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PubMed1992

An evolutionary Wolff's law for trabecular architecture.

A continuum model is proposed to describe the temporal evolution of both the density changes and the reorientation of the trabecular architecture given the applied stress state in the bone and certain material parameters of the bone. The data upon which the proposed model is to be based consist of experimentally determined remodeling rate coefficients and quantitative stereological and anisotropic elastic constant measurements of cancellous bone. The model shows that the system of differential equations governing the temporal changes in architecture is necessarily nonlinear. This nonlinearity is fundamental in that it stems from the fact that, during remodeling, the relationship between stress and strain is changing as the stress and strain variables themselves are changing. In order to preserve the remodeling property of the model, terms that are of the order strain times the changes in density and/or microstructural properties must be retained. If these terms were dropped, there would be no feedback mechanism for architectural adaptation and no adaptation of the trabecular architecture. There is, therefore, no linearized version of the model of the temporal evolution of trabecular architecture. An application of the model is illustrated by an example problem in which the temporal evolution of homogeneous trabecular architecture is predicted. A limitation of the proposed continuum model is the length scale below which it cannot be applied. The model cannot be applied in regions of cancellous bone where the trabecular bone architecture is relatively inhomogeneous or at a bone-implant interface.

Bone Density↗

PubMed2026

Architectural logic of the 3D genome: mechanisms of dysregulation and emerging cancer therapeutics.

The three-dimensional (3D) genome provides an essential layer of organization that shapes genome function in space and time. Chromatin compartments and topologically associating domains (TADs) arise from the interplay between intrinsic properties of chromatin and architectural factors, including cohesin and CTCF. Despite substantial progress in defining these structural features, whether 3D genome architecture plays a causal role in regulating processes such as transcription, DNA replication, and DNA repair, or instead reflects underlying regulatory activity, remains unresolved. Here, we use the distinction between chromatin-intrinsic features and architectural factors as a framework to evaluate evidence for causality in genome structure-function relationships. We extend this framework to cancer, where both intrinsic alterations (including noncoding mutations, structural variants, and changes in chromatin state) and architectural factor perturbations (such as mutations in architectural proteins and dysregulation of transcriptional machinery) disrupt genome organization and contribute to disease progression. These findings suggest that alterations in genome structure can, in some contexts, actively reshape oncogenic programs. A major limitation in applying 3D genome insights to cancer biology is the cost and complexity of omics assays. Recent advances in artificial intelligence (AI) and machine learning (ML) enable inference and prediction of 3D genome organization from sequence and epigenomic features, providing insight into the extent to which genome folding is encoded intrinsically versus dynamically regulated in architectural factors. This perspective provides a unified view of how genome structure is established, how it relates to function, and how its disruption contributes to tumorigenesis.

3D genome↗

PubMed1992

Architecture of selected muscles of the arm and forearm: anatomy and implications for tendon transfer.

The architectural features of twenty-one different forearm muscles (n = 154 total muscles) were studied. Muscles included the extensor digitorum communis to the index, middle, ring, and small fingers, the extensor digit quinti, the extensor indicis proprius, the extensor pollicis longus, the flexor digitorum superficialis, the flexor digitorum profundus, the flexor pollicis longus, the pronator quadratus, the palmaris longus, the pronator teres, and the brachioradialis. Muscle length, mass, fiber pennation angle, fiber length, and sarcomere length were determined with the use of laser diffraction techniques. From these values, physiologic cross-sectional area and fiber length/muscle length ratio were calculated. The individual digital extensor muscles were found to be relatively similar in architectural structure. Similarly, the deep and superficial digital flexors were very similar architecturally, with the exception of the small finger flexor digitorum superficialis, which was much smaller and shorter than the rest of the digital flexors. The brachioradialis and the pronator teres had dramatically different architectural properties. While the masses of the two muscles were nearly identical, the muscles had significantly different predicted contractile properties based on their different fiber arrangement. The brachioradialis, with its long fibers arranged at a small pennation angle, had a physiologic cross-sectional area that was only one third that of the pronator teres, with its short fibers that were more highly pennated. Using these architectural data and the statistical method of discriminant analysis, we provide additional information that might be useful in the selection of potential donor muscles to restore thumb flexion, thumb extension, finger extension, and finger flexion.

