Corticosteroids vs autologous blood injection for lateral epicondylitis: Study protocol for a cohort trial.

BACKGROUND: There is limited evidence to assess the evaluation of the safety and effectiveness of autologous blood injections in the treatment of lateral epicondylitis patients. For this study, the aim was to compare the efficiency of corticosteroid and autologous blood injections for the treatment of lateral epicondylitis in a retrospective cohort trial in our single center. METHODS: After being approved by the institutional review committee of Chongqing General Hospital (IRB# 2018.417.C, November 9, 2018), we performed a single-center, retrospective study between November 2018 and January 2020. All participants provided written informed consent. The criteria for inclusion in our experiment are as follows: over 18 years old; with the history of at least 6 months of lateral epicondylitis; and the palpation of lateral epicondyle tenderness; visual analog scale (≥4). In the group A, the patient were injected the autologous blood. In group B, the patients were immersed with 0.5% of bupivacaine (1 ml) and local corticosteroids (2 ml) at lateral epicondyle. The outcomes were composed of a visual analog scores of subjective pain severity over the past 24 hours as the primary result; and limb function in various tasks of daily activity measured with disabilities of the arm, shoulder, and hand quick questionnaire scores, the maximum grip strength and the modified scores of Nirschl, as secondary results. All the results were assessed before the injection and at 4 weeks and 8 weeks after the injection. For all examination, when the P value was less than .05, it would be defined to be a statistically significant difference. RESULTS: The results of this study would provide new information about the influence of autologous blood injections in treating the lateral epicondylitis. TRIAL REGISTRATION: This study protocol was registered in Research Registry (researchregistry6263).

p32 is a novel target for viral protein ICP34.5 of herpes simplex virus type 1 and facilitates viral nuclear egress.

As a large double-stranded DNA virus, herpes simplex virus type 1 (HSV-1) assembles capsids in the nucleus where the viral particles exit by budding through the inner nuclear membrane. Although a number of viral and host proteins are involved, the machinery of viral egress is not well understood. In a search for host interacting proteins of ICP34.5, which is a virulence factor of HSV-1, we identified a cellular protein, p32 (gC1qR/HABP1), by mass spectrophotometer analysis. When expressed, ICP34.5 associated with p32 in mammalian cells. Upon HSV-1 infection, p32 was recruited to the inner nuclear membrane by ICP34.5, which paralleled the phosphorylation and rearrangement of nuclear lamina. Knockdown of p32 in HSV-1-infected cells significantly reduced the production of cell-free viruses, suggesting that p32 is a mediator of HSV-1 nuclear egress. These observations suggest that the interaction between HSV-1 ICP34.5 and p32 leads to the disintegration of nuclear lamina and facilitates the nuclear egress of HSV-1 particles.