The mediation model of social status on the link between parental attachment, aggressive behavior, and psychological well-being: Evidence from two studies in Vietnamese adolescents and young adults.

Little is known about how insecure attachment affects aggressive behavior and well-being among Vietnamese youth. Using structural equation modeling, we investigate the mediating role of subjective social status (SSS) on the paths from insecure attachment to overt aggressive behavior (OAB) and psychological well-being (PW) in a sample of 1753 Vietnamese adolescents (Mage = 16.136, SD = 0.784) and test whether the results will be replicated in another sample of 601 Vietnamese young adults (Mage = 19.93, SD = 1.35). Participants complete a survey comprising demographic information, attachment styles, SSS, OAB, and PW questionnaires. Our main findings include: (a) anxious attachment positively related to OAB in both samples, (b) anxious attachment was only negatively associated with adolescents' PW, (c) avoidant attachment was positively correlated to OAB in adolescents but negatively correlated in young adults, and (d) avoidant attachment was negatively related to PW in both samples. In addition, (e) in adolescents, the mediation role of SSS was significant in all paths, but (f) SSS only mediated the link from avoidant attachment to PW of young adults. The present study suggests that aggressive behavior might not be associated with social status or attachment in the same way in adolescents compared to young adult Vietnamese samples.

Vimentin promotes collective cell migration through collagen networks via increased matrix remodeling and spheroid fluidity.

The intermediate filament (IF) protein vimentin is associated with many diseases with phenotypes of enhanced cellular migration and aggressive invasion through the extracellular matrix (ECM) of tissues, but vimentin's role in in-vivo cell migration is still largely unclear. Vimentin is important for proper cellular adhesion and force generation, which are critical to cell migration; yet the vimentin cytoskeleton also hinders the ability of cells to squeeze through small pores in ECM, resisting migration. To identify the role of vimentin in collective cell migration, we generate spheroids of wide-type and vimentin-null mouse embryonic fibroblasts (mEFs) and embed them in a 3D collagen matrix. We find that loss of vimentin significantly impairs the ability of the spheroid to collectively expand through collagen networks and remodel the collagen network. Traction force analysis reveals that vimentin null spheroids exert less contractile force than their wild-type counterparts. In addition, spheroids made of mEFs with only vimentin unit length filaments (ULFs) exhibit similar behavior as vimentin-null spheroids, suggesting filamentous vimentin is required to promote 3D collective cell migration. We find the vimentin-mediated collective cell expansion is dependent on matrix metalloproteinase (MMP) degradation of the collagen matrix. Further, 3D vertex model simulation of spheroid and embedded ECM indicates that wild-type spheroids behave more fluid-like, enabling more active pulling and reconstructing the surrounding collagen network. Altogether, these results signify that VIF plays a critical role in enhancing migratory persistence in 3D matrix environments through MMP transportation and tissue fluidity.

Vimentin supports cell polarization by enhancing centrosome function and microtubule acetylation.

Cell polarity is important for controlling cell shape, motility and cell division processes. Vimentin intermediate filaments are important for cell migration and cell polarization in mesenchymal cells and assembly of vimentin and microtubule networks is dynamically coordinated, but the precise details of how vimentin mediates cell polarity remain unclear. Here, we characterize the effects of vimentin on the structure and function of the centrosome and the stability of microtubule filaments in wild-type and vimentin-null mouse embryonic fibroblasts. We find that vimentin mediates the structure of the pericentriolar material, promotes centrosome-mediated microtubule regrowth and increases the level of stable acetylated microtubules in the cell. Loss of vimentin also impairs centrosome repositioning during cell polarization and migration processes that occur during wound closure. Our results suggest that vimentin modulates centrosome structure and function as well as microtubule network stability, which has important implications for how cells establish proper cell polarization and persistent migration.

Safety and efficacy of autologous adipose tissue-derived stem cell transplantation in aging-related low-grade inflammation patients: a single-group, open-label, phase I clinical trial.

