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Whether diseased motor neurones in sporadic amyotrophic lateral sclerosis (ALS) die via apoptosis is unknown. Because this relates primarily to difficulties in utilizing post-mortem tissue from end-stage disease, motor neurone degeneration in ALS spinal cord was compared with that of a model of a chronic motor neurone degeneration. Degenerating motor neurones in ALS, identified by ubiquitin immunoreactivity, did not demonstrate the morphological characteristics of apoptosis and were not c-Jun immunoreactive or TUNEL positive. A temporal analysis of spinal motor neurone death in the chronic AlCl3 neurotoxicity model of motor neurone degeneration was also undertaken. AlCl3 was administered intracisternally every 4 weeks and, at intervals of 51, 107, 156 and 267 days, evidence of apoptosis was sought by morphology, TUNEL hybridization or DNA laddering. Double-labelling immunostudies were also performed with antibodies to either c-Jun, ubiquitin or high molecular weight neurofilament (NFH) with TUNEL hybridization. Although significant neurone loss was evident, apoptosis was not found. These studies demonstrate a lack of apoptosis in ALS spinal motor neurones and suggest that this observation does not relate to the utilization of post-mortem tissue in which apoptotic neurones may have been lost.

We discuss analytically the vacuum structure and chiral-symmetry breaking in 1+1 dimensional lattice QCD with naive and Wilson fermions, using a unitary transformation and the variational method developed recently. As an example, the chiral order parameter is evaluated systematically for any coupling constant and fermion mass by including the multilink-terms in the transformation. The expected scaling behavior is observed. Our results are consistent with the continuum predictions.

Background: Traditionally considered a motor neuron–selective disorder, the clinical manifestations of ALS can include a frontotemporal dementia. Although the pathologic substrate of cognitive impairment remains to be defined, the presence of ubiquitin-immunoreactive (Ub+) intraneuronal inclusions in cortical regions has been suggested to constitute a pathologic marker of this process. Methods: The authors compared the neuropathological features of four cognitively impaired patients with ALS, four cognitively intact patients with ALS, and four neurologically normal patients. The extent and load of Ub+ neuronal inclusions, Ub+ dystrophic neurites, and superficial linear spongiosis (SLS) was determined among a number of cortical, hippocampal, and subcortical regions. Results: Although Ub+, alpha-synuclein-negative, and tau-negative neuronal inclusions were observed in both cognitively impaired and cognitively intact patients with ALS, their density and extent was greater among the former, with the difference greatest in the cingulate gyrus. Ub+ neurites were observed in a similar distribution. Only the presence of SLS, affecting the first and second cortical layers, reliably distinguished between the cognitively impaired and cognitively intact ALS subpopulations. In three of four cognitively impaired patients with ALS, SLS was associated with transcortical microglial activation, in the absence of detectable differences in astrocytosis, density of calbindin or parvalbumin neurons, or optical density of synaptophysin and SNAP-25. Conclusions: Although intraneuronal Ub+ inclusions and dystrophic neurites are observed in both ALS subpopulations, the presence of cognitive impairment was associated with a greater distribution and load of both neuropathologic features, suggesting a disease continuum. Moreover, cognitive impairment was uniformly associated with superficial linear spongiosis, a pathologic feature common to several forms of frontotemporal dementia.

To explore the possible neuroprotective role of microglia after a peripheral nerve lesion, the present study used athymic mice shown to have a lower number of microglia to highlight some functions of microglia not normally obvious in animals with a normal number of such cells. Observation of semithin sections showed that unoperated 5-day-old athymic mice had a significant lower number of microglial cells around sciatic motoneurons, compared to their BALB/c littermates. After right sciatic nerve cut at mid-thigh level, motoneuron loss occurred faster at 5 and 10 days after operation in neonatal athymic mice than BALB/c mice. The motoneuron loss by 15 days after nerve cut was, however, the same in both strains of mice. Microglial reaction after sciatic neurectomy, as revealed by Mac-1 immunohistochemistry, was obviously less in intensity and number in athymic mice than in BALB/c mice. The results indicated a neuroprotective function of microglia, which, when not present in adequate numbers, could result in a faster motoneuron death. The study also showed that while microglia were reduced in number in athymic mice, there was no significant difference in the number of astrocytes and oligodendrocytes in the spinal cord of the athymic mice, compared to that in BALB/c mice. This indicates that the development of astrocytes and oligodendrocytes in the spinal cord may not be affected by a reduced number of microglia.

The trace elements Zn, Cu, Fe, and ordinary elements K, Na, Ca, Mg in serum of 711 patients with heart disease (HD) were determined with GGX-II atomic absorption spectrophotometer and flame photometer. It was found that the contents of K, Ca/Mg in HD were significantly lower than those in the control, while the content of Na, Mg, Zn, Fe, and Zn/Cu, Na/K were significantly higher than those in the control. There was a significantly negative correlation between K, Ca/Mg and blood pressure (BP), between Zn/Cu and HDL-ch, and a significantly positive correlation between Na, Zn, Fe, Zn/Cu, Na/K and BP, between Fe and Hct, between Zn/Cu and Hct, TG, VLDL-ch.