The role of platelet-activating factor in the biocompatibility of hemodialysis membranes.
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Biomedical subjects
Publications and source records attributed to S David.
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The gene encoding the lactose transport protein (lacS) of Leuconostoc lactis NZ6009 has been cloned from its native lactose plasmid, pNZ63, by functional complementation of lactose permease-deficient Escherichia coli mutants. Nucleotide sequence analysis revealed an open reading frame with the capacity to encode a protein of 639 amino acids which had limited but significant identity to the lactose transport carriers (LacS) of Streptococcus thermophilus (34.5%) and Lactobacillus bulgaricus (35.6%). This similarity was present both in the amino-terminal hydrophobic carrier domain, which is homologous to the E. coli melibiose transporter, and in the carboxy-terminal enzyme IIA-like regulatory domain. The flanking regions of DNA surrounding lacS were also sequenced. Preceding the lacS gene was a small open reading frame in the same orientation encoding a deduced 95-amino-acid protein with a sequence similar to the amino-terminal portion of beta-galactosidase I from Bacillus stearothermophilus. The lacS gene was separated from the downstream beta-galactosidase genes (lacLM) by 2 kb of DNA containing an IS3-like insertion sequence, which is a novel arrangement for lac genes in comparison with that in other lactic acid bacteria. The lacS gene was cloned in an E. coli-Streptococcus shuttle vector and was expressed both in a lacS deletion derivative of S. thermophilus and in a pNZ63-cured strain, L. lactis NZ6091. The role of the LacS protein was confirmed by uptake assays in which substantial uptake of radiolabeled lactose or galactose was observed with L. lactis or S. thermophilus plasmids harboring an intact lacS gene. Furthermore, galactose uptake was observed in NZ6091, suggesting the presence of at least one more transport system for galactose in L. lactis.
OBJECTIVES: A cross-sectional epidemiologic survey was conducted among prison staff in France to investigate the relationships between work conditions and mental health. METHODS: The sample included men and women 20 to 64 years of age belonging to all categories of prison personnel (prison guards, administrative staff, socioeducational workers, technicians, health care workers, and managers). A postal self-administered questionnaire was used to assess sociodemographic factors, work conditions, and physical and mental disorders. Multiple logistic regression analyses were conducted to determine the effects of work conditions and social relationships on the mental health of prison staff. RESULTS: The results presented in this report only concern depressive symptomatology (measured by the French version of the Center for Epidemiologic Studies Depression Scale), anxiety (measured by the state version of the State-Trait Anxiety Inventory), and sleep disorders. The percentage of mental disorders was higher among prison staff than that determined for other occupational samples. Guards comprised the prison staff least affected by these symptoms. CONCLUSIONS: The results show that, in our sample, the factors concerning the subjective evaluation of work conditions and social support were more closely related to mental disorders than work conditions. In addition, seniority was associated with depressive symptoms and anxiety among the men.
A cross-sectional epidemiological survey was conducted among prison staff in France to investigate the relationships between working conditions and health. The sample included men and women 20 to 64 years old belonging to all categories of prison personnel: prison guards, administrative staff, socioeducational workers, technicians, health care workers, and managers (n = 4587, response rate 45.7%). A mailed self-administered questionnaire was used to assess sociodemographic characteristics, working conditions, and physical and mental disorders. Multiple logistic regression analyses were conducted to determine the effects of working conditions and social relationships on health of prison staff. However, the results reported here only concern 17 health disorders: body mass index, sick leave, medication use, accidents, digestive disorders, lower extremities and back disorders, hypertension, hemorrhoids, arthritis, skin disorders, urinary infections, chronic bronchitis, cholesterol, gastric ulcer, respiratory infections, ocular disorders. The living non professional conditions mostly associated with health disorders were financial difficulties (OR: 1.9 for digestive disorders, 1.8 for gastric ulcer, 1.7 for medication use) and irregularity of meals (OR = 1.5 for digestive disorders, and hypertension). In the occupational environment, the factors most associated with health disorders are seniority (OR = 4.2 for arthritis, 2.3 for cholesterol) and constraints (OR = 1.7 for lower extremities disorders). In spite of some limits associated to this kind of study, relationships between occupational and non occupational factors and physical health conditions were observed; the results also pointed out the protective role of the social relationships for health conditions.
