Temperature Dependence of the Dynamic Contact Angles of Water on a Smooth Stainless-Steel Surface under Elevated Pressures.

The temperature dependence of the dynamic contact angles (DCAs) of water on a metallic surface remains unclear, especially under elevated pressures. Here in this work, the advancing and receding contact angles (RCAs), as well as the contact angle hysteresis (CAH), of water on stainless-steel 316 (SS316) surfaces were studied using the dynamic sessile drop method for temperatures up to 300 °C and pressures up to 10 MPa. It was found that the temperature dependence of the DCAs exhibits a different pattern as compared to the piecewise linear decline of static contact angles. The advancing contact angle (ACA) remains nearly constant and does not decrease until the temperature becomes close to the saturated temperature. The decrease in ACA is attributed to evaporation, which reduces the advancement of energy barrier. The RCA linearly declines below 120 °C and remains stable above 120 °C. The increasing temperature enhances the pinning effect and changes the droplet receding mode. Under all pressures tested, the CAH demonstrates a "increase-constant-decrease" trilinear relationship with temperature. Furthermore, the mean solid surface entropy and solid-gas interfacial tension of SS316 were estimated to be 0.1152 mJ/(m2·°C) and 61.49 mJ/m2, respectively.

Access to colorectal cancer screening in populations in China, 2020: A coverage-focused synthesis analysis.

In populations in China, colorectal cancer (CRC) screening can be mainly accessed through organized screening, opportunistic screening, and physical examination. This screening intervention is found to be effective but the exact coverage rate is difficult to measure. Based on data from published articles, official websites, and available program reports, the screening coverage rate and related indicators were quantified. A rapid review was then conducted to estimate the overall and the breakdown coverage rates of the sub-type screening services, by leveraging the numbers of articles and the by-type median sample sizes. Up to 2020, two central government-funded and four provincial/municipal-level organized CRC screening programs have been initiated and included in this analysis. For populations aged 40-74, the estimated coverage rate of organized programs in China was 2.7% in 2020, and the 2-year cumulative coverage rate in 2019-2020 was 5.3% and the 3-year cumulative coverage rate in 2018-2020 was 7.7%. The corresponding coverage rates of 50-74-year-olds were estimated to be 3.4%, 7.1%, and 10.3%, respectively. Based on the rapid review approach, the overall screening coverage rate for 40-74 years, considering organized screening programs, opportunistic screening, and physical examinations, was then estimated to be 3.0% in China in 2020. However, comparing the findings of this study with the number of health check-ups reported in the local national health statistics yearbooks suggests that the number of CRC physical examinations may be underestimated in this study. The findings suggest that further efforts are needed to improve population access to CRC screening in China. Furthermore, evidence for access to opportunistic CRC screening and physical examination is limited, and more quantitative investigation is needed.

Discovery of BMP10 as a new gene underpinning congenital heart defects.

OBJECTIVE: Aggregating evidence convincingly establishes the predominant genetic basis underlying congenital heart defects (CHD), though the heritable determinants contributing to CHD in the majority of cases remain elusive. In the current investigation, BMP10 was selected as a prime candidate gene for human CHD mainly due to cardiovascular developmental abnormalities in Bmp10-knockout animals. The objective of this retrospective study was to identify a new BMP10 mutation responsible for CHD and characterize the functional effect of the identified CHD-causing BMP10 mutation. METHODS: Sequencing assay of BMP10 was fulfilled in a cohort of 276 probands with various CHD and a total of 288 non-CHD volunteers. The available family members from the proband harboring an identified BMP10 mutation were also BMP10-genotyped. The effect of the identified CHD-causative BMP10 mutation on the transactivation of TBX20 and NKX2.5 by BMP10 was quantitatively analyzed in maintained HeLa cells utilizing a dual-luciferase reporter assay system. RESULTS: A novel heterozygous BMP10 mutation, NM_014482.3:c.247G>T;p.(Glu83*), was identified in one proband with patent ductus arteriosus (PDA), which was confirmed to co-segregate with the PDA phenotype in the mutation carrier's family. The nonsense mutation was not observed in 288 non-CHD volunteers. Functional analysis unveiled that Glu83*-mutant BMP10 had no transactivation on its two representative target genes TBX20 and NKX2.5, which were both reported to cause CHD. CONCLUSION: These findings provide strong evidence indicating that genetically compromised BMP10 predisposes human beings to CHD, which sheds light on the new molecular mechanism that underlies CHD and allows for antenatal genetic counseling and individualized precise management of CHD.

