1,721,089 research outputs found
Metabolic Syndrome and Autophagy: Focus on HMGB1 Protein
No full textMetabolic syndrome (MetS) affects the population worldwide and results from several factors such as genetic background, environment and lifestyle. In recent years, an interplay among autophagy, metabolism, and metabolic disorders has become apparent. Defects in the autophagy machinery are associated with the dysfunction of many tissues/organs regulating metabolism. Metabolic hormones and nutrients regulate, in turn, the autophagy mechanism. Autophagy is a housekeeping stress-induced degradation process that ensures cellular homeostasis. High mobility group box 1 (HMGB1) is a highly conserved nuclear protein with a nuclear and extracellular role that functions as an extracellular signaling molecule under specific conditions. Several studies have shown that HMGB1 is a critical regulator of autophagy. This mini-review focuses on the involvement of HMGB1 protein in the interplay between autophagy and MetS, emphasizing its potential role as a promising biomarker candidate for the early stage of MetS or disease’s therapeutic target
Correction: Might Fibroblasts from Patients with Alzheimer’s Disease Reflect the Brain Pathology? A Focus on the Increased Phosphorylation of Amyloid Precursor Protein Tyr682 Residue, (Brain Sci, (2021), 11, 103, 10.3390/brainsci1101010)
No full textIn the original article [1], there was a mistake in “Figure 3”. During the assembly of Figure 3, Western blot panels labeled with APPpTyr, APP, and β-actin were mistakenly used for familiar patients with AD, AD, and healthy controls. This error also affected the optical density analysis of the APPpTyr levels reported in Figure 1 and Figure 3B, where the values corresponding to Figure 3 needed to be replaced. In contrast, APP and β-actins optical density analyses were performed on the correct panels that are now reported in Figure 3 and did not require changes in the corresponding Figure 3C–E. Nonetheless, these errors did not influence the overall significance of the results, which remain consistent with those reported and discussed in this article. The corrected “Figure 1 and Figure 3” appear below. The authors apologize for any inconvenience caused and state that the scientific conclusions are unaffected. The original article has been updated
Plasma levels of n-3 polyunsaturated fatty acids and cognitive decline: possible role of depressive symptoms and apolipoprotein E genotyping
No full textRole of biphosphonates and lymphatic drainage type Leduc in the complex regional pain syndrome (shoulder-hand syndrome).
No full textEffectiveness of Switching Therapy from Complexing Protein-containing Botulinum Toxin Type A to a Formulation with Low Immunogenicity in Spasticity after Stroke: A case report.
No full textObjective: Some patients receiving botulinum toxin type A therapy develop immunological resistance due to the production of neutralizing antibodies against the neurotoxin, thus partially or completely reducing the therapeutic effect. Case report: We report here neurophysiological and clinical findings for a 58-year-old man treated with botulinum toxin type A for spasticity after ischaemic stroke, who became a secondary non-responder patient. Subsequent treatment with a different preparation of botulinum toxin type A had a great therapeutic effect on his spasticity. The muscles injected and the dosages were the same for each treatment, but evaluation with the Modified Ashworth Scale after treatment with the second preparation showed a reduction of approximately 2 points compared with the first examination. The clinical results were also supported by extensor digitorum brevis testing of the right muscle, which showed a reduction in compound muscle action potential, whereas it was unchanged in the non-injected muscle. No side-effects were reported, and after 1 year of treatment with this formulation clinical benefits were still evident. Conclusion: The neurophysiological and clinical results obtained in this patient suggest that switching therapy from a complexing protein-containing product to a product potentially free of complexing proteins, which has low immunogenicity, may be a viable therapeutic option in secondary non-responder patients
Botulinum toxin type A in the treatment of painful adductor muscle contracture after total hip arthroplasty
No full textDystonia is a set of disorders characterized by abnormal postures and unwanted muscle spasms that interfere with motor performance. Focal dystonias, the most common, affect just 1 body part. A 25-year-old woman had a focal hand dystonia with pain and muscle spasms in the right hand after surgical treatment for thumb duplication. According to Wassel's classification, she was type II, with duplication of the distal phalanx. She had undergone Bilhaut-Cloquet surgery to remove a radial supernumerary thumb. During repetitive movements, she reported pain and muscle cramping in the right thumb and wrist. Force was rated, according to the Medical Research Council scale, from grades 0 to 5, and the patient had a score of 4. No sign of joint instability was found in her hand, and normal active and passive range of motion were found for interphalangeal or metacarpophalangeal joints of right thumb. However, right thenar muscle hypoplasia was found. Repetitive activity acted as an environmental trigger for the reconstructed thumb on thenar muscle hypoplasia as residual anatomical modification. Surface electromyography showed movements suggestive of dystonia. After 5 days of treatment with botulinum toxin type A, with both the flexor pollicis longus and the abductor pollicis brevis of right hand injected with a dose of 20 microM each, the patient reported a regression of most signs and symptoms. Two-month follow-up revealed that clinical effects of botulinum toxin type A were still present
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