Academic literature on the topic 'Tissue surface density'

Risk studies have identified cross-contamination during beef fabrication as a knowledge gap, particularly as to how and at what levels Escherichia coli O157:H7 transfers among meat and cutting board (or equipment) surfaces. The objectives of this study were to determine and model transfer coefficients (TCs) between E. coli O157:H7 on beef tissue and high-density polyethylene (HDPE) cutting board surfaces. Four different transfer scenarios were evaluated: (i) HDPE board to agar, (ii) beef tissue to agar, (iii) HDPE board to beef tissue to agar, and (iv) beef tissue to HDPE board to agar. Also, the following factors were studied for each transfer scenario: two HDPE surface roughness levels (rough and smooth), two beef tissues (fat and fascia), and two conditions of the initial beef tissue inoculation with E. coli O157:H7 (wet and dry surfaces), for a total of 24 treatments. The TCs were calculated as a function of the plated inoculum and of the cells recovered from the first contact. When the treatments were compared, all of the variables evaluated interacted significantly in determining the TC. An overall TC-per-treatment model did not adequately represent the reduction of the cells on the original surface after each contact and the interaction of the factors studied. However, an exponential model was developed that explained the experimental data for all treatments and represented the recontamination of the surfaces with E. coli O157:H7. The parameters for the exponential model for cross-contamination with E. coli O157:H7 between beef tissue and HDPE surfaces were determined, allowing for the use of the resulting model in quantitative microbial risk assessment.

Eukaryotic cells in living tissues form dynamic patterns with spatially varying orientational order that affects important physiological processes such as apoptosis and cell migration. The challenge is how to impart a predesigned map of orientational order onto a growing tissue. Here, we demonstrate an approach to produce cell monolayers of human dermal fibroblasts with predesigned orientational patterns and topological defects using a photoaligned liquid crystal elastomer (LCE) that swells anisotropically in an aqueous medium. The patterns inscribed into the LCE are replicated by the tissue monolayer and cause a strong spatial variation of cells phenotype, their surface density, and number density fluctuations. Unbinding dynamics of defect pairs intrinsic to active matter is suppressed by anisotropic surface anchoring allowing the estimation of the elastic characteristics of the tissues. The demonstrated patterned LCE approach has potential to control the collective behavior of cells in living tissues, cell differentiation, and tissue morphogenesis.

Synthetic sports surfaces are increasingly subject to standardization of athlete-surface and ball-surface interactions (playability parameters). Such standardizations have led to an increase in the level of the engineering and predictability of these surfaces, and as such may be beneficial also for natural turf. In warm and temperate climates, many natural turf sports surfaces are established with warm-season (C4) turfgrass species due to their suitability to the environment in such areas. This study was aimed at evaluating the Féderation Internationale de Football Association (FIFA)-standard playing characteristics of different sports turf surfaces obtained from three commonly used C4 turfgrass species: 1) ‘Tifway 419’ hybrid bermudagrass (Cynodon dactylon var. dactylon × C. transvaalensis), 2) ‘Zeon’ manilagrass (Zoysia matrella), and 3) ‘Salam’ seashore paspalum (Paspalum vaginatum) for factors concerning leaf tissue (silica, lignin, water content) and canopy structure (shoot density, leaf architecture, stolon density, etc.). Results showed that surfaces of different C4 turfgrass species generate different playability parameters, with seashore paspalum being a harder faster surface, manilagrass being a softer slower surface, and hybrid bermudagrass showing intermediate characteristics. These playing quality results were associated with certain specific canopy biometrical/morphological parameters such as shoot density, horizontal stem density (HSD), leaf section, and, to a lesser extent, to certain plant tissue compounds (lignin, silica).

Our aim was to use stereology to quantify the volume fraction of osteocyte lacunes, volume fraction of large blood vessels, numerical density of osteocyte lacunes, volume of osteocyte lacunae and bone surface in series of micro-CT images representing samples of spongy and compact bone of human tibia. The spongy bone had a smaller volume fraction of osteocyte lacunes, a greater numerical density of bone lacunes, a smaller volume of the lacunes within the same bone volume and a greater bone surface density when compared to the compact bone. Stereology provided us with data on hierarchical organization of bone structural heterogeneity with reasonable time costs.

Surface properties, including topography and chemistry, are of prime importance in establishing the response of tissues to biomaterials. Microfabrication techniques have enabled the production of precisely controlled surface topographies that have been used as substrata for cells in culture and on devices implanted in vivo. This article reviews aspects of cell behavior involved in tissue response to implants with an emphasis on the effects of topography. Microfabricated grooved surfaces produce orientation and directed locomotion of epithelial cells in vitro and can inhibit epithelial downgrowth on implants. The effects depend on the groove dimensions and they are modified by epithelial cell–cell interactions. Fibroblasts similarly exhibit contact guidance on grooved surfaces, but fibroblast shape in vitro differs markedly from that found in vivo. Surface topography is important in establishing tissue organization adjacent to implants, with smooth surfaces generally being associated with fibrous tissue encapsulation. Grooved topographies appear to have promise in reducing encapsulation in the short term, but additional studies employing three-dimensional reconstruction and diverse topographies are needed to understand better the process of connective-tissue organization adjacent to implants. Microfabricated surfaces can increase the frequency of mineralized bone-like tissue nodules adjacent to subcutaneously implanted surfaces in rats. Orientation of these nodules with grooves occurs both in culture and on implants. Detailed comparisons of cell behavior on micromachined substrata in vitro and in vivo are difficult because of the number and complexity of factors, such as population density and micromotion, that can differ between these conditions.

Childhood obesity is a complex health problem, and not many studies have been done on adipose tissue remodeling in early childhood. The aim of this study was to examine extracellular matrix remodeling in the adipose tissue of healthy male children depending on their weight status. Subcutaneous and visceral adipose tissue was obtained from 45 otherwise healthy male children who underwent elective surgery for hernia repairs or orchidopexy. The children were divided into overweight/obese (n = 17) or normal weight groups (n = 28) depending on their body mass index (BMI) z-score. Serum was obtained for glucose, testosterone, triglyceride, total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL) measurements. Sections of adipose tissue were stained with hematoxylin and eosin to determine the adipocytes’ surface area, and Masson’s trichrome stain was used to detect the adipocytes’ collagen content. Immunohistochemistry for CD163+ cells was also performed. The results showed that male children in the overweight group had higher serum triglyceride levels, greater adipocyte surface area and collagen content in their subcutaneous adipose tissue, more crown-like structures in fat tissues, and more CD163+ cells in their visceral adipose tissue than males in the normal weight group. In conclusion, in male children, obesity can lead to the hypertrophy of adipocytes, increased collagen deposition in subcutaneous adipose tissues, and changes in the polarization and accumulation of macrophages.

