Contribution of computational model for assessment of heart tissue local stress caused by suture in LVAD implantation.

STUDY: Implantation of a Left Ventricular Assist Device (LVAD) may produce both excessive local tissue stress and resulting strain-induced tissue rupture that are potential iatrogenic factors influencing the success of the surgical attachment of the LVAD into the myocardium. By using a computational simulation compared to mechanical tests, we sought to investigate the characteristics of stress-induced suture material on porcine myocardium. METHODS: Tensile strength experiments (n = 8) were performed on bulk left myocardium to establish a hyperelastic reduced polynomial constitutive law. Simultaneously, suture strength tests on left myocardium (n = 6) were performed with a standard tensile test setup. Experiments were made on bulk ventricular wall with a single U-suture (polypropylene 3-0) and a PTFE pledget. Then, a Finite Element simulation of a LVAD suture case was performed. Strength versus displacement behavior was compared between mechanical and numerical experiments. Local stress fields in the model were thus analyzed. RESULTS: A strong correlation between the experimental and the numerical responses was observed, validating the relevance of the numerical model. A secure damage limit of 100 kPa on heart tissue was defined from mechanical suture testing and used to describe numerical results. The impact of suture on heart tissue could be accurately determined through new parameters of numerical data (stress diffusion, triaxiality stress). Finally, an ideal spacing between sutures of 2 mm was proposed. CONCLUSION: Our computational model showed a reliable ability to provide and predict various local tissue stresses created by suture penetration into the myocardium. In addition, this model contributed to providing valuable information useful to design less traumatic sutures for LVAD implantation. Therefore, our computational model is a promising tool to predict and optimize LVAD myocardial suture.

Astrocytic alterations induced by HTLV type 1-infected T lymphocytes: a role for Tax-1 and tumor necrosis factor alpha.

In the neurological disease associated with HTLV-1 infected T lymphocytes infiltrated within the CNS are suspected of playing a prominent role in pathogenesis via inflammatory cytokines and the viral protein Tax-1. We hypothesized that T lymphocytes initiate functional perturbation in astrocytes, resulting in neuronal alteration as glial cells have a crucial role in CNS homeostasis. In particular, astrocytes manage the steady state level of glutamate and continuously provide metabolite precursors to neurons and oligodendrocytes. Using a model system of HTLV-1-infected T cells-astrocytes interaction, we show that after contact with T cells, astrocyte acquire a phenotype typical of gliosis: secretion of proinflammatory cytokines (TNF-alpha, IL-1alpha, IL-6) and matrix metalloproteinases (MMP-9, MMP-3). The concomitant increase in the expression of MMPs and of their endogenous inhibitors (TIMP-1 and TIMP-3) suggests a perturbation in MMP/TIMP balance. This may alter the extracellular matrix and, in turn, the cell environment. At a functional level, glutamate transport and catabolism are impaired in astrocytes. A decrease in glutamate uptake is associated with downregulated expression of glutamate transporters GLAST and GLT1. The expression of astrocytic enzyme of glutamate metabolism is modified with up-regulation of glutamine synthetase and down-regulation of glutamate dehydrogenase. The involvement of Tax-1 in these alterations, directly or indirectly via TNF-alpha, is shown. Altered glutamate uptake and catabolism associated with impairment in cell connectivity via MMP/TIMP imbalance could compromise the functional integrity of the CNS in general and that of neurons and oligodendrocytes in particular.

[Sensitivity to bacteriophage ES18 of strains of "S. dublin", "S. enteritidis" and "S. blegdam" and related serotypes (author's transl)]. / Sensibilité au bactériophage ES18 de cultures de Salmonella dublin, S. enteritidis et S. blegdam et de sérotypes apparentés

Sensitivity to bacteriophage ES18 may be used as an additional test for identification of strains of some serotypes of Salmonella. In the D group, the great majority (100/103) of the strains of S. enteritidis (H = g,m:-) and 7/7 strains of S. blegdam (H = G,m,q:-) are resistant. On the contrary, all the studied strains (111) of S. dublin (H = g,p:-) either Vi+ or Vi- are sensitive, as those of S. gallinarum-pullorum (61). Two strains of S. kiel (possibly derivated from S. dublin) are sensitive as that serotype, whereas 20 strains of S. paratyphi A, possessing the same O factors, are resistant.

Photoageing shows histological features of chronic skin inflammation without clinical and molecular abnormalities.

BACKGROUND: Photodamage is characterized by degradation of collagen and accumulation of abnormal elastin in the superficial dermis. Mast cells and macrophages, which are found in higher numbers in photoaged skin, have been implicated in this process. OBJECTIVES: To analyse the phenotype of haematopoietic-derived infiltrating cells in photodamaged skin. METHODS: Chronically sun-exposed (preauricular) and control sun-protected (postauricular) skin was recovered from eight healthy subjects undergoing cosmetic surgery (facial lifting). RESULTS: Histological analysis showed that sun-exposed skin harboured more infiltrating mononuclear cells than sun-protected skin. Cellular infiltrates were found at the periphery of areas of elastolysis around hair follicles in sun-exposed sites, whereas they were found in the interfollicular dermis around blood vessels and around hair follicles in sun-protected samples. Immunohistochemical analysis revealed an increased number of mast cells, macrophages and CD4+ CD45RO+ T cells in sun-exposed dermis as well as a higher number of CD1a+ dendritic cells in sun-exposed epidermis, compared with the sun-protected samples. Thus photoageing displays histological features of chronic skin inflammation. However, no molecular sign of inflammation was observed and we even found a decreased expression of interleukin-1beta mRNA in sun-exposed compared with sun-protected sites. Furthermore, the patients' skin looked normal and did not display any clinical inflammation. CONCLUSIONS: Collectively, these data show that chronic ultraviolet irradiation induces alterations of innate immune cells which are recruited in sun-exposed skin without being activated.

Decreased expression of keratinocyte beta1 integrins in chronically sun-exposed skin in vivo.

BACKGROUND: Chronic exposure to ultraviolet (UV) radiation induces changes in the skin structure which are mostly found in the superficial dermis and at the dermal-epidermal junction. Keratinocytes and fibroblasts contribute both to the synthesis and to the degradation of the molecules important for the integrity of this skin site. While several studies have reported on alterations of dermal components and of the functions of fibroblasts in vivo and in vitro after UV exposure, recent data suggested that keratinocytes could be the main skin cell type involved in the photoageing process. OBJECTIVES: In this study, we analysed the expression of two keratinocyte molecules namely, beta1 integrin (a proliferation marker) and involucrin (a differentiation marker) in sun-exposed and sun-protected facial skin of 16 healthy patients undergoing facial lifting. METHODS: Methods included histology, immunohistochemistry and quantitative reverse transcriptase-polymerase chain reaction analysis. RESULTS: Sun-exposed skin displayed the characteristic morphological and molecular features of dermal photoageing, compared with sun-protected skin, including dermal elastosis, diminished fibrillin and type VII collagen expression. Analysis of the epidermis in sun-exposed vs. sun-protected skin showed no histological differences, but dramatic changes in the expression of beta1 integrin and involucrin. In sun-exposed skin, expression of beta1 integrin protein by epidermal basal cells was reduced, paralleling a downregulation of beta1 integrin mRNA, whereas involucrin protein expression was greatly enhanced in the superficial epidermal cell layers. Interestingly, the ratio between involucrin and beta1 integrin protein expression was consistently increased in sun-exposed skin sites. CONCLUSIONS: Collectively these results demonstrate that epidermal homeostasis is impaired by chronic UV exposure, and define beta1 integrin expression as a molecular marker of the epidermal photoageing process.