Impacts of gene variants on drug effects-the foundation of genotype-guided pharmacologic therapy for long QT syndrome and short QT syndrome.

The clinical significance of optimal pharmacotherapy for inherited arrhythmias such as short QT syndrome (SQTS) and long QT syndrome (LQTS) has been increasingly recognised. The advancement of gene technology has opened up new possibilities for identifying genetic variations and investigating the pathophysiological roles and mechanisms of genetic arrhythmias. Numerous variants in various genes have been proven to be causative in genetic arrhythmias. Studies have demonstrated that the effectiveness of certain drugs is specific to the patient or genotype, indicating the important role of gene-variants in drug response. This review aims to summarize the reported data on the impact of different gene-variants on drug response in SQTS and LQTS, as well as discuss the potential mechanisms by which gene-variants alter drug response. These findings may provide valuable information for future studies on the influence of gene variants on drug efficacy and the development of genotype-guided or precision treatment for these diseases.

Increased extracellular matrix stiffness regulates myofibroblast transformation through induction of autophagy-mediated Kindlin-2 cytoplasmic translocation.

The extracellular matrix (ECM) mechanical properties regulate biological processes, such as fibroblast-myofibroblast transformation (FMT), which is a crucial component in pelvic organ prolapse (POP) development. The 'Kindlin-2' protein, expressed by fibroblasts, plays an important role in the development of the mesoderm, which is responsible for connective tissue formation; however, the role of Kindlin-2 in FMT remains to be explored. In this study, we aimed to explore the role of Kindlin-2 in FMT as it relates to POP. We found that ECM stiffness induces autophagy to translocate Kindlin-2 to the cytoplasm of L929 cells, where it interacts with and degrades MOB1, thereby facilitating Yes-associated protein (YAP) entry into the nucleus and influencing FMT progression. Stiffness-induced autophagy was inhibited when using an autophagy inhibitor, which blocked the translocation of Kindlin-2 to the cytoplasm and partially reversed high-stiffness-induced FMT. In patients with POP, we observed an increase in cytoplasmic Kindlin-2 and nuclear YAP levels. Similar changes in vaginal wall-associated proteins were observed in a mouse model of acute vaginal injury. In conclusion, Kindlin-2 is a key gene affecting ECM stiffness, which regulates FMT by inducing autophagy and may influence the development of POP.

Evaluation of the Efficacy of Sacubitril/Valsartan on Radiofrequency Ablation in Patients with Hypertension and Persistent Atrial Fibrillation.

OBJECTIVE: To evaluate whether the effect of radiofrequency ablation can be improved by using sacubitril/valsartan (S/V) to control blood pressure in hypertensive patients with persistent atrial fibrillation. METHODS: A total of 63 and 67 hypertension patients with persistent atrial fibrillation were enrolled in an S/V group and ACEI/ARB group, respectively. All patients underwent radiofrequency catheter ablation (RFCA). The blood pressure of the two groups was controlled within the range of 100-140 mmHg (high pressure) and 60-90 mmHg (low pressure). The clinical outcomes of the two groups were observed after 12 months of follow-up. RESULTS: No significant differences in blood pressure were observed between the S/V and ACEI/ARB groups. In addition, the recurrence rate of atrial fibrillation between the two groups was not different. The left atrial diameter was an independent predictor of recurrence (HR = 1.063, P = 0.008). However, in the heart failure subgroup, the recurrence rate of S/V was significantly lower than that of the ACEI/ARB group (P = 0.005), and Cox regression analysis showed that the recurrence risk of atrial fibrillation of the S/V group was 0.302 lower than that of the ACEI/ARB group. NT-proBNP, LVEF, and LAD were significantly improved in hypertension patients with heart failure when comparing cases before and at the end of follow-up. CONCLUSIONS: S/V is better than ACEI/ARB in reducing the recurrence of persistent atrial fibrillation in patients with hypertension and heart failure after RFCA.

Estrogen inhibits the differentiation of fibroblasts induced by high stiffness matrix by enhancing DNMT1 expression.

