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OBJECTIVES The Edwards Intuity valve is a rapid deployment aortic prosthesis that favours less invasive approaches. However, evidence about the clinical behaviour of their smaller sizes is scarce. Herein, we studied haemodynamic behaviours and clinical outcomes of small Intuity prostheses (19–21 mm) in comparison to larger Intuity prostheses (>21 mm). METHODS This is an observational study including patients implanted with an Edwards Intuity rapid deployment aortic prosthesis. Patients with prosthesis sizes 19–21 and >21 mm were included. Baseline and perioperative variables, as well as adverse events during the follow-up were recorded and compared between groups. RESULTS A total of 122 patients (37% female, mean age 75 ± 4.5 years) were included, of whom 54 (45%) were implanted with a small prosthesis and 68 (55%) with a prosthesis >21 mm. There were no significant differences between patients with small Intuity prostheses and patients with larger prostheses regarding in-hospital mortality (2% vs 4%, P = 0.43) or mortality during the follow-up (3.41 vs 2.45 per 100 patients-years; P = 0.58). Survival in the small Intuity valve group was 95% at 1 year and 83% at 6 years, whereas in the larger Intuity valve group was 96% at 1 year and 78% at 6 years. The presence of a small prosthesis did not influence mid-term survival (log-rank P-value = 0.62). CONCLUSIONS This study showed good clinical performance of Intuity aortic prostheses with appropriate mid-term survival in patients with the small aortic annulus. Thus, the Edwards Intuity rapid deployment aortic prosthesis may be considered as a potential option in patients with the small aortic annulus.

Resume Cette etude retrospective monocentrique s’est interessee aux anomalies chromosomiques limitees au placenta (ACLP) a priori d’origine meiotique (i.e. anomalies chromosomiques limitees au placenta de type 3 homogenes). A partir d’une serie de 14 967 biopsies de trophoblaste effectuees dans notre centre de medecine fœtale, dix ACLP de type 3 homogenes ont ete mises en evidence. Ces anomalies impliquaient uniquement les chromosomes 15, 16 ou 22. Les grossesses compliquees d’une ACLP de type 3 homogene etaient associees a des termes de naissance prematures et des hypotrophies neonatales. Ainsi, lorsqu’une anomalie chromosomique limitee au placenta est suspectee, cette etude souligne la necessite de bien caracteriser son type afin de prevenir un tres probable retard de croissance intra-uterin associe aux ACLP de type 3 homogenes et adapter la prise en charge obstetricale le cas echeant.

Journal de Gynecologie Obstetrique et Biologie de la Reproduction - Vol. 35 - N° 7 - p. 711-719

NDP kinases are the non-specific enzymes which catalyse the synthesis of the NTPs through a transfer reaction using ATP as phosphoryl donor. In addition to their enzymatic activity, they display other not yet explained functions related to cell growth, differentiation and apoptosis, embryonic development, tumour progression and metastasis. In this study, the expression patterns of the three highly related NDP kinases A, B and C isoforms were investigated in the developing human trophoblast. Both NDP kinase A and B were found to be primarily present in the villous and extravillous cytotrophoblasts, while NDP kinase C was found almost exclusively in the syncytiotrophoblast layer. This suggests that NDP kinase A and B could be a marker for the mononuclear stage of differentiation of villous trophoblasts, while NDP kinase C could be a marker of the syncytiotrophoblast layer.

L’utilisation de plus en plus frequente du diagnostic prenatal permet de reveler des anomalies gonosomiques, en particulier le syndrome de Klinefelter, non associees a des anomalies echographiques fœtales. Les caracteristiques cliniques et biologiques du syndrome de Klinefelter sont bien connues. Il n’en est pas de meme des fonctions intellectuelles dont l’evaluation est essentiellement, determinee a partir d’etudes anciennes biaisees. Des etudes recentes demontrent que les facultes intellectuelles de ces sujets, bien que legerement abaissees sont proches de la normale. Des etudes recentes montrent que le principal mode de recrutement des sujets 47,XXY, en post natal, est le bilan d’infertilite. La decouverte d’un fœtus XXY genere toujours une anxiete majeure chez le couple. L’absence de malformation et de retard mental devrait permettre la poursuite de la grossesse. L’annonce de l’anomalie est determinante. Le taux d’interruption est plus important quand c’est l’obstetricien qui fait cette annonce. Des etudes recentes et notre etude, bien que peu importante, confirment cette constatation. La tendance actuelle est de ne pas proposer d’interruption medicale pour un “Klinefelter” tout en sachant l’impossibilite de predire quelle sera la gravite du syndrome.

