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BACKGROUND: Hydroxyapatite has been widely used in the studies on bone materials due to its good histocompatibility and bone conductivity. But pure hydroxyapatite has no antibacterial properties. Therefore, the antibacterial modification of hydroxyapatite is of great importance.OBJECTIVE: To review the research progress of the antibacterial modification of hydroxyapatite. METHODS: A computer-based retrieval of Science Direct online, PubMed, and CNKI databases was performed for the articles published before 2019. The key words were “antibacterial mechanism, hydroxyapatite, silver, gold, copper, cobalt, chitosan, strontium, zinc, gallium, magnesium, selenium, titanium” in English and Chinese, respectively. The irrelevant, repeated and old articles were excluded. RESULTS AND CONCLUSION: There are many ways to modify hydroxyapatite, but the main way is to add metal antibacterial particles. Silver, gold, copper, cobalt, chitosan, strontium, zinc, gallium, magnesium, selenium and titanium can be added into hydroxyapatite to make it have antibacterial activity. There are still some limitations in the research of antibacterial materials: the release curve of antibacterial Ions in hydroxyapatite has not been well regulated. There are few antibacterial materials, let alone used for implants in vivo. More nontoxic substances with good antibacterial properties need to be found. Due to the toxicity of antibacterial Ions, there is no uniform standard for the optimal concentration of each kind of antibacterial ion.
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Introduction: Elevated plasma level of homocysteine (eHcy) is associated with increased prevalence of peripheral neuropathy (PN) in diabetic patients. However, it is not known whether eHcy is an independent risk factor for the development of PN. Methods: We retrospectively reviewed clinic and laboratory data of patients with PN, and patients with headaches serving as controls. The study consisted of two separate cohorts in two different settings. Setting-A was designed to address whether the isolated eHcy is relevant to PN and setting-B to analyze various risk factors in patients with PN. Results: Fifty seven and 217 subjects with PN and 42 and 252 individuals with headache were included in the setting-A and setting-B, respectively. A significantly elevated level of homocysteine was observed in the patients with PN in both setting-A and setting-B (11.3±7.1 and 13.4±14.6 mmol/L, mean±SD) than in the patients with headaches (8.6±2.8 and 8.1±2.5, P=.02 and P=.02, respectively). In addition, significantly increased frequency of eHcy was observed in PN (21% and 38% in setting- A and setting-B) than that in headache controls (4.5% and 4.8%; P= .05 and P= .002, respectively). Conclusion: eHcy may potentially act as an independent risk factor for the development of PN.
ABSTRACT
<p><b>BACKGROUND</b>Atrial fibrillation (AF) is accompanied by atrial structural remodeling. Calpain activity is induced during AF. To test a causal relationship between calpain activation and atrial structural changes, N-acetyl-Leu-Leu-Met (ALLM), a calpain inhibitor, was utilized in a canine AF model.</p><p><b>METHODS</b>Fifteen dogs were randomly divided into 3 groups: sham-operated group, control group and calpain inhibitor group; each with 5 dogs. Sustained AF was induced by rapid right atrium pacing at 600 beats per minute for 3 weeks. ALLM was administered at a dosage of 1.0 mg x kg(-1) x d(-1) in the calpain inhibitor group. Three weeks later, the proteolysis, protein expression of TnT and myosin, calpain I localization and expression and structural changes were examined in left atrial free walls, right atrial free walls and the interatrial septum respectively. Atrial size and contractile function were also measured by echocardiography.</p><p><b>RESULTS</b>Long-term rapid atrial pacing induced marked structural changes such as enlarged atrial volume, myolysis, degradation of TnT and myosin, accumulation of glycogen and changes in mitochondrial shape and size, which were paralleled by an increase in calpain activity. The positive correlation between calpain activity and the degree of myolysis (r(s) = 0.90 961, P < 0.0001) was demonstrated. In addition to structural abnormalities, pacing-induced atrial contractile dysfunction was observed in this study. The pacing-induced atrial structural alterations and loss of contractility were partially prevented by the calpain inhibitor ALLM.</p><p><b>CONCLUSIONS</b>Activation of calpain represents key features in the progression towards overt structural remodeling. Calpain inhibitor, ALLM, suppressed the increased calpain activity and reversed structural remodeling caused by sustained atrial fibrillation in the present model. Calpain inhibition may therefore provide a possibility for therapeutic intervention in AF.</p>
Subject(s)
Animals , Dogs , Atrial Fibrillation , Pathology , Calpain , Cysteine Proteinase Inhibitors , Pharmacology , Disease Models, Animal , Heart Atria , Pathology , Myosins , Troponin TABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of 4OH-Tamoxifen (OHT) on proliferation and apoptosis of primary cultured prostate stromal cells.</p><p><b>METHODS</b>Primarily cultured prostate stromal cells in vitro were treated with various concentrations (10(-8) mol/L - 10(-5) mol/L) of estradiol (E2), diethylstilbestrol (DES), OHT and the mixture of E2 (10(-8) mol/L - 10(-6) mol/L) with OHT (10(-7) mol/L) and then MTT and TUNEL were used to detect their proliferation and apoptosis respectively.</p><p><b>RESULTS</b>There was a significant difference (P < 0.05) between OHT and estrogens in the effects on the apoptosis and proliferation of the primarily cultured prostate stromal cells. OHT suppressed proliferation of the prostate stromal cells at the concentrations from 10(-7) mol/L to 10(-5) mol/L (P < 0.05), and this effect was concentration related (r = -0.383, P = 0.005); OHT (10(-7) mol/L) suppressed the proliferation stimulation effect of E2 at the concentrations from 10(-8) mol/L to 10(-6) mol/L (P < 0.05). OHT induced apoptosis at the concentrations from 10(-8) mol/L to 10(-5) mol/L (P < 0.05), and this effect was concentration related (r = 0.349, P = 0.012). The apoptosis induced by OHT could not be reversed by E2 at the concentrations from 10(-8) mol/L to 10(-5) mol/L (P > 0.05).</p><p><b>CONCLUSION</b>OHT can obviously suppressed the proliferation and promote the apoptosis of primarily cultured prostate stromal cells, which might not be totally attributed to the competitive inhibition of the estrogen receptor.</p>