Surgical repair of Achilles tendon rupture. Comparison of surgical with conservative treatment

Achilles tendon suture combined with a triceps surae tendon tip-over graft was performed in 314 patients with acute rupture of the Achilles tendon between 1980 and 1991. Analysis of these cases showed a low tissue complication rate compared with that reported in the literature. An average of 8.1 years after repair, 223 patients were examined using Holz's scale of clinical assessment after Achilles tendon repair. The results were 'good' in 87.4%, 'fair' in 11.2% and 'poor' in 1.4%. The re-rupture rate was very low (0.4%). These results are better than the re-rupture rate after surgical repair with solely end-to-end suture or after conservative immobilizing or conservative functional treatment. In conclusion, these data show that the fascial reinforcement is a valuable complement to the tendon suture.     

A new animal model for molecular biological analysis of the implant-tissue interface: spatial expression of type XII collagen mRNA around a titanium oral implant

The objective of this study was to develop an animal model to investigate the molecular biological healing events at the tissue-implant surface occurring in the alveolar bone. Newly designed mini-titanium implants (2mm in length and 1 mm in diameter) were placed in the maxilla of retired-breeder male Sprague-Dawley rats. The implants were placed in freshly drilled holes in the maxillary bone, or in an area close to the roots of the maxillary first molar. The healing phase in each group was studied histologically at 28 days and at 56 days by means of non-decalcified polymethylmethacrylate-embedded sections and decalcified paraffin-embedded sections. Initial osseointegration was observed at 28 days, with mature osseointegration seen at 56 days. Specimens with implants placed immediately adjacent to the root showed fibrous healing at the implant-tissue surface. As a pilot study, the expression of type XII collagen, a molecular marker specific to the mature periodontal ligament (PDL), was studied by in situ hybridization. There was an absence of type XII expression close to the implant surface, whereas there was a zone of type XII collagen expression closest to the bony wall. Our preliminary results indicated a significant molecular variation in the fibrous-implant interface. This model will be useful in studies of the wound-healing patterns of the extracellular matrix around oral implants specifically relevant to alveolar bone osseointegration and potential formation of PDL.     

Localization of carboxy-terminal type II procollagen peptide (pCOL-II-C) and type II collagen in the repair tissue of full-thickness articular cartilage defect

Apoptosis and aging share common mechanisms in oxidative stress and mitochondrial involvement. Treatment of cultured neuroblastoma cells with a radical initiator induced apoptosis; raise in hydrogen peroxide and release of cytochrome c from mitochondria preceded collapse of mitochondrial potential and cell death. In rat hepatocytes treated with adriamycin incubation with exogenous Coenzyme Q10 counteracted the drug-induced increase of hydrogen peroxide and the fall of the mitochondrial potential, thus demonstrating the quinone antioxidant effect. Complex I activity and its rotenone sensitivity decreased in brain cortex non-synaptic mitochondria from old rats; a 5 kb mitochondrial DNA deletion was found only in the old rats. A similar behavior was found in human platelets from old individuals. The postulated energy decline was confirmed by the inhibitor sensitivities of platelet aggregation and lactate production. The lack of the 5 kb deletion in platelets throws doubts on mitochondrial DNA lesions as the only causes of mitochondrial dysfunction in aging.     

Induction of plasminogen activator inhibitor type 1 and type 1 collagen expression in rat cardiac microvascular endothelial cells by interleukin-1 and its dependence on oxygen-centered free radicals

BACKGROUND: Ischemia with or without reperfusion induces the release of diverse products from monocytes, including cytokines such as interleukin-1 (IL-1). To determine whether these phenomena modulate fibrinolysis and potentially exacerbate impairment of the macrocirculation, microcirculation, or both, we characterized the effects of IL-1 on the expression of fibrinolytic system and matrix proteins in rat cardiac microvascular endothelial cells (CMECs). METHODS AND RESULTS: Confluent CMECs were exposed to IL-1 in serum-free medium for 24 hours, and cell-conditioned medium was assayed for plasminogen activator inhibitor type 1 (PAI-1), the primary physiological inhibitor of plasminogen activators, and for type 1 collagen with Western blotting. IL-1 (2 ng/mL) specifically increased the accumulation of PAI-1 (4.4 +/- 0.6-fold; mean +/- SD; n = 9) without affecting tissue plasminogen activator (t-PA) or urokinase plasminogen activator (u-PA) levels, which remained unchanged. IL-1 increased the accumulation of collagen in conditioned media by 3.5 +/- 0.7-fold (n = 6). Conversely, the accumulation of both PAI-1 and collagen induced by IL-1 was inhibited with an IL-1 receptor antagonist (200 ng/mL; n = 6) and with cycloheximide (10 micrograms/mL; n = 6), implying that protein synthesis was a requirement for the effect. To determine whether the IL-1 effect was mediated by induction of oxygen-centered free radical production, known to be induced by IL-1, we exposed the cells to the hydroxyl radical scavenger tetramethylthiourea (10 mmol/L) and observed abolition of the IL-1-induced increase in the expression of PAI-1 and collagen (n = 6). Conversely, superoxides (generated with 10 mU/mL xanthine oxidase plus 0.6 mmol/L hypoxanthine, and 100 mumol/L hydrogen peroxide) induced the accumulation of PAI-1 and collagen (n = 6). IL-1 (1 microgram/kg body wt) and lipopolysaccharide (50 micrograms/kg body wt) administered in vivo increased PAI-1 protein in rat hearts as detected with Western blotting and PAI-1 immunostaining of rat heart microvessels, indicating the effects delineated in vitro were paralleled by effects in vivo. CONCLUSIONS: These results indicate that IL-1-induced oxygen-centered free radicals stimulate elaboration of PAI-1 and collagen by CMECs. Accordingly, microvascularly mediated inhibition of fibrinolysis may predispose to the persistence of microvascular thrombi, thereby contributing to impaired microcirculatory function, the no-reflow phenomenon, and cardiac dysfunction after ischemia and reperfusion.     

