Objective To understand the latest research developments of the formation mechanism of psammoma body in human tumors and related issues. Methods Related domestic and foreign literatures were widely referred, analyzed, and reviewed. Results Psammoma body is unique pathological calcification in some tumors, which is arranged in concentric, laminar circles microscopically. Psammoma body is commonly seen in thyroid papillary carcinoma, meningiomas, ovarian serous papillary carcinoma, and so on. Conclusions Although arranged in concentric, laminar circles microscopically in tumor, the formation process of psammoma body is not entirely the same in different tumors. A comprehensive and objective understanding of psammoma body would be useful in cancer diagnosis and treatment.
Abstract: Objective To evaluate a new type of treatment that reduces calcification of glutaraldehydetreated bovine jugular venous conduit (BJVC). Methods Fresh bovine jugular veins were treated with glutaraldehyde, followed by Triton X-100 and epoxy chloropropane (EC+Tr group). We compared the group’s appearance, histology, shrinkage temperature, tensile strength, and elongation at break with those of a fresh group, and with a group treated with glutaraldehyde only (GA group). We then implanted the EC+Tr and GA group BJVCs subcutaneously into the backs of SD rats and left them for eight weeks (n=8). The morphologic properties and inflammatory response of the test specimens were evaluated by HE staining. The tissue calcium content was determined by atomic absorption spectrophotometer. Results The shrinkage temperature, tensile strength, and elongation at break of the EC+Tr group were significantly higher than those of the fresh group (86.15±0.92 ℃ vs. 69.94±0.92 ℃,t=35.239, P=0.000; 5.31±0.14 mPa vs.3.15±0.95 mPa,t=6.362, P=0.000; 265.11%±27.80% vs. 16521%±25.06%,t=7.550, P=0.000) and of the GA group (86.15±0.92 ℃ vs. 82.73±1.28 ℃, t=6.137, P=0.000; 5.31±0.14 mPa vs. 4.52±0.56 mPa,t=3.871, P=0.002; 265.11%±27.80% vs.237.85%±17.41%,t=2.351,P=0.034). The tissue structure of the subcutaneously implanted EC+Tr veins remained intact;degradation was slight and they contained few inflammatory cells. The calcium content of the EC+Tr group was lower than that of the GA group (51.22±2.69 μg/mg vs. 73.24±3.82 μg/mg, t=11.545，P=0.000). Conclusion Treatment with Triton X-100 and epoxy chloropropane modification with glutaraldehydetreated bovine jugular venous conduit was an effective way to prepare BJVC that avoided calcification.
Abstract: Objective To induce calcification in aortic valvular interstitial cells (VICs) in vitro and observe the shift of cellular phenotype during the process. Methods Porcine aortic VICs were isolated and expanded by collagenase methods. Fluorescent staining was performed to identify the interstitial cells. VICs at 48 passages were used for experiments. The cells were divided into two groups: the experimental group in which cells were cultured in osteogenic media supplemented with βglycerophosphate, vitamin C and dexamethasone, and the control group in which cells were cultured in normal media. After 2 weeks, calcified nodules were quantified. Calcium deposit was stained and measured by Alizarin Red S staining and assay. Real time reverse transcription polymerase chain reaction (RTPCR) was performed to measure expression of alpha smooth muscle actin (α-SMA) and calcification related factors such as osteocalcin, osteopontin and Corebinding factor α1/Runx2 (Cbfα1/Runx2). Results VICs were successfully harvested from porcine aortic valves, identified by positive staining of α-SMA, vimentin and negative staining of Von Willebrand factor (vWF). VICs could calcify after 2 weeks of osteogenic induction with calcified nodules formed. Quantification of calcified nodules and calcification deposit were significantly higher (Plt;0.05) in the experimental group than those in the control group (156.25±17.38 vs. 2.50±1.29, 17.52±2.04 vs. 1.00±0.22). Real Time RT-PCR indicated that expression of α-SMA, as well as calcification related markers like osteocalcin, osteopontin and Cbfα1/Runx2 was much higher in the experimental group than those in the control group (Plt;0.05). Conclusion VICs are activated during the progress of calcification with phenotype shifting to contraction and ossification, which might be the pathological basis of valvular calcification.
