Acupuncture for Benign prostatic hyperplasia (BPH) pays attention to the syndrome differentiation theory, but also emphasizes the differentiation of the meridians, to obtain the better effective. At present, the clinical treatment of BPH is mainly based on deep acupuncture with filiform needle, electroacupuncture, warm acupuncture and moxibustion and comprehensive treatment of acupuncture and moxibustion, especially the comprehensive treatment of warm acupuncture combined with needle, Traditional Chinese Medicine and western medicine. Acupuncture treatment of BPH can reduce the prostate volume of patients, improve their lower urinary tract symptoms, improve their quality of life, without sever adverse events. BPH patients are often accompanied by emotional problems. It is suggested that acupuncture "treating spirit" should be further developed in clinical treatment to promote the application of acupuncture in the treatment of this disease.

IL-34 can promote osteoclast differentiation and activation, which may contribute to steroidinduced osteonecrosis of the femoral head (ONFH). Animal model was constructed in both BALB/c and IL-34 deficient mice to detect the relative expression of inflammation cytokines. Micro-CT was utilized to reveal the internal structure. In vitro differentiated osteoclast was induced by culturing bone marrow-derived macrophages with IL-34 conditioned medium or M-CSF. The relative expression of pro-inflammation cytokines, osteoclast marker genes, and relevant pathways molecules was detected with quantitative real-time RT-PCR, ELISA, and Western blot. Up-regulated IL-34 expression could be detected in the serum of ONFH patients and femoral heads of ONFH mice. IL-34 deficient mice showed the resistance to ONFH induction with the up-regulated trabecular number, trabecular thickness, bone value fraction, and down-regulated trabecular separation. On the other hand, inflammatory cytokines, such as TNF-α, IFN-γ, IL-6, IL-12, IL-2, and IL-17A, showed diminished expression in IL-34 deficient ONFH induced mice. IL-34 alone or works in coordination with M-CSF to promote osteoclastogenesis and activate ERK, STAT3, and non-canonical NF-κB pathways. These data demonstrate that IL-34 can promote the differentiation of osteoclast through ERK, STAT3, and non-canonical NF-κB pathways to aggravate steroid-induced ONFH, and IL-34 can be considered as a treatment target.