Detection and Evaluation for High-Quality Cardiopulmonary Resuscitation Based on a Three-Dimensional Motion Capture System: A Feasibility Study.

High-quality cardiopulmonary resuscitation (CPR) and training are important for successful revival during out-of-hospital cardiac arrest (OHCA). However, existing training faces challenges in quantifying each aspect. This study aimed to explore the possibility of using a three-dimensional motion capture system to accurately and effectively assess CPR operations, particularly about the non-quantified arm postures, and analyze the relationship among them to guide students to improve their performance. We used a motion capture system (Mars series, Nokov, China) to collect compression data about five cycles, recording dynamic data of each marker point in three-dimensional space following time and calculating depth and arm angles. Most unstably deviated to some extent from the standard, especially for the untrained students. Five data sets for each parameter per individual all revealed statistically significant differences (p < 0.05). The correlation between Angle 1' and Angle 2' for trained (rs = 0.203, p < 0.05) and untrained students (rs = -0.581, p < 0.01) showed a difference. Their performance still needed improvement. When conducting assessments, we should focus on not only the overall performance but also each compression. This study provides a new perspective for quantifying compression parameters, and future efforts should continue to incorporate new parameters and analyze the relationship among them.

Effects of habit formation interventions on physical activity habit strength: meta-analysis and meta-regression.

BACKGROUND: Interventions aimed at promoting physical activity (PA) behavior through habit formation pathways are gaining popularity, as they differ from conventional interventions that rely on intention pathways. Past research has established a positive correlation between PA habits and behavior. However, the efficacy of current interventions designed to form PA habits and improve PA automaticity is not yet fully ascertained. Additionally, the intervention components that significantly impact the effectiveness of these interventions are yet to be determined. METHODS: This systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We conducted a search of three databases (PubMed, Embase, and Cochrane Library) from January 2000 to December 2022, with a focus on interventions for developing PA habits. Two independent authors conducted paper selection, quality assessment, data extraction, and coding of behavior change techniques (BCTs). The effect size of interventions was calculated using standardized mean difference. Subgroup analyses were carried out based on follow-up duration, delivery method, sample characteristics, and theory. Furthermore, we employed meta-regression to investigate the association between BCTs and PA habits. RESULTS: Ten eligible studies with relatively high quality were included in the final data set. Characteristics of studies varied in intervention sample and delivery way. The habit formation interventions significantly increased PA habit (SMD = 0.31, 95% CI 0.14-0.48, P < .001) compared to the control groups. Subgroup analysis demonstrated that the duration of follow-up ≤ 12 weeks have a higher effect size on PA habit than the duration > 12 weeks. Meta-regression revealed that problem solving has a significant positive association with effectiveness improvement (ß = 0.36, 95% CI 0.17-0.55), while social reward is linked with a reduction in effectiveness (ß = -0.40, 95% CI -0.74-0.06). CONCLUSIONS: Our findings reveal that habit formation interventions are effective in fostering PA habit. Future studies could leverage the insights form this study to optimize the intervention design and achieve better effectiveness.

Activated SIRT1 contributes to DPT-induced glioma cell parthanatos by upregulation of NOX2 and NAT10.