Body composition, mitochondrial volume density, and mitochondrial membrane surface area were measured in six species of mammals representing a 100-fold weight range (18-2,067 g). The mammals examined included three eutherian species, two marsupial, and one monotreme species. The tissues examined were liver, kidney, brain, lung, heart, and skeletal muscle (gastrocnemius). Allometric equations were derived for tissue weight, and the allometric exponents ranged from 0.69 (brain) to 1.01 (skeletal muscle). Allometric relationships for mitochondrial membrane surface area were also determined both per milliliter tissue and per total tissue. Small mammals had a higher mitochondrial membrane surface area per milliliter tissue than large mammals in all tissues examined. These differences were significant in liver, kidney, brain, and heart. Total mitochondrial membrane surface area per tissue had allometric exponents ranging from 0.55 (kidney) to 0.78 (skeletal muscle). When total mitochondrial membrane surface area was summated for the major internal organs examined (liver, kidney, heart, and brain), the allometric equation was mitochondrial membrane surface area (m2) = 3.04 body wt0.59 (g). This was similar to the exponent of standard metabolic rate against body weight in the species examined (i.e., 0.62). The inclusion of skeletal muscle and lung into the summated mitochondrial membrane surface area increased the exponent to 0.76. This is compared with the relationship between maximal O2 consumption and body size in mammals.

Abstract Tissue factor, which is expressed in vascular lesions, increases thrombin production, blood coagulation, and smooth muscle cell proliferation. We demonstrate that oxidized low-density lipoprotein (LDL) induces surface tissue factor pathway activity (ie, activity of the tissue factor:factor VIIa complex) on human and rat smooth muscle cells. Tissue factor messenger RNA (mRNA) was induced by oxidized LDL or native LDL; however, native LDL did not markedly increase tissue factor activity. We hypothesized that oxidized LDL mediated the activation of the tissue factor pathway via an oxidant-dependent mechanism, because antioxidants blocked the enhanced tissue factor pathway activity by oxidized LDL, but not the increased mRNA or protein induction. We separated total lipid extracts of oxidized LDL using high-performance liquid chromatography (HPLC). This yielded 2 major peaks that induced tissue factor activity. Of the known oxysterols contained in the first peak, 7α- or 7β-hydroxy or 7-ketocholesterol had no effect on tissue factor pathway activity; however, 7β-hydroperoxycholesterol increased tissue factor pathway activity without induction of tissue factor mRNA. Tertiary butyl hydroperoxide also increased tissue factor pathway activity, suggesting that lipid hydroperoxides, some of which exist in atherosclerotic lesions, activate the tissue factor pathway. We speculate that thrombin production could be elevated via a mechanism involving peroxidation of cellular lipids, contributing to arterial thrombosis after plaque rupture. Our data suggest a mechanism by which antioxidants may offer a clinical benefit in acute coronary syndrome and restenosis.

Tissue factor, which is expressed in vascular lesions, increases thrombin production, blood coagulation, and smooth muscle cell proliferation. We demonstrate that oxidized low-density lipoprotein (LDL) induces surface tissue factor pathway activity (ie, activity of the tissue factor:factor VIIa complex) on human and rat smooth muscle cells. Tissue factor messenger RNA (mRNA) was induced by oxidized LDL or native LDL; however, native LDL did not markedly increase tissue factor activity. We hypothesized that oxidized LDL mediated the activation of the tissue factor pathway via an oxidant-dependent mechanism, because antioxidants blocked the enhanced tissue factor pathway activity by oxidized LDL, but not the increased mRNA or protein induction. We separated total lipid extracts of oxidized LDL using high-performance liquid chromatography (HPLC). This yielded 2 major peaks that induced tissue factor activity. Of the known oxysterols contained in the first peak, 7α- or 7β-hydroxy or 7-ketocholesterol had no effect on tissue factor pathway activity; however, 7β-hydroperoxycholesterol increased tissue factor pathway activity without induction of tissue factor mRNA. Tertiary butyl hydroperoxide also increased tissue factor pathway activity, suggesting that lipid hydroperoxides, some of which exist in atherosclerotic lesions, activate the tissue factor pathway. We speculate that thrombin production could be elevated via a mechanism involving peroxidation of cellular lipids, contributing to arterial thrombosis after plaque rupture. Our data suggest a mechanism by which antioxidants may offer a clinical benefit in acute coronary syndrome and restenosis.

В даній магістерській дисертаційній роботі проведено аналітичне дослідження ультразвукового засобу технологічного контролю поверхневої густини тканин. Проведений аналіз показав, що для забезпечення випуску якісних тканин необхідно проведення оперативного технологічного контролю їх поверхневої густини. В теперішній час застосовуються переважно руйнівні контактні методи контролю поверхневої густини тканин, які засновані на вирізанні та зважуванні зразків тканин, тоді як безконтактні не використовуються хоча мають ряд суттєвих переваг у порівнянні з контактними. Як показав проведений у першому розділі дисертації аналіз, для оперативного технологічного контролю поверхневої густини тканин, доцільним є застосування ультразвукових методів контролю. У другому розділі дисертації розглянуті особливості розповсюдження ультразвукових хвиль в тканинах, які пов’язані з розмірами пор та іншими структурними показниками тканин, які впливають на проходження ультразвукових хвиль скрізь тканину та відбиття від неї. Проведено дослідження проходження ультразвукової хвилі крізь контрольовані тканини з різними розмірами пор і відбиття від них та отримані аналітичні залежності для розрахунку та аналізу взаємодії ультразвукових хвиль з нитками тканин з різними акустичними опорами. Отримано аналітичні залежності, які пов’язують амплітудні співвідношення ультразвукових хвиль як із зміною самих діаметрів ниток основи та утоку, так і безпосередньо з поверхневою густиною тканини. Доведено, що згасанням ультразвукових коливань для більшості тканин можна знехтувати, а вибором співвідношення об’ємної густини тканини та довжиною ультразвукової хвилі в тканині можна знизити вплив згасання на амплітудні співвідношення ультразвукових хвиль. Показано, що при збільшенні тривалості ультразвукового імпульсного сигналу зменшуються амплітудна та фазова похибки в порівнянні з безперервним сигналом. Тому необхідно вибирати тривалість ультразвукового імпульсного сигналу такою, щоб не відбувалось перевідбиттів ультразвукових хвиль від поверхні тканини та поверхонь п’єзоперетворювачів. В третьому проведена розробка ультразвукового засобу технологічного контролю поверхневої густини тканин та його експериментальні дослідження.
In this master's dissertation an analytical study of the ultrasonic means of technological control of tissue surface density. The analysis showed that to ensure the release of quality fabrics it is necessary to carry out operational technological control of their surface density. Currently, mainly destructive contact methods of tissue surface density control are used, which are based on cutting and weighing tissue samples, while non-contact ones are not used, although they have a number of significant advantages over contact ones. As shown by the analysis conducted in the first section of the dissertation, for the operational technological control of tissue surface density, it is advisable to use ultrasonic control methods. The second section of the dissertation discusses the peculiarities of the propagation of ultrasonic waves in tissues, which are related to the pore size and other structural parameters of tissues that affect the passage of ultrasonic waves through the tissue and reflection from it. A study of the passage of ultrasonic waves through controlled tissues with different pore sizes and reflections from them and obtained analytical dependences for the calculation and analysis of the interaction of ultrasonic waves with tissue threads with different acoustic resistances. Analytical dependences are obtained, which relate the amplitude ratios of ultrasonic waves both with the change of the diameters of the warp and weft threads, and directly with the surface density of the fabric. It has been shown that the attenuation of ultrasonic vibrations can be neglected for most tissues, and the choice of the ratio of the bulk density of the tissue and the length of the ultrasonic wave in the fabric can reduce the effect of attenuation on the amplitude ratio of ultrasonic waves. It is shown that as the duration of the ultrasonic pulse signal increases, the amplitude and phase errors decrease in comparison with the continuous signal. Therefore, it is necessary to choose the duration of the ultrasonic pulse signal so that there are no reflections of ultrasonic waves from the surface of the fabric and the surfaces of the piezoelectric transducers. In the third development of ultrasonic means of technological control of surface density of fabrics and its experimental researches is carried out.

