An elderly woman with dyspnoea and bronchorrhoea. Bronchioloalveolar carcinoma.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to P Gil.
Explore the source record for details and available documents.
OBJECTIVE: The purpose of this study was to assess the value of imaging studies--conventional abdominal radiographs, sonography, and CT--in the diagnosis of gastrointestinal bezoars. METHODS AND METHODS: A review was made of the radiologic findings of 17 consecutive patients with surgically verified gastrointestinal bezoars over a period of 51 months. RESULTS: Twelve patients had a history of previous gastric surgery. In no patient was a bezoar clinically suspected. Phytobezoars were recorded in 16 patients and a trichobezoar in only one. A total of 33 bezoars were identified at surgery. Two patients had isolated gastric bezoars, whereas 15 patients had bezoars located in the small bowel. Among the latter group, associated gastric bezoars were found in eight patients, and five patients had multiple intestinal bezoars. Abdominal radiographs revealed bezoars in three patients, sonography revealed bezoars in 15, and CT revealed bezoars in all 17. Seven patients had associated gastric bezoars revealed at CT versus only two patients with gastric bezoars revealed at sonography. CT revealed multiple intestinal bezoars in five patients whereas sonography revealed them in only two patients. CONCLUSION: Both sonography and CT are reliable methods for diagnosing gastrointestinal bezoars. CT is more accurate, however, and exhibits a quite characteristic bezoar image; in addition, this imaging technique is able to reveal the presence of additional gastrointestinal bezoars.
A study is made of the diagnostic utility of echography in clinically suspected appendicitis, and its influence upon patient management and outcome. A total of 374 consecutive patients with possible appendicitis were prospectively evaluated by ultrasound. Two groups were established: group A (high clinical probability, > or =0.70) and group B (moderate clinical probability, 0.20-0.60). In group-A patients (n = 105, 28%), prevalence of appendicitis = 0.90) underwent surgery regardless of the echographic findings. In group B (n = 269, 72%), prevalence of appendicitis = 0.28) surgery was performed in the event of positive echography, whereas negative echographic findings did not definitively discard appendicitis. The diagnostic utility of echography was evaluated by applying the Pauker-Kasirer threshold approach to clinical decision making. The influence of ultrasound upon outcome was in turn evaluated by contrasting the total appendectomized patients (190 of 374) with a series of 181 individuals subjected to appendectomy prior to the introduction of echography. The probability of appendicitis in the presence of positive echography was 0.95 in group A (sensitivity = 0.92) and 0.89 in group B (sensitivity = 0.91). The probability of appendicitis in the event of negative ultrasound was 0.58 in group A (specificity = 0.55) and 0.03 in group B (specificity = 0.95) . In 46% of cases the echographic findings led to a change in therapeutic regimen. In addition, the incidence of negative appendectomies was significantly reduced (19.3 vs 11.6% with echography; p = 0.03), as was the delay in establishing a diagnosis (under 6 h in 68.5 vs 84.2% with echography; p = 0.002) and the number of medical acts required (three in 71.3 vs 84.1% with echography; p = 0.001). There was no significant reduction in the incidence of perforated appendicitis (17.1 vs 17.9% with echography), in the number of postoperative complications (13.8 vs 7.6% with echography), or in the days of hospital stay (4.44 vs 4.80 with echography). Echography proved useful in group B, and was generally of little utility in group A. The technique had a positive influence on treatment, with management reorientation in a considerable number of patients, and on outcome, since ultrasound contributed to establishing an earlier diagnosis, with a reduction of unnecessary appendectomies.
Photomorphogenesis of higher plants is regulated by photoreceptors including the red/far-red light-absorbing phytochromes, blue-UV/A sensing cryptochromes and as yet uncharacterized UV/B receptors. Specific phototransduction pathways that are controlled by either individual or interacting photoreceptors mediate regulation. Phytochrome B (phyB) is the major red light-sensing photoreceptor. Phototransduction mediated by this light sensor has been shown to include light-dependent nuclear import and interaction of phyB with transcription factor-like proteins in the nucleus. Here we report that nuclear import of phyB and physiological responses regulated by this photoreceptor exhibit very similar wavelength- and fluence rate-dependence. Nuclear import of phyB is insensitive to single red, blue and far-red light pulses. It is induced by continuous red light and to a lesser extent by continuous blue light, whereas far-red light is completely ineffective. The data presented indicate that light-dependent partitioning of phyB exhibits features characteristic of blue light responsiveness amplification, a phenomenon that is thought to be mediated by interaction of phyB with CRY1.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Wells' syndrome (WS) (eosinophilic cellulitis) is characterized by the presence of oedematous skin lesions associated with eosinophilia of the tissues. It has recently been observed that in patients with this disease, increased eosinophil cation protein (ECP) and interleukin (IL) -5 can be detected in peripheral blood, with T lymphocytes that have mRNA for this lymphokine. We present a patient with WS in whom we found a close correlation between clinical activity, eosinophils in blood and bone marrow, and ECP and IL-5 levels in peripheral blood and tissues. We underline the major part played by IL-5 in this disease.
