Approach and treatment of the adult acquired flatfoot deformity

Adult acquired flatfoot deformity (AAFD), embraces a wide spectrum of deformities. AAFD is a complex pathology consisting both of posterior tibial tendon insufficiency and failure of the capsular and ligamentous structures of the foot. Each patient presents with characteristic deformities across the involved joints, requiring individualized treatment. Early stages may respond well to aggressive conservative management, yet more severe AAFD necessitates prompt surgical therapy to halt the progression of the disease to stages requiring more complex procedures. We present the most current diagnostic and therapeutic approaches to AAFD, based on the most pertinent literature and our own experience and investigations.     

Endograft infection following emergency repair for abdominal aortic aneurysm dissection and the undervalued role of the bowel reservoir

Endograft infection after emergency endovascular aortic repair (EVAR) procedure has received less attention than other complications, and usually occurs soon after endograft positioning. Consequently, clear guidelines for the prevention and treatment of endograft infection have yet to come. We report a case of an 85‐year‐old patient treated with an emergency EVAR procedure for a fissured abdominal aortic aneurysm, whose immediate follow up was complicated by a prolonged upper gastrointestinal occlusion. Six months, later he developed an endograft infection due to intestinal flora. After exclusion of all other possible causes, bacterial translocation from the bowel appeared the only plausible mechanism. This case highlights the importance of the gastrointestinal tract as a potential source of endograft infection, and suggests how a clinical condition representing potential reservoir of infection should be managed properly.     

SRC homology-2-containing protein tyrosine phosphatase-1 restrains cell proliferation in human medullary thyroid carcinoma

Medullary thyroid carcinoma (MTC) is a rare tumor originating from thyroid parafollicular C cells, where, in the inherited form, constitutive activation of the RET protooncogene is responsible for unrestrained cell proliferation. We previously demonstrated that somatostatin (SRIF) reduces cell growth in the human MTC cell line TT, which expresses all SRIF receptor (SSTR) subtypes and responds differently to selective SSTR agonists. The antiproliferative mechanism of SRIF and its analogs in MTC is still unclear. Src homology-2-containing protein tyrosine phosphatase-1 (SHP-1), a cytoplasmic protein tyrosine phosphatase (PTP), is activated by somatotropin release-inhibiting factor and reduces mutated RET autophosphorylation in a heterologous system. In this study, we explore the role of PTP activation, in particular of SHP-1, in TT cells, where RET is constitutively activated. In TT cells, SRIF stimulated the PTP activity of SHP-1, which was associated with proliferation inhibition and with reduction in the MAPK pathway activation. Blockade of PTP activity with sodium orthovanadate induced cell proliferation and MAPK phosphorylation and blunted the inhibitory effects of SRIF. Moreover, SHP-1 associates with SSTR2 depending on its activation. By using a MAPK kinase inhibitor, we demonstrated that TT cell growth depends on MAPK pathway activation. Furthermore, in TT cells overexpressing SHP-1, cell proliferation and MAPK signaling were strongly down-regulated, whereas in TT cells transfected with a dominant negative form of SHP-1, cell proliferation and MAPK signaling were markedly induced. Our data demonstrate that SRIF inhibitory effects on TT cell proliferation are mediated, at least in part, by SHP-1, which acts through a MAPK-dependent mechanism.     

Prediction of Falls in Subjects Suffering From Parkinson Disease,Multiple Sclerosis,and Stroke

Objective

To compare the risk of falls and fall predictors in patients with Parkinson disease (PD), multiple sclerosis (MS), and stroke using the same study design.

Circulating intercellular adhesion molecule 1 predicts non-specific elevation of α1-fetoprotein

Molecules governing cellular interactions have been suggested to be involved in the spurious elevation of 1-fetoprotein (AFP) in non-neoplastic liver disease. To explore this controversial issue, we measured AFP, circulating intercellular adhesion molecule 1 (cICAM-1), and common liver function tests in 111 patients (71 male, 40 female). Eighty-four patients had non-neoplastic chronic liver disease and 27 had hepatocellular carcinoma. The concentration of cICAM-1 was determined immunoenzymatically. In patients with non-neoplastic chronic liver disease, univariate analysis demonstrated a significant correlation between AFP and cholinesterase (R=–0.397,P<0.001), aspartate aminotransferase (R=0.421,P<0.001), bilirubin (R=0.231,P<0.05) and cICAM-1 (R=0.430,P<0.001). Multivariate analysis among these variables and AFP indicated cICAM-1 to be the strongest independent predictor of AFP. We conclude that cICAM-1 compares favourably with liver function tests in predicting non-specific AFP variations in non-neoplastic chronic liver disease, suggesting a link between targeting of the inflammatory damage to the hepatocyte and development of neoplasia.Abbreviations AFP 1-fetoprotein - cICAM-1 circulating intercellular adhesion molecule 1