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Objectives This review presents a comprehensive overview of the rapidly evolving digital healthcare industry, aiming to provide a broad understanding of the recent landscape and directions for the future of digital healthcare. Methods This review examines the key trends in sectors of the digital healthcare industry, which can be divided into four main categories: digital hardware, software solutions, platforms, and enablers. We discuss electroceuticals, wearables, standalone medical software, non-medical health management services, telehealth, decentralized clinical trials, and infrastructural systems such as health data systems. The review covers both global and domestic perspectives, addressing definitions, significance, revenue trends, major companies, regulations, and socioenvironmental factors. Results Diverse growth patterns are evident across digital healthcare sectors. The applications of electroceuticals are expanding. Wearables are becoming more ubiquitous, facilitating continuous health monitoring and data collection. Artificial intelligence in standalone medical software is demonstrating clinical efficacy, with regulatory frameworks adapting to support commercialization. Non-medical health management services are expanding their scope to address chronic conditions under professional guidance. Telemedicine and decentralized clinical trials are gaining traction, driven by the need for flexible healthcare solutions post-pandemic. Efforts to build robust digital infrastructure with health data are underway, supported by data banks and data aggregation platforms. Conclusions Advancements in digital healthcare create a dynamic, transformative landscape, integrating, complementing, and offering alternatives to traditional paradigms. This evolution is driven by continuous innovation, increased stakeholder participation, regulatory adaptations promoting commercialization, and supportive initiatives. Ongoing discussions about optimal digital technology integration and effective healthcare strategy implementation are essential for progress.

Cardiovascular disease remains a global health concern. Stem cell therapy utilizing human cardiac progenitor cells (hCPCs) shows promise in treating cardiac vascular disease. However, limited availability and senescence of hCPCs hinder their widespread use. To address these challenges, researchers are exploring innovative approaches. In this study, a bioengineered cell culture plate was developed to mimic the natural cardiac tissue microenvironment. It was coated with a combination of extracellular matrix (ECM) peptide motifs and mussel adhesive protein (MAP). The selected ECM peptide motifs, derived from fibronectin and vitronectin, play crucial roles in hCPCs. Results revealed that the Fibro-P and Vitro-P coated plates significantly improved hCPC adhesion, proliferation, migration, and differentiation compared to uncoated plates. Additionally, long-term culture on the coated plates delayed cellular senescence and maintained hCPC stemness. These enhancements were attributed to the activation of integrin downstream signaling pathways. The findings suggest that the engineered ECM peptide motif-MAP-coated plates hold potential for enhancing the therapeutic efficacy of stem cell-based therapies in cardiac tissue engineering and regenerative medicine.

Abstract Small molecule can be utilized to restore the effectiveness of existing major classes of antibiotics against antibiotic‐resistant bacteria. In this study, it is demonstrated that celastrol, a natural compound, can modify the bacterial cell wall and subsequently render bacteria more suceptible to β‐lactam antibiotics. It is shown that celastrol leads to incomplete cell wall crosslinking by modulating levels of c‐di‐AMP, a secondary messenger, in methicillin‐resistant Staphylococcus aureus (MRSA). This mechanism enables celastrol to act as a potentiator, effectively rendering MRSA susceptible to a range of penicillins and cephalosporins. Restoration of in vivo susceptibility of MRSA to methicillin is also demonstrated using a sepsis animal model by co‐administering methicillin along with celastrol at a much lower amount than that of methicillin. The results suggest a novel approach for developing potentiators for major classes of antibiotics by exploring molecules that re‐program metabolic pathways to reverse β‐lactam‐resistant strains to susceptible strains.

