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To update evidence-based best practice guidelines for surgical care in weight loss surgery (WLS). Systematic search of English-language literature on WLS in MEDLINE, EMBASE, and the Cochrane Library between April 2004 and May 2007. Use of key words to narrow the search for a selective review of abstracts, retrieval of full articles, and grading of evidence according to systems used in established evidence-based models. Evidence-based best practice recommendations from the most recent literature on surgical methods and technologies, risks and benefits, outcomes, and surgeon qualifications and credentialing. We identified >135 articles; the 65 most relevant were reviewed in detail. Regular updates of evidence-based recommendations for best practices in WLS are required to address rapid changes in surgical techniques and patient demographics. Key factors in patient safety include surgical risk factors, type of procedure, surgeon training, and facility certification.

Expression of HLA-G on the surface of malignant hematopoietic cells isolated from leukemia patients was analyzed by flow cytometry using monoclonal antibodies (mAbs) recognizing both, intact HLA-G complex (87G, 01G and MEM-G9) as well as HLA-G free heavy chain (4H84, MEM-G/1 and MEM-G/2). Prerequisite of HLA-G detection by mAbs specific to free heavy chain was mild acid treatment, which dissociates intact HLA-G complex. All mAbs, with the exception of 4H84 mAb, did not indicate the presence of HLA-G antigen in leukemia cells. Positive staining with 4H84 mAb was detected in acid-treated cells isolated from 16 out of 30 patients. Intensity of staining increased after IFN-g pre-incubation in most cases. Immunoblot analyses and RT-PCR, however, failed to detect HLA-G antigen or HLA-G transcripts in cells that bind 4H84 mAb after acid-treatment. The binding of 4H84 mAb can be explained by the acid-induced cross-reactivity of this HLA-G specific mAb with classical HLA class I molecules [15]. The results described here further demonstrate that the HLA-G molecule is not expressed in freshly isolated human leukemia cells.

