Guillain-barré syndrome: A series observed at riyadh armed forces hospital january 1984–January 1994

A consecutive series of 47 hospitalized cases of Guillain-Barré syndrome seen over a 10-year period was analysed with respect to: (1) age and sex; (2) antecedent events and seasonal distribution; (3) patterns of clinical presentation; (4) CSF and neurophysiological findings; (5) results of treatment with plasma exchange; and (6) outcome. Twenty-two were children, 20 middle-aged and 5 aged; 37 were male and 10 were female. The most frequent antecedent event was upper respiratory tract infections; a seasonal peak incidence was found in winter. Clinical, CSF and neurophysiological findings concurred with those in the Western literature; 79% of the cases were severe. Plasma exchange performed within the first 2 weeks of onset benefitted in the short-term outcome, i.e. improvement by 1 grade at 4 weeks, but the long-term benefit, i.e. the ability to regain independent locomotion, was questionable. Plasma exchange helped in curtailing the time to walking unaided but had no benefit on the duration of artificial ventilation. Factors associated with an adverse outcome were: age over 15 years, severity of motor electrodiagnostic findings (especially a decreased distal CMAP amplitude and EMG signs of acute denervation), requirement for ventilation and slow progression (>3 weeks) to maximum deficit. After a mean follow-up of 11 months, 55% of the patients regained independent locomotion, which is a comparatively low proportion.     

Deamination of adenosine by extracts of Penicillium politans NRC-510

Cell-free extracts of nitrate-grown Penicillium politans NRC-510 could catalyze the hydrolytic deamination of adenosine to inosine maximally at pH 6.0 and 45 degrees C. However the same extracts could not catalyze the N-glycosidic bond cleavage of adenosine at pH 4.0, 6.0 and 8.0. Incubation of the extracts at 55 degrees C for 30 minutes caused about 31% loss in activity whereas incubation of the extracts at 60 degrees C for 15 minutes caused a complete loss of enzyme activity. Results indicated the absence of the involvement of sulfhydryl groups in the catalytic site of adenosine deaminase. The enzyme is inhibited by ethylene diamine tetraacetate indicating that adenosine deaminase is a metalloenzyme. MnCl2 and MgCl2 had a remarkable activating effect, whereas HgCl2, CaCl2 and ZnSO4 showed an inhibitory effect on enzyme activity. Dialyzing the extracts for 24 hours significantly increase deaminase activity by about 33%. The apparent K(m) value was calculated for adenosine and found to be 3.63 x 10(-3) M, which indicates high affinity of adenosine deaminase for its substrate adenosine.     

A morphological transition in the pleomorphic bacterium Ramlibacter tataouinensis TTB310

We provide microscopic evidence that motile rod-shaped forms of Ramlibacter tataouinensis TTB310 are formed from dividing cyst-like cells. Careful estimation of the size of the two morphotypes was conducted using optical and transmission electron microscopy (TEM). The cyst-like cell was shown to be a sphere with a diameter Dc=850 nm. The rod-shaped form was a round-ended cylinder with length Lr=2.91 microm and diameter Dr=239 nm. The membrane area of the two morphotypes was the same. However, the formation of rods from cysts involved loss of two-thirds of the cell volume. TEM showed that, prior to division and transition into rods, cysts contained condensed cytoplasmic material. These results suggest that the morphological transition occurs by pure reshaping of cells.     

Epidemiology and genetic characterization of HIV-1 isolates in the general population of Djibouti (Horn of Africa)

During a national survey in 2002 in Djibouti, serum samples were collected using a valid sampling scheme from 2423 Djiboutians representing the general population of urban and rural districts. The HIV-1 seroprevalence was 2%. The HIV-1 polymerase gene from 53 untreated patients was amplified. Phylogenetic analysis of 34 isolates revealed a majority of subtype C (73%) as well as other subtypes, including CRF02_AG recombinants (18%), subtype D (6%), and subtype A (3%).     

Cross-linking of surface IgM or IgD causes differential biological effects in spite of overlap in tyrosine (de)phosphorylation profile.

Although displaying similar amounts of surface IgM and IgD, ECH 408-1 cells only succumb to apoptosis after cross-linking of IgM (not IgD), suggesting that different signaling pathways couple to both receptors. Immunoprecipitation studies revealed the presence of several proteins selectively associated with IgM and IgD, thus ruling out that the lack of inhibitory signaling mediated by IgD might be due to membrane expression in the absence of associated proteins belonging to the B cell receptor complex. 32P metabolic labeling and immunoprecipitation studies demonstrated that IgM and IgD are associated with phosphoproteins of 32-33 kDa in an isotype-specific fashion. Kinetic analyses of tyrosine kinase activity showed that cross-linking of surface IgM or IgD resulted in the rapid (1-3 min) phosphorylation of several protein substrates on tyrosine residues, followed by a dephosphorylation step. Isotype-specific changes of the phosphorylation status specifically affected molecules in the 32-33 kDa range, i.e. IgM (not IgD) cross-linking affected a approximately 32-kDa protein, whereas IgD (not IgM) cross-linking induced phosphorylation of a protein exhibiting a slightly lower mobility (33 kDa). These results suggest that isotype-specific immunoglobulin-associated molecules could be involved in the second messenger cascade leading to different biological effects upon IgM and IgD cross-linking.     

Testosterone suppresses protective responses of the liver to blood-stage malaria

Testosterone induces a lethal outcome in otherwise self-healing blood-stage malaria caused by Plasmodium chabaudi. Here, we examine possible testosterone effects on the antimalaria effectors spleen and liver in female C57BL/6 mice. Self-healing malaria activates gating mechanisms in the spleen and liver that lead to a dramatic reduction in trapping activity, as measured by quantifying the uptake of 3-mum-diameter fluorescent polystyrol particles. However, testosterone delays malaria-induced closing of the liver, but not the spleen. Coincidently, testosterone causes an approximately 3- to 28-fold depression of the mRNA levels of nine malaria-responsive genes, out of 299 genes tested, only in the liver and not in the spleen, as shown by cDNA arrays and Northern blotting. Among these are the genes encoding plasminogen activator inhibitor (PAI1) and hydroxysteroid sulfotransferase (STA2). STA2, which detoxifies bile acids, is suppressed 10-fold by malaria and an additional 28-fold by testosterone, suggesting a severe perturbation of bile acid metabolism. PAI1 is protective against malaria, since disruption of the PAI1 gene results in partial loss of the ability to control the course of P. chabaudi infections. Collectively, our data indicate that the liver rather than the spleen is a major target organ for testosterone-mediated suppression of resistance against blood-stage malaria.