To transition the construction industry towards sustainable practices, we challenge wasteful methods and non-renewable systems by harnessing local biological materials and augmenting them to describe contemporary forms. Our work enhances the primarily compressive material properties of sand-based compounds to develop a construction method for tension–compression anticlastic shellular structures. We have developed a novel bilayer system with multiscale induced behavior called ChitoSand, made primarily of a sand matrix, incorporating chitosan biopolymer as a microstructural binder, short flax fibers to boost tensile capacity at the mesoscale, and citric acid to increase plasticity, which is then underlaid by a sewn burlap fabric base layer to raise the bending capacity at the macroscale. This produces a fully biodegradable material system that we paired with anticlastic geometry calculations to enhance effective material use and structural form. We then developed an earthen construction workflow that uses reusable pneumatic formwork holding the ChitoSand bilayer composite during hardening in ambient conditions. This research yields a tension–compression system with modern geometry and a minimized environmental footprint.

Abstract Backgrounds Alzheimer’s disease is the most common cause of dementia, and currently, there is no disease-modifying treatment. Favorable functional outcomes and reduction of amyloid levels were observed following transplantation of mesenchymal stem cells (MSCs) in animal studies. Objectives We conducted a phase I clinical trial in nine patients with mild-to-moderate Alzheimer’s disease dementia to evaluate the safety and dose-limiting toxicity of three repeated intracerebroventricular injections of human umbilical cord blood–derived MSCs (hUCB-MSCs). Methods We recruited nine mild-to-moderate Alzheimer’s disease dementia patients from Samsung Medical Center, Seoul, Republic of Korea. Four weeks prior to MSC administration, the Ommaya reservoir was implanted into the right lateral ventricle of the patients. Three patients received a low dose (1.0 × 107 cells/2 mL), and six patients received a high dose (3.0 × 107 cells/2 mL) of hUCB-MSCs. Three repeated injections of MSCs were performed (4-week intervals) in all nine patients. These patients were followed up to 12 weeks after the first hUCB-MSC injection and an additional 36 months in the extended observation study. Results After hUCB-MSC injection, the most common adverse event was fever (n = 9) followed by headache (n = 7), nausea (n = 5), and vomiting (n = 4), which all subsided within 36 h. There were three serious adverse events in two participants that were considered to have arisen from the investigational product. Fever in a low dose participant and nausea with vomiting in another low dose participant each required extended hospitalization by a day. There were no dose-limiting toxicities. Five participants completed the 36-month extended observation study, and no further serious adverse events were observed. Conclusions Three repeated administrations of hUCB-MSCs into the lateral ventricle via an Ommaya reservoir were feasible, relatively and sufficiently safe, and well-tolerated. Currently, we are undergoing an extended follow-up study for those who participated in a phase IIa trial where upon completion, we hope to gain a deeper understanding of the clinical efficacy of MSC AD therapy. Trial registration ClinicalTrials.gov NCT02054208. Registered on 4 February 2014. ClinicalTrials.gov NCT03172117. Registered on 1 June 2017

Bone maintenance: regulating cells that break down bone A gene-controlling protein called Spi-C promotes the development of bone-processing cells called osteoclasts; details of the molecular mechanisms involved will aid understanding of Spi-C’s role in bone health and disease. Osteoclasts degrade bone during the normal process of bone remodeling, balanced by the activity of osteoblast cells that form new bone. Excessive osteoclast activity can cause the bone loss associated with various bone diseases including early-onset osteoporosis. Researchers in South Korea led by Soo Young Lee at Ewha Womans University and Na Kyung Lee at Soonchunhyang University, Asan, found that Spi-C promotes osteoclast development by activating genes that code for key proteins of a signaling pathway known to be crucial for bone health. Drugs that interfere with Spi-C activity may therefore offer a new approach for treating bone disease.

