An experimental study on transplantation of articular cartilage

Summary Behaviour and fate of the transplanted articular cartilage were studied in 180 adult rabbits, using the scanning electron microscope, histological staining and autoradiographic examination.The junction between the host cartilage and the transplanted cartilage was covered with thin connective tissue layers which extended from the edges 4 weeks after transplantation.After the 24th week of transplantation the cartilage tissue appeared to be degenerating at the periphery of the graft.However, in the middle portion of the graft surviving cartilage cells were observed using ³⁵S autoradiography.

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Résumé Comportement et évolution du cartilage articulaire transplanté ont été étudiés chez 180 lapins adultes par microscopie électronique, colorations histologiques et autoradiographies.Quatre semaines après la transplantation, une fine couche de tissue conjonctif qui s'étend depuis les bords recouvre la jonction entre le cartilage du receveur et le cartilage transplanté.Vingt-quatre semaines après la transplantation, le tissu cartilagineux commence à dégénérer à la périphérie du greffon. Cependant, à la partie centrale de celuici, des cellules cartilagineuses survivantes peuvent être mises en évidence grâce à l'autoradiographie au S³⁵.

     

Silent and clinically overt stroke in older Japanese subjects with white-coat and sustained hypertension

BACKGROUND: Whether white-coat hypertension in older subjects is a benign condition or is associated with an increased risk for stroke remains uncertain. White-coat hypertension as a risk factor for stroke was investigated in relation to silent cerebral infarct in the older Japanese population. METHODS: The prognosis for stroke was studied in 958 older Japanese subjects [147 normotensives (NT), 236 white-coat hypertensives (WCHT), and 575 sustained hypertensives (SHT)] in whom ambulatory blood pressure monitoring was performed in the absence of antihypertensive treatment. Silent cerebral infarct was also assessed using brain magnetic resonance imaging in 585 subjects (61%). RESULTS: Silent cerebral infarcts were found in 36% of NT (n = 70), 42% of WCHT (n = 154), and 53% of SHT (n = 361), and multiple silent cerebral infarcts(presence of > or = 2 silent cerebral infarcts) were found in 24% of NT, 25% of WCHT, and 39% of SHT. During a mean 42-month-follow-up period, clinically overt strokes occurred in 62 subjects [NT 3(2.0%), WCHT 5(2.1%), SHT 54(9.4%)], with 14 fatal cases [NT 1(0.7%), WCHT 0(0%), SHT 13 (2.3%)]. Cox regression analysis showed that age (p = 0.0001) and SHT [RR(95% confidence interval): 4.3 (1.3-14.2), p = 0.018] were independent stroke predictors, whereas WCHT was not significant. Adding presence/absence of silent cerebral infarct at baseline into this model, the RR (95% confidence interval) for silent cerebral infarct was 4.6 (2.0-10.5) (p = 0.003), and that of SHT was 5.5 (1.8-18.9) vs WCHT (p = 0.004) and 3.8 (0.88-16.7) vs NT (p = 0.07). CONCLUSIONS: The incidence of stroke in WCHT is similar to that of NT, and one fourth the risk in SHT in older subjects. Although silent cerebral infarct is a strong predictor of stroke, the difference in stroke prognosis between SHT and WCHT was independent of silent cerebral infarct. It is clinically important to distinguish WCHT from SHT even after assessment of target organ damage in the elderly.     

Preconditioning with hyperbaric oxygen and hyperoxia induces tolerance against spinal cord ischemia in rabbits

BACKGROUND: The aim of this study was to determine if the ischemic tolerance could be induced in the spinal cord by pretreatment with hyperbaric oxygen (HBO) and what components of HBO (hyperoxia, hyperbaricity, and combination of these two) were critical in the induction of tolerance against ischemic injury. METHODS: In experiment 1, 21 rabbits were randomly assigned to one of three groups (n = 7 each): animals in the control group received no HBO before spinal cord ischemia; animals in the HBO-1 and HBO-2 groups received HBO (2.5 atmosphere absolute [ATA], 100% O2) pretreatment 1 h/day for 3 and 5 days before ischemia, respectively. In experiment 2, 48 rabbits were randomly assigned to one of four groups (n = 12 each): the control group received no HBO (21% O2, 1 ATA, 1 h/day, 5 days) before spinal cord ischemia; the HB group received 1-h treatment in 21% O2 at 2.5 ATA each day for 5 days; the HO group received 1-h treatment in 100% oxygen at 1 ATA each day for 5 days; and the HBO group received HBO (2.5 ATA, 100% O2) treatment 1 h/day for 5 days. Twenty-four hours after the last treatment, spinal cord ischemia was induced by an infrarenal aorta clamping for 20 min. Forty-eight hours after reperfusion, hind-limb motor function and histopathology of the spinal cord were examined in a blinded fashion. RESULTS: In experiment 1, the neurologic outcome in the HBO-2 group was better than that of the control group (P = 0.004). The number of normal neurons in the anterior spinal cord in the HBO-2 group was more than that of the control group (P = 0.021). In experiment 2, the neurologic and histopathologic outcomes in the HBO group were better than that of the control group (P < 0.01). The histopathologic outcome in the HO group was better than that in the control group (P < 0.05). CONCLUSIONS: Serial exposure to high oxygen tension induced ischemic tolerance in spinal cord of rabbits. Simple hyperbaricity (2.5 ATA, 21% O2) did not induce ischemic tolerance.     

Laser capture microdissection and microarray expression analysis of lung adenocarcinoma reveals tobacco smoking- and prognosis-related molecular profiles

Recent expression profile analyses revealed that lung adenocarcinomas can be divided into several subgroups with diverse pathological features. Because cellular heterogeneity of tumors can confound these analyses, we used laser capture microdissection and microarray expression analysis to characterize the molecular profiles of lung adenocarcinomas. We found 45 genes delineating smokers and nonsmokers that were located at chromosomal loci frequently altered in non-small cell lung cancers, and 27 genes, which were differentially expressed between survivors and nonsurvivors 5 years after surgery. These results are consistent with the hypothesis that the abnormal expression of genes involved in maintaining the mitotic spindle checkpoint and genomic stability, e.g., hBUB3, hZW10, and APC2, contribute to the molecular pathogenesis and tumor progression of tobacco smoke-induced adenocarcinoma of the lung.     

Aberrant methylation and histone deacetylation of cyclooxygenase 2 in gastric cancer.

Cyclooxygenase 2 plays a critical role in the development of gastrointestinal cancers in both human and animal models. About 80% of the gastric cancer showed a high level of expression of cyclooxygenase 2, but a subset of cases do not express without unknown reason. Aberrant methylation of CpG island of COX-2 was examined by using a series of gastric cancer cell lines and primary gastric cancers. Two out of 8 cell lines (25%) and 11 out of 93 (12%) primary cancers showed aberrant methylation of the 5' region of COX-2. Methylation of COX-2 was closely associated with loss of expression and treatment of methylation inhibitor, 5-deoxy-2'-azacytidine restored the expression of COX-2. A combined treatment of 5-deoxy-2'-azacytidine and a histone deacetylese inhibitor, trichostatin A, restored re-expression of the gene synergistically and chromatin immunoprecipitation analysis revealed that histone of methylated COX-2 promoter is deacetylated, indicating the role of cytosine methylation and histone deacetylation in the silencing of the gene. These results indicate that a subset of gastric cancer with COX-2 methylation evolves through the pathway that is independent of COX-2 expression and that COX-2 inhibitor may not be useful to induce apoptosis in these cases.