Prosthetic reconstruction after surgical resection of fibrous dysplasia of the maxillary and palatine bone.

Fibrous dysplasia is a rare disorder of the bone. It is seen in two main forms of presentation: monostotic and the polyostotic. A case of monostotic fibrous dysplasia of the maxillary and palatine bones in a 22-year old man who received prosthetic reconstruction is presented with a review of the literature.

Metabolism and DNA single strand breaks induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and its analogues in primary culture of rat hepatocytes.

Previous studies have shown that the tobacco specific nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is hepatocarcinogenic and results in alkylation of hepatic DNA in F344 rats. In this study, we have characterized the metabolism of NNK in cultured rat hepatocytes and have established the relationship between various metabolic pathways and the induction of DNA single strand breaks. DNA fragmentation by NNK and two other related N-nitrosamines, N'-nitrosonornicotine and nitrosodimethylamine, were compared. Metabolism of [5-3H]NNK (4.5 microM) by carbonyl reduction, alpha-carbon hydroxylation, and pyridine N-oxidation was linear from 0 to 6 h and with 0 to 2 x 10(6) hepatocytes. Using the alkaline elution assay, we observed that NNK induces DNA single strand breaks (SSB) in a dose (1-10 mM) and time (0.5-6 h) dependent manner. SSB induced by NNK (5 mM; rate of elution between 3 and 9 h, 0.117) are rejoined partially within 2 h (rate, 0.039) and totally 12 h after exposure. NNK N-oxide (5 mM) produces a smaller number of SSB (rate, 0.017) than NNK (rate, 0.105) suggesting that pyridine N-oxidation of NNK is a deactivation pathway. Hydrolysis of carbethoxy-nitrosaminomethane and 4-(N-carbethoxy-N-nitrosamino)-1-(3-pyridyl)butanone yields methyldiazohydroxide and 4-(3-pyridyl)-4-oxobutyl-diazohydroxide, respectively. These two alkylating intermediates are generated during alpha-carbon hydroxylation of NNK. After treatment of hepatocytes with 5 microM carbethoxynitrosaminomethane and 1 mM 4-(N-carbethoxyl-N-nitrosamino)-1-(3-pyridyl)butanone, the rates of DNA elution were 0.092 and 0.120, respectively. Carbonyl reduction of NNK leads to 4-(methylnitrosamino)-1-(3-pyridyl)butan-1-ol (NNAl). Reaction of NNK with methyl magnesium iodide gives 1-MeNNAl with 82% yield, NNAl but not 1-MeNNAl can be reoxidized to NNK. Both 5 mM NNAl (rate, 0.073) and 5 mM 1-MeNNAl (rate, 0.054) induce SSB indicating that NNAl does not require reconversion to NNK to be activated to DNA damaging intermediates. alpha-Methylene hydroxylation of NNK results in an equimolar formation of methyldiazohydroxide and 4-oxo-4-(3-pyridyl)-butanal. This aldehyde, at a concentration of 1 mM, induces the same frequency of SSB (rate, 0.116) as 5 mM NNK (0.105) and could possibly play a role in the carcinogenicity of NNK.(ABSTRACT TRUNCATED AT 400 WORDS)

Cytotoxicity, sister-chromatid exchanges and DNA single-strand breaks induced by 4-oxo-4-(3-pyridyl)butanal, a metabolite of a tobacco-specific N-nitrosamine.

The tobacco-specific N-nitrosamine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is metabolized by alpha-carbon hydroxylation to reactive diazohydroxides and aldehydes. The aim of this study was to determine the relative ability of one NNK-derived aldehyde, 4-oxo-4-(3-pyridyl)butanal, to induce cytotoxicity, sister-chromatid exchanges (SCEs) and DNA single-strand breaks (SSBs) in V79 cells. Our data demonstrate that this aldehyde is cytotoxic for V79 cells (IC50 = 0.4 mM) and induces SCEs at concentrations ranging from 0.01 to 0.5 mM. DNA SSBs were observed at concentrations ranging from 0.05 to 1 mM and were repaired within 8 h. When V79 cells were cultured with primary hepatocytes, there was a reduction in the frequency of SCEs induced by the aldehyde. This suggests that hepatocytes can partially deactivate the aldehyde. Our results suggest that this aldehyde is one of the reactive intermediates generated during NNK metabolism.

Facial palsy associated with leptospirosis.

INTRODUCTION: The authors report a rare case of facial palsy associated with leptospirosis. CASE REPORT: A 60-year-old man was admitted to ICU with severe leptospirosis. On the eighth day of hospitalisation, he developed left peripheral facial palsy with a favourable course in response to corticosteroids. DISCUSSION: Several types of neurological complications of leptospirosis have been reported: encephalitis, myelitis, stroke, cerebral arteritis, mononeuritis, polyradiculoneuropathy, and cranial nerve palsy. Peripheral facial palsy is a rare complication of leptospirosis. CONCLUSION: This case illustrates the possible association between leptospirosis and facial palsy.