PURPOSE: To evaluate the microleakage of CAD-CAM porcelain inlay restorations cemented with four different dual cure resin cements. MATERIALS AND METHODS: Thirty human extracted caries-free molar teeth were prepared with a Class II MOD cavity design. One proximal box ended on enamel and the other on root surface dentin. The teeth were divided into six groups of five samples each. Two groups were restored with a direct placement composite resin to serve as a control. The other four groups were restored with CAD/CAM-generated ceramic inlays that were cemented with four dual cure resin cements. All specimens were thermocycled. Microleakage of the restorations was assessed by dye penetration. RESULTS: Compared to direct placement resin composite which demonstrated an excellent enamel marginal seal, CAD/CAM-generated porcelain inlays produced excellent marginal seals at both the enamel and dentin interfaces.
A patient with primary non-hodgkins lymphoma of the paranasal sinuses presenting as rhinoorbital myiasis is reported. The myiasis causing species was identified as Chrysomia bezziana Villeneuve. This case demonstrates the extreme destruction caused by myiasis and the inadequacy of therapeutic options available in such patients.
Axon growth inhibitory proteins associated with central nervous system (CNS) myelin are responsible in part for the absence of long distance axon regeneration in the adult mammalian CNS. We have recently reported that myelin-associated glycoprotein (MAG), which is also present in peripheral nerves, is a potent inhibitor of neurite growth. This was surprising given the robust regenerative capacity of peripheral nerves. We now provide evidence that myelin purified from peripheral nerve also has neurite growth inhibitory activity. However, this activity can be masked by laminin, which is a constituent of the Schwann cell basal lamina. We also report that laminin, which is largely absent from the normal adult mammalian CNS, when added to purified CNS myelin, can override the neurite growth inhibitory activity in CNS myelin. These results have important implications for the development of strategies to foster axon regeneration in the adult mammalian CNS where multiple growth inhibitors exist.
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The citrate permease determinant (citP) in several Leuconostoc strains was demonstrated to be plasmid encoded by curing experiments and hybridization studies with a DNA fragment containing the citP gene from Lactococcus lactis subsp. lactis biovar diacetylactis NCDO176. Cloning and nucleotide sequence analysis of Leuconostoc lactis NZ6070 citP revealed almost complete identity to lactococcal citP.
In Klebsiella pneumoniae, six genes, constituting the pqqABCDEF operon, which are required for the synthesis of the cofactor pyrroloquinoline quinone (PQQ) have been identified. The role of each of these K. pneumoniae Pqq proteins was examined by expression of the cloned pqq genes in Escherichia coli, which cannot synthesize PQQ. All six pqq genes were required for PQQ biosynthesis and excretion into the medium in sufficient amounts to allow growth of E. coli on glucose via the PQQ-dependent glucose dehydrogenase. Mutants lacking the PqqB or PqqF protein synthesized small amounts of PQQ, however. PQQ synthesis was also studied in cell extracts. Extracts made from cells containing all Pqq proteins contained PQQ. Lack of each of the Pqq proteins except PqqB resulted in the absence of PQQ. Extracts lacking PqqB synthesized PQQ slowly. Complementation studies with extracts containing different Pqq proteins showed that an extract lacking PqqC synthesized an intermediate which was also detected in the culture medium of pqqC mutants. It is proposed that PqqC catalyzes the last step in PQQ biosynthesis. Studies with cells lacking PqqB suggest that the same intermediate might be accumulated in these mutants. By using pqq-lacZ protein fusions, it was shown that the expression of the putative precursor of PQQ, the small PqqA polypeptide, was much higher than that of the other Pqq proteins. Synthesis of PQQ most likely requires molecular oxygen, since PQQ was not synthesized under anaerobic conditions, although the pqq genes were expressed.
The paper reviews the changes in ameloblast ultrastructure, concomitant with the changes in its functions across the major stages of amelogenesis. It describes the mechanisms associated with the major events in biosynthesis and degradation of the major enamel proteins (amelogenins and tuftelin/enamelins) and with the presecretory and postsecretory mechanisms leading to the heterogeneity of these extracellular matrix proteins. The gene structure, chromosomal localization, protein, primary structure and possible function, and the involvement of the different proteins in X-linked (amelogenin) and possibly in autosomally linked (tuftelin) amelogenesis imperfecta, the most common hereditary disease of enamel, are also discussed.