Somatic GATA4 mutation contributes to tetralogy of Fallot.

Tetralogy of Fallot (TOF) is the most prevalent cyanotic congenital heart pathology and causes infant morbidity and mortality worldwide. GATA-binding protein 4 (GATA4) serves as a pivotal transcriptional factor for embryonic cardiogenesis and germline GATA4 mutations are causally linked to TOF. However, the effects of somatic GATA4 mutations on the pathogenesis of TOF remain to be ascertained. In the present study, sequencing assay of GATA4 was performed utilizing genomic DNA derived from resected heart tissue specimens as well as matched peripheral blood specimens of 62 patients with non-familial TOF who underwent surgical treatment for TOF. Sequencing of GATA4 was also performed using the heart tissue specimens as well as matched peripheral venous blood samples of 68 sporadic cases who underwent heart valve displacement because of rheumatic heart disorder and the peripheral venous whole blood samples of 216 healthy subjects. The function of the mutant was explored by dual-luciferase activity analysis. Consequently, a new GATA4 mutation, NM_002052.5:c.708T>G;p.(Tyr236*), was found in the heart tissue of one patient with TOF. No mutation was detected in the heart tissue of the 68 cases suffering from rheumatic heart disorder or in the venous blood samples of all 346 individuals. GATA4 mutant failed to transactivate its target gene, myosin heavy chain 6. Additionally, this mutation nullified the synergistic transactivation between GATA4 and T-box transcription factor 5 or NK2 homeobox 5, two genes causative for TOF. Somatic GATA4 mutation predisposes TOF, highlighting the significant contribution of somatic variations to the molecular pathogenesis underpinning TOF.

Estimating the economic burden of colorectal cancer in China, 2019-2030: A population-level prevalence-based analysis.

BACKGROUND: Colorectal cancer (CRC) is one of the most common cancers worldwide. Comprehensive data on the economic burden of CRC at a population-level is critical in informing policymaking, but such data are currently limited in China. METHODS: From a societal perspective, the economic burden of CRC in 2019 was estimated, including direct medical and nonmedical expenditure, disability, and premature-death-related indirect expenditure. Data on disease burden was taken from the GBD 2019 and analyzed using a prevalence-based approach. The per-person direct expenditure and work loss days were from a multicenter study; the premature-death-related expenditure was estimated using a human capital approach. Projections were conducted in different simulated scenarios. All expenditure data were in Chinese Yuan (CNY) and discounted to 2019. RESULTS: In 2019, the estimated overall economic burden of CRC in China was CNY170.5 billion (0.189% of the local GDP). The direct expenditure was CNY106.4 billion (62.4% of the total economic burden), 91.4% of which was a direct medical expenditure. The indirect expenditure was CNY64.1 billion, of which 63.7% was related to premature death. The predicted burden would reach CNY560.0 billion in 2030 given constant trends for disease burden; however, it would be alternatively reduced to

[Matrine inhibits inflammatory response induced by TNF-α in human umbilical vein endothelial cells through miR-25-3p-mediated Klf4 pathway].

