Trabecular Layer Research Articles

High ejection fraction of the left ventricular trabecular layer of the human heart

AbstractNumerous diagnostic criteria for excessive trabeculation, or “noncompaction,” score the extent of the trabecular layer. Whether the trabeculations themselves have a poor or good contractility is largely unknown. We retrospectively analyzed cardiac magnetic resonance (CMR) of patients with excessive trabeculation of the left ventricle (LV). The LV was labeled into four regions: compact wall, central cavity (CC), trabeculations, and intertrabecular recesses (IR). For each label we calculated the systolic fractional volume change (SFVC) in short‐axis images (n = 15) and systolic fractional area change (SFAC) in four‐chamber images (n = 30). We measured the ejection fraction (EF) of IR, CC, and total cavity. Three methods to calculate EF of the total cavity were compared: trabeculations included (per guidelines), IR excluded (Jacquier criterion), and trabeculations contoured and excluded (contour‐EF). The SFVC and SFAC of the compact wall were similar with SFVC and SFAC of trabeculations. In contrast, the IR were more diminished in systole by comparison with the CC, having lower SFVC (39% vs. 56%) and SFAC (37% vs. 72%). EF of the IR was also greater than EF of the CC (61% vs. 44%). Excluding IR from the total cavity or including trabeculations negatively impacts the EF (44% and 40%, respectively, vs. 51% for contour‐EF). The trabecular layer operates at a high EF.

The changing morphology of the ventricular walls of mouse and human with increasing gestation.

That the highly trabeculated ventricular walls of the developing embryos transform to the arrangement during the fetal stages, when the mural architecture is dominated by the thickness of the compact myocardium, has been explained by the coalescence of trabeculations, often erroneously described as 'compaction'. Recent data, however, support differential rates of growth of the trabecular and compact layers as the major driver of change. Here, these processes were assessed quantitatively and visualized in standardized views. We used a larger dataset than has previously been available of mouse hearts, covering the period from embryonic day 10.5 to postnatal day 3, supported by images from human hearts. The volume of the trabecular layer increased throughout development, in contrast to what would be expected had there been 'compaction'. During the transition from embryonic to fetal life, the rapid growth of the compact layer diminished the proportion of trabeculations. Similarly, great expansion of the central cavity reduced the proportion of the total cavity made up of intertrabecular recesses. Illustrations of the hearts with the median value of left ventricular trabeculation confirm a pronounced growth of the compact wall, with prominence of the central cavity. This corresponds, in morphological terms, to a reduction in the extent of the trabecular layer. Similar observations were made in the human hearts. We conclude that it is a period of comparatively slow growth of the trabecular layer, rather than so-called compaction, that is the major determinant of the changing morphology of the ventricular walls of both mouse and human hearts.

Effect of skull porosity on ultrasound transmission and wave mode conversion at large incidence angles.

Transcranial ultrasound imaging and therapy depend on the efficient transmission of acoustic energy through the skull. Multiple previous studies have concluded that a large incidence angle should be avoided during transcranial-focused ultrasound therapy to ensure transmission through the skull. Alternatively, some other studies have shown that longitudinal-to-shear wave mode conversion might improve transmission through the skull when the incidence angle is increased above the critical angle (i.e., 25° to 30°). The effect of skull porosity on the transmission of ultrasound through the skull at varying incidence angles was investigated for the first time to elucidate why transmission through the skull at large angles of incidence is decreased in some cases but improved in other cases. Transcranial ultrasound transmission at varying incidence angles (0°-50°) was investigated in phantoms and ex vivo skull samples with varying bone porosity (0% to 28.54%±3.36%) using both numerical and experimental methods. First, the elastic acoustic wave transmission through the skull was simulated using micro-computed tomography data of ex vivo skull samples. The trans-skull pressure was compared between skull segments having three levels of porosity, that is, low porosity (2.65%±0.03%), medium porosity (13.41%±0.12%), and high porosity (26.9%). Next, transmission through two 3D-printed resin skull phantoms (compact vs. porous phantoms) was experimentally measured to test the effect of porous microstructure alone on ultrasound transmission through flat plates. Finally, the effect of skull porosity on ultrasound transmission was investigated experimentally by comparing transmission through two ex vivo human skull segments having similar thicknesses but different porosities (13.78%±2.05% vs. 28.54%±3.36%). Numerical simulations indicated that an increase in transmission pressure occurs at large incidence angles for skull segments having low porosities but not for those with high porosity. In experimental studies, a similar phenomenon was observed. Specifically, for the low porosity skull sample (13.78%±2.05%), the normalized pressure was 0.25 when the incidence angle increased to 35°. However, for the high porosity sample (28.54%±3.36%), the pressure was no more than 0.1 at large incidence angles. These results indicate that the skull porosity has an evident effect on the transmission of ultrasound at large incidence angles. The wave mode conversion at large, oblique incidence angles could enhance the transmission of ultrasound through parts of the skull having lower porosity in the trabecular layer. However, for transcranial ultrasound therapy in the presence of highly porous trabecular bone, transmission at a normal incidence angle is preferable relative to oblique incidence angles due to the higher transmission efficiency.

