PDZK1 is correlated with DCE-MRI perfusion parameters in high-grade glioma.

OBJECTIVE: This study investigated the relationship between PDZK1 expression and Dynamic Contrast-Enhanced MRI (DCE-MRI) perfusion parameters in High-Grade Glioma (HGG). METHODS: Preoperative DCE-MRI scanning was performed on 80 patients with HGG to obtain DCE perfusion transfer coefficient (Ktrans), vascular plasma volume fraction (vp), extracellular volume fraction (ve), and reverse transfer constant (kep). PDZK1 in HGG patients was detected, and its correlation with DCE-MRI perfusion parameters was assessed by the Pearson method. An analysis of Cox regression was performed to determine the risk factors affecting survival, while Kaplan-Meier and log-rank tests to evaluate PDZK1's prognostic significance, and ROC curve analysis to assess its diagnostic value. RESULTS: PDZK1 was upregulated in HGG patients and predicted poor overall survival and progression-free survival. Moreover, PDZK1 expression distinguished grade III from grade IV HGG. PDZK1 expression was positively correlated with Ktrans 90, and ve_90, and negatively correlated with kep_max, and kep_90. CONCLUSION: PDZK1 is upregulated in HGG, predicts poor survival, and differentiates tumor grading in HGG patients. PDZK1 expression is correlated with DCE-MRI perfusion parameters.

Exploring the clinical and cellular mechanisms of LncRNA-KCNQ1OT1/miR-29a-3p/SOCS3 molecular axis in cases of unexplained recurrent spontaneous abortion.

OBJECTIVE: The objective of this study is to explore the functions and mechanisms of the LncRNA-KCNQ1OT1/miR-29a-3p/SOCS3 molecular pathway in the context of unexplained recurrent spontaneous abortion (URSA). METHODS: We conducted qRT-PCR to assess the levels of LncRNA-KCNQ1OT1, miR-29a-3p, and SOCS3 in both abortion tissues from women who experienced URSA and healthy early pregnant women. A dual-luciferase assay was employed to investigate whether miR-29a-3p targets SOCS3. Furthermore, RNA IP and RNA Pull-Down assays were employed to confirm the interaction between KCNQ1OT1 and SOCS3 with miR-29a-3p. RNA FISH was used to determine the cellular localization of KCNQ1OT1. Additionally, trophoblast cells (HTR8/SVneo) were cultured and the CCK-8 assay was utilized to assess cell proliferation, while flow cytometry was employed to analyze cell apoptosis. RESULTS: Compared to abortion tissues obtained from healthy early pregnant individuals, those from women who experienced URSA displayed a notable downregulation of KCNQ1OT1 and SOCS3, accompanied by an upregulation of miR-29a-3p. Suppression of KCNQ1OT1 resulted in the inhibition of cell proliferation and the facilitation of apoptosis in HTR8/SVneo cells. Our findings suggest that KCNQ1OT1 may exert a regulatory influence on SOCS3 through a competitive binding mechanism with miR-29a-3p. Notably, KCNQ1OT1 exhibited expression in both the cytoplasm and nucleus, with a predominant localization in the cytoplasm. Furthermore, we observed a negative regulatory relationship between miR-29a-3p and SOCS3, as the miR-29a-3p mimic group demonstrated significantly reduced cell proliferation and an increased rate of apoptosis when compared to the negative control (NC mimic) group. Additionally, the SOCS3 Vector group exhibited a substantial improvement in proliferation capability and a marked reduction in the apoptosis rate in comparison to the NC Vector group. The miR-29a-3p mimic + SOCS3 Vector group demonstrated a remarkable enhancement in proliferation and a reduction in apoptosis when compared to the miR-29a-3p mimic group. CONCLUSION: The competitive binding of miR-29a-3p to LncRNA-KCNQ1OT1 appears to result in the elevation of SOCS3 expression, consequently fostering the proliferation of trophoblast cells while concomitantly suppressing apoptosis.