Objective To investigate whether the placental expression of P-glycoprotein shows a quantitative difference during pregnancy. Study design Villous tissue was collected from chorionic villus samples (13–14 weeks of gestation; n =33 and 20–25 weeks of gestation; n =4) and from full-term placentas (38–41 weeks of gestation; n =28). P-glycoprotein was detected by western blot analysis and quantified by densitometry. Results We showed for the first time a significant and progressive two-fold decrease in the mean expression of P-glycoprotein between early and late samples, with a major overlap of values. Conclusion As P-glycoprotein appears to be involved in drug extrusion, these data suggest that the placenta's ability to protect the fetus from xenobiotics is greater in early pregnancy than at term.

Chromosomal analysis of 25 colonic adenomatous polyps was performed by a direct method similar to that used in prenatal diagnosis of chromosomal aberration on chorionic villi. Fourteen lesions showed an abnormal karyotype. Two changes were recurrent: trisomy 7 (observed in eight cases) and trisomy 13 (observed in seven cases). No monosomy of the short arm of chromosome 17 was observed even at the level of two polyps with in situ carcinoma lesions.

SUBJECT. Massive Chronic Intervillositis is an infrequent inflammation lesion of the placenta, characterized by lymphohistiocytic intervillous infiltration, associated with fibrinoid deposition. The purpose of this study was to evaluate the perinatal outcome of pregnancies complicated by such lesions.We conducted a descriptive retrospective multicentric analysis of a series of pregnancies for which placenta or products of abortion were analyzed between January 1995 and September 2005, at the University Hospital of Bordeaux. After re-examining the histology slides, we performed a semi-quantitative graduation of the cell infiltration and fibrinoid deposition.Twenty-five women were included (one twin-pregnancy and two histologic recurrences). We found three spontaneous abortions before 22 weeks, four intrauterine fetal deaths and three neonatals deaths. Seven of eight elective inductions pregnancies, were performed for intrauterine growth restriction less than 2.5 percentile. The rate of pregnancy loss was 55% and the perinatal mortality was 29%. 77% of fetuses are small for gestational age. Three mothers were pre-eclamptic. 21% of the fetuses had a congenital malformation. Only 32% of the fetuses were alive one week after birth. Histologically, 25% were associated with lesions of Villitis of Unknown Etiology. 77% of the cell infiltration was grade 3 and seemed to be correlated with severe growth restriction. We describe 3 cases of antenatal diagnosis of Chronic Intervillositis, realised after immunofixation on chorionic villous sampling.Massive Chronic Intervillositis is a recurrent lesion with a poor prognosis complicated by spontaneous abortion, intrauterine growth restriction and perinatal fetal death. Currently, there is no treatment. Chorionic villous sampling in severe growth restriction might be useful in order to obtain at the same time the fetal karyotype and an histological probe of the placenta.

Uniparental disomy (UPD) for several human chromosomes is associated with clinical abnormalities. We report the case of a 2-year-old boy with severe intrauterine and post-natal growth retardation (IUGR/PNGR) and highly variable sweat chloride concentrations. The patient was identified as heterozygous for the F508del mutation of the CFTR (cystic fibrosis transmembrane conductance regulator) gene. Unexpectedly, the signal corresponding to the maternally inherited F508del allele appeared much more intense than the paternally derived wild allele. Molecular analysis including polymorphic marker studies, microsatellites and single-nucleotide polymorphisms subsequently showed that the boy was a carrier of a de novo mosaic maternal isodisomy of a chromosome 7 segment while there was a biparental inheritance of the rest of the chromosome. This is the first report of a mosaic partial UPD7. The matUPD7 segment at 7q21-qter extends for 72.7 Mb. The karyotype (550 bands) of our patient was normal, and fluorescence in situ hybridization with probes mapping around the CFTR gene allowed us to rule out a partial duplication. The detection of this chromosomal rearrangement confirms the hypothesis that the 7q31-qter segment is a candidate for the localization of human imprinted genes involved in the control of IUGR and PNGR. It also emphasizes the importance of searching for UPD7 in severe, isolated and unexplained IUGR and PNGR.

