify CECs in peripheral blood samples. "In situ" expression of the Vascular Endothelial Growth Factor (VEGF) and Metalloproteinase 9 (MMP-9) transcripts was quantified in a Real Time-PCR analysis. Circulating VEGF concentration was determined by an ELISA assay. Results Arterial wall from diabetic patients, compared with non diabetic subjects, revealed a higher incidence of serious lesions (60% vs 47%) and a lower number of capillaries (65% vs 87%). Mean number of CECs/ml was significantly increased in all patients, compared to healthy controls (p=0.001). Compared to healthy subjects, VEGF transcripts expression resulted significantly higher in diabetic patients and in all patients (p<0.05) and a similar result was obtained in the MMP-9 transcripts expression. Serum VEGF concentration was significantly increased in PAOD patients correlated with controls (p=0.0431). Conclusions Our study demonstrates that in all patients considered, probably, regressive phenomenons prevail on reparative ones, causing an inesorable and progressive degeneration of the vascular wall, worse by diabetes. The vascular damage can be monitored by determining CECs number and its severity and development are emphasized by the MMP-9 transcripts expression. The "in situ" VEGF increased expression seems to be the evidence of a parietal cells bid to induce local angiogenesis. This reparing mechanism could induce the EPCs mobilitation by means the release of VEGF from the arterial wall. The mechanism, however, is ineffective like demonstrated by the EPCs reduced number and activities observed in patients suffering PAOD and critical ischaemia.