Submodelling approach to screw-to-bone interaction in additively manufactured subperiosteal implant structures.

Thanks to new digital technologies, complex cases of severe maxillary atrophy may now be treated with additively manufactured subperiosteal implant structures (AMSISs). However, there are few studies addressing this topic and most of them focus on the mechanical behaviour of the AMSIS itself without considering its interaction with the maxilla bone. The aim of this study is to provide a methodology based on finite element analysis (FEA) to evaluate the effect of interaction between the maxilla bone and the screws fixing the AMSIS. The mechanical performance of an AMSIS was examined via a FEA based on submodelling. Significant differences were encountered in displacements and reaction forces when bone-screw interaction was considered. Stress in the cortical layer was found to be close to the maximum strength while the trabecular layer seems to have no effect on the results; stresses in the AMSIS are lower than the fatigue stress limit. Finally, the comparison of stresses between models with and without osseointegration shows how stresses drop once osseointegration is complete. The proposed submodelling approach considerably reduces the computational effort and enables both a detailed model of the interaction between the thread of the screws and the bone and an accurate evaluation of displacement and stress fields on the interface. The results have shown that stresses in the cortical bone are highly affected by the initial geometry of the thread inside the bone, which demonstrates the importance of modelling the effect of the thread.

AGE ASSESSMENT OF THE DYNAMICS OF MORPHOLOGICAL REARRANGEMENT OF BONE TISSUE OF THE ARTICULAR PROCESSES OF THE HUMAN LOWER JAW DEPENDING ON THE LOSS OF THE MASTICATORY TEETH

Aim: To analyze morphometric changes in the structure of bone tissue of the mandibular articular processes and establish their densitometric dependence on the masticatory teeth loss in people of I-II periods of adulthood. Materials and methods: We analyzed 136 digital CT recordings of human temporomandibular joints. The research subjects were divided into three groups based on the degree of dentition defect acquisition: the first - a limited defect, the second - a final defect, and the third - a preserved dentition (control); by age into two periods of adulthood of postnatal human ontogenesis. Digital statistical analysis of the bone density is presented as M±σ (mean and standard deviation). We compared the experimental groups with the control group using nonparametric statistical analysis. Results: Changes in the vertical dimension of occlusion due to limited masticatory teeth loss acquire variable morphometric features, causing an interrelated process of bone atrophy of the cellular part and the trabecular layer of the mandibular processes. The density of bone tissue of the cortical layer of the articular-fossa quadrant (A-Fh/q) of the articular head of the mandibular process increases on the right with limited defects and decreases with final defects. Indicators of bone densitometry of A-Fh/q on the left is characterized by a decrease with limited defects for individuals of the I-st period of adulthood and an increase in the final defects in the II-nd on the left and right. Conclusions: Multifactorial pathomorphological compensatory processes ensure bone density, but with a change in values on the right and a decrease on the left. Morphometric values of trabecular layers, the most vulnerable areas of the neck and base of the mandibular articular processes, indicate the reconstruc¬tion of their bone tissue with limited defects; in the first period of the adulthood, they decrease with a significant predominance on the left.