It has been widely accepted that mesenchymal stem cells (MSCs) can evade the immune surveillance of the recipient. However, emerging research cast doubt on whether MSCs are intrinsically immune-privileged. Previously, we observed that the transplantation of human MSCs (hMSCs) into the mouse parenchyma attracted a high infiltration of leukocytes into the injection tract. Thus, in order to reduce the immune responses generated by hMSCs, the aim of this study was to assess which immunosuppressant condition (dexamethasone only, tacrolimus only, or dexamethasone and tacrolimus together) would not only reduce the overall immune response but also enhance the persistence of MSCs engrafted into the caudate putamen of wild-type C57BL/6 mice. According to immunohistochemical analysis, compared to the hMSC only group, the administration of immunosuppressants (for all three conditions) reduced the infiltration of CD45-positive leukocytes and neutrophils at the site of injection. The highest hMSC persistence was detected from the group that received combinatorial administrations of dexamethasone and tacrolimus. Moreover, compared to the immunocompetent WT mouse, higher MSC engraftment was observed from the immunodeficient BALB/c mice. The results of this study support the use of immunosuppressants to tackle MSC-mediated immune responses and to possibly prolong the engraftment of transplanted MSCs.

We have recently reported on how transplantation of human mesenchymal stem cells (MSCs) into the mouse parenchyma generated immune responses. To facilitate the clinical translation of MSC-based AD therapy, the safety and efficacy of human derived MSCs (hMSCs) must be confirmed in the pre-clinical stage. Thus, it is imperative to investigate measures to reduce immune responses exerted via xenotransplantation. In this study, immunosuppressants were co-administered to mice that had received injections of hMSCs into the parenchyma. Prior to performing experiments using transgenic AD mice (5xFAD), varying immunosuppressant regimens were tested in wild-type (WT) mice and the combination of dexamethasone and tofacitinib (DexaTofa) revealed to be effective in enhancing the persistence of hMSCs. According to transcriptome sequencing and immunohistochemical analyses, administration of DexaTofa reduced immune responses generated via transplantation of hMSCs in the parenchyma of 5xFAD mice. Significant mitigation of amyloid burden, however, was not noted following transplantation of hMSCs alone or hMSCs with DexaTofa. The efficacy of the immunosuppressant regimen should be tested in multiple AD mouse models to promote its successful application and use in AD stem cell therapy.

Previously we conducted a Phase I/IIa clinical trial in nine patients with mild to moderate Alzheimer’s disease (AD). Unexpectedly, all patients who were given injections of human-umbilical cord-blood-derived mesenchymal stem cells (hUCB-MSCs) developed fever which subsided after 24 h. Several possible causes of transient fever include bacterial infection, inflammatory reaction from the cell culture media composition, or the cells themselves. To delineate these causes, first we compared the levels of several cytokines in the cerebrospinal fluid (CSF) of AD patients who received saline (placebo) or hUCB-MSC injections, respectively. Compared to the placebo group, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and c-reactive protein (CRP) levels were increased in the hUCB-MSC group. Negative bacterial culture results of the CSF samples and the fact that the same hUCB-MSC administration procedure was used for both the placebo and hUCB-MSC groups ruled out the bacterial infection hypothesis. However, it was not yet clear as to whether the transplanted cells or the composition of the cell culture media generated the transient fever. Therefore, we carried out intracerebroventricular (ICV) injections of hUCB-MSCs in a 5xFAD mouse model of AD. Interestingly, we discovered that pro-inflammatory cytokine levels were higher in the hUCB-MSC group. Taken together, our data suggest that the cause of transient inflammatory response observed from both the clinical trial and mouse study was due to the transplanted hUCB-MSCs.

This study aimed to investigate the effects of exercise-induced muscle fatigue in the unaffected knee joint on postural control and kinematic changes in stroke patients. Forty participants (20 stroke patients, 20 age-matched healthy participants) were recruited. To induce fatigue, maximum voluntary isometric contractions were performed in the unaffected knee joint in a Leg Extension Rehab exercise machine using the pneumatic resistance. We measured static and dynamic balance and lower-limb kinematics during gait. Changes in postural control parameters anteroposterior sway speed and total center of pressure distance differed significantly between the stroke and control groups. In addition, changes in gait kinematic parameters knee and ankle angles of initial contact differed significantly between stroke (paretic and non-paretic) and control groups. Muscle fatigue in the unaffected knee and ankle impaired postural control and debilitates kinematic movement of ipsilateral and contralateral lower limbs, and may place the fatigued stroke patients at greater risk for falls.