This manuscript reports a fetus of 24 weeks gestation, detected on echography to have congenital anomalies: intra-uterine growth retardation, facial dysmorphism, ventricular septal defect with aortic displacement and 8-mm nuchal skinfold thickness. Karyotype was performed. Post termination of pregnancy autopsy showed additionnal internal organ anomalies included: absent gall bladder and thyroid isthmus agenesis. To our knowledge, these anomalies have never been described in trisomic 22 fetuses. This case suggests that chromosome 22 could play a role in thyroid development.

Two CMOS application-specific integrated circuit (ASIC) families are presented. The first ASIC family with 1.0 mu m channel length, is based on a sea-of-cells (SOC) architecture and a double-level-metal (DLM) structure. It offers chip density up to 100 K wirable circuits and higher I/O pin count using plastic-flat-pack (PFP) packaging. The second ASIC family with 0.5 mu m channel length offers up to 75 K wirable gates with boundary scan I/Os and array built-in self-test (ABIST). Single-chip-module (SCM), and multiple-chip-module (MCM) pin-in-hole packages are used to save space at the card level. Specific features are described, focusing on the complementarity offering of these two families and on the design tradeoffs between high-density and high-speed ASIC applications. >

Journal de Gynecologie Obstetrique et Biologie de la Reproduction - Vol. 40 - N° 5 - p. 481-482

Nitric oxide (NO) is a very small lipophilic molecule which rapidly diffuses and reaches the cytoplasmic components, and results in the activation of diverse biological function. It has been already reported that cultured osteoblasts synthesize NO in response to proinflammatory cytokines and lipopolysaccaride. In terms of the action of NO on bone metabolism, cytokine-induced NO by osteoblast inhibits bone resorption through inducing the apoptosis of osteoclast progenitor cells and suppressing the osteoclast activity. Also, NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine is reported to induce a dose-dependent inhibitory effect on the proliferation of osteoblast-like cell lines MG63 and ROS 17/2.8, which indicate that NO may stimulate cell proliferation. On the other hand, cytokine-induced NO is reported to reduce osteoblast activity significantly in high concentration, as was evidenced by inhibition of DNA synthesis, cell proliferation, alkaline phosphatase activity, and osteocalcin production. Thus, the effect of NO on osteoblast activities is still controversial. In the present study, S-nitroso-N-acetyl-dl-penicillamine(SNAP), NO donor enhanced DNA synthesis of MC3T3-E1 in vitro. This activation seems to be mediated by NO directly because specific NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO) partially attenuated the osteoblast proliferation induced by SNAP. On the other hand, the guanylate cyclase inhibitor, LY83583, failed to abolish the effect of SNAP on DNA synthesis of osteoblasts and 8-bromo cyclic guanosine 3',5'-monophosphate(cGMP), substituting for the accumulation of intracellular cGMP in osteoblasts, did not enhance the incorporation of 3H-thymidine(3H-TdR). It is, then, suggested that osteoblast proliferation might be enhanced by NO independently apart from the activation of cytoplasmic guanylate cyclase and cGMP-dependent mechanisms.

In order to investigate the mechanism of anti-rheumatic action of mizoribine (MZR), antiproliferative effect of MZR on synovial fibroblasts obtained from rheumatoid arthritis (RA) patients were examined. To examine the effect of MZR on DNA synthesis, total radioactivity of 3H-thymidine (3H-TdR) incorporated into the synovial fibroblasts was measured. Also quantification of DNA fragmentation of synovial fibroblasts in the cultured supernatant and cell associated Bcl-2 protein, which is suspected of interfering with apoptosis, were performed with enzyme-linked immunosorbent assay. MZR suppressed 3H-TdR incorporation into synovial fibroblasts in a dose dependent fashion. Significant inhibition (P0.01) was attained at the concentration of more than 1 microgram/ml of MZR. However, induction of DNA fragmentation which is characteristic of apoptosis, were observed at only 10 micrograms/ml of MZR over 72 h-incubation significantly. In terms of the Bcl-2 expression of synovial fibroblasts, up to 10 micrograms/ml of MZR has no effect on the expression of this protooncogene bcl-2 expression. These results suggest that MZR might suppress the growth of rheumatoid pannus by inhibition of synovial fibroblast proliferation partially through the induction of apoptosis of synovial fibroblast without modulating Bcl-2 expression.