Arm↗

PubMed2026

Pervasive context-dependent effects in the genetic architecture of complex and quantitative traits revealed by a powerful multiparent mapping population in yeast.

The genetic dissection of complex traits remains a major challenge in basic and biomedical research, but is essential for understanding the molecular pathways that shape phenotypic variation and for developing predictive models of trait and disease susceptibility. Here, we leverage a novel multiparent mapping population of budding yeast, CYClones, comprising 9,344 haploid strains derived from eight genetically diverse founders (~270,000 SNVs, ~ 1 per 44 bp, capturing 56% of common variants and 32% of all variants with a minor allele frequency greater than 0.005 in the global population), to identify quantitative trait loci (QTL) and systematically investigate the genetic architecture of growth rates across ten environmental conditions. In total, we identified 349 QTL (ranging from 18 to 49 QTL per growth condition) that explained between 60% and 100% of narrow sense heritability across traits. The high power and resolution of CYClones revealed that growth traits exhibited distinct, condition-specific genetic architectures with extensive allelic heterogeneity, where a QTL was the result of multiple tightly linked causal variants. We also observed pleiotropy among QTL with complex, trait-dependent allele effects that are also consistent with allelic heterogeneity. Genetic complexity varied widely, with some traits showing nearly Mendelian architectures, while others were highly polygenic. Introgressed loci played a prominent role in the landscape of growth rate QTL, including a QTL localized to a 2.4 kb interval in the PCA1 cadmium transporter that explains 72% of variation in cadmium resistance and is largely driven by an introgression, and a non-additive interaction between the GAL3 regulator and introgressed GAL1/7/10 alleles, extending a previously described three-locus GAL-pathway incompatibility to a four-locus interaction. In both cadmium and galactose conditions, we show that allelic variation at a small number of loci stratifies the population into regulatory or physiological subgroups, each with distinct genetic architectures, a specific manifestation of epistasis we term allele-dependent stratification. Collectively, our results provide novel insights into the genetics of growth rates in budding yeast, the architectural features of genetic complexity, and demonstrate that CYClones is a powerful platform for revealing the molecular basis of complex trait variation.

Quantitative Trait Loci↗

PubMed2026

Genetic architectures of brain-related traits are shaped by strong selective constraints.

Genome-wide association studies (GWAS) have identified hundreds of significant loci for psychiatric disorders, yet the strength of these associations remains modest compared to other human complex traits with similar numbers of hits. Whether this pattern reflects statistical artifacts or real biological differences-and, if the latter, what underlies it-remains unclear. In addition to psychiatric disorders, we find that other traits with functional enrichment in the central nervous system (CNS), whether binary or quantitative, also share similar genetic architectures, characterized by GWAS hits of limited statistical significance and generally higher allele frequencies. In comparing the architecture of binary and quantitative traits, we adjust for statistical power in their respective studies. After this adjustment, we fit an evolutionary model of architecture and show that CNS-enriched traits have large mutational target sizes, with contributing variants and genes experiencing stronger selection than those for other traits. Our findings reveal heterogeneity among complex traits and provide insights into traits that more effectively capture fitness-relevant processes. More broadly, our results suggest that the genetic architectures of complex traits are shaped by the tissues through which these traits are mediated.

Humans↗

PubMed1992

Design and control of the head retractor muscle in a turtle, Pseudemys (Trachemys) scripta: I. Architecture and histochemistry of single muscle fibers.

