Fluorescence spectroscopy on a series of aqueous solutions of poly(acrylic acid) containing a luminescent label showed that polymers with molar mass, Mn < 16.5 kDa did not exhibit a pH responsive conformational change, which is typical of higher molar mass poly(acrylic acid). Below this molar mass, polymers remained in an extended conformation, regardless of pH. Above this molar mass, a pH-dependent conformational change was observed. Diffusion-ordered nuclear magnetic resonance spectroscopy confirmed that low molar mass polymers did not undergo a conformational transition, although large molar mass polymers did exhibit pH-dependent diffusion.
Previous studies demonstrated age- and height-related slowing of nerve conduction velocity (NCV) and reduction in nerve response amplitude. Unfortunately, many studies examined discontinuous populations, preventing regression analysis. The correlation coefficients of available studies vary widely, preventing clear conclusions. We retrospectively examined 3969 clinically normal subjects ranging in age from 20 to 95 years from a total of 22,420 electrodiagnostic studies done between 1986 and 1998. The correlation of NCV with height was stronger than with age. Regression equations using both factors account for 12--27% of the variance. Responses were seen in the majority of patients aged 70 years and older, but the percentage of normals who had no response increased with advancing age. Age was strongly inversely correlated with the amplitudes of both sensory and motor responses, accounting for 7--16% of the variance. Regression equations using both height and age improved this correlation, accounting for 7--22% of the variance. Therefore, both height and age must be taken into consideration when normal values are developed.
Of 40 patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), 28 completed a controlled three-month trial of prednisone. Prednisone was shown to cause a small but significant improvement over no treatment in scored neurological disability, some measures of computer-assisted sensory detection threshold, graded muscle strength, and some attributes of nerve conduction. No subset of patients was more likely than another to be responsive to prednisone; those with a progressive course were as likely to be responsive as recurrent cases. This finding provides further justification for classifying progressive with recurrent cases as CIDP and demonstrates that prednisone treatment should not be withheld from patients with progressive disease.
The findings highlight the value of qualitative research in the psychopharmacological investigation of psychedelics. They describe perceived connections between drug- and non-drug factors, and provide suggestions for future research trial design and clinical applications.
Recent randomized controlled trials of psilocybin-assisted psychotherapy for patients with cancer suggest that this treatment results in large-magnitude reductions in anxiety and depression as well as improvements in attitudes toward disease progression and death, quality of life, and spirituality. To better understand these findings, we sought to identify psychological mechanisms of action using qualitative methods to study patient experiences in psilocybinassisted psychotherapy. Semistructured interviews were conducted with 13
We compared anti-GM1 IgM antibody titers in patients with various neurologic diseases and in normal subjects. We found increased titers in patients with lower motor neuron disease, sensorimotor neuropathy, or motor neuropathy with or without multifocal conduction block. In patients with other diseases, titers are similar to those in normal individuals, suggesting that anti-GM1 antibody levels are not increased nonspecifically after neural injury or inflammatory diseases. Anti-GM1 antibodies in many of the patients occur as monoclonal gammopathies, predominantly of lambda light-chain type, but the antibodies are sometimes polyclonal with normal or increased serum IgM concentrations. Most of the anti-GM1 antibodies appear to react with the Gal(beta 1-3)GalNAc epitope which is shared with asialo-GM1 and GD1b, but in some patients the antibodies are more specific for GM1 and associated with motor neuropathy. Patients with motor or sensorimotor peripheral neuropathy or lower motor neuron disease should be tested for anti-GM1 antibodies or anti-Gal(beta 1-3)GalNAc antibodies, as therapeutic reduction in antibody concentrations was reported to result in clinical improvement in some patients.
Ciguatera is a type of marine food poisoning produced by the consumption of ciguatoxic reef fish. The disease is of significant concern in many tropical areas where it has been known for centuries. Although mortality from ciguatera is low, morbidity is high and symptoms may be debilitating and prolonged. Ciguatera produces characteristic gastrointestinal, neurological, and to a lesser extent, cardiovascular symptoms. Though the symptoms are relatively well documented, the disease often goes unreported or misdiagnosed. The toxins responsible for ciguatera are produced by marine dinoflagellates associated with coral reefs. The toxins are ingested by and accumulate in the fishes which when consumed by man ultimately cause ciguatera. Recent advances in toxin pharmacology have identified ciguatoxin as a sodium channel agonist and have begun to address other aspects of ciguatera on the molecular level. Treatment with mannitol relieves the symptoms; the precise mechanism or mechanisms of action have not been proven. Immunoassays are being developed for detecting even negligible amounts of toxins in suspect fish flesh.
Even when all known factors affecting the determination of nerve conduction velocity are controlled, large individual variations persist. In 40 normal controls, we found that peroneal and sural conduction velocities varied inversely with body height (P less than 0.001). This height effect is not due to temperature differences, and it explains almost 50% of the intersubject variability in conduction velocity. We hypothesize that the height influence reflects abrupt, rather than gradual, tapering of axons distally. This mode of tapering may help explain the decrements in conduction velocity from proximal to distal nerve segments and from upper to lower extremities, which have long been observed in clinical electromyography. Clinical recognition of this height effect is important lest one label as abnormal an individual with mildly slowed peripheral nerve conduction velocity solely related to large stature.
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