Differential mortality: some comparisons between England and Wales, Finland and France, based on inequality measures

Inequalities in mortality between social classes or socioeconomic groups were compared in three European countries, using similar sources of data from large national cohort studies. People registered at a census in 1971 (1975 for France) or a sample of them, were followed until 1980 or 1981. The Gini coefficient, a measure widely used in economics, allowed the comparison of various situations involving different numbers and group sizes. It was applied to age groups 35-44, and 45-54 for men only. According to this measure, inequalities were of the same order in England and Wales and Finland, and greater in France. Differences between the three countries concerning the principal causes of death leading to inequalities were cardiovascular diseases in England and Wales, accidents and cardiovascular diseases in Finland, and cancer and cirrhosis in France.     

Carbon Monoxide Mass Exposure in a Pediatric Population

Abstract. Objectives:To describe the outcomes of a mass carbon monoxide (CO) intoxication, and to calculate the CO half-life in a pediatric school-aged population.
Methods:A retrospective chart review was performed based on Regional Poison Center database information, hospital laboratory data, and medical records of the pediatric patients who sought care at one of 3 St. Louis area hospitals, after exposure to high levels of CO. Exposures occurred on January 5, 1996, after evidence of a CO leak was discovered at an area elementary school. Charts were reviewed for major demographics, symptoms reported, carboxyhemoglobin (COHb) levels and times, and level of effect.
Results:Information about 177 (35%) of the 504 children in attendance at school that day was available. Mean age was 8.7 ± 1.8 years (range 4–12 years). Symptoms were present in 155 (88%) of the 177 children for whom data were available. Initial COHb levels were obtained for 147 (83.1%) of the 177 children. First mean COHb level was 7.0% (95% CI = 6.6–7.5%). Second COHb level was obtained for 26 children with a mean of 2.7% (95% CI = 2.2–3.2%). Calculated half-life of COHb, on 100% 0₂ at 1 atm, was 44.0 minutes (95% CI = 39.6–48.2 minutes).
Conclusion:Some children had symptoms at COHb levels that traditionally have been considered nontoxic. The elimination of COHb was found to be more rapid in this population of children than reported in other studies.     

A murine cytomegalovirus-neutralizing monoclonal antibody exhibits autoreactivity and induces tissue damage in vivo.

The autoreactivity of murine cytomegalovirus (MCMV)-neutralizing monoclonal antibody (mAb) AC1 was examined in vitro and in vivo. Both mAb AC1 and a human antiserum reactive with U1-small nuclear ribonucleoprotein (U1-snRNP) stained uninfected mouse embryo fibroblasts (MEF) in a speckled nuclear pattern and reacted with 70,000 molecular weight (MW) MEF nuclear antigens by immunoblotting, suggesting that mAb AC1 cross-reacted with the 70,000 MW component of U1-snRNP. However, only mAb AC1 cross-reacted with an additional epithelial cytoplasmic autoantigen present in cultured HEp2 cells. On tissue sections from uninfected mice, mAb AC1 predominantly reacted with a component of central and peripheral nervous systems, although cross-reactivity with the stratum spinosum of the skin and the outer sheath of hair follicles was also observed. Immunoblotting revealed that mAb AC1 reacted with phosphorylated epitopes present on a 98,000 MW MCMV structural protein and the 200,000 MW mouse neurofilament protein (NFP). Treatment of uninfected mice with mAb AC1 resulted in a severe interstitial pneumonia with greatly thickened and congested alveolar septa. Severe oedema of the hypodermis and a mild mesangial proliferative glomerulonephritis were also observed. These results demonstrate that a mAb reacting with a MCMV structural phosphoprotein which can protect mice against the dissemination of MCMV, can also promote the development of autoimmune disease. Therefore, the production of such cross-reactive antibodies may be an important mechanism in the development of autoimmunity following viral infection.     