This study aimed to analyze the effect of matrine on tumor necrosis factor-α(TNF-α)-induced inflammatory response in human umbilical vein endothelial cells(HUVECs) and explore whether the underlying mechanism was related to the miR-25-3p-mediated Krüppel-like factor 4(Klf4) pathway. The HUVEC cell inflammation model was induced by TNF-α stimulation. After 24 or 48 hours of incubation with different concentrations of matrine(0.625, 1.25, and 2.5 mmol·L~(-1)), CCK-8 assay was used to detect cell proliferation. After treatment with 2.5 mmol·L~(-1) matrine for 48 h, the expression of TNF-α, interleukin-6(IL-6), interleukin-1ß(IL-1ß), and Klf4 mRNA and miR-25-3p was detected by real-time fluorescence-based quantitative PCR, and the protein expression of TNF-α, IL-6, IL-1ß, and Klf4 was detected by Western blot. The anti-miR-25-3p was transfected into HUVECs, and the effect of anti-miR-25-3p on TNF-α-induced cell proliferation and inflammatory factors was detected by the above method. The cells were further transfected with miR-25-3p and incubated with matrine to detect the changes in proliferation and expression of related inflammatory factors, miR-25-3p, and Klf4. The targeting relationship between miR-25-3p and Klf4 was verified by bioinformatics analysis and dual luciferase reporter gene assay. The results displayed that matrine could inhibit TNF-α-induced HUVEC proliferation, decrease the mRNA and protein expression of TNF-α, IL-6, and IL-1ß, increase the mRNA and protein expression of Klf4, and reduce the expression of miR-25-3p. Bioinformatics analysis showed that there were specific complementary binding sites between miR-25-3p and Klf4 sequences. Dual luciferase reporter gene assay confirmed that miR-25-3p negatively regulated Klf4 expression in HUVECs by targeting. The inhibition of miR-25-3p expression can reduce TNF-α-induced cell proliferation and mRNA and protein expression of TNF-α, IL-6, and IL-1ß. MiR-25-3p overexpression could reverse the effect of matrine on TNF-α-induced cell proliferation and the mRNA and protein expression of TNF-α, IL-6, IL-1ß, and Klf4. This study shows that matrine inhibits the inflammatory response induced by TNF-α in HUVECs through miR-25-3p-mediated Klf4 pathway.

Discovery of TBX20 as a Novel Gene Underlying Atrial Fibrillation.

Atrial fibrillation (AF), the most prevalent type of sustained cardiac dysrhythmia globally, confers strikingly enhanced risks for cognitive dysfunction, stroke, chronic cardiac failure, and sudden cardiovascular demise. Aggregating studies underscore the crucial roles of inherited determinants in the occurrence and perpetuation of AF. However, due to conspicuous genetic heterogeneity, the inherited defects accounting for AF remain largely indefinite. Here, via whole-genome genotyping with genetic markers and a linkage assay in a family suffering from AF, a new AF-causative locus was located at human chromosome 7p14.2-p14.3, a ~4.89 cM (~4.43-Mb) interval between the markers D7S526 and D7S2250. An exome-wide sequencing assay unveiled that, at the defined locus, the mutation in the TBX20 gene, NM_001077653.2: c.695A>G; p.(His232Arg), was solely co-segregated with AF in the family. Additionally, a Sanger sequencing assay of TBX20 in another family suffering from AF uncovered a novel mutation, NM_001077653.2: c.862G>C; p.(Asp288His). Neither of the two mutations were observed in 600 unrelated control individuals. Functional investigations demonstrated that the two mutations both significantly reduced the transactivation of the target gene KCNH2 (a well-established AF-causing gene) and the ability to bind the promoter of KCNH2, while they had no effect on the nuclear distribution of TBX20. Conclusively, these findings reveal a new AF-causative locus at human chromosome 7p14.2-p14.3 and strongly indicate TBX20 as a novel AF-predisposing gene, shedding light on the mechanism underlying AF and suggesting clinical significance for the allele-specific treatment of AF patients.

[Construction of a Mouse Model for Myeloproliferative Neoplasms and an Evaluation System].

