A chemo-mechanical model for describing sorption hysteresis in a glassy polyurethane.

Hysteretic sorption and desorption of water is observed from 0 to 95% relative humidity and 298-333 K on a glassy polyurethane foam. It is postulated that sorption-induced swelling of the glassy polyurethane increases the concentration of accessible hydrogen-bonding adsorption sites for water. The accessibility of sites is kinetically controlled due to the restricted thermal motions of chains in the glassy polymer, causing a difference in accessible site concentrations during sorption and desorption. This discrepancy leads to hysteresis in the sorbed concentrations of water. A coupled chemo-mechanical model relating volumetric strain, adsorption site concentration, and sorbed water concentration is employed to describe water sorption hysteresis in the glassy polyurethane. This model not only describes the final mass uptake for each relative humidity step, but also captures the dynamics of water uptake, which exhibit diffusion and relaxation rate-controlled regimes.

Upregulation of circRNA_0023685 promotes gastric cancer progression via a circRNA-miRNA-mRNA interaction network.

Circular RNAs (circRNAs) have been extensively studied for their critical roles as noncoding RNAs (ncRNAs) in gastric cancer (GC). In this study, we focused on the expression, function and molecular mechanism of circRNA_0023685 in gastric cancer (GC) to provide new ways for the diagnosis and treatment of GC. Firstly, a novel differentially expressed circRNA, circRNA_0023685, was identified, and its differential expression in GC plasma, tissue, and cell lines was further verified by RT-qPCR. Next, circRNA_0023685 was verified to promote the proliferation, migration and apoptosis of GC cells in vitro. CircRNA_0023685 was also proved to enhance the growth of GC tumors in xenograft models. Finally, for excavating the mechanism to promote GC, downstream microRNAs (miRNAs) and mRNAs were screened by bioinformatics analyses. After intersecting the target genes and genes enriched in GO analysis, a circRNA competing endogenous RNAs (ceRNAs) network was built. A protein-protein interaction (PPI) network was then constructed to find the candidate gene, APP. Our study confirmed that the highly expressed circRNA_0023685 could promote GC, which provided a new clinical diagnostic biomarker and therapeutic target for GC.

Exploring the challenge of early gastric cancer diagnostic AI system face in multiple centers and its potential solutions.

BACKGROUND: Artificial intelligence (AI) performed variously among test sets with different diversity due to sample selection bias, which can be stumbling block for AI applications. We previously tested AI named ENDOANGEL, diagnosing early gastric cancer (EGC) on single-center videos in man-machine competition. We aimed to re-test ENDOANGEL on multi-center videos to explore challenges applying AI in multiple centers, then upgrade ENDOANGEL and explore solutions to the challenge. METHODS: ENDOANGEL was re-tested on multi-center videos retrospectively collected from 12 institutions and compared with performance in previously reported single-center videos. We then upgraded ENDOANGEL to ENDOANGEL-2022 with more training samples and novel algorithms and conducted competition between ENDOANGEL-2022 and endoscopists. ENDOANGEL-2022 was then tested on single-center videos and compared with performance in multi-center videos; the two AI systems were also compared with each other and endoscopists. RESULTS: Forty-six EGCs and 54 non-cancers were included in multi-center video cohort. On diagnosing EGCs, compared with single-center videos, ENDOANGEL showed stable sensitivity (97.83% vs. 100.00%) while sharply decreased specificity (61.11% vs. 82.54%); ENDOANGEL-2022 showed similar tendency while achieving significantly higher specificity (79.63%, p < 0.01) making fewer mistakes on typical lesions than ENDOANGEL. On detecting gastric neoplasms, both AI showed stable sensitivity while sharply decreased specificity. Nevertheless, both AI outperformed endoscopists in the two competitions. CONCLUSIONS: Great increase of false positives is a prominent challenge for applying EGC diagnostic AI in multiple centers due to high heterogeneity of negative cases. Optimizing AI by adding samples and using novel algorithms is promising to overcome this challenge.

Acetylation coordinates the crosstalk between carbon metabolism and ammonium assimilation in Salmonella enterica.

