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Videolaparoscopic surgery exposes the abdominal organs to the mechanical effect of pneumoperitoneum at pressure values between 12 and 15 mm Hg, which are considered safe. Nevertheless, experimental data have shown that this pressure range can represent a hemodynamic risk factor as it may induce a decrease in the venous return to the right ventricle, a decrease in cardiac output, and activation of the sympathetic nervous system and renin angiotensin system. We report two cases of acute renal failure that occurred soon after videolaparoscopy in young female patients without any evidence of ongoing renal disease. Patient A was 29 years old and was submitted to videolaparoscopic surgery in a follow-up program after surgical treatment of ovarian cancer; patient B was 15 years old and was submitted to the surgical removal of a monolateral ovarian cyst. In neither of the cases was it necessary to perform hemodialysis. Patient A underwent a renal biopsy under ultrasound guidance; optic microscopy showed only in ra- and extraglomerular capillary congestion. In both cases the acute renal failure resolved completely and the patients where discharged with normal renal function. Taking in to account that normal renal venous pressure levels are around 4 mmHg we think that a) a 15 mmHg pneumoperitoneum may represent a risk factor during videolaparoscopic surgery mainly if the patient's extracellular volume is not properly expanded; b) administration of nonsteroidal anti-inflammatory drugs in order to prevent surgical pain may inhibit vasodilatory prostaglandin availability; c) onset of oliguria during the surgical procedure suggests that extracellular volume expansion is required.

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One of the complications of arteriovenous fistulas in chronic hemodialyzed patients is the onset of an aneurysm which can be at risk of rupture. Traditional surgical repair is not always feasible and may not be successful in these cases, leading therefore to the loss of a functioning vascular access and requiring in any case the temporary use of a central venous catheter to allow regular hemodialysis sessions. We applied to this kind of aneurysm the same experience developed in the management of major arterial aneurysms and we considered endografting repair a good alternative in this case. In this paper we present the successful treatment of an arteriovenous fistula aneurysm using that technique. A distal radio-cephalic arteriovenous fistula in one of our patients presented an aneurysm with high risk of rupture. The endografting repair with percutaneous insertion of a WallgraftTM endoprosthesis was well tolerated and the vascular access could be used the day after, without the need for a central venous catheter insertion.

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UNLABELLED: Seroma is one of the most frequent complications of PTFE vascular grafts and its etiology is still unclear. CASE REPORT: A 51 year-old male on regular dialytic treatment for seven years underwent the surgical implantation of a vascular prosthesis of homologous safena due to the thrombosis of his native artero-venous fistula. Several years earlier the patient had suffered the amputation of the left forearm because of electric shock. A few months later the vascular prosthesis was replaced with a PTFE vascular graft as a result of aneurysm formation and thrombosis. During the following days a non pulsating swelling occurred near the arterial anasto-mosis. Ultrasonography, doppler sonography and aspiration confirmed the diagnosis of seroma and it was surgically removed. Some weeks later a new seroma was observed in the same site and associated with a skin ulcer. A new surgical removal had no benefit and about one month later a perigraft collection was found along with signs of bacterial infection. For this reason the patient underwent the surgical excision of the PTFE graft and a vascular access was warranted by placing a Tesio TM catheter. Usually surgery is considered mandatory in seromas larger than 2 cm in diameter and showing continuous growth. In our patient the poor vascular status might have suggested a more conservative management even with a seroma diameter of about 7 cm. Nevertheless the high risk of systemic infection prompted us to remove the PTFE graft.

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Sclerosing encapsulating peritonitis (SEP) is a serious complication of long-term continuous ambulatory peritoneal dialysis (CAPD), very likely related to a persisting expression of the transforming growth factor beta1 (TGFbeta1) gene on peritoneal mesothelial cells. We report the case of a 67-year-old uremic woman who developed SEP eight years after being placed on CAPD, complicated by eight episodes of bacterial peritonitis. CAPD was therefore stopped and the patient transferred to hemodialysis. The diagnosis of SEP was confirmed by physical findings (vomiting, abdominal pain with palpable mass, ileus, cachexia) and CT data. The patient was treated with tamoxifen (10 mg/day) for three months, and gradually recovered, a subsequent CT showing a significant reduction of the thickness of peritoneal and intestinal loops. Tamoxifen probably interferes with TGFbeta1 and may be useful in the treatment of this CAPD complication.

