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，疾病进展过程中，人类和小鼠的OA软中FOS阳性的软细胞增多。

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

这是一个元音二字符音节：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.

如果你问 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.

节长期以来一直被认为是“磨损”过程的结果，致节软丧失。

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

这里我们显示FOS蛋白节软中的表达增加。

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

人类中，发现FOS启动子中的两个单核苷酸多态性与膝节的易感性有。

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.

节（OA）是最常见的节疾病，其发病率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.

方法 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)的小鼠的节软切片中的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，节初期，软细胞维持着软的结构和功能完整性，并能感知微环境的变化，尽管潜的软保护机制仍然不明。

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，软基质基因如COL2A1、COL9A3、COL11A2和软寡聚基质蛋白（COMP）的突变，这些基因由节软细胞产生，会致软发育不良并伴早期发病的节。

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节的强风险因素，同时也是膝节节的风险因素，这些情况下，低级别的慢性症和全身代谢改变会扰乱节组织的稳态。

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.

膝节有较大比例（40%）是可遗传的，全基因组联研究显示，大多数节风险变异位于非编码序列中，并且与骼和软发育相基因附近富集。