Evaluation of the effect of CaD on the bone structure and bone metabolic changes in senile osteoporosis rats based on MLP–ANN methods

2019 ◽  
Vol 10 (12) ◽  
pp. 8026-8041 ◽  
Author(s):  
Xiufeng Tang ◽  
Yingying Gao ◽  
Yuheng Chen ◽  
Xiaoxi Li ◽  
Ping Yu ◽  
...  

Senile osteoporosis (SOP) is a related disease of systematic degenerative changes in bones during natural aging.

2007 ◽  
Vol 42 (11) ◽  
pp. 1099-1108 ◽  
Author(s):  
Peter Pietschmann ◽  
Monika Skalicky ◽  
Michaela Kneissel ◽  
Martina Rauner ◽  
Günther Hofbauer ◽  
...  

Author(s):  
Ahmed Abdulaziz G. Ibrahim ◽  
Ali Mohammed A. Alahmari ◽  
Abdullah Hassan F. Alsuayri ◽  
Abdullah Misfer M. Algomshah ◽  
Saeed Ghanem S. Almlfi ◽  
...  

Cervical spondylosis is a term that encompasses a wide range of progressive degenerative changes that affect all components of the cervical spine (i.e., intervertebral discs, facet joints, Luschka joints, flava ligaments, and laminae). It is a natural aging process and occurs in most people after the age of five. Most people with radiographic spondylotic changes in the cervical spine  remain asymptomatic, and 25% of those under  40, 50% of those over  40, and 85% of those over  60 show some evidence of degenerative changes , including changes in  the environment. Uncovertebral joints, facet joints, posterior longitudinal ligament (PLL) and yellow ligament lead to  narrowing of the spinal canal and intervertebral foramina. As a result, the spinal cord, spinal vasculature, and nerve roots can become compressed, leading to the three clinical syndromes that occur with cervical spondylosis: axial neck pain, cervical myelopathy, and cervical radiculopathy. Cervical spondylosis is usually diagnosed for clinical reasons only, but imaging is also required. Treatment for cervical spondylosis can be medical or surgical, depending on whether the patient has symptoms of myelopathy, radicular pain, or neck pain.


2021 ◽  
Vol 15 (1) ◽  
pp. 191-195
Author(s):  
Zurab Khabadze ◽  
Oleg Mordanov ◽  
Georgiy Davreshyan ◽  
Mariya Balashova ◽  
Alexander Prokopenko ◽  
...  

Aim: This study aimed at assessing the degenerative changes in the Temporomandibular Joint (TMJ)in elderly patients with posterior edentulous maxilla and mandibula according to Cone-Beam Computed Tomography (CBCT) data. Materials and Methods: The study included 32 patients (64 temporomandibular joints) aged from 50 to 81 years (mean age 62 ± 7.9 years; 16 males and 16 females). TMJs were visualized on reconstructed parasagittal, paracoronal, and axial sections of the joint. The following changes in bone tissue were evaluated: condyle flattening, erosion, sclerosis, subchondral cysts, osteophytes. Joint space was evaluated as well. Results and Discussion: 100% of patients had at least one sign of degenerative changes in TMJ at least on one side. In 19 patients, degenerative symptoms were found only on one side. The most common sign was subchondral cysts. It was noted that the number of degenerative symptoms in male patients was statistically more than in the female group. On the right side, the anterior, superior, and posterior joint spaces had the following values: 2.35 mm, 2.95 mm, and 4.84 mm, respectively. On the left side, the anterior, superior, and posterior joint spaces had the following values: 2.14 mm, 2.3 mm, and 4.1 mm, respectively. Conclusion: Both edentulousness and aging affect the bone structure of TMJ in both genders.


2020 ◽  
Vol 245 (17) ◽  
pp. 1571-1583 ◽  
Author(s):  
Wei-Hua Lee ◽  
Vijesh J Bhute ◽  
Hitoshi Higuchi ◽  
Sakae Ikeda ◽  
Sean P Palecek ◽  
...  

