Maybe catching up on the " OA, " I dunno.

也许赶上“OA” ，我不知道。

All OA approval processes should be approved three times a day.

所有OA审批流程应每天审批三次。

Results FOS-positive chondrocytes were increased in human and murine OA cartilage during disease progression.

结果显示，在疾病进展过程中，人类和小鼠的OA软骨中FOS阳性的软骨细胞增多。

This is a vowel digraph syllable: ai, ay, ee, ea, oa, ow.

这是一元音二字符音节：ai、ay、ee、ea、oa、ow。

And if you ask The OA and Homer, near-death experiences can also lead to some unique dance movements.

如果你 OA 和荷马，濒死体验也会致一些独特的舞蹈动作。

OA has long been considered the consequence of a 'wear and tear' process leading to loss of articular cartilage.

骨关节长期以来一直被认为是“磨损”过程的结果，致关节软骨丧失。

Here we show that FOS protein expression is increased in OA cartilage.

这里我们显示FOS蛋白在骨关节软骨中的表达增加。

In humans two single nucleotide polymorphisms in the FOS promoter were found to be associated with knee-OA susceptibility.

在人类中，发现FOS启动子中的两单核苷酸多态性与膝骨关节的易感性有关。

Osteoarthritis (OA) is the most common joint disease and its prevalence is growing in developed countries due to population ageing, more frequent biomechanical trauma and obesity.

骨关节（OA）是最常见的关节疾病，其发病率在发达国家中由于人口老龄化、更频繁的生物力学创伤和肥胖而不断增加。

Methods c-Fos expression was evaluated by immunohistochemistry on articular cartilage sections from patients with OA and mice subjected to the destabilisation of the medial meniscus (DMM) model of OA.

法 通过免疫组化评估了来自OA患者和接受内侧半月板不稳(OA的DMM模型)的小鼠的关节软骨切片中的c-Fos表达。

This implies that chondrocytes maintain the structural and functional integrity of cartilage and sense microenvironmental changes during OA onset, although the underlying cartilage protective mechanisms remain elusive.

这表明，在骨关节初期，软骨细胞维持着软骨的结构和功能完整性，并能感知微环境的变化，尽管潜在的软骨保护机制仍然不明。

Importantly, mutations in cartilage matrix genes such as COL2A1, COL9A3, COL11A2 and cartilage oligomeric matrix protein (COMP), which are produced by articular chondrocytes, cause chondrodysplasia with early-onset OA.

重要的是，软骨基质基因如COL2A1、COL9A3、COL11A2和软骨寡聚基质蛋白（COMP）的突变，这些基因由关节软骨细胞产生，会致软骨发育不良并伴早期发病的骨关节。

Obesity and metabolic syndrome are recognized as strong risk factors for hand OA, but also knee OA, where low-grade chronic inflammation and systemic metabolic alterations disrupt joint tissue homoeostasis.

肥胖和代谢综合征被认为是手部骨关节的强风险因素，同时也是膝关节骨关节的风险因素，在这些情况下，低级别的慢性症和全身代谢改变会扰乱关节组织的稳态。

A large fraction (40%) of knee OA is heritable and genome-wide association studies indicated that most OA risk variants are located in non-coding sequences, and enriched close to genes involved in bone and cartilage development.

膝骨关节有较大比例（40%）是可遗传的，全基因组关联研究显示，大多数骨关节风险变异位于非编码序列中，并且在与骨骼和软骨发育相关基因附近富集。