We are using the head retractor muscle (RCCQ) of a turtle, Pseudemys scripta, to analyze the neuromuscular mechanisms by which organisms vary the force and timing of muscle contraction. Previously we demonstrated that RCCQ comprises three histochemically defined fiber types: fast glycolytic (Fg), fast oxidative glycolytic (FOG), and slow oxidative (SO). In the present paper we report the 1) architectural features of single muscle fibers in RCCQ, including their lengths, diameters, and taper characteristics, 2) histochemical profiles of single muscle fibers, and 3) quantitative relations between our architectural and histochemical variables. Single fibers in RCCQ exhibit an order of magnitude variation in length (4-60 mm). Approximately 40% span the full muscle. The remaining fibers generally attach to bone or tendon at one end, and the other end tapers intramuscularly; rarely a fiber may taper at both ends. The maximum (untapering) diameters of single fibers are bimodally distributed, forming two diameter classes. Fibers also vary in the percentage of their total length that tapers and in the shape of the tapering region. Large diameter muscle fibers generally are longer and have shorter, more blunted tapers than small diameter fibers. The large diameter fibers are almost all Fg types; these fibers have a median diameter of 59.3 microns, and they account for approximately 60% of total fibers in RCCQ. FOG and SO fibers generally have small diameters (median: 32.5 microns and 35.8 microns), and they typically account for 30% and 10% of total fibers. We use these relations to draw inferences about the attachments and architecture of glycolytic (Fg) and oxidative (FOG, SO) fiber types. Taken together, our data suggest that single muscle fibers in RCCQ may be architecturally as well as histochemically specialized to perform different roles in head retraction. In the accompanying paper we report the efferent innervation of these fibers and consider some of the neural control problems posed by these diverse fiber types.

Animals↗

PubMed1992

Control of bone architecture by functional load bearing.

The continuing ability of the skeleton to withstand functional loads without damage requires that bone mass and architecture are adjusted according to the loads experienced. Load bearing is the only functional influence that requires a particular bone architecture, and functionally engendered strains within the bone tissue provide the only feedback containing the necessary information on the relationship between current architecture and prevailing load history. The specific strain-related objectives of the adaptive modeling and remodeling response to load bearing have not been adequately defined. They appear to be different for cortical and cancellous bone and vary according to cortical location. Experiments suggest that adaptive modeling and remodeling is sensitive to dynamic but not static strain change and that the osteogenic response to a period of dynamic strain is quickly saturated but is higher when the rate of change in strain is high and the distribution of strain unusual. Presumably it is the cumulative effect of this osteogenic response to load bearing that normally maintains bone mass above that seen in disuse situations. Through their independent effects on bone cell behavior, nutritional and hormonal factors can enable, enhance, limit, or frustrate full expression of the osteogenic response to strain change. However, such systemic factors do not appear to be able to engender or successfully imitate the sustained cumulative local response to load bearing that normally maintains functionally appropriate bone mass and architecture. Experiments in vivo and in vitro suggest that in osteocytes and surface osteoblasts the almost immediate response to strain change is increased production of prostacyclin. Surface osteoblasts also produce prostaglandin E.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2026

Muscle mechanical and architectural adaptations in response to different endurance training modalities in older adults.

INTRODUCTION: This study examined the effects of various cycling endurance training modalities, matched for total workload, on muscle mechanical and architectural characteristics in older adults. METHODS: Fifty healthy participants (25 females, 59-79 yrs) were randomly assigned to five age and sex matched groups: one control and four workload-matched training groups (moderate-intensity continuous, heavy-intensity continuous, high-intensity interval, and heavy-intensity continuous in eccentric cycling). Training consisted of three weekly sessions over 8 weeks, with evaluations conducted at the beginning and end of the intervention with maximal voluntary isometric contractions at five different knee angles (90, 75, 60, 45, 30°) and maximal concentric and eccentric isokinetic contractions at five different knee angular velocities (45, 90, 150, 210, 250°/s). Maximum voluntary isometric torque (Tmax) and optimal knee angle (KAopt) were obtained from the isometric contractions; eccentric torque (Tecc) and maximum concentric knee angular velocity (Vmax) were obtained from the isokinetic contractions. The muscle architecture of vastus lateralis (VL) at rest (muscle thickness, pennation angle, and fascicle length) was investigated as well. RESULTS: No statistical differences were detected between groups or time points in VL architecture, in KAopt and in Vmax. A main effect of time was observed for Tmax (p < 0.001, η2p = 0.458) and Tecc (p = 0.002, η2p = 0.191) in all the investigated training groups. The within-group comparisons indicate significant increases in Tmax in the training groups, but not in the control group. CONCLUSIONS: Commonly applied endurance exercises improve muscle mechanical capacity (Tmax and Tecc) in older adults, with no structural (architectural) muscle remodelling, when matched for workload.

