Clinical/occlusal scores and jaw-muscle EMGs were recorded in 24 TMD symptomatic (group S) and 20 normal (group N) subjects to evaluate the significance of EMG parameters and their clinical associations. Results indicated: (1) integrated EMG activity (IEMG) was larger at the rest position (RP) in anterior temporalis (Ta) but smaller at maximal voluntary clenching (MVC) in masseter (Ma) and Ta, and the ratios of IEMG at 70%MVC to the corresponding bite force (70%BF) were greater in group S; (2) mean power frequency (MPF) were almost the same in both groups but its shift was more rapid in group S; (3) silent period duration (SPD) was longer in group S; (4) asymmetry indices for SPD and silent period latency (SPL) were larger in group S; (5) muscle pain was associated negatively with IEMG at MVC and 70%BF but positively with IEMGs at RP and 70%MVC, and impaired jaw movements were associated negatively with the above EMG values; (6) muscle pain was positively associated with SPD in Ma, while joint pain and sound showed positive and negative associations with SPD, respectively; (7) associations between occlusion and EMG parameters were found more in group N. These findings verify: (1) jaw elevators in TMD may have hyper-tonic activities and a weak functional efficiency; (2) jaw muscles in TMD may become easily fatigued following a functional effort, and less relaxed following a muscle twitch; (3) the severity of pain could not be reflected in EMG activities, but impaired jaw movement may increase tonic activity and decrease functional effort; (4) TMD symptoms may alter the functional adaptation of jaw-muscle activities and occlusion.

Xeno nucleic acids (XNAs) are a group of chemically modified nucleic acid analogues that have been applied to various biological technologies such as antisense oligonucleotides, siRNAs and aptamers.

Parkinson’s disease (PD) is a neurodegenerative disease caused by the loss of dopaminergic neurons in the substantia nigra. A characteristic pathological feature of PD is cytoplasmic accumulation of α-synuclein (SNCA) protein. Multiplication of the SNCA gene in familial PD and pathological accumulation of SNCA protein during progression of sporadic PD suggest that increased SNCA protein levels increase the risk of PD. Thus, reducing SNCA expression levels could delay PD onset or modify the disease course. For efficient knock down, we designed and synthesized an amido-bridged nucleic acids (AmNA)-modified antisense oligonucleotide (ASO) that targeted SNCA with improved stability and cellular uptake in vivo . AmNA-ASO efficiently downregulated SNCA at both the mRNA and protein level in vitro and in vivo . Notably, AmNA-ASO was efficiently delivered into the mouse brain by intracerebroventricular injection without the aid of additional chemicals. Furthermore, administration of AmNA-ASO ameliorated neurological defects in PD model mice expressing human wild type SNCA. Taken together, these findings suggest that AmNA-ASO is a promising therapeutic strategy for SNCA-associated pathology in PD.