This study investigated the effect of transcranial direct current stimulation (tDCS) polarity depending on lateralized function of task property in normal individuals performing visuomotor and simple repetitive tasks. Thirty healthy participants with no neurological disorders were recruited to participate in this study. Participants were randomly allocated into active or control condition. For the active condition, tDCS intensity was 2 mA with stimulation applied for 15 minutes to the right hemisphere (tDCS condition). For the sham control, electrodes were placed in the same position, but the stimulator was turned off after 30 seconds (sham condition). The tapping and tracking task tests were performed before and after for both conditions. Univariate analysis revealed significant difference only in the tracking task. For direct comparison of both tasks within each group, the tracking task had significantly higher Z score than the tapping task in the tDCS group (P < 0.05). Thus, our study indicates that stimulation of the right hemisphere using tDCS can effectively improve visuomotor (tracking) task over simple repetitive (tapping) task.

Transcranial direct current stimulation (tDCS), an emerging technique for non-invasive brain stimulation, is increasingly used to induce changes in cortical excitability and modulate motor behavior, especially for upper limbs. The purpose of this study was to investigate the effects of tDCS of the primary motor cortex on visuomotor coordination based on three levels of task difficulty in healthy subjects. Thirty-eight healthy participants underwent real tDCS or sham tDCS. Using a single-blind, sham-controlled crossover design, tDCS was applied to the primary motor cortex. For real tDCS conditions, tDCS intensity was 1 mA while stimulation was applied for 15 minutes. For the sham tDCS, electrodes were placed in the same position, but the stimulator was turned off after 5 seconds. Visuomotor tracking task, consisting of three levels (levels 1, 2, 3) of difficulty with higher level indicating greater difficulty, was performed before and after tDCS application. At level 2, real tDCS of the primary motor cortex improved the accurate index compared to the sham tDCS. However, at levels 1 and 3, the accurate index was not significantly increased after real tDCS compared to the sham tDCS. These findings suggest that tasks of moderate difficulty may improve visuomotor coordination in healthy subjects when tDCS is applied compared with easier or more difficult tasks.

Mesenchymal stem cells (MSCs) have a promising role as a therapeutic agent for neurodegenerative diseases such as Alzheimer's disease (AD). Prior studies suggested that intra-arterially administered MSCs are engrafted into the brain in stroke or traumatic brain injury (TBI) animal models. However, a controversial standpoint exists in terms of the integrity of the blood brain barrier (BBB) in transgenic AD mice. The primary goal of this study was to explore the feasibility of delivering human umbilical cord-blood derived mesenchymal stem cells (hUCB-MSCs) into the brains of non-transgenic WT (C3H/C57) and transgenic AD (APP/PS1) mice through the intra-arterial (IA) route. Through two experiments, mice were infused with hUCB-MSCs via the right internal carotid artery and were sacrificed at two different time points: 6 hours (experiment 1) or 5 minutes (experiment 2) after infusion. In both experiments, no cells were detected in the brain parenchyma while MSCs were detected in the cerebrovasculature in experiment 2. The results from this study highlight that intra-arterial delivery of MSCs is not the most favorable route to be implemented as a potential therapeutic approach for AD.

