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The perimammary zone is a critical area for healing, due to high incidence of dehiscences, expecially sternal ones. Although deep sternal wound complications are nowadays less common after cardiac surgery, in some at risk patients, dehiscences still represent important complications of major cardiac or vascular surgeries and they are directly correlated to an increased risk of patient's morbidity and mortality. A heavy breast represents a source of tension on the perimammary wound, inhibiting or delaying a complete recovery. We report the case of a 66-year-old female patient with a critical post-surgical sternal dehiscence and multiple chronic comorbidities. The dehiscence was managed with a routinely performed primary intention closure combined with an innovative breast cerclage. To our opinion, this is the first reported description of a breast cerclage used as an expedient to reduce tension on the wound and minimize the risk of relapse, allowing a rapid and complete healing. This novel technique has proved to be effective and satisfactory in the achievement of both a functional and aesthetic results and we are confident that it could become a fully-fledged wound healing issue in chest wall reconstruction.

We present a successful split-thickness skin allograft for a chronic cutaneous graft-versus-host disease of the thigh in an immunosuppressed patient, treated for acute myeloid leukemia with allogenic bone marrow stem cells transplant.

Splanchnic artery occlusion (SAO) shock is a severe form of circulatory shock produced by ischemia and reperfusion of the splanchnic organs. The occlusion and reperfusion of the splanchnic arteries causes activation and adhesion of polymorphonuclear neutrophils (PMNs), release of proinflammatory substances and the formation of both species of oxygen and nitrogen derivatives free radicals. Olprinone is a specific phosphodiesterase-III inhibitor that has many properties; one of which is anti-inflammatory actions at therapeutic concentrations clinically used for heart failure. In this study, we wanted to evaluate the pharmacological action of olprinone (a PDEIII inhibitor) on SAO shock in mice.SAO shock was induced by clamping both the superior mesenteric artery and the celiac trunk, resulting in a total occlusion of these arteries for 30 min. After this period of occlusion, the clamps were removed. Olprinone was given at a dose of 0.2 mg/kg i.p. 15 min before reperfusion.Our results indicated that olprinone up-regulated cAMP in injured ileum tissue, and decreased the ileum tissue damage after 1 h of reperfusion in SAO shock mice. Moreover, olprinone decreased NF-kappaB expression; the nitration of tyrosine residues; the phosphorylation of p38 MAPK and JNK; cytokine production (TNF-alpha and IL-1beta); ICAM-1 and P-selectin expression and apoptosis in the injured ileum.These results could imply a future use of olprinone in the therapy of ischemia and reperfusion shock.

Aim: The aim of the present study was to examine the effects of 3,5-dicaffeoyl-4-malonylquinic acid (CA1), extract from Centella Asiatica, in rats subjected to experimental colitis.Results: Colitis was induced in rats by intracolonic instillation of dinitrobenzene sulphonic acid (DNBS). CA1 was administered daily orally (0.2 or 2 mg/kg). Four days after DNBS administration, treatment with CA1 significantly reduced the appearance of diarrhoea and the loss of body weight. This was associated with a significant reduction in colonic MPO activity. CA1 also reduced NF-κB activation, the pro-inflammatory cytokines release, the appearance of I-NOS, nitrotyrosine, PARP and proMMP-9 and -2 activity in the colon and reduced the up-regulation of ICAM-1 and the expression of P-Selectin.Conclusions: The results of this study suggested that administration of CA1 may be beneficial for treatment of inflammatory bowel disease.

Permanent functional deficits following spinal cord injury (SCI) arise from both mechanical injury and from secondary tissue reactions involving inflammation. The mitogen-activated protein kinases (MAPKs) play a critical role in cell signaling and gene expression. MAPK family includes three major members: extracellular signal regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), representing three different signaling cascades. Moreover, various studies have clearly shown that high-mobility group box 1 (HMGB1) protein is implicated as a putative danger signal involved in the pathogenesis of a variety of inflammatory conditions including autoimmunity, cancer, trauma and hemorrhagic shock, and ischemia-reperfusion injury. Recently, we have reported that the pineal secretory product melatonin exerts important anti-inflammatory effects in an experimental model of SCI induced by the application of vascular clips (force of 24 g) to the dura after a four-level T5-T8 laminectomy. However, no reports are available on the effect of melatonin on MAPK signaling pathways and HMGB1 expression in SCI. The aim of the present study was to evaluate whether the melatonin protective effect observed in SCI is related to the regulation of MAPK signaling pathways and HMGB1 in mice. In this study we demonstrate the efficacy of treatment with the melatonin in SCI in mice in reducing (a) motor recovery, (b) activation of MAPKs p38, JNK and ERK1/2, (c) tumor necrosis factor-alpha expression, and (d) expression of HMGB1. We propose that melatonin's ability to reduce SCI in mice is also related to a reduction in MAPK signaling pathways and HMGB1 expression.

