Objective To study the changes of life span and pathology in superoxide dismutase 1 (SOD1)-G93A mice after intracardiac transplantation of human mesenchymal stem cells (hMSCs).Methods hMSCs were isolated from bone marrow cells obtained from healthy donors and cultured.The purity and morphology were assessed by flow cytometry (FCM).hMSCs (3×10~6) resuspended in 0.2 ml DMEM was injected into the heart of 8 week-old SOD1-G93A mice.In non-transplantion control SOD1-G93A mice, only DMEM was injected.The mice were evaluated for signs of motor deficit with 4-point scoring system previously described by Weydt et al.The age of onset and life span in mice were assessed.The pathological change including number of motor neurons was investigated by Nissl staining.Immunofluorescence staining with specific human nuclear antibody was used to confirm the transplant of hMSCs in mice.Results The onset symptoms in untreated SOD1-G93A mice appeared at (156.56±3.60) days of age and the average life span was (188.32±3.51) days.hMSCs transplantation delayed the onset of ALS type symptoms about 16 days (x~2=10.888, P=0.001) and prolonged the life span about 14 days compared to the untreated SOD1-G93A littermates((202.19±4.09) days vs (188.32±3.51) days, x~2=3.917, P=0.04).The loss of motor neurons in untreated mice was earlier and more severe than in hMSCs transplanted mice.At 20 weeks, the number of motor neurons in transplanted mice was significantly higher than those in untreated mice.Human specific nuclear antigen in brain and spinal cord was detected in transplanted SOD1-G93A mice.Conclusion hMSCs can be implanted for a long-term into central nervous system by intracardiac transplantation and the transplantation can prolong life span, and delay the onset of the disease and motor neuron loss in SOD1-G93A mice.

Objective To study the biological function of Topical Oxygen Therapy(TOT) and Infrared Light-Emitting Diode(LED) therapy and mechanism of combination of both therapy in wound healing.To develop a device combined with TOT and LED therapy.Methods Wound models were made using rabbits which were grouped in four groups such as control group,TOT group,LED group and combined group by random.Except control group,the other groups were carried on TOT,LED and TOT+LED therapy respectively.Wound healing situations were observed.Results TOT+LED therapy could cut the wound healing time whose mechanism was to form composition force in the processing of wound healing by prompting inside growth factors and outside factors.Conclusion The therapy combined with TOT and LED can facilitate the wound healing.The theory of the wound healing device is feasible according to the results of the experiments.

OBJECTIVE:To observe the efficacy and safety of prednisone combined with human immunoglobulin(pH4)for intra-venous injection in the treatment of idiopathic thrombocytopenic purpura. METHODS:85 patients with idiopathic thrombocytopenic purpura were divided into control group(42 cases)and observation group(43 cases). Control group received 1.6 mg/(kg·d)Predni-sone tablet,orally,for continuous 4 weeks;observation group received 400 mg/(kg·d)human immunoglobulin(pH4)for intravenous injection,intravenous injection,for continuous 5 d,then 1.6 mg/(kg·d)Prednisone tablet,orally,for continuous 4 weeks. All pa-tients were given Adrenal color hydrazone tablet,Vitamin C tablet and other conventional treatment. Clinical efficacy,platelet number, T lymphocyte subsets(CD3+,CD3+CD4+,CD3+CD8+,CD19+),TNF-α,IL-6 before and after treatment,time of platelet number reached normal and reached peak value,peak value of platelet number and the incidence of adverse reactions in 2 groups were ob-served. RESULTS:The total effective rate and peak value of platelet number in observation group were significantly higher than control group,time of platelet number reached normal and reached peak value were significantly shorter than control group,the differences were statistically significant(P<0.05). Before treatment,there were no significant differences in platelet number,T lymphocyte sub-sets,IL-6 and TNF-αlevel in 2 groups(P>0.05);after treatment,platelet number,CD3+and CD3+CD4+in 2 groups were significant-ly higher than before,and observation group was higher than control group,IL-6,TNF-αlevel,CD3+CD8+and CD19+were signifi-cantly lower than before,and observation group was lower than control group,the differences were statistically significant(P<0.05). And there was no significant difference in the incidence of adverse reactions in 2 groups(P>0.05). CONCLUSIONS:Prednisone com-bined with human immunoglobulin(pH4) for intravenous injection shows better efficacy than prednisone alone in the treatment of idio-pathic thrombocytopenic purpura,it can increase platelet number,adjust immune function,and do not increase the incidence of ad-verse reactions.