Enteric bacteria use up to 15% of their cellular energy for ammonium assimilation via glutamine synthetase (GS)/glutamate synthase (GOGAT) and glutamate dehydrogenase (GDH) in response to varying ammonium availability. However, the sensory mechanisms for effective and appropriate coordination between carbon metabolism and ammonium assimilation have not been fully elucidated. Here, we report that in Salmonella enterica, carbon metabolism coordinates the activities of GS/GDH via functionally reversible protein lysine acetylation. Glucose promotes Pat acetyltransferase-mediated acetylation and activation of adenylylated GS. Simultaneously, glucose induces GDH acetylation to inactivate the enzyme by impeding its catalytic centre, which is reversed upon GDH deacetylation by deacetylase CobB. Molecular dynamics (MD) simulations indicate that adenylylation is required for acetylation-dependent activation of GS. We show that acetylation and deacetylation occur within minutes of "glucose shock" to promptly adapt to ammonium/carbon variation and finely balance glutamine/glutamate synthesis. Finally, in a mouse infection model, reduced S. enterica growth caused by the expression of adenylylation-mimetic GS is rescued by acetylation-mimicking mutations. Thus, glucose-driven acetylation integrates signals from ammonium assimilation and carbon metabolism to fine-tune bacterial growth control.

CircRNA DICAR as a novel endogenous regulator for diabetic cardiomyopathy and diabetic pyroptosis of cardiomyocytes.

In this study, we identified that a conserved circular RNA (circRNA) DICAR, which was downregulated in diabetic mouse hearts. DICAR had an inhibitory effect on diabetic cardiomyopathy (DCM), as the spontaneous cardiac dysfunction, cardiac cell hypertrophy, and cardiac fibrosis occurred in DICAR deficiency (DICAR+/-) mice, whereas the DCM was alleviated in DICAR-overexpressed DICARTg mice. At the cellular level, we found that overexpression of DICAR inhibited, but knockdown of DICAR enhanced the diabetic cardiomyocyte pyroptosis. At the molecular level, we identified that DICAR-VCP-Med12 degradation could be the underlying molecular mechanism in DICAR-mediated effects. The synthesized DICAR junction part (DICAR-JP) exhibited a similar effect to the entire DICAR. In addition, the expression of DICAR in circulating blood cells and plasma from diabetic patients was lower than that from health controls, which was consistent with the decreased DICAR expression in diabetic hearts. DICAR and the synthesized DICAR-JP may be drug candidates for DCM.

Predictive value of ferroptosis-related biomarkers for diabetic kidney disease: a prospective observational study.

AIMS: To explore the predictive value of ferroptosis-related (FR) biomarkers for diabetic kidney disease (DKD) in patients with type 2 diabetes mellitus (T2DM). METHODS: This prospective observational study enrolled patients with T2DM at the Second Hospital of Jilin University between December 2021 and March 2022. DKD was measured by the urinary albumin-to-creatinine ratio. Receiver operating characteristic curve (ROC) analysis was performed to assess the predictive value of ferroptosis-related biomarkers for DKD.The risk factors for massive proteinuria were performed by multivariable logistic regression analysis. RESULTS: Finally, 118 patients (53.0 ± 12.2 years, 76 males) were enrolled, 52 of them without DKD (had normal proteinuria), while 66 with DKD. (Forty-one had microproteinuria, and 25 had massive proteinuria.) FR biomarkers, including acyl-CoA synthase long chain family member 4 (ACSL4), malondialdehyde (MDA), and reactive oxygen species (ROS), were significantly higher in the massive proteinuria group than in the other groups, while glutathione peroxidase 4 (GPX4) was significantly lower (all P < 0.05). The area under the ROC of the combination of GPX4, ACSL4, MDA, and ROS for predicting DKD was 0.804 (P < 0.001). Additionally, multivariate logistic regression analysis showed that the course of disease and ferritin levels were independent risk factors for massive proteinuria, while high serum iron, transferrin, and GPX4 levels were independent protective factors for massive proteinuria in patients with T2DM (all P < 0.05). CONCLUSIONS: The GPX4, ACSL4, MDA, and ROS combination might have a good predictive value for DKD. Additionally, the course of disease, ferritin levels, serum iron, transferrin, and GPX4 were independently associated with massive proteinuria.

Muse cells decrease the neuroinflammatory response by modulating the proportion of M1 and M2 microglia in vitro.