Modulation of intestinal metabolites by calorie restriction and its association with gut microbiota in a xenograft model of colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) is a common malignant tumor, and its occurrence and development are closely related to dysbiosis of gut microbes. Previously, we found calorie restriction altered the composition of the microbial community in a colorectal cancer mouse model and inhibited in vivo growth of CRC cells. Here, we aim to further investigate alteration in the intestinal metabolites and explore the interplay between gut microbiota and intestinal metabolites upon calorie restriction. METHODS: Human colorectal cancer HCT116 cells were used to establish a colorectal cancer xenograft mouse model. The changes of intestinal metabolites in the ad libitum group and calorie restriction group were investigated through untargeted metabolomics analysis. The integrative analysis of gut microbiota and metabolites to elucidate the associations between gut microbiota and intestinal metabolites. RESULTS: Compared with the mice in the ad libitum group, mice upon calorie restriction exhibited downregulation of Isoleucyl-Valine, and upregulation of D-Proline, 1-Palmitoylphosphatidylcholine, and 4-Trimethylammoniobutanoic acid. Additionally, an integrative analysis of gut microbiota and metabolites revealed that Lactobacillus, Parabacteroides and rC4-4 genus were upregulated in the calorie restriction group and positively correlated with D-Proline, 4-Trimethylammoniobutanoic acid or 1-Palmitoylphosphatidylcholine, while negatively correlated with Isoleucyl-Valine. In contrast, the Nitrospirae and Deferribacteres phylum exhibited opposite trends. CONCLUSION: Calorie restriction affects the abundance of gut microbes such as Nitrospirae phylum and Lactobacillus genus in mouse model of colorectal cancer, leading to changes in the metabolites such as D-Proline、Isoleucyl-Valine, which contributes to the suppression of in vivo growth of CRC by calorie restriction.

Differential roles of highly expressed PFKFB4 in colon adenocarcinoma patients.

Colon adenocarcinoma (COAD) is a common malignant tumor, and the role of the protein PFKFB4 in glycolysis and pentose phosphate pathways is crucial. Researchers investigated the clinical significance of PFKFB4 in COAD by studying its expression in 79 tissue samples using immunohistochemistry. We found that PFKFB4 expression was significantly higher in COAD patients, particularly in the sigmoid colon. Interestingly, high PFKFB4 expression was associated with both improved overall survival (OS) and worse progression-free survival (PPS) in COAD patients. Further analysis revealed that genes associated with PFKFB4 were linked to various metabolic pathways, including amino acid biosynthesis, glycolysis, gluconeogenesis, glucose metabolism, and inflammatory response. PFKFB4 expression also showed correlations with the infiltration of different immune cell types in COAD patients, such as CD8+ T cells, CD4+ T cells, regulatory T cells (Tregs), macrophages, neutrophils, dendritic cells, active mast cells, and resting NK cells. Overall, the relationship between PFKFB4 expression and the prognosis of COAD is complex and diverse, possibly playing different roles at different stages of the disease. Moreover, its mechanism might involve interactions with various metabolic pathways and immune infiltration in the tumor microenvironment. These findings provide valuable insights into the potential role of PFKFB4 as a biomarker or therapeutic target in COAD.

Orientational Water Bonding on Pt(111): Beyond the Frontier Orbital Principle.

For decades, our understanding of water-metal bonding has been dominated by the frontier orbital principle in which globally stable water-metal interactions are ruled by HOMO interacting with metal surfaces. Using density functional theory calculations, herein, we have revealed that the frontier orbital principle cannot be applied to metastable water bonding on Pt(111), where the decisive role of HOMO is replaced by HOMO-1 in terms of the greatest orbital shifts and depopulations as the two different bonding indicators. Unlike the stable water configuration in which both HOMO-1 and HOMO prefer to overlap with metal states through σ-like orbital interactions, metastable configurations exhibit delicate competition or balance between σ-like and π-like orbital interactions exerted by HOMO-1 and HOMO, respectively. These findings have significantly deepened our understanding of orbital roles in water-metal bonding interactions and bridged the gap between theoretical understanding of electrified waters at electrochemical interfaces and water science on metal surfaces.

The People's War Against Pandemic: protocol for a randomized control trial based on a virtual interactive training system intervention to improve the emergency preparedness of public for major emerging infectious diseases.