Ongoing developments in the field of medical imaging modalities have pushed the frontiers of modern medicine and biomedical engineering, prompting the need for new applications to improve diagnosis, treatment and prevention of diseases. Biomedical data visualization and modeling rely predominately on manual processing and utilization of voxel and facet based homogeneous models. Biological structures are naturally heterogeneous and in order to accurately design and biomimic biological structures, properties such as chemical composition, size and shape of biological constituents need to be incorporated in the computational biological models. Our proposed approach involves generating a density point cloud based on the intensity variations in a medical image slice, to capture tissue density variations through point cloud densities. The density point cloud is ordered and approximated with a set of cross-sectional least-squares B-Spline curves, based on which a skinned B-Spline surface is generated. The aim of this method is to capture and accurately represent density variations within the medical image data with a lofted surface function. The fitted B-Spline surface is sampled at uniformly distributed parameters, and our preliminary results indicate that the bio-CAD model preserves the density variations of the original image based point cloud. The resultant surface can thus be visualized by mapping the density in the parametric domain into color in pixel domain. The B-Spline function produced from each image slice can be used for medical visualization and heterogeneous tissue modeling. The process can be repeated for each slice in the medical dataset to produce heterogeneous B-Spline volumes. The emphasis of this research is placed on accuracy and shape fidelity needed for medical operations.

Cette thèse vise à caractériser des polymères imprimés tridimensionnellement (3D) sur des matériaux textiles PET via une méthode de dépôt de polymère fondu connu sur le nom de Fused Deposition Modeling (FDM) utilisant à la fois des polymères non conducteurs et conducteurs. Les propriétés mécaniques et électriques ont été optimisées par le biais de modèles statistiques et améliorées grâce à des pré et post-traitements ou le développement de mélanges de polymères. Ce travail de recherche apporte de nouveaux résultats sur le développement de textiles techniques par l'impression 3D de polymères fonctionnels. Le procédé FDM a été considéré dans cette thèse pour son fort potentiel en termes de flexibilité, d'efficacité des ressources, de production sur mesure et d'écologie par rapport aux procédés de finition textile conventionnels existants, par exemple, les impressions numériques et sérigraphiques. Le principal enjeu de cette technologie est de garantir des propriétés électriques et mécaniques optimisées (flexion, flexibilité, traction, abrasion, etc.) du polymère imprimé en 3D sur les textiles afin d’être utilisé dans l'industrie textile. Par conséquent, le développement de nouveaux polymères imprimés en 3D sur des matériaux PET avec des propriétés améliorées est nécessaire.Dans un premier temps, de l’'acide polylactique (PLA) non conducteur et du PLA contenant 2.5% de noir de carbone ont été imprimé en 3D sur des tissus en PET. Les polymères conducteurs ont été fabriqués par le procédé d'extrusion à voie fondu. Les propriétés mécaniques, notamment d’adhésion, de traction, de déformation, de résistance au lavage et d’abrasion ont été déterminées. Ensuite, la relation entre les caractéristiques structurelles et thermiques du textile et la température du plateau de l’imprimante 3D et ces propriétés par le biais de modèles statistiques a été déterminée. De plus, différents pré-traitements sur textiles incluant le plasma atmosphérique, le greffage d'acide acrylique et l'application d'adhésifs ont été suggérés pour améliorer les propriétés d’adhésion du PLA imprimé en 3D sur les tissus en PET. Enfin, de nouveaux mélanges biophasiques utilisant du polyéthylène basse densité (LDPE) et un élastomère à base de propylène (PBE) contenant de nanotubes de carbone à parois multiples (CNT) et de noir de carbone à haute structure (KB) ont été développés et fabriqués pour améliorer la flexibilité, le la contrainte et la déformation à la rupture et les propriétés électriques du PLA imprimé en 3D sur le tissu PET. La morphologie, les propriétés thermiques et rhéologiques de chaque mélange sont également determinées afin de comprendre le comportement du matériau et l’amélioration de ses propriétés mécaniques et électriques.Les résultats ont démontré que la structure textile définie par sa densité en trame, son motif et la composition des fils de trame et de chaîne a un impact significatif sur l'adhésion, la déformation, l'abrasion et les propriétés de traction du PLA imprimé en 3D sur les tissus en PET. Des compromis doivent être trouvés car les textiles poreux, rugueux possédant de faible conductivité thermique ont montré de meilleures propriétés de lavage, d’adhésion et de traction et une moins bonne résistance à la déformation et à l'abrasion. Des modèles statistiques entre les propriétés textiles et le PLA imprimé en 3D sur des matériaux PET et les propriétés ont été développés avec succès et utilisés pour les optimiser. L'application d'adhésifs sur des tissus en PET traité avec de l'acide acrylique greffé a considérablement amélioré la résistance d'adhésion. Par ailleurs, les mélanges LDPE / PBE de phases co-continues et contenant du CNT et de KB localisés à l'interface ou dans la phase LDPE a révélé améliorer considérablement la déformation et les propriétés de traction et électriques des imprimés 3D sur textiles
This thesis aims at characterizing tridimensional (3D) printed polymers onto PET textile materials via fused deposition modeling (FDM) that uses both non-conductive and conductive polymers, optimizing their mechanical and electrical properties through statistical modeling and enhancing them with pre and post-treatments and the development of polymer blends. This research work supports the development of technical textiles through 3D printing that may have functionalities. The FDM process was considered in this thesis for its strong potential in terms of flexibility, resource-efficiency, cost-effectiveness tailored production and ecology compared to the existing conventional textile finishing processes, for instance, the digital and screen printings. The main challenge of this technology is to warranty optimized electrical and mechanical (bending, flexibility, tensile, abrasion, etc.) properties of the 3D printed polymer onto textiles for the materials to be used in textile industry. Therefore, the development of novel 3D printed polymers onto PET materials with improved properties is necessary. First of all, 3D printed non-conductive Polylactic Acid (PLA) and PLA filled with 2.5wt% Carbon-Black filled onto PET fabrics were purchased and manufactured through melt extrusion process respectively, to characterize their mechanical properties including adhesion, tensile, deformation, wash ability and abrasion. Then, the relationship between the textile structural characteristics and thermal properties and build platform temperature and these properties through statistical modeling was determined. Subsequently, different textile pre-treatments that include atmospheric plasma, grafting of acrylic acid and application of adhesives were suggested to enhance the adhesion properties of the 3D printed PLA onto PET fabrics. Lastly, novel biophasic blends using Low-Density Polyethylene (LDPE) / Propylene- Based Elastomer (PBE) filled with multi-walled carbon nanotubes (CNT) and high-structured carbon black (KB) were developed and manufactured to improve the flexibility, the stress and strain at rupture and the electrical properties of the 3D printed PLA onto PET fabric. The morphology, thermal and rheological properties of each blends are also accessed in order to understand the material behavior and enhanced mechanical and electrical properties.The findings demonstrated that the textile structure defined by its weft density and pattern and weft and warp yarn compositions has a significant impact on the adhesion, deformation, abrasion, tensile properties of 3D printed PLA onto PET fabrics. Compromises have to be found as porous and rough textiles with low thermal properties showed better wash-ability, adhesion and tensile properties and worse deformation and abrasion resistance. Statistical models between the textile properties and the 3D printed PLA onto PET materials and the properties were successfully developed and used to optimize them. The application of adhesives on treated PET with grafted acrylic acid did significantly improve the adhesion resistance and LDPE/PBE blends filled with CNT and KB that have co-continuous LDPE and PBE phases as well as CNT and KB selectively located at the interface and in the LDPE phase revealed enhanced deformation and tensile and electrical properties

