Artificial Intelligence Rehabilitation Evaluation and Training System for Degeneration of Joint Disease

Degeneration of joint disease is one of the problems that threaten global public health.Currently,the therapies of the disease are mainly conservative but not very effective.To solve the problem,we need to find effective,convenient and inexpensive therapies.With the rapid development of artificial intelligence,we innovatively propose to combine Traditional Chinese Medicine(TCM)with artificial intelligence to design a rehabilitation assessment system based on TCM Daoyin.Our system consists of four subsystems:the spine movement assessment system,the posture recognition and correction system,the background music recommendation system,and the physiological signal monitoring system.We incorporate several technologies such as keypoint detection,posture estimation,heart rate detection,and deriving respiration from electrocardiogram(ECG)signals.Finally,we integrate the four subsystems into a portable wireless device so that the rehabilitation equipment is well suited for home and community environment.The system can effectively alleviate the problem of an inadequate number of physicians and nurses.At the same time,it can promote our TCM culture as well.

Streptozotocin induced Alzheimer's disease like changes and the underlying neural degeneration and regeneration mechanism

Alzheimer’s disease（AD）is a neurodegenerative disorder which is remarkably characterized by pathological hallmarks that include neurofibrillary tangles,neuronal loss extracellular senile plaques containing aggregated amyloid beta（Aβ）,and neurofibrillary tangles composed of the hyperphosphorylated form of the microtubule protein tau.It is the most common form of dementia which is characterized by severe neurodegenerative changes such as loss of neurons and synapses in brain（Kamat et al.,2014）.

Degree of dopaminergic degeneration measured by ^(99m)Tc-TRODAT-1 SPECT/CT imaging

To prevent and treat Parkinson＇s disease in its early stages,it is essential to be able to detect the degree of early dopaminergic neuron degeneration.Dopamine transporters（DAT） in the striatum regulate synaptic dopamine levels,and striatal ^99mTc-TRODAT-1 single-photon emission computed tomography（-SPECT） imaging is a marker for presynaptic neuronal degeneration.However,the association between the degree of dopaminergic degeneration and in vivo ^99mTc-TRODAT-1 SPECT imaging is unknown.Therefore,this study investigated the association between the degree of 6-hydroxydopamine（6-OHDA）-induced dopaminergic degeneration and DAT imaging using^99mTc-TRODAT-1 SPECT in rats.Different degrees of nigrostriatal dopamine depletion were generated by injecting different doses of 6-OHDA（2,4,and 8 μg） into the right medial forebrain bundle.The degree of nigrostriatal dopaminergic neuron degeneration was assessed by rotational behavior and immunohistochemical staining.The results showed that striatal ^99mTc-TRODAT-1 binding was significantly diminished both in the ipsilateral and the contralateral sides in the 4 and 8 μg 6-OHDA groups,and that DAT ^99mTc-TRODAT-1 binding in the ipsilateral striatum showed a high correlation to apomorphine-induced rotations at 8 weeks post-lesion（r = –0.887,P 〈 0.01）.There were significant correlations between DAT ^99mTc-TRODAT-1 binding in the ipsilateral striatum and the amount of tyrosine hydroxylase immunoreactive neurons in the ipsilateral substantia nigra in the 2,4,and 8 μg 6-OHDA groups at 8 weeks post-lesion（r = 0.899,P 〈 0.01）.These findings indicate that striatal DAT imaging using ^99mTc-TRODAT-1 is a useful technique for evaluating the severity of dopaminergic degeneration.

Coexistent Charcot-Marie-Tooth type 1A and type 2 diabetes mellitus neuropathies in a Chinese family

Charcot-Marie-Tooth disease type 1A（CMT1A） is caused by duplication of the peripheral myelin protein 22（PMP22） gene on chromosome 17. It is the most common inherited demyelinating neuropathy. Type 2 diabetes mellitus is a common metabolic disorder that frequently causes predominantly sensory neuropathy. In this study, we report the occurrence of CMT1 A in a Chinese family affected by type 2 diabetes mellitus. In this family, seven individuals had duplication of the PMP22 gene, although only four had clinical features of polyneuropathy. All CMT1 A patients with a clinical phenotype also presented with type 2 diabetes mellitus. The other three individuals had no signs of CMT1 A or type 2 diabetes mellitus. We believe that there may be a genetic link between these two diseases.