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Biomedical subjects

S Miot

Publications and source records attributed to S Miot.

14 recordsLinked to original sources
PubMed2006

Cartilage tissue engineering by expanded goat articular chondrocytes.

In this study we investigated whether expanded goat chondrocytes have the capacity to generate cartilaginous tissues with biochemical and biomechanical properties improving with time in culture. Goat chondrocytes were expanded in monolayer with or without combinations of FGF-2, TGF-beta1, and PDGFbb, and the postexpansion chondrogenic capacity assessed in pellet cultures. Expanded chondrocytes were also cultured for up to 6 weeks in HYAFF-M nonwoven meshes or Polyactive foams, and the resulting cartilaginous tissues were assessed histologically, biochemically, and biomechanically. Supplementation of the expansion medium with FGF-2 increased the proliferation rate of goat chondrocytes and enhanced their postexpansion chondrogenic capacity. FGF-2-expanded chondrocytes seeded in HYAFF-M or Polyactive scaffolds formed cartilaginous tissues with wet weight, glycosaminoglycan, and collagen content, increasing from 2 days to 6 weeks culture (up to respectively 2-, 8-, and 41-fold). Equilibrium and dynamic stiffness measured in HYAFF M-based constructs also increased with time, up to, respectively, 1.3- and 16-fold. This study demonstrates the feasibility to engineer goat cartilaginous tissues at different stages of development by varying culture time, and thus opens the possibility to test the effect of maturation stage of engineered cartilage on the outcome of cartilage repair in orthotopic goat models.

Animals↗
PubMed2005

Crossed retroperitoneal approach to the internal iliac artery: a preliminary anatomical study.

The internal iliac arteries (IIA), and especially the distal segment, course very deep in the pelvis and are generally difficult to access surgically. The recent development of simple and reliable methods to investigate proximal ischemia of the lower extremities has led to discovery of more candidates for elective revascularization of the IAA. The classic approaches to the IAA, i.e., the transperitoneal and homolateral retroperitoneal routs have certain disadvantages. We present a new crossed retroperitoneal approach to the IAA and the results of such method in six cadavers. In all six cases, the entire IAA could be exposed without any particular problems. This novel approach to the IAA seems to be both simple and reproducible.

Aged↗
PubMed2003

[Lactate measurements and acid-base balance in cord blood].

OBJECTIVE: To compare two techniques of lactate measurements in cord blood: either by electrochemical strip method with Lactate Pro of KDK in the umbilical artery alone (series 1) or by enzymatic method with Rapid lab Analyzer of Bayer in the two vessels (series 2) with acid base balance being also determined. SUBJECTS AND METHODS: Series 1 included 353 neonates with a mean gestational age of 37 (+/- 3.6) weeks and series 2 included 410 newborns with a mean gestational age of 38 (+/- 3.1) weeks. RESULTS: Data was presented as mean and SD. In the first series mean umbilical artery lactate concentration was 3.71 (+/- 1.81) mmol/l. In the second series mean umbilical artery blood gas and lactate levels were as follows: pH = 7.25 (+/- 0.9), pCO2 = 6.55 (+/- 1.39) kPa; BD = 6.61 (+/- 3.33) mmol/l, lactate 3.92 (+/- 1.81) mmol/l. The 3rd percentile of pH was 7.05 whereas the 97th percentile of lactate was 7.54 mmol/l. There was a close correlation between lactate and pH, and lactate and BD. Lactate concentration was higher in case of instrumental delivery compared to spontaneous one: 4.65 versus 3.76 mmol/l (p = 0.0001, Student test). No perfect correlation was found between lactate level and neonatal outcome but there was not a significant number of neonates with immediate complication. CONCLUSION: Lactate measurements obtained with single use strip method are valuable and easy to perform.

Acid-Base Equilibrium↗
PubMed2001

No complement receptor 1 stumps on podocytes in human glomerulopathies.

BACKGROUND: Type one complement receptor (CR1) is the only physiological inhibitor of complement on podocytes. CR1 is lost in different glomerulopathies, in particular in lupus nephritis, in which it has been suggested that CR1 is removed by proteolysis from the cell membrane. METHODS: To define whether proteolytic cleavage of CR1 on podocytes is a general phenomenon, we analyzed the expression of CR1 in different glomerulopathies using a monoclonal antibody against epitopes present on the extracellular portion of the molecule and a polyclonal antibody directed at the intracellular tail of CR1. The two antibodies were applied on sequential serial histologic sections of renal biopsy. RESULTS: In normal glomeruli, the two antibodies provided similar results, that is, strong staining of podocytes, and both were shown to recognize specifically CR1. Decreased expression of the extracellular portion of CR1 was observed in lupus nephritis (8/8), focal and segmental glomerulosclerosis (FSGS; 7/7), IgA nephritis (6/6), membranous glomerulonephritis (3/3), and minimal change disease (3/3). In each case, the decreased expression was accompanied by a simultaneous decrease of the expression of the intracellular tail of CR1 (Spearman's correlation coefficient rs = 0.951, P < 0.001). This observation was confirmed by analyzing focal glomerular lesions on sequential serial sections. CONCLUSION: These data indicate that there are no CR1 stumps on podocytes, even in lupus nephritis, and suggest that the CR1 loss on podocytes is not due to consumption but to decreased synthesis. A loss of CR1 synthesis might render podocytes highly sensitive to complement attack.