Prosthetic reconstruction after surgical resection of fibrous dysplasia of the maxillary and palatine bone / Reconstrucción prostética tras la resección quirúrgica de la displasia fibrosa del hueso maxilar y el palatino

Fibrous dysplasia is a rare disorder of the bone. It is seen in two main forms ofpresentation: monostotic and the polyostotic. A case of monostotic fibrous dysplasia of the maxillary and palatine bones in a 22-year old man who received prosthetic reconstruction is presented with a review of the literature.

La displasia fibrosa es un trastorno raro del hueso. Se le ve en dos formas principales: la monostótica y la poliostótica. Junto con la correspondiente revisión de la literatura, se presenta un caso de displasia fibrosa monostótica de los huesos maxilar y palatino en un hombre de 22 anos que recibió una reconstrucción prostética.

Batch cultures of recombinant Lactococcus lactis subsp. lactis in a stirred fermentor. I. Effect of plasmid content on bacterial growth and on genetic stability in pure cultures.

The effect of plasmid introduction into Lactococcus lactis subsp. lactis IL2661 on the growth of this strain and on plasmid stability was studied in pure batch cultures. The plasmids used (coding for erythromycin or chloramphenicol resistance) were the following: pIL205 (42 kb), pIL252 (4.6 kb, 6-9 copies), pIL253 (4.8 kb, 45-85 copies) and pE194 (inserted in the chromosome). Growth and acidification of L. lactis subsp. lactis IL2661 were similar to those of the derived recombinant lactococci. The maximal population at the end of the fermentation (9 h) was about 1.1 +/- 0.3 x 10(10) cfu/ml, and maximal growth rate 0.92 +/- 0.07 h-1. Growth yield and lactic acid concentrations were 3.9 +/- 0.8 x 10(11) cfu/g lactose consumed and 25.6 +/- 2.3 g/l, respectively. Different levels of plasmid stability were detected. Plasmid pE194, and plasmids pIL252 and pIL253 in the absence of pIL205, were stable after 10 h of culture. A slight loss (1-2%) of pIL205 was observed in all strains. In the presence of pIL205, plasmids pIL252 and pIL253 were maintained in only 56-95% of the cells. This result suggested an incompatibility between pIL205 and pIL252 or pIL253.

Batch cultures of recombinant Lactococcus lactis subsp. lactis in a stirred fermentor. II. Plasmid transfer in mixed cultures.

The transfer of plasmids was studied in a stirred fermentor in the course of mixed batch cultures combining recombinant strains of Lactococcus lactis subsp. lactis (donor strains) with L. lactis subsp. lactis CNRZ 268M3 (recipient strain). Donor strains contained one or two of the following plasmids (coding for erythromycin or chloramphenicol resistance): pIL205 (self-transmissible), pIL252, pIL253 (non-transmissible but mobilizable by pIL205, respectively small and large copy number) and pE194 (inserted in the chromosome). Only self-transmissible plasmid pIL205 was transferred, with frequencies ranging from 10(-7) to 10(-8) after 12 h of fermentation. These frequencies were 60-400 times lower than in unstirred M17 broth and 100,000 times lower than on agar medium. In the latter case, non-transmissible plasmids pIL252 and pIL253 were mobilized by pIL205 with a frequency of about 10(-5) - 10(-6).

Characterization of activation and deactivation pathways of 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) in rat hepatocytes.

We have characterized the metabolism of 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butanone (NNK) in cultured rat hepatocytes and have established the relationship between various metabolic pathways and single-strand breaks (SSB) in DNA. Metabolism of [5-3H]-NNK by carbonyl reduction, alpha-carbon hydroxylation and pyridine N-oxidation was linear from 0.5 to 6 h with 0.25-2 x 10(6) hepatocytes. Using an alkaline elution assay, we observed that NNK induces SSB in DNA in a dose- and time-dependent manner. SSB induced by NNK were rejoined partially within 2 h and totally by 12 h after exposure. NNK-N-oxide produced a smaller number of SSB than NNK, suggesting that pyridine N-oxidation of NNK is a deactivation pathway. Carbonyl reduction of NNK led to 4-(N-nitrosomethylamino)-1-(3-pyridyl)-1-butan-1-ol (NNAl). Reaction of NNK with methyl magnesium iodide gave 4-(N-nitrosomethylamino)-1-(methyl)-1-(3- pyridyl)butanol-1-ol (1-MeNNAl) 82% yield. NNAl, but not 1-MeNNA1, can be reoxidized to NNK. Doses of 5 mM NNAl and 1-MeNNAl both induced SSB, indicating that NNAl does not require reconversion to NNK to be activated to DNA damaging intermediates. alpha-Methylene hydroxylation resulted in the formation of 4-oxo-4-(3- pyridyl)butanal. At equimolar concentration (5 mM), the aldehyde was more damaging than NNK to hepatocyte DNA. The results of this study demonstrate that NNK is activated by rat hepatocytes and that metabolites formed by alpha-carbon hydroxylation induce SSB.

[Wegener's granulomatosis. Apropos of a case]. / Granulomatose de Wegener. A propos d'un cas.

A rare case of granulomatosis of Wegener is rapported in this study. One patient presented with ENT and pulmonary symptoms. The differential diagnosis with tuberculosis was raised. Based on a literature review, the authors discuss clinical, pathological and imaging features of the condition and its management.