Modulation of collagen gene expression by cytokines: stimulatory effect of transforming growth factor-beta1, with divergent effects of epidermal growth factor and tumor necrosis factor-alpha on collagen type I and collagen type IV

Transforming growth factor-beta1 (TGF-beta1) is well recognized as a potent mediator of both fibrillar (collagen type I) and basement membrane (collagen type IV) production. However, tissue injury is characterized by the concomitant expression of many cytokines and/or growth factors in addition to TGF-beta1, and the ultimate extent of extracellular-matrix (ECM) deposition may reflect the interacting effects of TGF-beta1 and these other cytokines and/or growth factors. We, therefore, sought to determine whether other cytokines and/or growth factors, known to be produced after tissue injury, are capable either alone or in combination with TGF-beta1 of modulating collagen gene expression. Collagen type I and collagen type IV gene expression was assessed in NIH-3T3 cells, a murine fibroblast-like cell line that responds to TGF-beta1, with increases in both collagen type I and collagen type IV production. TGF-beta1 coordinately induced production of collagen type IV messenger ribonucleic acid (mRNA) to a level 3.8-fold above its baseline value (p < 0.001) and collagen type I mRNA to a level 2.6-fold above its baseline value (p < 0.001). Of the other cytokines and/or growth factors tested, only epidermal growth factor (EGF) had significant effects on collagen mRNA expression. We report the novel observation that EGF significantly induced collagen type IV mRNA (3.0-fold; p < 0.001) but did not alter collagen type I mRNA expression. Platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and insulin-like growth factor-1 (IGF-1) did not alter the expression of mRNA for collagen type IV or collagen type I. Addition of TGF-beta1 to cytokine- and/or growth factor-treated cells increased both collagen type IV and collagen type I mRNA levels. However, collagen type IV mRNA levels were similar in cultures given TGF-beta1 alone and cultures given TGF-beta1 with other cytokines and/or growth factors; there were no additive, synergistic, or antagonistic effects after coadministration of TGF-beta1 and other cytokines and/or growth factors. With regard to collagen type I mRNA expression, all cytokines and/or growth factors tested, with the exception of TNF-alpha, had no effect on collagen type I mRNA levels in TGF-beta1-treated cultures. Importantly, TNF-alpha antagonized the stimulatory effect of TGF-beta1 on collagen type I mRNA levels. These observations support a dominant role for TGF-beta1 in stimulating coordinate expression of collagen type I and collagen type IV mRNAs by NIH-3T3 cells; EGF and TNF-alpha are capable of inducing divergent expression of the genes for these two types of collagen.     

Sequential changes in laminin and type IV collagen in the infarct zone--immunohistochemical study in rat myocardial infarction

The T1-weighted volumetric magnetic resonance images of 31 patients with intractable temporal lobe epilepsy, and 13 control subjects matched for age and sex, were subjected to semiautomated threshold analysis. The method used proved to be relatively fast and reliable. An index of temporal lobe interhemispheric asymmetry was extracted by thresholding high-signal (white matter) pixels. Patients had significantly more asymmetrical indices for white matter and hippocampal volumes that did control subjects, and the two indices were significantly correlated, providing evidence for the validity of the white matter index. Differences in both indices were consistent with decreased tissue on the side of the focus. In classification analyses a combination of these two indices correctly predicted the side of focus at a greater rate than did either used alone. Findings provide support for the hypothesis that seizure activity is associated with atrophy in both mesial and lateral temporal lobe structures.     

Composition and organization of the extracellular matrix of vein walls: collagen networks

As there are few recent reports concerning the structure and exact composition of the extracellular matrix from human normal and varicose veins, we carried out comparative immunohistochemical analysis of vessel wall using conventional and confocal laser scanning immunofluorescence techniques. The present report is a rapid review of the structure and function of the 19 known collagen types and our first results on the distribution of collagen types VI, XII and XIV and laminin (glycoprotein from basement membrane) in vein walls. Type VI collagen is concentrated in the sub-endothelium and widely distributed in the media and adventice. For the first time, we demonstrated that both FACIT (fibril-associated) collagens XII and XIV were present in the vein wall, but at different anatomic sites.     

