This paper introduces Professor WANG Jihong's clinical experience in treating refractory lateral epicondylitis using the Wang's crescent technique of blade needle. Based on the classical theories of Huangdi Neijing (the Yellow Emperor's Inner Classic) such as the "twelve sinew meridians" "short needling" and "shu needling", Professor WANG applies a self-designed blade needle with crescent needling method. This approach forms a distinctive treatment philosophy characterized by "sinew meridians as the foundation, selecting points at the pain site; using chicken-claw needling technique deliverd at both internal and external; integration of heaven, earth, and man, using both short and shu needling; treating tendon injuries and inflammation with the crescent technique of blade needle". It embodies the therapeutic concept of "treating tendons and bones simultaneously, harmonizing yin and yang", and shows unique advantages in the treatment of this condition.
Acupuncture Therapy/methods* ; Humans ; Tennis Elbow/therapy* ; Male ; Middle Aged ; Adult ; Needles ; Female ; Acupuncture Points

Abstract Skin, the largest organ of the human body, serves as the primary barrier against environmental hazards. Skin aging is a complex process influenced by both intrinsic factors, such as endogenous physiological changes, and extrinsic factors, including environmental exposures, reflecting the internal health status of the body. During skin aging, various cell types exhibit diverse responses to aging-related stimulations. This paper systematically reviews the roles of cells in the pathogenesis of skin aging and explores potential therapeutic strategies for mitigating this process. Furthermore, based on the biological activities of cells during skin aging, we elucidate the interaction mechanisms among cells within the skin microenvironment.

The global prevalence of diabetes among adults is increasing year by year,with diabetes mellitus type 2(T2DM)being the most common form.T2DM is a chronic disease characterized by insulin resistance and insufficient insulin secretion,often accompanied by disturbances in glucose,protein,and lipid metabolism.Impaired wound healing is one of the major complications of T2DM.Studies have shown that wound healing in T2DM patients are regulated by macrophages and are closely related to their phenotype,activity,and abundance.Macrophages of different phenotypes play distinct roles in various stages of T2DM wound healing:M1 macrophages are involved in the early inflammatory response and pathogen clearance,while M2 macrophages contribute to anti-inflammatory responses and wound repair during later stages.Dysregulation of macrophage phenotype switching affects wound inflammatory response,skin cell function,and extracellular matrix(ECM)synthesis,ultimately leading to impaired healing.Significant progress has been made in understanding the interactions between macrophage metabolic changes and phenotype switching,and this dynamic relationship might play a synergistic role in regulating the wound healing process in T2DM.This review summarizes the functional roles of macrophages in both normal and T2DM-associated wound healing,discusses alterations in glucose,lipid,and amino acid metabolism in macrophages under pathological conditions,and explores how these metabolic shifts regulate wound healing.Furthermore,it examines the therapeutic potential of targeting macrophage metabolism to improve wound healing outcomes.

The global prevalence of diabetes among adults is increasing year by year,with diabetes mellitus type 2(T2DM)being the most common form.T2DM is a chronic disease characterized by insulin resistance and insufficient insulin secretion,often accompanied by disturbances in glucose,protein,and lipid metabolism.Impaired wound healing is one of the major complications of T2DM.Studies have shown that wound healing in T2DM patients are regulated by macrophages and are closely related to their phenotype,activity,and abundance.Macrophages of different phenotypes play distinct roles in various stages of T2DM wound healing:M1 macrophages are involved in the early inflammatory response and pathogen clearance,while M2 macrophages contribute to anti-inflammatory responses and wound repair during later stages.Dysregulation of macrophage phenotype switching affects wound inflammatory response,skin cell function,and extracellular matrix(ECM)synthesis,ultimately leading to impaired healing.Significant progress has been made in understanding the interactions between macrophage metabolic changes and phenotype switching,and this dynamic relationship might play a synergistic role in regulating the wound healing process in T2DM.This review summarizes the functional roles of macrophages in both normal and T2DM-associated wound healing,discusses alterations in glucose,lipid,and amino acid metabolism in macrophages under pathological conditions,and explores how these metabolic shifts regulate wound healing.Furthermore,it examines the therapeutic potential of targeting macrophage metabolism to improve wound healing outcomes.

OBJECTIVETo study the effect of heme oxygenase-1 (HO-1) on peribiliary vascular plexus (PVP) in rat bile duct ischemia/reperfusion injury.

METHODSTotal 128 male SD rats were randomly divided into saline group (Saline), empty virus group (Adv), induced group (Adv-HO-1) and suppressed group (HO-1 siRNA), and there were 32 rats in each group. Rats were injected using 0.5 ml of saline, empty adenovirus, HO-1 adenovirus and siRNA adenovirus (2×10(9) TU/rat) via the dorsal penile vein 24 hours before surgery. Liver function was analyzed at 1 hour and 1, 7, 14 days after reperfusion. HO-1, hypoxiainducible factor-1α (HIF-1α), stromal cell derived factor-1α (SDF-1α) and vascular endothelial growth factor (VEGF) protein content was analyzed by Western blot. The endothelial progenitor cells (EPCs) ratio in the liver and peripheral blood was detected by flow cytometry. Small vascular around the bile duct was observed by α-smooth muscle actin and von Willebrand factor double immunofluorescence staining.

RESULTSReduced liver injury and higher expression of HIF-1α, SDF-1α and VEGF in the induced group after surgery (q = 5.68-7.52, P < 0.01). EPCs ratio in the liver and peripheral blood was significantly higher in the induced group than saline group (q = 12.14 and 15.26, P < 0.01), and the suppressed group at 7 days after surgery were less than saline group significantly (q = 4.83 and 5.07, P < 0.01). In comparison to the suppressed group, higher density of small vascular around the bile duct was seen in the liver tissue of induced group.

CONCLUSIONSHO-1 can induce the expression of HIF-1α, SDF-1α and VEGF, and mobilize the release of EPCs to the peripheral from the bone marrow. EPCs migrate to the liver and promote damaged PVP repair and regeneration.

Animals ; Bile Ducts ; blood supply ; Chemokine CXCL12 ; metabolism ; Endothelial Cells ; cytology ; Heme Oxygenase (Decyclizing) ; physiology ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Male ; Neovascularization, Physiologic ; RNA, Small Interfering ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; physiopathology ; Stem Cells ; cytology ; Vascular Endothelial Growth Factor A ; metabolism