Antibodies, Monoclonal↗
PubMed2000

Molecular cloning of the critical region for glomerulopathy with fibronectin deposits (GFND) and evaluation of candidate genes.

Glomerulopathy with fibronectin deposits (GFND, MIM 601894) is an autosomal dominant kidney disease that leads to terminal renal failure at a median age of 47 years. It represents a distinct entity of membranoproliferative glomerulonephritis (MPGN) type III and is characterized by the unique feature of massive glomerular deposits of fibronectin. We have recently localized a gene locus for GFND to human chromosome 1q32 by total genome linkage analysis in a large kindred, within a 4.1-cM critical interval between markers D1S2872 and D1S2891. This interval contains a cluster of genes for "regulators of complement activation" (RCA), which represent strong candidates for GFND. To identify positional candidate genes for GFND within the critical genetic interval, we here report the cloning of the entire critical GFND region in a complete YAC and partial PAC contig. We constructed a high-resolution transcriptional map, thereby defining positional and functional candidate genes for the disease. To evaluate their role in GFND, we performed functional studies on RCA proteins in GFND patients from the large kindred, as well as mutational analysis of the genes for complement receptor-2 (CR2), membrane cofactor protein (MCP), and decay accelerating factor (DAF). Although no loss-of-function mutation has been identified as yet, these data provide a basis for the examination of candidate genes for GFND and other genes for MPGN, which localize to the vicinity of the GFND region.

Adult↗
PubMed1999

Elastase and metalloproteinase activities regulate soluble complement receptor 1 release.

Complement receptor 1 (CR1) is cleaved from the surface of polymorphonuclear cells (PMN) in the membrane-proximal region to yield a soluble fragment (sCR1) that contains the functional domains. The enzymes involved in this cleavage are produced by the PMN itself, since in vitro stimulation of purified PMN is followed by sCR1 release. Purified human neutrophil elastase (HNE) cleaved CR1 from erythrocytes and urinary vesicles originating from podocytes and enhanced tenfold the cleavage of CR1 from activated PMN. The largest fragment released from PMN by HNE was identical in size to CR1 shed spontaneously. The CR1 fragments cleaved from erythrocytes were functional. The shedding of sCR1 by activated PMN was inhibited by phenylmethylsulfonyl fluoride (80 +/- 10%), alpha1-antiprotease (50 +/- 5%) and elafin (60 +/- 5%). Furthermore the cleavage was blocked by the metalloprotease inhibitor 1,10-phenanthroline (70 +/- 6 %) as well as by a monoclonal antibody against human neutrophil collagenase MMP8 (40 +/- 10%). Maximal inhibition of sCR1 shedding was obtained by a combination of 1,10-phenanthroline with elafin (86 +/- 6%). These inhibitors had no effect on L-selectin shedding, indicating that the cleavage of CR1 was specific. In conclusion, elastase or elastase-like activity may be responsible for the shedding of functional sCR1 in vivo, and this activity is controlled by the local release of PMN metalloproteases and alpha1antiprotease.

Complement C3b↗
PubMed1996

Molecular cloning of a hemopexin-like cDNA from rainbow trout liver.

Hemopexin is an abundant heme-binding serum protein synthesized in the liver and for which the sequence is determined only for mammals. Little is known about fish heme-binding proteins. We have cloned a rainbow trout complementary DNA that encodes a 445 amino acid polypeptide exhibiting an overall 30% homology with human hemopexin and 69% with the goldfish warm temperature acclimation-related 65-kDa protein. Structural homology, deduced from hydrophobic cluster analysis (HCA), was strong between the trout and human proteins since global HCA scores of 76% were obtained when the N- or C-terminal halves of the two proteins were compared. Moreover, several characteristics of hemopexin were found in the trout protein; finally, the trout hemopexin-like messenger RNA was specifically expressed in the liver. We conclude that the trout protein is a good candidate for a true fish hemopexin.

Amino Acid Sequence↗
PubMedDate not supplied

[Cesarean section for failed vacuum extraction: risk factors and maternal and neonatal outcomes].

OBJECTIVE: To evaluate risk factors associated with failed attempts of vacuum extraction and their outcomes. PATIENTS AND METHODS: All trial vacuum extractions (metal Minicup) from 1992 to 2000 in Besançon University Hospital Center were retrospectively analysed, namely 2447 cases. Univariate and multivariate analyses of failed vacuum extraction risk factors and descriptive analyse of outcomes were performed. RESULTS: The rate of failed vacuum extractions was 3.47% (85/2447). A multivariate analysis showed the following independent risks factors in failed extraction: extraction above pelvic level + 2 (OR = 1.8; CI 95%: 1.1-3), newborn weight (OR = 2.9; CI 95%: 1.8-4.9), parity >2 (OR = 0.08; CI 95%: 0.01-0.6). In case of failed vacuum extraction, newborns had a significantly higher rate of Apgar score <7 at 1 min (P = 0.0002), but not at 5 min. These newborns were most regularly admitted in pediatric care units (P = 0.01). CONCLUSION: The failed trial attempt vacuum extraction rate stays low. These failed instrumental extractions are more common in an extraction above pelvic + 2, a high fetal weight and an arrest during the second stage of labor. There is an increased adverse neonatal outcome. Clinical fetal weight estimation and diagnosis of presentation level in mother pelvis must be performed before vacuum extraction.

Adolescent↗