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Biomedical subjects

B Jany

Publications and source records attributed to B Jany.

At least 19 recordsLinked to original sources
PubMed2004

[Post-traumatic endocapsular blood effusion].

A rare complication after extracapsular surgery of the cataract, blood effusion is often a fortuitous discovery when a drop in visual acuity occurs. The subject reported herein is a 76-Year-old patient who presented an endocapsular blood effusion with no liquid level 1 Year after the extracapsular surgery of the cataract, discovered while examining a decrease in visual acuity. Questioning led to the discovery of eye trauma due to Nd: YAG laser posterior capsulotomy 3 Months before, which had progressed spontaneously and favorably for 2 Months, with a reduction of the effusion and better visual acuity. The bleeding seems to have come from a vascular injury due to a direct contusion, with blood possibly coming from the ciliary body, the iridocorneal angle, or the vitreous. The liquid effusion may have been caught at the back by the implant and enclosed in the area located between the capsular bag and the anterior hyaloid, without intravitreous diffusion. Most of reported cases in the literature discuss observations made on an intact posterior capsule, which appeared during or after close surgery. The treatment was simple supervision. Some Authors propose a Nd: YAG laser capsulotomy in case resorption is too slow.

Aged↗
PubMed2001

Identification of disease genes by expression profiling.

The human genome has been completely sequenced. The development of innovative methodologies and tools to understand the functions of human genes in health and disease will allow the data of the human genome project to be utilized. This paper reviews methods that can be used to detect and isolate genes that are specifically expressed in certain diseases or that are specific to cell types. First, classical methods, such as differential screening of complementary deoxyribonucleic acid libraries and subtractive techniques, are described. Methods based on polymerase chain reaction (PCR), such as differential display PCR or serial analysis of gene expression, will then be discussed. Finally, recent developments in gene chip technology and basic principles of functional genomics will be illustrated. Future developments will link the results of genomic approaches to data obtained by other systematic methods, such as proteomics (i.e. the systematic, large scale analysis of proteins), and will allow the production of a detailed molecular characterization of diseases, disease stages, tissues, or cell types. Methods to detect disease or cell type-specific gene expression patterns will play an important role in the future of basic research, as well as the development of novel diagnostic procedures and identification of therapeutic targets.

DNA Fingerprinting↗
PubMed2000

[Smokers with chronic bronchitis and emphysema. Utilize the entire therapy spectrum!].

In the majority of cases, chronic obstructive bronchitis is due to inhalative cigarette smoking. Not only does it cause high costs, but it also has a poor prognosis. The pathogenesis of the illness is now considered to be chronic, mainly neutrophilic, inflammation of the airways and the peripheral parts of the lungs--chronic hypersecretion is a common feature of the disease. Successful treatment requires the giving up of inhalative cigarette smoking. Pharmacological options include anticholinergics, beta sympathomimetics, theophylline and inhalative or systemic corticosteroids. Long-acting beta sympathomimetics such as formoterol, and salmeterol, and still experimental long-acting parasympatholytics, represent significant advances. Such additional measures as vaccination, long-term administration of oxygen and, more recently, surgical procedures such as lung volume reduction to treat severe pulmonary emphysema are described.

Bronchitis↗
PubMed1998

[A patient with muscle pain after a journey to the tropics. Myocardial involvement in proximal myotonic myopathy].

HISTORY AND ADMISSION FINDINGS: A 36-year-old man reported feeling generally unwell and experiencing shooting and tearing pain, especially in the thighs and over the precordium, just after returning from a five-week holiday in Central Africa. An active sportsman in his youth (fencing) he was known to have incomplete right bundle branch block in the ECG and a raised concentration of gamma-glutamyl transferase, of unknown aetiology. Physical examination on admission was negative except for discrete weakness on head bending and slightly delayed finger stretching after making a fist. INVESTIGATIONS: Multiple tests excluded tropical diseases. There were abnormal T waves in leads III and V1 of the ECG. Serum concentrations of creatine kinase (CK; maximally 822 U/l), gamma-glutamyl transaminase (gamma-GT; 446 U/l), glutamyl-pyruvate transaminase (GPT; 510 U/l) and of glutamate-oxalate transaminase (GOT; 108 U/l) were all elevated. Erythrocyte sedimentation rate and C-reactive protein were within normal limits. TREATMENT AND COURSE: At first the suspected diagnosis was myocarditis and he was placed on bed-rest, monitored and treated symptomatically. Because the levels of CK, gamma-GT, GPT and GOT improved only transiently, there were no signs of inflammatory disease and the muscle pains continued, biopsies of skeletal muscle and the liver were done. They revealed nonspecific liver changes and a noninflammatory myopathy. As congenital myopathy was suspected he was transferred to the neurology department where the diagnosis of proximal myotonic myopathy (PROMM) was established. CONCLUSION: We assume that an unknown viral infection triggered the illness that, in addition to the usual nonspecific symptoms, accentuated the signs of the existing multi-system proximal myotonic myopathy.