OBJECTIVE: To construct a myeloproliferative neoplasms (MPN) transplanted mouse model with JAK2-V617F, MPLW515L or CALR-Type I gene mutation, and establish a systematic evaluation system to verify the success of model construction. METHODS: The bone marrow c-kit+ cells of the mice were obtained by the following steps: The mice were killed by cervical dislocation, the femur, tibia and ilium were separated, and the bone marrow cells were collected. The c-kit+ cells were sorted after incubation with CD117 magnetic beads. The method of constructing mouse primary mutant cells is as follows: A gene mutation vector with a GFP tag was constructed by the retroviral system, and the retroviral vector was packaged into the Platinum-E cells to obtain the virus supernatant, and then used it to infect the c-kit+ cells of mice. The MPN mouse model was constructed as follows: the mouse primary c-kit+ cells containing the mutant genes were collected after infection, and then transplanted them via the tail vein into the female recipient mice of the same species which were irradiated with a lethal dose of gamma rays (8.0 Gy). The MPN mouse model was evaluated as follows: After transplantation, the peripheral blood of the mice was regularly collected from the tail vein to perform the complete blood count test, and the size of spleen and the degree of bone marrow fibrosis were estimated. RESULTS: The mouse c-kit+ cells with the mutant genes were successfully obtained from the bone marrow. MPN mouse model was successfully constructed: The peripheral blood cells of the MPN-transplanted mice carried exogenous implanted GFP-positive cells, and the white blood cells (WBC), platelet (PLT) and hematocrit (HCT) were all increased; the body weight loss, and the water and food intake were reduced in the transplanted mice; further pathological analysis showed that the transplanted mice displayed splenomegaly and bone marrow fibrosis. These results suggested that the MPN mouse model was successfully constructed. According to the common and different characteristics of the three MPN mouse model, a preliminary evaluation system for judging the success of MPN mouse model construction was summarized, which mainly included the following indicators, for example, the proportion of GFP-positive cells in the peripheral blood of mice; WBC, PLT and HCT; the degree of spleen enlargement and the bone marrow fibrosis. CONCLUSION: The MPN mouse model with JAK2-V617F, MPLW515L or CALR-Type I gene mutation is successfully established by retroviral system, which can provide an important experimental animal model for the research of MPN pathogenesis and drug-targeted therapy.

Targeting PPARs for therapy of atherosclerosis: A review.

Atherosclerosis, a chief pathogenic factor of cardiovascular disease, is associated with many factors including inflammation, dyslipidemia, and oxidative stress. Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors and are widely expressed with tissue- and cell-specificity. They control multiple genes that are involved in lipid metabolism, inflammatory response, and redox homeostasis. Given the diverse biological functions of PPARs, they have been extensively studied since their discovery in 1990s. Although controversies exist, accumulating evidence have demonstrated that PPAR activation attenuates atherosclerosis. Recent advances are valuable for understanding the mechanisms of action of PPAR activation. This article reviews the recent findings, mainly from the year of 2018 to present, including endogenous molecules in regulation of PPARs, roles of PPARs in atherosclerosis by focusing on lipid metabolism, inflammation, and oxidative stress, and synthesized PPAR modulators. This article provides information valuable for researchers in the field of basic cardiovascular research, for pharmacologists that are interested in developing novel PPAR agonists and antagonists with lower side effects as well as for clinicians.

Discovery of GJC1 (Cx45) as a New Gene Underlying Congenital Heart Disease and Arrhythmias.

As the most prevalent type of birth malformation, congenital heart disease (CHD) gives rise to substantial mortality and morbidity as well as a socioeconomic burden. Although aggregating investigations highlight the genetic basis for CHD, the genetic determinants underpinning CHD remain largely obscure. In this research, a Chinese family suffering from autosomal dominant CHD (atrial septal defect) and arrhythmias was enrolled. A genome-wide genotyping with microsatellite markers followed by linkage assay as well as sequencing analysis was conducted. The functional effects of the discovered genetic mutation were characterized by dual patch-clamp electrophysiological recordings in N2A cells and propidium iodide uptake assays in HeLa cells. As a result, a novel genetic locus for CHD and arrhythmias was located on chromosome 17q21.31-q21.33, a 4.82-cM (5.12 Mb) region between two markers of D17S1861 and D17S1795. Sequencing assays of the genes at the mapped locus unveiled a novel heterozygous mutation in the GJC1 gene coding for connexin 45 (Cx45), NM_005497.4:c.550A>G;p.R184G, which was in co-segregation with the disease in the whole family and was not observed in 516 unrelated healthy individuals or gnomAD. Electrophysiological analyses revealed that the mutation significantly diminished the coupling conductance in homomeric cell pairs (R184G/R184G) and in cell pairs expressing either R184G/Cx45 or R184G/Cx43. Propidium iodide uptake experiments demonstrated that the Cx45 R184G mutation did not increase the Cx45 hemichannel function. This investigation locates a new genetic locus linked to CHD and arrhythmias on chromosome 17q21.31-q21.33 and indicates GJC1 as a novel gene predisposing to CHD and arrhythmias, implying clinical implications for prognostic risk assessment and personalized management of patients affected with CHD and arrhythmias.

Targeting macrophages in atherosclerosis using nanocarriers loaded with liver X receptor agonists: A narrow review.