INTRODUCTION AND HYPOTHESIS: Pelvic organ prolapse(POP) is a multifactorial connective tissue disorder caused by damage to the supporting structures of the pelvic floor. Evidence from several studies suggests that anterior vaginal wall stiffness is higher in patients with POP, but the mechanisms involved remain unknown. METHODS: Tissue from the anterior vaginal wall of patients with POP or other benign diseases was obtained. The modulus of elasticity of the anterior vaginal wall was measured using a microindenter. Cells were cultured in vitro on acrylamide gels of different stiffness and treated with DNMT1 inhibitor, microtubule polymerisation inhibitor and estrogen. Western blot or immunohistochemical staining was performed to detect DNA Methyltransferase 1, α-smooth muscle actin(α-SMA) expression, and connective tissue growth factor(CTGF) expression. CONCLUSION: Estrogen can inhibit high stiffness matrix-induced fibroblast differentiation, by enhancing DNMT1 expression. This study may help to elucidate the complex crosstalk between fibroblasts and their surrounding matrix under healthy and pathological conditions and provide new insights into the options for material-related therapeutic applications.

Ferrostatin-1 alleviates the damage of C2C12 myoblast and mouse pelvic floor muscle induced by mechanical trauma.

Ferroptosis is a special form of regulated cell death, which is reported to play an important role in a variety of traumatic diseases by promoting lipid peroxidation and devastating cell membrane structure. Pelvic floor dysfunction (PFD) is a kind of disease affecting the quality and health of many women's lives, which is closely related to the injury of the pelvic floor muscle. Clinical findings have discovered that there is anomalous oxidative damage to the pelvic floor muscle in women with PFD caused by mechanical trauma, but the specific mechanism is still unclear. In this study, we explored the role of ferroptosis-associated oxidative mechanisms in mechanical stretching-induced pelvic floor muscle injury, and whether obesity predisposed pelvic floor muscle to ferroptosis from mechanical injury. Our results, in vitro, showed that mechanical stretch could induce oxidative damage to myoblasts and trigger ferroptosis. In addition, glutathione peroxidase 4 (GPX4) down-regulation and 15-lipoxygenase 1(15LOX-1) up-regulation exhibited the same variational characteristics as ferroptosis, which was much more pronounced in palmitic acid (PA)-treated myoblasts. Furthermore, ferroptosis induced by mechanical stretch could be rescued by ferroptosis inhibitor (ferrostatin-1). More importantly, in vivo, we found that the mitochondria of pelvic floor muscle shrank, which were consistent with the mitochondrial morphology of ferroptosis, and GPX4 and 15LOX-1 showed the same change observed in cells. In conclusion, our data suggest ferroptosis is involved in the injury of the pelvic floor muscle caused by mechanical stretching, and provide a novel insight for PFD therapy.

SHP-1 alleviates atrial fibrosis in atrial fibrillation by modulating STAT3 activation.

Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1) has a well-established role in myocardial infarction, yet its involvement in atrial fibrosis and atrial fibrillation (AF) has not been elucidated. As cardiac arrhythmias caused by AF are a major global health concern, we investigated whether SHP-1 modulates AF development. The degree of atrial fibrosis was examined using Masson's trichrome staining, and SHP-1 expression in the human atrium was assessed using quantitative polymerase chain reaction (qPCR), immunohistochemistry (IHC), and western blotting (WB). We also examined SHP-1 expression in cardiac tissue from an AF mouse model, as well as in angiotensin II (Ang II)-treated mouse atrial myocytes and fibroblasts. We found that SHP-1 expression was reduced with the aggravation of atrial fibrosis in clinical samples of patients with AF. SHP-1 was also downregulated in the heart tissue of AF mice and Ang II-treated myocytes and fibroblasts, compared with that in the control groups. Next, we demonstrated that SHP-1 overexpression alleviated AF severity in mice by injecting a lentiviral vector into the pericardial space. In Ang II-treated myocytes and fibroblasts, we observed excessive extracellular matrix (ECM) deposition, reactive oxygen species (ROS) generation, and transforming growth factor beta 1 (TGF-ß1)/mothers against decapentaplegic homolog 2 (SMAD2) pathway activation, all of which were counteracted by the overexpression of SHP-1. Our WB data showed that STAT3 activation was inversely correlated with SHP-1 expression in samples from patients with AF, AF mice, and Ang II-treated cells. Furthermore, administration of colivelin, a STAT3 agonist, in SHP-1-overexpressing, Ang II-treated myocytes and fibroblasts resulted in higher levels of ECM deposition, ROS generation, and TGF-ß1/SMAD2 activation. These findings indicate that SHP-1 regulates AF fibrosis progression by modulating STAT3 activation and is thus a potential treatment target for atrial fibrosis and AF.

