ABSTRACT
The normal function of vascular endothelial cells is an important foundation for maintaining vascular permeability， restricting inflammatory activities of the vascular wall， and balancing the coagulation and fibrinolytic system. Endothelial dysfunction caused by persistent damage from pathological factors is considered as an early and prominent event of diabetic macroangiopathy. In traditional Chinese medicine， the classical theory of "restraining excessiveness to acquire harmony" was originally a condensed generalization of the rule of generation， restriction， replacement and evolution in the natural world， revealing the internal regulation mechanism of the stable operation of things. Then it gradually evolved into an important rule to explain the physiological phenomena and pathological mechanism of human body and guide the treatment. Corresponding to the nature， the body homeostasis also requires to achieve a state of strong viscera function and inexhaustible Qi and blood generation under the rule of restriction and generation. The pathogenesis of diabetic macroangiopathy is the process of "the predominant one failing to restrict and the hyperactive one becoming harmful". The loss of restriction and generation of the five organs leads to powerless Qi transformation and， as a result， the Qi， blood and body fluid cannot be dispersed. Therefore， the Qi， blood and body fluid turn into phlegm and blood stasis， such as glucose and lipid metabolism disorder， oxidative stress， inflammatory response and high blood viscosity， and finally block the veins. Excessive phlegm and blood stasis cannot be resolved， instead they become harmful and invade the blood vessel， causing endothelial dysfunction and further resulting in diabetic macroangiopathy. Under the guidance of the theory of "restraining excessiveness to acquire harmony"， the method of "harmonizing viscera， eliminating pathogen and removing turbidity" can effectively regulate the function of vascular endothelial cells， thus playing a positive role in preventing and treating diabetic macroangiopathy. The mechanism may be related to reducing oxidative stress， inhibiting inflammation， limiting vascular smooth muscle proliferation， and reducing platelet adhesion.
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AIM:To compare the clinical effect of 23G and 25G+ vitrectomy for treatment of proliferative diabetic retinopathy (PDR).METHODS: A total of 128 PDR patients (195 eyes) requiring vitrectomy in our hospital from November 2013 to May 2016 were randomly divided into 25G+ group and 23G group, 64 cases (97 eyes) in 25G+ group and 64 cases (98 eyes) in 23G group.In 25G+ group, patients were treated by 25G+ vitrectomy.In 23G group, patients were treated by 23G vitrectomy.The visual acuity, as well as intraocular pressure (IOP), iatrogenic injury and complications in two groups were recorded before and 1d, 1wk, 1mo after treatment.The operation time was compared between two groups.RESULTS: The operation time in 25G+ group was lower than that in 23G group (P0.05).IOP in 25G+ group before surgery had no significant difference compared with those after surgery at 1d,1wk, and 1mo(P>0.05), which it was the same in 23G group.IOP of two groups in the same period had no significant difference (P>0.05).The incidence rate of iatrogenic injury in 25G+ group was 4.1%, which was significant lower than that of 23G group (13.3%) (P<0.05).The incidence rate of complication in 25G+ group was 3.1%, which was significant lower than that of 23G group (11.2%) (P<0.05).CONCLUSION: Both 23G and 25G+ vitrectomy are safe and effective treatment for PDR.However, 25G+ vitrectomy is the better choice for PDR for the shorter operation time, lower incidence rate of iatrogenic injury and fewer surgical complications.
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Objective: To investigate the phenotypic characteristics and functional capability differences of mouse bone marrow-derived dendritic cells after stimulation with Mycobacterium tuberculosis in the presence or absence of vitamin D3. Methods: Mouse bone marrow-derived cells were cultured with GM-CSF (20 ng/mL). Then, one was added with 100 nmol/L of 25(OH)D3, while the other did not. On day 6, 5 μg/mL of BCG was added to stimulate the cells for 24 h. On day 7, suspension cells were harvested for phenotypic and functional analyses. Results: The percentages of CD86 dendritic cells (DCs) in the control group and 25(OH)D3 group were 66.97% ± 8.29% and 52.18% ± 8.52%, respectively; the mean fluorescence intensities of MHC-II in the control group and 25(OH)D3 group were 1 102.16 ± 371.02 and 681.62 ± 292.71. The expression levels of MHC- II and CD86 on the surface of the DCs in 25(OH)D3 group were significantly lower than those of the control group. The ability of the DCs to stimulate proliferation of T-lymphocytes was also significantly lower than that of the control group. Conclusions: These findings suggest that 25(OH)D3 modulates the immune response by affecting the maturation and function of DCs in Mycobacterium tuberculosis period.
ABSTRACT
OBJECTIVE@#To investigate the phenotypic characteristics and functional capability differences of mouse bone marrow-derived dendritic cells after stimulation with Mycobacterium tuberculosis in the presence or absence of vitamin D3.@*METHODS@#Mouse bone marrow-derived cells were cultured with GM-CSF (20 ng/mL). Then, one was added with 100 nmol/L of 25(OH)D3, while the other did not. On day 6, 5 μg/mL of BCG was added to stimulate the cells for 24 h. On day 7, suspension cells were harvested for phenotypic and functional analyses.@*RESULTS@#The percentages of CD86 dendritic cells (DCs) in the control group and 25(OH)D3 group were 66.97% ± 8.29% and 52.18% ± 8.52%, respectively; the mean fluorescence intensities of MHC-II in the control group and 25(OH)D3 group were 1 102.16 ± 371.02 and 681.62 ± 292.71. The expression levels of MHC- II and CD86 on the surface of the DCs in 25(OH)D3 group were significantly lower than those of the control group. The ability of the DCs to stimulate proliferation of T-lymphocytes was also significantly lower than that of the control group.@*CONCLUSIONS@#These findings suggest that 25(OH)D3 modulates the immune response by affecting the maturation and function of DCs in Mycobacterium tuberculosis period.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the efficacy of individualized anti-tuberculosis chemotherapy guided by drug susceptibility testing for spinal tuberculosis through analyses on the post-operative follow-up outcomes.</p><p><b>METHODS</b>The diagnoses of spinal tuberculosis were established by clinical, radiological and histological evaluation in 132 patients who were admitted from August 2005 to January 2010, 62 patients (37 male and 25 female) with follow-up more than 12 months in this study. The average age was 33.6 years (ranging from 4 - 67 years). The infected samples were collected during surgery. After processed in a routine laboratory procedure, the samples were inoculated into vials of the BACT/ALERT 3D system. The drug susceptibility testing was performed using absolute concentration method, which included 11 first-line and second-line drugs. Four or five anti-tuberculosis drug regimen was chosen according to the results of drug susceptibility testing. All the patients were followed up a month later, and then once 3 months in the following 11 months, and subsequently at intervals of half a year. The clinical status, erythrocyte sedimentation rate (ESR), roentgenogram, MRI and 3D-CT were concerned to estimate the progress of tuberculosis.</p><p><b>RESULTS</b>The culture positive rate was 45.2% (28/62). The average detection time was 42 d (ranging from 28 - 58 d). The drug susceptibility testing showed a total drug resistance level of 24.2%:12.9% for isoniazid, 4.8% for rifampicin, 3.2% for ethambutol, 9.7% for streptomycin, 6.4% for pasiniazid, 14.5% for levofloxacin, 1.6% for rifapentine. The mean follow-up period was 21 months (ranging from 12 - 44 months). According to Bridwell criteria, grade I bony fusion was obtained in all patients in 8 - 12 months.</p><p><b>CONCLUSION</b>Guided by drug susceptibility testing, individualized anti-tuberculosis chemotherapy for 12 to 18 months is effective for spinal tuberculosis.</p>