[Sudden death due to primary systemic amyloidosis].
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Biomedical subjects
Publications and source records attributed to M Rochet.
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We report the complete sequence of two cosmids, SPBC19C7 (34815 bp insert, Accession No. AL023859) and SPBC15D4 (33203 bp insert, Accession No. AL031349), localized on chromosome II of the S. pombe genome. Twelve open reading frames (ORFs) were identified in SPBC19C7 and 16 in SPBC5D4. Two known genes were found on each cosmid: cyr1 and uve1 on SPBC19C7, encoding adenylate cyclase and a UV-endonuclease, respectively, and gpt and pho2 on SPBC15D4, encoding an N-acetylglucosamine-1-phosphate transferase and a4-nitrophenylphosphatase, respectively. Five ORFs similar to known proteins were found on SPBC19C7, and six on SPBC15D4. They include putative genes for a ubiquitin protein ligase, a prolyl-tRNA synthetase, a tRNA splicing endonuclease, a voltage-gated chloride channel, a mannosyl transferase, a kinesin-like protein, a histone transcriptional regulator, an N-acetyltransferase, a cystathionine gamma-synthase and a TFIID subunit. Two ORF products of SPBC15D4 do not have clear homologues: one encodes a putative transcriptional regulator with a binuclear zinc domain and the other a protein with six transmembrane domains. Two ORFs from SPBC15D4 are similar to unknown ORFs, one from Saccharomyces cerevisiae and the other from Caenorhabditis elegans. Finally, two ORFs of SPBC19C7 and six of SPBC15D4 correspond to orphan genes. The frequent occurrence of introns and the short and degenerated intron-exon boundaries consensus sequences significantly complicated ORF predictions. Two potential ORF-free regions spanning several kb were predicted, and a clustering of ORFs transcribed in the same orientation was observed.
We report the complete sequence of two cosmids, SPCC895 (38457 bp insert, EMBL Accession No. AL035247) and SPCC1322 (42068 bp insert, EMBL Accession No. AL035259), localized on chromosome III of the Schizosaccharomyces pombe genome. Fourteen Coding DNA sequences (CDSs) were identified in SPCC895 and 17 in SPCC1322. Two known genes were found in each cosmid: map2 and gms1 on SPCC895, encoding the mating type P-factor precursor and an UDP-galactose transporter, respectively, and bub1 and ade6 in SPCC1322, encoding a protein kinase and a phosphoribosylaminoimidazole carboxylase, respectively. The fission yeast K RNA gene has been localized to SPCC895. Three ribosomal proteins have been predicted among these two cosmids. Nine CDSs similar to known proteins were found on SPCC895, and seven on SPCC1322. They include putative genes for an uridylate kinase, a proteasome catalytic component, an ion transporter, a checkpoint protein, a translation initiation protein, a SNARE complex protein, a protein involved in cytoskeletal organization, a spindle pole body-associating protein, pre-mRNA splicing factor RNA helicase, a 3'-5' exonuclease for RNA 3' ss-tail, an UTP-glucose-1-phosphate uridylyltransferase, a leukotriene A(4) hydrolase, a member of the RanBP7-importin beta-Cse1p superfamily, a Ca(++)-calmodulin-dependent serine/threonine protein kinase and a prohibitin antiproliferative protein. One CDS is predicted to be an integral membrane protein. One CDS from SPCC895 is similar to a CDS of unknown function from Saccharomyces cerevisiae and three from SPCC1322 are similar to CDSs of unknown function from Candida albicans, S. cerevisiae and Sz. pombe, respectively. Finally, one CDS of SPCC895 and three of SPCC1322 correspond to orphan genes.
This retrospective study was performed to evaluate the interest of cytology in the diagnosis of pulmonary carcinomas. Bronchial samples were collected from 330 patients known to display a macroscopic lesion which was detected by bronchoscopy. Cytological analysis of the bronchial brushings and washings, removed at the first fibroscopy, allowed the diagnosis of malignancy in 92% of the cases analyzed whereas the biopsy confirmed the malignancy in 77% of the cases. In conclusion cytological studies gave information on malignity and classification in 90% of the cases. However histological classification only could guarantee the choice of the best treatment regimen.
NotI and SfiI genomic restriction maps were used to detect and characterize a ring chromosome II in a Schizosaccharomyces pombe strain with a meiotic defect on chromosome II. The ring chromosome was formed by an intrachromosomal fusion near, or at, the very ends of chromosome II.
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A 78 year old woman with a history of maxillary ameloblastoma from age of 38 years was found on routine examination to have a pulmonary image of the balloon release type. The lesion was atypical with respect to its clinical tolerance and slow progression. Pathology of several nodules removed by surgical lung biopsy confirmed the benign nature and identity of the maxillary and pulmonary lesions. The diagnosis was therefore pulmonary metastases from a benign ameloblastoma. The age of the patient and slow course of the lesion, combined with the absence of any functional disorder, was the basis for the decision not to operate on the pulmonary lesion. The concept of benign metastatic ameloblastoma is analyzed and findings compared with data in the literature.
We report the observation of a 78 year old patient who had a plexiform ameloblastoma since the age of 38. A systematic pulmonary radiographic examination revealed multiple dense nodules like "cannon ball secondaries". However the histology of these pulmonary nodules, obtained by open lung biopsy, was identical with the primary tumour and showed no evidence of malignancy. The dispersion to the lungs was probably explained by inhalation of tumour cells, itself favoured by 8 surgical curettages. The progress of these pulmonary lesions was as slow as the primary tumour. No therapeutic trial was attempted on the grounds of age, perfect clinical tolerance and the absence of any known therapeutic protocol which would be active.
A bronchial P cell carcinoid, which was negative for all hormones immunocyto chemically tested, showed a globular intracytoplasmic inclusion in almost every cell. The inclusions were not clearly distinguishable using the haematoxylin- eosin- safran procedure; they were best demonstrated with the Masson trichrome stain and the Grimelius technique and were easily detected in 1 micron thick Epon sections as target-like structures. On electron microscopy, they were found to be composed of filamentous aggregates entrapping a few endosecretory granules, which showed degenerative changes. The filaments, 8-10 nm in diameter, lacked any periodicity; they were randomly dispersed in the central area and arranged in broken concentric swirls at the periphery of the inclusions. The globules lacked the tinctorial properties of amyloid, but showed a strong immunostaining for keratin-like proteins. A systematic investigation of 12 APUDomas of bronchial or duodenopancreatic origin, using both light and electron microscopy, identified a few filamentous bodies in one case, a somatostatin cell tumour of ampulla of Vater. In both cases, the structures appeared similar to those previously reported in growth hormone cell pituitary adenomas as well as in a few bronchial or gut carcinoids. Whatever their nature, morphological data suggest that they are related to abnormalities in the secretory function, involving the Golgi apparatus, the endosecretory granules and the microtubular microfilamentous system.
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A case of Wegener's granulomatosis starting as a localized pseudo-tumoral lung lesion and following a fulminating course is reported. The histological diagnosis required thoracotomy. New pulmonary lesions developed post-operatively, together with severe renal failure which was responsible for the patient's death 5 weeks after the thoracotomy. The authors describe the lesions characteristic of the disease and their pathogenesis and discuss the relationship between Wegener's syndrome and other granulomatous angiitis.
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