Objective To study the relationship between parathyroid hormone(PTH)level and central arterial stiffness in patients with high risk of coronary artery disease(CAD) and preserved renal function.Methods Seventy-seven patients with at least one risk factor of coronary artery disease (CAD) were divided into increased arterial stiffness group(n=35) and control group(n=42),based on whether the noninvasive pulse wave analysis index of the central pulse pressure(CPP) was higher than 40mmHg or not.Coronary artery angiography was performed in all cases.Serum intact PTH,calcium,phosphor,and highly sensitive C reactive protein (hsCRP) was assessed by radioimmunoassay.Coronary angiography was also performed.Results The patients in increased arterial stiffness group were elder and had higher serum uric acid compared with those in the control group.Forty-four patients were confirmed to have CAD; CAD patients in the stiffness group (n=23) had significantly higher serum iPTH level compared with those in the control group(n=21) (P40 mmHg)after adjustment for age,BMI,hs-CRP,and male gender.Conclusion CAD patients with increased central arterial stiffness and preserved renal function have higher serum PTH level.The serum PTH level is positively correlated with central arterial stiffness,and is the independent risk factor for increased arterial stiffness.

Objective To investigate the effects of different fine particulate matter (PM2.5) components (water-soluble, organic, water-soluble+organic) in vivo on the NOS/NO system in the endothelial cells from rat thoracic aortas. Methods Three PM2.5 components were used to inject by vein in rat tail. ELISA and immunohistochemical technique were used to examine the change of NOS/NO system in the blood-serum and the endothelial cells from rat thoracic aorta. Results Compared with control group, three PM2.5 components increased NO level of rat blood-serum [control, (38.00±5.40) μmol/L; water-soluble group, (44.66±16.59) μmol/L, t =3.58, P< 0.05; organic groups, (58.28±12.30) μmol/L, t =12.85, P <0.01; mixtural component group, (84.02+19.24) μmol/L, t =31.39, P<0.01]; increased iNOS level of rat blood-serum [control, (17.47±5.33) U/ml; water-soluble group, (21.87±4.63) U/ml, t =4.92, P <0.05; organic groups, (25.27±6.58) U/ml, t = 6.22, P<0.05; Mixtural component group, (32.79±5.86) U/ml, t =32.84, P <0.01]. Mixtural component decreased eNOS level of rat blood-serum [(12.58±4.59) pg/ml vs (17.47±2.97) pg/ml, t =5.91, P <0.05], no significant difference on eNOS level of blood-serum among other component groups (P >0.05). Three components decreased the expression of eNOS protein in the endothelial cells from rat thoracic aorta(control, 164.68±4.80; water-soluble group, 185.43±5.63, t =4.26, P <0.05; organic groups, 194.07±9.77, t =5.26, P <0.05; Mixtural component group, 209.24±15.43, t =43.19, P <0.01), increased the expression of iNOS protein (control, 160.17±5.79; water-soluble group, 134.78±8.22, t =5.21, P <0.05; organic groups, 134.78±8.22, t =5.98, P <0.05; Mixtural component group, 81.62 ±10.59, t =34.98, P <0.01) in the endothelial cells from rat thoracic aortas.Conclusion Three components of PM2.5 induced the dysfunction of endothelial cells and disorder of NOS/NO system in the endothelial cells.

A comparative observation about histological and histochemical study were made onthe preservating methods of local ischemic kidney of dogs.The methods of this exp-eriment were divided into five groups:A.Local hypothermia;B.Hypothermic perfu-sion solution 500ml,4℃,containing Procaine 450 mg and Heparin 100 mg,infusedinto renal artery;C.Hypothermic perfusion solution 500ml,4℃,containing 20% Ma-nniton 32ml,25% MgSO_4 0.36 ml,Heparin 100 ml,infused into renal artery;D.Localhypothermia and heparin 30 mg injected into the same vessel.E.Local room tem-perature.The specimens were taken from the kidneys of the experimental dogs atvarious period after treated with every method.The results were as follows;A,D and E group presented irreversible histological changes within 4 hoursaftertreatment.Four hours later,the reaction of SDH,ATPase,AlPase werenegative.It suggested that the kidney damage was serious,as well as expressed thatthe effect of these preservating methods for ischemic kidney are not satisfactory.In B group,the histological and histochemical alteration is very light and almostreversible,during 60 days after treatment.In C group,hypothermic perfusionsolution containing Mannitol,MgSO_4 etc either during experiment or follow observa-tion for 60 days,no histological and histochemical alterations were found.It indica-ted that this method is an ideal perservating technique for ischemic kidney.