CD34 positive (CD34+) cells contain all hematopoietic progenitors from stem cells to committed precursors. Therefore the transplantation of purified bone marrow or blood CD34+ cells is sufficient for hematopoietic recovery after a myeloablative radiochemotherapy. Using different techniques, CD34+ progenitors can be induced to undergo terminal differentiation in a stroma-free liquid culture system in the presence of cytokines. In the present study, we have evaluated the functional potential of CD34+ blood progenitors after ex-vivo expansion cultures. CD34+ cells were isolated from 16 samples (PBSC n = 8 and Cord Blood (CB) n = 8) using either ISOLEX 50 (n=6), CEPRATE LC CD34 kit (n = 6) or MICROCELLECTOR T-25 Stem Cell kit (n = 4). CD34+ cells were cultured for seven days in the presence of 500 UI/ML of IL-1, 10 ng/ml of IL-3 and 10 ng/ml of SCF. We obtained an 8-fold expansion of nucleated cells. We observed a 59-fold expansion of GM-CSF responsive committed precursors, a 4.4-fold expansion of IL-1+IL-3+SCF+Epo responsive multilineage progenitors and a 2.2-fold expansion of the 5-FU resistant quiescent progenitors. We did not observe any significant difference in the amplification/expansion parameters between cultures initiated with CD34+ cells from PBSC or CB. Our data show that cytokine mediated ex-vivo expansion of blood CD34+ cells can produce a large number of committed precursors without affecting the compartment of the most immature progenitors. These results suggest that cytokine-mediated amplification technology could be of great interest in the autologous transplantation setting.
Over 1500 treatments of hemofiltration with on-line preparation of substitution fluid were performed in 16 patients. Two patients were treated for over 40 months. On-line preparation of the solution allowed use of bicarbonate as a buffer. 73-74 L/session were infused in pre-dilution modality, at a rate of about 370 ml/min, and the treatment length was above 4 hrs. The good quality of on-line prepared solution was confirmed by the negativity of microbiological tests and by the absence of clinical or sub-clinical reactions in patients. Urea clearance was calculated by equations considering either plasma flow or whole blood flow. Results were 196-197 ml/min and 186-183 ml/min, respectively. The latter was nearer to the value of directly measured clearance (182-173 ml/min). Kt/V urea was about 1 per session and PCR ranged between 1.3 and 1.4 g/kg/day. A high vascular stability was also observed. Since sodium balance may, at least in part, account for better vascular stability, sodium sieving coefficient was measured during the treatment. The sodium-retaining effect of the increase of protein concentration within the filter, due to the ultrafiltration, was less relevant in pre-dilution hemofiltration if compared to post-dilution hemofiltration. It has been calculated that to obtain a sodium balance similar to that of the hemodialysis (HD), the sodium concentration of infusion solution should be about 2 mEq/L higher than HD dialysis solution. However, difficulty in performing accurate balance studies prevents a general agreement on these conclusions.
Coronary spasm may occur with angiographically normal and diseased coronary arteries. General anesthesia has been described only rarely as a triggering event for coronary artery spasm, and only once before in the presence of angiographically normal coronary arteries. We have now seen three patients presenting with acute ST-segment elevation following induction of general anesthesia with enzyme evidence of myocardial necrosis in two patients. Cardiac catheterization was performed in all three patients with one of the procedures performed on an emergency basis owing to hemodynamic compromise. All three patients demonstrated angiographically normal coronary arteries. The electrocardiograms and coronary arteriograms are presented, and possible mechanisms for the injury pattern seen on the electrocardiogram are discussed. Coronary vasospasm causing an acute injury pattern on the electrocardiogram can be caused by general anesthesia and has to be recognized promptly and treated appropriately to prevent more serious complications.
Astrocytes purified from the neonatal rat brain were cultured for up to 3 weeks prior to being treated with agents that can induce reactive changes in astrocytes. These agents included dibutyryl cAMP, interleukin-1 beta, and macrophage conditioned media. After treating astrocytes for 3 days, the agents were removed and the ability of the astrocytes to support neurite growth was assessed by plating neonatal rat cerebellar cortical neurons. All the agents increased the ability of astrocytes to support the growth of long neurites. This was particularly evident with astrocytes treated with dibutyryl cAMP and LPS macrophage-conditioned medium. These results provide direct evidence that the reactive changes induced in astrocytes in this in vitro model might aid the growth of neurites. Similar changes may underlie the injury-induced axonal sprouting that occurs in vivo.