Humans↗

PubMed2026

Shared genetic architecture between major depression and intrinsic brain functional connectome organization.

BACKGROUND: Major depression (MD) is increasingly understood as a disorder characterized by widespread abnormalities in intrinsic brain functional network organization. Although both MD and brain functional connectome architecture are highly heritable, the genetic architecture underlying their relationship remains poorly characterized. METHODS: We integrated genome-wide association studies of MD with 191 ICA-based resting-state functional connectome traits to investigate their shared genetic architecture. These traits captured intrinsic connectome organization across amplitude, functional connectivity, and global connectivity domains. Cross-trait genetic analyses were used to assess pleiotropic overlap between traits. Locus-level and gene-based analyses integrating multi-omics evidence were performed to characterize the biological relevance of shared genetic signals. RESULTS: We identified significant genetic overlap between MD and 148 of 191 brain functional connectome traits. Cross-trait analyses revealed widespread shared genetic signals organized into 627 genomic loci across amplitude, functional connectivity, and global connectivity measures. Among these, 193 loci showed evidence consistent with shared causal variants based on colocalization analyses. Gene-level integration mapped these loci to 1459 protein-coding genes (390 unique genes). Multi-layer prioritization identified 17 high-confidence genes supported by convergent genomic, transcriptomic, and proteomic evidence, with enrichment in neurodevelopmental and lipid-related metabolism pathways. CONCLUSIONS: This study provides a multi-scale characterization of the shared genetic architecture between MD and intrinsic brain functional connectome organization, revealing that shared genetic signals between MD and brain functional systems are distributed across multiple functional levels and converge at the molecular level.

Connectome↗

PubMed1992

Polysomnography in newborns and young infants: sleep architecture.

Sleep architecture derived from long-term polysomnographic recordings during the first year of life is characterized by clear developmental trends against a backdrop of variability. Variability is due to differences in state definitions and data collection and analysis strategies but probably also to an intrinsic characteristic of the maturing central nervous system (functional plasticity). Changes in sleep and wakefulness probably constitute nonspecific responses to a variety of stimuli. The variability has frustrated efforts to use specific features of sleep architecture for diagnostic or prognostic purposes. At present, polysomnographic studies of sleep architecture independent from EEG and cardiorespiratory studies are not indicated for diagnosing specific medical conditions or prognoses of good/adverse outcomes. For accurate interpretation for cardio-respiratory data, however, studies of sleep and wakefulness are indispensable. Furthermore, the study of neonatal seizures, in particular the coherence of state-defining variables or the evolution of sleep morphology, may benefit from attention to sleep architecture. Initial findings from some laboratories suggest that the very feature of excessive instability, which can be measured by repetitive long-term polysomnographic monitoring, signals a poor prognosis. In addition, fragmented sleep and the evolving interrelationship between ultradian and circadian rhythms may contain useful information that has yet to be mined. The advent of computer technologies can make the clinical laboratory into a setting where both research and clinical studies contribute to an elucidation of risk for sudden infant death syndrome and sequelae of neonatal seizures.

Circadian Rhythm↗

PubMed1992

A three-dimensional architecture for a parallel processing photosensing array.

A three-dimensional architecture for a photosensing array has been developed. This silicon based architecture consists of a 10 x 10 array of photosensors with 80 microns diameter, through chip interconnects to the back side of a 500 microns thick silicon wafer. Each photosensor consists of a 300 x 300 microns pn-junction photodiode. The following processes were used to create this photosensing architecture: 1) thermomigration of aluminum pads through an n-type silicon wafer; 2) creation of pn-junction photosensors on one side of the wafer; and 3) creation of aluminum pad ohmic contacts to the thermomigrated, through chip interconnects and the substrate on the back side of the wafer. The electrical and optical characteristics of the three-dimensional architecture indicates that it should be well suited as a photosensing framework around which a "silicon retina" could be built.