Both periosteal cell proliferation and endochondral ossification accompanied are characteristic of the fracture healing process. This process is regulated by various kinds of soluble factors including prostanoids, cytokines and growth factors. In particularly, basic fibroblast growth factor (bFGF) stimulates the mesenchymal cell proliferation and differentiation in the periosteum and leads to the fracture healing. Recently, newly synthesized pyrimidine compound, 2-piperadino-6-methyl-5-oxo-5,6-dihydro (7H) pyrrolo [3,4-d] pyrimidine maleate (MS-818) has been reported to augment the biological effect of bFGF in vitro. Therefore, we have studied the effect of MS-818 on fracture healing process in which bFGF has been reported to play an important role. In the rat fracture model, 5 mg/kg MS-818 which had been administered intraperitoneally for fourteen consecutive days enhanced the cartilage matrix formation. In the bone defect model, in which we can find only membranous ossification without chondrogenesis, cartilage matrix formation was observed in seven days after 1 microgram of human bFGF containing polymer pellet was embedded in the defect site. Chondrogenesis induced by bFGF was enhanced significantly after 5 micrograms MS-818 containing pellet was implanted with bFGF pellet. These results suggest that MS-818 might promote the fracture healing process through enhancement of the effect of bFGF on endochondral ossification.

While the unphysiological mechanical load is a central etiologic factor of disc degeneration, biologic factors including nitric oxide (NO) seems to play an important role in this condition. It is, therefore, investigated whether NO is related to the degeneration of intervertebral disc by way of inducing the disc cell apoptosis. Twelve herniated lumbar disc and eight control specimens were obtained from the patients underwent surgery. Apoptotic cells were identified by TUNEL procedure and the percent apoptotic cell index (ACI%) of each sample was calculated. Detection of iNOS expression was performed by immunohistochemical analysis. Disc cell monolayer culture was prepared from the surgical specimen of the patients with lumbar disc herniation. NO generation of the disc cells was measured by Griess reaction. Cell proliferation was detected by measuring the incorporation of 3H-Thymidine. The extent of fragmented DNA induced by NO donor, NOC-18, was also measured by an enzyme-linked immunosorbent assay. The incidence of apoptotic cell death (ACI%) was greater in the herniated group (61.3 +/- 24.5%) than that of control group (5.6 +/- 6.8%; P0.001). iNOS positive disc cells were detected in all the samples. NO production of disc cells was enhanced by the stimulation of IL-1 alpha. Suppression of 3H-Thymidine incorporation and DNA fragmentation in the disc cells were promoted by treatment of 100 microM NOC-18. These results suggest that disc cells are able to release NO and NO may play an important role in the pathogenesis of disc degeneration through the induction of apoptosis of disc cells in situ.

Both nitric oxide (NO) and prostaglandin E2 (PGE2) are known to play an important role in cartilage metabolism. The present study investigated the novel intercellular mechanism of inducible NO synthase (iNOS) induction mediated by PGE2 in articular chondrocytes. Bovine articular chondrocytes were stimulated by cyclic adenosine monophosphate (cAMP) elevating agents like PGE2 in the presence of interleukin-1 alpha (IL-1 alpha). NO generation was measured by using the Griess reaction. Inducible NOS mRNA was semi-quantitated by reverse transcription-polymerase chain reaction (RT-PCR). While little NO was released from articular chondrocytes in the presence of PGE2 or direct adenylate cyclase activator such as forskolin, synergistic augmentation of NO generation was observed when chondrocytes were stimulated by PGE2 or forskolin in combination with IL-1 alpha. Further expression of iNOS mRNA by stimulation of PGE2 in the presence of IL-1 alpha simultaneously was also detected by RT-PCR in comparison with the mRNA induction by IL-1 alpha stimulation alone. These results indicated that PGE2 might modulate the articular cartilage metabolism by augmentation of chondrocyte NO synthesis in inflammatory process through cAMP-protein kinase A system.