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Anti-HLA class I monoclonal antibody 01.65 inhibits the proliferative response of PHA-activated human T lymphocytes from peripheral blood mononuclear cells. The recruitment rate in the cell cycle is slack and the G1 and S phases are prolonged. Among the early events after PHA activation, only the calcium-dependent PKC activity appears to be modified: particulate PKC is completely depleted while cytosolic residual PKC is reduced by 80% after MAb 01.65 treatment. We have carried out in greater detail the study of c-myc gene regulation by MAb 01.65 and the results are as follows: (i) c-myc RNA transcription is normally initiated and finished, suggesting a post-transcriptional regulation of c-myc gene expression; (ii) no alteration in c-myc mRNA stability has been documented; (iii) steady-state levels of c-myc mRNA expression by Northern blot analysis and PCR amplification are decreased in the cytoplasmic compartment, while in the nuclear compartment they appear to be increased. Nuclear accumulation of mature mRNA after MAb 01.65 and PKC inhibitor (H7 and StSp) treatment appears to be the most probable mechanism involved. The possible implications of this are discussed.

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Neutrophil accumulation and the consequent production of oxygen-derived free radicals are involved in the pathogenesis of Ischemia-Reperfusion syndrome. In this study we investigated whether a treatment with Vitamin E, which has antioxidant properties, could attenuate the tissue damage by interfering with the influx of neutrophils within the ischemic and reperfused human skeletal muscle. To this purpose, patients undergoing aortic cross-clamping during the surgical repair of aortic abdominal aneurysm were studied as a model of ischemia-reperfusion of the lower limb muscles. Muscle biopsies from the right femoral quadriceps of patients not receiving and receiving Vitamin E pretreatment before surgery were taken: a) after the induction of anaesthesia, as control samples, and b) after a period of ischemia followed by 30 min of reperfusion. The tissue samples were either routinely processed for morphological study and immunohistochemical analysis to detect an altered expression of specific endothelial adhesion proteins, such as E-selectin and ICAM-1. The results obtained showed that Vitamin E administration was able to prevent the accumulation of neutrophils within the ischemic and reperfused muscle. This beneficial effect of Vitamin E was due to its ability to hinder the expression of E-selectin and ICAM-1, molecules known to increase the adhesiveness of endothelium to circulating neutrophils. After treatment with Vitamin E a marked attenuation of the reperfusion injury was also evident. In conclusion, Vitamin E treatment may be considered a valuable tool for protection against the ischemia-reperfusion damage of human skeletal muscle.

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PURPOSE: The biochemical and morphological alterations induced in lower limb skeletal muscle by ischemia-reperfusion (I-R) during aortic surgery and the effect of vitamin E pretreatment were investigated. METHODS: Two groups of patients undergoing aortic aneurysm resection, one untreated and one treated with vitamin E, were examined. Quadricep muscle biopsies were taken after induction of anesthesia, at the end of ischemia, and after reperfusion. The malondialdehyde (MDA) content and morphology of biopsies were examined to assess peroxidative processes. RESULTS: Ischemia did not induce an increase in MDA content but did increase neutrophil infiltration in muscle fibers of untreated patients. Reperfusion led to a significant increase in MDA content and to intermyofibrillar edema and mitochondrial swelling. The MDA content was not increased during ischemia and neutrophil infiltration was minimal in vitamin E treated patients. At reperfusion, the MDA content, the ultrastructural injuries and neutrophil infiltration were significantly reduced by the treatment. CONCLUSIONS: Vitamin E is effective in reducing the oxidative muscle damage occurring after a period of I-R.

