218 research outputs found
IPLEX and the Telephone Game: the difficulty in separating myth from reality on the internet
No full text
Detection of serum reverse transcriptase activity in patients with ALS and unaffected blood relatives
No full textThese results confirm that patients with ALS have a significantly higher prevalence of serum reverse transcriptase (RT) activity than that seen in unrelated control subjects. The finding of a similarly increased prevalence in blood relatives of ALS patients raises the possibility that the observed RT activity might be due to an inherited endogenous retrovirus
Altered fractal dynamics of gait: reduced stride-interval correlations with aging and Huntington’s disease
No full text Hausdorff, Jeffrey M., Susan L. Mitchell, Renée Firtion, C. K. Peng, Merit E. Cudkowicz, Jeanne Y. Wei, and Ary L. Goldberger. Altered fractal dynamics of gait: reduced stride-interval correlations with aging and Huntington’s disease. J. Appl. Physiol. 82(1): 262–269, 1997.—Fluctuations in the duration of the gait cycle (the stride interval) display fractal dynamics and long-range correlations in healthy young adults. We hypothesized that these stride-interval correlations would be altered by changes in neurological function associated with aging and certain disease states. To test this hypothesis, we compared the stride-interval time series of 1) healthy elderly subjects and young controls and of 2) subjects with Huntington’s disease and healthy controls. Using detrended fluctuation analysis, we computed α, a measure of the degree to which one stride interval is correlated with previous and subsequent intervals over different time scales. The scaling exponent α was significantly lower in elderly subjects compared with young subjects (elderly: 0.68 ± 0.14; young: 0.87 ± 0.15; P < 0.003). The scaling exponent α was also smaller in the subjects with Huntington’s disease compared with disease-free controls (Huntington’s disease: 0.60 ± 0.24; controls: 0.88 ± 0.17; P < 0.005). Moreover, α was linearly related to degree of functional impairment in subjects with Huntington’s disease ( r = 0.78, P < 0.0005). These findings demonstrate that stride-interval fluctuations are more random (i.e., less correlated) in elderly subjects and in subjects with Huntington’s disease. Abnormal alterations in the fractal properties of gait dynamics are apparently associated with changes in central nervous system control. </jats:p
Phase II/III randomized trial of TCH346 in patients with ALS
No full textBACKGROUND: TCH346 exerts antiapoptotic effects by binding to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and blocking the apoptotic pathway in which GAPDH is involved. Apoptosis is considered to be a key pathogenic mechanism in neurodegenerative diseases including ALS.
METHODS: Patients were randomly assigned in a double-blind fashion to receive either placebo or one of four doses of TCH346 (1.0, 2.5, 7.5, or 15 mg/day) administered orally once daily for at least 24 weeks. The primary outcome measure was the rate of change in the revised ALS functional rating scale (ALSFRS-R). The trial design included a 16-week lead-in phase to determine each patient''s rate of disease progression. The between treatment comparison was adjusted for the individual pretreatment rates of progression. The study was powered to detect a 25% reduction in the rate of decline of the ALSFRS-R as compared with placebo. Secondary outcome measures included survival, pulmonary function, and manual muscle testing (MMT).
RESULTS: Five hundred ninety-one patients were enrolled at 42 sites in Europe and North America. There were no differences in baseline variables. There were no significant differences between placebo and active treatment groups in the mean rate of decline of the ALSFRS-R or in the secondary outcome measures (survival, pulmonary function, and MMT).
CONCLUSION: The trial revealed no evidence of a beneficial effect of TCH346 on disease progression in patients with ALS
Deficient production of nonerythroid cells by transplanted marrow of anemic wwv mice. Abstr.
No full textPeculiar immunobiology of bone marrow allografts. I. Graft rejection by irradiated responder mice.
No full textMice are capable of rejecting H-2-incompatible bone marrow grafts after a single lethal exposure to X-rays. The onset of rejection begins 18-24 hr after transplantation and is completed by 96 hr. Maturation of this type of allograft reactivity does not occur until the 22nd day of life. In adult mice, the resistance to marrow allografts can be weakened by administration of cyclophosphamide or dead cultures of Corynebacterium parvum, but not heterologous anti-thymocyte serum. Sublethal exposures to X-rays 7 or 14 days before transplantation also weaken resistance. There is considerable interstrain variation in the ability of mice to resist allografts, even when H-2 differences between hosts and donor are kept identical. Although H-2 incompatibility is a necessary prerequisite for resistance, additional genetic factors influence the outcome of marrow allografts, presumably by controlling recognition. The regulator genes are determinant specific and the alleles for resistance or responder status appear to be dominant. The responder phenotype is expressed by hemopoietic cells and not by the environment. Accordingly, resistance is conferred to otherwise susceptible mice upon transfer of bone marrow cells but not of serum. The production and differentiation of effector cells for marrow graft rejection are thymus independent. In conclusion, bone marrow allografts elicit a particular transplantation reaction, previously unknown, in irradiated mice. Peculiar features of this reaction are the lack of proliferation of host lymphoid cells, tissue specificity, thymus independence, and regulation by genetic factors which apparently do not affect the fate of other grafts
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