海藻化工以氢氧化钙作为钙化剂的新型钙化工艺研究

研究了海藻化工中以氢氧化钙作为钙化剂的新型钙化工艺,使用氢氧化钙+氯化钙作为褐藻酸钠的钙化剂替代传统的单一氯化钙。确定的双钙钙化工艺条件：每升褐藻酸钠胶液（褐藻酸钠质量浓度为2.5 g/L）,添加氯化钙溶液29.0 mL（质量分数为5%）,添加氢氧化钙溶液13.75 mL（质量分数为5%）,复合钙化剂中氯化钙与氢氧化钙物质的量比为1.19∶1。与传统工艺相比,新型钙化工艺褐藻酸钠的产率未有明显变化,得到的褐藻酸钠粘度稍有降低,粘度由275.1 mPa·s降低至241.3 mPa·s;氯化钙使用量降低40%以上,总钙添加量减少19%。双钙钙化工艺实现了对钙化废水的再利用,废水中钙质量浓度经处理由483 mg/L降到20 mg/L左右,电导率由6.84 mS/cm降至4.28 mS/cm;经脱钙处理的钙化废水回用后对产品褐藻酸钠的产率和粘度没有显著影响。新工艺操作简单,不仅有效减少了钙化废水中离子的引入,同时可以实现低成本地脱钙,脱钙后的废水可以作为冲稀水回收利用,减少了水资源的消耗,为海藻化工行业的减排提供了一条新的工艺途径。     

Regulation effect of osteoblasts towards osteocytes by silk fibroin encapsulation

Herein, the rational design micromilieus involved silk fibroin (SF)-based materials have been used to encapsulate the osteoblasts, forming an extracellular coated shell on the cells, which exhibited the high potential to shift the regulation of osteoblasts to osteocytes by encapsulation cues. SF coating treated cells showed a change in cell morphology from osteoblasts-like to osteocytes-like shape compared with untreated ones. Moreover, the expression of alkaline phosphatase (ALP), collagen I (Col I) and osteocalcin (OCN) further indicated a potential approach for inducing osteoblasts regulation, which typically accelerates calcium deposition and cell calcification, presenting a key role for the SF encapsulation in controlling osteoblasts behavior. This discovery showed that SF-based cell encapsulation could be used for osteoblasts behavior regulation, which offers a great potential to modulate mammalian cells’ phenotype involving alternating surrounding cues.     

The Protective Effects of the Autophagic and Lysosomal Machinery in Vascular and Valvular Calcification: A Systematic Review

Background: Autophagy is a highly conserved catabolic homeostatic process, crucial for cell survival. It has been shown that autophagy can modulate different cardiovascular pathologies, including vascular calcification (VCN). Objective: To assess how modulation of autophagy, either through induction or inhibition, affects vascular and valvular calcification and to determine the therapeutic applicability of inducing autophagy. Data sources: A systematic review of English language articles using MEDLINE/PubMed, Web of Science (WoS) and the Cochrane library. The search terms included autophagy, autolysosome, mitophagy, endoplasmic reticulum (ER)-phagy, lysosomal, calcification and calcinosis. Study characteristics: Thirty-seven articles were selected based on pre-defined eligibility criteria. Thirty-three studies (89%) studied vascular smooth muscle cell (VSMC) calcification of which 27 (82%) studies investigated autophagy and six (18%) studies lysosomal function in VCN. Four studies (11%) studied aortic valve calcification (AVCN). Thirty-four studies were published in the time period 2015–2020 (92%). Conclusion: There is compelling evidence that both autophagy and lysosomal function are critical regulators of VCN, which opens new perspectives for treatment strategies. However, there are still challenges to overcome, such as the development of more selective pharmacological agents and standardization of methods to measure autophagic flux.     

Calcification-Based Cancer Diagnosis and Therapy

In nature, calcium deposition is a common biological process in mammals that shapes mechanical structures and creates the functions of bones and teeth, and causes calculi formation. Spontaneous tumor calcification and regional lymph node calcification in colorectal cancer, lung cancer, and glioblastoma have been proven to be benign prognostic factors in the clinic. In line with this concept, we introduce the idea and lead the compound development of artificially inducing bionic calcification around the surface of cancer cells. This process is shown to have excellent effects in the inhibition of growth and metastases of cervical, breast, and lung tumors, as well as superb performance in early-stage diagnosis. Therefore, we predict that this concept may open the door for cancer targeting calcification therapy and diagnosis and provide an outlook for a new avenue in anticancer drug development.     