Adult↗
PubMed1997

Localization and up-regulation of mucin (MUC2) gene expression in human nasal biopsies of patients with cystic fibrosis.

Using digoxigenin-UTP-labelled human HAM-1 (92 bp) or SMUC41 (850 bp) cRNA probes, the expression and localization of MUC2 gene transcripts were determined by in situ hybridization in human nasal tissues obtained as biopsies from 12 patients with cystic fibrosis (CF): all had been part of a gene therapy trial in which CFTR cDNA-liposome complexes had been delivered by topical application to eight and liposome alone to four as a placebo control. For comparison, there were nasal tissues taken at surgical resection from four non-CF subjects and a further four biopsies taken from normal healthy volunteer controls. Both SMUC41 and HAM-1 probes provided a strong signal. MUC2 mRNA transcripts were present in serous and mucous acini of submucosal glands, ciliated and basal cells of the surface epithelium, and occasional mononuclear inflammatory cells. The percentages (mean +/- SEM) of serous and mucous acini showing positivity for MUC2 gene expression in the four samples surgically resected from non-CF subjects were 25.4 +/- 5.6 and 26.7 +/- 3.3 per cent, respectively. Compared with the non-CF subjects, the mean percentage of acini showing MUC2 gene expression in the four placebo-treated CF subjects was significantly higher for serous (80.5 +/- 12.7 per cent; P < 0.05, t-test), but not for mucous acini (53.1 +/- 16.8 per cent; P = 0.38). In CF and non-CF groups, where present, MUC2 positivity was strongly expressed and constituted approximately 84 per cent of the cell area in serous acini, whereas it was less obvious and was confined to the perinuclear area of cells in mucous acini. A significantly greater proportion of the surface epithelium was positive for MUC2 mRNA transcripts in the CF subjects (89.0, +/- 1.4 per cent) than in the surgically resected tissues of the four non-CF subjects (19.4, +/- 4.0 per cent) (P = 0.02). In the eight CFTR-cDNA-treated subjects, there was an overall trend to reduction, but no statistically significant alteration of MUC2 gene expression. It is concluded that the MUC2 gene is expressed at three- to four-fold higher levels in CF nasal mucosa than in non-CF nasal tissue and that it is expressed in a variety of cells additional to submucosal mucus-secreting glands.

Adult↗
PubMed1995

[Sarcoidosis in monozygotic twins].

Identical (monozygotic) female twins both simultaneously developed acute sarcoidosis with unusual manifestations. Additional to pulmonary involvement they both also had hypercalcaemia with compensated renal failure. When seen at the age of 33 years, these findings were more marked in one of them (case 2) than in the other, and she also had granulomatous conjunctivitis, while in the other one (case 1) the dominant sign was widespread lymph node enlargement. Both were also found by magnetic resonance imaging to have multiple lesions in the white matter, interpreted as the morphological correlate of neurosarcoidosis. But they caused clinical symptoms (visual disorder, unsteady gait) in only one sister (case 1). Treatment with prednisolone largely normalized the lung functions in case 2, completely in case 1, and renal functions in both. But when the daily prednisolone dose was reduced to below 10 mg, the pulmonary symptoms recurred. These observations indicate that even in chronic sarcoidosis acute episodes may occur, with involvement of multiple organs and other rare complications. The manifestations of the underlying disease in identical twins and the similarities of its course in the two sisters underline the possible role of genetic factors in the pathogenesis of sarcoidosis.

Acute Disease↗
PubMed1995

Activation of the transcription factor NF-kappa B in human tracheobronchial epithelial cells by inflammatory stimuli.

Recent studies have shown that surface epithelial cells play a major role in the defence and inflammatory reactions of the airways. How extracellular stimuli lead to increased gene expression in these epithelial cells is not well known. In this study, we asked whether the multiunit transcription factor, nuclear factor (NF)-kappa B, which regulates the expression of genes involved in defense and immune processes, is activated in airway epithelial cells following stimulation with inflammatory mediators and hydrogen peroxide. In addition, we studied whether this would be followed by upregulation of the NF-kappa B target gene product granulocyte-macrophage colony-stimulating factor (GM-CSF). Activation of NF-kappa B in the SV40 transformed human tracheobronchial epithelial cell line 1HAEo- was measured by electrophoretic mobility shift assays. GM-CSF concentrations in cell culture supernatants were determined by enzyme-linked immunosorbent assays. NF-kappa B was rapidly activated by exposure of cells to interleukin-1 beta (IL-1 beta), phorbol myristate acetate (PMA), and tumour necrosis factor-alpha (TNF). Exposure to H2O2 platelet activating factor (PAF) and lipopolysaccharide (LPS) did not lead to increased NF-kappa B activation. Co-stimulation of IL-1 beta with H2O2 led to augmentation and prolongation of the effect on NF-kappa B activation compared to stimulation with IL-1 beta alone. GM-CSF concentrations increased following stimulation with IL-1 beta and H2O2, and the effect of IL-1 beta/H2O2 co-stimulation on GM-CSF concentrations was additive. These results suggest that NF-kappa B may represent an important transcription factor, controlling the expression of cytokine genes in airway epithelial cells.