Cytoplasmic presence of Hsp60, which is principally a nuclear gene-encoded mitochondrial chaperonin, has frequently been stated, but its role in intracellular signaling is largely unknown. In this study, we demonstrate that the cytosolic Hsp60 promotes the TNF-alpha-mediated activation of the IKK/NF-kappaB survival pathway via direct interaction with IKKalpha/beta in the cytoplasm. Selective loss or blockade of cytosolic Hsp60 by specific antisense oligonucleotide or neutralizing antibody diminished the IKK/NF-kappaB activation and the expression of NF-kappaB target genes, such as Bfl-1/A1 and MnSOD, which thus augmented intracellular ROS production and ASK1-dependent cell death, in response to TNF-alpha. Conversely, the ectopic expression of cytosol-targeted Hsp60 enhanced IKK/NF-kappaB activation. Mechanistically, the cytosolic Hsp60 enhanced IKK activation via upregulating the activation-dependent serine phosphorylation in a chaperone-independent manner. Furthermore, transgenic mouse study showed that the cytosolic Hsp60 suppressed hepatic cell death induced by diethylnitrosamine in vivo. The cytosolic Hsp60 is likely to be a regulatory component of IKK complex and it implicates the first mitochondrial factor that regulates cell survival via NF-kappaB pathway.

The safety and efficacy of both cell and gene therapies have been demonstrated in numerous preclinical and clinical trials. Chimeric antigen receptor T (CAR-T) cell therapy, which leverages the technologies of both cell and gene therapies, has also shown great promise for treating various cancers. Advancements in pertinent fields have also highlighted challenges faced while manufacturing cell and gene therapy products. Potential problems and obstacles must be addressed to ease the clinical translation of individual therapies. Literature reviews of representative cell-based, gene-based, and cell-based gene therapies with regard to their general manufacturing processes, the challenges faced during manufacturing, and QC specifications are limited. We review the general manufacturing processes of cell and gene therapies, including those involving mesenchymal stem cells, viral vectors, and CAR-T cells. The complexities associated with the manufacturing processes and subsequent QC/validation processes may present challenges that could impede the clinical progression of the products. This article addresses these potential challenges. Further, we discuss the use of the manufacturing model and its impact on cell and gene therapy. [ABSTRACT FROM AUTHOR]

Objectives: The aim of this study was to determine whether exercises can change the cervical angle and respiratory function in smartphone users. Methods: Thirty healthy volunteers were recruited. The subjects were randomly divided into an exercise group and a control group. All participants used a smartphone for 1 hour while maintaining a sitting posture. Then, each group performed their assigned activity. The exercise group performed two types of exercises and the control group maintained routine activities for 20 minutes. To investigate the changes in cervical angle and respiratory function, we measured the craniovertebral angle by using a spirometer. Results: Statistically significant differences were noted in the craniovertebral angle, forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), FEV1/FVC ratio, peak expiratory flow, maximal inspiratory pressure, and maximal expiratory pressure of the two groups (p < 0.05). Conclusion: Our findings showed that proper exercise could be a good method of improving the cervical angle and respiratory function in smartphone users. [ABSTRACT FROM AUTHOR]

Background: Decreased hemoglobin levels increase the risk of developing dementia among the elderly. However, the underlying mechanisms that link decreased hemoglobin levels to incident dementia still remain unclear, possibly due to the fact that few studies have reported on the relationship between low hemoglobin levels and neuroimaging markers. We, therefore, investigated the relationships between decreased hemoglobin levels, cerebral small-vessel disease (CSVD), and cortical atrophy in cognitively healthy women and men.Methods: Cognitively normal women (n = 1,022) and men (n = 1,018) who underwent medical check-ups and magnetic resonance imaging (MRI) were enrolled at a health promotion center. We measured hemoglobin levels, white matter hyperintensities (WMH) scales, lacunes, and microbleeds. Cortical thickness was automatically measured using surface based methods. Multivariate regression analyses were performed after controlling for possible confounders.Results: Decreased hemoglobin levels were not associated with the presence of WMH, lacunes, or microbleeds in women and men. Among women, decreased hemoglobin levels were associated with decreased cortical thickness in the frontal (Estimates, 95% confidence interval, -0.007, (-0.013, -0.001)), temporal (-0.010, (-0.018, -0.002)), parietal (-0.009, (-0.015, -0.003)), and occipital regions (-0.011, (-0.019, -0.003)). Among men, however, no associations were observed between hemoglobin levels and cortical thickness.Conclusion: Our findings suggested that decreased hemoglobin levels affected cortical atrophy, but not increased CSVD, among women, although the association is modest. Given the paucity of modifiable risk factors for age-related cognitive decline, our results have important public health implications. [ABSTRACT FROM AUTHOR]