Macrophages are involved in the whole process of atherosclerosis, which is characterized by accumulation of lipid and inflammation. Presently, clinically used lipid-lowering drugs cannot completely retard the progress of atherosclerosis. Liver X receptor (LXR) plays a key role in regulation of lipid metabolism and inflammation. Accumulating evidence have demonstrated that synthetic LXR agonists can significantly retard the development of atherosclerosis. However, these agonists induce sever hypertriglyceridemia and liver steatosis. These side effects have greatly limited their potential application for therapy of atherosclerosis. The rapid development of drug delivery system makes it possible to delivery interested drugs to special organs or cells using nanocarriers. Macrophages express various receptors which can recognize and ingest specially modified nanocarriers loaded with LXR agonists. In the past decades, a great progress has been made in this field. These macrophage-targeted nanocarriers loaded with LXR agonists are found to decrease atherosclerosis by reducing cholesterol accumulation and inflammatory reactions. Of important, these nanocarriers can alleviate side effects of LXR agonists. In this article, we briefly review the roles of macrophages in atherosclerosis, mechanisms of action of LXR agonists, and focus on the advances of macrophage-targeted nanocarriers loaded with LXR agonists. This work may promote the potential clinical application of these nanocarriers.

[Research progress on the modulation mechanism of electroacupuncture for learning and memory impairment after ischemic stroke].

Electroacupuncture may play a role in treatment of learning and memory impairment after ischemic stroke by regulating phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway, cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA)/cAMP response element binding protein (CREB) signaling pathway, nerve growth factor (NGF)/tyrosine kinase-A (TrkA) signaling pathway, Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway, Notch signaling pathway, erythropoietin-producing hepatocyte (Eph)/ephrin signaling pathway. The interactions among these pathways should be further explored in treatment of learning and memory impairment after ischemic stroke.

Benign lymphoepithelial cyst of parotid gland without human immunodeficiency virus infection: A case report.

BACKGROUND: Benign lymphoepithelial cyst (BLEC) of the parotid gland is a rare benign embryonic-dysplastic cystic tumor in the anterolateral neck that occurs most commonly in human immunodeficiency virus (HIV)-positive adults and rarely in non-acquired immune deficiency syndrome patients. The main presentation is a slow-growing, painless mass, and secondary infection may cause acute inflammatory symptoms. CASE SUMMARY: A 44-year-old Chinese male patient presented with a 1-year history of a mass in the left side of the neck. On physical examination, a mass similar in size and shape to a quail egg was found in the left parotid gland. The mass was tough, without tenderness, and easily moveable. The results of HIV tests, including antibody and nucleic acid tests and CD4+ T cell examination, were negative. Imaging examination revealed a left parotid gland mass. The patient underwent surgical treatment, and BLEC was diagnosed based on postoperative pathology. After 2 years of follow-up, the patient survived well without related discomfort. CONCLUSION: The detailed characteristics of a BLEC in a patient without HIV infection contribute to an improved understanding of this rare disease.

Rice glycosyltransferase gene UGT2 functions in salt stress tolerance under the regulation of bZIP23 transcription factor.

KEY MESSAGE: Rice glycosyltransferase gene UGT2 was identified to play a crucial role in salt tolerance. The transcription factor OsbZIP23 was demonstrated to regulate the UGT2 expression under stress conditions. UDP-glycosyltransferases (UGTs) play key roles in modulating plant responses to environmental challenges. In this study, we characterized a novel glycosyltransferase, UGT2, which plays an important role in salt stress responses in rice (Oryza sativa L). We found that seedlings overexpressing UGT2 exhibited better growth than wild type in shoot and root under hydroponic culture with salt stress treatments, while ugt2ko mutant lines suffered much more growth inhibition. When the soil-grown UGT2 transgenic plants were subjected to salt stress, we also found that ugt2ko mutant lines were severely withered and most of them died, while the overexpression lines grew well and had higher survival rate. Compared with wild-type plants, UGT2 overexpression greatly increased the expression levels of the reactive oxygen species scavenging genes and stress-responsive genes. Furthermore, the upstream regulatory mechanism of the UGT2 gene was identified and we found that a bZIP transcription factor, OsbZIP23, can bind to the UGT2 promoter and enhance the UGT2 transcription levels. This work reveals that OsbZIP23-UGT2 module may play a major role in regulating the salt stress tolerance in rice.