BACKGROUND: Inflamm-aging is associated with the rate of aging and is significantly related to diseases such as Alzheimer's disease, Parkinson's disease, atherosclerosis, heart disease, and age-related degenerative diseases such as type II diabetes and osteoporosis. This study aims to evaluate the safety and efficiency of autologous adipose tissue-derived mesenchymal stem cell (AD-MSC) transplantation in aging-related low-grade inflammation patients. METHODS: This study is a single-group, open-label, phase I clinical trial in which patients treated with 2 infusions (100 million cells i.v) of autologous AD-MSCs were initially evaluated in 12 inflamm-aging patients who concurrently had highly proinflammatory cytokines and 2 of the following 3 diseases: diabetes, dyslipidemia, and obesity. The treatment effects were evaluated based on plasma cytokines. RESULTS: During the study's follow-up period, no adverse effects were observed in AD-MSC injection patients. Compared to baseline (D-44), the inflammatory cytokines IL-1α, IL-1ß, IL-8, IL-6, and TNF-α were significantly reduced after 180 days (D180) of MSC infusion. IL-4/IL-10 at 90 days (D90) and IL-2/IL-10 at D180 increased, reversing the imbalance between proinflammatory and inflammatory ratios in the patients. CONCLUSION: AD-MSCs represent a potential intervention to prevent age-related inflammation in patients. TRIAL REGISTRATION: ClinicalTrials.gov number is NCT05827757, first registered on 13th Oct 2020.

Enhanced extracellular matrix remodeling due to embedded spheroid fluidization.

Tumor spheroids are in vitro three-dimensional, cellular collectives consisting of cancerous cells. Embedding these spheroids in an in vitro fibrous environment, such as a collagen network, to mimic the extracellular matrix (ECM) provides an essential platform to quantitatively investigate the biophysical mechanisms leading to tumor invasion of the ECM. To understand the mechanical interplay between tumor spheroids and the ECM, we computationally construct and study a three-dimensional vertex model for a tumor spheroid that is mechanically coupled to a cross-linked network of fibers. In such a vertex model, cells are represented as deformable polyhedrons that share faces. Some fraction of the boundary faces of the tumor spheroid contain linker springs connecting the center of the boundary face to the nearest node in the fiber network. As these linker springs actively contract, the fiber network remodels. By toggling between fluid-like and solid-like spheroids via changing the dimensionless cell shape index, we find that the spheroid rheology affects the remodeling of the fiber network. More precisely, fluid-like spheroids displace the fiber network more on average near the vicinity of the spheroid than solid-like spheroids. We also find more densification of the fiber network near the spheroid for the fluid-like spheroids. These spheroid rheology-dependent effects are the result of cellular motility due to active cellular rearrangements that emerge over time in the fluid-like spheroids to generate spheroid shape fluctuations. Our results uncover intricate morphological-mechanical interplay between an embedded spheroid and its surrounding fiber network with both spheroid contractile strength and spheroid shape fluctuations playing important roles in the pre-invasion stages of tumor invasion.

153Sm-labeled Fe3O4@lapatinib nanoparticles as a potential therapeutic agent for breast cancer: synthesis, quality control, and in vivo evaluation.

The present study introduces Fe3O4-coated lapatinib-labeled 153Sm nanoparticles (denoted as Fe3O4@lapatinib-153Sm) as a promising avenue for advancing breast cancer treatment. The radiolabeled nanoparticles combine various attributes, offering enhanced therapeutic precision. The integration of lapatinib confers therapeutic effects and targeted delivery. The inherent magnetic characteristics of Fe3O4 nanoparticles contribute to improved imaging contrast and targeted localization. Incorporating the gamma-emitting 153Sm isotope permits single-photon emission computed tomography imaging and radiation dose evaluation, while its beta-emitting nature ensures targeted cancer cell eradication. The synthesis of Fe3O4@lapatinib-153Sm was meticulously optimized by investigating the effects of parameters on radiolabeling efficiency. Physicochemical attributes were scrutinized using several analytical techniques. In-depth in vivo assessment evaluated the biocompatibility, toxicity, and biodistribution in a murine model, illuminating clinical utility. Optimal conditions (153SmCl3 concentration of 10 mCi mL-1, pH 7.4, a reaction time of 30 min, and a temperature of 25 °C) achieved >99% labeling efficiency and radiochemical purity. The TEM analysis indicated that the diameter of Fe3O4@lapatinib-153Sm nanoparticles ranged from 10 to 40 nm. Vibrating-sample magnetometry verified their superparamagnetic behaviour with a saturation magnetization of 41.4 emu g-1. The synthesized radiopharmaceutical exhibited high sterility and in vitro stability. Acute toxicity studies showed the mild effects of Fe3O4@lapatinib-153Sm at a dose of 20 mCi kg-1, with no observed mortality. Notably, lesions from Fe3O4@lapatinib-153Sm use recovered naturally over time. Radiation doses below 20 mCi kg-1 were recommended for clinical trials. The biodistribution study in BT474 xenograft mice revealed rapid clearance of Fe3O4@lapatinib-153Sm within 48 h. Significant accumulation occurred in the liver, spleen, and tumor tissue, while minimal accumulation was found in other tissues. Future steps involve studying biocorona formation and therapeutic efficacy on tumour models, refining its clinical potential.