Neuroinflammation hinders repair of the central nervous system (CNS). Stem cell transplantation is a very promising approach for treatment of CNS injuries. However, it is difficult to select seed cells that can both facilitate nerve regeneration and improve the microenvironment in the CNS. In this study, we isolated multilineage-differentiating stress-enduring (Muse) cells from bone marrow mesenchymal stem cells. We explored the anti-inflammatory effect and mechanism of Muse cells in vitro by coculture of Muse cells with lipopolysaccharide-stimulated microglia. Our results showed that Muse cells effectively reduced the transcription and secretion of tumor necrosis factor α and interleukin-1ß and increased the expression of transforming growth factor-ß and interleukin-10 in microglia. In addition, Muse cells decreased the number of M1 microglia and increased the proportion of M2 microglia in an inflammatory environment more effectively than bone marrow mesenchymal stem cells. We also show that Muse cells inhibited the protein expression of toll-like receptor 4 (TLR4) and myeloid differentiation primary response protein (MyD88) and inhibited the expression of the phosphorylated forms of transcription factor p65, nuclear factor (NF)-κB inhibitor alpha, and p38 mitogen-activated protein kinase (MAPK) in microglia. Therefore, we suggest Muse cells cause antineuroinflammatory effects by inhibition of the TLR4/MyD88/NF-κB and p38 MAPK signaling pathways in microglia. Our results shed light on the function of Muse cells in relation to CNS diseases and provide insight into the selection of seed cells.

Never-in-Mitosis A-Related Kinase 8 (NEK8) Regulates Adipogenesis, Glucose Homeostasis, and Obesity.

Background: Adipogenesis is a complex biological process and the leading main cause of obesity. We evaluated the role of never-in-mitosis A-related kinase 8 (NEK8) in adipocyte development and insulin sensitivity in the present study. Methods: NEK8 expression was manipulated using a specific shRNA or the NEK8-full-length expressing recombinant plasmids. The interaction between NEK8 and Tafazzin (TAZ, an oncogenic transcriptional regulator) was examined by Co-immunoprecipitation (Co-IP) and confocal immunofluorescence staining. Western blot assay was performed to determine the protein expression. The in vivo role of NEK8 was explored in a mouse model of high-fat diet- (HFD-) induced insulin resistance. Results: During adipogenesis, the expression of NEK8 was elevated while TAZ was downregulated. Overexpression of NEK8 promoted lipid accumulation and expression of markers for adipocyte differentiation. Mechanically, NEK8 interacted with TAZ and suppressed its expression in adipocytes. Functionally, lentiviral-mediated NEK8 inhibition ameliorates HFD-induced insulin resistance in adipocytes. Conclusion: These findings suggest that NEK8 plays a critical role in adipocyte proliferation, providing novel insight into the link between NEK8 and type 2 diabetes- (T2DM-) related obesity.

Evaluation of subsurface transport processes of delayed gas signatures applicable to underground nuclear explosions.

Radioactive gas signatures from underground nuclear explosions (UNEs) result from gas-migration processes occurring in the subsurface. The processes considered in this study either drive or retard upward migration of gases from the detonation cavity. The relative importance of these processes is evaluated by simulating subsurface transport in a dual-permeability medium for the multi-tracer Noble Gas Migration Experiment (NGME) originally intended to study some aspects of transport from a UNE. For this experiment, relevant driving processes include weak two-phase convection driven by the geothermal gradient, over pressuring of the detonation cavity, and barometric pumping while gas sorption, dissolution, radioactive decay, and usually diffusion represent retarding processes. From deterministic simulations we found that over-pressuring of the post-detonation chimney coupled with barometric pumping produced a synergistic effect amplifying the tracer-gas reaching the surface. Bounding simulations indicated that the sorption and dissolution of gases, tending to retard transport, were much smaller than anticipated by earlier laboratory studies. The NGME observations themselves show that differences in gas diffusivity have a larger effect on influencing upward transport than do the combined effects of tracer-gas sorption and dissolution, which is consistent with a Sobol' sensitivity analysis. Both deterministic simulations and those considering parametric uncertainties of transport-related properties predict that the excess in concentration of SF[Formula: see text] compared to [Formula: see text]Xe as might be captured in small volumetric samples should be much smaller than the order-of-magnitude contrast found in the large-volume gas samples taken at the site. While extraction of large-volume subsurface gas samples is shown to be capable of distorting in situ gas compositions, the highly variable injection rate of SF[Formula: see text] into the detonation cavity relative to that of [Formula: see text]Xe at the start of the field experiment is the most likely explanation for the large difference in observed concentrations.

Intestinal fatty acid binding protein: A rising therapeutic target in lipid metabolism.

