Separation of bacterial capsular and lipopolysaccharides by preparative electrophoresis

Preparative gel electrophoresis was used to separate and purify extracellular, capsular and lipopolysaccharides (EPSs, CPSs, and LPSs, respectively) from crude bacterial extracts. The procedure effectively separates CPS from LPSs. In addition discreet size ranges of these various polysaccharides can be isolated. The 'rough' (R-type), 'smooth' (S-type), and 'semi-smooth' LPSs were separated from one another. In addition different size classes of 'semi-smooth', or S-type LPS, can be separated. This procedure was demonstrated for diverse bacterial species, including the soil bacteria Rhizobium fredii, and the enteric bacterial species, Salmonella enteritidis and Proteus mirabilis. In the latter case, it was also possible to separate capsular polysaccharide from its lipid-bound form.     

Lamotrigine may limit pathological excitation in the hippocampus by modulating a transient potassium outward current

Actions of the new antiepileptic drug lamotrigine were characterised using whole cell patch clamp recordings from rat CA1 pyramidal cells in vitro. The results suggest that lamotrigine, besides its previously described effect on the fast sodium inward current and calcium currents, modulates the transient potassium outward current ID. This may be an effective mechanism to inhibit pathological excitation.     

Mode of action of lufenuron on larval cat fleas (Siphonaptera: Pulicidae)

Adult cat fleas, Ctenocephalides felis (Bouché), were fed suboptimal in vitro concentrations of lufenuron in blood to allow hatching of flea larvae for cytological study. At concentrations of 0.125, 0.25, and 0.5 ppm, larval hatch was 64, 15, and 4%, respectively. Larvae hatching from eggs laid by adults fed lufenuron at concentrations of 0.025, 0.08, or 0.125 ppm did not differ significantly from the control. However, many larvae from the 0.08-ppm group and higher concentrations died during the 1st instar. Examination of these larvae revealed that they were dying from desiccation caused by bleeding from microscopic lesions in the cuticle or the inability to complete the molt to the next instar. Electron micrographs showed that lufenuron often disrupted formation of the endocuticle resulting in the deposition of an amorphous mass of randomly oriented chitin microfibrils. Other larvae formed normal endocuticle but were unable to digest the old endocuticle or produce new procuticle after apolysis. Failure of larvae to digest old cuticle or form new cuticle was caused by degeneration of the epidermal cells needed for the synthesis of molting fluid and chitin.     

Convulsions due to increased permeability of the blood-brain barrier in experimental cerebral malaria can be prevented by splenectomy or anti-T cell treatment

Experimental cerebral malaria (ECM) can be induced in C57B1 mice by infection with Plasmodium berghei K173 parasites. Behavioral changes shortly before they die of ECM may reflect disturbance of the integrity of the blood-brain barrier (BBB). Folic acid elicits strong convulsive activity if the permeability of the BBB is increased. Administration of folic acid to mice during development of ECM induced convulsions. Interventions known to prevent fatal outcome from ECM, such as splenectomy or treatment with anti-CD4 or anti-CD8 monoclonal antibodies, also prevented sensitivity to folic acid-induced convulsions. In addition, infected mice with ECM and sensitive to folic acid-induced convulsions, recovered from this sensitivity after treatment with anti-T cell antibodies within 4 h. These data suggest that disturbance of the permeability of the BBB can be reversed and depends on the involvement of T cells.     

Dynamic contrast perception assessed by pattern masking

The perceived contrast of a pulsed grating varies markedly with the exposure duration and spatial frequency of the grating. We studied dynamic changes in perceived grating contrast with a pattern-masking paradigm. We measured masking of a brief, localized test pattern (a D6 stimulus, 30 ms in duration) by fixed-contrast cosine grating patterns of varying duration (50-500 ms). The cosine mask pattern had spatial frequency of either 1 or 6 cycles per degree (cpd) at a contrast of 0.3. The D6 test pattern was centered on a light bar of the mask and was either positive peak contrast (same-polarity test and mask) or negative peak contrast (opposite-polarity test and mask). In Experiment 1, the test and mask had simultaneous onset. With a 6-cpd mask, the same-polarity test-threshold elevation versus mask-duration function increases monotonically. For a 1-cpd mask, the same-polarity threshold-mask-duration function is nonmonotonic, with peak masking effect produced by a grating pulse of 80-100 ms. These masking effects are closely congruent with known dynamic contrast effects. With negative tests, masking-duration functions are elevated from same-polarity functions and are essentially similar in shape for 1- and 6-cpd masks. The elevated thresholds suggest inhibitory interaction between ON and OFF pathways, with a similar time course across spatial frequency. In Experiment 2, the D6 test was delayed from mask onset by 33 ms. Positive contrasts only were employed. For 1-cpd stimuli, the delay of test greatly reduced masking at all mask durations and eliminated the nonmonotonic function. This suggests that for low-spatial-frequency patterns, perceived contrast is determined by an early peak component of the neural response. But for 6-cpd stimuli, masking of the delayed test was somewhat greater at all mask durations, consistent with a gradually increasing underlying neural response to the grating. Finally, in Experiment 3, same-polarity masking effects at both spatial frequencies were replicated with negative-contrast test and mask (OFF pathway mediation). This indicates that the ON and OFF pathways have similar response dynamics.     

Increased incidence of congenital malformations in children with transient thyroid-stimulating hormone elevation on neonatal screening

Huntington's disease is an autosomal-dominant inherited progressive neurodegenerative disease associated with an expanded trinucleotide repeat (CAG) sequence on the short arm of chromosome 4. The disease is considered rare in Africans. We report five black South African families of different ethnic origin with proven expansions typical of Huntington's disease and discuss the possible origins of the disease in Africa.