Implication of transcription factor FOXD2 dysfunction in syndromic congenital anomalies of the kidney and urinary tract (CAKUT).

Congenital anomalies of the kidney and urinary tract (CAKUT) are the predominant cause for chronic kidney disease below age 30 years. Many monogenic forms have been discovered due to comprehensive genetic testing like exome sequencing. However, disease-causing variants in known disease-associated genes only explain a proportion of cases. Here, we aim to unravel underlying molecular mechanisms of syndromic CAKUT in three unrelated multiplex families with presumed autosomal recessive inheritance. Exome sequencing in the index individuals revealed three different rare homozygous variants in FOXD2, encoding a transcription factor not previously implicated in CAKUT in humans: a frameshift in the Arabic and a missense variant each in the Turkish and the Israeli family with segregation patterns consistent with autosomal recessive inheritance. CRISPR/Cas9-derived Foxd2 knockout mice presented with a bilateral dilated kidney pelvis accompanied by atrophy of the kidney papilla and mandibular, ophthalmologic, and behavioral anomalies, recapitulating the human phenotype. In a complementary approach to study pathomechanisms of FOXD2-dysfunction-mediated developmental kidney defects, we generated CRISPR/Cas9-mediated knockout of Foxd2 in ureteric bud-induced mouse metanephric mesenchyme cells. Transcriptomic analyses revealed enrichment of numerous differentially expressed genes important for kidney/urogenital development, including Pax2 and Wnt4 as well as gene expression changes indicating a shift toward a stromal cell identity. Histology of Foxd2 knockout mouse kidneys confirmed increased fibrosis. Further, genome-wide association studies suggest that FOXD2 could play a role for maintenance of podocyte integrity during adulthood. Thus, our studies help in genetic diagnostics of monogenic CAKUT and in understanding of monogenic and multifactorial kidney diseases.

Safety assessment, radioiodination and preclinical evaluation of antinuclear antibody as novel medication for prostate cancer in mouse xenograft model.

This study aims to provide in vitro and in vivo data to support the utilization of antinuclear antibodies (ANAs) as novel tools for the diagnosis and treatment of prostate cancers. The hematological, biochemical, and histological toxicities of ANAs were assessed at the doses of 5 and 50 µg per mouse. Radiolabeling study was then conducted with ANA and 131I using the chloramine T method, and the biodistribution and treatment efficacy were subsequently investigated in a PC3 xenograft model. No changes in clinical behavior or signs of intoxication, necrosis, or malignancy were observed in ANA-treated mice. 131I-ANA was obtained in very high yield and radiochemical purity, at 94.97 ± 0.98% and 98.56 ± 0.29%, respectively. They achieved immunoreactivity fraction of 0.841 ± 0.17% with PC-3 cells. Levels of radiolabeled ANAs were 1.15-10.14 times higher in tumor tissues than in other examined organs at 24 h post-injection. The tumor growth inhibition rates were 28.33 ± 5.01% in PC3 xenografts mice treated with 131I-ANAs compared with controls and a nearly twofold improvement in median survival was observed. These results demonstrate that radioimmunotherapy of radiolabeled natural ANAs may be an effective treatment for prostate tumors.

A novel diphenylbutenoid-type compound from the rhizomes of Zingiber montanum (J.Koenig) Link ex A.Dietr. (Zingiberaceae).