Transformation of tetracycline by multipurpose Fe-Mn-Cu nano-composite oxide: Dual-synergies and dual-mechanisms.

The interaction between tetracycline (TTC) and mixed metallic oxides remains unclear, and even complexation usually is ignored. This study firstly distinguished the triple functions of adsorption, transformation and complexation in presence of Fe-Mn-Cu nano-composite metallic oxide (FMC) on TTC. Rapid adsorption and faint complexation initiated the transformation that dominated the entire reactions at 180 min, which completed TTC removal (up to 99.04%) synergistically within 48 h. Environmental factors (dosage, pH and coexisting ions) had small influence on TTC removal, which primarily depended on the stable transformation characteristics of FMC. Kinetic models incorporating pseudo-second-order kinetics and transformation reaction kinetics demonstrated that the surface sites of FMC promoted electron transfer process through chemical adsorption and electrostatic attraction. ProtoFit program coupled with characterization methods concluded that Cu-OH was the main reaction site of FMC where the protonated surface favored to generate·O2-. Meanwhile, three metal ions developed simultaneous mediated transformation reactions on TTC in liquid phase, and·O2- induced the production of·OH. The transformed products were subjected to toxicity assessment, which had lost antimicrobial properties toward Escherichia coli. Insights gained from this study can refine the dual mechanisms of multipurpose FMC in solid and liquid phases underlying TTC transformation.

Prime editing: advances and therapeutic applications.

Clustered regularly interspaced short palindromic repeats-associated protein 9 (CRISPR-Cas)-mediated genome editing has revolutionized biomedical research and will likely change the therapeutic and diagnostic landscape. However, CRISPR-Cas9, which edits DNA by activating DNA double-strand break (DSB) repair pathways, is not always sufficient for gene therapy applications where precise mutation repair is required. Prime editing, the latest revolution in genome-editing technologies, can achieve any possible base substitution, insertion, or deletion without the requirement for DSBs. However, prime editing is still in its infancy, and further development is needed to improve editing efficiency and delivery strategies for therapeutic applications. We summarize latest developments in the optimization of prime editor (PE) variants with improved editing efficiency and precision. Moreover, we highlight some potential therapeutic applications.

Structural Fusion Yields Guest Acceptors that Enable Ternary Organic Solar Cells with 18.77 % Efficiency.

The design and selection of a suitable guest acceptor are particularly important for improving the photovoltaic performance of ternary organic solar cells (OSCs). Herein, we designed and successfully synthesized two asymmetric silicon-oxygen bridged guest acceptors, which featured distinct blue-shifted absorption, upshifted lowest unoccupied molecular orbital energy levels, and larger dipole moments than symmetric silicon-oxygen-bridged acceptor. Ternary devices with the incorporation of 14.2 wt % these two asymmetric guest acceptors exhibited excellent performance with power conversion efficiencies (PCEs) of 18.22 % and 18.77 %, respectively. Our success in precise control of material properties via structural fusion of five-membered carbon linkages and six-membered silicon-oxygen connection at the central electron-donating core unit of fused-ring electron acceptors can attract considerable attention and bring new vigor and vitality for developing new materials toward more efficient OSCs.

Sex Pheromone Receptor-Derived Peptide Biosensor for Efficient Monitoring of the Cotton Bollworm Helicoverpa armigera.

The cotton bollworm, Helicoverpa armigera (H. armigera), causes damage to a wide range of cultivated crops and is one of the pests with the greatest economic importance for global agriculture. Currently, the detection of H. armigera is based on manual sampling. A low limit of detection (LOD), convenient, and real-time monitoring method is urgently needed for its early warning and efficient management. Here, we characterized the amino acid sequence in the sex pheromone receptors (SPRs) recognizing the pheromone components of H. armigera by three-dimensional (3D) modeling and molecular docking. Next, sex pheromone receptor-derived peptides (SPRPs) were synthesized and conjugated to nanotubes by chemical connection. The modified nanotubes were used to fabricate a sensor capable of real-time monitoring of gaseous sex pheromone compounds with a low LOD (∼10 ppb for Z11-16:Ald) and selectivity, and the sensor was able to detect a single live H. armigera. Furthermore, the developed biosensor allowed direct monitoring of the pheromone release dynamics by female H. armigera and showed that the release was instantly reduced in response to light. Here, we report the first demonstration of a biosensing method for detecting gaseous sex pheromones and live H. armigera. The findings show the great potential of the SPRP sensor for broad applications in insect biology study and infestation monitoring.