Fatty acid binding proteins (FABPs) are key proteins in lipid transport, and the isoforms are segregated according to their tissue origins. Several isoforms, such as adipose-FABP and epidermal-FABP, have been shown to participate in multiple pathologic processes due to their ubiquitous expression. Intestinal fatty acid binding protein, also termed FABP2 or I-FABP, is specifically expressed in the small intestine. FABP2 can traffic lipids from the intestinal lumen to enterocytes and bind superfluous fatty acids to maintain a steady pool of fatty acids in the epithelium. As a lipid chaperone, FABP2 can also carry lipophilic drugs to facilitate targeted transport. When the integrity of the intestinal epithelium is disrupted, FABP2 is released into the circulation. Thus, it can potentially serve as a clinical biomarker. In this review, we discuss the pivotal role of FABP2 in intestinal lipid metabolism. We also summarize the molecular interactions that have been reported to date, highlighting the clinical prospects of FABP2 research.

Cerebral Ischemic Complications After Surgical Revascularization for Moyamoya Disease: Risk Factors and Development of a Predictive Model Based on Preoperative Nutritional Blood Parameters.

Objectives: Cerebral ischemic complications are common after revascularization in patients with moyamoya disease (MMD). Risk factors from specific laboratory variables have only been assessed by limited research. This study was to investigate the association between postoperative cerebral ischemia and nutritional blood parameters and examine predictive values of such risk factors in adults. Methods: Preoperative demographics and nutritional blood parameters of patients with MMD who received revascularization at our institution from 2012 to 2021 were retrospectively reviewed. Univariate analysis and multivariable logistic regression were used to identify independent risk factors for the onset of postoperative cerebral ischemic complications. Predictive values were tested and a model incorporating these independent risk factors was created using the R program. Area under the receiver operating characteristic curve (AUC) was used for testing its discriminability. Results: Postoperative cerebral ischemic complications occurred in 32 patients of 100 included procedures. Surgery on the left hemisphere, lower admission modified Rankin Scale (mRS) score, aberrant nutritional parameters including low white blood cell (WBC), and high total cholesterol (TC) were significantly associated with cerebral ischemic complications after revascularization. The intriguing role of WBC might be explained by altered immunomodulation. The AUC of this model with novel nutritional parameters yielded a value of 0.811, presenting better predictive accuracy. Additionally, the model was visualized in the form of a nomogram and translated into a user-friendly calculator to generate individual risk. Conclusions: Surgical side, admission mRS score, WBC, and TC were independent risk factors for postoperative cerebral ischemic complications. The model composed of these four parameters was promising to be adopted in clinical practice.

Fecal Signatures of Streptococcus anginosus and Streptococcus constellatus for Noninvasive Screening and Early Warning of Gastric Cancer.

BACKGROUND & AIMS: Most patients with gastric cancer (GCa) are diagnosed at an advanced stage. We aimed to investigate novel fecal signatures for clinical application in early diagnosis of GCa. METHODS: This was an observational study that included 1043 patients from 10 hospitals in China. In the discovery cohort, 16S ribosomal RNA gene analysis was performed in paired samples (tissues and feces) from patients with GCa and chronic gastritis (ChG) to determine differential abundant microbes. Their relative abundances were detected using quantitative real-time polymerase chain reaction to test them as bacterial candidates in the training cohort. Their diagnostic efficacy was validated in the validation cohort. RESULTS: Significant enrichments of Streptococcus anginosus (Sa) and Streptococcus constellatus (Sc) in GCa tumor tissues (P < .05) and feces (P < .0001) were observed in patients with intraepithelial neoplasia, early and advanced GCa. Either the signature parallel test Sa∪Sc or single signature Sa/Sc demonstrated superior sensitivity (Sa: 75.6% vs 72.1%, P < .05; Sc: 84.4% vs 64.0%, P < .001; and Sa∪Sc: 91.1% vs 81.4%, P < .01) in detecting early GCa compared with advanced GCa (specificity: Sa: 84.0% vs 83.9%, Sc: 70.4% vs 82.3%, and Sa∪Sc: 64.0% vs 73.4%). Fecal signature Sa∪Sc outperformed Sa∪CEA/Sc∪CEA in the discrimination of advanced GCa (sensitivity: 81.4% vs 74.2% and 81.4% vs 72.3%, P < .01; specificity: 73.4% vs 81.0 % and 73.4% vs 81.0%). The performance of Sa∪Sc in the diagnosis of both early and advanced GCa was verified in the validation cohort. CONCLUSION: Fecal Sa and Sc are noninvasive, accurate, and sensitive signatures for early warning in GCa. (ClinicalTrials.gov, Number: NCT04638959).

Glutamate dehydrogenase enables Salmonella to survive under oxidative stress and escape from clearance in macrophages.

