To clarify dynamic change of quality of life (QOL) in patients with stroke after treatment, and to explore the predictors associated with return to work (RTW) within 48 weeks. Patients diagnosed with stroke were enrolled. All patients enrolled were asked to fill in the Short Form 36 Health Survey. For patients with stroke, SF-36 questionnaires were measured repeatedly 4 weeks after treatment. We used phone call to find out if the patient was RTW. The investigation time was 48 weeks. Patients with stroke had lower scores in terms of physiological dimensions, such as physical functional, role limitations due to physical problems, and general health ( P < .001). While patients with strokes scored significantly lower in all mental dimensions including vitality, social functioning, role limitations due to emotional problems, and mental health ( P < .001). After 4-weeks treatment, we found that, except for bodily pain, scores in dimensions like physical functioning, role limitations due to physical problems, and general health had increased significantly ( P < .001). Multivariate logistic regression analysis was conducted, and the result showed that older age ( P = .04) and singleness ( P = .03) were risk factors associated with QOL improvement in stroke patients after treatment. Outcomes of stroke patients within 48 weeks were explored. The results showed that 108 out of 136 patients RTW within 48 weeks. Average days it took for patients with cerebral infarction to return to work were 77 ± 79, significantly less than patients with cerebral hemorrhage (206 ± 159 days) and patients with subarachnoid hemorrhage (117 ± 113 days, P < .001). Multivariate analysis indicated that only QOL improvement ( P = .04) and subtype of stroke ( P = .01) were independent factors associated with RTW within 48 weeks. QOL of stroke patients was significantly reduced. After treatments, the physiological quality of stroke patients increased, but the psychological quality remained low. In addition, patients with cerebral hemorrhage and patients with no significant improvement in QOL are independent risk factors for RTW. Therefore, for this subgroup of the population, early diagnosis, close follow-up and monitor of the psychological state should be provided to avoid the occurrence of adverse events.

Introduction: The polarization state of microglia affects the progress of neuropathic pain. MiR-155 modulates polarization of microglia, while its role in neuropathic pain has not been well studied. Material and methods: We separately used lipopolysaccharide (LPS) and interleukin 4 (IL-4) for constructing an M1/M2 polarization model in BV-2 cells. The levels of CD86, iNOS, CD206, Arg and miR-155 were measured by western blot or qRT-PCR, as needed. Subsequently, BV-2 cells were transfected with miR-155 mimics or inhibitor to explore the effects of miR-155 on polarization states. We also constructed a neuropathic pain model by applying spinal nerve ligation (SNL) in Wistar rats with miR-155 agomir or antagomir injection. The withdrawal threshold was measured by Von Frey fibre needle. The levels of interleukin 1β (IL-1β), tumour necrosis factor α (TNF-α) and the proportion of M1-polarized microglia in primary microglia from rats were measured by ELISA and flow cytometry. Results: LPS induced M1 polarization in BV-2 cells with increasing of CD86, iNOS and miR-155, while IL-4 induced M2 polarization in BV-2 cells with increasing of CD206, Arg and decreasing of miR-155. MiR-155 mimics upregulated CD86 and downregulated CD206, whereas miR-155 inhibitor downregulated CD86 and upregulated CD206. MiR-155 antagomir increased the withdrawal threshold, decreased the production of IL-1β, TNF-α and the proportion of M1-polarized microglia in primary microglia. Conclusions: Results demonstrate that suppression of miR-155 attenuates neuropathic pain by inducing an M1 to M2 switch in microglia. Our findings provide a new perspective to understand the function of miR-155 in microglia.

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Spleen tyrosine kinase (SYK) has an important role in immunoreceptor signaling, and SYK inhibition has accordingly attenuated immune-mediated injury in several models. Therefore, the present study examined the effect of SYK inhibition with the selective spleen tyrosine kinase inhibitor P505-15 in experimental rheumatoid arthritis (RA) using a murine model of collagen-induced arthritis (CIA). Treatment with the selective SYK inhibitor P505-15, a small molecule kinase inhibitor selective for SYK, led to a reduction in arthritis score and attenuated histological damage. P505-15 reduced cartilage destruction and macrophage infiltration in CIA mice. In addition, P505-15-treated mice showed lower circulating levels of type II-collagen immunoglobulin (Ig)G1 and IgG2 and pro-inflammatory cytokines. Importantly, P505-15 treatment markedly reduced the interleukin 1β-stimulated inflammatory response in human RA synovial cells. Given these encouraging results, a key function for SYK in the development of RA was identified, highlighting that SYK may be a potential therapeutic target for human RA.