Lumbar disc herniation (LDH) is the disease which is the major cause of radiculopathy. In terms of the pathogenesis of disease, it is reported that prostaglandinE2 (PGE2) plays an important role to induce radiculopathy. Arachidonate cascade, which is the process of PGE2 synthesis, is mainly regulated by two kinds of enzymes, phospholipaseA2 (PLA2) and cyclooxy genase (COX). Previously, PLA2 was recognized as the rate-limiting enzyme of this cascade, and some authors reported the clinical significance of PLA2 at the site of LDH concerning the radicular pain. Recently, COX was elucidated to consist of 2 types of isoform, a constitutive form of COX-1 and an inducible form of COX-2. COX-2 has been focused as a key enzyme to regulate PGE2 synthesis and plays an important role in inflammation, because COX-2 was induced in many types of cells by the stimulation of inflammatory cytokines such as interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). However, it is not fully discussed whether or not, COX-2 is induced in lumbar disc tissue and if it plays a significant role in the pathogenesis of LDH. To clarify the role of COX-2 in the pathomechanism of radiculopathy of LDH, we have investigated the expression of COX-2, IL-1 beta and TNF alpha in herniated lumbar disc tissue. Immunohistologically, they were detected in the cytosol of chondrocytes constituting the disc tissue. RT-PCR showed that herniated lumbar disc-derived cells expressed mRNA of COX-2, IL-1 beta and TNF alpha in the presence of inflammatory cytokines in vitro. The disc-derived cells also produced much PGE2 by stimulating of inflammatory cytokines at the same time and this PGE2 production was distinctly suppressed by a selective inhibitor of COX-2, 6-methoxy-2-naphtyl acetic acids (6MNA). These results suggest that COX-2 and inflammatory cytokines might play a causative role in the radiculopathy of LDH through upregulating PGE2 synthesis.

Many attempts have described a standard experimental model for fracture non-union in laboratory conditions, but the majority of them produced after an experimental osteotomy, so it is different from clinical disturbed fracture healing. The purpose of this study is to establish a standard method for producing fracture non-union with only muscle interposed into the fracture site in rats. Bilateral tibial fractures were made in forty-eight male Wister rats by three point bending and we surgically interposed the distal end of the tibialis anterior muscle into the fracture site. They were sacrificed at 1, 2, 3, 6, 12, 24, 48, and 96 weeks after fracture. The rentgenograms were obtained, and the fractured tibias were harvested in each time period and investigated histologically and immunohistochemically. The rentgenogram at six weeks, in the non-union rats, showed abundant callus at each end of the fracture fragments, but no bridging callus. The histological finding with hematoxylin and eosin, at this point, shows no bridging soft callus, and small isolated regions of cartilage were observed only where the bone was not covered by the muscle. The proliferating cell nuclear antibody immunostaining which is associated with cell proliferation was abruptly lost in chondrocytes at two weeks. This early disappearance of chondrocytes without endochondral ossification may be a significant etiological factor in the development of a non-union. This non-union model is technically simple and reproducible, and dose not require periosteal stripping or surgical osteotomy to produce an artificial bone gap.

Seven patients with subcutaneus of the extensor pollicis longus tendon (EPL) in rheumatoid arthritis were studied. There were one man and six women. The mean age of the patients was 56. 9 years, with a range of 47 to 83 years. The duration of the disease was from 0.2 to 6 years, its average 3 years. An interval between rupture of the tendon and operation was 9 days to 18 months. Tendon transfers of the extensor indicis proprius tendons were performed in 3 cases, sutures in 2 cases and free tendon graft of the palmaris longus in one case. All cases showed very active tenosynovitis around the EPLs, which were ruptured near Lister's tubercle. The histopathological findings of the ruptured EPL revealed that synovial proliferative tissue with chronic inflammatory cells infiltration were invading into the tenion tissue directly. The synovial granulatins might weaken the tendon and repetitive mechanical stress on the tendon at Lister's tubercle could result in the rupture of EPLs.

Mutations in ion channels have been shown to be responsible for a variety of neurological and muscular diseases. The voltage-gated chloride channel CLCN3 was recently mapped to chromosomal region 4q32. We are analysing a young female patient with Wolf-Hirschhorn syndrome and chorea associated with an inversion-deletion of chromosome 4 [46XX,inv(4)del(4)(qter--q33::p15.32--q33]. Considering that chorea in this patient might be due to the disruption of a gene at either of the 4p15.32 or 4q33 breakpoints, CLCN3 was considered as a candidate gene. We showed by FISH analysis with a CLCN3 YAC that the gene was not broken by the inv-del event, and was therefore an unlikely candidate. Using high resolution techniques, we refined the localisation of CLCN3 to 4q33.