Gynecological prevention and control model based on ward rearrangement and zoning management in pandemic period of COVID-19.

By April 25, 2020, the outbreak of COVID-19 caused 2,719,897 confirmed cases and 18,7705 deaths globally, remarkably more than severe acute respiratory syndrome (SARS) (8273 cases, 775 deaths) and middle east respiratory syndrome (MERS) (1139 cases, 431 deaths) in 2003 and 2013, respectively. Gynecology is a specialty department with many critical and severe patients. Consequently, it is of preeminent importance to formulate the in-patient management process. Rearranging the gynecological wards and managing ward partition, as well as the medical protection measures in specialized areas, are suitable for the current prevention and control for COVID-19 pandemic and the therapeutic requirements of patients. To effectively minimize nosocomial infections during the COVID-19 pandemic period, our department implemented a novel prevention strategy based on the ward redesign and partition management. With this model, our department effectively protected the safety and health of patients and medical care staff from cross and nosocomial infection in the hospital. Now we would like to share the experience and strategies we implemented as following.

Restoration of NAD+ homeostasis protects C2C12 myoblasts and mouse levator ani muscle from mechanical stress-induced damage.

Excessive mechanical traction damages the levator ani muscle (LAM), increasing the incidence of pelvic floor dysfunction (PFD). In this study, we explored the effects of oxidized nicotinamide adenine dinucleotide (NAD+) on the damage to both muscle cells and LAM tissue induced by mechanical stress (MS) at the cellular and animal levels. The cell damage model was established using a four-point bending system. The LAM damage model was established using vaginal distention and traction. Exogenous addition of PJ34, an inhibitor of poly (ADP-ribose) polymerase-1 (PARP-1), and the nicotinamide mononucleotide (NMN) precursor of NAD+ increased NAD+ levels. ATP content and mitochondrial membrane potential were measured to assess mitochondrial function. NAD+ levels, cell viability, and PARP-1 activity were detected using commercial kits. DNA damage in cells was detected with immunofluorescence staining, and LAM damage was detected with tissue TUNEL staining. PARP-1 activity and DNA damage of LAM were detected by immunohistochemistry. A small amount of DNA damage and PARP-1 activation did not affect NAD+ levels, while excessive DNA damage and PARP-1 activation led to an imbalance of NAD+ homeostasis. Furthermore, increasing NAD+ levels in vivo and in vitro could rescue mitochondrial dysfunction and damage to both muscle cells and LAM tissue induced by MS. In conclusion, MS can induce damage to both C2C12 cells and LAM tissue. Restoring NAD+ homeostasis can rescue this damage by improving mitochondrial function.

An immunogenic cell injury module for the single-cell multiplexed activity metabolomics platform to identify promising anti-cancer natural products.

Natural products constitute and significantly impact many current anti-cancer medical interventions. A subset of natural products induces injury processes in malignant cells that recruit and activate host immune cells to produce an adaptive anti-cancer immune response, a process known as immunogenic cell death. However, a challenge in the field is to delineate forms of cell death and injury that best promote durable antitumor immunity. Addressing this with a single-cell chemical biology natural product discovery platform, like multiplex activity metabolomics, would be especially valuable in human leukemia, where cancer cells are heterogeneous and may react differently to the same compounds. Herein, a new ten-color, fluorescent cell barcoding-compatible module measuring six immunogenic cell injury signaling readouts are as follows: DNA damage response (γH2AX), apoptosis (cCAS3), necroptosis (p-MLKL), mitosis (p-Histone H3), autophagy (LC3), and the unfolded protein response (p-EIF2α). A proof-of-concept screen was performed to validate functional changes in single cells induced by secondary metabolites with known mechanisms within bacterial extracts. This assay was then applied in multiplexed activity metabolomics to reveal an unexpected mammalian cell injury profile induced by the natural product narbomycin. Finally, the functional consequences of injury pathways on immunogenicity were compared with three canonical assays for immunogenic hallmarks, ATP, HMGB1, and calreticulin, to correlate secondary metabolite-induced cell injury profiles with canonical markers of immunogenic cell death. In total, this work demonstrated a new phenotypic screen for discovery of natural products that modulate injury response pathways that can contribute to cancer immunogenicity.