Influence of mechanical stimuli and zoledronic acid on the femoral morfology in rats with obesity and limited mobility models

The aim. Investigate the long-term effect of WBV and bisphosphonate (zoledronic acid) on the morphological structure and mineral density of the rat femora. Materials and methods. Rats were divided into control and three experimental groups: I - experimental group - high-calorie diet + limited mobility (HCD + LM), II - experimental group - HCD + LM + whole body vibration (WBV 3 m/s2). III - experimental group - HCD + LM + administration of zoledronic acid (HCD + LM + Zol. at a dose of 0.025 mg / kg). Bone mineral density determination, scanning electron microscopy of trabecular meshwork and immunohistological examination were performed. Results. The application of the model of a high-calorie diet with limited mobility leads to the loss of the mineral component of trabeculae up to 16.2%. The trabecular layer thinned to 13.9% compared to the control group, and the intertrabecular spaces expanded. Under the influence of whole-body vibration, there was an increase in BMD in the femora compared to the group HCD + LM, and bone density remained at the control level until the 16th week of the experiment. In group III, the rate of bone formation increased, the ratio of bone to trabecular volume was significantly higher compared to the group HCD + LM. Starting from the 8th week, it increased by 8.1% and 13% at the end of the experiment, respectively.Conclusions. A high-calorie diet with limited mobility reduces the mineral density of the trabeculae in the femoral bone. Zoledronic acid effectively improves mineralization but leads to impairment of the morphology of the bone growth plate. The research results indicate that WBV can be an effective non-pharmacological method of maintaining bone health in young people.

Abstract P2112: Human Genetics And Engineered Heart Tissues Link Frail MYH7 Alleles To Delayed Maturation And Ventricular Noncompaction

Background: Up to 1% of humans are born with a congenital heart defect. Among those defects is a condition known as left ventricular noncompaction (LVNC), which is defined as the ratio of trabeculated myocardium to compact myocardium exceeding 2.3:1. The process of compaction occurs when the layer of compact cardiomyocytes (CMs) proliferates, while CMs in the trabecular layer quiesce. This differential expansion of the CM layers reduces the trabecular invaginations into the cardiac lumen. Deficient compact CM proliferation or excessive trabecular CM proliferation converge on a similar presentation, collectively referred to as noncompaction. Family and population genetics studies have implicated deleterious variants in sarcomere genes as highly correlated with LVNC (PMID: 18506004, PMID: 3350056); specifically, MYH7 truncations and missense variants that fall within the first 600 amino acids of the beta myosin heavy chain head region. Hypothesis: Reduced contractility in certain MYH7 head domain missense or truncating variants disrupts cardiomyocyte terminal maturation, leading to excessive trabeculation. Results: We identified individuals and families with MYH7 Lys234Asn and Arg243His. Variant carriers had LVNC often in the setting of dilated cardiomyopathy, similar to what has been described with MYH7 truncations. We engineered MYH7 truncations in human induced pluripotent stem cells (hiPSCs) which were differentiated into engineered heart tissues (EHTs) to model the developing heart. In EHTs with MYH7 truncations contractility was reduced by 50%, EHT size increased by 17%, and CM proliferation increased by 40% in EHTs heterozygous for MYH7 truncations (N=6 each). Conclusions and Future Directions: Our observations of impaired differentiation, reduced contractility, and decreased compaction are consistent with LVNC phenotypes. We propose a general model where diminished contractility delays sarcomere maturation, extending the proliferation time of trabecular cardiomyocytes and resulting in excessive trabeculae.

Endothelial Loss of ETS1 Impairs Coronary Vascular Development and Leads to Ventricular Non-Compaction.