Though cisplatin (cis-diamminedichloroplatinum; CDDP) has been widely used for the treatment of malignant tumors, the mechanism of its action has not been well understood. Neovascularization, which accompanies tumor growth and metastasis, is required for cell proliferation in order to supply both oxygen and nutrients. We have studied in this investigation the effect of CDDP on endothelial cell (EC) proliferation in vitro and on rabbit corneal neovascularization in vivo. DNA synthesis of human umbilical EC was inhibited by CDDP in a dose-dependent fashion. Significant inhibition was observed at concentration over 10(-8) M, which is attainable in the serum of treated patients. Rabbit corneal neovascularization in vivo was also suppressed by intravenous injection of 0.5 mg/kg of CDDP for 10 days. These results suggest that CDDP might have an indirect anti-neoplastic effect through the suppression of neovascularization required for the tumor growth.

A case of antenatal hydrothorax was observed. The aetiology could not be determined before birth. At birth an extra-lobe lung sequestation was treated surgically after 3 weeks in the intensive care unit. The surgical cure was successful with no sequellae. This favourable outcome is unusual in this type of pathology and can be explained by the fact that the sequestration was isolated in a fetus with only minimal anasarca. Indications for prenatal pleural drainage are discussed.

Determine the pathogenesis of fetal nuchal oedema and cystic hygromas of the neck and establish prenatal prognosis factors.Retrospective study of 49 cases including 35 early diagnoses (10 to 14 weeks gestation) and 14 late diagnosis (after 15 weeks). Chorial villosity biopsy was performed for fetal karyotype.The global rate of genetic or chromosomic abnormalities in the fetuses was 47%. The fetuses with nuchal associated with other echographic anomalies had a high risk of chromosomic aberrations (80%). Fetuses with nuchal oedema alone during the first trimester had a higher risk of trisomy 21 proportionally with the age of the mother and paradoxically no trisomy 21 was found in women under 30 years of age. When early nuchal oedema regressed spontaneously in an euploid fetus, echographic surveillance can be proposed to detect possible polymalformation syndromes discovered late. Cystic hygromas of the neck were diagnosed from 15 weeks gestation and were always pathologic.Interpreting nuchal images in the fetus must take into account the echographic term at discovery and its isolated or associated nature. Further studies are needed to determine indications for chorial villosity biopsy in mothers under 30 with a fetus with isolated nuchal oedema which regresses spontaneously during the first trimester.

Background The prognosis of gastric cancer with peritoneal metastasis is extremely poor. Neither systemic chemotherapy nor surgery alone prolongs survival of patients significantly. Methods Patients diagnosed with advanced gastric cancer underwent staging laparoscopy and received chemotherapy when peritoneal dissemination and/or cancer cells on peritoneal cytology were confirmed. The chemotherapy regimen consisted of S-1, weekly intravenous and intraperitoneal paclitaxel, which was verified in our phase II trial (Ann Oncol 2009). S-1 was administered at 80 mg/m2/day for 14 consecutive days, followed by 7 days rest. Paclitaxel was administered intravenously at 50 mg/m2 and intraperitoneally at 20 mg/m2 on days 1 and 8. Clinical response of chemotherapy was assessed by computed tomography, gastroendoscopy, peritoneal cytology and second-look laparoscopy. Radical gastrectomy was carried out when macroscopic curative resection was made achievable by chemotherapy. Chemotherapy was restarted after operation as soon as possible. Overall survival, relapse free survival, morbidity and mortality of gastrectomy were evaluated. Results Out of 100 patients with peritoneal metastasis who received chemotherapy, 60 patients underwent gastrectomy after response to chemotherapy, including 54 with macroscopic metastasis and 6 with positive peritoneal cytology only. A median of three courses were administered preoperatively (range 1–16). Total or distal gastrectomy with lymphnode dissection was carried out in 54 or 6 patients, respectively. The median survival time was 34.5 months. The median relapse-free survival was 16.7 months. The first site of relapse was the peritoneum in 24 patients and the other organ site in 17 patients. Postoperative complications included anastomotic leakage and pancreatic fistula in two patients each, which were healed conservatively. There were no treatment-related deaths. Conclusions Gastrectomy combined with S-1, intravenous and intraperitoneal paclitaxel is safe and active for gastric cancer patients with peritoneal metastasis.