Matrix metalloproteinases (MMPs) are associated with matrix turnover in both physiological and pathological conditions. Several data indicate that MMPs play an important role in the pathogenesis of colitis. Various evidence has documented that the pineal secretory product melatonin exerts an important anti-inflammatory effect in different experimental models including colitis. However, no reports are available on the relationship between the activity and expression of MMPs and anti-inflammatory effect of melatonin. The aim of the present study was to evaluate whether melatonin prevents the experimental colitis in rats by regulating MMP-9 and MMP-2 activity and expression. Colitis was induced by intracolonic instillation of dinitrobenzene sulphonic acid (DNBS). Four days after DNBS administration, colon TNF-alpha production was associated with colon damage. Biochemical methods and zymography were used to analyse MMP-9 and MMP-2 activities in colon tissues from DNBS-injured rats. Our studies reveal that melatonin prevented colon injury and lipid peroxidation in rats at 4 days after DNBS-induced colitis. Melatonin also reduced proMMP-9 and MMP-2 activities that were induced in the colon tissues by DNBS administration. Reduced MMP-9 and MMP-2 activities were associated with reduced expression of TNF-alpha. We conclude that melatonin's ability to reduce DNBS-induced colon injury in rats is related to a reduction in proMMP-9 and MMP-2 activities and expression.

The matrix metalloproteinases (MMPs) are important enzymes that regulate developmental processes, maintain normal physiology in adulthood and have reparative roles at specific stages after an insult to the nervous system. MMPs, particularly MMP-9/gelatinase B, promote early inflammation and barrier disruption after spinal cord injury (SCI). Recently, we have reported that the pineal secretory product melatonin exerts important anti-inflammatory effects in an experimental model of SCI induced by the application of vascular clips (force of 24 g) to the dura after a four-level T5-T8 laminectomy. However, no reports are available on the relationship between the activity of MMPs and melatonin's anti-inflammatory effects. The aim of the present study was to evaluate whether the protective effect of melatonin observed in SCI is related to the regulation of MMP-9 and MMP-2 in mice. Biochemical and zymographic methods were used to analyze MMP-9 and -2 expression and activities in spinal cord tissue from SCI-treated mice at 24 hr after the trauma. Our studies reveal that melatonin reduced SCI and lipid peroxidation in spinal cord at 24 hr after SCI. Melatonin also diminished proMMP-9 and -2 activities that were induced in the spinal cord tissues at 24 hr after SCI. The reduced activities of MMP-9 and -2 were associated with depressed expression of TNF-alpha. We propose that melatonin's ability to reduce SCI in mice is also related to a reduction in MMP-9 and MMP-2 activity and expression.

Background and purpose: 5-lipoxygenase (5-LO) is the key enzyme in leukotriene (LT) biosynthesis from arachidonic acid (AA). Here, we examined the role of the 5-LO-product, cysteinyl-LT (Cys-LT), with a 5-LO inhibitor (zileuton) and a Cys-LT, receptor antagonist (montelukast), in the inflammatory response and tissue injury associated with spinal cord injury (SCI). Experimental approach: SCI was induced in mice by the application of vascular clips to the dura via a two-level T6 to T7 laminectomy for 1 min. Cord inflammation was assessed histologically and by measuring inflammatory mediators (ELISA) and apoptosis by annexin V, TUNEL, Fas ligand staining and Bax and Bcl-2 expression (immunohistochemistry and western blots). Motor function in hindlimbs was assessed by a locomotor rating scale, for 10 days after cord injury. Key results: SCI in mice resulted in tissue damage, oedema, neutrophil infiltration, apoptosis, tumour necrosis-α (TNF-α) and cyclooxygenase-2 (COX-2) expression, prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) production, and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation in injured tissue. Treatment of the mice with zileuton or montelukast reduced the spinal cord inflammation and tissue injury, neutrophil infiltration, TNF-α, COX-2 and pERK1/2 expression, PGE2 and LTB4 production, and apoptosis. In separate experiments, zileuton or montelukast significantly improved the recovery of limb function over 10 days. Conclusions and implications: Zileuton and montelukast produced a substantial reduction of inflammatory events associated with experimental SCI. Our data underline the important role of 5-LO and Cys-LT in neurotrauma. British Journal of Pharmacology (2008) 153, 568–582; doi:10.1038/sj.bjp.0707577; published online 3 December 2007

To evaluate the role of the hepatic perfusion in the assessment of the colorectal cancer.For this research 18 patients affected by colorectal cancer were enrolled. All the patients were submitted to the evaluation of the Doppler Perfusion Index (DPI) which represents the ratio of hepatic arterial to total liver blood flow.The correlation between the evaluation of the Doppler Perfusion Index and the occurrence of the liver metastases did not show false negative but has highlighted 6 false positive, achieved a good sensitivity and very low specificity.A review of the literature and the results obtained in our study suggest that DPI may be helpful in detection of hepatic metastases.