Jacobsen syndrome is a rare chromosomal disorder caused by deletions in the long arm of human chromosome 11, resulting in multiple developmental defects including congenital heart defects. Combined studies in humans and genetically engineered mice implicate that loss of ETS1 (E26 transformation specific 1) is the cause of congenital heart defects in Jacobsen syndrome, but the underlying molecular and cellular mechanisms are unknown. To determine the role of ETS1 in heart development, specifically its roles in coronary endothelium and endocardium and the mechanisms by which loss of ETS1 causes coronary vascular defects and ventricular noncompaction. ETS1 global and endothelial-specific knockout mice were used. Phenotypic assessments, RNA sequencing, and chromatin immunoprecipitation analysis were performed together with expression analysis, immunofluorescence and RNAscope in situ hybridization to uncover phenotypic and transcriptomic changes in response to loss of ETS1. Loss of ETS1 in endothelial cells causes ventricular noncompaction, reproducing the phenotype arising from global deletion of ETS1. Endothelial-specific deletion of ETS1 decreased the levels of Alk1 (activin receptor-like kinase 1), Cldn5 (claudin 5), Sox18 (SRY-box transcription factor 18), Robo4 (roundabout guidance receptor 4), Esm1 (endothelial cell specific molecule 1) and Kdr (kinase insert domain receptor), 6 important angiogenesis-relevant genes in endothelial cells, causing a coronary vasculature developmental defect in association with decreased compact zone cardiomyocyte proliferation. Downregulation of ALK1 expression in endocardium due to the loss of ETS1, along with the upregulation of TGF (transforming growth factor)-β1 and TGF-β3, occurred with increased TGFBR2/TGFBR1/SMAD2 signaling and increased extracellular matrix expression in the trabecular layer, in association with increased trabecular cardiomyocyte proliferation. These results demonstrate the importance of endothelial and endocardial ETS1 in cardiac development. Delineation of the gene regulatory network involving ETS1 in heart development will enhance our understanding of the molecular mechanisms underlying ventricular and coronary vascular developmental defects and will lead to improved approaches for the treatment of patients with congenital heart disease.

Papillary muscle avulsion following balloon mitral valvotomy evaluated with three-dimensional echocardiography

BackgroundPercutaneous balloon mitral valvotomy is a common therapeutic approach for rheumatic mitral stenosis. Avulsion of the papillary muscle is a rare but serious complication of balloon mitral valvotomy. The papillary muscles are derived from the trabecular layer of the developing ventricular walls. When subjected to a force, avulsion of papillary muscle from the trabecular layer may occur.Case presentationIn this case report, we describe a patient with rheumatic mitral stenosis, who experienced avulsion of the mitral papillary muscle from the left ventricular wall after undergoing balloon mitral valvotomy. Papillary muscle alvusion resulted in severe mitral regurgitation, which was finally treated by mitral valve replacement.ConclusionWe successfully diagnosed avulsion of the papillary muscle following balloon mitral valvotomy. Three-dimensional transthoracic echocardiography provides more information on mitral apparatus structure than two-dimensional transthoracic echocardiography.

COMPARATIVE ANALYSIS OF DENS ITOMETRIC DETERMINATION OF BONE TISSUE IN THE CASE OF LOSS OF THE MASTICATORY TEETH OF THE MANDIBLE

Conducting densitometric studies aimed at objectifying and improving the accuracy of estimating the structural parameters of the bone become fundamental in the rehabilitation of patients to meet their functional, prosthetic and aesthetic needs. Today, the results of bone density analysis determine the priority in choosing a new method of direct implantation with immediate load or search for an alternative to existing ones that guarantee the predictability of the result concerning the physiological terms of osteogenesis, directed bone regeneration and other reconstructive surgical interventions. Based on 243 computed tomographic digital scans taken by the VaTech PaX-I 3D Green extraoral system, bone density was analyzed in conventional grayness units (CGU) in the projection of the missing 3.7, 3.6, 4.6, 4.7 teeth and 136 studies were selected as objects for this work, which provide proper information and signifi cant cognitive importance. The maximum mineralization of bone tissue in the toothless distal areas of the lower jaw, both on the left and right sides, was established in individuals of the fi rst study group (25-45 years) with values of pronounced density on sagittal sections of horizontal planes in the projection of 3.6 tooth M=1246.6±63.13 CGU and in projection 4.6 tooth, where M=1158.8±47.04 CGU. The lowest values of bone density were determined in individuals of the third study group (61-75 years) on sagittal sections of vertical planes in projections of 3.7 tooth, where M=736.8±42.63 CGU, and 4.7 tooth, where M=778.8±51.79 CGU. The result of the analysis of this work confi rms the hypothesis of age-related dependence of changes in bone density on the time of tooth loss. It was found that early loss of the masticatory teeth leads to high indicators, with an increase in bone density towards distalization of the terminal defect of dentition. Conversely, the lack of functional action on bone tissue leads to a decrease in its density in the age aspect, and, accordingly, the exhaustion of the trabecular layer, which contributes to the progression of atrophic processes.