OBJECTIVETo design and fabricate the custom-made titanium mandibular condyle by the reverse engineering technology combined with selective laser melting (SLM) technology and to explore the mechanical properties of the SLM-processed samples and the application of the custom-made condyle in the temporomandibular joint (TMJ) reconstruction.

METHODSThe three-dimensional model of the mandibular condyle was obtained from a series of CT databases. The custom-made condyle model was designed by the reverse engineering software. The mandibular condyle was made of titanium powder with a particle size of 20-65 µm as the basic material and the processing was carried out in an argon atmosphere by the SLM machine. The yield strength, ultimate strength, bending strength, hardness, surface morphology and roughness were tested and analyzed. The finite element analysis (FEA) was used to analyze the stress distribution.

RESULTSThe complex geometry and the surface of the custom-made condyle can be reproduced precisely by the SLM. The mechanical results showed that the yield strength, ultimate strength, bending strength and hardness were (559±14) MPa, (659±32) MPa, (1 067±42) MPa, and (212±4)HV, respectively. The surface roughness was reduced by sandblast treatment.

CONCLUSIONSThe custom-made titanium condyle can be fabricated by SLM technology which is time-saving and highly digitized. The mechanical properties of the SLM sample can meet the requirements of surgical implant material in the clinic. The possibility of fabricating custom-made titanium mandibular condyle combined with the FEA opens new interesting perspectives for TMJ reconstruction.

Dental Materials ; Finite Element Analysis ; Hardness ; Humans ; Lasers ; Mandibular Condyle ; Prostheses and Implants ; Prosthesis Design ; Titanium

Objective To investigate the effect of intestinal mucosal Toll-like receptor 4/nuclear factor κB (TLR4/NF-κB) signaling pathway on renal damage in pseudo-sterile IgA nephropathy (IgAN) mice. Methods C57BL/6 mice were randomly divided into experimental group (pseudosterile mouse model group), control group (IgAN mouse model group), pseudosterile mouse blank group, and normal mouse blank group. Pseudosterile mice were established by intragastric administration of quadruple antibiotics once a day for 14 days. The pseudosterile IgAN mouse model was set up by combination of oral bovine serum albumin (BSA) administration and staphylococcal enterotoxin B (SEB) injection. The pathological changes of renal tissue were observed by immunofluorescence staining and PAS staining, and the intestinal mucosa barrier damage indicators lipopolysaccharide(LPS), soluble intercellular adhesion molecule 1(sICAM-1) and D-lactate(D-LAC) were analyzed by ELISA. Biochemical analysis was used to test 24 hour urine protein, serum creatinine and blood urea nitrogen. The mRNA and protein levels of Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and nuclear factor κB (NF-κB) were detected by reverse transcription PCR and Western blot analysis. Results The kidney damage of pseudosterile IgAN mice was more severe than that of IgAN mice, and the expressions of intestinal mucosal barrier damage markers (LPS, sICAM-1 and D-LAC) were significantly increased in pseudosterile IgAN mice. In addition, the expressions of TLR4, MyD88, and NF-κB level were all up-regulated in the intestinal tissues of IgAN pseudosterile mice. Conclusion Intestinal flora disturbance leads to intestinal mucosal barrier damage and induces activation of TLR4 signaling pathway to mediate renal injury in IgAN.
Animals ; Mice ; Mice, Inbred C57BL ; Glomerulonephritis, IGA ; NF-kappa B ; Toll-Like Receptor 4/genetics* ; Lipopolysaccharides ; Myeloid Differentiation Factor 88/genetics* ; Kidney ; Intestinal Mucosa ; Infertility ; Disease Models, Animal