Biocompatibility studies of the Anaconda stent-graft and observations of nitinol corrosion resistance.

PURPOSE: To validate the deployment, in vivo performance, biostability, and healing capacity of the Anaconda self-expanding endoprosthesis in a canine aortic aneurysm model. METHODS: Aneurysms were surgically created in 12 dogs by sewing a woven polyester patch onto the anterior side of the thoracic or abdominal aorta. Anaconda prostheses were implanted transfemorally for prescheduled periods (1 or 3 months). Aneurysm exclusion and stent-graft patency were monitored angiographically. Healing was assessed with histological analysis and scanning electron microscopy (SEM). Textile analysis determined the physical and chemical stability of the woven polyester material, while the biostability of the nitinol wires was evaluated with SEM and spectroscopy. RESULTS: All prostheses were intact at explantation. After 1 month, endothelial-like cells were migrating in a discontinuous manner both proximally and distally over the internal collagenous pannus at the device-host boundary. After 3 months, endothelialization had reached the midsections of the devices, with a thicker collagenous internal capsule. Patches of endothelial-like cells were sharing the luminal surface with thrombotic deposits. However, the wall of the device at the level of the aneurysm was generally poorly healed, with multiple thrombi scattered irregularly over the luminal surface. The polyester fabric was intact except for some filaments that were ruptured adjacent to the sutures and some abrasion caused by the nitinol wires. No evidence of corrosion was found on the nitinol stents. CONCLUSIONS: This Anaconda stent-graft has demonstrated its ability to exclude arterial aneurysms. The device used in this study was an experimental prototype, and the manufacturer has incorporated new immobilization features into the model for clinical use. The constituent materials appear to be suitable in terms of biocompatibility, biofunctionality, and short-term durability.     

Research on antibacterial and antifungal agents. III. Synthesis and antimicrobial activity of 2-methyl-5-aryl-3-furoic acids and 2-methyl-3-imidazolylmethyl-5-aryl furans

The synthesis and microbiological activities of 2-methyl-5-aryl-3-furoic acids and 2-methyl-3-imidazolyl-methyl-5-aryl-3-furans are reported. Antimicrobial data in comparison with pyrrolnitrin showed an interesting antifungal activity but a very poor antibacterial activity. The presence of an imidazole nucleus does not increase antifungal activity. The introduction of a substituent in the para position of the aryl at a C5 of the furan ring affects antifungal activity.     

Differential expression of extracellular matrix metalloproteinase inducer (CD147) in normal and ulcerated corneas: role in epithelio-stromal interactions and matrix metalloproteinase induction

Extracellular matrix metalloproteinase inducer (EMMPRIN) was originally identified on the tumor cell surface as an inducer of matrix metalloproteinase (MMP) production in neighboring fibroblasts. Here we demonstrate a role for EMMPRIN in MMP induction during corneal wound healing. MMP and EMMPRIN expression was analyzed in normal and ulcerated human corneas, as well as in corneal epithelial and stromal cells in culture using confocal microscopy, zymography, immunoblots, and real-time polymerase chain reaction. In normal cornea EMMPRIN was predominantly expressed in the epithelium but was markedly induced in the anterior stroma of ulcerated corneas. This coincided with MMP-2 induction that co-localized with EMMPRIN at the epithelio-stromal boundary. The role of epithelial-stromal interaction in MMP induction was investigated in an in vitro co-culture system and demonstrated an induction and co-localization of EMMPRIN and MMP-2 in the fibroblasts at the interface with epithelial cells. Direct contact of fibroblasts with EMMPRIN-containing purified epithelial cell membranes also induced MMP-1, MMP-2, and EMMPRIN and this was inhibited by a blocking anti-EMMPRIN antibody, suggesting that EMMPRIN was primarily responsible for this induction. These findings, and the up-regulation of EMMPRIN by epidermal growth factor and transforming growth factor-beta, demonstrate a role for EMMPRIN in wound healing and suggest that sustained local up-regulation of EMMPRIN and MMPs in chronic situations in which healing is delayed may lead to excessive matrix degradation and corneal melts.     