Artificial Organs↗

PubMed2025

Genomic structural equation modeling elucidates the shared genetic architecture of allergic disorders.

BACKGROUND: The intricate shared genetic architecture underlying allergic disorders-including allergic asthma, atopic dermatitis, contact dermatitis, allergic rhinitis, allergic conjunctivitis, allergic urticaria, anaphylaxis, and eosinophilic esophagitis-remains incompletely characterized. METHODS: Our study employed genomic structural equation modeling (Genomic SEM) to define the common factor representing the shared genetic architecture of allergic disorders. Coupled with diverse post-GWAS analytical methods, we aimed to discover susceptible loci and investigate genetic associations with external traits. Furthermore, we explored enriched genetic pathways, cellular layers, and genomic elements, and investigated putative plasma protein biomarkers. Polygenic risk score (PRS) analyses, leveraging our integrated GWAS data, were conducted to assess chromosomal-level risk associations for allergic disorders. RESULTS: A well-fitted genomic SEM integrated GWAS data, revealing the shared genetic architecture of allergic disorders. We identified a total of 2038 genome-wide significant SNP loci (p < 5e-8), including 31 previously unreported loci. Fine-mapping of variants and gene sets pinpointed 2 causal variants and 31 candidate susceptible genes. Genetic correlation analyses further illuminated the shared genetic architecture underlying multiple traits, notably psychiatric disorders. Preliminary findings identified four putative causal plasma protein biomarkers. CONCLUSION: Notably, this study presents the first comprehensive genetic characterization of allergic disorders through a GWAS analysis of an unmeasured composite phenotype, providing novel insights into shared etiological pathways across these conditions.

Humans↗

PubMed2025

Simple scaling laws control the genetic architectures of human complex traits.

Genome-wide association studies have revealed that the genetic architectures of complex traits vary widely, including in terms of the numbers, effect sizes, and allele frequencies of significant hits. However, at present we lack a principled way of understanding the similarities and differences among traits. Here, we describe a probabilistic model that combines the effects of mutation, drift, and stabilizing selection at individual sites with a genome-scale model of phenotypic variation. In this model, the architecture of a trait arises from the distribution of selection coefficients of mutations and from two scaling parameters. We fit this model for 95 highly polygenic quantitative traits of different kinds from the UK Biobank. Notably, we infer that all these traits have fairly similar, though not identical, distributions of selection coefficients. This similarity suggests that differences in architectures of highly polygenic traits arise mainly from the two scaling parameters: the mutational target size and heritability per site, which vary by orders of magnitude among traits. When these two scale factors are accounted for, we find that the architectures of all 95 traits are very similar.

Humans↗

PubMed2026

Deconvolution of evolutionary architecture unmasks a high-risk, subclonal-rich subtype in treatment-naive small cell lung cancer.