Densitometric assessment in the justification of rehabilitation of patients with atrophy of the bone tissue of the mandible, on the right side

Densitometric methods for determining bone density are increasingly becoming fundamental in research and a priority in clinical applications in medical practice. Rehabilitation of patients with bone atrophy becomes impossible without assessing its density and, at the same time, is an important component in the diagnosis and planning of reconstructive surgery, in particular, prognosticity in the use of osteoplastic materials or osteointegration of dental implants. The aim of the study was to conduct a densitometric assessment to substantiate the rehabilitation of patients with atrophy of the mandible, on the right side, in the age groups of 25 to 75 years. Computed tomography digital scan scans obtained using the Vatech PaX-I 3D Green extra-oral radiography system and processed by the standardized X-ray diagnostic software Ez3D-I Original ver.5.1.9.0. Using the tools of the horizontal option panel, in particular the keys of the interface “profile”, the density of bone tissue with interpretation in conventional units of grayness (CUG) in the projection of 4.6, 4.7 teeth was investigated. To obtain qualitatively homogeneous values, we used nonparametric methods of statistical analysis of comparison of age groups – using the multidimensional Kruskal-Wallis test as an alternative intergroup analysis of variance, for simultaneous comparison of three samples. It is proved that during the statistical analysis of bone density using the Mann-Whitney U test in the studied areas of the mandible on the right, the total average number of M experimental (E) groups compared to the average number of the control group (C), high reliability in vertical (VP) measurements and confirmed p<0.05. Thus, it is proved that the early loss of the masticatory group of teeth, in the first group of studies (25-45 years), leads to high rates, with increasing bone density in the direction of distalization of the final defect of the dentition. Conversely, the lack of functional action on bone tissue in the second (46-60 years) and third (61-75 years) groups of the study, leads to a decrease in its density, and, consequently, to the devastation of the trabecular layer, which contributes to the progression of atrophic processes.

Left Ventricular Noncompaction Is Associated with Valvular Regurgitation and a Variety of Arrhythmias.

Left ventricular noncompaction (LVNC) is a type of cardiomyopathy characterized anatomically by prominent ventricular trabeculation and deep intertrabecular recesses. The mortality associated with LVNC ranges from 5% to 47%. The etiology of LVNC is yet to be fully understood, although decades have passed since its recognition as a clinical entity globally. Furthermore, critical questions, i.e., whether LVNC represents an acquired pathology or has a congenital origin and whether the reduced contractile function in LVNC patients is a cause or consequence of noncompaction, remain to be addressed. In this study, to answer some of these questions, we analyzed the clinical features of LVNC patients. Out of 9582 subjects screened for abnormal cardiac functions, 45 exhibit the characteristics of LVNC, and 1 presents right ventricular noncompaction (RVNC). We found that 40 patients show valvular regurgitation, 39 manifest reduced systolic contractions, and 46 out of the 46 present different forms of arrhythmias that are not restricted to be caused by the noncompact myocardium. This retrospective examination of LVNC patients reveals some novel findings: LVNC is associated with regurgitation in most patients and arrhythmias in all patients. The thickness ratio of the trabecular layer to compact layer negatively correlates with fractional shortening, and reduced contractility might result from LVNC. This study adds evidence to support a congenital origin of LVNC that might benefit the diagnosis and subsequent characterization of LVNC patients.

MORPHOMETRIC ANALYSIS OF TOPOGRAPHIC VARIABILITY OF THE LEFT AND RIGHT MANDIBULAR CANALS IN CASE OF LOSS OF THE MASTICATORY TEETH

The aim: To study the topographic variability of the left and right mandibular canals in case of bone atrophy caused by the loss of the masticatory teeth. Materials and methods: 136 digital scans were selected for morphometric analysis, 68 for each side taken with the Vatech PaX-i 3D Green extra-oral radiography system. The readout of absolute morphometric values, laying the left and right MC was performed in the projection of 3.7, 3.6, 4.6, 4.7 teeth using standardized Ez3D-I software. Results: The alveolar part is characterized by distance to the alveolar ridge, and primarily exposed to pronounced atrophic processes of bone tissue. Distance to the lingual ridge directly proportionally indicates the morphological transposition vector of the mandibular canals for the distance to the buccal ridge, by the same length to its reduction. Morphometric analysis on a short toothless segment determines the variability of laying the mandibular canals but it is characterized by constant regular values of the ridge of the mandibular base. Conclusions: Dentition defects, moving towards the missing teeth, lead to a decrease in the biophysical stimulus on bone tissue, causing pronounced morphological changes with the loss of significant volume and restructuring of its trabecular layer, which synchronously affects the topographic variability of the left and right MC.

