OBJECTIVETo investigate a new method to construct tissue-engineering bone that will be applicable clinically.

METHODSThe cultured 5th generation rabbit bone marrow stroma osteoblasts (MSO) was dissolved in 3% sodium alginate solution (the final concentration of sodium alginate in the solution being 1%, and MSO, 5x10(6)/L), and then inoculated into prepared true bone ceramic (TBC) and gelatinized the bone by dribbling with calcium gluconate. The standard bone defect models were made in 48 adult New Zealand rabbit's both radius. Among the 48 rabbits, 24 were in Groups A and B, in which the left radius was implanted with gelatinized MSO-TBC (Group A) and right radius implanted with autograft-bone (Group B); and the other 24 were in control group whose left radius was implanted with non-gelatinized MSO-TBC (Group C) and right radius implanted with gelatinized TBC (Group D). Outcomes of the implanted bones were assessed by radiology, pathological histology, osteogenetic quantitative analysis, and biomechanics at 2, 4, 8, 12 weeks postoperatively.

RESULTSIn Groups A and B, a satisfactory bone reparation and bony union was noted within 12 weeks. In Groups C and D, bone reparation was not satisfied compared with Group A in terms of ostogenetic quantity and biomechanics.

CONCLUSIONSGelatinized MSO-TBC is an ideal artificial active bone that overcomes TBC shortcomings of fragileness and smooth surface that is not eligible for seed cell's adhesion. It is promising to put into clinical use extensively.

Animals ; Biomass ; Bone Diseases ; diagnostic imaging ; pathology ; therapy ; Bone Marrow Cells ; cytology ; Bone Substitutes ; Ceramics ; Disease Models, Animal ; Female ; Gelatin ; Male ; Osteoblasts ; cytology ; transplantation ; Osteogenesis ; Rabbits ; Radiography ; Radius ; diagnostic imaging ; injuries ; pathology ; surgery ; Stromal Cells ; cytology ; transplantation ; Tissue Engineering ; methods ; Treatment Outcome

OBJECTIVETo study the relation of the structural remodeling processes and activation of calpain I.

METHODSFifteen dogs were randomly divided into three groups. The dogs in pacing group (n=5) and inhibitor group (n=5) were subjected to 3 weeks of rapid atrial pacing at 600 beats/min, control dogs (n=5) were in sham-operated group. The dogs in inhibitor group were administered intravenous N-Acetyl-Leu-Leu-Met (ALLM), a calpain inhibitor, and in pacing group and sham-operated group were administered intravenous DMSO. The activity of calpain I was measured by hydrolyzing Suc-Leu-Leu-Val-Tyr-7-amino-4-methyl-coumarin. The ultrastructure of atrium was examined by light and electron microscopy. TnT expression was assessed by Western blot. Echocardiography examination was performed in all the three groups.

RESULTSCalpain I activity was significantly increased in pacing group (2.3-fold, P<0.01), and decreased in inhibitor group (1.1-fold, P>0.05), compared to sham-operated group respectively. The percentages of myolysis were (76.7 +/- 5.9)% and (20.8 +/- 8.1)% in pacing group and inhibitor group respectively (P<0.01). TnT expression decreased in the rapid pacing-induced persistent atrial fibrillation, and these effects were inhibited by calpain I inhibitor ALLM. The area and volume of left atrium tended to increase after 3 weeks ALLM treatment in inhibitor group, but the change was not as prominent as in pacing group (P<0.05).

CONCLUSIONSALLM can decrease calpain I activity, and prevent canine atrial cardiomyocyte structural remodeling during atrial fibrillation. This study provided a capacity of atrial cardiomyocyte protection.

Animals ; Atrial Fibrillation ; metabolism ; physiopathology ; Atrial Function, Left ; Calpain ; antagonists & inhibitors ; metabolism ; Cardiac Pacing, Artificial ; Disease Models, Animal ; Dogs ; Heart Atria ; ultrastructure ; Myocardium ; metabolism ; Troponin T ; metabolism

BACKGROUNDAtrial 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.

METHODSFifteen 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.

RESULTSLong-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.

CONCLUSIONSActivation 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.

