Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5767781 | PMC |
| http://dx.doi.org/10.5114/kitp.2017.72235 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
GBA is the major risk gene for Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB), two common α-synucleinopathies with cognitive deficits. We investigated the role of mutant GBA in cognitive decline by utilizing Gba (L444P) mutant, SNCA transgenic (tg), and Gba-SNCA double mutant mice. Notably, Gba mutant mice showed early cognitive deficits but lacked PD-like motor deficits or α-synuclein pathology.
View Article and Find Full Text PDFSurgical parathyroidectomy in pregnancy for severe secondary hyperparathyroidism associated with end-stage kidney disease.
BMJ Case Rep
January 2025
Maternity Services, The Royal Women's Hospital, Parkville, Victoria, Australia.
Secondary hyperparathyroidism (SHPT) is common in patients with end-stage kidney disease (ESKD) on kidney replacement therapy, which leads to abnormalities of bone and mineral metabolism. Patients conceiving on kidney replacement therapy add a further layer of complexity to the management of their SHPT. Existing literature in cases of primary hyperparathyroidism (PHPT) has linked untreated hyperparathyroidism to increased maternal and fetal morbidity, including hypertensive disorders of pregnancy, fetal growth restriction and neonatal hypocalcaemia.
View Article and Find Full Text PDFChronotherapy with Cinacalcet has a striking effect on inhibition of parathyroid gland proliferation in rats with secondary hyperparathyroidism.
PLoS One
January 2025
Nephrological Department, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.
Secondary hyperparathyroidism (sHPT) is a significant clinical complication of CKD leading to bone abnormalities and cardiovascular disease. Current treatment based on activating the parathyroid calcium-sensing receptor (CaSR) using calcimimetics such as Cinacalcet, aims to decrease plasma PTH levels and inhibit the progression of parathyroid hyperplasia. In the present study, we found significant diurnal rhythmicity of Casr, encoding the Cinacalcet drug target in hyperplastic parathyroid glands (p = 0.
View Article and Find Full Text PDFCharacterization of Dystrophin Dp71 Expression and Interaction Partners in Embryonic Brain Development: Implications for Duchenne/Becker Muscular Dystrophy.
Mol Neurobiol
January 2025
Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-Cho, Kawaramachi Hirokoji, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Duchenne/Becker muscular dystrophy (DMD/BMD) manifests progressive muscular dystrophy and non-progressive central nervous disorder. The neural disorder is possibly caused by abnormalities in the developmental period; however, basic research to understand the mechanisms remains underdeveloped. The responsible gene, Dmd (dystrophin), generates multiple products derived from several gene promoters.
View Article and Find Full Text PDFTooth Anomalies in Patients With Nonsyndromic Orofacial Cleft: A Systematic Review and Meta-Analysis.
Oral Dis
January 2025
Department of Oral Diagnosis, School of Dentistry, University of Campinas, Piracicaba, São Paulo, Brazil.
Objective: To evaluate the frequency of tooth anomalies (TA) in the deciduous and permanent dentition of patients with nonsyndromic orofacial clefts (NSOC), both inside and outside the cleft area.
Methods: The following databases were searched for the relevant literature: Cochrane, OVID, SciELO, Embase, Livivo, PubMed, Scopus, and Web of Science. The risk of bias was analyzed using the Joanna Briggs Institute.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!