Parthanatos is a type of programmed cell death dependent on hyper-activation of poly (ADP-ribose) polymerase 1 (PARP-1). SIRT1 is a highly conserved nuclear deacetylase and often acts as an inhibitor of parthanatos by deacetylation of PARP1. Our previous study showed that deoxypodophyllotoxin (DPT), a natural compound isolated from the traditional herb Anthriscus sylvestris, triggered glioma cell death via parthanatos. In this study, we investigated the role of SIRT1 in DPT-induced human glioma cell parthanatos. We showed that DPT (450 nmol/L) activated both PARP1 and SIRT1, and induced parthanatos in U87 and U251 glioma cells. Activation of SIRT1 with SRT2183 (10 µmol/L) enhanced, while inhibition of SIRT1 with EX527 (200 µmol/L) or knockdown of SIRT1 attenuated DPT-induced PARP1 activation and glioma cell death. We demonstrated that DPT (450 nmol/L) significantly decreased intracellular NAD+ levels in U87 and U251 cells. Further decrease of NAD+ levels with FK866 (100 µmol/L) aggravated, but supplement of NAD+ (0.5, 2 mmol/L) attenuated DPT-induced PARP1 activation. We found that NAD+ depletion enhanced PARP1 activation via two ways: one was aggravating ROS-dependent DNA DSBs by upregulation of NADPH oxidase 2 (NOX2); the other was reinforcing PARP1 acetylation via increase of N-acetyltransferase 10 (NAT10) expression. We found that SIRT1 activity was improved when being phosphorylated by JNK at Ser27, the activated SIRT1 in reverse aggravated JNK activation via upregulating ROS-related ASK1 signaling, thus forming a positive feedback between JNK and SIRT1. Taken together, SIRT1 activated by JNK contributed to DPT-induced human glioma cell parthanatos via initiation of NAD+ depletion-dependent upregulation of NOX2 and NAT10.

Could we prove the nursing outcomes utilising clinical data warehouse? Effectiveness of pressure ulcer intervention in Korean tertiary hospital.

The use of Clinical Data Warehouse (CDW)  for research and quality improvement has become more frequent in the last 10 years. In this study, we used CDW to determine the effectiveness of pressure ulcer interventions offered by ward nurses and wound care nursing specialists. A retrospective clinical outcomes study that utilise CDW has been carried out. We identified 1415 patients who were evaluated as pressure ulcer risk group from 1 July 2019 to 31 December 2019. Kaplan-Meier survival analyses were used to estimate the time to occurrence of pressure ulcers. We compared the survival curves of each group by applying the log-rank test for significance. The overall median time to occurrence for both groups was 13 days (95% CI range: 11-14 days). The control group showed a longer median time (14 days) to occurrence than the case group (12 days). In the pressure ulcer stage I, the case group showed a longer median time (14 days) to occurrence than the control group (8 days), indicating that the intervention provided by the wound care nursing specialist was effective in stage I, and delayed the occurrence of pressure ulcers. The findings may be used as preliminary data for the utilisation of the CDW in the field of nursing research in the future. Also, facilitating the accessibility of the wound care nursing specialist in the general wards should be effective to decrease the incidence rates.

Taxifolin blocks monosodium urate crystal-induced gouty inflammation by regulating phagocytosis and autophagy.

Gout is a chronic disease caused by monosodium urate (MSU) crystal deposition in the joints and surrounding tissues. We examined the effects of Taxifolin, a natural flavonoid mainly existing in vegetables and fruits, on MSU-induced gout. Pretreatment with Taxifolin significantly reduced IL-1ß, Caspase-1 and HMGB1 levels, upregulation of autophagy-related protein, LC3, as well as improved phagocytosis of macrophages. This study indicated that Taxifolin-attenuated inflammatory response in MSU-induced acute gout model by decreasing pro-inflammatory cytokine production and promoting the autophagy and phagocytic capacity of macrophages. Dietary supplementation with Taxifolin induces the autophagy and attenuated inflammatory response, which in consequence modulates acute gout. A preventive strategy combining dietary interventions with Taxifolin may offer a potential therapeutic alternative to pharmacological treatment to reduce inflammatory response to gout.

FOXO3a protects glioma cells against temozolomide-induced DNA double strand breaks via promotion of BNIP3-mediated mitophagy.