The article examines the role of witness testimony in cases related to patent arbitration. Topics discussed include ways to deal with common evidentiary issues arising in arbitration proceedings such as evidence admissibility, relevance and materiality, custom and past practice; witness' credibility and nondisciplinary arbitration; and fundamental fairness in making evidentiary rulings.

This study investigated the prevalence of pain in the ipsilateral upper-limb in stroke patients. 229 stroke patients (133 men, 96 women; M age = 59.0 yr., SD = 12.4) were assessed with the Pain Behaviors Scales and their motor weakness was measured with the Motricity Index. Results indicated that over 27% of patients experienced pain in at least one joint of the ipsilateral upper limb. Shoulder pain was the most common. Further analysis indicated that the occurrence of pain in the ipsilateral upper limb was higher among women, among patients who used a cane, and among patients with a greater weakness of the affected lower limb. [ABSTRACT FROM AUTHOR]

Cytoplasmic presence of Hsp60, which is principally a nuclear gene-encoded mitochondrial chaperonin, has frequently been stated, but its role in intracellular signaling is largely unknown. In this study, we demonstrate that the cytosolic Hsp60 promotes the TNF-α-mediated activation of the IKK/NF-κB survival pathway via direct interaction with IKKα/β in the cytoplasm. Selective loss or blockade of cytosolic Hsp60 by specific antisense oligonucleotide or neutralizing antibody diminished the IKK/NF-κB activation and the expression of NF-κB target genes, such as Bfl-1/A1 and MnSOD, which thus augmented intracellular ROS production and ASK1-dependent cell death, in response to TNF-α. Conversely, the ectopic expression of cytosol-targeted Hsp60 enhanced IKK/NF-κB activation. Mechanistically, the cytosolic Hsp60 enhanced IKK activation via upregulating the activation-dependent serine phosphorylation in a chaperone-independent manner. Furthermore, transgenic mouse study showed that the cytosolic Hsp60 suppressed hepatic cell death induced by diethylnitrosamine in vivo. The cytosolic Hsp60 is likely to be a regulatory component of IKK complex and it implicates the first mitochondrial factor that regulates cell survival via NF--κB pathway. [ABSTRACT FROM AUTHOR]

Background: The importance of infection with COVID-19 is being emphasized in dentistry with high risks such as aerosols. The purpose of this study is to investigate the knowledge and practice of infection control, stress and coping, and turnover of dental hygienists.Methods: Questionnaire was conducted knowledge and practice of infection control, occupational stress and coping, turnover. Survey data was investigated about 149 dental hygienists from February to March 2021 Data were analyzed t-test, ANOVA, Pearson’s correlation using statistical programs of PASW Statistics ver. 21.0.Results: Regarding occupational stress, relationship conflict was higher in the group with less than 2 years of experience (p＜ 0.05). Job anxiety, organizational system, inadequate compensation, and workplace culture were highly surveyed in the 3 to 5 year of experience. The group with more than 6 years of experience had the highest perception of lack of job autonomy (p＜0.05). The group with higher knowledge of infection control had lower mean inappropriate rewards and stress (p＜0.05). The group with high infection control performance had a lower average in items such as job instability, organizational system, inadequate compensation, workplace culture, and stress. And problem-focused coping ability was found to be high (p＜0.05). Infection control knowledge and performance were positively correlated (r=0.251, p＜0.01), infection control practice and stress were negatively correlated (r=−0.264, p＜0.01), and stress and emotional coping were positively correlated (r=0.367, p＜0.01). Stress was positively correlated with turnover rate (r=0.549, p＜0.01).Conclusion: Infection control training was required to reduce occupational stress. Occupational stress was highly correlated with turnover, a holistic and systemic organizational operation and improvement of the quality of medical care were required to reduce stress.