A Genomics-Based Model for Prediction of Severe Bioprosthetic Mitral Valve Calcification

Severe bioprosthetic mitral valve calcification is a significant problem in cardiovascular surgery. Unfortunately, clinical markers did not demonstrate efficacy in prediction of severe bioprosthetic mitral valve calcification. Here, we examined whether a genomics-based approach is efficient in predicting the risk of severe bioprosthetic mitral valve calcification. A total of 124 consecutive Russian patients who underwent mitral valve replacement surgery were recruited. We investigated the associations of the inherited variation in innate immunity, lipid metabolism and calcium metabolism genes with severe bioprosthetic mitral valve calcification. Genotyping was conducted utilizing the TaqMan assay. Eight gene polymorphisms were significantly associated with severe bioprosthetic mitral valve calcification and were therefore included into stepwise logistic regression which identified male gender, the T/T genotype of the rs3775073 polymorphism within the TLR6 gene, the C/T genotype of the rs2229238 polymorphism within the IL6R gene, and the A/A genotype of the rs10455872 polymorphism within the LPA gene as independent predictors of severe bioprosthetic mitral valve calcification. The developed genomics-based model had fair predictive value with area under the receiver operating characteristic (ROC) curve of 0.73. In conclusion, our genomics-based approach is efficient for the prediction of severe bioprosthetic mitral valve calcification.     

Calcific mitral stenosis in the hemodialysis patient

The dialysis patient is prone to elevations in the calcium phosphorus product and hyperparathyroidism, which contributes to valvular and vascular calcification. We present the case of a young lady on chronic dialysis that developed mitral calcification complicated by severe mitral stenosis, caseous calcification and retinal embolization. She subsequently required mitral valve replacement.     

Long-term effects of magnesium carbonate on coronary artery calcification and bone mineral density in hemodialysis patients: A pilot study

Observational data suggest that elevated magnesium levels in dialysis patients may prevent vascular calcification and in vitro magnesium can prevent hydroxyapatite crystal growth. However, the effects of magnesium on vascular calcification and bone mineral density have not been studied prospectively. Seven chronic hemodialysis patients participated in this open label, prospective pilot study to evaluate the effects of a magnesium-based phosphate binder on coronary artery calcification (CAC) scores and vertebral bone mineral density (V-BMD) in patients with baseline CAC scores >30. Magnesium carbonate/calcium carbonate (elemental Mg: 86 mg/elemental Ca 100 mg) was administered as the principal phosphate binder for a period of 18 months and changes in CAC and V-BMD were measured at baseline, 6, 12, and 18 months. Serum magnesium levels averaged 2.2±0.4 mEq/L (range: 1.3–3.9 mEq/L). Phosphorus levels (4.5±0.6 mg/dL) were well controlled throughout the 18 months study. Electron beam computed tomography results demonstrated a small not statically significant increase in absolute CAC scores, no significant change in median percent change, and a small none significant change in V-BMD. Magnesium may have a favorable effect on CAC. The long-term effect on bone mineral density remains unclear. Larger studies are needed to confirm these findings.     

Simple evaluation of aortic arch calcification by chest radiography in hemodialysis patients

Vascular calcification is associated with a poor prognosis in dialysis patients. It can be assessed with computed tomography but simple inoffice techniques may provide useful information. We compared the results obtained with a simple noninvasive technique with those obtained using multidetector computed tomography for aortic arch calcification volume (AoACV) in chronic hemodialysis (HD) patients. The enrolled study subjects were 63 (32 men and 31 women) maintenance HD patients. Calcification of the aortic arch was semiquantitatively estimated with a AoAC score (AoACS) on plain chest radiology. The AoACV was increased, with a mean value of 6.6 ranging from 0% to 36.5%. The coefficient of intraobserver variation was less than 2.5%. Aortic arch calcification score was highly correlated with AoACV (r=0.635, P<0.001). Multiple regression analysis showed age (F value=12.62, P<0.001) and pulse pressure (F value=4.54, P=0.037) to be significant independent determinants of AoACS. In conclusion, a simple measurement of AoACS may be useful for inoffice imaging to choose a therapeutic regimen in HD patients.     

石灰湿法燃煤烟气脱硫过程CO2钙化问题分析研究

采用模拟燃煤烟气方法．研究了石灰湿法燃煤烟气脱硫过程中CO2钙化问题，指出了烟气脱硫过程中CaCO3的生成量与脱硫液初始pH值、SO2初始浓度、温度的关系．得出抑制CaCO3生成的条件．为减缓石灰湿法燃煤烟气脱硫存在的结垢现象．对石灰湿法燃煤烟气脱硫系统的实际应用具有一定的指导和借鉴价值。     

Changes in circulating biomarkers during a single hemodialysis session

The hemodialysis (HD) procedure induces an inflammatory response potentially contributing to cardiovascular disease. Here we investigated the acute impact of HD on circulating biomarkers. Circulating biomarkers (small solutes, middle molecular‐sized peptides, and proteins) related to inflammation, oxidative stress, and vascular calcification (VC) were measured before and after a single session of HD in 45 clinically stable patients. Concentrations were corrected for ultrafiltration‐induced hemoconcentration. Among vascular calcification‐related biomarkers, osteoprotegerin and fetuin‐A remained unchanged while fibroblast growth factor‐23 (FGF23) decreased by ?19%. Changes of FGF23 and changes of phosphate correlated (ρ = 0.61, P < 0.001). While C‐reactive protein did not change, interleukin‐6 (IL‐6) increased by 14% and pentraxin 3 (PTX3) increased by 45%. IL‐6 and PTX3 appear to be valid biomarkers of the intradialytic inflammatory response. VC‐related markers were in general not affected by the single HD session; however, the observed correlation between acute changes of FGF‐23 and phosphate during HD warrants further studies.