Estimating disability-adjusted life years for breast cancer and the impact of screening in female populations in China, 2015-2030: an exploratory prevalence-based analysis applying local weights.

BACKGROUND: Most cancer disability-adjusted life year (DALY) studies worldwide have used broad, generic disability weights (DWs); however, differences exist among populations and types of cancers. Using breast cancer as example, this study aimed to estimate the population-level DALYs in females in China and the impact of screening as well as applying local DWs. METHODS: Using multisource data, a prevalence-based model was constructed. (1) Overall years lived with disability (YLDs) were estimated by using numbers of prevalence cases, stage-specific proportions, and local DWs for breast cancer. Numbers of females and new breast cancer cases as well as local survival rates were used to calculate the number of prevalence cases. (2) Years of life lost (YLLs) were estimated using breast cancer mortality rates, female numbers and standard life expectancies. (3) The prevalence of and mortality due to breast cancer and associated DALYs from 2020 to 2030 were predicted using Joinpoint regression. (4) Assumptions considered for screening predictions included expanding coverage, reducing mortality due to breast cancer and improving early-stage proportion for breast cancer. RESULTS: In Chinese females, the estimated number of breast cancer DALYs was 2251.5 thousand (of 17.3% were YLDs) in 2015, which is predicted to increase by 26.7% (60.3% among those aged ≥ 65 years) in 2030 (2852.8 thousand) if the screening coverage (25.7%) stays unchanged. However, if the coverage can be achieved to 40.7% in 2030 (deduced from the "Healthy China Initiative"), DALYs would decrease by 1.5% among the screened age groups. Sensitivity analyses found that using local DWs would change the base-case values by ~ 10%. CONCLUSION: Estimates of DALYs due to breast cancer in China were lower (with a higher proportion of YLDs) than Global Burden of Disease Study numbers (2527.0 thousand, 8.2% were YLDs), suggesting the importance of the application of population-specific DWs. If the screening coverage remains unchanged, breast cancer-caused DALYs would continue to increase, especially among elderly individuals.

Case report: Transcatheter pulmonary valve-in-valve implantation in a deteriorated self-expandable valve caused by infective endocarditis.

Background: Infective endocarditis is a complication with high mortality in patients with congenital heart disease, particularly for those with bioprosthetic valve. Case summary: We report a case of a 54-year-old female with a history of tetralogy of Fallot who had been surgically repaired using a transannular patch due to severe pulmonary insufficiency with right heart enlargement and presented with worsening dyspnea. She had received transcatheter pulmonary valve implantation (TPVI) 5 years ago. Unfortunately, bioprosthesis-associated infective endocarditis occurred due to dental caries. Given persistent antibiotic medication, she became clinically stable with prosthesis functional recovery. However, dysfunctional bioprosthesis was still detected 3 years later, which was successfully treated by valve-in-valve TPVI with the help of modified buddy wire technique. At a 12-month follow-up after valve-in-valve TPVI, she was completely recovered with improved symptoms of heart failure. Conclusion: This is the first report of valve-in-valve TPVI of a self-expandable valve in a degenerated self-expandable valve. The case highlights increased surveillance for infective endocarditis of transcatheter pulmonary valve should be emphasized. Subsequent valve-in-valve TPVI is an effective treatment for valve failure in defined conditions improving the hemodynamics.

Molecular Thermal Motion Modulated Room-Temperature Phosphorescence for Multilevel Encryption.

The stimulus-responsive room-temperature phosphorescence (RTP) materials have become an increasingly significant topic in the fields of bioimaging, sensing, and anticounterfeiting. However, this kind of materials is scarce to date, especially for the ones with delicate stimulus-responsive behavior. Herein, a universal strategy for multilevel thermal erasure of RTP via chromatographic separation of host-guest doping RTP systems is proposed. The tunable host-guest systems, matrix materials, heating temperature, and time are demonstrated to allow precise six-level data encryption, QR code encryption, and thermochromic phosphorescence encryption. Mechanistic study reveals that the thermal-responsive property might be attributed to molecular thermal motion and the separation effect of the silica gel, which provides expanded applications of host-guest RTP materials such as cold chain break detection. This work offers a simple yet universal way to construct advanced responsive RTP materials.