Higher spatial resolution improves the interpretation of the extent of ventricular trabeculation.

The ventricular walls of the human heart comprise an outer compact layer and an inner trabecular layer. In the context of an increased pre‐test probability, diagnosis left ventricular noncompaction cardiomyopathy is given when the left ventricle is excessively trabeculated in volume (trabecular vol >25% of total LV wall volume) or thickness (trabecular/compact (T/C) >2.3). Here, we investigated whether higher spatial resolution affects the detection of trabeculation and thus the assessment of normal and excessively trabeculated wall morphology. First, we screened left ventricles in 1112 post‐natal autopsy hearts. We identified five excessively trabeculated hearts and this low prevalence of excessive trabeculation is in agreement with pathology reports but contrasts the prevalence of approximately 10% of the population found by in vivo non‐invasive imaging. Using macroscopy, histology and low‐ and high‐resolution MRI, the five excessively trabeculated hearts were compared with six normal hearts and seven abnormally trabeculated and excessive trabeculation‐negative hearts. Some abnormally trabeculated hearts could be considered excessively trabeculated macroscopically because of a trabecular outflow or an excessive number of trabeculations, but they were excessive trabeculation‐negative when assessed with MRI‐based measurements (T/C <2.3 and vol <25%). The number of detected trabeculations and T/C ratio were positively correlated with higher spatial resolution. Using measurements on high resolution MRI and with histological validation, we could not replicate the correlation between trabeculations of the left and right ventricle that has been previously reported. In conclusion, higher spatial resolution may affect the sensitivity of diagnostic measurements and in addition could allow for novel measurements such as counting of trabeculations.

BONE MINERAL DENSITY OF THE RATS TIBIA AFTER MODELING OF ARTIFICIAL MENOPAUSE AND INFLUENCE OF WHOLE BODY VIBRATION

Early deficiency of female sex hormones provokes bone loss in various parts of the skeleton, which further requires therapeutic correction. However, it is known that vibrational oscillations are anabolic for the trabecular layer of bone, which have been studied in both animal models and humans under physiological norms. It is likely that this anabolic reaction does not occur evenly throughout the skeleton, on the one hand, due to the cushioning properties of muscle tissue, ligaments, joints, and resonance, on the other.&#x0D; The aim of the study is to assess the condition and mineral density of the tibia under the condition of artificial menopause and the influence of non-physiological whole body vibration (WBV) with acceleration 0,3 g.&#x0D; Material and methods. The experiments were performed on 54 adult female Wistar rats. Rats were divided into three groups: control group (n=18) – SHAM surgery, experimental group I (n=18) - rats with ovariectomy, experimental group II (n=18) - rats after ovariectomy + WBV. Rats of were subjected to total vibration with acceleration of 0,3 g for 30 minutes 5 days a week for 24 weeks. At the 8th, 16th and 24th week of the experiment CT-densitometry of the tibia was performed.&#x0D; Results. The greatest loss of bone tissue was observed in experimental group I at the 24th week of the experiment, which decreased by 23.5% compared with the control group. At the 8th week of the study, the rate did not change statistically, and at the 16th - decreased to 8.1%. In experimental group II, bone density did not decrease statistically at the 8th and 16th week of our study, however, at the 24th week decreased by -16% to the control group, and compared with group I, increased by +11,2 % on the 24th day. The cortical layer of the tibial bone tissue did not change statistically in the experimental groups in relation to the control group. Factors that can affect the anabolic response in the tissues of the musculoskeletal system are the parameters of vibration, in particular the frequency and level of vibration acceleration. In our experimental study, we observed a decrease in bone mineral density in rats with ovariectomy and compared with ovariectomized rats subjected to vibration. We observed a positive correlation between whole body vibration and bone mass increase, which may be due to the effect of increased mechanical stress on the skeleton. We also demonstrated the negative effect of time after ovariectomy on bone density in experimental rats. The use of vibration maintained normal bone mineral density for a long time, and until the 16th week of the experiment, but at the 24th week, rate decreased significantly compared with the control group, but was higher than in group I. Analysis of CT scans showed high values of mineral density in experimental group II (ovariectomy + WBV) compared with experimental group I.&#x0D; Conclusions. The obtained results allow us to conclude that the WBV inhibits the accelerated remodeling after ovariectomy and prevents the rapid loss of bone tissue for a long time. To this end, mechanical vibrations should be used in the early menopause to maintain normal bone mineral mass. This therapy can be used alone and as an adjunct to osteoporosis medication. Therefore, early detection of osteopenia and timely appropriate treatment is important, which, in addition to antiresorptive drug treatment, should include lifestyle changes and exercise.