BACKGROUND: The frequent occurrence and increasing severity of major emerging infectious diseases (MEIDs) have posed considerable public health, economic and social issues worldwide. The emergency preparedness of public is inadequate to respond to and recover from MEIDs. Due to the limitation of time, space and resources, it is also difficult to carry out large-scale emergency preparedness training related to MEIDs. Then we developed a virtual interactive training system to improve emergency preparedness of public, including preparation of legal compliance, emergency knowledge, emergency capacity, economic estimation, material reserve and physical and mental health. METHODS: A protocol for conducting a randomized controlled trail to evaluate the People's War against Pandemic, a virtual interactive training system aimed to improve emergency preparedness of public for MEIDs. During the intervention, participants need to complete the storyline task at least once a day, watch at least one article and one video in the knowledge corner, and complete a retest of wrong choices in the intelligent evaluation module. The primary outcome is emergency preparedness of public for MEIDs. The secondary outcome is prevention and control knowledge of MEIDs. DISCUSSION: The People's War Against Pandemic may be an effective approach to provide public with a panoramic understanding of the response to MEIDs, so as to promote their comprehensive preparation and finally achieve effective response. TRIAL REGISTRATION: This study was funded in 2021 and registered in the Chinese Clinical Trial Registry (registration number: ChiCTR2200060919) in June 2022. Recruitment and enrollment of participants began in July 2022.

High Glucose-Induced Kidney Injury via Activation of Necroptosis in Diabetic Kidney Disease.

Diabetic kidney disease (DKD) is a major microvascular complication of diabetes mellitus (DM) and is closely associated to programmed cell death. However, the complex mechanisms of necroptosis, an alternative cell death pathway, in DKD pathogenesis are yet to be elucidated. This study indicates that necroptosis is involved in DKD induced by high glucose (HG) both in vivo and in vitro. HG intervention led to the activation of RIPK1/RIPK3/MLKL signaling, resulting in renal tissue necroptosis and proinflammatory activation in streptozotocin/high-fat diet- (STZ/HFD-) induced diabetic mice and HG-induced normal rat kidney tubular cells (NRK-52E). We further found that in HG-induced NRK-52E cell, necroptosis might, at least partly, depend on the levels of reactive oxygen species (ROS). Meanwhile, ROS participated in necroptosis via a positive feedback loop involving the RIPK1/RIPK3 pathway. In addition, blocking RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS generation, could effectively protect the kidney against HG-induced damage, decrease the release of proinflammatory cytokines, and rescue renal function in STZ/HFD-induced diabetic mice. Inhibition of RIPK1 effectively decreased the activation of RIPK1-kinase-/NF-κB-dependent inflammation. Collectively, we demonstrated that high glucose induced DKD via renal tubular epithelium necroptosis, and Nec-1 or NAC treatment downregulated the RIPK1/RIPK3/MLKL pathway and finally reduced necroptosis, oxidative stress, and inflammation. Thus, RIPK1 may be a therapeutic target for DKD.

Calorie restriction remodels gut microbiota and suppresses tumorigenesis of colorectal cancer in mice.

Colorectal cancer (CRC) is one of the most common cancers worldwide and the consumption of a high-calorie diet is one of its risk factors. Calorie restriction (CR) slows tumor growth in a variety of cancers, including colorectal cancer; however, the mechanism behind this remains unknown. In the present study, CR effectively reduced the tumor volume and weight in a xenograft BALB/c male nude mouse model. In addition, tumor immunohistochemistry revealed that the CR group had significantly higher expression of Bax (P<0.001) and significantly lower levels of Bcl2 (P<0.0001) and Ki67 (P<0.001) compared with control group. Furthermore, data from 16S ribosomal (r)RNA sequencing implied that CR was able to reprogram the microbiota structure, characterized by increased Lactobacillus constituent ratio (P<0.05), with amelioration of microbial dysbiosis caused by CRC. Further receiver operating characteristic curves demonstrated that the bacteria Bacteroides [area under the curve (AUC)=0.800], Lactobacillus (AUC=0.760) and Roseburia (AUC=0.720) served key roles in suppression of CRC in the mouse model. The functional prediction of intestinal flora indicated 'cyanoamino acid metabolism' (P<0.01), 'replication initiation protein REP (rolling circle plasmid replication)' (P<0.01), 'tRNA G10 N-methylase Trm11' (P<0.01) and 'uncharacterized protein with cyclophilin fold, contains DUF369 domain' (P<0.05) were downregulated in CR group. These findings implied that CR suppressed CRC in mice and altered the gut microbiota.

Perturbative vibration of the coupled hydrogen-bond (O:H-O) in water.