Bones are multifunctional passive organs of movement that supports soft tissue and directly attached muscles. They also protect internal organs and are a reserve of calcium, phosphorus and magnesium. Each bone is covered with periosteum, and the adjacent bone surfaces are covered by articular cartilage. Histologically, the bone is an organ composed of many different tissues. The main component is bone tissue (cortical and spongy) composed of a set of bone cells and intercellular substance (mineral and organic), it also contains fat, hematopoietic (bone marrow) and cartilaginous tissue. Bones are a tissue that even in adult life retains the ability to change shape and structure depending on changes in their mechanical and hormonal environment, as well as self-renewal and repair capabilities. This process is called bone turnover. The basic processes of bone turnover are: • bone modeling (incessantly changes in bone shape during individual growth) following resorption and tissue formation at various locations (e.g. bone marrow formation) to increase mass and skeletal morphology. This process occurs in the bones of growing individuals and stops after reaching puberty • bone remodeling (processes involve in maintaining bone tissue by resorbing and replacing old bone tissue with new tissue in the same place, e.g. repairing micro fractures). It is a process involving the removal and internal remodeling of existing bone and is responsible for maintaining tissue mass and architecture of mature bones. Bone turnover is regulated by two types of transformation: • osteoclastogenesis, i.e. formation of cells responsible for bone resorption • osteoblastogenesis, i.e. formation of cells responsible for bone formation (bone matrix synthesis and mineralization) Bone maturity can be defined as the completion of basic structural development and mineralization leading to maximum mass and optimal mechanical strength. The highest rate of increase in pig bone mass is observed in the first twelve weeks after birth. This period of growth is considered crucial for optimizing the growth of the skeleton of pigs, because the degree of bone mineralization in later life stages (adulthood) depends largely on the amount of bone minerals accumulated in the early stages of their growth. The development of the technique allows to determine the condition of the skeletal system (or individual bones) in living animals by methods used in human medicine, or after their slaughter. For in vivo determination of bone properties, Abstract 10 double energy X-ray absorptiometry or computed tomography scanning techniques are used. Both methods allow the quantification of mineral content and bone mineral density. The most important property from a practical point of view is the bone’s bending strength, which is directly determined by the maximum bending force. The most important factors affecting bone strength are: • age (growth period), • gender and the associated hormonal balance, • genotype and modification of genes responsible for bone growth • chemical composition of the body (protein and fat content, and the proportion between these components), • physical activity and related bone load, • nutritional factors: – protein intake influencing synthesis of organic matrix of bone, – content of minerals in the feed (CA, P, Zn, Ca/P, Mg, Mn, Na, Cl, K, Cu ratio) influencing synthesis of the inorganic matrix of bone, – mineral/protein ratio in the diet (Ca/protein, P/protein, Zn/protein) – feed energy concentration, – energy source (content of saturated fatty acids - SFA, content of polyun saturated fatty acids - PUFA, in particular ALA, EPA, DPA, DHA), – feed additives, in particular: enzymes (e.g. phytase releasing of minerals bounded in phytin complexes), probiotics and prebiotics (e.g. inulin improving the function of the digestive tract by increasing absorption of nutrients), – vitamin content that regulate metabolism and biochemical changes occurring in bone tissue (e.g. vitamin D3, B6, C and K). This study was based on the results of research experiments from available literature, and studies on growing pigs carried out at the Kielanowski Institute of Animal Physiology and Nutrition, Polish Academy of Sciences. The tests were performed in total on 300 pigs of Duroc, Pietrain, Puławska breeds, line 990 and hybrids (Great White × Duroc, Great White × Landrace), PIC pigs, slaughtered at different body weight during the growth period from 15 to 130 kg. Bones for biomechanical tests were collected after slaughter from each pig. Their length, mass and volume were determined. Based on these measurements, the specific weight (density, g/cm3) was calculated. Then each bone was cut in the middle of the shaft and the outer and inner diameters were measured both horizontally and vertically. Based on these measurements, the following indicators were calculated: • cortical thickness, • cortical surface, • cortical index. Abstract 11 Bone strength was tested by a three-point bending test. The obtained data enabled the determination of: • bending force (the magnitude of the maximum force at which disintegration and disruption of bone structure occurs), • strength (the amount of maximum force needed to break/crack of bone), • stiffness (quotient of the force acting on the bone and the amount of displacement occurring under the influence of this force). Investigation of changes in physical and biomechanical features of bones during growth was performed on pigs of the synthetic 990 line growing from 15 to 130 kg body weight. The animals were slaughtered successively at a body weight of 15, 30, 40, 50, 70, 90, 110 and 130 kg. After slaughter, the following bones were separated from the right half-carcass: humerus, 3rd and 4th metatarsal bone, femur, tibia and fibula as well as 3rd and 4th metatarsal bone. The features of bones were determined using methods described in the methodology. Describing bone growth with the Gompertz equation, it was found that the earliest slowdown of bone growth curve was observed for metacarpal and metatarsal bones. This means that these bones matured the most quickly. The established data also indicate that the rib is the slowest maturing bone. The femur, humerus, tibia and fibula were between the values of these features for the metatarsal, metacarpal and