FOXO3a (forkhead box transcription factor 3a) is involved in regulating multiple biological processes in cancer cells. BNIP3 (Bcl-2/adenovirus E1B 19-kDa-interacting protein 3) is a receptor accounting for priming damaged mitochondria for autophagic removal. In this study we investigated the role of FOXO3a in regulating the sensitivity of glioma cells to temozolomide (TMZ) and its relationship with BNIP3-mediated mitophagy. We showed that TMZ dosage-dependently inhibited the viability of human U87, U251, T98G, LN18 and rat C6 glioma cells with IC50 values of 135.75, 128.26, 142.65, 155.73 and 111.60 µM, respectively. In U87 and U251 cells, TMZ (200 µM) induced DNA double strand breaks (DSBs) and nuclear translocation of apoptosis inducing factor (AIF), which was accompanied by BNIP3-mediated mitophagy and FOXO3a accumulation in nucleus. TMZ treatment induced intracellular ROS accumulation in U87 and U251 cells via enhancing mitochondrial superoxide, which not only contributed to DNA DSBs and exacerbated mitochondrial dysfunction, but also upregulated FOXO3a expression. Knockdown of FOXO3a aggravated TMZ-induced DNA DSBs and mitochondrial damage, as well as glioma cell death. TMZ treatment not only upregulated BNIP3 and activated autophagy, but also triggered mitophagy by prompting BNIP3 translocation to mitochondria and reinforcing BNIP3 interaction with LC3BII. Inhibition of mitophagy by knocking down BNIP3 with SiRNA or blocking autophagy with 3MA or bafilomycin A1 exacerbated mitochondrial superoxide and intracellular ROS accumulation. Moreover, FOXO3a knockdown inhibited TMZ-induced BNIP3 upregulation and autophagy activation. In addition, we showed that treatment with TMZ (100 mg·kg-1·d-1, ip) for 12 days in C6 cell xenograft mice markedly inhibited tumor growth accompanied by inducing FOXO3a upregulation, oxidative stress and BNIP3-mediated mitophagy in tumor tissues. These results demonstrate that FOXO3a attenuates temozolomide-induced DNA double strand breaks in human glioma cells via promoting BNIP3-mediated mitophagy.

[Association between time of birth and resuscitation outcomes in extremely preterm infants].

OBJECTIVE: To study whether there are differences in the resuscitation process and early outcomes between the extremely preterm infants delivered on off-hours (6 pm to 8 am of working days, weekends, and national holidays) and those delivered on working hours. METHODS: A retrospective analysis was performed on the medical data of extremely preterm infants who were born in the Peking University Third Hospital from January 1, 2010 to December 31, 2020 and transferred to the neonatal intensive care unit (NICU). According to the time of birth, they were divided into two groups:working hours (n=77) and off-hours (n=98). The resuscitation process and early outcomes were compared between the two groups. RESULTS: Compared with the working hours group, the off-hours group had a significantly lower proportion of infants with the use of full-dose dexamethasone before delivery (P < 0.05) and a significantly higher proportion of infants with a 1-minute Apgar score of < 7, positive pressure ventilation, or tracheal intubation (P < 0.05). The incidence rates of neonatal respiratory distress syndrome and intrauterine pneumonia in the off-hours group were significantly higher than those in the working hours group (P < 0.05). CONCLUSIONS: Extremely preterm infants delivered on off-hours tend to have a low Apgar score at 1 minute after birth, with a higher proportion of infants requiring positive pressure ventilation or tracheal intubation during resuscitation than those delivered on working hours, and they tend to develop neonatal respiratory distress syndrome and intrauterine pneumonia. This suggests that it is important to make adequate preparations in terms of personnel and supplies for resuscitation of extremely preterm infants after birth and that NICUs should develop a detailed management plan for extremely preterm infants at each period of time before, during, and after birth.

The Purpose of Bedside Robots: Exploring the Needs of Inpatients and Healthcare Professionals.