Perturbation Raman spectroscopy has underscored the hydrogen bond (O:H-O or HB) cooperativity and polarizability (HBCP) for water, which offers a proper parameter space for the performance of the HB and electrons in the energy-space-time domains. The OO repulsive coupling drives the O:H-O segmental length and energy to relax cooperatively upon perturbation. Mechanical compression shortens and stiffens the O:H nonbond while lengthens and softens the HO bond associated with polarization. However, electrification by an electric field or charge injection, or molecular undercoordination at a surface, relaxes the O:H-O in a contrasting way to the compression with derivation of the supersolid phase that is viscoelastic, less dense, thermally diffusive, and mechanically and thermally more stable. The HO bond exhibits negative thermal expansivity in the liquid and the ice-I phase while its length responds in proportional to temperature in the quasisolid phase. The O:H-O relaxation modifies the mass densities, phase boundaries, critical temperatures and the polarization endows the slipperiness of ice and superfluidity of water at the nanometer scale. Protons injection by acid solvation creates the H↔H anti-HB and introduction of electron lone pairs derives the O:⇔:O super-HB into the solutions of base or H2O2 hydrogen-peroxide. The repulsive H↔H and O:⇔:O interactions lengthen the solvent HO bond while the solute HO bond contracts because its bond order loss. Differential phonon spectroscopy quantifies the abundance, structure order, and stiffness of the bonds transiting from the mode of pristine water to the perturbed states. The HBCP and the perturbative spectroscopy have enabled the dynamic potentials for the relaxing O:H-O bond. Findings not only amplified the power of the Raman spectroscopy but also substantiated the understanding of anomalies of water subjecting to perturbation.

MIIP functions as a novel ligand for ITGB3 to inhibit angiogenesis and tumorigenesis of triple-negative breast cancer.

Migration and invasion inhibitory protein (MIIP) has been identified as a tumor suppressor in various cancer types. Although MIIP is reported to exert tumor suppressive functions by repressing proliferation and metastasis of cancer cells, the detailed mechanism is poorly understood. In the present study, we found MIIP is a favorable indicator of prognosis in triple-negative breast cancer. MIIP could inhibit tumor angiogenesis, proliferation, and metastasis of triple-negative breast cancer cells in vivo and in vitro. Mechanistically, MIIP directly interacted with ITGB3 and suppressed its downstream signaling. As a result, ß-catenin was reduced due to elevated ubiquitin-mediated degradation, leading to downregulated VEGFA production and epithelial mesenchymal transition. More importantly, we found RGD motif is essential for MIIP binding with ITGB3 and executing efficient tumor-suppressing effect. Our findings unravel a novel mechanism by which MIIP suppresses tumorigenesis in triple-negative breast cancer, and MIIP is thus a promising molecular biomarker or therapeutic target for the disease.

China's Vaccine Diplomacy and Its Implications for Global Health Governance.

The COVID-19 pandemic has wreaked havoc on global economy and human communities. Promoting the accessibility and affordability of vaccine via diplomacy is the key to mitigating the pandemic crisis. China has been accused of seeking geopolitical objectives by launching vaccine diplomacy. The definition of vaccine diplomacy is neutral by nature. China's vaccine diplomacy is based on its holistic approach to national security and the importance China attaches to the "Belt and Road" Initiative. With a whole-of-government approach on both the bilateral and multilateral levels and marketization of vaccines, China's vaccine diplomacy has immense implications for global health governance, in that it helps to narrow the global immunization vaccination gap and to promote human-right-based approach to global health governance. However, the sustainability of China's vaccine diplomacy is questionable because of the Sino-American geopolitical competition and doubts over the efficacy of China's vaccines. The escalation of power rivalry between China and the U.S. and the concerns over the efficacy of China's vaccines forebode the gloomy future of China's vaccine diplomacy.

Epigallocatechin Gallate Induces the Demethylation of Actinin Alpha 4 to Inhibit Diabetic Nephropathy Renal Fibrosis via the NF-KB Signaling Pathway In Vitro.