The authors reviewed forty-three surgically managed cases of cubital tunnel syndrome treated during the past twelve years. Surgery had been performed on thirty-one men and twelve women. Their average age was 46.8 years old. The etiology of cubital tunnel syndrome had been determined as follows: There were twenty-three cases of osteoarthritis of the elbow joint. There were four cases of isolated cubitus valgus deformity. There were three cases of isolated cubitus varus deformity. There were three cases of rheumatoid arthritis. One patient had sustained trauma to the cubital tunnel. In nine other patients there were various causes but no joint malalignment. The selection of the surgical technique for the correction of cubital tunnel syndrome was a function of the etiology of the condition. Cubital tunnel syndrome from osteoarthritis was surgically managed with a modified King technique. Ulnar neuropathy with a cubitus valgus deformity was managed with an ulnar nerve anterior transposition. Ulnar neuropathy with a cubitus varus deformity was managed with a neurolysis. The surgical outcome for cubital tunnel syndrome in patients with an angular deformity at the elbow frequently was not optimum. However, although some patients remained symptomatic, the majority of postoperative patients did obtain improved motor strength and conduction velocities. This confirmed the efficacy of surgical management regardless of the cubital tunnel syndrome etiology.

During a 4-year period, 29 fetal nuchal edemas were observed, associated with other ultrasound abnormalities in 7 cases (24%). Fetal karyotypes were abnormal in 10 cases: 6 trisomy 21; 3 trisomy 18, and 1 Turner's syndrome. Isolated fetal nuchal edema was associated with aneuploidy in 4 cases: 3 trisomy 21, and 1 trisomy 18. The average age of the women carrying a fetus with nuchal edema associated or not with a trisomy 21 was 38.3 and 30.8 years, respectively. These results are similar to those found in the literature. It would appear that maternal age is a better marker in trisomy 21 screening than isolated fetal nuchal edema.

We report on a case of fetal goitrous hypothyroidism confirmed by the study of fetal thyroid function. Two injections of intra amniotic levo-thyroxine were performed at 35 and 36 WA. The serial ultra sonographic examination showed the disappearance of the fetal goiter. A healthy baby were delivered by cesarean section at 37 WA. At birth, the thyroid gland was slightly enlarged and the neonatal thyroid hormones were within the normal range. This case suggests that cordocentesis is a reliable method of assessing the status of the fetal thyroid, and that even as early as 35 WA a prenatal treatment of fetal goitrous hypothyroidism is possible by amniocentesis.

A chromosomal study of 42 colonic adenomatous polyps was performed using a technique of direct chromosome analysis derived from the prenatal procedure for diagnosing chromosomal alterations from chorionic villi sampling. Abnormal karyotypes were found in 22 cases. Trisomy 7, the most frequently found alteration, was found in 13 cases, followed by trisomy 13 (nine cases). Monosomy 18 was observed in two cases; in one of these, that of a polyp which had degenerated into an intra-mucosal adenocarcinoma, it was associated with 17p monosomy. Interestingly, these two types of alterations (trisomy 7 versus 18 and 17p monosomy) were not found together in the same lesion. This suggests that there could be two distinct chromosomal behaviors which might be related to the two cytogenetic groups described for colorectal adenocarcinoma. However, the respective frequencies of such cytogenetic groups varied inversely between adenomas and adenocarcinomas, thus suggesting that they evolve differently.

A possible role for immune complexes in the degradation of cartilage (rheumatoid arthritis and antigen induced arthritis) has been modelled in vitro by studying interactions between cultured bovine chondrocytes and monomeric (M) or heat aggregated (HA) IgG. Concentrations of IgG used were within the range of values reported in the synovial fluids of rheumatoid joints. ELISA and rosetting assays revealed Fc receptor mediated binding of MIgG and HAIgG to chondrocytes that had been cultured, but not to freshly isolated cells. Both forms of IgG stimulated the production of metalloprotease, but only HAIgG boosted generation of superoxide anion and reduced proteoglycan synthesis. HAIgG also stimulated cells to produce immunoreactive interleukin 1 although no biological activity was apparent. It is concluded that the equivalent behavior of chondrocytes in vivo, triggered by immune complexes, could contribute or lead directly to matrix degradation.

A survey carried out on lymphocyte chromosome preparations from 50 normal patients showed that the usual occurrence of C-anaphases is related to mitotic aggregations. This rule was not verified in variant and mutant patients exhibiting a high rate of C-anaphases.