The maternal tolerance to the semiallogeneic fetus is still a central theme in reproductive immunology. During placentation, fetally-derived, genetically dissimilar tissue and cells come into close contact with maternal tissue and cells, thus forming the so-called feto-maternal interface. The most extensive contact between fetally-derived and maternal blood cells is formed by the villous trophoblastic barrier, where the syncytiotrophoblast surface permanently floats in maternal blood. Further contact is made by some extravillous cytotrophoblast cells, either located at villous tips, in so-called cell islands, or the endovascular trophoblast population within the uteroplacental spiral arteries. The third contact zone is the so-called junctional zone within the decidua where the invading extravillous trophoblast cells encounter all maternal tissue leukocytes, which are mainly NK cells, macrophages and T cells; this junctional zone extends at the edge of the placenta to the amnio-chorionic membranes where the chorionic laeve trophoblast has intimate contact with decidua tissue. It is worth mentioning that evidence has shown that even in healthy pregnancies fetal and maternal lymphoid cells are able to transgress the trophoblastic barrier, which, anatomically, seems completely impermeable. Because of this intimate contact of foreign cells to the foreign immune system it is important to define the antigenic status of the placental cells, in particular with respect to antigens of the Major Histocompatibility complex. The role of the highly polymorphic classical class I molecules HLA -A, -B, -C, which are expressed on almost all somatic cells, is the induction of a specific immune response by presenting peptide antigens to T cells. In contrast, the non-classical HLA class I molecules HLA-G and HLA-E are thought to be involved in the induction of immune tolerance by acting as ligands for inhibitory receptors present on NK cells and macrophages. The non-classical HLA-E is also expressed ubiquitously, but HLA-G expression is characterized by a unique tissue expression mainly in the human placenta. A further feature of HLA-G is that its mRNA has undergone alternative splicing, resulting in at least 6 different isoforms, encoding different proteins: 4 membrane-bound and 2 soluble forms, which could simultaneously maintain different functions depending on their molecular structure. In our immunohistochemical study we investigated the expression of classical and non-classical HLA class I proteins in human placenta using various mAbs, which were kindly provided by the groups of A. Ziegler, D. Geraghty, O. Genbacev, MT. McMaster, A. King, YW. Loke and Ph. Le Bouteiller. For HLA-A,-B detection we used the antibody LA45; for detection of HLA-C,-B mAbs Tü149 and HC10. HLA-C expression alone was detected with mAb L31. HLA-G expression was studied using antibodies 4H84, G233, 87G, 16G1 and BFL.1. For HLA-E staining we used antibodies DT9 and V16. The classical HLA class I proteins are expressed in all non-trophoblastic cells including the fetal and maternal cells. Comparison of HLA-A and HLA-B staining intensities within the villous stroma indicates that during first trimester of pregnancy the fetal HLA-B proteins are expressed before HLA-A appears. Among the trophoblast populations, the syncytiotrophoblast does not show any HLA class I staining, but the extravillous cells express high amounts of HLA-G together with HLA-C. King and co-workers have shown recently, using methods other than immunohistochemistry, that first trimester extravillous trophoblast cells are also likely to express HLA-E. By contrast we did not detect HLA-E in any trophoblasts with antibodies DT9 and V16. There is still an ongoing and also controversial discussion about which kinds of cells in the placenta, other than extravillous trophoblast, express which kind of the HLA-G isoforms. Depending on the antibodies and the different immunohistochemical techniques used, different results have been described: Antibody 16G1 specific for soluble HLA-G labels syncytiotrophoblast, antibody BFL.1 endothelial cells of chorionic fetal blood vessels and antibody 87G Hofbauer cells. All these HLA-G labelings, apart from extravillous trophoblasts, are in complete contrast to the reaction pattern (merely extravillous trophoblast) given by antibody 4H84, which recognizes all HLA-G isoforms -including the soluble ones- through an epitope located on the a 1-domain of HLA-G. Future studies employing isoform-specific antibodies, which are not yet available for all of the possible isoforms, will elucidate the function and expression pattern of HLA-G in the human placenta.

The teratocarcinoma cell line 833K and its relatively cisplatin-resistant subline 833K/63CP 10 were used to assess the cytotoxicity of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ), cisplatin, and 4-hydroxyperoxycyclophosphamide quantitatively. The results showed that paclitaxel had marked cytotoxicity against teratocarcinoma, particularly in the cells that were relatively cisplatin resistant. These studies suggested synergy in cytotoxicity for paclitaxel, cisplatin, and 4-hydroxyperoxycyclophosphamide. A phase II trial of paclitaxel was conducted in patients with previously treated germ cell tumors with restricted prior treatment. The paclitaxel dose was 250 mg/m2 given by 24-hour continuous infusion. In 31 patients treated with paclitaxel, eight (26%) achieved a major (complete or partial) response. The antitumor activity of paclitaxel in the phase II trial has led us to further study it as a part of combination therapy. Since the in vitro studies showed synergistic cytotoxicity, combination studies of paclitaxel, ifosfamide, and platinum are under way as salvage treatment for patients with germ cell tumors.

150 patients with adenovirus type 8 infection where treated at random, in a prospective study. Based upon a quantifiable conjunctivitis severity score we tried to find out where there are differences in treatment. The best results were seen using polyvinylpyrrolidone-iodine (Betaisodona) although it could not prevent totally subepithelial corneal infiltrates. The combination of exogenous interferon alpha with polyvinylpyrrolidone-iodo-drops or trifluorothymidine-drops was less successful. We could not show any prophylactic effect of interferon on uninflamed fellow eyes. Treatment with vasoconstrictor did not show any therapeutic or prophylactic potency. This group of patients must be seen as a control group and the results of effective therapy should significantly differ from the results in this group. Topical corticosteroids should be reserved for severe symptomatic cases and those with iritis and pseudomembranous conjunctivitis. Giving topical corticosteroids in combination with antibiotics we did not find any influence on the incidence of subepithelial keratitis or the number of corneal infiltrates. The mean duration of acute keratoconjunctivitis using this therapy was longer than the mean duration in the control group with vasoconstrictor.