Actinin alpha 4 (ACTN4) is expressed in the kidney podocytes. ACTN4 gene methylation in patients with diabetic nephropathy (DN) remains high. Underlying mechanism of epigallocatechin-3-gallate (EGCG) inducing ACTN4 demethylation, and its inhibitory effect on DN renal fibrosis remains unclear. Methods: Human podocyte cell line, HPC, was treated with high glucose to establish model of DN. The levels of cytokines, vascular endothelial growth factor (VEGF) and interleukin (IL)-8, and fibrosis markers, alpha smooth muscle actin (α-SMA) and fibronectin (FN), were determined using enzyme-linked immunosorbent assay. HPC cells were treated with EGCG, and cell viability was determined by MTT assay, ACTN4 gene methylation was analyzed by MSP. mRNA and protein expression levels were measured using RT-qPCR and Western blotting, respectively. Results: Actinin alpha 4 gene promoter was hypermethylated in the high glucose-treated groups. EGCG reversed the hypermethylated status of ACTN4, along with the upregulation of ACTN4 levels and downregulation of DNA methyltransferase 1 (DNMT1), NF-κB p65, p-NF-κB p65, IκB-α, VEGF, IL-8, α-SMA, and FN levels (P<.05). Conclusion: Epigallocatechin-3-gallate reduced hypermethylation of ACTN4 in HPC cells by downregulating DNMT1 expression and restoring ACTN4 expression, contributing to the upregulation of the NF-KB p65, p-NF-KB p65, IKB-α, VEGF, IL-8, α-SMA, and FN levels (P<.05).

Chronic Ethanol Consumption Induces Osteopenia via Activation of Osteoblast Necroptosis.

Chronic high-dose alcohol consumption impairs bone remodeling, reduces bone mass, and increases the risk of osteoporosis and bone fracture. However, the mechanisms underlying alcohol-induced osteoporosis are yet to be elucidated. In this study, we showed that excess intake of ethyl alcohol (EtOH) resulted in osteopenia and osteoblast necroptosis in mice that led to necrotic lesions and reduced osteogenic differentiation in bone marrow mesenchymal stem cells (BMMSCs). We found that EtOH treatment led to the activation of the RIPK1/RIPK3/MLKL signaling, resulting in increased osteoblast necroptosis and decreased osteogenic differentiation and bone formation both in vivo and in vitro. We further discovered that excessive EtOH treatment-induced osteoblast necroptosis might partly depend on reactive oxygen species (ROS) generation; concomitantly, ROS contributed to necroptosis of osteoblasts through a positive feedback loop involving RIPK1/RIPK3. In addition, blocking of the RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 kinase in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS, could decrease the activation of osteoblast necroptosis and ameliorate alcohol-induced osteopenia both in vivo and in vitro. Collectively, we demonstrated that chronic high-dose alcohol consumption induced osteopenia via osteoblast necroptosis and revealed that RIPK1 kinase may be a therapeutic target for alcohol-induced osteopenia.

Applying machine learning to balance performance and stability of high energy density materials.

The long-standing performance-stability contradiction issue of high energy density materials (HEDMs) is of extremely complex and multi-parameter nature. Herein, machine learning was employed to handle 28 feature descriptors and 5 properties of detonation and stability of 153 HEDMs, wherein all 21,648 data used were obtained through high-throughput crystal-level quantum mechanics calculations on supercomputers. Among five models, namely, extreme gradient boosting regression tree (XGBoost), adaptive boosting, random forest, multi-layer perceptron, and kernel ridge regression, were respectively trained and evaluated by stratified sampling and 5-fold cross-validation method. Among them, XGBoost model produced the best scoring metrics in predicting the detonation velocity, detonation pressure, heat of explosion, decomposition temperature, and lattice energy of HEDMs, and XGBoost predictions agreed best with the 1,383 experimental data collected from massive literatures. Feature importance analysis was conducted to obtain data-driven insight into the causality of the performance-stability contradiction and delivered the optimal range of key features for more efficient rational design of advanced HEDMs.

Effect of the IDO Gene on Pregnancy in Mice with Recurrent Pregnancy Loss.