Objective To study the relationships between pathological grade of Henoch-Schonlein purpura nephritis (HSPN) and levels of serum transforming growth factor-beta 1 (TGF-β1),monocyte chemoattractant protein 1 (MCP-1),interleukin (IL)-17 and prognosis in adults.Methods 98 HSPN patients treated in our hospital from June 2015 to December 2017 were selected as the study group,65 IgA nephritis patients were selected as the IgA nephritis group,and 60 healthy people who came to our hospital for physical examination during the same period were selected as the control group.The levels of TGF-β1,MCP-1 and IL-17 in serum of the three groups were detected,and the Cox regression analysis was used to analyze the risk factors affecting the patient's condition.Results The levels of serum TGF-β1,MCP-1 and IL-17 in the study group were significantly higher than those in IgA nephritis group and control group (P ＜ 0.05).The levels of serum TGF-β1,MCP-1 and IL-17 in IgA nephritis group were significantly higher than those in control group (P ＜ 0.05).There was no significant difference in age,sex,hemoglobin,albumin,urinary protein and renal phenotype among groups (P ＜ 0.05).Platelets of type Ⅲ were significantly lower than those of type Ⅱ (P ＜0.05);C-reactive protein (CRP) level of type Ⅳ,Ⅴ and Ⅵ was significantly higher than that of type Ⅱ (P ＜ 0.05).The degree of glomerulosclerosis in patients with type Ⅲ,Ⅳ,Ⅴ and Ⅵ was significantly higher than that in patients with type Ⅱ,and the degree of glomerulosclerosis in patients with type Ⅴ and Ⅵ was also significantly higher than that in patients with type Ⅲ (P ＜ 0.05).The formation of crescents in patients with type Ⅲ,Ⅳ,Ⅴ and Ⅵ was significantly higher than that in patients with type Ⅱ,and the formation of crescents in patients with type Ⅳ,Ⅴ and Ⅵ was also significantly higher than that in patients with type Ⅲ (P ＜ 0.05).The levels of serum TGF-β1,MCP-1 and IL-17 were the lowest in type Ⅱ patients and the highest in type Ⅴ and Ⅵ patients.The levels of TGF-β1,MCP-1 and IL-17 in type Ⅲ,Ⅳ,Ⅴ and Ⅵ were significantly higher than those in type Ⅱ (P ＜0.05),and the level of TGF-β1 in type Ⅳ,Ⅴ and Ⅵ was significantly higher than that in type Ⅲ (P ＜ 0.05);Serum IL-17 level of type Ⅴ and Ⅵ was significantly higher than that of type Ⅲ (P ＜ 0.05).Cox regression analysis showed that TGF-β1 and IL-17 were risk factors for pathological grading.Conclusions The higher the pathological grade of Henoch-Schonlein purpura nephritis in adults,the higher the levels of serum TGF-β1 and IL-17.TGF-β1 and IL-17 are the risk factors affecting the pathological grade of Henoch-Schonlein purpura nephritis.

Madelung′s disease is a rare lipid metabolic disorder with unclear mechanism, characterized by the formation of diffuse uncapsulated lipomas in face, neck, shoulder and other body areas. This disease mainly affect middle-aged male, and is related to alcohol abuse. The treatment nowadays is only palliative surgery with a high recurrence rate, including lipectomy and liposuction. Both of them have advantages and disadvantages.

Recent studies on male infertility reveal a growing worry: more infertile men are dealing with inflammation in the testis. Analyzing testicular biopsies from infertile men highlights a significant presence of inflammation. This connection, supported by clinical and pathological evidence, emphasizes that testicular inflammation hampers sperm production, leading to lasting declines in sperm count and quality. However, the exact reasons behind male infertility due to orchitis, a type of testicular inflammation, are still uncertain. Understanding these fundamental aspects of molecular signals and cellular mechanisms in testicular inflammation is crucial. Our review delves into recent literature with a dual objective: elucidating potential mechanisms involving immune cells, non-immune cells, and cytokines that link orchitis to male infertility, while also paving the way for precise interventions and solutions to address the challenges of male infertility.

Recent studies on male infertility reveal a growing worry: more infertile men are dealing with inflammation in the testis. Analyzing testicular biopsies from infertile men highlights a significant presence of inflammation. This connection, supported by clinical and pathological evidence, emphasizes that testicular inflammation hampers sperm production, leading to lasting declines in sperm count and quality. However, the exact reasons behind male infertility due to orchitis, a type of testicular inflammation, are still uncertain. Understanding these fundamental aspects of molecular signals and cellular mechanisms in testicular inflammation is crucial. Our review delves into recent literature with a dual objective: elucidating potential mechanisms involving immune cells, non-immune cells, and cytokines that link orchitis to male infertility, while also paving the way for precise interventions and solutions to address the challenges of male infertility.

Recent studies on male infertility reveal a growing worry: more infertile men are dealing with inflammation in the testis. Analyzing testicular biopsies from infertile men highlights a significant presence of inflammation. This connection, supported by clinical and pathological evidence, emphasizes that testicular inflammation hampers sperm production, leading to lasting declines in sperm count and quality. However, the exact reasons behind male infertility due to orchitis, a type of testicular inflammation, are still uncertain. Understanding these fundamental aspects of molecular signals and cellular mechanisms in testicular inflammation is crucial. Our review delves into recent literature with a dual objective: elucidating potential mechanisms involving immune cells, non-immune cells, and cytokines that link orchitis to male infertility, while also paving the way for precise interventions and solutions to address the challenges of male infertility.

Recent studies on male infertility reveal a growing worry: more infertile men are dealing with inflammation in the testis. Analyzing testicular biopsies from infertile men highlights a significant presence of inflammation. This connection, supported by clinical and pathological evidence, emphasizes that testicular inflammation hampers sperm production, leading to lasting declines in sperm count and quality. However, the exact reasons behind male infertility due to orchitis, a type of testicular inflammation, are still uncertain. Understanding these fundamental aspects of molecular signals and cellular mechanisms in testicular inflammation is crucial. Our review delves into recent literature with a dual objective: elucidating potential mechanisms involving immune cells, non-immune cells, and cytokines that link orchitis to male infertility, while also paving the way for precise interventions and solutions to address the challenges of male infertility.

Recent studies on male infertility reveal a growing worry: more infertile men are dealing with inflammation in the testis. Analyzing testicular biopsies from infertile men highlights a significant presence of inflammation. This connection, supported by clinical and pathological evidence, emphasizes that testicular inflammation hampers sperm production, leading to lasting declines in sperm count and quality. However, the exact reasons behind male infertility due to orchitis, a type of testicular inflammation, are still uncertain. Understanding these fundamental aspects of molecular signals and cellular mechanisms in testicular inflammation is crucial. Our review delves into recent literature with a dual objective: elucidating potential mechanisms involving immune cells, non-immune cells, and cytokines that link orchitis to male infertility, while also paving the way for precise interventions and solutions to address the challenges of male infertility.