Magnetic resonance imaging of the brain stem

Magnetic resonance imaging of 30 normal volonteers' posterior fossae was performed on a CGR Magniscan machine with a magnetic field strength of 0.5 Tesla. We chose the inversion recovery signal with a Tr of 2,000 ms, a TE of 21 ms and an inverse time of 500 ms. This sequence gives a better definition of the grey matter, the white matter and the CSF. To study the brain stem we suggest 8 horizontal and 3 sagittal sections.     

Membrane attack complex of complement and 20 kDa homologous restriction factor (CD59) in myocardial infarction

In order to investigate the mechanism of deposition of the complement membrane attack complex (MAC) in cardiomyocytes in areas of human myocardial infarction, the 20 kDA homologous restriction factor of complement (HRF20; CD59) and complement components (C1q, C3d and MAC) were analysed immunohistochemically using specific antibodies. Myocardial tissues obtained at autopsy from nine patients who died of acute myocardial infarction were fixed in acetone and embedded in paraffin. The ages of the infarcts ranged from about 3.5 h to 12 days. In cases of myocardial infarction of 20 h or less, MAC deposition was shown in the infarcted cardiomyocytes without loss of HRF20. Where the duration was 4 days or more, the cardiomyocytes with MAC deposition in the infarcted areas also showed complete loss of HRF20. Outside the infarcts, HRF20 in the cardiomyocytes was well preserved without MAC deposition. The present study suggests that the initial MAC deposition in dead cardiomyocytes can occur as a result of degradation of plasma-membrane by a mechanism independent of complement-mediated injury to the membrane. Loss of HRF20 from dead cardiomyocytes may not be the initial cause of MAC deposition, but may accelerate the deposition process of MAC in later stages of infarction.     

Conservation of genes encoding HLA-B5 and B35 cross-reactive group antigens in various races

HLA-B5 and B35 CREG antigens include HLA-B35, B51, B52, B53, and B78. Recent studies suggest that the genes encoding the HLA-B5, B35 CREG, and HLA-B58 antigens share a common ancestor. We sequenced the exons of the genes encoding HLA-B51, B53, and B58 from American black individuals and the gene HLA-B52 encoding from an Arabic individual, and compared them with previously reported sequences of HLA-B51 (B^*5101) and HLA-B52 (B^*5201) from Japanese, HLA-B53 (B^*5301) from an Algerian, and HLA-B58 (B^*5801) from a Sardinian. The sequences of the genes from the American black and Arabic individuals were identical to those from the other races. These findings support the hypothesis that these antigens have evolved prior to divergence of the major ethnic groups.     

The expression of B7-H1 on keratinocytes in chronic inflammatory mucocutaneous disease and its regulatory role

PD-1 and its ligands, B7-H1/PD-L1 and B7-DC/PD-L2, have been identified recently as CD28-B7 family molecules that are implicated in immune regulation. Lichen planus (LP) is a T cell-mediated chronic inflammatory mucocutaneous disease. We investigated the expression and function of PD-1 and its two ligands in LP. Immunohistochemical examination revealed the abundant expression of PD-1 and B7-H1 in infiltrating T cells and macrophages, and lower-level expression of B7-DC on macrophages in the subepithelium. Interestingly, substantial expression of B7-H1 on keratinocytes (KCs) was found close to the numerous T cell infiltrates in the subepithelium. Unstimulated cultured KCs expressed both B7-H1 and B7-DC, and their expression was upregulated by proinflammatory cytokines, particularly IFN-gamma. The T-cell proliferative responses and IFN-gamma production that were induced by IFN-gamma-treated KCs were augmented preferentially by anti-B7-H1 mAb, but not by anti-B7-DC mAb. These results indicate the regulatory role of B7-H1 on KCs in the interactions with T cells. Our results suggest that the induction of B7-H1 on KCs may play an important role in tolerance induction in the inflamed oral mucosa and skin.     