Oxidative stress and the production of reactive oxygen species (ROS) are a biological threat to bacteria, which induce the synthesis of proteins and production of antioxidants to combat it. Herein, we report that glutamate dehydrogenase (GDH) of Salmonella can assimilate ammonium into glutamate and promote the generation of glutathione (GSH) to combat oxidative damage. Oxidation induces the transcription of gdhA, which encodes GDH, and activates the enzymatic activity of GDH. The ΔgdhA mutant Salmonella strain showed decreased levels of GSH and reduced survival in macrophages, and this growth deficiency could be partially restored by overexpression of GDH and complementation with its downstream metabolites. Therefore, GDH plays a critical role in the growth of Salmonella in oxidative environments, especially under low energy supply.

Knockdown of the DJ-1 (PARK7) gene sensitizes pancreatic cancer to erlotinib inhibition.

The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor erlotinib, in combination with gemcitabine, has been shown to be a promising therapy in the treatment of pancreatic cancer. Our previous study showed that DJ-1 promotes invasion and metastasis of pancreatic cancer cells by activating SRC/extracellular signal-regulated kinase (ERK)/uPA. The aim of this study was to evaluate whether knockdown of DJ-1 expression can sensitize pancreatic cancer cells to erlotinib treatment. Knockdown of DJ-1 expression accelerated erlotinib-induced cell apoptosis and improved the inhibitory effect of erlotinib on pancreatic cancer cell proliferation (for the BxPC-3, PANC-1, and MiaPACa-2 cell lines, regardless of KRAS mutation status) in vitro and in xenograft tumor growth in vivo. Knockdown of DJ-1 decreased K-RAS expression, membrane translocation, and activity in BxPC-3 cells. Knockdown of DJ-1 also decreased K-RAS, H-RAS, and N-RAS expression in PANC-1 and MiaPACa-2 cells. Knockdown of DJ-1 synergistically inhibited AKT and ERK1/2 phosphorylation with erlotinib in pancreatic cancer cells. These findings indicate that DJ-1 may activate the RAS pathway, reinforcing erlotinib drug resistance. Therefore, blocking DJ-1 in combination with the EGFR tyrosine kinase inhibitor erlotinib may be an attractive therapeutic target in pancreatic cancer.

The effect of miR-471-3p on macrophage polarization in the development of diabetic cardiomyopathy.

AIMS: The imbalance of M1/M2 macrophage ratio promotes the occurrence of diabetic cardiomyopathy (DCM), but the precise mechanisms are not fully understood. The aim of this study was to investigate whether miR-471-3p/silent information regulator 1 (SIRT1) pathway is involved in the macrophage polarization during the development of DCM. METHODS: Immunohistochemical staining was used to detect M1 and M2 macrophages infiltration in the heart tissue. Flow cytometry was used to detect the proportion of M1 and M2 macrophages. Expression of miR-471-3p was quantified by real time quantitative-PCR. Transfection of miRNA inhibitor into RAW264.7 cells was performed to investigate the underlying mechanisms. Bioinformatics methods and western blotting were used to explore the target gene of miR-471-3p and further confirmed by dual luciferase reporter assay. KEY FINDINGS: We observed that M1 macrophages infiltration in the heart of tissue in DCM while M2 type was decreased. M1/M2 ratio was increased significantly in bone marrow-derived macrophages (BMDMs) from db/db mice and in RAW264.7 cells treated with advanced glycation end products (AGEs). Meanwhile, miR-471-3p was significantly upregulated in RAW264.7 cells induced by AGEs and inhibition of miR-471-3p could reduce the inflammatory polarization of macrophages. Bioinformatics analysis identified SIRT1 as a target of miR-471-3p. Both dual luciferase reporter assay and western blotting verified that miR-471-3p negatively regulated SIRT1 expression. SIRT1 agonist resveratrol could downregulate the increased proportion of M1 macrophages induced by AGEs. CONCLUSION: Our results indicated that the development of DCM was related to AGEs-induced macrophage polarized to M1 type through a mechanism involving the miR-471-3p/SIRT1 pathway.

Immunohistochemical analysis of HNF4A and ß-catenin expression to predict low-grade dysplasia in the colitis-neoplastic sequence.