rib bones. The rate of increase in bone mass and length differed significantly between the examined bones, but in all cases it was lower (coefficient b <1) than the growth rate of the whole body of the animal. The fastest growth rate was estimated for the rib mass (coefficient b = 0.93). Among the long bones, the humerus (coefficient b = 0.81) was characterized by the fastest rate of weight gain, however femur the smallest (coefficient b = 0.71). The lowest rate of bone mass increase was observed in the foot bones, with the metacarpal bones having a slightly higher value of coefficient b than the metatarsal bones (0.67 vs 0.62). The third bone had a lower growth rate than the fourth bone, regardless of whether they were metatarsal or metacarpal. The value of the bending force increased as the animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. The rate of change in the value of this indicator increased at a similar rate as the body weight changes of the animals in the case of the fibula and the fourth metacarpal bone (b value = 0.98), and more slowly in the case of the metatarsal bone, the third metacarpal bone, and the tibia bone (values of the b ratio 0.81–0.85), and the slowest femur, humerus and rib (value of b = 0.60–0.66). Bone stiffness increased as animals grew. Regardless of the growth point tested, the highest values were observed for the humerus, tibia and femur, smaller for the metatarsal and metacarpal bone, and the lowest for the fibula and rib. Abstract 12 The rate of change in the value of this indicator changed at a faster rate than the increase in weight of pigs in the case of metacarpal and metatarsal bones (coefficient b = 1.01–1.22), slightly slower in the case of fibula (coefficient b = 0.92), definitely slower in the case of the tibia (b = 0.73), ribs (b = 0.66), femur (b = 0.59) and humerus (b = 0.50). Bone strength increased as animals grew. Regardless of the growth point tested, bone strength was as follows femur > tibia > humerus > 4 metacarpal> 3 metacarpal> 3 metatarsal > 4 metatarsal > rib> fibula. The rate of increase in strength of all examined bones was greater than the rate of weight gain of pigs (value of the coefficient b = 2.04–3.26). As the animals grew, the bone density increased. However, the growth rate of this indicator for the majority of bones was slower than the rate of weight gain (the value of the coefficient b ranged from 0.37 – humerus to 0.84 – fibula). The exception was the rib, whose density increased at a similar pace increasing the body weight of animals (value of the coefficient b = 0.97). The study on the influence of the breed and the feeding intensity on bone characteristics (physical and biomechanical) was performed on pigs of the breeds Duroc, Pietrain, and synthetic 990 during a growth period of 15 to 70 kg body weight. Animals were fed ad libitum or dosed system. After slaughter at a body weight of 70 kg, three bones were taken from the right half-carcass: femur, three metatarsal, and three metacarpal and subjected to the determinations described in the methodology. The weight of bones of animals fed aa libitum was significantly lower than in pigs fed restrictively All bones of Duroc breed were significantly heavier and longer than Pietrain and 990 pig bones. The average values of bending force for the examined bones took the following order: III metatarsal bone (63.5 kg) <III metacarpal bone (77.9 kg) <femur (271.5 kg). The feeding system and breed of pigs had no significant effect on the value of this indicator. The average values of the bones strength took the following order: III metatarsal bone (92.6 kg) <III metacarpal (107.2 kg) <femur (353.1 kg). Feeding intensity and breed of animals had no significant effect on the value of this feature of the bones tested. The average bone density took the following order: femur (1.23 g/cm3) <III metatarsal bone (1.26 g/cm3) <III metacarpal bone (1.34 g / cm3). The density of bones of animals fed aa libitum was higher (P<0.01) than in animals fed with a dosing system. The density of examined bones within the breeds took the following order: Pietrain race> line 990> Duroc race. The differences between the “extreme” breeds were: 7.2% (III metatarsal bone), 8.3% (III metacarpal bone), 8.4% (femur). Abstract 13 The average bone stiffness took the following order: III metatarsal bone (35.1 kg/mm) <III metacarpus (41.5 kg/mm) <femur (60.5 kg/mm). This indicator did not differ between the groups of pigs fed at different intensity, except for the metacarpal bone, which was more stiffer in pigs fed aa libitum (P<0.05). The femur of animals fed ad libitum showed a tendency (P<0.09) to be more stiffer and a force of 4.5 kg required for its displacement by 1 mm. Breed differences in stiffness were found for the femur (P <0.05) and III metacarpal bone (P <0.05). For femur, the highest value of this indicator was found in Pietrain pigs (64.5 kg/mm), lower in pigs of 990 line (61.6 kg/mm) and the lowest in Duroc pigs (55.3 kg/mm). In turn, the 3rd metacarpal bone of Duroc and Pietrain pigs had similar stiffness (39.0 and 40.0 kg/mm respectively) and was smaller than that of line 990 pigs (45.4 kg/mm). The thickness of the cortical bone layer took the following order: III metatarsal bone (2.25 mm) <III metacarpal bone (2.41 mm) <femur (5.12 mm). The feeding system did not affect this indicator. Breed differences (P <0.05) for this trait were found only for the femur bone: Duroc (5.42 mm)> line 990 (5.13 mm)> Pietrain (4.81 mm). The cross sectional area of the examined bones was arranged in the following order: III metatarsal bone (84 mm2) <III metacarpal bone (90 mm2) <femur (286 mm2). The feeding system had no effect on the value of this bone trait, with the exception of the femur, which in animals fed the dosing system was 4.7% higher (P<0.05) than in pigs fed ad libitum. Breed differences (P<0.01) in the coross sectional area were found only in femur and III metatarsal bone. The value of this indicator was the highest in Duroc pigs, lower in 990 animals and the lowest in Pietrain pigs. The cortical index of individual bones was in the following order: III metatarsal bone (31.86) <III metacarpal bone (33.86) <femur (44.75). However, its value did not significantly depend on the intensity of feeding or the breed of pigs.

