BackgroundLaparoscopic appendectomy is not yet unanimously considered the “gold standard” in the treatment of acute appendicitis because of its higher operative time, intra-abdominal abscess risk, and costs compared to open appendectomy. This study aimed to compare outcomes and cost of laparoscopic and open appendectomy in a district hospital.MethodsA retrospective analysis of 230 patients who underwent appendectomy at the Division of General Surgery of the Civil Hospital of Ragusa, Italy, from May 2008 to May 2012 was performed. The variables analyzed included patients data (age, gender, previous abdominal surgery, preoperative WBC count, duration of symptoms, ASA risk score), rate of uncomplicated or complicated appendicitis, operative time, postoperative complications, length of hospital stay, and total costs. The patients were divided in two groups according to the surgical approach and compared for each variable. The results were analyzed using the t Student test for quantitative variables, and the Chi-square test with Yates correction and Fisher exact test for categorical.ResultsLaparoscopic appendectomy was performed in 139 patients, open appendectomy in 91. Two cases (1.4%) were converted to open procedure and included in the laparoscopic group data. Patient data and rate of complicated appendicitis were similar in the two study groups. There was no statistical difference (p = 0.476) in the mean operative time between the laparoscopic (52.2 min; range, 20–155) and open appendectomy (49.3 min; range, 20–110) groups. The overall incidence of minor and major complications was significantly lower (p = 0.006) after laparoscopic appendectomy (2.9%, 4 cases) than after open appendectomy (13.2%, 12 cases); rate of intra-abdominal abscess were similar. The length of hospital stay was significantly shorter (p = 0.001) in laparoscopic group (2.75 days; range, 1–8) than in open group (3.87 days; range, 1–19). The mean total cost was 2282 Euro in laparoscopic group and 2337 Euro in open group, with a no significant difference of 55 Euro (p = 0.812).ConclusionLaparoscopic appendectomy is associated with fewer complications, shorter hospital stay, and similar operative time, intra-abdominal abscess rate, and total costs, compared with open appendectomy. Therefore, laparoscopic appendectomy can be recommended as preferred approach in acute appendicitis.

Our cohort study showed that SCT is safe and effective for reconstruction of the first segment of the subclavian artery. The systematic review suggested that rates of patency and freedom from clinical symptoms are higher with SCT than with CSB.

Evidence from randomized and nonrandomized trials and from cohort studies support the use of CSF drainage as an adjunct to prevent paraplegia when this adjunct is used in centers with large experience in the management of TAAA.

Right-sided aortic arch is a rare variant of the thoracic vascular anatomy that may be accompanied by an aberrant origin of the left subclavian artery. We report a true aneurysm of the distal arch and descending thoracic aorta in a patient with right-sided arch and review previous descriptions of aneurysms of anomalous right-sided aortas. In our patient, the left subclavian artery originated at the junction between the distal arch and the descending thoracic aorta located in the right chest and was aneurysmal (Kommerell's diverticulum); the thoracic aorta was also aneurysmal. Extra-anatomic left subclavian-to-carotid transposition was performed before the intrathoracic procedure. Subsequently, a right thoracotomy provided adequate exposure for repairing the aortic aneurysm and oversewing the aneurysmal origin of the subclavian artery. Because the distal aortic arch was involved, deep hypothermia and circulatory arrest were used. Only five previous instances of true aneurysms of a right-sided aortic arch have been reported; four of these patients underwent operative repair (via bilateral thoracotomy, median sternotomy, or right thoracotomy). We believe that a right thoracotomy provides good exposure and avoids the morbidity associated with bilateral thoracotomy. The reconstruction of the subclavian artery has not previously been reported in this setting. Performing subclavian reconstruction as an extrathoracic procedure before the intrathoracic repair would be expected to reduce the subsequent risk of distal ischemia or subclavian steal without increasing the overall morbidity associated with the procedure.