Mitochondria are dynamic organelles that undergo fission and fusion. While they are essential for cellular metabolism, the effect of dysregulated mitochondrial dynamics on cellular metabolism is not fully understood. We previously found that transmembrane protein 135 ( Tmem135) plays a role in the regulation of mitochondrial dynamics in mice. Mice homozygous for a Tmem135 mutation ( Tmem135FUN025/FUN025) display accelerated aging and age-related disease pathologies in the retina including the retinal pigment epithelium (RPE). We also generated a transgenic mouse line globally overexpressing the Tmem135 gene ( Tmem135 TG). In several tissues and cells that we studied such as the retina, heart, and fibroblast cells, we observed that the Tmem135 mutation causes elongated mitochondria, while overexpression of Tmem135 results in fragmented mitochondria. To investigate how abnormal mitochondrial dynamics affect metabolic signatures of tissues and cells, we identified metabolic changes in primary RPE cell cultures as well as heart, cerebellum, and hippocampus isolated from Tmem135FUN025/FUN025 mice (fusion > fission) and Tmem135 TG mice (fusion < fission) using nuclear magnetic resonance spectroscopy. Metabolomics analysis revealed a tissue-dependent response to Tmem135 alterations, whereby significant metabolic changes were observed in the heart of both Tmem135 mutant and TG mice as compared to wild-type, while negligible effects were observed in the cerebellum and hippocampus. We also observed changes in Tmem135FUN025/FUN025 and Tmem135 TG RPE cells associated with osmosis and glucose and phospholipid metabolism. We observed depletion of NAD+ in both Tmem135FUN025/FUN025 and Tmem135 TG RPE cells, indicating that imbalance in mitochondrial dynamics to both directions lowers the cellular NAD+ level. Metabolic changes identified in this study might be associated with imbalanced mitochondrial dynamics in heart tissue and RPE cells which can likely lead to functional abnormalities. Impact statement Mitochondria are dynamic organelles undergoing fission and fusion. Proper regulation of this process is important for healthy aging process, as aberrant mitochondrial dynamics are associated with several age-related diseases/pathologies. However, it is not well understood how imbalanced mitochondrial dynamics may lead to those diseases and pathologies. Here, we aimed to determine metabolic alterations in tissues and cells from mouse models with over-fused (fusion > fission) and over-fragmented (fusion < fission) mitochondria that display age-related disease pathologies. Our results indicated tissue-dependent sensitivity to these mitochondrial changes, and metabolic pathways likely affected by aberrant mitochondrial dynamics. This study provides new insights into how dysregulated mitochondrial dynamics could lead to functional abnormalities of tissues and cells.


Author(s):  
Jay W. Cha ◽  
Perry J. Melnick

Hereditary ochronosis in very few cases has been examined electron microscopically or histochemically. In this disease homogentisic acid, a normal intermediary of tyrosine metabolism, forms in excessive amounts. This is believed to be due to absence or defective activity of homogentisic acid oxidase, an enzyme system necessary to break the benzene ring and to further break it down to fumaric and acetoacetic acids. Ochronotic pigment, a polymerized form of homogentisic acid, deposits mainly in mesenchymal tissues. There has been a question whether the pigment originates from the collagenous tissues, or deposits passively, where in contrast to melanin it induces degenerative changes.


Author(s):  
Sidney D. Kobernick ◽  
Edna A. Elfont ◽  
Neddra L. Brooks

This cytochemical study was designed to investigate early metabolic changes in the aortic wall that might lead to or accompany development of atherosclerotic plaques in rabbits. The hypothesis that the primary cellular alteration leading to plaque formation might be due to changes in either carbohydrate or lipid metabolism led to histochemical studies that showed elevation of G-6-Pase in atherosclerotic plaques of rabbit aorta. This observation initiated the present investigation to determine how early in plaque formation and in which cells this change could be observed.Male New Zealand white rabbits of approximately 2000 kg consumed normal diets or diets containing 0.25 or 1.0 gm of cholesterol per day for 10, 50 and 90 days. Aortas were injected jin situ with glutaraldehyde fixative and dissected out. The plaques were identified, isolated, minced and fixed for not more than 10 minutes. Incubation and postfixation proceeded as described by Leskes and co-workers.


2006 ◽  
Vol 5 (12) ◽  
pp. 30
Author(s):  
KERRI WACHTER
Keyword(s):  

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