Current-distance relations of axons mediating circling elicited by midbrain stimulation

Stimulation of mediocaudal midbrain in rats produces ipsiversive circling due to the stimulation of longitudinal axons. The refractory periods of these axons were measured by delivering trains of conditioning and testing pulses via a single electrode at various conditioning-testing (C-T) intervals. As C-T interval increased from 0.3 to 2.0 ms, the frequency required to produce a constant amount of circling halved. The current-distance relations of these axons were measured by placing two electrodes lateral to one another, and delivering conditioning pulses via one electrode and testing pulses via the second electrode. The required frequency decreased less at C-T intervals in the refractory period range using two electrodes rather than using a single electrode. This partial refractoriness suggests that only part of the axons were stimulated by both electrodes. The refractoriness increased as current increased or as interelectrode distance decreased. The overlap in the fields of stimulation at each current was calculated from the refractoriness observed in single and double electrode experiments. The results suggest that the axons mediating circling have a wide range of thresholds rather than a single threshold. The current required to activate an axon is roughly equal to K X r2, were K is a constant and r is the radial distance from electrode to axon. K must range from 400 to at least 3000 microA/mm2, to account for the circling data. For axons mediating medial forebrain bundle self-stimulation3, K must range from 1000 to at least 6400 microA/mm2. Estimation of the K distribution allows calculation of the effects of electrode size, placement and current on the recruitment of axons with different thresholds.     

An evaluation of symptom and chest radiographic screening in tuberculosis prevalence surveys.

SETTING: A tuberculosis (TB) prevalence survey was performed in 2002 in two urban communities in Cape Town, South Africa. The population was 36,334 in 2001, and the TB notification rate was 341 per 100,000 population for new smear-positive TB in 2002. OBJECTIVE: To evaluate the relative contributions of symptom and chest radiographic (CXR) screening in the detection of subjects with smear- and/or culture-positive TB in prevalence surveys. DESIGN: Information on symptoms, CXR abnormalities, sputum smear and culture was gathered from a random cluster sample of 1170 adults (aged > or = 15 years). Smear and/or culture-positive TB was used as the gold standard. RESULTS: Of 1170 adults, 29 had bacteriologically positive TB (smear- and/or culture-positive). The presence of any abnormalities on CXR had the highest sensitivity for detecting subjects with bacteriologically positive TB (0.97, 95%CI 0.90-1.00). Specificity for any abnormalities on CXR was 0.67 (95%CI 0.64-0.70). The specificity of any of five TB-related symptoms was 0.68 (95%CI 0.65-0.71). Individual symptoms had low sensitivities, ranging from 0.10 for fever to 0.54 for cough of > or = 2 weeks. CONCLUSION: In this TB prevalence survey, CXR screening, but not symptom screening, was a sensitive alternative to sputum examination of all participants.     

Reduced stimulation of helper T cells by Ki-ras transformed cells.

A number of viral genes and cellular oncogenes inhibit major histocompatibility complex (MHC) antigen expression at the cell surface. In the case of inhibition of class I MHC antigens by viral genes this results in a reduced recognition by antigen-specific cytotoxic T cells. The activated Ki-ras cellular oncogene carried by the Ki-murine sarcoma virus (Ki-MuSV) in contrast inhibits class II MHC (or Ia) antigen expression on transformed cells. We have studied how transformation with Ki-ras affects recognition by alloreactive helper T cells. We found that the Ki-ras inhibition of class II MHC antigen expression led to greatly reduced stimulation of alloreactive T cells to proliferate and to secrete interferon-gamma (IFN-gamma). These findings support our hypothesis that the ability of an oncogene to reduce class II MHC antigen expression is crucial to its ability to produce tumour cells.