From the EtOAc-soluble extract of the rhizomes of Zingiber montanum (J.Koenig) Link ex A.Dietr., a novel diphenylbutenoid, montadinin A (1) and a previously unreported phenylbutenoid compound, 1-(3,4-dimethoxyphenyl)but-3-en-2-ol (7), in natural source were isolated. Additionally, seven known phenylbutenoids were also identified. The structures of all compounds were elucidated through NMR spectroscopic interpretation. Compounds cis-3-(3,4-dimethoxyphenyl)-4-[(E)-3,4-dimethoxystyryl]cyclohex-1-ene (2), cis-4-[(E)-3,4-dimethoxystyryl]-3-(2,4,5-trimethoxyphenyl)cyclohex-1-ene (3), trans-3-(3,4,-dimethoxyphenyl)-4-[(E)-2,4,5-trimethoxystyryl]cyclohex-1-ene (5), and cis-3-(3,4-dimethoxyphenyl)-4-[(Z)-2,4,5-trimethoxylstyryl]cyclohex-1-ene (6) showed weak cytotoxicity against HepG2 cells with IC50 values of 122.9, 127.3, 257.5, and 168.5 µM, respectively.

Extracellular vimentin is sufficient to promote cell attachment, spreading, and motility by a mechanism involving N-acetyl glucosamine-containing structures.

Vimentin intermediate filaments form part of the cytoskeleton of mesenchymal cells, but under pathological conditions often associated with inflammation, vimentin filaments depolymerize as the result of phosphorylation or citrullination, and vimentin oligomers are secreted or released into the extracellular environment. In the extracellular space, vimentin can bind surfaces of cells and the extracellular matrix, and the interaction between extracellular vimentin and cells can trigger changes in cellular functions, such as activation of fibroblasts to a fibrotic phenotype. The mechanism by which extracellular vimentin binds external cell membranes and whether vimentin alone can act as an adhesive anchor for cells is largely uncharacterized. Here, we show that various cell types (normal and vimentin null fibroblasts, mesenchymal stem cells, and A549 lung carcinoma cells) attach to and spread on polyacrylamide hydrogel substrates covalently linked to vimentin. Using traction force microscopy and spheroid expansion assays, we characterize how different cell types respond to extracellular vimentin. Cell attachment to and spreading on vimentin-coated surfaces is inhibited by hyaluronic acid degrading enzymes, hyaluronic acid synthase inhibitors, soluble heparin or N-acetyl glucosamine, all of which are treatments that have little or no effect on the same cell types binding to collagen-coated hydrogels. These studies highlight the effectiveness of substrate-bound vimentin as a ligand for cells and suggest that carbohydrate structures, including the glycocalyx and glycosylated cell surface proteins that contain N-acetyl glucosamine, form a novel class of adhesion receptors for extracellular vimentin that can either directly support cell adhesion to a substrate or fine-tune the glycocalyx adhesive properties.

Exploring the Mechanism of Subjective Social Status on Compulsive Shopping Behavior: A Moderated Mediation Model of Self-compassion and Depression.

The present study aimed to explore the mediating role of depression in the relationship between subjective social status (SSS) and compulsive shopping behavior (CSB) and whether self-compassion (SC) played a moderating role in this model. The study was designed based on the cross-sectional method. The final sample includes 664 Vietnamese adults (Mage = 21.95, SD = 5.681 years). Participants completed an online survey, including questionnaires about SSS, CSB, depression, SC, and basic demographic information. First, the study results showed that SSS did not directly affect CSB (p > .05, 95% CI includes zero). Second, a mediating role of depression and a moderating role of SC in the research model was discovered (p < .001, 95% CI does not contain zero). Results indicated that individuals with a higher SSS experienced lower depression. Moreover, during a depressive episode, having a higher level of SC increases CSB. The study highlighted meaningful recommendations to promote consumers' mental health and healthy shopping behaviors.

Autophagy Inhibitor Chloroquine Downmodulates Hepatic Stellate Cell Activation and Liver Damage in Bile-Duct-Ligated Mice.

Hepatic stellate cell (HSC) activation via the autophagy pathway is a critical factor in liver fibrogenesis. This study tests the hypothesis that chloroquine (CQ) treatment can prevent autophagy and HSC activation in vitro and in vivo in bile-duct-ligated (BDL) mice. Sham-operated and BDL mice were treated with either PBS or CQ in two 60 mg/kg doses the day (D) before and after surgery. On day 2 (2D), HSCs were isolated, and their biological activities were evaluated by measuring intracellular lipid content, α-sma/collagen, and expression of autophagy lc3, sqstm1/p62 markers. The treatment efficacy on liver function was evaluated with serum albumin, transaminases (AST/ALT), and hepatic histology. Primary HSCs were treated in vitro for 24 h with CQ at 0, 2.5, 5, 10, 30, and 50 µM. Autophagy and HSC activation were assessed after 2D of treatment. CQ treatment improved serum AST/ALT, albumin, and bile duct proliferation in 2D BDL mice. This is associated with a suppression of HSC activation, shown by higher HSC lipid content and collagen I staining, along with the blockage of HSC autophagy indicated by an increase in p62 level and reduction in lc3 staining. CQ 5 µM inhibited autophagy in primary HSCs in vitro by increasing p62 and lc3 accumulation, thereby suppressing their in vitro activation. The autophagy inhibitor CQ reduced HSC activation in vitro and in vivo. CQ improved liver function and reduced liver injury in BDL mice.

