Objective To summarize the molecular biological research progress of non-coding RNAs modulating osteoarthritis (OA), and provide a reference basis for biological study and clinical treatment of OA. Methods Recent domestic and foreign related literature about the regulation of OA pathological process by non-coding RNAs was widely reviewed. Results Non-coding RNAs can be divided into three types based on the length of RNA. A lot of non-coding RNAs participating in OA pathological process are screened out by high throughput sequencing technology and microarray technology, and it is verified that these non-coding RNAs involve in the regulation of OA by RT-PCR. The mechanism of OA mediated target is clarified by knocking-down and overexpressing of the most prominent expressed non-coding RNAs in OA. There are the complicated gene expressed network topology in non-coding RNAs, and between non-coding RNAs and coding RNAs. It provides a basis for clearing the effect of gene structure and function, and finding the definite therapeutic target of OA. Conclusion There is preliminary study on molecular biological mechanism of non-coding RNAs mediating OA, but the key structure or sequence of non-coding RNAs, formation and interaction of effecting composite structure about mediating OA are unknown, and it needs further study.
Objective To summarize the research progress of intraductal papillary mucinous neoplasms (IPMNs). Method The domestic and international published literatures related to IPMNs in recent years were collected and reviewed． Results Based on the site of tumor involved, IPMNs were classified into main duct, branch duct, and mixed types. According to the histologic features, IPMNs were divided into intestinal, pancreatobiliary, gastric, and oncocytic types. The pathological and clinical presentations of IPMNs were vary, and multiple imaging approaches including endoscopic retrograde cholangiopancreatography (ERCP), endoscopic ultrasonography (EUS), CT, magnetic resonance cholangiopancreatography (MRCP) combined with MRI, could display morphologic and functional characteristics of IPMNs. In additon, the risk of malignancy in IPMNs could be evaluated and the functions of some genes (including KRAS, BRAF, GNAS, and so on) in the development process of IPMNs had been confirmed. Conclusion IPMNs is a kind of disease different from other tumors of the pancreas in clinicopathologic features, imaging performance, and molecular biology changes, and how to link the above three aspects needs to be further studied.
ObjectiveTo understand the progress of molecular biology research on the pathogenesis of hemorrhoids. MethodThe literatures relevant to reseaches on the molecular biology of hemorrhoid pathogenesis in recent years had been reviewed. ResultsThe generally accepted theories of hemorrhoids included anal cushion downward movement theory, varicose vein theory, and vascular proliferation theory. The molecular biological studies related to the theory of anal cushion downward movement found that the increased expression of matrix metalloproteinase-9 and the abnormal expression of smooth muscle actin could damage the supporting tissue of anal cushion, causing the downward movement and prolapse of anal cushion, and then formed hemorrhoids; The molecular biology researches related to varicose vein theory found that the increase of nitric oxide synthase and transient receptor potential vanilloid 1 could promote the production of nitric oxide, causing varicose veins, and then leaded to the pathogenesis of hemorrhoids; The molecular biology researches related to vascular proliferation theory found that the low expressions of miR-412-5p and miR-4729, and the overexpressions of vascular endothelial growth factor and fibroblast growth factor were related to the vascular proliferation of hemorrhoids. In addition, the secondary inflammatory reaction after the onset of hemorrhoids also played an important role in the occurrence and development of hemorrhoids. ConclusionsThe occurrence and development of hemorrhoids is the result of the intersection and interaction of various mechanisms such as anal cushion downward movement, varicose veins, vascular proliferation, and secondary inflammatory reaction. The molecular biology research on the pathogenesis of hemorrhoids is helpful to better explain the occurrence of hemorrhoids from a microcosmic perspective, and lay a foundation for further exploring the etiology of hemorrhoids.
Primary cardiac tumors, which originate from the heart, are uncommon and can be classified as benign or malignant, with the majority being benign. Malignant primary cardiac tumors have a poor prognosis. Benign ones may also cause severe hemodynamic and electrophysiological consequences, but the prognosis is generally good if they are detected early and treated properly. In recent years, researches on the genetic and molecular causes of primary cardiac tumors have yielded some promising breakthroughs, with some of them already being translated into clinical practice. This article reviews research progress and its use in precise diagnosis and targeted therapy from the perspective of DNA, RNA, and protein changes, as well as prospects the promising research directions in the future.
Objective To review the research progress of pathological changes of glenohumeral capsule in patients with recurrent shoulder anterior dislocation (RSAD). Methods The literature on shoulder capsules, both domestic and international, was reviewed. The anatomy, histology, and molecular biology characteristics of the glenohumeral capsule in RSAD patients were summarized. Results Anatomically, the glenohumeral capsule is composed of four distinct parts: the upper, lower, anterior, and posterior sections. The thickness of these sections is uneven, and the stability of the capsule is further enhanced by the presence of the glenohumeral and coracohumeral ligaments. Histologically, the capsule tissue undergoes adaptive changes following RSAD, which improve its ability to withstand stretching and deformation. In the realm of molecular biology, genes associated with the regulation of structure formation, function, and extracellular matrix homeostasis of the shoulder capsule’s collagen fibers exhibit varying degrees of expression changes. Specifically, the up-regulation of transforming growth factor β1 (TGF-β1), TGF-β receptor 1, lysyl oxidase, and procollagen-lysine, 2-oxoglutarate 5-dioxygenase 1 facilitates the repair of the joint capsule, thereby contributing to the maintenance of shoulder joint stability. Conversely, the up-regulation of collagen type Ⅰ alpha 1 (COL1A1), COL3A1, and COL5A1 is linked to the recurrence of shoulder anterior dislocation, as these changes reflect the joint capsule’s response to dislocation. Additionally, the expression of tenascin C and fibronectin 1 may play a role in the pathological processes occurring during the early stages of RSAD. ConclusionGlenohumeral capsular laxity is both a consequence of RSAD and a significant factor contributing to its recurrence. While numerous studies have documented alterations in the shoulder capsule following RSAD, further research is necessary to confirm the specific pathological anatomy, histological, and molecular biological changes involved.