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BACKGROUND: A new intubating transilluminated device (Trachlight) has been recently proposed as an alternative to tracheal intubation with direct laryngoscopy. OBJECTIVE: 1) To evaluate Trachlight device in orotracheal intubation and to assess its operation and complications. 2) To compare the time consumption of transillumination intubation in respect to direct laryngoscopy on the same patients. METHODS: The first study was performed on 50 patients undergoing elective surgery and submitted to Trachlight intubation alone; speed of intubation, number of attempts and all complications were recorded and related to Mallampati classes. In the second study 16 patients undergoing to elective surgery were enrolled. Each patient was classified according to both the Mallampati classes and the Cormack classes. Each patient was submitted to two tracheal intubations: the first with the Trachlight and the second with conventional direct laryngoscopy performed by the same anesthesiologist. The time to intubation and the number of attempts were recorded and related to the Mallampati and Cormack classes. RESULTS: In the first study time of intubation with Trachlight was 20.93 +/- 13.02s (mean +/- SD) without statistical differences in respect to the Mallampati classes. In the second study the times to intubation were without any statistical difference independently of the technique of intubation and of the Mallampati or Cormack classes. CONCLUSIONS: Orotracheal intubation using Trachlight appears to be an effective and easy to learn technique, being also easy, safe and fast to carry out. The comparison with direct laryngoscopy showed the same speed and effectiveness even on patients with difficult intubation.

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Only recently, in our laboratory of experimental surgery, we started with a protocol for orthotopic liver transplantation (OLT) in a pig model. This was felt as mandatory for experimental purposes as well as for future clinical applications at our center. We report herein our own experience with 41 OLTx. Intraoperative "lethal" complications occurred in up to 32% (14/41) whereas postoperative complications occurred in the remainders at different intervals of time with a maximum survival of 30 days. No attention was paid to prevent rejection-infection episodes. The main cause of death was the primary non-function (PNF) or dis-function (PDF) manifested either intra or postoperatively in 16 out the 41 OLTx (39%). Intraoperative technical errors accounted for up to 9% (4/41 OLTx). Acute hemorrhage gastritis and gastric perforations occurred postoperatively in 6 animals (14%) and represent one of the peculiar aspects of OLT in pig model.

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Membranous glomerulonephritis is the most common glomerular disease associated with malignancy, the association of minimal change glomerulopathy with solid tumor is still uncommon. We report a 72-year-old man with nephrotic syndrome due to minimal change glomerular disease; an accurate seek of underlying malignancy revealed a cecum adenocarcinoma. We had a complete remission of nephrotic syndrome after surgery of carcinoma.

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Toluene diisocyanate (TDI) is the most common cause of occupational asthma in western countries. The aim of this study was to investigate whether genetic factors are involved in toluene diisocyanate-induced asthma. We studied the frequency of human leucocyte antigen (HLA) class II genetic markers in three groups of subjects: 1) subjects with TDI-induced asthma (n = 30); 2) exposed subjects with no history of TDI-induced asthma (n = 12); and 3) normal subjects not exposed to TDI (n = 126). Venous blood samples were collected from the three groups and the polymorphic second exon of DQA and DQB genes was amplified by the polymerase chain reaction (PCR) method. Evaluation of HLA class II gene products in TDI-induced asthma cases showed a positive association with HLA-DQB1 * 0503 and a negative association with HLA-DQB1 * 0501 alleles, which differed at residue 57 for a single amino acid, i.e. aspartic acid in DQB1 * 0503 and valine in DQB1 * 0501. No significant difference was found in the distribution of DQA1 alleles between asthmatics and controls. Our results confirm the hypothesis that HLA-DQB1 * 0503 has a role in conferring susceptibility to TDI-induced asthma and that residue 57 of HLA-DQB1 is a potentially critical location.

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We describe a female patient with Vohwinkel syndrome (mutilating palmoplantar keratoderma), who in addition showed cleft lip and palate, microcephaly, facial asymmetry, and other anomalies.

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Stimulation by platelet-derived growth factor (PDGF) is known to increase the number of IGF-I binding sites in cells in culture. We show here that PDGF also increases the levels of IGF-1 receptor mRNA. Using cell lines stably transfected with an expression plasmid in which the reporter luciferase gene is under the control of the rat IGF-1 receptor gene promoter, we find that PDGF increases the activity of this promoter. A short IGF-1 receptor gene promoter, comprising about 100 base pairs of the sequence immediately upstream of the initiation of transcription site, is sufficient for a response to the stimulatory action of PDGF. These results suggest that an increase in RNA levels and in promoter activity may play an important role in the increase in IGF-1 receptor levels that occurs after stimulation by PDGF.

