A METHOD OF TESTING IMPLANTED CARDIAC PACEMAKERS

In some patients with complete heart block electrical pacing has become an accepted form of treatment, and this has been well reviewed (Chardack, Gage, and Greatbatch, 1960; Chardack 1964; Zoli et al., 1961; Portal et al., 1962). The quoted battery life of pacemakers available co-mercially is from 2 to 5 years. However, experience with our first 10 cases has shown that earlier replacement of the units is sometimes necessary because of premature battery failure and either gradual or sudden failure of another component. These failures cause changes in one or more of the following output characteristics of the pacemaker: rate, amplitude, and pulse width. Measure-ment of these characteristics is easily made with the pacemaker outside the body, but after the unit is implanted this presents some difficulty. Pulse rate of the unit can be obtained from the electro-cardiogram, but output voltage and pulse width are more difficult to measure. One commercial model * provides two subcutaneous testing electrodes to which needles can be attached under local anmsthetic, but it is possible for these wires to break while the unit is functioning correctly (Par-sonnet et al., 1963). The standard electrocardiogram from a patient with an implanted pacemaker shows the stimu-lating pulses (Fig. 1), but their wave form is not accurately reproduced because of the limited fre

The Structure of the Vote in the 2004 Presidential Election

This article examines the structure underlying the vote in the 2004 presidential election. Specifically the study uses correlation and factor analysis to discern the extent to which the structure of the vote in 2004 was similar to that of prior elections. The analysis reveals that the structure of the state-by-state vote in 2004 demonstrated a remarkably high level of continuity with recent presidential elections. Indeed at the aggregate level, the stability exhibited in the presidential vote now rivals that found during the zenith of the New Deal party system. This suggests that those who continue to talk about dealignment and ongoing electoral volatility have missed an important development in the contemporary American party system: the stability underlying the presidential vote not only in 2004 but over the past three decades of party competition. © 2005 Policy Studies Organization

Glia-dependent TGF-β signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis

Autoimmune encephalomyelitis, a mouse model for multiple sclerosis, is characterized by the activation of immune cells, demyelination of axons in the CNS, and paralysis. We found that TGF-β1 synthesis in glial cells and TGF-β–induced signaling in the CNS were activated several days before the onset of paralysis in mice with autoimmune encephalomyelitis. While early production of TGF-β1 was observed in glial cells TGF-β signaling was activated in neurons and later in infiltrating T cells in inflammatory lesions. Systemic treatment with a pharmacological inhibitor of TGF-β signaling ameliorated the paralytic disease and reduced the accumulation of pathogenic T cells and expression of IL-6 in the CNS. Priming of peripheral T cells was not altered, nor was the generation of TH17 cells, indicating that this effect was directed within the brain, yet affected the immune system. These results suggest that early production of TGF-β1 in the CNS creates a permissive and dangerous environment for the initiation of autoimmune inflammation, providing a rare example of the brain modulating the immune system. Importantly, inhibition of TGF-β signaling may have benefits in the treatment of the acute phase of autoimmune CNS inflammation

The Neuroprotective Functions of Transforming Growth Factor Beta Proteins

Transforming growth factor beta (TGF-β) proteins are multifunctional cytokines whose neural functions are increasingly recognized. The machinery of TGF-β signaling, including the serine kinase type transmembrane receptors, is present in the central nervous system. However, the 3 mammalian TGF-β subtypes have distinct distributions in the brain suggesting different neural functions. Evidence of their involvement in the development and plasticity of the nervous system as well as their functions in peripheral organs suggested that they also exhibit neuroprotective functions. Indeed, TGF-β expression is induced following a variety of types of brain tissue injury. The neuroprotective function of TGF-βs is most established following brain ischemia. Damage in experimental animal models of global and focal ischemia was shown to be attenuated by TGF-βs. In addition, support for their neuroprotective actions following trauma, sclerosis multiplex, neurodegenerative diseases, infections, and brain tumors is also accumulating. The review will also describe the potential mechanisms of neuroprotection exerted by TGF-βs including anti-inflammatory, -apoptotic, -excitotoxic actions as well as the promotion of scar formation, angiogenesis, and neuroregeneration. The participation of these mechanisms in the neuroprotective effects of TGF-βs during different brain lesions will also be discussed