Background and objectives: Frozen shoulder is a common painful disease of the shoulder joint characterized by structural changes in the shoulder joint, restricting both active and passive shoulder joint activities. Proprioceptive neuromuscular facilitation (PNF) effectively improved and maintained the range of motion; however, it is not clear whether it can improve the shoulder joint structure in patients with frozen shoulder. This pilot study used magnetic resonance imaging (MRI) observation to assess the improvement of the local structure of the shoulder joint upon PNF treatment to elucidate a target based on structure for the treatment of frozen shoulder. Materials and methods: Forty-eight patients with frozen shoulder were randomly divided into the traditional manual therapy group and the PNF technique group. Changes in the thicknesses of the coracohumeral ligament (CHL) and capsule in axillary recess (CAR) of the shoulder joint were observed via MRI upon admission and at 4 weeks after treatment. A visual analog scale (VAS) and passive shoulder range of motion (ROM) at abduction, anteflexion and external rotation position were used to evaluate the improvement of shoulder joint pain and function in the initial, mid-term, and discharge of the two groups of patients. Results: The primary outcome results shown that the PNF joint mobilization significantly reduced the thickness of the CHL (p = 0.0217) and CAR (p = 0.0133). Compared with simple joint mobilization, The mid-term and discharge rehabilitation assessment results showed that PNF has a better effect on shoulder pain. At the mid-term evaluation, the ROM of the PNF group was significantly better than that of the Control group in the three directions (p < 0.05). Conclusion: As an adjunctive therapy, PNF can improve the shoulder joint structure of patients with frozen shoulder and is an effective treatment strategy for frozen shoulder.

Migrasomes are migration‐dependent membrane‐bound vesicular structures that contain cellular contents and small vesicles. Migrasomes grow on the tips or intersections of the retraction fibers after cells migrate away. The process of releasing migrasomes into the extracellular space is named as “migracytosis”. After releasing, they can be taken up by the surrounding cells, or rupture and further release their contents into the extracellular environment. Physiologically, migrasomes provide regional cues for organ morphogenesis during zebrafish gastrulation and discard the damaged mitochondria in response to mild mitochondrial stresses. Pathologically, migrasomes are released from podocyte during early podocyte stress and/or damage, from platelets after infection with severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), from microglia/macrophages of the ischemic brain, and from tumor necrosis factor α (TNFα)‐activated endothelial cells (ECs); thus, this newly discovered extracellular vesicle is involved in all these pathological processes. Moreover, migrasomes can modulate the proliferation of cancer cell via lateral transferring mRNA and protein. In this review, we will summarize the biogenesis, release, uptake, and rupture of migrasomes and discuss its biological roles in development, redox signalling, innate immunity and COVID‐19, cardio‐cerebrovascular diseases, renal diseases, and cancer biology, all of these highlight the importance of migrasomes in modulating body homeostasis and diseases.

Stroke is one of the main causes of disease‑related mortality worldwide. Buyang Huanwu Decoction (BHD) has been used to protect against stroke and stroke‑induced disability for several years in China. Studies have shown that BHD can relieve neuronal damage in rats with cerebral ischemia/reperfusion (I/R) injury. However, the mechanism remains unclear. A middle cerebral artery occlusion and reperfusion (MCAO‑R) model was used in the present study. The animals were treated with BHD (5, 10 and 20 g/kg) or rapamycin. Infarct size and modified neurological severity score were calculated on day 5 following MCAO‑R surgery. Cellular changes around the ischemic penumbra were revealed by hematoxylin and eosin and Nissl staining. The protein expression levels of nestin, brain‑derived neurotrophic factor (BDNF), doublecortin on the X chromosome (DCX) and autophagy‑related proteins (beclin 1, LC3‑II and p62) in the peri‑ischemic area of the brain were detected. The results demonstrated that post‑surgical treatment with BHD reduced the brain infarct size and improved neurological deficits in MCAO‑R rats. BHD protected against MCAO‑R‑induced neuronal impairment and promoted neurogenesis, increased the protein expression of nestin, BDNF and DCX and markedly enhanced autophagy by increasing beclin 1 and LC3‑II and decreasing p62. Meanwhile, BHD promoted the expression of sirtuin 1 (SIRT1), an important regulator of autophagy. In conclusion, the present study suggested that post‑surgical treatment with BHD could protect rat brains from I/R injury, potentially through the SIRT1/autophagy pathway.

Background The panicle is the most important organ in rice, and all the panicle-related traits are correlated with rice grain yield. Understanding the underlying genetic mechanisms controlling panicle development is very important for improving rice production. Methods Nine panicle-related traits including heading date, panicle length, number of primary branches, number of secondary branches, number of grains per panicle, number of panicles per plant, number of filled grains per plant, seed-setting rate, and grain yield per plant were investigated. To map the quantitative trait loci (QTLs) for the nine panicle-related traits, a PCR-based genetic map with 208 markers (including 121 simple sequence repeats and 87 InDels) and a high-density linkage map with 18,194 single nucleotide polymorphism (SNP) markers were both used. Results Using a recombinant inbred line population derived from an indica variety Huanghuazhan and a japonica line Jizi 1560, a total of 110 and 112 QTLs were detected for panicle-related traits by PCR-based genetic map and by high-density linkage map, respectively. Most of the QTLs were clustered on chromosomes 1, 2, 3, 6, and 7 while no QTLs were detected on chromosome 10. Almost all the QTLs with LOD values of more than 5.0 were repeatedly detected, indicating the accuracy of the two methods and the stability of the QTL effects. No genes for panicle-related traits have been previously reported in most of these regions. QTLs found in JD1006–JD1007 and RM1148–RM5556 with high LOD and additive values deserved further research. The results of this study are beneficial for marker-assisted breeding and provide research foundation for further fine-mapping and cloning of these QTLs for panicle-related traits.