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A peptide inhibiting either corpuscolate or purified PKC has been identified from microsomes of PHA-activated human PBMC but it is not detectable in microsomes of resting PBMC. The peptide was obtained from a microsomal preparation in an oligomeric form that could be transformed into a monomeric form by beta-MSH. The active peptide (IN) was retained on a PC-11 chromatographic column and could be eluted with NaCl. IN is ineffective on PKC-dependent protamine phosphorylation of protamine and on Ca2+ and phospholipid-independent activity generated by mild hydrolysis with trypsin of PKC. Ca2+ binding is permissive for IN activity. IN inhibits particulate PKC in PHA-activated PBMC, but is ineffective after TPA activation. All these data indicate that IN acts at the regulatory domain of PKC.

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Blood lead corrected for hematocrit (PbC) was measured in 115 hemodialysis (HD) patients. Information was collected with a questionnaire about personal and environmental factors thought to influence blood Pb levels. HD patients had significantly higher mean blood Pb than healthy subjects (p < 0.001). A non-negligible percentage of the HD population (13%) had values over 30 micrograms/dl, the threshold for risk in occupational exposure, and 4% over 40 micrograms/dl which reflects Pb intoxication. No association was found between sex, age, duration of HD and PbC. The prevalence of high diastolic blood pressure was associated with PbC over 30 micrograms/dl (p < 0.01). Also, at blood Pb levels generally considered as 'nontoxic' (less than 40 micrograms/dl), we found a low correlation with diastolic blood pressure (r = 0.19, p = 0.049). A correlation was found between PbC and parathyroid hormone (r = 0.22, p = 0.01) and between PbC and mean corpuscular volume (r = -0.21, p = 0.02). The patients with individual risk factors (smoke, alcohol consumption and alkyl Pb from air contamination) had PbC levels higher than patients without (p = 0.001). The patients with environmental risk factors (professional exposure, tap water consumption and older houses) had PbC levels higher than patients without (p = 0.01). Patients with past occupational exposure had the highest mean PbC levels (34.1 micrograms/dl = 1.65 nM/ml).

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Studies of the mode of inheritance of affective disorders have been reviewed. The overall picture which emerges does not seem to involve specific modes of inheritance. Linkage studies based on the single gene hypothesis, support X-linkage for a bipolar variant, as well as possible linkage to chromosomes 6 and 11. The more recent approach of linkage studies using large numbers of RFLP markers scattered throughout the genome looks promising, though it may still give rise to misinformation. Several confounding factors have been suggested such as genetic and phenotypic heterogeneity, as well as the lack of well defined diagnostic criteria.

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It is known that anti-HLA Class I antibodies inhibit the proliferative response of PHA-activated T-lymphocytes. We found that plastic- or sepharose-linked anti-HLA Class I monoclonal antibody 01.65 does not inhibit either [3H]Thymidine incorporation or recruitment in the cell cycle, nor does it reduce the expression of c-myc mRNA and the membrane expression of Interleukin-2 Receptor and Transferrin Receptor. Furthermore, particulate Protein Kinase C is not affected by anchored anti-HLA Class I monoclonal antibody 01.65. We suggest that anti-HLA Class I monoclonal antibody may act through crosslinking or internalization of HLA Class I antigens.

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Anti-HLA class I monoclonal antibody (mAb) 01.65 inhibited phytohaemagglutinin (PHA)-induced human lymphocyte proliferation. The inhibitory effect was inversely correlated to the strength of the proliferative response. It was increased when lymphocytes were stimulated with suboptimal doses of PHA but it disappeared with supraoptimal doses. Proliferation inhibition was achieved by prolonging the cell cycle time and by slowing down its recruitment rate. The former effect was not restricted to the G1-phase but also included the S phase. These results support the idea that HLA class I molecules are important in the PHA-induced proliferation of human T-lymphocytes.

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