Bronchi↗
PubMed1993

Characterization of a rat airway cDNA encoding a mucin-like protein.

The purpose of this study was to isolate airway mucin cDNAs for use in studies of mucin biosynthesis in rat models of human airway disease. To this end, we screened a rat airway cDNA library with the human intestinal mucin cDNA SMUC 41 and obtained 7 positive clones. Preliminary characterization of each of these led us to focus on the clone expressing the 390 bp cDNA RAM 7s. Evidence indicating that RAM 7s encodes part of a rat airway mucin gene is that RAM 7s: (a) hybridizes in plaque lifts to SMUC 41, (b) hybridizes in Northern blots to large, polydisperse transcripts, (c) has a sequence encoding threonine-rich tandem repeats and (d) shows appropriate tissue-specific expression of cognate mRNA. The repetitive peptide encoded by RAM 7s includes five copies of the consensus sequence TTTTIITI. Because this sequence is different from those reported for two cDNAs previously isolated from rat intestinal libraries, we tentatively conclude that RAM 7s encodes part of a previously unidentified rat mucin gene.

Amino Acid Sequence↗
PubMed1993

[Molecular cloning of human respiratory tract mucin and studies of mucin gene expression in tracheobronchial epithelium of the rat].

Mucus hypersecretion is an important symptom of chronic airway diseases such as Chronic Bronchitis, Asthma, and Cystic Fibrosis. The cellular and molecular pathogenesis of hypersecretion is poorly understood. Airway mucin is a marker of chronic hypersecretion. By characterising an airway mucin cDNA, we were able to show that human airway epithelium and the intestine express the same mucin gene MUC2. It is also expressed in Cystic Fibrosis tracheobronchial epithelium. In an animal model of hypersecretion, viral infection and sulfur dioxide exposition lead to a dramatic accumulation of mucin mRNA in the airway epithelium. This could represent an important initial step in the pathogenesis of tracheobronchial hypersecretion.

Animals↗
PubMed1991

Mucin gene expression in rat airways following infection and irritation.

Airway mucus hypersecretion occurs in response to infection and irritation and poses an important and poorly understood clinical problem. In order to gain insight into its pathogenesis, we have focused on an mRNA encoding the major mucus glycoprotein, mucin. Northern blots showed that mucin mRNA was abundant in the intestine of specific pathogen free rats whereas it was undetectable in the airways of these rats until pathogen-free conditions were suspended and rats acquired Sendai (Parainfluenza I) virus infections. Airway mucin hybridization signals in rats that were both infected with Sendai virus and exposed to SO2 were more intense than those in rats with infection alone. These results suggest that pathogen-and irritant-induced hypersecretion may be partly controlled at the level of mucin mRNA.

Animals↗
PubMed1991

Mucin in disease. Modification of mucin gene expression in airway disease.

Mucus hypersecretion is a characteristic feature of several human airway diseases, including chronic bronchitis, cystic fibrosis, and asthma. Although its pathogenesis is poorly understood, hypersecretion apparently results from the abnormally large number of mucous cells found in hypersecretory airways. The factors giving rise to these mucous cells are unknown, but experimental evidence supports possible roles for both mitosis (mucous cell hyperplasia) and differentiation (mucous cell metaplasia). On the basis of the hypothesis that differentiation would require activation of mucin mRNA transcription, we have used mucin cDNA to monitor mucin mRNA levels in an animal model of chronic bronchitis. We first showed that a mucin gene (SMUC or MUC-2) cloned from the human intestine is also expressed in the human airways and is the same or homologous to genes expressed in other human mucin-producing organs. We next showed that a homologue of the SMUC gene is expressed in several animal species, including the rat. Finally, we showed that the induction of experimental chronic bronchitis by SO2 in rats is accompanied by the induction (from near zero baseline) of airway mucin mRNA. The induction by irritants of high steady-state levels of mucin mRNA may represent one of the early events in mucous cell differentiation and hypersecretion.

Animals↗
PubMed1990

The serous cell.

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Animals↗
PubMed1990

Plasticity in the airway epithelium.

Normal cell turnover as well as the response to injury require cell proliferation and differentiation. The airway epithelium maintains these processes throughout adult life. Controlled homeostatically, cell proliferation and differentiation usually restore, as an end point, the pseudostratified architecture of the normal mucociliary epithelium. After injury, however, cell proliferation and differentiation sometimes establish, as an end point, regions of metaplastic cells. In this brief review, we have tried to summarize research findings that 1) describe the development of metaplastic lesions in morphological terms, 2) identify cells the proliferation of which forms the basis of these lesions, and 3) identify molecular changes within these cells that control development of the metaplastic phenotype.

Animals↗