We report three cases of ruptured mycotic thoracoabdominal aortic aneurysms (TAAAS) and a review of the literature. Escherichia coli and Streptococcus pneumoniae (2 patients) were the responsible organisms. Surgical management consisted of wide debridement of necrotic tissue and in situ repair with a Dacron graft. Antibiotics were administered intravenously in the hospital and continued orally after discharge for at least 6 weeks, until clinical and laboratory parameters were normalized. A review of the literature showed that Gram-negative microorganisms are found in 47% of mycotic TAAAs. A trend toward increased mortality for these organisms, compared with Gram-positive microorganisms, was observed (P =.09). Lifelong antimicrobial therapy is controversial. No difference in survival or recurrence rate was found between series advocating lifelong therapy and those suggesting prolonged (6 weeks to 12 months) therapy (median follow-up period, 18 and 19 months, respectively). In situ repair with synthetic material can be successful if prompt confirmation of infection is obtained, all possibly infected tissue is resected, and antibiotic therapy based on sensitivity data is administered for a prolonged period. A short-term survival rate as high as 82% can be expected with this strategy, but data on long-term survival rates are limited. Polytetrafluoroethylene-expanded grafts, homografts, and antibiotic-bonded grafts may offer advantages over Dacron grafts, but data are insufficient to draw conclusions. Careful long-term follow-up is an important element of the treatment of these patients. We suggest antibiotic treatment until biochemical parameters of inflammation (white cell count, erythrocyte sedimentation rate, or C-reactive protein) return to normal and a computerized tomography scan every 3 months for 1 year, then annually.

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The embryonic microenvironment is well known to be non-permissive for tumor development because early developmental signals naturally suppress the expression of proto-oncogenes. In an analogous manner, mimicking an early embryonic environment during embryonic stem cell culture has been shown to suppress oncogenic phenotypes of cancer cells. Exosomes derived from human embryonic stem cells harbor substances that mirror the content of the cells of origin and have been reported to reprogram hematopoietic stem/progenitor cells via horizontal transfer of mRNA and proteins. However, the possibility that these embryonic stem cells-derived exosomes might be the main effectors of the anti-tumor effect mediated by the embryonic stem cells has not been explored yet. The present study aims to investigate whether exosomes derived from human embryonic stem cells can reprogram malignant cancer cells to a benign stage and reduce their tumorigenicity. We show that the embryonic stem cell-conditioned medium contains factors that inhibit cancer cell growth and tumorigenicity in vitro and in vivo. Moreover, we demonstrate that exosomes derived from human embryonic stem cells display anti-proliferation and pro-apoptotic effects, and decrease tumor size in a xenograft model. These exosomes are also able to transfer their cargo into target cancer cells, inducing a dose-dependent increase in SOX2, OCT4 and Nanog proteins, leading to a dose-dependent decrease of cancer cell growth and tumorigenicity. This study shows for the first time that human embryonic stem cell-derived exosomes play an important role in the tumor suppressive activity displayed by human embryonic stem cells.

BackgroundHorizontal transfer of malignant traits from the primary tumor to distant organs, through blood circulating factors, has recently become a thoroughly studied metastatic pathway to explain cancer dissemination. Recently, we reported that oncosuppressor gene-mutated human cells undergo malignant transformation when exposed to cancer patients’ sera. We also observed that oncosuppressor mutated cells would show an increased uptake of cancer-derived exosomes and we suggested that oncosuppressor genes might protect the integrity of the cell genome by blocking integration of cancer-derived exosomes. In the present study, we tested the hypothesis that cancer patients’ sera-derived exosomes might be responsible for the malignant transformation of target cells and that oncosuppressor mutation would promote their increased uptake. We also sought to unveil the mechanisms behind the hypothesized phenomena.MethodsWe used human BRCA1 knockout (BRCA1-KO) fibroblasts as target cells. Cells were treated in vitro with cancer patients’ sera or cancer patients’ sera-derived exosomes. Treated cells were injected into NOD-SCID mice. Immunohistochemical analyses were performed to determine the differentiation state of the xenotransplants. Mass spectrometry analyses of proteins from cancer exosomes and the BRCA1-KO fibroblasts’ membrane were performed to investigate possible de novo expression of molecules involved in vesicles uptake. Blocking of the identified molecules in vitro was performed and in vivo experiments were conducted to confirm the role of these molecules in the malignant transformation carried out by cancer-derived exosomes.ResultsCells treated with exosomes isolated from cancer patients’ sera underwent malignant transformation and formed tumors when transplanted into immunodeficient mice. Histological analyses showed that the tumors were carcinomas that differentiated into the same lineage of the primary tumors of blood donors. Oncosuppressor mutation promoted the de novo expression, on the plasma membrane of target cells, of receptors, responsible for the increased uptake of cancer-derived exosomes. The selective blocking of these receptors inhibited the horizontal transfer of malignant traits.ConclusionThese findings strengthen the hypothesis that oncogenic factors transferred via circulating cancer exosomes, induce malignant transformation of target cells even at distance. Oncosuppressor genes might protect the integrity of the cell genome by inhibiting the uptake of cancer-derived exosomes.Electronic supplementary materialThe online version of this article (10.1186/s13046-017-0587-0) contains supplementary material, which is available to authorized users.