We report the occurrence of Townes-Brocks syndrome (TBS) in an infant with a two break reciprocal translocation between chromosome 5 and chromosome 16. The occurrence of both abnormalities in the same subject could be due to chance. However, it is of interest to note that a familial case of TBS associated with an inv(16) with the same breakpoint at 16q12.1 has been reported. We suggest the possible disruption of the TBS gene at this breakpoint.

Cartilage from patients with rheumatoid arthritis and from animals with antigen-induced arthritis is frequently contaminated with complement-containing immune complexes. A possible role for complement activation in cartilage degradation was modeled in vitro by exposing cultured bovine chondrocytes to homologous serum, and determining cytotoxicity by monitoring the release of intracellular 51Cr. Complement activation was found to be cytotoxic, having maximal effect at 20-30% serum by 18 h. Serum toxicity was ablated by heat (50 degrees C, 20 min) or methylamine treatment but not by EGTA, suggesting that in these experiments activation occurred by the alternate route. The implications of the results are discussed in relation to ultrastructural evidence for the involvement of complement in the pathogenesis of cartilage degradation in inflammatory arthritis.

The authors report their experience of 790 villous specimens taken either early (for 430 cases) or late (360 cases) between 10 and 37 weeks of amenorrhea (WA) using a transabdominal syringe. In the early choriocentesis cases, they conclude that use of the transabdominal route after 12.5 WA, regardless of the position of the chorion, makes it possible significantly to reduce the rate of fetal loss which becomes similar to that for amniocentesis. Placentocentesis has been used at later stages, either for high-risk couples as an alternative to amniocentesis (183 cases), or in cases of ultrasound abnormalities (177 cases) as an alternative to amniocentesis or cordocentesis. Placentocentesis makes it possible to obtain the fetal karyotype very rapidly within 1 to 2 days.

In order to investigate the clinical and pathological features of arthritis mutilans, the clinical history, activity of inflammation, histological findings and treatment have been studied on the basis of follow-up of rheumatoid arthritis (RA) patients with arthritis mutilans. A high incidence of arthritis mutilans was observed in rheumatoid patients who have a younger onset, longer history and higher activity of RA without specific pathophysiological features. Joint destruction may further progress in arthritis mutilans despite intensive treatment with disease modifying anti-rheumatic drugs (DMARDs), and multi-joint replacement may be required in the patients with this type of arthritis.

Our study relates to damage of articular cartilage by deposition of immune complexes. Addition of IgG to cultured chondrocytes affected their metabolism--boosting metalloprotease synthesis, generating superoxide anion (O2-), and reducing the synthesis of sulfated glycosaminoglycans (S-GAG). Heat aggregation of the IgG enhanced its effect on O2- and S-GAG. Some interleukin 1 beta (38 pg/ml) was detected by ELISA after exposure to heat aggregated IgG. There was no cytotoxic effect due to IgG alone, but addition of complement (5% bovine serum) caused significant loss of intracellular 51Cr, which was further increased by addition of heat aggregated IgG. Similar responses of chondrocytes in vivo might account for immune complex mediated damage of cartilage.

The authors report their experience with fine needle chorionic villus sampling carried out transabdominally. Six hundred antenatal karyotype diagnoses were made using this method. The indications were: maternal age: 509 (85%), previous chromosomal abnormalities: 57 (9.5%), parental chromosomal abnormalities: 19 (3%), X chromosome linked diseases: 9 (1.5%), others: 6 (1%). The patients were divided into two groups according as to whether the test was carried out before or after 12 weeks of amenorrhea (Group 1 and Group 2). Each group was divided into two sub-groups according to whether the amniotic membranes were broken or not. The test was carried out using a 20 gauge needle under ultrasound control with a to-and-fro movement using continuous aspiration. The success rate was 98.4%. Minor complications were rare. Contractions 9 (1.5%), spotting 4 (0.6%), small haematomas 13 (2.1%), loss of amniotic fluid 4 (0.6%). The level of unintentional abortions depended on the duration of the pregnancy and whether the amniotic cavity or not was entered. In group 1 (before or at 12 weak amenorrhea) there were 2 abortions out of 124 cases (1.6%) and if the needle entered the amniotic cavity 10 out of 57 cases (17.5%). In group 2 (after 12 weeks of amenorrhea) there was no ill effect from going into the amniotic cavity to the rest of the pregnancy. The abortion rates was 6 out of 419 (1.43%). There were no false positive or negative results.(ABSTRACT TRUNCATED AT 250 WORDS)