Abstract: Objective To summarize the 17-year clinical experience of coronary artery bypass grafting (CABG). Methods From April 1987 to May 2004, total 253 patients with coronary artery disease underwent CABG. The operation were performed in 217 patients under cardiopulmonary bypass (CPB) with moderate hypothermia, because of calcified ascending aorta, partial replacement of ascending aorta wall with apiece of Gore-Tex graft for the proximal anastomosis were done in 10 patients. Off-pump coronary artery bypass grafting (OPCAB) were performed in 30 patients. The operation under CPB with heart beating were performed in 6 patients. Cardiac valvular operations were performed in 15patients. Left atrium myxoma operation was performed in 1 patient. Left ventricular aneurysm plasty operation were performed in 10 patients. Results Total mortality rate was 7.9% (20/253). There was significant difference between the mortality rate of the first 10 years (16.0%,8/50) and that of the last 7 years (5.9%,12/203; χ2=5.62，Plt;0.05). The causes of death were: 3 patients died on table because of low cardiac output after valvular replacement though emergent CABG were conducted, 2 patients died of multiple organ failure after valvular replacement and emergent CABG had undergone, 3 patients died of ventricular fibrillation during closing the sternum, 6 patients died of multiple organ failure caused of severe lung infection, 2 patients died of ventricular fibrillation after operation, and 4 patients died of acute renal failure. One hundred and fiftyseven patients (67.4%, 157/233) were followed up, follow-up time was 6 months to 15 years. Three of them died of unknown causes, most of them have improved life quality. There were 87 patients in New York Heart Association (NYHA) class Ⅰ, 49 patients in NYHA class Ⅱ, 16 patients in NYHA classⅢ, and 2 patients in NYHA classⅣ. Conclusion When the experience of surgery and postoperative care is matured, CABG is a safe method for treatment of coronary artery disease. Partial replacement of ascending aorta wall with GoreTex graft for proximal anastomosis of the graft is acandidate method for the treatment of patients with calcified ascending aorta.
Objective To investigate the management during offpump coronary artery bypass grafting (OPCAB) for patients with ascending aorta atherosclerosis and to find appropriate treatment for minimizing the postoperative cerebrovascular accidents. Methods 236 patients with ascending aorta atherosclerosis were retrospectively analyzed underwent OPCAB in this hospital from Sep.2004 to Dec.2007, 4 of them received “No-touch” technique, 35 of them had the proximal anastomoses with the Enclose assistant, and 197 of them had the proximal anastomoses with the assistant of Heartstring. Hemodynamic indexes were consecutively monitored, blood streams of grafts was monitored by transit time flow measurement (TTFM) to evaluate the quality. Results Distal anastomoses 881，proximal anastomoses 267, the blood stream of 881 grafts was monitored, the mean flow was 16.2±18.7 ml/min, and the pulsatility index (PI) were 4.9±2.3, indicating the good quality of all grafts. The change of hemodynamic indexes including mean artery pressure (MAP, 78.1±10.4 mmHg vs. 80.9±8.1 mmHg）, pulmonary capillary wedge pressure (PCWP, 11.9±3.6 vs. 10.9±2.1 mmHg）, mean pulmonary artery pressure (MPAP, 17.3±4.3 mmHg vs. 15.3±2.8 mmHg）, cardiac output (CO, 4.2±1.2 L/min vs. 4.5±1.6 L/min）, center vinous pressure (CVP, 9.2±2.3cmH2O vs. 9.3±1.8 cmH2O）, heart rate (HR, 71.4±14.0 beats/min vs. 73.4±16.5 beats/min）, there were no statistically difference between before and after proximal anastomoses (Pgt;0.05). Two patients died of low cardio output during operation, 4 patients with transient ischemic attack were improved by 2 months medical therapy, and others had no postoperative complications as perioperative myocardial infarction etc, and the time of stay hospital was 10.5±4.2d. Followup 3-24 months for 185 patients, all living patients had no myocardial or cerebrovascular accidents, the symptoms were alleviated and myocardiac function improved. Conclusion Assessing the degree of the ascending aorta atherosclerosis sufficiently before and during the operation, choosing different operational strategy, and decreasing the manipulation of aorta can decrease the incidence of cerebrovascular accident and get better clinical result.