A Preclinical Study on Brugada Syndrome with a CACNB2 Variant Using Human Cardiomyocytes from Induced Pluripotent Stem Cells.

Aims: Some gene variants in the sodium channels, as well as calcium channels, have been associated with Brugada syndrome (BrS). However, the investigation of the human cellular phenotype and the use of drugs for BrS in presence of variant in the calcium channel subunit is still lacking. Objectives: The objective of this study was to establish a cellular model of BrS in the presence of a CACNB2 variant of uncertain significance (c.425C > T/p.S142F) using human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) and test drug effects using this model. Methods and results: This study recruited cells from a patient with Brugada syndrome (BrS) and recurrent ventricular fibrillation carrying a missense variant in CACNB2 as well as from three healthy independent persons. These cells (hiPSC-CMs) generated from skin biopsies of healthy persons and the BrS patient (BrS-hiPSC-CMs) as well as CRISPR/Cas9 corrected cells (isogenic control, site-variant corrected) were used for this study. The hiPSC-CMs from the BrS patient showed a significantly reduced L-type calcium channel current (ICa-L) compared with the healthy control hiPSC-CMs. The inactivation curve was shifted to a more positive potential and the recovery from inactivation was accelerated. The protein expression of CACNB2 of the hiPSC-CMs from the BrS-patient was significantly decreased compared with healthy hiPSC-CMs. Moreover, the correction of the CACNB2 site-variant rescued the changes seen in the hiPSC-CMs of the BrS patient to the normal state. These data indicate that the CACNB2 gene variant led to loss-of-function of L-type calcium channels in hiPSC-CMs from the BrS patient. Strikingly, arrhythmia events were more frequently detected in BrS-hiPSC-CMs. Bisoprolol (beta-blockers) at low concentration and quinidine decreased arrhythmic events. Conclusions: The CACNB2 variant (c.425C > T/p.S142F) causes a loss-of-function of L-type calcium channels and is pathogenic for this type of BrS. Bisoprolol and quinidine may be effective for treating BrS with this variant.

Nervous system manifestations related to COVID-19 and their possible mechanisms.

In December 2019, the novel coronavirus disease (COVID-19) due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection broke. With the gradual deepening understanding of SARS-CoV-2 and COVID-19, researchers and clinicians noticed that this disease is closely related to the nervous system and has complex effects on the central nervous system (CNS) and peripheral nervous system (PNS). In this review, we summarize the effects and mechanisms of SARS-CoV-2 on the nervous system, including the pathways of invasion, direct and indirect effects, and associated neuropsychiatric diseases, to deepen our knowledge and understanding of the relationship between COVID-19 and the nervous system.

Ligation-assisted homologous recombination enables precise genome editing by deploying both MMEJ and HDR.

CRISPR/Cas12a is a single effector nuclease that, like CRISPR/Cas9, has been harnessed for genome editing based on its ability to generate targeted DNA double strand breaks (DSBs). Unlike the blunt-ended DSB generated by Cas9, Cas12a generates sticky-ended DSB that could potentially aid precise genome editing, but this unique feature has thus far been underutilized. In the current study, we found that a short double-stranded DNA (dsDNA) repair template containing a sticky end that matched one of the Cas12a-generated DSB ends and a homologous arm sharing homology with the genomic region adjacent to the other end of the DSB enabled precise repair of the DSB and introduced a desired nucleotide substitution. We termed this strategy 'Ligation-Assisted Homologous Recombination' (LAHR). Compared to the single-stranded oligo deoxyribonucleotide (ssODN)-mediated homology directed repair (HDR), LAHR yields relatively high editing efficiency as demonstrated for both a reporter gene and endogenous genes. We found that both HDR and microhomology-mediated end joining (MMEJ) mechanisms are involved in the LAHR process. Our LAHR genome editing strategy, extends the repertoire of genome editing technologies and provides a broader understanding of the type and role of DNA repair mechanisms involved in genome editing.

Smartphone-Based Electrochemical Biosensors for Directly Detecting Serum-Derived Exosomes and Monitoring Their Secretion.