Animals ; Atrial Fibrillation ; pathology ; Calpain ; antagonists & inhibitors ; Cysteine Proteinase Inhibitors ; pharmacology ; Disease Models, Animal ; Dogs ; Heart Atria ; pathology ; ultrastructure ; Myosins ; analysis ; Troponin T ; analysis

Objective: To observe the short- and long-term clinical outcomes of fraction flow reserve (FFR)-guided percutaneous coronary intervention (PCI) in coronary artery disease (CAD) patients with SYNTAX score≥33 unsuitable for coronary artery bypass grafting (CABG). Methods: A total of 117 CAD patients admitted in our hospital from 2012-01 to 2015-06 were enrolled. Since SYNTAX score≥33, EuroSCORE>6, the patients were unsuitable for CABG and treated in 2 groups: Medication group, n=20 and PCI group, during FFR-guided PCI procedure, patients received ROTA or IVUS according to physician's experience, n=97. All patients were followed-up for at least 12 months. Meanwhile, taking "coronary stent and bypass", "CABG and PCI" as key words, we searched relevant documents in VIP Chinese science and technology journal full-text database, WanFang medical database, ChinaNet and Chinese biomedical literature database from 2012-01-01 to 2015-12-31, patients' outcomes were compared with the above references to explore the clinical benefit. Results: ① PCI group and Medication group had similar SYNTAX score and EuroSCORE, P>0.05. The common pathogenesis was LAD involvement, chronic occlusion was 31.3% (5/16) in patients with partial revascularization.②PCI group had 18.6% (18/97) incidence of major adverse cardiac and cerebral events (MACCE), 2 patients died during follow-up period and 9 received revascularization; Medication group had 60% (12/20) incidence of MACCE, 3 patients died during follow-up period; the difference between 2 groups showed statistical meaning, P<0.05.③There were 22 relevant documents retrieved as comparison; in our research, PCI group had similar incidence of MACCE to the documents, P>0.05; Medication group had increased incidence of MACCE than the documents, P<0.05. Conclusion: FFR-guided PCI could bring clinical benefit in CAD patients with SYNTAX score≥33 unsuitable for CABG.

BACKGROUNDWe hypothesize that increased atrial oxidative stress and inflammation may play an important role in atrial nerve sprouting and heterogeneous sympathetic hyperinnervation during atrial fibrillation (AF). To test the hypothesis, we examined whether the antioxidant and anti-inflammatory treatment with probucol attenuates atrial autonomic remodeling in a canine model of AF produced by prolonged rapid right atrial pacing.

METHODSTwenty-one dogs were divided into a sham-operated group, a control group and a probucol group. Dogs in the control group and probucol group underwent right atrial pacing at 400 beats per minute for 6 weeks, and those in the probucol group received probucol 1 week before rapid atrial pacing until pacing stopped. After 6-week rapid atrial pacing, general properties including left atrial structure and function, atrial hemodynamics and the inducibility and duration of AF were measured in all the groups. Atrial oxidative stress markers and serum C-reactive protein (CRP) concentration were estimated. The degree of nerve sprouting and sympathetic innervation at the right atrial anterior wall (RAAW) and the left atrial anterior wall (LAAW) were quantified by immunohistochemistry, atrial norepinephrine contents were also detected. Atrial beta-nerve growth factor (beta-NGF) mRNA and protein expression at the RAAW and LAAW were assessed by real-time quantitative RT-PCR and Western blotting respectively.

RESULTSAtrial tachypacing induced significant nerve sprouting and heterogeneous sympathetic hyperinnervation, and the magnitude of nerve sprouting and hyperinnervation was higher in the RAAW than in the LAAW. Atrial beta-NGF mRNA and protein levels were significantly increased at the RAAW and LAAW, and the upregulation of beta-NGF expression was greater at the RAAW than at the LAAW in the control group. The beta-NGF protein level was positively correlated with the density of sympathetic nerves in all groups. Probucol decreased the increase of CRP concentration and attenuated atrial oxidative stress caused by atrial tachypacing. In addition, probucol could effectively inhibit atrial beta-NGF upregulation, significantly attenuate atrial nerve sprouting and heterogeneous sympathetic hyperinnervation, and dramatically reduce the inducibility and duration of AF.

CONCLUSIONSThe atrial over-expression of beta-NGF possibly caused by increased oxidative stress and inflammation may be the main mechanism underlying atrial autonomic remodeling during AF. Probucol attenuates atrial autonomic remodeling possibly by its antioxidant and anti-inflammatory actions.