Hfq-dependent regulation of OmpA synthesis is mediated by an antisense RNA

This paper shows that the small RNA MicA (previously SraD) is an antisense regulator of ompA in Escherichia coli. MicA accumulates upon entry into stationary phase and down-regulates the level of ompA mRNA. Regulation of ompA (outer membrane protein A), previously attributed to Hfq/mRNA binding, is lost upon deletion of the micA gene, whereas overexpression of MicA inhibits the synthesis of OmpA. In vitro, MicA binds to the ompA mRNA leader. Enzymatic and chemical probing was used to map the structures of MicA, the ompA mRNA leader, and the complex formed upon binding. MicA binding generates a footprint across the ompA Shine-Dalgarno sequence, consistent with a 12 + 4 base-pair interaction, which is additionally supported by the effect of mutations in vivo and by bioinformatics analysis of enterobacterial micA/ompA homolog sequences. MicA is conserved in many enterobacteria, as is its ompA target site. In vitro toeprinting confirmed that binding of MicA specifically interferes with ribosome binding. We propose that MicA, when present at high levels, blocks ribosome binding at the ompA translation start site, which-in line with previous work-secondarily facilitates RNase E cleavage and subsequent mRNA decay. MicA requires the presence of the Hfq protein, although the mechanistic basis for this remains unclear.     

Human epithelial thymic tumours: heterogeneity in immunostaining of epithelial cell markers and thymic hormones.

Different hormones (thymulin, thymosin alpha 1, vasopressin), antigenic markers of cortical and subcapsular/medullary thymic areas and tumour associated antigens were studied on paraffin or frozen section and cultures of human epithelial thymic tumours ('thymomas'). Thymulin, thymosin alpha 1 and for the first time vasopressin are found in most tumours. The epithelial cells of five 'thymomas' had markers of both cortical (TE3) and subcapsular/medullary thymic regions (A2B5 and/or TE4 and/or anti-p19). Leu-7, a marker of subcapsular epithelial cells was positive only in two tumours. The histological classification into cortical and medullary tumours does not correspond to our immunofluorescence results. The presence of these markers does not support the theory of different embryologic origin of the cortical and subcapsular/medullary epithelial cells. Transferrin receptors were detected on only some epithelial cells of thymic 'carcinomas'. Adenocarcinoma related antigen and carcino embryonic antigen only stained a few epithelial cells of all the tumours. There is no expected correlation between the presence of epidermal growth factor receptors on cell membranes and the number of proliferative cells stained by the anti-Ki67 antibodies. Immunostainings were heterogeneous according to the epithelial thymic tumours, independent of histological classification and not yet useful for prognosis.     

Immunoreactivity of aqueous extracts of rat and mouse tissue with anti-thymosin alpha 1, anti-bovine thymopoietin and anti-thymulin antibodies. Studies using immunoblotting

Anti-thymosin alpha 1 monoclonal antibodies recognized, on immunoblots, 1 to 2 bands corresponding to molecules of 34 and 35 Kd when using aqueous extracts of thymus, spleen, kidney, liver, brain, pituitary and adrenal glands from rats or mice. Anti-bovine thymopoietin polyclonal antibodies, in the same conditions, labelled analogous 34, 35 and 35.5 Kd molecules in brain and thymus extracts but also a 40 Kd molecules in thymus and a 90 Kd in brain extracts. Anti-synthetic thymulin monoclonal antibodies recognized irregularly and poorly a 52 Kd molecule from thymus and brain extracts. These results suggest that thymopoietin, thymulin and specially Thymosin alpha 1 are first synthesized in large precursors. Finally, other organs seem capable of synthesizing thymosin alpha 1 and probably thymopoietin, but for thymulin, the results are too irregular to conclude.