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

The behaviour and properties of roots are central subjects in this book. A number of biochemical and physiological properties have already been described, for individual roots, in chapters 2, 5, 7, and 8. However, the macroscopic properties of root systems are of very great importance, to an extent that may not be immediately apparent from the point of view of the laboratory. These properties include the root/shoot ratio, the root system dimensions, its topological properties, and its distribution in the soil profile. The property of greatest practical importance is the way in which root length density (length per unit volume of soil) is distributed in the soil, because this defines the spatial limits to the efficiency of a root system in absorbing water and nutrients. For these reasons, we have collected material relating to root system properties here in a separate chapter. This may be particularly helpful to readers because there are very few single-part recent publications that deal with this subject. It appears logical to start with a discussion of how much root a plant possesses, its dependence upon the allocation of fixed carbon, and the efficiency with which this is used to form root tissue. Carbon is the basic currency of plants, and the way in which they distribute and use it is part of their growth strategy. The allocation of carbon in plants has been extensively researched within the above-ground part, but not the below-ground part, because of the difficult access to the root system, and the difficulty of separating the root, root surface and soil processes. It is important to understand the way in which carbon is allocated to both the root system as a whole, and then to the different parts of the root system, its symbiotic partners, exudates and other root products. Some broader issues are also relevant. Some of the carbon allocated to the root could be wasted, from the point of view of the plant or the farmer (Gregory 1994a).

Breast thermography is an emerging adjunct tool to mammography in early breast cancer detection due to its non-invasiveness and safety. Steady-state infrared imaging proves promising in this field as it is not affected by tissue density. The main aim of the present study is to develop a computational thermal model of breast cancer using real breast surface geometry and internal tumor specification. The model depicting the thermal profile of the subject's aggressive ductal carcinoma is calibrated by variation of blood perfusion and metabolic heat generation rate. The subject's IR image is used for validation of the simulated temperature profile. The thermal breast model presented here may prove useful in monitoring the response of tumor post-chemotherapy for female subjects with similar breast cancer characteristics.

In discussing humidity in the preceding chapter, the concept of equilibrium between water and its vapour has been introduced as a thermodynamic concept. The concept of vaporisation of other liquids such as volatile anaesthetic agents follows on naturally from that, but first of all it will be worth taking a detour through a discussion on solubility of gases and vapours in their own and other liquids [Davis 2003]. To maintain simplicity in the discussion on humidity, no mention was made of the presence of air or other gas above the surface of the water, only the water vapour. Depending on the solubility of the gas in the liquid, a variable amount of the gas dissolves in the liquid, whether that be air in water or carbon dioxide in blood. As will be discussed in the section on vaporisation, some molecules of gas enter the liquid and some leave it, depending on their individual kinetic energies, until equilibrium is reached. If the pressure inside the container with the gas or vapour and liquid is increased, then the partial pressure of the gas above the liquid surface increases; this increases the population density of gas molecules, resulting in more of the gas molecules dissolving in the liquid. Henry’s Law states that for a fixed temperature the solubility of a gas in a liquid is proportional to its partial pressure in equilibrium with the liquid. Note the condition of constant temperature because, in addition, solubility decreases with increased temperature. This occurs because an increase in the thermal energy of the dissolved gas molecules increases the partial pressure of the gas and encourages it to come out of solution (see below on vaporisation). Thus gas bubbles are more apparent in liquids that are heated. A historical clinical example of the relevance of ambient pressure and nitrogen solubility in body tissues is in decompression sickness associated with tunnel workers. Modern examples include underwater diving and, to a lesser extent, aviators and space walking astronauts. Nitrogen is a compressible gas and goes into solution in body tissue spaces under compression if the miner, tunnel worker, or diver is breathing ambient air.

The story of statins starts with cholesterol because statins are a class of drugs that reduce low-density lipoprotein (LDL) cholesterol, the “bad” cholesterol. LDL cholesterol, in turn, is a major risk factor for coronary heart disease, the leading cause of death worldwide and projected to remain so through 2025. About 1.5 million Americans suffer heart attacks each year, and heart disease has emerged as the biggest cause of death in the United States, killing 911,000 people in 2003. Before the 1940s, the average lifespan in America was 47 years, and heart disease did not contribute to mortality to a large extent because people often died of infections. Currently, an average American lives to celebrate her 77th birthday. As a consequence, heart-related disease has risen to be the number one killer. Coronary heart disease manifests in many forms: angina, arrhythmia, atrial fibrillation, congestive heart failure, hypertension, atherosclerosis, myocardial infarction (heart attack), and sudden cardiac death. Atherosclerosis, or blockage in arteries, results when a buildup of cholesterol, inflammatory cells, and fibrous tissue called plaques forms on an artery wall. If these plaques rupture, they can block blood flow to critical organs such as the heart or brain and can lead to heart attack or stroke. Despite the many different forms of cardiovascular disease, the molecule cholesterol is a common denominator for most of them. Therefore, in order to understand coronary heart disease, we first need to take a look at the cholesterol molecule. According to Roman mythology, Janus is the guardian of portals and patron of beginnings and endings. Just like the two-faced Roman god, cholesterol is a double-edged sword for the human body. On the one hand, it is an essential building block for many crucial ingredients the body needs. On the other hand, it can be lethal when it forms plaques on the surface of the arteries and subsequently causes coronary heart disease. Make no mistake, cholesterol is vital to our existence. It is most abundant in our brains—23% of total body cholesterol resides there, making up 1/10th of the solid substance of the brain.

Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to extracellular vesicles (mainly microvesicles) a role in all stages of atherosclerosis development and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

Dendritic spines, sometimes also called dendritic thorns, are tiny, specialized protoplasmic protuberances that cover the surface of many neurons. First described by Ramón y Cajal (1909; 1991) in light-microscopic studies of Golgi stained tissue, they are among the most striking subneuronal features of many neurons. Indeed, the presence of a high density of dendritic spines allows the unambiguous classification of neuronal types into spiny and aspiny, sparsely spiny, or smooth neurons. Over 90% of all excitatory synapses that occur in the cortex are located on dendritic spines. Spines can be found in all vertebrates as well as in invertebrates (e.g., the dendrites of Kenyon cells in the mushroom bodies in the olfactory system of the insect brain). The intimate association of spines with synaptic traffic suggests some crucial role in synaptic transmission and plasticity. Because of their submicrometer size (see below), physiological hypotheses as to the function of dendritic spines have only very recently become accessible to the experimentalist. For the previous two decades, spine properties have been investigated through analytical and computational studies based on morphological data, providing a very fertile ground for the crosspollination of theory and experiment. (For a very readable historical account of this see Segev et al., 1995.) The recent technical advances in the direct visualization of calcium dynamics in dendrites and spines are now permitting direct tests of some of these theoretical inferences (Guthrie, Segal, and Kater, 1991; Müller and Connor, 1991; Yuste and Denk, 1995; Denk, Sugimori, and Llinás, 1995; Svoboda, Tank, and Denk, 1996). As discussed in this chapter and, more extensively, in Chap. 19, the theoretical models that have endowed spines with active properties giving rise to all-or-none behavior (Perkel and Perkel, 1985; Shepherd et al., 1985; Segev and Rail, 1988; Baer and Rinzel, 1991) have, in general, been confirmed experimentally. Historically, the possibility of implementing synaptic memory by modulating the electroanatomy of spines was recognized early on (Chang, 1952) and was subsequently analyzed in depth by Rail (1970, 1974, 1978) and many others. Because small changes in the spine morphology can lead to large changes in the amplitude of the EPSP induced by the excitatory synapse on the spine, spines have been considered to contribute to the modulation of synaptic “weight” during long-term potentiation (see Chap. 13).