Animals ; Antioxidants ; therapeutic use ; Atrial Fibrillation ; drug therapy ; Blotting, Western ; C-Reactive Protein ; metabolism ; Cardiac Pacing, Artificial ; adverse effects ; Disease Models, Animal ; Dogs ; Electrocardiography ; Female ; Heart Atria ; Immunohistochemistry ; Male ; Nerve Growth Factor ; genetics ; metabolism ; Norepinephrine ; metabolism ; Probucol ; therapeutic use ; Reverse Transcriptase Polymerase Chain Reaction

Adult ; Aged ; Angioplasty, Balloon, Coronary ; adverse effects ; methods ; Emergencies ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; therapy ; Radial Artery

Besides UCP1-dependent thermogenesis pathways, UCP1-independent thermogenesis pathways also could increase heat production in adipose tissue to combat obesity. N-Acyl amino acids (NAAs) have been suggested as novel endogenous uncouplers to induce mitochondria UCP1-independent thermogenesis in adipose tissue. Here, we use mouse skeletal muscle C2C12 cells which lack of UCP1 as UCP1 negative cell models. Comparing with its corresponding common fatty acid—oleate, one of the NAAs—N-Oleoylglycine (NOGly), which is highly expressed in the plasma of HFD mice, is selected to study their effects and mechanisms on mitochondrial thermogenesis. We found that 60 μmol / L oleate could induce mitochondrial oxidative phosphorylation protein levels, as well as increase mitochondria thermogenesis-related genes (COX8b, DIO2, UCP3) expression (P < 0. 05) . However, 60 μmol / L NOGly damaged the production and oxidative phosphorylation of mitochondria, significantly down-regulated expression of thermogenic genes (PGC1a, COX8b, COX2, DIO2, UQCRFS1and UCP3) (P< 0. 01), induced the production of reactive oxygen species (ROS) in the mitochondria, and enhanced the oxidative stress in cells. Our study found that oleate can induce UCP1-independent thermogenesis under 60 μmol / L addition dose, whereas NOGly does not due to the induction of oxidative stress in cells.

Objective: To search for an optimal strategy for the treatment of penile and scrotal gangrene by analyzing the clinical effect of vacuum sealing drainage (VSD) as an adjuvant treatment on this disease. METHODS: We retrospectively analyzed the clinical data about 4 cases of penile and scrotal gangrene treated by VSD as an adjuvant treatment from January 2015 to June 2016. The 4 patients all underwent early extensive and radical debridement of gangrene of the scrotum and penis and received intravenous injection of two broad-spectrum antibiotics, followed by VSD for wound drainage and irrigation. RESULTS: Adequate wound drainage was achieved in all the 4 cases, the gangrene range rapidly localized and testicular necrosis avoided. The wound surface healed satisfactorily after cleansing and suturing. The patients were followed up for 3 months after discharged from the hospital and none experienced recurrence. CONCLUSIONS VSD combined with early adequate debridement can effectively localize the gangrene range, significantly reduce the frequency of changing dressings and shorten the hospitalization time of the patient, and therefore is a very effective adjuvant treatment of penile and scrotal gangrene.
Debridement ; Gangrene ; therapy ; Genital Diseases, Male ; pathology ; prevention & control ; therapy ; Humans ; Male ; Negative-Pressure Wound Therapy ; methods ; Penis ; pathology ; Retrospective Studies ; Scrotum ; pathology ; Testis ; pathology ; Treatment Outcome ; Vacuum

BACKGROUNDPrevious studies revealed that culprit vessels of ST-segment elevation myocardial infarction (STEMI) were often related to mild or moderate stenosis. However, recent studies suggested that severe stenosis was primarily found in culprit lesions. The objective of this study was to analyze the stenosis severity of culprit lesions in STEMI patients and to clarify the paradoxical results.

METHODSA total of 489 consecutive STEMI patients who underwent primary percutaneous coronary intervention were retrospectively studied from January 2012 to December 2014. The patients were divided into three groups based on stenosis severity using quantitative coronary analysis: Group A, 314 cases, stenosis ≥70%; Group B, 127 cases, stenosis 50-70%; and Group C, 48 cases, stenosis ≤50%. The clinical, demographic, and angiographic data of all groups were analyzed.

RESULTSPatients in Group A exhibited a significantly higher prevalence of history of angina pectoris (95.9% vs. 62.5%, P< 0.001), multivessel disease (73.2% vs. 54.2%, P = 0.007), and lower cardiac ejection fraction (53.3 ± 8.6 vs. 56.8 ± 8.4, P= 0.009) than those in Group C. Multivariable analysis revealed that history of angina pectoris (odds ratio [OR]: 13.89, 95% confidence interval [CI]: 6.21-31.11) and multivessel disease (OR: 2.32, 95% CI: 1.25-4.31) were correlated with severe stenosis of the culprit lesion in Group A.

CONCLUSIONSMost culprit lesions in STEMI patients were severe stenosis. These patients exhibited a higher prevalence of angina history and multivessel diseases.

Aged ; Coronary Angiography ; Coronary Thrombosis ; diagnosis ; pathology ; therapy ; Female ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Myocardial Infarction ; complications ; pathology ; therapy ; Percutaneous Coronary Intervention ; Retrospective Studies