ABSTRACT
OBJECTIVES: To compare the clinical effect of combined therapy of acupotomy and electroacupuncture (EA) with the simple application of EA on knee osteoarthritis (KOA), and their influence on knee function. METHODS: Sixty-eight KOA patients were randomly divided into 2 groups, an acupotomy group and an EA group. In the acupotomy group, the combined therapy of acupotomy and EA was adopted. In the EA group, EA was simply used, delivered once every two days, 3 treatments a weekï¼and the duration of treatment was 4 weeks. In the acupotomy group, besides the treatment as the EA group, acupotomy was combined once weekly, and the duration of treatment was 4 weeks. Separately, before and after treatment, and in 4 and 12 weeks after treatment completion (1-month and 3-month follow-up), the results of the timed up and go test (TUG), the 9-step stair climb test (9-SCT) and the knee function (Western Ontario and McMaster University osteoarthritis index visualization scale ï¼»WOMACï¼½) were measured in the two groups. RESULTS: By the intention-to-treat analysis, the results of TUG, 9-SCT and WOMAC scores were reduced after treatment and in 1-month and 3-month follow-up when compared with those before treatment in the patients of the two groups (P<0.05). Compared with the EA group at the same time point, TUG results were decreased after treatment and in 1-month follow-up, and WOMAC score was reduced after treatment in the acupotomy group. WOMAC score in 1-month follow-up was reduced when compared with that before treatment within the acupotomy group (P<0.05). CONCLUSIONS: Either the simple application of EA or the combined therapy of acupotomy and EA can improve knee function, but the combined therapy obviously increases the walking speed and relieves the symptoms such as joint pain and morning stiffness. The treatment with acupotomy and EA is safe and effective on KOA and the long-term effect is satisfactory.
Subject(s)
Acupuncture Therapy , Electroacupuncture , Osteoarthritis, Knee , Humans , Osteoarthritis, Knee/therapy , Osteoarthritis, Knee/physiopathology , Female , Male , Middle Aged , Aged , Treatment Outcome , Combined Modality Therapy , Knee Joint/physiopathology , Acupuncture PointsABSTRACT
Recurrent respiratory tract infections (RRTIs) are one of the most common pediatric diseases. Although the pathogenesis of pediatric RRTIs remains unknown, ineffective B cell-dominated humoral immunity has been considered as the core mechanism. During the course of pediatric RRTIs, B cell-dominated humoral immunity has changed from "protector" of respiratory system to "bystander" of respiratory tract infections. Under physiological condition, Tfh cells are essential for B cell-dominated humoral immunity, including regulating GC formation, promoting memory B cell (MB)/plasma cell (PC) differentiation, inducting immunoglobulin (Ig) class switching, and selecting affinity-matured antibodies. However, in disease states, Tfh cells are dysfunctional, which can be reflected by phenotypes and cytokine production. Tfh cell dysfunctions can cause the disorders of B cell-dominated humoral immunity, such as promoting B cell presented apoptosis, abrogating total Ig production, reducing MB/PC populations, and delaying affinity maturation of antigens-specific antibodies. In this review, we focused on the functions of B and Tfh cells in the homeostasis of respiratory system, and specifically discussed the disorders of humoral immunity and aberrant Tfh cell responses in the disease process of pediatric RRTIs. We hoped to provide some clues for the prevention and treatment of pediatric RRTIs.
ABSTRACT
Inflammatory bowel diseases (IBDs), including ulcerative colitis and Crohn's disease, are characterized by chronic idiopathic inflammation of gastrointestinal tract. Although the pathogenesis of IBD remains unknown, intestinal immune dysfunction has been considered as the core pathogenesis. In the intestinal immune system, T helper 1 (Th1) and Th17 cells are indispensable for intestine homeostasis via preventing pathogenic bacteria invasion, regulating metabolism and functions of intestinal epithelial cells (IECs), and promoting IEC self-renewal. However, during the development of IBD, Th1 and Th17 cells acquire the pathogenicity and change from the maintainer of intestinal homeostasis to the destroyer of intestinal mucosa. Because of coexpressing interferon-γ and interleukin-17A, Th17 cells with pathogenicity are named as pathogenic Th17 cells. In disease states, Th1 cells impair IEC programs by inducing IEC apoptosis, recruiting immune cells, promoting adhesion molecules expression of IECs, and differentiating to epithelial cell adhesion molecule-specific interferon γ-positive Th1 cells. Pathogenic Th17 cells induce IEC injury by triggering IBD susceptibility genes expression of IECs and specifically killing IECs. In addition, Th1 and pathogenic Th17 cells could cooperate to induce colitis. The evidences from IBD patients and animal models demonstrate that synergistic action of Th1 and pathogenic Th17 cells occurs in the diseases development and aggravates the mucosal inflammation. In this review, we focused on Th1 and Th17 cell programs in homeostasis and intestine inflammation and specifically discussed the impact of Th1 and Th17 cell pathogenicity and their synergistic action on the onset and the development of IBD. We hoped to provide some clues for treating IBD.
Although treatment methods have been comprehensively optimized, the death risk of inflammatory bowel disease (IBD) patients is higher than that of healthy control subjects and still gradually increasing. Even so, the pathogenesis of IBD remains poorly understood. A better understanding of the roles of T helper 1 and pathogenic T helper 17 cells in the pathogenesis of IBD may provide some promising clues for treating IBD.