BACKGROUND: Intratumoral heterogeneity (ITH) drives therapeutic resistance in small cell lung cancer (SCLC). However, conventional single-sample analysis has limited horizontal, cross-patient comparisons, leaving the overarching evolutionary architecture in treatment-naive tumors poorly understood. This study aims to deconvolve these architectures to identify clinically relevant evolutionary subtypes. METHODS: We analyzed whole-exome sequencing data from 41 treatment-naive SCLC patients. To overcome the cross-patient comparability bottleneck, we developed a novel probabilistic framework using a refined Gaussian Mixture Model (GMM). This standardized subclonal structures into four hierarchical strata, enabling the identification of evolutionary subtypes via unsupervised clustering. To address the scarcity of SCLC public data, prognostic concordance was robustly explored in The Cancer Genome Atlas (TCGA) lung squamous cell carcinoma (LUSC) based on shared smoking etiology, with lung adenocarcinoma (LUAD) serving as a negative control. RESULTS: The cohort robustly segregated into "Clonal-dominant" (Group 1, n=28) and "Subclonal-rich" (Group 2, n=13) subtypes. Group 1 evolution was primarily driven by tobacco signatures (SBS4). Conversely, Group 2 exhibited late-stage acquisition of a DNA mismatch repair deficiency (MMRd) signature (SBS15), fueling trace subclonal diversification. Clinically, Group 2 demonstrated a significantly lower objective response rate (ORR) to platinum-based regimens (25.0% vs. 81.3%, P=0.02). Furthermore, the Subclonal-rich architecture independently predicted inferior overall survival (OS) [adjusted hazard ratio (adj. HR) =2.93, P=0.02], driven predominantly by limited-stage disease. Cross-cancer analysis validated this histology-dependent, high-heterogeneity adverse pattern in early-stage LUSC but not in LUAD. CONCLUSIONS: This hypothesis-generating study demonstrates that a "Subclonal-rich" architecture, driven by acquired MMRd, identifies high-risk, chemo-resistant SCLC. Our GMM approach suggests that pre-existing heterogeneity may serve as a potential, histology-dependent prognostic marker that warrants prospective validation for tailoring future therapeutic regimens.

Gaussian Mixture Model (GMM)↗

PubMed1991

[Microvascular architecture of the human tongue carcinoma--a scanning electron microscopic study].

Vascular architecture of tumors in experimental animals has been studied in detail. However, the reports on architecture of the capillaries in human carcinoma in the head and neck regions are few nowadays. In this paper architecture of the blood vessels reproduced by using methacrylate casting medium in human carcinoma of the tongue was studied by scanning electron microscopy. Tortous capillaries and loop-like vessels were observed at the proliferative area of the tumor on the surface of the tongue. There were avascular zones around the vessels of the tumor characterizing irregular proliferation. The vessels of sinusoidal, tapering, distorted and disrupted characters were seen in the muscle layer of the tongue. Ruptured vessels and viable tumor-cells were observed at the areas surrounding necrotic lesions. These findings elucidated combination of various kinds of architectures of vessels in various stages of tumor-growing. Existence of the avascular area suggests that proliferation of tumor-cells proceeds before proliferation of the capillaries. Both avascular and necrotic changes in the structure might reduce the effects of anti-cancer agents.

Capillaries↗

PubMed2026

Shared genetic architecture between ADHD and intelligence varies across ADHD subtypes.

BACKGROUND: Attention-deficit/hyperactivity disorder (ADHD) is a heterogeneous neurodevelopmental condition frequently accompanied by cognitive difficulties. Although previous genetic studies have demonstrated substantial overlap between ADHD and intelligence, most have treated ADHD as a single phenotype. However, whether this shared genetic architecture differs across ADHD subtypes remains unclear. METHODS: We conducted a genome-wide cross-trait analysis integrating large-scale genome-wide association study (GWAS) datasets of overall ADHD, its subtypes-childhood ADHD, persistent ADHD, and late-diagnosed ADHD-and intelligence (total N > 300,000). Genome-wide genetic correlations, polygenic overlap, local genetic correlations, and variant-level associations between ADHD phenotypes and intelligence were evaluated to characterize their shared genetic architecture. Shared variants were identified through cross-trait enrichment analyses and subsequently mapped to genes for functional annotation and gene-set enrichment. Bidirectional associations were evaluated using two-sample Mendelian randomization with sensitivity analyses. Additional GWAS datasets were used to validate the robustness of shared loci by assessing the consistency of effect directions. RESULTS: All ADHD phenotypes showed significant negative genetic correlations with intelligence (rg ranging from -0.3442 to -0.4205). Despite these modest genome-wide correlations, cross-trait analyses revealed substantial genetic overlap, including polygenic overlap, local genetic correlations, and variant-level associations. We identified 184 loci jointly associated with ADHD traits and intelligence, including 64 novel loci, whereas no shared loci were detected for persistent ADHD under the current analysis. Functional annotation revealed biologically distinct enrichment patterns across subtypes: childhood ADHD loci were linked to early neurodevelopmental processes, while late-diagnosed ADHD loci were enriched in synapse-related and neuronal signaling pathways. Mendelian randomization analyses suggested bidirectional associations, with stronger evidence supporting a directional association from intelligence to ADHD risk. Furthermore, these shared loci showed largely consistent effect directions across additional GWAS datasets, providing support for the robustness of the findings. CONCLUSIONS: The shared genetic architecture between ADHD and intelligence varies across ADHD subtypes, highlighting distinct biological pathways underlying cognitive heterogeneity in ADHD. These findings suggest that the relationship between ADHD liability and general cognitive ability is not uniform across ADHD subtypes and may inform future research on risk stratification and early identification in child and adolescent psychiatry.