The aim of this study is to investigate the effect of the IDO (indoleamine 2,3-dioxygenase) gene on pregnancy outcome in mice with recurrent pregnancy loss (RPL) and its mechanism of action in the maternal-fetal interface. An RPL model was established via natural mating of female CBA/J mice with male DBA/2 mice; thereafter, the female mice were randomly divided into groups treated with LV-EGFP (enhanced green fluorescent protein)-IDO (lentivirus vector carrying IDO-EGFP gene), LV-EGFP (negative control lentivirus vector), or phosphate-buffered saline (control). The mice were sacrificed at 13.5 days of pregnancy, and the embryo absorption rate was determined. Peripheral blood regulatory T cells (Tregs) from the pregnant mice were detected using flow cytometry. Placental and decidual tissue IDO expression was detected using immunofluorescence and Western blotting. Inflammatory cell infiltration of the placental and decidual tissue was observed using hematoxylin-eosin (HE) staining. The LV-EGFP-IDO group had a significantly lower embryo absorption rate than the LV-EGFP and control groups (P = 0.0006 and P = 0.0049, respectively) and significantly more Tregs than the LV-EGFP and control groups (P = 0.0151 and P = 0.0392, respectively). Placental and decidual IDO protein levels correlated positively with peripheral blood Treg expression levels. The LV-EGFP-IDO group had significantly higher placental and decidual IDO protein levels than the LV-EGFP and control groups (P < 0.005), and it had significantly less inflammatory cell infiltration than the LV-EGFP and control groups. The IDO gene may reduce the embryo absorption rate in an RPL mouse model, possibly improving pregnancy outcome by upregulating Tregs and reducing the inflammatory response.

Strategies for Achieving Balance between Detonation Performance and Crystal Stability of High-Energy-Density Materials.

Performance-stability contradiction of high-energy-density materials (HEDMs) is a long-standing puzzle in the field of chemistry and material science. Bridging the gap that exists between detonation performance of new HEDMs and their stability remains a formidable challenge. Achieving optimal balance between the two contradictory factors is of a significant demand for deep-well oil and gas drilling, space exploration, and other civil and defense applications. Herein, supercomputers and latest quantitative computational strategies were employed and high-throughput quantum calculations were conducted for 67 reported HEDMs. Based on statistical analysis of large amounts of physico-chemical data, in-crystal interspecies interactions were identified to be the one that provokes the performance-stability contradiction of HEDMs. To design new HEDMs with both good detonation performance and high stability, the proposed systematic and comprehensive strategies must be satisfied, which could promote the development of crystal engineering of HEDMs to an era of theory-guided rational design of materials.

Unexpected Solute Occupancy and Anisotropic Polarizability in Lewis Basic Solutions.

Density functional computation revealed that in YOH solvation (Y = Li, Na, and K), the Y+ cation locates eccentrically at the interstitial hollow site to form the Y+·4H2O unit, and the hydroxyl adds an excessive electron lone pair ":" to form a OH-·H2O unit where the hydroxide stays in the the center. The surrounding four oriented H2O neighbors interact with the Y+ through Y+ ↔ H+ repulsion and Y+:O2- attraction, causing the Y+ eccentric dislocation by some 0.80 Å. The ":" turns one O:H-O bond into the O: ⇔ :O super hydrogen bond by altering H2O·4H2O into HO-·4H2O. The repulsive Y+ ↔ H+ enlarges its separation and the attractive Y+:O shortens itself, showing the anisotropic polarization of the Y+ cation. The anisotropic Y+ polarizability, O: ⇔ :O compressibility, and the H-O bond contraction of the solute OH- distorts the solute bonding network and disperses the O:H-O segmental phonon frequencies, as confirmed spectroscopically.

Hydration of Hofmeister ions.

Water dissolves salt into ions and then hydrates the ions to form an aqueous solution. Hydration of ions deforms the hydrogen bonding network and triggers the solution with what the pure water never shows such as conductivity, molecular diffusivity, thermal stability, surface stress, solubility, and viscosity, having enormous impact to many branches in biochemistry, chemistry, physics, and energy and environmental industry sectors. However, regulations for the solute-solute-solvent interactions are still open for exploration. From the perspective of the screened ionic polarization and O:H-O bond relaxation, this treatise features the recent progress and a perspective in understanding the hydration dynamics of Hofmeister ions in the typical YI, NaX, ZX2, and NaT salt solutions (Y = Li, Na, K, Rb, Cs; X = F, Cl, Br, I; Z = Mg, Ca, Ba, Sr; T = ClO4, NO3, HSO4, SCN). Phonon spectrometric analysis turned out the f(C) number fraction of bonds transition from the mode of deionized water to the hydrating. The linear f(C) ∝ C form features the invariant hydration volume of small cations that are fully-screened by their hydration H2O dipoles. The nonlinear f(C) ∝ 1 - exp.(-C/C0) form describes that the number insufficiency of the ordered hydrating H2O dipoles partially screens the anions. Molecular anions show stronger yet shorter electric field of dipoles. The screened ionic polarization, inter-solute interaction, and O:H-O bond transition unify the solution conductivity, surface stress, viscosity, and critical energies for phase transition.