Le Controle D'activité du Vaccin Antipoliomyélitique

Conclusions Les limites de validité de la méthode de détermination de la valeur antigénique du poliovaccin ont été vérifiées en se basant sur une expérience de 3 ans. Cette étude a permis de déterminer les limites entre lesquelles un test peut être reconnu comme valable et significatif. En fonction de ces données, un test simplifié est proposé. Dans ce test, le rapport d'antigénicité est établi rapidement au moyen d'un nomogramme. La méthode utilisée dans notre laboratoire a servi à rechercher le degré de stabilité de l'antigène poliomyélitique. De ces résultats, il ressort que la période de conservation du poliovaccin ne devrait pas dépasser 1 an. Au terme de cette période, le vaccin a perdu environ 50% de son activité antigénique initiale. La combinaison de l'antigène poliomyélitique à d'autres antigènes et son absorption sur aluminium n'interfèrent pas avec la technique de détermination. La stabilité des vaccins combinés est variable, il est indiqué d'effectuer des essais de stabilité de ces préparations afin d'obtenir une standardisation de l'activité de l'antigène poliomyélitique dans ces vaccins. Communication présentée au 6^e Congrès de Standardisation Microbiologique, Wiesbaden, Septembre 1960.     

Antiviral Activity of Polyacrylic and Polymethacrylic Acids: II. Mode of Action in Vivo.

A marked virus-inhibiting potency is obtained in the serum after intraperitoneal injection of polyacrylic acid (PAA) and polymethacrylic acid (PMAA) in mice. Much higher antiviral levels were reached than for other related polymers including dextran sulfate, heparin, polyvinyl sulfate, pyran copolymer, polystyrene sulfonate, and macrodex. The broad antiviral action of PAA and PMAA was attributed both to a direct interference with the virus-cell interaction and the viral ribonucleic acid metabolism and to the formation of an interferon-like factor. Both polyanions differed in interferon-inducing ability: highest serum interferon titer was obtained 18 hr after the intraperitoneal injection of PAA. The mechanism of interferon production by PAA and PMAA is discussed. As described previously for Sindbis virus and endotoxin, the animals also became hyporeactive after injection of PAA.     

Granulomatous skin lesions complicating Varicella infection in a patient with Rothmund-Thomson syndrome and immune deficiency: case report

Acro-cardio-facial syndrome (ACFS) is a rare genetic disorder characterized by split-hand/split-foot malformation (SHFM), facial anomalies, cleft lip/palate, congenital heart defect (CHD), genital anomalies, and mental retardation. Up to now, 9 patients have been described, and most of the reported cases were not surviving the first days or months of age. The spectrum of defects occurring in ACFS is wide, and both interindividual variability and clinical differences among sibs have been reported. The diagnosis is based on clinical criteria, since the genetic mechanism underlying ACFS is still unknown. The differential diagnosis includes other disorders with ectrodactyly, and clefting conditions associated with genital anomalies and heart defects. An autosomal recessive pattern of inheritance has been suggested, based on parental consanguinity and disease's recurrence in sibs in some families. The more appropriate recurrence risk of transmitting the disease for the parents of an affected child seems to be up to one in four. Management of affected patients includes treatment of cardiac, respiratory, and feeding problems by neonatal pediatricians and other specialists. Prognosis of ACFS is poor.     

Effect of tocilizumab on ischemia-reperfusion-induced oxido-inflammatory renal damage and dysfunction in rats

Ischemia-reperfusion-induced (I/R) renal damage is a pathogenic process that starts with ischemia, then progresses through oxidative stress and inflammation. Tocilizumab (TCZ), a recombinant human monoclonal antibody produced against the IL-6 receptor, will be tested against renal I/R injury. TCZ is known to lower the levels of proinflammatory cytokines and oxidant mediators while raising the amounts of antioxidant molecules. Our purpose is to evaluate the biochemical and histological effects of TCZ against I/R-induced oxido-inflammatory kidney damage and dysfunction in rats. Animals were divided into 3 groups as renal I/R (RIR), I/R+ TCZ (IRT), and healthy group (HG). TCZ was administered at a dose of 8 mg/kg to the IRT group (n=6) of the animals, and distilled water as a solvent was administered intraperitoneally (ip) to the RIR (n=6) and HG (n=6) groups. Then, two hours of ischemia and six hours of reperfusion were applied to the left kidneys of IRT and RIR animals. TCZ significantly inhibited the increase in the levels of malondialdehyde (MDA), nuclear kappa B (NF-κB), tumour necrosis factor alpha (TNF-α), interleukin 1-β (IL-1β), IL-6, creatinine (Cr) and blood urea nitrogen (BUN) and decrease in total glutathione (tGSH) with I/R in renal tissue. TCZ also attenuated severe histopathological damage due to I/R in renal tissue. TCZ protected renal tissue from I/R-induced oxidative and inflammatory damage. These results indicate that TCZ may be useful in the treatment of renal I/R injury.     

In Vivo Expansion of Co-Transplanted T Cells Impacts on Tumor Re-Initiating Activity of Human Acute Myeloid Leukemia in NSG Mice

Human cells from acute myeloid leukemia (AML) patients are frequently transplanted into immune-compromised mouse strains to provide an in vivo environment for studies on the biology of the disease. Since frequencies of leukemia re-initiating cells are low and a unique cell surface phenotype that includes all tumor re-initiating activity remains unknown, the underlying mechanisms leading to limitations in the xenotransplantation assay need to be understood and overcome to obtain robust engraftment of AML-containing samples. We report here that in the NSG xenotransplantation assay, the large majority of mononucleated cells from patients with AML fail to establish a reproducible myeloid engraftment despite high donor chimerism. Instead, donor-derived cells mainly consist of polyclonal disease-unrelated expanded co-transplanted human T lymphocytes that induce xenogeneic graft versus host disease and mask the engraftment of human AML in mice. Engraftment of mainly myeloid cell types can be enforced by the prevention of T cell expansion through the depletion of lymphocytes from the graft prior transplantation.     

Immunohistochemical profile of CD markers in experimental neural tube defect

ABSTRACT

Neural tube defects (NTDs) are the second most common birth defects worldwide. Stem cells play a critical role in the mechanisms underlying NTDs. We established an experimental NTD model in rats using retinoic acid (RA). We used mesenchymal and hemopoietic stem cell markers to determine their distribution in the mesenchyme in and around the neuroepithelium during the embryonic and fetal periods in both cranial and caudal regions. Adult female rats were given RA on days 5 and 10 of gestation and olive oil was administered to the control group. On days 10.5 and 15.5, embryos in the experimental and control groups were removed from the uterus. Embryos were embedded in paraffin and serial sections of the cranial and caudal neural tube were examined. We found severe cranial and caudal defects including axial rotation in the experimental groups using histochemistry. We used CD44, CD56, CD73, CD90, CD105, CD271 antibodies as mesenchymal stem cell markers and CD14, CD45 as hemopoietic stem cell markers. More CD44, CD56, CD90, CD105 and CD14 were detected during the embryonic period than the fetal period. CD73 was more frequent during the fetal period, whereas CD271 and CD45 were not significantly different. When CD44, CD56, CD73, CD90, CD105, CD271 immunostaining was found, NTDs were decreased early and increased later. We found no significant difference between CD14 and CD45. Formation of NTDs was due to deterioration of the of the neuroepithelial and surrounding stem cells. One reason for the formation of NTDs is that stem cells may develop defective cell-cell or cell-matrix interactions.