Explore the source record for details and available documents.
In this retrospective study we aimed to assess the diagnostic yield of bronchoalveolar lavage (BAL) in kidney transplant patients who were suspected of having severe respiratory infection or in whom empirical antibiotic treatment had failed. All BAL procedures performed on kidney transplanted patients suspected of having respiratory infections between January 1, 1988 and July 31, 1996 were analyzed. BAL was carried out in the standard way and samples were sent for cytologic and bacteriologic study. Thirty-three patients with a mean age of 48.5 years were enrolled. All had been receiving immunosuppressive treatment and the mean time following transplantation was 320 days. Thirty-one had received antibiotic treatment before BAL. BAL was positive for 21 of the 33 patients (64%). Twenty-two pathogens were identified: 6 Pneumocystis carinii, 4 Cytomegalovirus, 3 Mycobacterium tuberculosis, 2 Aspergillus fumigatus, 2 Herpes simplex type I, 1 Streptococcus pneumoniae, 1 Staphylococcus aureus, 1 Streptococcus mitis, 1 Legionella pneumophila, 1 Legionella longbeachae. BAL was negative for 12 patients, of whom 8 were tentatively diagnosed of bacterial infection, 3 of acute pulmonary edema and one of pulmonary infarction. Based on the results, therapy was changed for 20 patients (61%), 19 (58%) because an unsuspected pathogen was identified and 1 because treatment could be simplified. The diagnostic yield of BAL is high (64%) in kidney transplant patients suspected of respiratory infection and is useful for managing such cases, as evidenced by the fact that a high proportion (19/33) of our patients were infected by pathogens not covered by empirical treatment.
We report three cases of thoracic actinomycosis whose symptoms were cutaneous tumors on the thorax. Clinical signs and images are described, along with diagnostic procedures. The excellent outcome after antibiotic treatment, which must last at least 6 months, is emphasized as well as the need to keep this disease in mind when certain symptoms and images coincide.
SAUR-AC1 is a small-auxin-up-RNA (SAUR) gene of Arabidopsis. Here we demonstrate that the SAUR-AC1 promoter region induces accumulation of a reporter transcript upon treatment with auxin and is preferentially active in elongating hypocotyls and certain other organs and tissues of transgenic Arabidopsis and tobacco plants. This study extends the utility of the SAUR-AC1 gene by providing a foundation for comparative analyses of SAUR promoter activity in auxin-responsive mutants of Arabidopsis.
Four pap genes (papA, papB, papC, papM) were found by sequencing near to snbA, a Streptomyces pristinaespiralis gene which was previously shown to encode one of the pristinamycin I (PI) synthetases. Analysis of the homologies observed from the deduced amino acid sequences suggested that these four genes could be involved in the biosynthesis of the PI precursor 4-dimethylamino-L-phenylalanine (DMPAPA). This was first verified when disruption of papA in S. pristinaespiralis led to a PI- phenotype, which was reversed by the addition of DMPAPA into the culture medium. Further confirmation was obtained when papM was overexpressed in Escherichia coli and the corresponding protein purified to homogeneity. It catalysed the two successive N-methylation steps of 4-amino-L-phenylalanine leading to DMPAPA via 4-methylamino-L-phenylalanine. These results allowed us to assign a function to each of the four pap genes and to propose a biosynthetic pathway for DMPAPA.
Explore the source record for details and available documents.
Streptomyces pristinaespiralis and S. virginiae both produce closely related hexadepsipeptide antibiotics of the streptogramin B family. Pristinamycins I and virginiamycins S differ only in the fifth incorporated precursor, di(mono)methylated amine and phenylalanine, respectively. By using degenerate oligonucleotide probes derived from internal sequences of the purified S. pristinaespiralis SnbD and SnbE proteins, the genes from two streptogramin B producers, S. pristinaespiralis and S. virginiae, encoding the peptide synthetase involved in the activation and incorporation of the last four precursors (proline, 4-dimethylparaaminophenylalanine [for pristinamycin I(A)] or phenylalanine [for virginiamycin S], pipecolic acid, and phenylglycine) were cloned. Analysis of the sequence revealed that SnbD and SnbE are encoded by a unique snbDE gene. SnbDE (4,849 amino acids [aa]) contains four amino acid activation domains, four condensation domains, an N-methylation domain, and a C-terminal thioesterase domain. Comparison of the sequences of 55 amino acid-activating modules from different origins confirmed that these sequences contain enough information for the performance of legitimate predictions of their substrate specificity. Partial sequencing (1,993 aa) of the SnbDE protein of S. virginiae allowed comparison of the proline and aromatic acid activation domains of the two species and the identification of coupled frameshift mutations.