Implication of FOXD2 dysfunction in syndromic congenital anomalies of the kidney and urinary tract (CAKUT).

Background: Congenital anomalies of the kidney and urinary tract (CAKUT) are the predominant cause for chronic kidney disease below 30 years of age. Many monogenic forms have been discovered mainly due to comprehensive genetic testing like exome sequencing (ES). However, disease-causing variants in known disease-associated genes still only explain a proportion of cases. Aim of this study was to unravel the underlying molecular mechanism of syndromic CAKUT in two multiplex families with presumed autosomal recessive inheritance. Methods and Results: ES in the index individuals revealed two different rare homozygous variants in FOXD2, a transcription factor not previously implicated in CAKUT in humans: a frameshift in family 1 and a missense variant in family 2 with family segregation patterns consistent with autosomal-recessive inheritance. CRISPR/Cas9-derived Foxd2 knock-out (KO) mice presented with bilateral dilated renal pelvis accompanied by renal papilla atrophy while extrarenal features included mandibular, ophthalmologic, and behavioral anomalies, recapitulating the phenotype of humans with FOXD2 dysfunction. To study the pathomechanism of FOXD2-dysfunction-mediated developmental renal defects, in a complementary approach, we generated CRISPR/Cas9-mediated KO of Foxd2 in ureteric-bud-induced mouse metanephric mesenchyme cells. Transcriptomic analyses revealed enrichment of numerous differentially expressed genes important in renal/urogenital development, including Pax2 and Wnt4 as well as gene expression changes indicating a cell identity shift towards a stromal cell identity. Histology of Foxd2 KO mouse kidneys confirmed increased fibrosis. Further, GWAS data (genome-wide association studies) suggests that FOXD2 could play a role for maintenance of podocyte integrity during adulthood. Conclusions: In summary, our data implicate that FOXD2 dysfunction is a very rare cause of autosomal recessive syndromic CAKUT and suggest disturbances of the PAX2-WNT4 cell signaling axis contribute to this phenotype.

Vimentin supports cell polarization by enhancing centrosome function and microtubule acetylation.

Cell polarity is important for controlling cell shape, motility, and cell division processes. Vimentin intermediate filaments are necessary for proper polarization of migrating fibroblasts and assembly of vimentin and microtubule networks is dynamically coordinated, but the precise details of how vimentin mediates cell polarity remain unclear. Here, we characterize the effects of vimentin on the structure and function of the centrosome and the stability of microtubule filaments in wild-type and vimentin-null mouse embryonic fibroblasts (mEFs). We find that vimentin mediates the structure of the pericentrosomal material, promotes centrosome-mediated microtubule regrowth, and increases the level of stable acetylated microtubules in the cell. Loss of vimentin also impairs centrosome repositioning during cell polarization and migration processes that occur during wound closure. Our results suggest that vimentin modulates centrosome structure and function as well as microtubule network stability, which has important implications for how cells establish proper cell polarization and persistent migration.

Dynamic remodeling of fiber networks with stiff inclusions under compressive loading.

