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The quest for reliable fluid biomarkers tracking synaptic disruption is supported by the evidence of a tight association between synaptic density and cognitive performance in neurodegenerative diseases (NDD), especially Alzheimer's disease (AD). Neurogranin (Ng) is a post-synaptic protein largely expressed in neurons involved in the memory networks. Currently, Ng measured in CSF is the most promising synaptic biomarker. Several studies show Ng elevated in AD dementia with a hippocampal phenotype as well as in MCI individuals who progress to AD. Ng concentrations are also increased in Creutzfeldt Jacob Disease where widespread and massive synaptic disintegration takes place. Ng does not discriminate Parkinson's disease from atypical parkinsonisms, nor is it altered in Huntington disease. CSF synaptosomal-associated protein 25 (SNAP-25) and synaptotagmin-1 (SYT-1) are emerging candidates. CSF Ng revealed a role as a diagnostic and prognostic biomarker in NDD. Ng increase seems to be very specific for typical AD phenotype, probably for a prevalent hippocampal involvement. Synaptic biomarkers may serve different context-of-use in AD and other NDD including prognosis, diagnosis, and tracking synaptic damage - a critical pathophysiological mechanism in NDD - thus representing reliable tools for a precision medicine-oriented approach to NDD. CSF Ng revealed a role as a diagnostic and prognostic biomarker in NDD. Ng increase seems to be very specific for typical AD phenotype, probably for a prevalent hippocampal involvement. Synaptic biomarkers may serve different context-of-use in AD and other NDD including prognosis, diagnosis, and tracking synaptic damage - a critical pathophysiological mechanism in NDD - thus representing reliable tools for a precision medicine-oriented approach to NDD.Phosphorus (P) is an essential macronutrient for all living organisms. Importantly, plants require a large amount of P to grow, and P deficiency causes huge losses in plant production. Although this issue can be mitigated by the appropriate use of phosphate (Pi) rock-derived P fertilizers, phosphate rock is a finite natural resource. Moreover, the increased demand for food as a result of our growing global population is another factor contributing to a prospective P crisis. While creating crops that are resilient to Pi deficiency presents great scientific challenge, the current progress in our understanding of how plants regulate Pi homeostasis offers some opportunities for further study. In this review, we present the published research supporting these opportunities, which are based on the molecular mechanisms that plants have evolved to respond to P deficiency. First, we focus on recent advances in P sensing and signaling pathways in the regulation of root system architecture. Next, we describe the mechanisms that regulate Pi transport and accumulation, in a Pi- (or other nutrient) dependent manner. Integrating these data will help to design an innovative strategy for improving Pi nutrition in plants. In addition, this will help with Pi scarcity, one of the challenges facing agriculture in the twenty first century. To determine alterations of chondroitin sulfate (CS) that reflect cartilage damage in an experimental osteoarthritis (OA) model as well as in human OA samples. Rats were subjected to anterior cruciate ligament transection (ACLT; OA) or a sham procedure and sacrificed 14, 28, or 70days after ACLT for histopathology and analysis of extracted CS. Cartilage samples from 14 patients undergoing hip or shoulder arthroplasty secondary to OA or fracture (control) were subjected to the same protocol. The CS content (µg/mg dry cartilage) after proteolysis was determined by densitometry, using agarose-gel electrophoresis. Molar mass (MM) and peak MM of CS were determined using high-performance size-exclusion chromatography (HPSEC). OA and sham joints at 70 d had 24 [22-24] and 3 [1-6] median histopathology scores, respectively (p<0.001). Relative CS content (77.7±8.3µg/mg) was significantly increased in OA samples 70 d after ACLT, as compared to sham (53.5±10.0µg/mg). Peak MM of CS was higher in OA than in sham samples (P<0.05). Similarly, CS content and peak MM were higher in cartilage from human OA patients, as compared to fracture samples, reproducing experimental data. Cartilage matrix from experimental and human OA samples has increased in the relative CS content. https://www.selleckchem.com/products/ly3537982.html Increase in the peak MM distinguishes CS of the extracellular matrix of OA from normal cartilage. Cartilage matrix from experimental and human OA samples has increased in the relative CS content. Increase in the peak MM distinguishes CS of the extracellular matrix of OA from normal cartilage. The objective of this study is to determine if the second-trimester serum afamin is a reasonable predictor of preeclampsia (PE). In this nested case-control study, all pregnant women were screened by second-trimester screening test between 15 and 20 weeks of gestation and serum samples were collected and stored at -80 °C for biochemical analysis. All available stored samples from pregnant women who subsequently developed PE were thawed and the concentrations of afamin in the serum were measured. Control cases, chosen randomly from the same cohort whose blood was collected and stored in the same period as with the study group, who did not develop PE. Afamin levels were expressed ng/mL. Logistic regression was used to calculate adjusted odds ratio (aORs) for the prediction of PE. A total of 39 women with PE and 46 controls were studied. Afamin levels were found to be significantly higher during the second trimester in women who developed PE compared to the control group. Afamin, at a cut-off level of 96.2 ng/mL, the aORs for PE was 28.6 (95% CI 7.458-110.193). After adjustment for BMI, age, smoking, the aORs for PE was 65.6 (95% CI 11.6-371.4; = .001). High levels of afamin in the early weeks of gestation in patients going on to develop PE later may be promising as a potential marker to predict PE in the first and second trimesters. High levels of afamin in the early weeks of gestation in patients going on to develop PE later may be promising as a potential marker to predict PE in the first and second trimesters.
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