Results of muscular x-ray computed tomography in 145 cases of neuromuscular disease

CT Scan examination in 145 cases of neuromuscular diseases yielded the following results: Diagnosis between myogenic and neurogenic process is inconstant and cannot be considered as absolute. In myogenic diseases the X ray density of muscle is early decreased with a preservation of muscle outline. In neurogenic diseases muscle volume is early decreased. Coexistence of atrophic and hypertrophic muscles indicates primarily muscle disease. Some patterns of involvement appear to be frequent. In Duchenne's dystrophy a contrast exists between atrophic "empty" or hypertrophic muscles during the ambulatory period and "ghostly" muscles during the terminal period. In facio-scapulo-humeral muscular dystrophy, tibialis anterior and hamstring muscles have often a decreased density and psoas muscles are normal or hypertrophic. In myotonic dystrophy a hypodense perifemoral crescent is frequently observed. Diagnosis between limb-girdle myopathy ("empty" muscles with preserved limits, hypertrophic muscles, hypodense gastrocnemius medialis muscles) and chronic spinal amyotrophy (irregular and atrophic muscles without selective involvement and hypertrophic muscles) is tentatively proposed but is not considered to be clear-cut. Muscle involvement has an asymmetric distribution in amyotrophic lateral sclerosis and is rather symmetric in peripheral neuropathies.     

Interaction of cyclosporin derivatives with the ATPase activity of human P-glycoprotein

1. P-glycoprotein, a 170–180 kDa membrane glycoprotein that mediates multidrug resistance, hydrolyses ATP to efflux a broad spectrum of hydrophobic agents. In this study, we analysed the effects of three MDR reversing agents, verapamil, cyclosporin A and [3′-keto-Bmt]-[Val^*]-cyclosporin (PSC 833), on the adenosine triphosphatase (ATPase) activity of human P-glycoprotein.
2. P-glycoprotein was immunoprecipitated with a monoclonal antibody (MRK-16) and the P-glycoprotein-MRK-16-Protein A-Sepharose complexes obtained were subjected to a coupled enzyme ATPase assay.
3. While verapamil activated the ATPase, the cyclosporin derivatives inhibited both the substrate-stimulated and the basal P-glycoprotein ATPase. No significant difference was observed between PSC 833 and cyclosporin A on the inhibition of basal P-glycoprotein ATPase activity. PSC 833 was more potent than cyclosporin A for the substrate-stimulated activity.
4. Kinetic analysis indicated a competitive inhibition of verapamil-stimulated ATPase by PSC 833.
5. The binding of 8-azido-[α-³²P]-ATP to P-glycoprotein was not altered by the cyclosporin derivatives, verapamil, vinblastine and doxorubicin, suggesting that the modulation by these agents of P-glycoprotein ATPase cannot be attributed to an effect on ATP binding to P-glycoprotein.
6. The interaction of the cyclosporin derivatives with ATPase of P-glycoprotein might present an alternative and/or additional mechanism of action for the modulation of P-glycoprotein function.

     

Retrospective estimation methods of pesticide occupational exposure]

The extensively growing use of pesticides in the last decades has led to great improvements in agriculture but also to threats for human health. Studying long term effects to assess individual exposures encounters difficulties in exposure assessment. This article summarizes retrospective methods for assessing occupational exposures to pesticides currently used in epidemiological studies. Questionnaires, environmental and biological monitoring constitute direct assessment of exposure, in an individual approach. But the validity of questionnaires is often poor and the metrology rarely reflects past exposures. Some indirect measures have been used together with job exposure matrices. To establish dose-response relationships is important to quantify the risk, but needs accurate exposure assessment based on quantitative indexes.     

Difficulties in senior center life: group behaviors

In the past, the literature regarding senior centers has generally directed itself towards environmental or ecological issues. This article, however, looks at problem behaviors which reportedly occur in senior centers. A review of some possible causes and examples of these behaviors, is presented, along with some suggestions for change. The authors feel that individual problem behaviors can best by changed by setting group goals in which all program participants may be acknowledged and rewarded.