Morphological features of bone tissue in "disuse atrophy" on the example of a segment of the human lower jaw: clinical experience of treatment

Current real-time science and technology techniques based on ENDORET PRGF technologies and the implementation of their results in practical medicine, provide ample opportunities for the use of cell autotransplantation for guided tissue regeneration, including in the treatment of "disuse atrophy" of the human lower jaw bone tissue with early tooth loss. The purpose of this work is to ensure the principles of biological feasibility and physiological capacity, technical rationality. The pathology in the distal segment of a lower limb, which is a vertical atrophy of bone tissue was confirmed by the methods of computed tomography, Vatech PaX-I 3D Green systems of extra-oral radiography with a scan size range of 16×9 cm, a focal spot of 0.5 mm (IEC60336) with a gray scale of 14 bits with a size of 0.2/0.3 voxel. Using ENDORET PRGF technology, according to the approved BTI protocol, autocellular grafts that have provided a positive result that meets the basic principles of the goal in restoring the mechanisms of physiological processes of normal quantitative and qualitative morphology of bone tissue, with its biological characteristics were obtained. The results of the study showed that bone tissue on a scale of shades of gray based on the classification of Hounsfield, is not characterized by a single biotype and in the area of missing 3.6 tooth belongs to the second biotype, and in the area of missing 3.7 tooth – to the first biotype by its density. The indicators of densitometric determination confirmed excessive mineralization of the trabecular layer, ie vertical atrophy of bone tissue, which is in the sagittal section in the projection of the missing 36 teeth – with a maximum number of 881 gray standard units (GSU), M=315 GSU (where, M is the average value of absolute number); sagittal section in the projection of the missing 37 teeth – with a maximum number of 1726 GSU, M=1173 GSU. This clinical experience with the use of autocellular grafts in the treatment of "disuse atrophy" of the bone tissue of the jaws, which is essentially scientifically-research in nature, based on modern, at the same time available technologies of cell engineering and technical progress, provides a predictable result of clinical observation and deserves further research and practical testing.

Gestational intermittent hyperoxia rescues murine genetic congenital heart disease in part

Cardiac development is a dynamic process, temporally and spatially. When disturbed, it leads to congenital cardiac anomalies that affect approximately 1% of live births. Genetic variants in several loci lead to anomalies, with the transcription factor NKX2-5 being one of the largest. However, there are also non-genetic factors that influence cardiac malformations. We examined the hypothesis that hyperoxia may be beneficial and can rescue genetic cardiac anomalies induced by an Nkx2-5 mutation. Intermittent mild hyperoxia (40% PO2) was applied for 10 h per day to normal wild-type female mice mated with heterozygous Nkx2-5 mutant males from gestational day 8.5 to birth. Hyperoxia therapy reduced excessive trabeculation in Nkx2-5 mutant mice compared to normoxic conditions (ratio of trabecular layer relative to compact layer area, normoxia 1.84 ± 0.07 vs. hyperoxia 1.51 ± 0.04) and frequency of muscular ventricular septal defects per heart (1.53 ± 0.32 vs. 0.68 ± 0.15); however, the incidence of membranous ventricular septal defects in Nkx2-5 mutant hearts was not changed. Nkx2-5 mutant embryonic hearts showed defective coronary vessel organization, which was improved by intermittent mild hyperoxia. The results of our study showed that mild gestational hyperoxia therapy rescued genetic cardiac malformation induced by Nkx2-5 mutation in part.

Tension heterogeneity directs form and fate to pattern the myocardial wall.