The ability of tissues to sustain and withstand mechanical stress is critical to tissue development and healthy tissue maintenance. The mechanical properties of tissues are typically considered to be dominated by the fibrous extracellular matrix (ECM) component of tissues. Fiber network mechanics can capture certain mechanical features of tissues, such as shear strain stiffening, but is insufficient in describing the compressive response of certain tissues and blood clots that are rich in extracellular matrix. To understand the mechanical response of tissues, we employ a contemporary mechanical model, a fibrous network of fibrin embedded with inert bead inclusions that preserve the volume-conserving constraints of cells in tissues. Combining bulk mechanical rheology and a custom imaging device, we show that the presence of inclusions alters the local dynamic remodeling of the networks undergoing uniaxial compressive strains and demonstrate non-affine correlated motion within a fiber-bead network, predicted to stretch fibers in the network and lead to the ability of the network to stiffen under compression, a key feature of real tissues. These findings have important implications for understanding how local structural properties of cells and ECM fibers impact the bulk mechanical response of real tissues. STATEMENT OF SIGNIFICANCE: To understand why real tissue stiffens under compression, we study a model tissue system which also stiffens: a fibrin network embedded with stiff beads. We design a device that images compression of both fiber and fiber-bead networks. Distinct from previous imaging studies, this setup can dynamically capture network deformation on scales larger than single fibers. From the videos, we see fluid flow and network remodeling are both critical to compression behavior. The fiber-bead network has faster fluid flow, reduced network recovery, and correlated motion during network relaxation. We hypothesize that the beads hinder network relaxation of stretched fibers, thus retaining the applied stress and exhibiting stiffening. Our findings reveal important details for modeling tissue mechanics towards optimizing healthcare.

Single-cell RNA sequencing analysis identifies one subpopulation of endothelial cells that proliferates and another that undergoes the endothelial-mesenchymal transition in regenerating pig hearts.

Background: In our previous work, we demonstrated that when newborn pigs undergo apical resection (AR) on postnatal day 1 (P1), the animals' hearts were completely recover from a myocardial infarction (MI) that occurs on postnatal day 28 (P28); single-nucleus RNA sequencing (snRNAseq) data suggested that this recovery was achieved by regeneration of pig cardiomyocyte subpopulations in response to MI. However, coronary vasculature also has a key role in promoting cardiac repair. Method: Thus, in this report, we used autoencoder algorithms to analyze snRNAseq data from endothelial cells (ECs) in the hearts of the same animals. Main results: Our results identified five EC clusters, three composed of vascular ECs (VEC1-3) and two containing lymphatic ECs (LEC1-2). Cells from VEC1 expressed elevated levels of each of five cell-cyclespecific markers (Aurora Kinase B [AURKB], Marker of Proliferation Ki-67 [MKI67], Inner Centromere Protein [INCENP], Survivin [BIRC5], and Borealin [CDCA8]), as well as a number of transcription factors that promote EC proliferation, while (VEC3 was enriched for genes that regulate intercellular junctions, participate in transforming growth factor ß (TGFß), bone morphogenic protein (BMP) signaling, and promote the endothelial mesenchymal transition (EndMT). The remaining VEC2 did not appear to participate directly in the angiogenic response to MI, but trajectory analyses indicated that it may serve as a reservoir for the generation of VEC1 and VEC3 ECs in response to MI. Notably, only the VEC3 cluster was more populous in regenerating (i.e., ARP1MIP28) than non-regenerating (i.e., MIP28) hearts during the 1-week period after MI induction, which suggests that further investigation of the VEC3 cluster could identify new targets for improving myocardial recovery after MI. Histological analysis of KI67 and EndMT marker PDGFRA demonstrated that while the expression of proliferation of endothelial cells was not significantly different, expression of EndMT markers was significantly higher among endothelial cells of ARP1MIP28 hearts compared to MIP28 hearts, which were consistent with snRNAseq analysis of clusters VEC1 and VEC3. Furthermore, upregulated secrete genes by VEC3 may promote cardiomyocyte proliferation via the Pi3k-Akt and ERBB signaling pathways, which directly contribute to cardiac muscle regeneration. Conclusion: In regenerative heart, endothelial cells may express EndMT markers, and this process could contribute to regeneration via a endothelial-cardiomyocyte crosstalk that supports cardiomyocyte proliferation.

Mechanobiology as a tool for addressing the genotype-to-phenotype problem in microbiology.

The central hypothesis of the genotype-phenotype relationship is that the phenotype of a developing organism (i.e., its set of observable attributes) depends on its genome and the environment. However, as we learn more about the genetics and biochemistry of living systems, our understanding does not fully extend to the complex multiscale nature of how cells move, interact, and organize; this gap in understanding is referred to as the genotype-to-phenotype problem. The physics of soft matter sets the background on which living organisms evolved, and the cell environment is a strong determinant of cell phenotype. This inevitably leads to challenges as the full function of many genes, and the diversity of cellular behaviors cannot be assessed without wide screens of environmental conditions. Cellular mechanobiology is an emerging field that provides methodologies to understand how cells integrate chemical and physical environmental stress and signals, and how they are transduced to control cell function. Biofilm forming bacteria represent an attractive model because they are fast growing, genetically malleable and can display sophisticated self-organizing developmental behaviors similar to those found in higher organisms. Here, we propose mechanobiology as a new area of study in prokaryotic systems and describe its potential for unveiling new links between an organism's genome and phenome.

