258 research outputs found

    Effect of antithrombotic therapy on postoperative outcome of 538 consecutive emergency laparoscopic cholecystectomies for acute cholecystitis. Two Italian center’s study

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    The risk of developing hemorrhagic complications during or after emergency cholecystectomy (EC) for acute cholecystitis (AC) in patients with antithrombotic therapy (ATT) remains uncertain. In this double-center study, we evaluated post-operative outcomes in patients with ATT undergoing EC. We retrospectively evaluated 538 patients who underwent laparoscopic EC for AC between May 2015 and December 2019 at two referral centers. 89 of them (17%) were on ATT. We defined postoperative complication rates, including bleeding, as our primary outcome. Mortality was higher in the ATT group. Morbidity was higher in the ATT group as well; however, the difference was not statistically significant. 12 patients (2%) experienced intraoperative blood loss over 500 ml and ten (2%) had postoperative bleeding complications. Two patients (< 1%) experienced both intraoperative and postoperative bleeding. On multivariate analysis, ATT was not significantly associated with worse postoperative outcomes. Antithrombotic therapy is not an independently associated factor of severe postoperative complications (including bleeding) or mortality. However, these patients still represent a challenging group and must be carefully managed to avoid postoperative bleeding complications

    Direct Transactivation of the Anti-apoptotic Gene Apolipoprotein J (Clusterin) by B-MYB

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    B-MYB is a ubiquitously expressed transcription factor involved in the regulation of cell survival, proliferation, and differentiation. In an attempt to isolate B-MYB-regulated genes that may explain the role of B-MYB in cellular processes, representational difference analysis was performed in neuroblastoma cell lines with different levels of B-MYB expression. One of the genes, the mRNA levels of which were enhanced in B-MYB expressing cells, was ApoJ/Clusterin(SGP-2/TRMP-2) (ApoJ/Clusterin), previously implicated in regulation of apoptosis and tumor progression. Here we show that the human ApoJ/Clusterin gene contains a Myb binding site in its 5\' flanking region, which interacts with bacterially synthesized B-MYB protein and mediates B-MYB-dependent transactivation of the ApoJ/Clusterin promoter in transient transfection assays. Endogenous ApoJ/Clusterin expression is induced in mammalian cell lines following transient transfection of a B-MYB cDNA. Blockage of secreted clusterin by a monoclonal antibody results in increased apoptosis of neuroblastoma cells exposed to the chemotherapeutic drug doxorubicin. Thus, activation of ApoJ/Clusterin by B-MYB may be an important step in the regulation of apoptosis in normal and diseased cell

    Paratesticular Mesenchymal Malignancies: A Single-Center Case Series, Clinical Management, and Review of Literature

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    Background: Primary soft tissue sarcomas arising from the male urinary and genital tract are rare tumors, only accounting for 1% to 2% of all malignancies of the genitourinary tract. Clinical management of advanced disease is lacking in standardized recommendations due to the rarity of the disease. To date, complete and extensive surgery represents the only curative and standardized approach for localized disease, while the impact of retroperitoneal lymphadenectomy and adjuvant treatments on clinical outcomes are still unclear. Similarly, a standardized systemic treatment for advanced metastatic disease is still missing. Cases Presentation: Four out of 274 patients have been identified in our sarcoma population. The mean age was 54 years (range = 45-73). The histotypes showed liposarcoma in 2 cases and leiomyosarcoma in the remaining 2 cases. In all 4 cases, the disease was localized at presentation, patients underwent complete surgery, and no adjuvant treatments were done. Three cases presented a recurrence of disease at a mean follow-up of 86 months (range = 60-106 months), more than 7 years. Two cases were treated with a second surgery and chemotherapy and 1 case only with chemotherapy. Discussion and Conclusions: Sharing data about clinical management of paratesticular mesenchymal tumors is a key issue due to the rarity of this tumor\u2019s subtype. In this article, we report the clinical history of 4 patients affected by paratesticular mesenchymal tumor. In particular, main issues of interest are the decision of postoperative treatment and systemic treatment at time of disease recurrence

    False in Name Only-Gastroduodenal Artery Pseudoaneurysm in a Recurrently Bleeding Patient: Case Report and Literature Review.

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    INTRODUCTION: Although the diagnosis of visceral pseudoaneurysm is unusual, it requires emergent attention due to the risk of rupture. We describe a 70-year old man with a gastroduodenal artery (GDA) pseudoaneurysm manifest as recurrent hæmorrhage. AREAS COVERED: We highlight the possible ætiologies, clinical presentations, diagnostic tools and treatment options for this condition. In this instance, the patient was successfully treated by selective angio-embolization. EXPERT COMMENTARY: A visceral pseudoaneurysm should be considered in patients with abdominal pain and GI hæmorrhage. At present, angio-embolization is first-line therapy

    Atypical presentation of acute idiopathic megacolon in a 14-year-old patient

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    In clinical practice the term "megacolon" is used to indicate a marked dilatation of the cecum and the sigmoid colon (>12 and 6.5 cm, respectively) (1). From a clinical standpoint, a megacolon can be classified as chronic or acute depending on its clinical presentation. Chronic megacolon typically refers to a congenital disorder in which the enteric nervous system (ENS) supplying the colon does not develop properly, thereby leaving the distal segments of the viscus without myenteric and submucosal ganglia (i.e. Hirschsprung's disease) (2). Other cases of non-aganglionic chronic megacolon can be secondary to variety of conditions such as Chagas' disease and neurodegenerative diseases (e.g. Parkinson's and Alzheimer's diseases), leading to or associated with ENS abnormalities (3). The acute form of megacolon, also referred to as Ogilvie's syndrome, is characterized by a predominant involvement of the cecum and right colon usually affecting elderly patients undergoing surgery (e.g. orthopedic procedures) or taking medications altering gut motility (e.g. opioids or antidepressants) (4). Some forms of acute megacolon, however, can be idiopathic in origin since no underlying etiology can be identified. Patients with acute idiopathic megacolon usually have a longstanding history of constipation, often accompanied by laxative abuse, and their clinical presentation is characterized by abdominal distension and severe pain with radiological evidence of stool impacted in the colon and rectum (1, 4). The case herein reported represents an unusual form of acute idiopathic megacolon characterized by massive descending and sigmoid colon distension complicated with a volvulus in a 14-year-old boy with no Hirschsprung's disease. In addition, just to increase the peculiarity of this case report, the patient had an unremarkable clinical record, and never suffered from chronic constipation in the past

    The tumour-suppressive function of CLU is explained by its localisation and interaction with HSP60

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    The product of the CLU gene promotes or inhibits tumourigenesis in a context-dependent manner. It has been hypothesised that different CLU isoforms have different and even opposing biological functions, but this theory has not been experimentally validated. Here we show that molecules involved in survival pathways are differentially modulated by the intracellular or secreted forms of CLU. Secreted CLU, which is selectively increased after transformation, activates the survival factor AKT, whereas intracellular CLU inhibits the activity of the oncogenic transcription factor nuclear factor kappa B. Furthermore, intracellular CLU is inactivated by the pro-proliferative and pro-survival activity of the chaperone protein HSP60 in neuroblastoma cells by forming a physical complex. Thus, localisation is key for CLU physiology, explaining the wide range of effects in cell survival and transformation
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