Mayerkendall1032

The aim of the study was to describe the bone metabolism status that underlies a hip fracture.

Estimated glomerular filtration rate (e-GFR), calcium (Ca), phosphorus (P), total (ALP) and bone specific alkaline phosphatase (b-ALP), intact parathyroid hormone (i-PTH), 25-hydroxy-vitamin D (25OHD), total procollagen type I amino-terminal propeptide (PINP), and N-terminal peptide of collagen I (NTx), measured at admission in 272 hip fracture patients, were ex post analyzed by K-means clustering and principal component analysis and were evaluated by a clinician.

Four components, mainly consisting of b-ALP, PINP, ALP, and NTx; e-GFR and P; i-PTH and 25OHD; and Ca explained about 70% of the variability. A total of 184 patients clustered around a centroid (A) with low 25OHD (13.2 ng/ml), well-preserved kidney function (e-GFR=67.19 ml/min/1.73m

), normal Ca, P, i-PTH and bone markers, with the exception of slightly increased NTx (24.82nMBCE). Cluster B (n=70) had increased i-PTH (93.38 pg/ml), moderately decreased e-GFR, very low 25OHD (8.68 ng/dl), and high bone turnover (b-ALP 28.46 U/L, PINP 69.87 ng/ml, NTx 31.3nMBCE). Cluster C (n=17) also had hyperparathyroidism (80.35 pg/ml) and hypovitaminosis D (9.15 ng/ml), low e-GFR(48.89 ml/min/1.73m

), and notably high ALP(173 U/L) and bone markers (b-ALP 44.64 U/L, PINP 186.98 ng/ml,NTx 38.28nMBCE). According to the clinician, 62 cases clearly had secondary hyperparathyroidism.

Based on serum measurements, the dominant patterns of bone metabolism were normal bone turnover with high normal NTx, and secondary hyperparathyroidism related to chronic kidney disease and hypovitaminosis D. The bone formation markers, e-GFR, NTx, and P composed the most important factors.

Based on serum measurements, the dominant patterns of bone metabolism were normal bone turnover with high normal NTx, and secondary hyperparathyroidism related to chronic kidney disease and hypovitaminosis D. The bone formation markers, e-GFR, NTx, and P composed the most important factors.Stroke is the leading cause of seizures and epilepsy in older adults. Patients who have larger and more severe strokes involving the cortex, are younger, and have acute symptomatic seizures and intracerebral haemorrhage are at highest risk of developing post-stroke epilepsy. Prognostic models, including the SeLECT and CAVE scores, help gauge the risk of epileptogenesis. Early electroencephalogram and blood-based biomarkers can provide information additional to the clinical risk factors of post-stroke epilepsy. The management of acute versus remote symptomatic seizures after stroke is markedly different. The choice of an ideal antiseizure medication should not only rely on efficacy but also consider adverse effects, altered pharmacodynamics in older adults, and the influence on the underlying vascular co-morbidity. Drug-drug interactions, particularly those between antiseizure medications and anticoagulants or antiplatelets, also influence treatment decisions. In this review, we describe the epidemiology, risk factors, biomarkers, and management of seizures after an ischaemic or haemorrhagic stroke. We discuss the special considerations required for the treatment of post-stroke epilepsy due to the age, co-morbidities, co-medication, and vulnerability of stroke survivors.Primary Sjögren's syndrome (SjS) is a systemic autoimmune disease most commonly diagnosed in middle-aged women. Although the disease can occur at all ages, it is diagnosed between 30 and 60 years of age in two-thirds of patients. In more than 20% of cases, the people are older than 65 years. see more In this review, we focus on the therapeutic management of primary SjS in older patients, following the recently published 2020 European League Against Rheumatism (EULAR) recommendations for the management of the disease with topical and systemic therapies. These recommendations are applicable to all patients with primary SjS regardless of age at diagnosis, although the therapeutic management in older patients requires additional considerations. Older patients are more likely to have pulmonary, liver, kidney, or heart-related comorbidities (even cognitive disturbances); caution is required when most drugs are used, including muscarinic agents, systemic corticosteroids and synthetic immunosuppressants. It is also important to monitor the use of eye drops containing steroids due to the increased risk of developing cataracts, a frequent ocular complication in the older population. In contrast, the majority of drugs that can be used topically (pilocarpine rinses, eye drops containing topical non-steroidal anti-inflammatory drugs (NSAIDs) or cyclosporine A, topical dermal formulations of NSAIDs) have shown an acceptable safety profile in older patients, as well as rituximab. A rigorous evaluation of the medical history of older patients is essential when drugs included in the EULAR guidelines are prescribed, with special attention to factors frequently related to ageing, such as polypharmacy, the existence of organ-specific comorbidities, or the enhanced susceptibility to infections.The placenta is important for pregnancy maintenance, and autophagy is documented to be essential for placental development. Autophagy is responsible for degrading and recycling cellular misfolded proteins and damaged organelles. Mitophagy is a selective type of autophagy, where the autophagic machinery engulfs the damaged mitochondria for degradation, and there is reciprocal crosstalk between autophagy and mitochondria. Within these processes, 5'-AMP-activated protein kinase (AMPK) plays an important role. However, the role of AMPK regulation in both autophagy and mitochondria in primary human trophoblasts is unknown. In this study, we address this question by investigating changes in mRNA expression and the abundance of autophagy- and mitochondria-related proteins in isolated human trophoblasts after treatment with AMPK agonists and antagonists. We found that compared to the control group, autophagy was slightly suppressed in the AMPK agonist group and significantly enhanced autophagy in the AMPK antagonist group. However, the expressions of genes related to autophagosome-lysosome fusion were reduced, while genes related to lysosomal function were unchanged in both groups. Furthermore, mitophagy and mitochondrial fusion/fission were both impaired in the AMPK agonist and antagonist groups. Although mitochondrial biogenesis was enhanced in both groups, the function of mitochondrial fatty acid oxidation was increased in the AMPK agonist group but decreased in the AMPK antagonist group. Overall, our study demonstrates that AMPK regulation negatively modulates autophagy and consequently affects mitophagy, mitochondrial fusion/fission, and function in primary human trophoblasts.