Unraveling the nexus of NAD+ metabolism and diabetic kidney disease: insights from murine models and human data.

Background: Nicotinamide adenine dinucleotide (NAD+) is a critical coenzyme involved in kidney disease, yet its regulation in diabetic kidney disease (DKD) remains inadequately understood.

Objective: Therefore, we investigated the changes of NAD+ levels in DKD and the underlying mechanism.

Methods: Alternations of NAD+ levels and its biosynthesis enzymes were detected in kidneys from streptozotocin-induced diabetic mouse model by real-time PCR and immunoblot.

Functional iron deficiency anemia was associated with higher mortality in chronic kidney disease patients: the NHANES III follow-up study.

Anemia, a common complication of chronic kidney disease (CKD), is associated with poor prognosis. However, it is not completely clear whether this association is caused by anemia per se or other comorbidities. Whether different types of iron deficiency anemia can predict the outcomes of CKD remains unclear.

Loss of Pinch Proteins Causes Severe Degenerative Disc Disease-Like Lesions in Mice.

Degenerative disc disease (DDD) is one of the most common skeletal disorders affecting aged populations. DDD is the leading cause of low back/neck pain, resulting in disability and huge socioeconomic burdens. However, the molecular mechanisms underlying DDD initiation and progression remain poorly understood.

Pip5k1c Loss in Chondrocytes Causes Spontaneous Osteoarthritic Lesions in Aged Mice.

Osteoarthritis (OA) is the most common degenerative joint disease affecting the older populations globally. Phosphatidylinositol-4-phosphate 5-kinase type-1 gamma (Pip5k1c), a lipid kinase catalyzing the synthesis of phospholipid phosphatidylinositol 4,5-bisphosphate (PIP2), is involved in various cellular processes, such as focal adhesion (FA) formation, cell migration, and cellular signal transduction. However, whether Pip5k1c plays a role in the pathogenesis of OA remains unclear.

The metabolites of NAD synthesis are a valuable predictor of acute kidney injury.

Background: Acute kidney injury (AKI) is often iatrogenic and potentially preventable. Reduced renal nicotinamide adenine dinucleotide (NAD) is reported to increase the susceptibility of AKI. The present study explored the predictive value of urinary NAD synthetic metabolites for AKI using two independent cohorts.

Osteoarthritis: pathogenic signaling pathways and therapeutic targets.

Osteoarthritis (OA) is a chronic degenerative joint disorder that leads to disability and affects more than 500 million population worldwide. OA was believed to be caused by the wearing and tearing of articular cartilage, but it is now more commonly referred to as a chronic whole-joint disorder that is initiated with biochemical and cellular alterations in the synovial joint tissues, which leads to the histological and structural changes of the joint and ends up with the whole tissue dysfunction. Currently, there is no cure for OA, partly due to a lack of comprehensive understanding of the pathological mechanism of the initiation and progression of the disease.

Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice.

The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint (TMJ) osteoarthritis (OA); however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ.

The hypoxia-inducible factor prolyl hydroxylase inhibitor FG4592 promotes natriuresis through upregulation of COX2 in the renal medulla.

The renal medulla is a key site for the regulation of renal sodium excretion. However, the molecular mechanism remains unclear. Cyclooxygenase 2 (COX2) is specifically expressed in the renal medulla and contributes to the maintenance of the electrolyte/water balance in the body.

Kindlin-2 deletion in osteoprogenitors causes severe chondrodysplasia and low-turnover osteopenia in mice.

Background: Our recent studies demonstrate that the focal adhesion protein Kindlin-2 exerts crucial functions in the mesenchymal stem cells, mature osteoblasts and osteocytes in control of early skeletal development and bone homeostasis in mice. However, whether Kindlin-2 plays a role in osteoprogenitors remains unclear.

Materials And Methods: Mice lacking Kindlin-2 expression in osterix (Osx)-expressing cells (i.

Universal adversarial examples and perturbations for quantum classifiers.

Quantum machine learning explores the interplay between machine learning and quantum physics, which may lead to unprecedented perspectives for both fields. In fact, recent works have shown strong evidence that quantum computers could outperform classical computers in solving certain notable machine learning tasks. Yet, quantum learning systems may also suffer from the vulnerability problem: adding a tiny carefully crafted perturbation to the legitimate input data would cause the systems to make incorrect predictions at a notably high confidence level.