Objective To establ ish a porcine model of articular full-thickness cartilage defect characterized byremaining cartilage calcified zone on femoral trochlea, so as to provide a considerable and comparative control group forinvestigating repair effects of tissue engineered scaffolds in articular cartilage defects with cartilage calcified zone remaining.Methods The full-thickness cartilage column defects (6 mm in diameter, 0.2-0.5 mm in depth) without damage on calcifiedcartilage zone were made on the femoral trochlea in 9 clean-grade 6-month-old Guizhou mini pigs by standard cartilage-defectmakingsuites. Microscopical observation was performed after modeling. Scanning were made by 3.0T MRI at 4 weeks. Thengeneral observation, stereomicroscope, and histological staining were used to observe cartilage repair. Results All animals wereal ive. No infection of incisions or patellar dislocations occurred; they were able to walk with partial weight-bearing immediatelyafter surgery and could move freely without limp at 1 week. Obvious signal discontinuity in trochlea and subchondral bone couldbe observed in MRI, without deep signal change in defects surrounding. Microscopical observation showed a few repair tissueand petechia at base of the defect with clear boundary. Nearly intact calcified zone of cartilage and zonal collapse of subchondralbone in defects could be observed with stereomicroscope. Under common microscope, no chondrocytes was found in defects,as well as negative staining of fast green-safranin O and alcian blue. Under polarized microscope, the bottom of defects werefilled with a l ittle of fibrous tissue presenting continuous and b l ight-refraction by sirius red staining. Conclusion Theanimal model of articular full-thickness cartilage defect on femoral trochlea by standard cartilage-defect-making suites can beapplied for the research of cartilage disease in early human osteoarthritis and function of calcified cartilage zone in pig.
To review the structure and function of the calcified cartilage zone and its role in the pathogenesis of osteoarthritis (OA). Methods Recent l iterature about calcified zone was reviewed and analyzed in terms of architecture, composition, biomechanics, and biological function. Results Calcified zone has particular structure and material properties, and functions as a semi permeable membrane; chondrocytes in the calcified zone retain some characteristics of growth plate cells, which play a crucial role in cartilage function maintenance and pathogenesis of OA. Therefore, reconstructionof the calcified zone at osteochondral conjunction has become one of the hot research in the fields of interface tissue engineering. Conclusion It is necessary to pay more attention to calcified cartilage zone, which is important for both the treatment of OA and the preparation of tissue engineered osteochondral composite.
To investigate the pathologic characteristics of the articular cartilage and subchondral bone from osteoarthritic knees, and to compare the structural parameters of articular cartilage and subchondral bone between the medial and lateral tibial plateau, so as to determine the role of calcified zone and subchondral bone in the pathogenesis of osteoarthritis (OA). Methods The tibial plateaus were taken from 30 patients undergoing total knee arthroplasty between October 2009 and May 2011. The subjects included 11 males and 19 females with an average age of 65.1 years (range, 55-78years). The mean disease duration was 16.6 years (range, 10-25 years); the mean varus angle of the diseased knee was 9.3° (range, 1-23°). After gross observation, the cartilage-bone samples were taken out from the most weight-bearing regions in the internal areas of the medial and lateral plateaus. The decalcified paraffin-embedded sections were prepared and stained with HE and Safranin O/fast green for cartilage assessment (Mankin score), staging, and bone histomorphometry; the pathologic features of the cartilage and subchondral bone were also observed. The thickness of total articular cartilage (TAC), articular calcified cartilage (ACC), subchondral bone plate (SCP), and the trabecular bone volume (BV/TV) were measured by Image Pro Plus 6.0 imaging system, then the ratio of ACC/TAC was calculated. Results Macroscopic results showed that articular cartilage degeneration was more severe in the medial plateau than in the lateral plateau; Mankin score of the medial plateau (12.4 ± 1.1) was significantly higher than that of the lateral plateau (8.3 ± 1.6) (t=12.173, P=0.000). In the 60 samples, 14 samples were at stage I, characterisd by fissures within the superficial zone, dupl icated tidemark, and thickend subchondral bone; 19 samples were at stage II, characterisd by fissures extending into the deep zone, multiple subchondral bone resorption pits, and obviously thickend subchondral bone; and 27 samples were at stage III, characterisd by full-thickness cartilage defects, endochondral ossification, and eburnated subchondral bone. The bone histomorphometric study showed that TAC thickness of the medial plateau was significantly lower than that of the lateral plateau (P lt; 0.05); the ratios of ACC/TAC, BV/TV, and SCP thickness of the medial plateau were significantly higher than those of the lateral plateau (P lt; 0.05). However, there was no significantdifference in the ACC thickness between the medial and lateral plateaus (P gt; 0.05). Conclusion The calcified zone andsubchondral bone may play an important role in the initiation and progression of OA.