Two genes involved in the biosynthesis of the depsipeptide antibiotics pristinamycins I (PI) produced by Streptomyces pristinaespiralis were cloned and sequenced. The 1.7-kb snbA gene encodes a 3-hydroxypicolinic acid:AMP ligase, and the 7.7-kb snbC gene encodes PI synthetase 2, responsible for incorporating L-threonine and L-aminobutyric acid in the PI macrocycle. snbA and snbC, which encode the two first structural enzymes of PI synthesis, are not contiguous. Both genes are located in PI-specific transcriptional units, as disruption of one gene or the other led to PI-deficient strains producing normal levels of the polyunsaturated macrolactone antibiotic pristinamycin II, also produced by S. pristinaespiralis. Analysis of the deduced amino acid sequences showed that the SnbA protein is a member of the adenylate-forming enzyme superfamily and that the SnbC protein contains two amino acid-incorporating modules and a C-terminal epimerization domain. A model for the initiation of PI synthesis analogous to the established model of initiation of fatty acid synthesis is proposed.
The concentration of malonaldehyde (MDA) was measured in human erythrocytes obtained from subjects suffering from senile dementia of the Alzheimer type (SDAT), non-demented elderly subjects, and from young controls by two methods: high-performance liquid chromatography (HPLC) and the thiobarbituric acid (TBA) test. The MDA concentration measured by HPLC showed significant differences between SDAT and young control groups (p < 0.01) and between SDAT and non-demented elderly groups (p < 0.01), respectively. Nevertheless, significant differences were not exhibited between young control and non-demented elderly. Moreover, the rate of accumulation of TBA-reactive substances was not significantly different among the three groups. Our results indicate that the HPLC method is highly specific and accurate and distinguishes between true MDA and other aldehydes that may react with TBA. Significant increases in the concentration of MDA of SDAT subjects were found in comparison with the two other groups, indicating that the measurement of MDA in erythrocytes could be used as a marker of oxidative damage in Alzheimer's disease.
Neurocutaneous syndromes constitute a large and complex group of diseases in which recent medical advances, particularly in the field of molecular biology and genetics, have afforded a deeper understanding of the way in which these diseases originate. In this article, we review the advances concerning pathogenic mechanisms. First, we discuss the malformations disorders of the central nervous system associated with skin disorders, which range from spinal and/or cranial dysraphism with skin lesions to fustrated forms of malformations of the neural tube, such us membranous aplasia cutis. Neurocutaneous vascular disorders can be due to malformational disease, such as in Sturge-Weber syndrome, as well as to autoimmune diseases. The analysis of mutations affecting the capacity for migration and differentiation of melanocyte precursors enables us to gain a better understanding of disorders of the cells of the neural crest, such as piebaldism and Waardenburg's syndrome. Mutations in tumor suppressor genes play an important part in the development of hamartomatous and neoplastic lesions in neurofibromatosis and tuberous sclerosis. Genetic mosaicism, both of the functional and the genomic kind, accounts for the great diversity of phenotypes and the distribution of neurocutaneous diseases. Lastly, neurocutaneous syndromes such as the paracrinopathies form an attractive hypothesis, which is as yet to be confirmed.
The small-auxin-up-RNA (SAUR) transcripts are rapidly induced by auxin and are among the most short-lived mRNAs in higher plants. In this study, we investigate the regulation of SAUR-AC1, a well characterized SAUR gene of Arabidopsis. Be examining the expression of chimeric genes in transgenic tobacco, we demonstrate that the promoter region of SAUR-AC1 mediates auxin induction. Sequences downstream of the promoter region were found to limit mRNA accumulation in a manner that was independent of auxin treatment. Both the coding region and the 3' untranslated region (UTR) of SAUR-AC1 independently contribute to this limitation. Effects on mRNA stability were assayed using chimeric genes under the control of the tetracycline-repressible Top10 promoter. mRNA half-life analysis following tetracycline treatment showed that the SAUR-AC1 coding region does not contain elements that decrease mRNA stability. In contrast, the 3' UTR was found to act as a potent mRNA instability determinant. This finding and the general utility of the Top10 system should provide the means to elucidate mRNA decay pathways that are potentially novel and specific for certain unstable transcripts.