Understanding the physiological bases of magnetoencephalography (MEG) and electroencephalography (EEG) provides the foundation for developing these techniques as tools for studying human brain functions because this information can serve as a guide for planning experimental studies and for interpreting the data. During the past 50 years, the concept of electrophysiology of neurons has been profoundly modified as new types of active conductance have been discovered in the dendrites and soma. The biophysical models of individual neurons and neuronal networks developed within the framework of modern electrophysiology have provided quantitatively accurate accounts of evoked magnetic fields, extracellular potentials, and intracellular potentials in principal neurons in the tissues within a single theoretical framework. These results are consistent with the conclusion that intracellular currents in active tissues produce both MEG and EEG signals in the cerebellum, hippocampus, and cerebral cortex. We now know that the calcium and potassium currents are the major currents shaping the waveforms of MEG and EEG and that the sodium and potassium currents generate the spikes and high-frequency signals detectable outside the brain. The current dipole moment density, defined as current dipole moment per unit surface area of the active cortex, is governed by the intracellular volume fraction and basic kinetics of the active conductances. This quantity, which is conserved across the evolutionary scale ranging from reptiles to humans, may serve as a useful physiological constraint in interpreting MEG and EEG signals. It is hoped that this foundation will help advance the research on human brain functions.

A volumetric graphics model of deformable human tissue with layers of varying stiffness was developed. The model uses spring-mass-damper to calculate haptic force feedback from various layers of tissue. A haptic epidural needle insertion simulation is developed with real-time tissue deformation when external forces are exerted. Voxelization is used to fill surface meshes with grids of spring-mass-damper assemblies. The modeled tissues include all the layers traversed during an epidural procedure, including skin, subcutaneous fat, Supraspinous and interspinous ligaments, ligamentum flavum and the epidural space. Tissue is modeled with volumetric information describing the stiffness and density of each layer. Spring-mass-damper modeling enables the calculation of compression and extension of springs between tissue masses, to simulate tissue stretching and relaxation movement. A haptic force feedback device is used to interact with the tissue model with a virtual needle. The resulting simulation gives a different feeling for each tissue layer. The haptic device allows the user to insert a needle though the modeled tissue layers feeling the various physical properties of each tissue layer during needle insertion. Tissues can be viewed in cross-section to see the progress and depth of the needle. Force feedback graphs were produced to compare the force from the operator’s thumb to the resultant force feedback from the device.

Bioceramics with porous microstructure has attracted intense attention in tissue engineering due to tissue growth facilitation in the human body. In the present work, a novel manufacturing process for producing hydroxyapatite (HA) aerogels with a high density shell inspired by human bone microstructure is proposed for bone tissue engineering applications. This method combines laser processing and traditional freeze casting in which HA aerogel is prepared by freeze casting and aqueous suspension prior to laser processing of the aerogel surface with a focused CO2 laser beam that forms a dense layer on top of the porous microstructure. Using the proposed method, HA aerogel with dense shell was successfully prepared with a microstructure similar to human bone. The effect of laser process parameters on surface and cross-sectional morphology and microstructure was investigated in order to obtain optimum parameters and have a better understanding of the process. Low laser energy resulted in fragile surface with defects and cracks due to low temperature and inability of laser to fully melt the surface while high laser energy caused thermal damage both to surface and microstructure. The range of 40–45 W laser power, 5 mm/s scanning speed, spot size of 1 mmm and 50 % overlap in laser scanning the surface yielded the best surface morphology and micro structure in our experiments.

An anteroapical transmural myocardial infarction was created in Dorset sheep and resulting scar tissues were excised two (Group A, n=5, 10.6 ± 1.2 weeks) and eight months (Group B, n=6, 36.8 ± 1.4 weeks) post infarction [1]. Samples were oriented in longitudinal and circumferential directions in a biaxial stretcher, preconditioned and tested in displacement control at room temperature in BDM solution. Stress-strain plots were obtained for samples. Histology was performed by cryo-sectioning specimens into 8 μm slices and staining using Hematoxylin & Eosin. Stress-strain analyses show that circumsferential direction was stiffer than longitudinal for Group A. Group B samples show a reverse trend and are stiffer than Group A. Stained sections show more collagen in the endocardial surface for Group B samples while Group A samples have added collagen in the epicardial side. A high density of fat cells was seen in Group B samples that may affect stiffness trends.

Articular cartilage (AC) functions as a load-bearing, low friction, and wear resistant material in diarthrodial joints. The distribution of AC matrix composition is highly depth-dependent. The fluid fraction in AC is 80% and decreases from surface to the depth of the tissue [1]. Collagen constitutes 70% of the tissue dry weight, and is highest in the superficial and deep zones and lowest in the middle zone [2]. Proteoglycans (PG’s) constitute 20–30% of the tissue dry weight. PG’s are lowest in the superficial zone, and highest in the middle zone. Although the PG content is lower in the deep zone than in the middle zone, the fixed charge density (FCD) is highest in the deep zone [3]. Apart from AC composition, its structure is also depth-dependent. In the superficial zone collagen fibers are densely packed, and are arranged parallel to the articular surface. In the middle zone collagen fibers are more randomly arranged. In the deep zone, the collagen fibers have their largest diameters and are arranged perpendicular to the subchondral bone (Fig. 1) [4].

Cryopreservation of tissues and organs, including artificial organs, could be one of the important steps in the medical service that brings the progress in the tissue engineering to realization. In this case, high viability of cryopreserved cells is critical to recovery after transplantation. In contrast, in the cryosurgery, which is expected to expand its application as a minimally invasive treatment of cancer, malignant cells should be destructed completely to prevent from recurrence. The appropriate freeze-thaw protocol is therefore needed to be established for cryopreservation or cryosurgery depending on specific type of tissues and organs. Although it is determined empirically, the underlying mechanism of cell injury by freezing has been explored for a long time to give a scientific basis of the process. The experiments with a cell suspension showed that the cell injury during slow freezing to a relatively higher sub-zero temperature was attributed to the mechanical stress from the extracellular ice, while the effect of elevated concentration of solutes became more crucial to cell damage at lower temperatures [1]. However, there are some studies that indicates the difference in the freeze tolerance between cell suspensions and attached monolayers, some of which indicated higher susceptibility of monolayers to freezing than cell suspension [2] and the other suggested reverse [3,4]. The goal of our study is thus to validate the difference in freezing injury between isolated cells and tissues that are more important in aforementioned applications and clarify the mechanism. We used cells adhered to a surface as a first simple model of cells in tissues. The cells adhered on a surface at low number density were used to highlight the effect of cell-to-surface interaction without cell-to-cell interactions. In the present study we first demonstrate that the survival of cells adhered on a surface is lower than those in the suspension after a freeze-thaw manipulation. Then the osmotic response to concentration increase was examined to clarify if the extent of dehydration is different between these two types of cells. The cells were observed by a laser confocal scanning microscope that allows real-time 3-D observation.