Exosomes are potential biomarkers, which play an important role in early diagnosis and prognosis prediction of cancer-related diseases. Nevertheless, direct quantification of exosomes in biological fluid, especially in point-of-care tests (POCTs), remains extremely challenging. Herein, we developed a sensitive and portable electrochemical biosensor in combination with smartphones for quantitative analysis of exosomes. The improved double-antibody sandwich method-based poly-enzyme signal amplification was adopted to detect exosomes. We could detect as low as 7.23 ng of CD63-positive exosomes in 5 µL of serum within 2 h. Importantly, we demonstrated that the biosensor worked well with microliter-level serum and cell culture supernatant. The biosensor holds great potential for the detection of CD-63-expressing exosomes in early diagnosis of prostate disease because CD63-positive exosomes were less detected from the prostate patient serum. Also, the biosensor was used to monitor the secretion of exosomes with the drug therapy, showing a close relationship between the secretion of exosomes and the concentration of cisplatin. The biosensing platform provides a novel way toward POCT for the diagnosis and prognosis prediction of prostate disease and other diseases via biomarker expression levels of exosomes.

Evaluating the performance of bridging-assembly chelating flocculant for heavy metals removal: Role of branched architectures.

A novel chelating flocculant with branched architectures, polyacrylamide grafted maleoyl chitosan-mercaptoacetic acid (PAM-g-M(CS-MA)), was successfully fabricated using maleic anhydride as the "bridge" between chitosan and polyacrylamide. The functional groups and structural characteristic information of copolymers were obtained via characterization analysis. Flocculation performance was systematically investigated via purifying a series of simulated wastewater containing Cu or Cd. The properties of the flocs were studied to give in-depth evidences for the role of chelation groups and branched architectures in flocculation. Results indicated that PAM-g-M(CS-MA) showed excellent flocculation capacity for heavy metals in high concentrations and was superior to other chelating flocculants. The maximum flocculation efficiency of Cu (93.90%) and Cd (92.47%) was achieved by PAM-g-M(CS-MA) at pH 7, dosage of 100 mg L-1 and stirring speed of 90 rpm. The flocculation mechanisms of PAM-g-M(CS-MA) were deeply explored through the analyses of floc properties. The strong synergistic chelation of mercapto, carboxyl, amide and hydroxyl groups predominated for the capturing of heavy metals; and the branched architectures facilitated the formation of large and stable flocs via adsorption and bridging-furl effect. This study provided a solid foundation for the fabrication of flocculants for heavy metal wastewater treatment.

Highly sensitive detection of multiple proteins from single cells by MoS2-FET biosensors.

Single-cell analysis of proteins is critical to gain precise information regarding the mechanisms that dictate the heterogeneity in cellular phenotypes and their differential response to internal and external stimuli. However, tools that allow sensitive and easy measurement of proteins in individual cells are still limited. The emerging semiconductor-based bioelectronics may provide a new approach to overcome the challenges in this field, however its utility in single-cell protein analysis has not been explored. In this study, we investigated multiple protein detection in single cells by MoS2 field effect transistors (MoS2-FETs) modified with specific biological probes. First, ß-actin antibody was connected to the surface of MoS2-FETs by covalent bonds, and the fabricated device was tested using ß-actin solution with concentrations from 10-9 to 10-3 µg/µL. Next, we examined the application of MoS2-FET for protein analysis in complex biological samples, and the device showed electrical signal response to human embryonic kidney cell line HEK293T in a dose-dependent manner. Furthermore, we applied this method to analyze individual liver cancer MHCC-97L cells, targeting four cellular proteins, including ß-actin, epidermal growth factor receptor, sirtuin-2, and glyceraldehyde-3-phosphate dehydrogenase. The devices modified with corresponding probes could identify the target proteins and showed cell number-dependent responses. As a proof of principle, we demonstrated sensitive and multiplexed detection of proteins in single cells using MoS2-FETs. The biosensor and this detection method are cost-efficient and user-friendly with broad application prospects in biological studies and clinical diagnosis.

Shear-Thinning and Designable Responsive Supramolecular DNA Hydrogels Based on Chemically Branched DNA.

A novel supramolecular DNA hydrogel system was designed based on a directly synthesized chemically branched DNA. For the hydrogel formation, a self-dimer DNA with two sticky ends was designed as the linker to induce the gelation of B-Y. By programing the linker sequence, thermal and metal-ion responsiveness could be introduced into this hydrogel system. This supramolecular DNA hydrogel shows shear-thinning, designable responsiveness, and good biocompatibility, which will simplify the hydrogel composition and preparation process of the supramolecular DNA hydrogel and accelerate its biomedical applications.