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To better understand the site of action of Botulinum Toxin (BTX) in spasticity, we studied 6 patients affected with upper limb post-stroke spasticity. Patients were injected with Botulinum Toxin type A (Botox®, Allergan SpA, Rome, Italy) in one or more arm muscles with total doses not to exceed 200U (mean 158U). Mean onset of stroke was 22 months. Tests before injection, 15 days and 30 days after included: (i) evaluation of tone (Ashworth score); (ii) active and passive range of motion at elbow and wrist; (iii) ratio Hmax/Mmax from flexor carpi radialis (FCR); (iv) H-reflex presynaptic inhibition during vibration (FCR); (v) functional score; (vi) reciprocal inhibition of the H-reflex (FCR); (vii) kinesiologic EMG. The clinical examination improved in all patients, and changes of the functional and Ashworth scores were significant (p<0.02). We observed an improved range of motion for active extension at the wrist and elbow. No significant changes in the Hmax/Mmax ratio, the H-reflex presynaptic inhibition during vibration, and in the reciprocal inhibition of the H-reflex were observed. Each patient described a subjective improvement and a sensation of increased “freedom” of their arm. The results suggest that the use of BTX in patients affected with spasticity does not act at the level of changes in presynaptic inhibition of alpha-motoneurons. [Copyright &y& Elsevier]

Background: Diabetes accelerates atherosclerosis through undefined molecular mechanisms. Hyperglycemia induces formation of advanced glycation end product (AGE)-modified low-density lipoprotein (LDL). Anti-AGE-LDL autoantibodies favor atherosclerosis (AS) progression in humans, while anti oxidized LDL immunization inhibits AS in hypercholesterolemic, non-diabetic mice. We here investigated if AGE-LDL immunization protects against AS in diabetic mice. Methods: After diabetes induction with streptozotocin and high fat diet, both low density lipoprotein receptor (LDLR)−/− and apoE female mice were randomized to: AGE-LDL immunization with aluminum hydroxide (Alum) adjuvant; Alum alone; or PBS. Results: AGE-LDL immunization: significantly reduced AS; induced specific plasma IgM and IgG antibodies; upregulated splenic Th2, Treg and IL-10 levels, without altering Th1 or Th17 cells; and increased serum high density lipoprotein(HDL) while numerically lowering HbA1c levels. Conclusions: Subcutaneous immunization with AGE-LDL significantly inhibits atherosclerosis progression in hyperlipidemic diabetic mice possibly through activation of specific humoral and cell mediated immune responses and metabolic control improvement. [ABSTRACT FROM AUTHOR]