Spleen preservation in a caudal pancreatic serous cystadenoma - case report.

Cystic lesions of the pancreas are relatively rare entities but have been increasingly diagnosed in recent years due to advanced imaging techniques. This category encompasses pancreatic pseudocyst as well as a wide range of pancreatic tumors with benign behavior, borderline or primary malignant. Serous cystadenoma of the pancreas represents the most common benign pancreatic tumor, with a very low but well recognized malignant potential. The clinical presentation varies according to its size; small tumors may be asymptomatic and discovered incidentally, while large tumors are more likely symptomatic. We report the case of a female patient presenting with non-specific left abdominal pain, who was diagnosed through a CT scan with a caudal pancreatic tumor. The patient underwent spleen-preserving distal pancreatectomy. The result of the histopathological examination revealed a serous cystadenoma.

Treatment of bilateral inguinal hernia -- minimally invasive versus open surgery procedure.

OBJECTIVES: The aim of this study is to evaluate and compare the treatment outcomes of the bilateral inguinal hernia repair in one stage using minimally invasive technique (totally extraperitoneal) and conventional surgery (Lichtenstein). MATERIALS AND METHODS: Records from all hospitalized cases in our institution between 2006 and 2011 that underwent surgery having the diagnosis of bilateral inguinal hernia were analysed. RESULTS: The study consists of two groups selected by means of the used procedure: the study arm which is laparoscopic (234 cases) and the control arm that consists of Lichtenstein procedure (91 cases). One conversion was recorded due to difficult dissection (0.4% of cases). There were complications reported in 2.5% cases in the laparoscopic group and 27.4% complications noted in the conventional group (p less then 0.01). Reinterventions were logged in 1.7% cases in the laparoscopic group and 2.1% reinterventions in the open group (p less then 0.01). The postoperative hospital stay was 2.1 days in the laparoscopic group and 4.7 days for the open procedure. Mortality was not recorded. CONCLUSIONS: In our department the procedure of choice for bilateral inguinal repair is the laparoscopic approach (TEP) which has a 10 fold decrease in complications rate than Lichtenstein operation and also a shortening by half of the hospital stay. Hernia recurrence is the same for both procedures.

Apoptosis of lung epithelial cells in response to TNF-alpha requires angiotensin II generation de novo.

Recent work from this laboratory demonstrated that apoptosis of pulmonary alveolar epithelial cells (AEC) in response to Fas requires angiotensin II (ANGII) generation de novo and binding to its receptor (Wang et al., 1999b, Am J Physiol Lung Cell Mol Physiol 277:L1245-L1250). These findings led us to hypothesize that a similar mechanism might be involved in the induction of AEC apoptosis by TNF-alpha. Apoptosis was detected by assessment of nuclear and chromatin morphology, increased activity of caspase 3, binding of annexin V, and by net cell loss inhibitable by the caspase inhibitor ZVAD-fmk. Purified human TNF-alpha induced dose-dependent apoptosis in primary type II pneumocytes isolated from rats or in the AEC-derived human lung carcinoma cell line A549. Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril; the inhibition of TNF-induced apoptosis was maximal at 50 microgram/ml saralasin (101% inhibition) and at 0.5 microgram/ml lisinopril (86% inhibition). In both cell culture models, purified TNF-alpha caused a significant increase in the mRNA for angiotensinogen (ANGEN), which was not expressed in unactivated cells. Transfection of primary cultures of rat AEC with antisense oligonucleotides against ANGEN mRNA inhibited the subsequent induction of TNF-stimulated apoptosis by 72% (P < 0.01). Exposure to TNF-alpha increased the concentration of ANGII in the serum-free extracellular medium by fivefold in A549 cell cultures and by 40-fold in primary AEC preparations; further, exposure to TNF-alpha for 40 h caused a net cell loss of 70%, which was completely abrogated by either the caspase inhibitor ZVAD-fmk, lisinopril, or saralasin. Apoptosis in response to TNF-alpha was also completely inhibited by neutralizing antibodies specific for ANGII (P < 0.01), but isotype-matched nonimmune immunoglobulins had no significant effect. These data indicate that the induction of AEC apoptosis by TNF-alpha requires a functional renin/angiotensin system (RAS) in the target cell. They also suggest that therapeutic control of AEC apoptosis in response to TNF-alpha is feasible through pharmacologic manipulation of the local RAS.

Angiotensin II induces apoptosis in human and rat alveolar epithelial cells.

Recent work from this laboratory demonstrated potent inhibition of apoptosis in human alveolar epithelial cells (AECs) by the angiotensin-converting enzyme inhibitor captopril [B. D. Uhal, C. Gidea, R. Bargout, A. Bifero, O. Ibarra-Sunga, M. Papp, K. Flynn, and G. Filippatos. Am. J. Physiol. 275 (Lung Cell. Mol. Physiol. 19): L1013-L1017, 1998]. On this basis, we hypothesized that apoptosis in this cell type might be induced by angiotensin II (ANG II) through its interaction with the ANG II receptor. Purified ANG II induced dose-dependent apoptosis in both the human AEC-derived A549 cell line and in primary type II pneumocytes isolated from adult Wistar rats as detected by nuclear and chromatin morphology, caspase-3 activity, and increased binding of annexin V. Apoptosis also was induced in primary rat AECs by purified angiotensinogen. The nonselective ANG II-receptor antagonist saralasin completely abrogated both ANG II- and angiotensinogen-induced apoptosis at a concentration of 50 microgram/ml. With RT-PCR, both cell types expressed the ANG II-receptor subtypes 1 and 2 and angiotensin-converting enzyme (ACE). The nonthiol ACE inhibitor lisinopril blocked apoptosis induced by angiotensinogen, but not apoptosis induced by purified ANG II. These data demonstrate the presence of a functional ANG II-dependent pathway for apoptosis in human and rat AECs and suggest a role for the ANG II receptor and ACE in the induction of AEC apoptosis in vivo.

Captopril inhibits apoptosis in human lung epithelial cells: a potential antifibrotic mechanism.

The angiotensin-converting enzyme inhibitor captopril has been shown to inhibit fibrogenesis in the lung, but the mechanisms underlying this action are unclear. Apoptosis of lung epithelial cells is believed to be involved in the pathogenesis of pulmonary fibrosis. For these reasons, we studied the effect of captopril on Fas-induced apoptosis in a human lung epithelial cell line. Monoclonal antibodies that activate the Fas receptor induced epithelial cell apoptosis as detected by chromatin condensation, nuclear fragmentation, DNA fragmentation, and increased activities of caspase-1 and -3. Apoptosis was not induced by isotype-matched nonimmune mouse immunoglobulins or nonactivating anti-Fas monoclonal antibodies. When applied simultaneously with anti-Fas antibodies, 50 ng/ml of captopril completely abrogated apoptotic indexes based on morphology, DNA fragmentation, and inducible caspase-1 activity and significantly decreased the inducible activity of caspase-3. Inhibition of apoptosis by captopril was concentration dependent, with an IC50 of 70 pg/ml. These data suggest that the inhibitory actions of captopril on pulmonary fibrosis may be related to prevention of lung epithelial cell apoptosis.