Humans↗

PubMed1976

Architecture of the marrow vasculature in three amphibian species and its significance in hematopoietic development.

Architecture of the bone marrow vasculature, particularly that of the femur, was analyzed in three amphibian species in relation to the early phylogeny of marrow hematopoiesis. A dye-injection method and histological techniques, including both serial sectioning and reconstruction methods, were used for this purpose. From these observations the following conclusions may be drawn. (1) Marrow hematopoiesis is absent from the femur of the urodelan (Triturus pyrrhogaster) and appears first in the femur of the primitive anuran (Xenopus laevis) (2) The site of primitive hematopoiesis (granulopoiesis) is the subendosteal region where the venous vascular net develops. (3) The primitive vascular architecture observed in the femur of Xenopus is characterized by the absence of a central vein. Subendosteal veins drain the blood from the bone marrow. A vein collateral to the primary artery appears in the femur of Rana catesbeiana, an advanced anuran, in which further development of both the subendosteal venous plexus and hematopoietic activity are noted. In both anura examined, the primitive blood sinuses form near the mid-shaft of the femur. The proliferation of mesenchymal elements containing dark pigment, presumably melanin, was also noted in this area. (4) The architecture of marrow vessels in Rana approaches the structure noted in mammalian bone marrow. (5) Fat tissue is observed in the urodelan bone marrow prior to the appearance of hematopoietic activity. This indicates that the formation of marrow fat is phylogenetically unrelated to the development of hematopoiesis. The present investigation on primitive hematopoiesis suggests that the development of hematopoietic activity is intimately related to the development of the marrow vasculature, particularly that of the subendosteal venous plexus. A favorable vascular arrangement may be necessary to allow active hematopoiesis.

Amphibians↗

PubMed1992

Effect of growth on architecture of rat semimembranosus lateralis muscle.

Architecture of semimembranosus lateralis muscle (SMl), an almost parallel-fibered muscle with bony origin and aponeurotic insertion of its muscle fibers, was studied in male Wistar rats of two age groups. Using photographic techniques and maximal stimulation active muscle architecture was determined at muscle optimum length. Muscle length increases were almost similar with fiber length increases (approximately 36%). Aponeurosis length increased (by 31%) as did angle of the aponeurosis with the line of pull (approximately 4 degrees). Angles of the proximal as well as distal fibers with the line of pull were unchanged. Increases in mean fiber diameter were estimated to be approximately 50%. It is likely that increased mean fiber diameter was accommodated at the bony origin by enlargement of its area. At the aponeurosis increased mean fiber diameter was accommodated by increased length of the aponeurosis as well as a change in fiber angle with the aponeurosis. This change in fiber angle proved to be different in the proximal and distal part of the aponeurosis. Under the assumption of a uniform change in fiber diameters, a gradient of length change along the aponeurosis occurs. It is concluded that growth in an almost parallel-fibered muscle with a bony attachment results in different architectural adaptations in the parts close to the bony attachment as compared to those close to the aponeurosis. This difference is due to the fact that adaptation of aponeurosis angle with the line of pull occurred, which was not the case for angle of the line of origin with the line of pull.

Animals↗