How diverse cell fates and complex forms emerge and feed backto each other to sculpt functional organs remains unclear. In the developing heart, the myocardium transitions from a simple epithelium to an intricate tissue that consists of distinct layers: the outer compact and inner trabecular layers. Defects in this process, which is known as cardiac trabeculation, cause cardiomyopathies and embryonic lethality, yet how tissue symmetry is broken to specify trabecular cardiomyocytes is unknown. Here we show that local tension heterogeneity drives organ-scale patterning and cell-fate decisions during cardiac trabeculation in zebrafish. Proliferation-induced cellular crowding at the tissue scale triggers tension heterogeneity among cardiomyocytes of the compact layer and drives those with higher contractility to delaminate and seed the trabecular layer. Experimentally, increasing crowding within the compact layer cardiomyocytes augments delamination, whereas decreasing it abrogates delamination. Using genetic mosaics in trabeculation-deficient zebrafish models-that is, in the absence of critical upstream signals such as Nrg-Erbb2 or blood flow-we find that inducing actomyosin contractility rescues cardiomyocyte delamination and is sufficient to drive cardiomyocyte fate specification, as assessed by Notch reporter expression in compact layer cardiomyocytes. Furthermore, Notch signalling perturbs the actomyosin machinery in cardiomyocytes to restrict excessive delamination, thereby preserving the architecture of the myocardial wall. Thus, tissue-scale forces converge on local cellular mechanics to generate complex forms and modulate cell-fate choices, and these multiscale regulatory interactions ensure robust self-organized organ patterning.

A New Approach Based on Glued Multi-Ultra High Molecular Weight Polyethylene Forms to Fabricate Bone Replacement Products.

Three types of glue based on thiol-ene reaction, polyvinyl alcohol (PVA)/cellulose, and phenol formaldehyde were prepared and applied on modified ultra-high molecular weight polyethylene (UHMWPE) samples grafted by cellulose. In comparison with unmodified UHMWPE samples, T-peel tests on the modified and grafted UHMWPE films showed an increase in the peel strength values for the glues based on thiol-ene reaction, PVA/cellulose, and phenol formaldehyde by 40, 29, and 41 times, respectively. The maximum peel strength value of 0.62 Kg/cm was obtained for the glue based on phenol formaldehyde. Mechanical tests for the cylindrical multi-UHMWPE forms samples, made of porous UHMWPE as a trabecular layer and an armored layer (cortical layer) that consists of bulk and UHMWPE films, indicated an improvement in the mechanical properties of these samples for all glue types, as a result of the UHMWPE films existence and the increase in the number of their layers. The maximum compressive yield strength and compressive modulus values for the armored layer (bulk and six layers of the UHMWPE films using the glue based on thiol-ene reaction) were 44.1 MPa (an increase of 17%) and 1130 MPa (an increase of 36%), respectively, in comparison with one armored layer of bulk UHMWPE. A hemocompatibility test carried out on these glues clarified that the modified UHMWPE grafted by cellulose with glues based on PVA/cellulose and thiol-ene reaction were classified as biocompatible materials. These multi-UHMWPE forms composites can be considered a promising development for joint reconstruction.

A Histological Study on Heart of &lt;i&gt;Pelophylax&lt;/i&gt; cf. &lt;i&gt;bedriagae&lt;/i&gt; (Anura: Ranidae)

A circulatory system become compulsory for the transport of nutrients and gases due to the growth of animals and the development of various organs. The heart of Pelophylax cf. bedriagae consisted of three chambers (two atria and one ventricle). Two atria were completely separated, however the ventricle were undivided. When looking dorsally on the heart, thin-walled sinus venosus was observed. The sinus venosus is responsible for initiating the heart beat and receives venous blood coming from caput, anterior legs, and body that then flows to the right atrium. Pacemaker cells and ganglion cells were main cells of the sinus venosus. The layer of the heart wall consisted of epicardium, myocardium and endocardium. The epicardium was the outer layer of heart. The myocardium was medium layer which was composed of an outer compact layer and inner trabecular layer. Ventricular trabeculae were lined by a thin layer of endocardial endothelium. The inner trabecular layer of ectothermic vertebrates is accepted as homologous to the Purkinje network. The atrioventricular valves were composed of loose connective tissue.