The indication for prophylactic temporary and permanent pacing during acute myocardial infarction (MI) complicated by bundle branch block is high risk of progression via a Type II pattern to second or third degree (high degree) AV block during hospitalization or follow-up. In this study, determinants of high degree AV block during hospitalization and sudden death or recurrent high degree block during the first year of follow-up were examined in 432 patients with MI and bundle branch block. Timing of onset of bundle branch block, the involved fascicles, and the PR interval were examined as determinants of risk of progression to high degree AV block during MI. At highest risk were 186 patients with blocks involving the right bundle and at least one fascicle of the left bundle which were not documented on prior electrocardiograms. Risk was similar with (38%) or without (31%) accompanying first degree AV block. Patients with transient high degree AV block during MI had a 28% incidence of sudden death or recurrent high degree block during the first year of follow-up. Patients not continuously paced had a higher incidence of sudden death or recurrent high degree block than patients continuously paced (65% vs 10%, P less than 0.001). Sudden death during follow-up also occurred in 13% of patients without high degree block during MI. A subgroup with 1) documented prior MI, 2) anterior or indeterminant acute MI, and 3) no symptoms of cardiac failure had a 35% risk of sudden death. The role of permanent pacing in this group is unknown. Thus, patients at high risk of high degree AV block should receive prophylactic temporary pacing. Patients who survive high degree block with MI should receive temporary and then permanent pacing. Patients without high degree AV block during MI who nervertheless have a high risk of sudden death may benefit from permanent pacing.

Fatty acid composition of mature human milk from Curacao (Netherlands Antilles), Surinam and Tanzania was determined by capillary gas chromatography. In the Curacaoan samples the cholesterol and alpha- and gamma-tocopherol concentrations were also determined. Remarkable differences were found in the fatty acid composition of breastmilk fat from the three countries. The differences in the levels of medium chain fatty acids between Curacao and Tanzania, and between Curacao and Surinam were significant. The mean sum of the essential fatty acids linoleic acid and linolenic acid showed the highest values in Curacao (16.1 g per cent). Mean values for Tanzania and Surinam were 14.9 and 12.7, respectively. The mean level of the docosahexaenoic acid was higher in the Curacaoan and Surinam samples compared with that from Tanzania. In the Curacaoan breastmilk samples the concentrations of cholesterol and alpha- and gamma-tocopherol were about twice as high as those reported for Western countries.

To provide an understanding of the clinical characteristics of patients with acute myocardial infarction (MI) and bundle branch block, experience from five centers was accumulated. Patients in whom bundle branch block first appeared after the onset of cardiogenic shock were excluded. In 432 patients, the most common types of block were left (38%) and right with left anterior fascicular block (34%). In 42% of the patients, bundle branch block was new. Progression to high degree (second or third degree) atrioventricular (AV) block via a Type II pattern occurred in 22% of the patients. Hospital and first year follow-up mortality rates were 28% and 28%, respectively. Only 46% of the patients developed pulmonary edema or shock (Killip Class III or IV), and hospital mortality was related to the amount of heart failure (8%, 7%, 27%, 83% for Killip Classes I-IV, respectively). Patients with progression to second degree or third degree AV block via a Type II pattern had increased hospital mortality compared with patients without this complication (47% vs 23%, P less than 0.001). In the absence of pulmonary edema or shock, patients with Type II second degree or third degree AV block still had a higher mortality rate than patients without advanced AV block (31% vs 2%, P less than 0.005), with nearly all the deaths due to abrupt development of AV block. Thus, in many patients MI with bundle branch block is associated with severe heart failure. However, this was not true for a majority of the patients, in whom therapy aimed at preventing morbidity and mortality due to the bradyarrhythmia of advanced AV block might be beneficial.