Investigating Stable and Dynamic Aspects of the Vietnamese Self-Compassion Scale using Generalisability Theory.

Objectives: Evaluating comprehensive reliability of the Vietnamese Self-Compassion Scale (VSCS) and its ability to distinguish between trait (stable) vs state (dynamic) aspects of self-compassion using Generalisability Theory (G-Theory) is necessary. This investigation contributes to both reliability and validity of research that uses the VSCS to measure self-compassion in Vietnamese adults. Methods: In a sample of 155 Vietnamese adults who completed the VSCS at three occasions that were each 2 weeks apart, a G-study was conducted to measure reliability and trait vs state aspects of each VSCS subscale and the short-form VSCS, and a D-study was conducted to examine the effects of removing subscales on overall scale reliability as well as evaluate trait vs state aspects of each item. Results: With G-coefficients of 0.93-0.98, both the complete and short-form VSCS (VSCS-SF) demonstrated excellent reliability in measuring trait self-compassion. Three of the six subscales-self-judgement, mindfulness, and kindness-also demonstrated excellent reliability, with G-coefficients of 0.82-0.85. Eighteen of the 26 items measured trait more than state. The remaining eight items reflected a mixture of trait and state, but this did not affect overall reliability. Conclusions: This study indicated that the VSCS, VSCS-SF, and three VSCS subscales reliably measured trait self-compassion, with scores generalisable across the Vietnamese population and occasions. Thus, overall self-compassion levels remained stable over time, which is useful for evaluating the effectiveness of an intervention because significant changes of self-compassion are likely to be long-lasting. Supplementary Information: The online version contains supplementary material available at 10.1007/s12671-022-01950-3.

Structural Characterization of Mannoglucan Isolated from Ophiocordyceps sobolifera and Its Antioxidant Activities.

A novel polysaccharide structure (PS-T80) was collected from Ophiocordyceps sobolifera biomass and characterized via a combination of chemical and spectral analyses. Employing high-performance gel permeation chromatography (HPGPC), the average molecular weight is proven to be 7.4 × 104 Da. Furthermore, a sugar composition analysis of the obtained polysaccharide suggests two main sugars, ß-d-glucose and α-d-mannose, at a molar ratio of 2:1, respectively, in the backbone. The structure analysis unveils that PS-T80 is a mannoglucan, possessing the repeating unit of [→3)-ß-d-Glcp-(1 → 3)-α-d-Manp-(1 → 3)-ß-d-Glcp-(1→] n . Such a configuration could be considered a novel polysaccharide. Impressively, in vitro antioxidant tests revealed that PS-T80 has a promising antioxidant activity. These results demonstrate that the obtained PS is a potential bioactive material for biomedical applications.

Design synthesis of Y-90 glass microspheres and study of their therapeutic effects on mouse liver cancer cell line Hep3B.

In this article, a system for synthesizing Y-90 glass microspheres (Y-90-GM) was successfully designed in the Da Lat nuclear reactor (Vietnam), and the therapeutic effects of Y-90-GM on mice liver cancer cell line Hep3B were studied. The effects of synthesis factors, including heating time, heating temperature, gas flow rate, sample conduit length and diameter, were investigated to establish the optimal parameters. The size and shape of Y-90-GM were checked by field emission scanning electron microscope, and the radioactivity measurement was performed on a dosimeter. The results indicated that the optimal conditions for the synthesis of Y-90-GM were determined as the heating temperature of 1600 °C, heating time of 2 h, conduit length and diameter of 50 cm and 3.6 cm, and gas/oxygen flow rate of 15 mph. The Y-90-GM samples obtained at the optimal parameters have a size of 18-30 µm with a density of 3.53 g cm-3 and a specific radioactivity of 630 mCi g-1. The results of the therapeutic study on mice liver cancer cell line Hep3B showed that after two weeks of treatment with Y-90-GM (1mCi/mouse), the tumor volume was reduced by about 30.7% and after 3 consecutive treatment cycles, the liver cancer tumor was completely reduced. It was demonstrated that Y-90-GM is promising radiopharmaceuticals in the treatment of liver cancer by the radioembolization method.