The meniscus is comprised of two semilunar disks resting between the articular surface of the tibial plateaus and femoral condyles within the knee joint of each leg [1–3]. Both the medial and lateral menisci play a vital role in maintaining the joint’s integrity by distributing loads, stabilizing and lubricating the joint, and proprioceptive functions [2,3]. While the meniscus is found in many animals, morphological variations are present between species, indicating differences in the biomechanics of the joint [1,2]. These anatomical variations have not been quantified and, thus, remain unlinked to further structural changes that occur with injury. The goals of this study were aimed towards characterizing the normal lapine meniscal tissue using regional comparisons for tissue area and cell density measurements. The preliminary data from this research will be used as a comparison against future animal injury models. It was hypothesized that a difference would be observed between anterior, central, and posterior divisions in the normal lapine meniscus.

The coexistence of fibrin and tissue macrophages is a common finding in the histopathology of chronic inflammatory diseases of the lung.Fibrin deposition may occur as a result of activation of the extrinsic coagulation system,initiated by procoagulants generated by alveolar macrophages.In this study human alveolar macrophages (LAM) obtained by lavage of healthy donors were shown to express procoagulant factors,thromboplastin (tissue factor) and a direct factor X activator,probably a thromboplastin/ factor VII complex.In contrast to blood monocytes, LAM were only slightly susceptible for in vitro induction of thromboplastin activity (11,3 ± 2,6 (SEM)-fold and 1,3 t 0,2-fold activity increase after endotoxin stimulation).LAM were separated into four subpopulations by density gradient centrifugation.The specific thromboplastin activity of subpopulation cells varied inversely with their density (3,08 ± 0,42 U/mg cell protein for the least dense vs.0.49 ± 0.03 for the most dense subpopulation ).Low-density subpopulations of LAM released membrane material to the culture medium,which was sedimentable in the u1tracentrifuge and which expressed procoagulant activities with the same characteristics as the LAM procoagu1 ants.These findings suggest that alveolar macrophages and the membrane vesicles shed from their surface can contribute to local fibrin deposition in the lungs by expressing procoagulant factors.

Dynamic compression of soft tissues affects tissue mechanical properties and metabolic activities. The effect is attributed, in part, to the movement of water and solutes in extracellular matrix, which alters the mechanical (e.g. fluid shear stress) and chemical (e.g. growth factors, cytokines and hormones) microenvironments for cells in the tissue. To quantify contributions of external dynamic loads on solute transport in extracellular matrix, we have applied a poroelastic theory to calculate the deformation of the matrix and the movement of the fluid. In the simplified two-dimensional model, the solid phase represented the matrix of collagens and proteoglycans and the liquid phase represented the interstitial fluid. Deformable matrix embedded with cells was immersed in a solution inside a well with rigid, impermeable walls. On top of the matrix, solution with known solute concentration existed. Solute moved into the matrix and was consumed by cells. Mechanical cyclic loads were applied over a central area on the top surface of the matrix, causing its deformation and extracellular fluid movement. Resulting cell density in the matrix changed with the time during the loading cycle and it varied with the location in the matrix as well. Movement of the extracellular fluid coupled with solute diffusion contributed to the overall solute transport in the matrix. Effects of different loading frequencies and amplitudes were investigated. Different sized molecules were also considered in the study. Results from the model confirmed experimental findings that cyclic loads facilitated solute transport in soft tissues. The effect was more significant for large sized molecules. Special attention was given to regions of the matrix where cells would initially remain metabolically inactive due to lower than the critical value of the solute concentration. Quantitative analysis of solute concentration distribution in the matrix made it possible to predict regions where cells became activated by the improved solute supply. The fact that more cells in tissues became metabolically active under dynamic loads exemplified most directly the effect of external dynamic loads on solute transport in soft tissues.

Despite recent need-based advances in orthopedic scaffold design, current implants are unsuitable as “total” scaffold replacements. Both mechanical requirements of stiffness/strength and biological stipulations dictating cellular behavior (attachment, differentiation) should be included. The amount of mechanical stimulation in the form of stresses, strains, and energies most suitable toward implant design is presently unknown. Additionally unknown is if whole-bone optimization goals such as uniform and non-uniform driving forces are applicable to a scaffold-bone interface. At the very least, scaffolds ready for implantation should exhibit mechanical distributions (dependent on loading type) on the surface within the typical mechanical usage window. Scaffold micro-architectures can be strategically shifted into that window. The overall goal of this study was to produce microarchitectures tailored to a more uniform mechanical distribution, while maintaining the morphological properties necessary to sustain its mechanical integrity. The mechanical adjustment stimuli investigated were von Mises stress, strain energy density, maximum principle strain, and volumetric strain. Scaffold models of a similar volume fraction were generated of three initial architectures (Rhombitruncated Cuboctahedron, hollow sphere, and trabecular-like bone cube) using high resolution voxel mapping. The resulting voxels were translated into finite element meshes and solved, with a specially written iterative solver created in Fortran90, under confined displacement boundary conditions. The result was verified against a commercial software. Once the mechanical distributions were identified one of two methods was chosen to alter the configuration of material in Cartesian space. The success of the alteration was judged through a diagnostic based on the histogram of mechanical values present on the surface of the micro-architecture. The first method used a compliant approach and, for the case of stress, reinforced locations on the surface with large stresses with extra material (strategically taken from the least stressed portions). The second method used a simulated annealing approach to randomly mutate the initial state in a “temperature” dependent manner. Results indicate that the mechanical distributions of the initial scaffold designs vary significantly. Additionally, the end state of the adjustment demonstrated anisotropy shifts toward the direction of loading. Moreover, the adjustment methods were found to be sensitive both to the mechanical parameter used for adjustment and the portion of the surface adjusted at each increment. In conclusion, scaffolds may be adjusted using a mechanical surface-based objective, as the surface of the scaffold is crucial toward its in vivo acceptance. This technique provides some mathematical specificity toward the whole of computer-aided tissue engineering.