Animal studies indicated that P1 promoter-driven hepatocyte nuclear factor 4 alpha (HFN4A) prevents carcinogenesis in colitis. But the function of total HNF4A protein has not been fully investigated, and it was assumed to be involved in the colitis-neoplastic sequence. The aim of this study was to determine the clinical value of total P1-/P2-driven HNF4A combined with ß-catenin in the colitis-neoplastic sequence. A total of 69 samples, including 4 normal colon tissues, 16 sporadic colorectal cancer (CRC) tissues, 35 inflammatory bowel disease (IBD) tissues, and 14 IBD-associated low-grade dysplasia tissues, were collected to assess P1-/P2-driven HNF4A and ß-catenin expressions by immunohistochemical assay. In addition, a colonic epithelial cell line Caco2 with stable P1-/P2-driven HNF4A knockdown was constructed. ß-Catenin expression and skeleton structure were determined in the transfected cells by western blot analysis and immunofluorescence assay respectively. Increased expression of nuclear P1-/P2-driven HNF4A was observed in the colitis-associated colorectal neoplasm and sporadic CRC samples, compared with that in colitis samples. The parallel alterations between cytoplasmic ß-catenin and nuclear P1-/P2-driven HNF4A were also verified. Silencing of P1-/P2-driven HNF4A expression in Caco2 cells decreased ß-catenin expression and F-actin formation. Our results confirmed the elevated expressions of nuclear P1-/P2-driven HNF4A and cytoplasmic ß-catenin in the colitis-neoplastic sequence, and both of them may be used as potential biomarkers to predict low-grade dysplasia.

The detrimental qualitative and quantitative alterations of circulating endothelial progenitor cells in patients with bronchiectasis.

BACKGROUND: Bronchiectasis is an independent risk factor for cardiovascular disease（CVD）and cardiac dysfunction. Endothelial progenitor cells (EPCs) play a crucial role in maintaining endothelial function, and is inversely correlated with cardiovascular risk factors or cardiac dysfunction. However, the relationship between EPCs and bronchiectasis is unknown. METHODS: Twenty-nine patients with stable bronchiectasis and 15 healthy controls were recruited. Fasting venous blood were collected for determining circulating EPC number and activity as well as systemic inflammatory cytokines. RESULTS: The number and migratory or proliferative activity of circulating EPCs in bronchiectasis patients were significantly reduced (p < 0.001). In high E-FACED group, the number of circulating EPCs evaluated by cell culture assay and EPC proliferation were decreased (p < 0.05). Similarly, the number and function of circulating EPCs were both reduced in low forced expiratory volume in 1 s (FEV1) or high mMRC group (p < 0.05). There was a significant correlation between circulating EPCs and bronchiectasis disease severity, according to the E-FACED score (p < 0.05), particularly to FEV1 (p < 0.05) and mMRC dyspnea score (p < 0.05). The count and activity of EPCs inversely correlated with hsCRP levels and IL-6 levels (p < 0.01). CONCLUSIONS: Deficiencies in the number and function of circulating EPCs are present in patients with bronchiectasis. The changes are related to disease severity and may be partly attributed to systemic inflammation. The current findings may provide novel surrogate evaluation biomarkers and potential therapeutic target for bronchiectasis.

Predicting 3D moisture sorption behavior of materials from 1D investigations.

Moisture in materials can be a source of future outgassing and exacerbate unwanted changes in physical and chemical properties. Here, we investigate the effect of sample size and shape on the moisture transport phenomena through a combined experimental and modeling approach. Several different materials varying in size and shape were investigated over a wide range of relative humidities (0-90%) and temperatures ([Formula: see text]) using gravimetric type dynamic vapor sorption (DVS). A dynamic triple-mode sorption model, developed previously, was employed to describe the experimental results with good success; the model includes absorption, adsorption, pooling (clustering) of species, and molecular diffusion. Here we show that the full triple-mode sorption model is robust enough to predict the dynamic uptake and outgassing of 3-dimensional (3D) samples using parameters derived from quasi-1D samples. This successful demonstration on three different materials (filled polydimethylsiloxane (PDMS), unfilled PDMS, and ceramic inorganic composite) illustrates that the model is robust at describing the scale-independent physics and chemistry of moisture sorption and diffusion materials. This work demonstrates that while sorption mechanisms manifest in testing of all sample sizes, some of these mechanisms were so subtle that they were overlooked in our initial modeling and assessment, illustrating the importance of multi-scale experiments in the development of robust predictive capabilities. Our study also outlines the challenges and viable solutions for global optimization of a multi-parameter model. The ability to quantify moisture sorption and diffusion, independent of scale, using 1D lab-scale experiments enables prediction of long-term bulk materials behavior in real applications.