The previous results suggest that peroxisome proliferator-activated receptor-alpha (PPAR)-α, an intracellular transcription factor activated by fatty acids, plays a role in control of inflammation. There is persuasive epidemiological and experimental evidence that dietary polyphenols have anti-inflammatory activity. In this regard, it has been demonstrated that verbascoside (VB) functions as intracellular radical scavenger and reduces the microscopic and macroscopic signs of experimental colitis. With the aim to characterize the role of PPAR-αin VB-mediated anti-inflammatory activity, we tested the efficacy of VB in an experimental model of inflammatory bowel disease induced by dinitrobenzene sulfonic acid, comparing mice lacking PPAR-α(PPAR-αKO) with wild type (WT) mice. Results indicate that VB-mediated anti-inflammatory activity is weakened in PPAR-αKO mice, compared to WT controls, especially in the inhibition of neutrophil infiltration, intestinal permeability and colon injury. These results indicate that PPAR-αcan contribute to the anti-inflammatory activity of VB in inflammatory bowel disease.

Aim and background. In breast cancer, as in almost all neoplastic diseases, the prog -nosis is strictly related to the invasive capacity, local and distant, that characterizesthe growth of all tumors. Since the mechanisms that regulate replication of the neo -plastic cells, with consequent capacity to metastasize, are not completely known,identification of new markers represents the gold standard of research in the stratifi -cation of patients with such a pathology. Osteopontin, a specific phosphoglycopro -tein isolated from extracellular bone matrix and actively involved in mechanisms ofbone reabsorption, appears to play a key role in osteoclastogenesis at the level of theskeleton in some pathologic situations. It has been found that patients with metasta -tic bone lesions from breast or prostate cancer present, with respect to subjects with -out repetitive bone lesions, elevated serum levels of the protein, indicating that os -teopontin could play an important role in the development and progression of theneoplastic disease at the bone level.Methods and study design . The authors studied 26 patients with breast cancer, eval -uating as a marker also serum osteopontin levels.Resultsandconclusions. The results, although obtained on a small number of patients,showed that osteopontin evaluation in breast cancer patients can be a particularly in -teresting method of research in staging of the disease as well as in the prognosis, there -by attributing a role of a biotumoral marker also in the follow-up of the therapy.IntroductionBreast cancer is the main cause of death of women in the western world. However,owing to the possibility of an early diagnosis, in a high percentage of cases it is possi -ble to obtain good results in terms of cure and long-term survival. Unfortunately,when metastatic lesions are present, the prognosis is very poor. Extensive researchthroughout the last century has emphasized the prognostic significance of a numberof pathological factors, which include the size of the primary tumor, the histologicalgrade, and the appearance of tumor deposits in the draining lymph nodes of the pri -mary breast carcinoma. In spite of the progress observed in the study of tumorgrowth, one of the main limitations of modern oncology is the lack of knowledge onthe mechanisms that rule the kinetics of replication of neoplastic cells and particu -larly of its metastasizing capacity.Among the many studies carried out to identify the mechanisms underlying the ba -sis of tumor growth and secondary replication, interesting are those that havedemonstrated that osteopontin – a 44-kDa phosphotylated glycoprotein with theamino acid sequence Arg-Gly-Asp that elicits binding of integrin and is secreted bythe autocrine system of the cells of some aggressive multiple myeloma

The case of a giant sigmoid diverticulum complicated by a volvulus of the bowel is reported. After an exhaustive literature review, the Authors analyse the aetiopathogenetic, physiopathological and clinical aspects of this rare condition, considering its diagnostic and therapeutic implications. The Authors describe surgical problems and therapeutic management, pointing out that without an accurate study by radiological imaging, it is very difficult to diagnose the condition, particularly when no specific symptoms have been observed.

Glucocorticoids (GCs) are effective anti-inflammatory agents widely used in therapeutic approach to treatment of inflammatory bowel disease (IBD). Previous results suggest that peroxisome proliferator-activated receptor [alpha] (PPAR-[alpha]), an intracellular transcription factor activated by fatty acids, plays a role in control of inflammation. With the aim to characterize the role of PPAR-[alpha] in GC-mediated anti-inflammatory activity, we tested the efficacy of dexamethasone (DEX), a synthetic GC specific for GR, in an experimental model of IBD induced by dinitrobenzene sulfonic acid, comparing mice lacking PPAR-[alpha] (PPAR-[alpha]KO) with wild-type (WT) mice. Results indicate that DEX-mediated anti-inflammatory activity is weakened in PPAR-[alpha]KO mice as compared with WT controls. In particular, DEX was less effective in PPAR-[alpha]KO compared with WT mice, as evaluated by inhibition of proinflammatory cytokines production, cell migration, oxidative stress, apoptosis, and colon injury. These results indicate that PPAR-[alpha] can contribute to the anti-inflammatory activity of GCs in IBD.