The rhizomes of Alpinia galanga (Thai ginger) have been used extensively as a spice in Southeast Asian and Arabian cuisines and reported to possess a wide range of biological properties, such as antioxidant, antimicrobial, and antibacterial. However, the specific molecular and cellular mechanisms underlying the anti-tumor effects induced by Thai ginger and its corresponding active compounds have been poorly characterized. We found that upon EtOH extraction, Thai ginger extract exhibits cytotoxic activity (IC50 < 10 μg/mL) and triggers cell death via caspase-dependent apoptosis in human ovarian cancer cells. Among the three major compounds isolated from the extract, 1′-acetoxyeugenol acetate (AEA) exhibited potent cytotoxic activity in human ovarian cancer cells, SKOV3 and A2780. AEA induced apoptotic cell death through the activation of caspases-3 and -9. Notably, AEA enhanced the intracellular levels of reactive oxygen species (ROS), and the application of an antioxidant markedly reversed AEA-induced apoptosis of ovarian cancer cells. The knockdown of p47phox, a subunit of NADPH oxidase, suppressed both the pro-apoptotic and ROS-inducing effects of AEA. Additionally, the activation of the mitogen-activated protein kinase (MAPK) pathway by AEA through ROS regulation was found to be involved in AEA-induced apoptosis. Altogether, these results suggest that AEA exhibits potent apoptosis-inducing activity through the activation of the intrinsic pathway via ROS-mediated MAPK signaling in human ovarian cancer cells.

Purpose: This study sought to use child and parent counselling to investigate aspects of maladjustment in parent–child and peer relationships of children who had been exposed to excessive private education in early life. Method: The Case study method was used for three children and their mothers, analyzing the process of transformation in awareness of the issue of excessive education, based on the content of the counselling session. Result: The process of change in awareness of problems due to their experiences of excessive private education experiences was divided into five domains and 13 categories. The participants showed that they were aware of the problems in their relationship and consequently made changes to their lives. Conclusion: This study found that counselling helped alleviate the aforementioned problems, which suggests the need for preventive interventions on parent–child relationship in the context of the negative effects of excessive private education.

Cardiac progenitor cells (CPCs) are resident stem cells present in a small portion of ischemic hearts and function in repairing the damaged heart tissue. Intense oxidative stress impairs cell metabolism thereby decreasing cell viability. Protecting CPCs from undergoing cellular apoptosis during oxidative stress is crucial in optimizing CPC-based therapy. Histochrome (sodium salt of echinochrome A—a common sea urchin pigment) is an antioxidant drug that has been clinically used as a pharmacologic agent for ischemia/reperfusion injury in Russia. However, the mechanistic effect of histochrome on CPCs has never been reported. We investigated the protective effect of histochrome pretreatment on human CPCs (hCPCs) against hydrogen peroxide (H2O2)-induced oxidative stress. Annexin V/7-aminoactinomycin D (7-AAD) assay revealed that histochrome-treated CPCs showed significant protective effects against H2O2-induced cell death. The anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and Bcl-xL were significantly upregulated, whereas the pro-apoptotic proteins BCL2-associated X (Bax), H2O2-induced cleaved caspase-3, and the DNA damage marker, phosphorylated histone (γH2A.X) foci, were significantly downregulated upon histochrome treatment of hCPCs in vitro. Further, prolonged incubation with histochrome alleviated the replicative cellular senescence of hCPCs. In conclusion, we report the protective effect of histochrome against oxidative stress and present the use of a potent and bio-safe cell priming agent as a potential therapeutic strategy in patient-derived hCPCs to treat heart disease.