Functional organization of the rat amygdala with respect to avoidance behavior.

Conducted tests with approximately 100 adult female albino Holtzman Sprague-Dawley rats. Bilateral electrolytic lesions in the periamygdaloid piriform cortex of Ss produced marked disruptive effects on the acquisition of active avoidance responses in a 1-way as well as a 2-way test situation, significantly impaired passive avoidance behavior, and inhibited feeding in a novel environment. Lesions in each of the 6 major subdivisions of the amygdala (cortical, medial, central, intercalated, lateral, and basolateral nuclei) consistently produced facilitatory effects on active avoidance behavior in 1-way as well as 2-way situations. Passive avoidance behavior was impaired in Ss with lesions in the central, intercalated, and basolateral nuclei. Damage to the anterior amygdaloid area or the nuclei of the lateral olfactory tract did not reliably affect active or passive avoidance behavior. (34 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Differential expression of type XIV collagen/undulin by human mammary gland intralobular and interlobular fibroblasts

Immunolocalisation of type XIV collagen/undulin in the human mammary gland revealed greater deposition in the interlobular stroma than in the intralobular stroma. The interlobular stroma is located between the breast lobules and their associated intralobular stroma. Fibroblasts isolated from the interlobular stroma synthesised 3- to 5-fold more type XIV collagen/undulin than intralobular fibroblasts, but synthesised type I and type IV collagens in similar amounts. The differential expression of type XIV collagen/undulin was maintained with passage in culture. The results suggest a role for type XIV collagen/undulin in stabilising dense collagen fibrils. The maintenance of two types of structurally distinct stromas may be important during developmental processes in the mammary gland.     

Androgens and the organization of sex differences in active avoidance behavior in the rat.

Performed 3 experiments to clarify the role of androgens in the development of sex differences in the acquisition of active avoidance behavior in a total of 248 male and 231 female Holtzman albino rats. Gonadectomy in adulthood did not affect the performance of either sex regardless of the length of the postoperative recovery interval. Neonatal castration also failed to improve the avoidance performance of males, but prenatal exposure to the antiandrogen cyproterone acetate combined with neonatal gonadectomy produced males whose avoidance acquisition and open field activity scores were indistinguishable from those of control females. Prenatal exposure to endogenous androgens was sufficient to organize the avoidance behavior characteristic of normal males, but there is no compelling evidence that exposure to androgens during the prenatal period was critical to this effect. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Double dissociation and hierarchical organization of strategy switches and reversals in the rat PFC.

Prelimbic–infralimbic cortex (PL-IL) and orbitofrontal cortex (OFC) influence behavioral flexibility in the rat. The authors tested the effects of PL-IL or OFC infusion with the GABA agonist muscimol in the context of 2 flexible responding tasks: strategy switching and reversal. Muscimol infusion into PL-IL impaired retention of strategy switches but not reversals, whereas muscimol infusion into OFC impaired retention of reversals but not switches. However, whereas training in repeated reversals did not remove the requirement of PL-IL for switch retention (E. L. Rich & M. L. Shapiro, 2007), training in repeated switches did remove the requirement of OFC for reversal retention. Thus, activity during strategy switches was sufficient to initiate learning and remove the requirement of OFC in later reversals. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Angiotensin converting enzyme inhibition reduces the expression of transforming growth factor-beta1 and type IV collagen in diabetic vasculopathy

OBJECTIVE: The purpose of this study was to assess the role of transforming growth factor (TGF)-beta1 in the development of diabetes-associated mesenteric vascular hypertrophy and in the antitrophic effect of angiotensin converting enzyme inhibitors. DESIGN AND METHODS: Streptozotocin-induced diabetic and control Sprague-Dawley rats were randomly allocated to treatment with the angiotensin converting enzyme inhibitor ramipril or to no treatment and were killed 1 or 3 weeks after the streptozotocin injection. Blood was collected and mesenteric vessels removed. Mesenteric vascular weight was measured and TGF-beta1 and alpha1 (type IV) collagen messenger (m)RNA levels were analysed by Northern analysis. Immunohistochemical analyses for TGF-beta1 and type IV collagen were also performed. RESULTS: The diabetic rats had increased mesenteric vessel weight at 3 weeks but not at 1 week and a concomitant rise in mesenteric TGF-beta1 and in alpha1 (type IV) collagen mRNA levels. Ramipril treatment attenuated mesenteric vessel hypertrophy and prevented the increase in TGF-beta1 and alpha1 (type IV) collagen mRNA levels after 3 weeks of diabetes. The immunohistochemical analysis revealed that diabetes was associated with increased TGF-beta1 and type IV collagen protein and extracellular matrix accumulation in mesenteric vessels, and this increase was reduced by ramipril treatment. CONCLUSIONS: These results support the concept that TGF-beta is involved in the changes associated with diabetic vascular disease, and suggest a mechanism by which angiotensin converting enzyme inhibitors exert their antitrophic effects.