Robotic systems are used to support inpatients and healthcare professionals and to improve the efficiency and quality of nursing. There is a lack of scientific literature on how applied robotic systems can be used to support inpatients. This study uses surveys and focus group interviews to identify the necessary aspects and functions of bedside robots for inpatients. A total of 90 healthcare professionals and 108 inpatients completed the questionnaire, and four physicians and five nurses participated in the focus group interviews. The most highly desired functionalities were related to patient care and monitoring, including alerting staff, measuring vital signs, and sensing falls. Nurses and physicians reported different needs for human-robot interaction. Nurses valued robotic functions such as nonverbal expression recognition, automatic movement, content suggestion, and emotional expressions. The results of the patients' open-ended questions and healthcare professionals' focus groups indicate that the purpose of the robots should primarily be treatment and nursing. Participants believe bedside robots would be helpful but have concerns regarding safety and utility. This study attempts to determine which aspects of robots may increase their acceptance. Our findings suggest that if robots are used in healthcare institutions, they may improve the effectiveness of care.

Management of Gout-associated MSU crystals-induced NLRP3 inflammasome activation by procyanidin B2: targeting IL-1ß and Cathepsin B in macrophages.

Gout, the most prevalent inflammatory arthritis worldwide, released interleukin-1ß (IL-1ß) and Cathepsin B inflammatory mediators that constitute the hallmark of the disease. Herein we aimed to investigate whether procyanidin B2 (PCB2), a natural dietary compound, can suppress MSU crystals-stimulated gouty inflammation. Treated with lipopolysaccharide (LPS) plus MSU, both mouse peritoneal macrophages (MPM) and mouse bone marrow-derived macrophages (BMDM) released a large amount of mature IL-1ß compared to those treated with MSU or LPS alone, while IL-1ß release was blocked by TLR4 and its downstream effector inhibitors. In two mouse models of gout, oral administration of PCB2 suppressed MSU crystals-induced increasing expression of IL-1ß, Cathepsin B and NLRP3 in the air pouch skin and paws, accompanied with the downregulation prostaglandin E2 (PGE2) in pouch exudates. Inflammatory immune cell infiltration including macrophages and neutrophils were significantly blocked by PCB2 in air pouch skin and paws of mice gout groups. PCB2 also suppressed the release of IL-1ß and Cathepsin B induced by MSU plus LPS in MPM. Our results suggest that the inhibitory effects of PCB2 on NLRP3 inflammasome may alleviate inflammatory response in gout, and this might be a promising anti-inflammatory mechanism of PCB2 against the inflammation in gout.

RSL3 induced autophagic death in glioma cells via causing glycolysis dysfunction.

RSL3 is a type of small molecular compound which can inactivate glutathione peroxidase 4 (GPX4) and induce ferroptosis, but its role in glioma cell death remains unclear. In this study, we found RSL3 inhibited the viabilities of glioma cells and induced glioma cell death in a dose-dependent manner. In vitro studies revealed that RSL3-induced cell death was accompanied with the changes of autophagy-associated protein levels and was alleviated by pretreatment of 3-Methyladenine, bafilomycin A1 and knockdown of ATG5 with siRNA. The ATP and pyruvate content as well as the protein levels of HKII, PFKP, PKM2 were decreased in cells treated by RSL3, indicating that RSL3 induced glycolysis dysfunction in glioma cells. Moreover, supplement of exterior sodium pyruvate, which was a final product of glycolysis, not only inhibited the changes of autophagy-associated protein levels caused by RSL3, but also prevented RSL3-induced cell death. In vivo data suggested that the inhibitory effect of RSL3 on the growth of glioma cells was associated with glycolysis dysfunction and autophagy activation. Taken together, RSL3 induced autophagic cell death in glioma cells via causing glycolysis dysfunction.

A Typology of Future Health Services by Exploring Core Concepts and Values: A Q-methodology Approach.

Recent rapid development of medical and information technology has enabled the use of appropriate techniques for the delivery of healthcare. This project involved prediction of the meaning and structure of future health services, which are now commonly described through various keywords, without establishment of the concepts. The objectives of this study were to identify key concepts and values about future health services and to categorize the prediction of those from the perspectives of the concerned professionals using Q-methodology with 50 selected Q-statements. A total of 53 participants performed the Q-sort task using the 50 statements; collected data were analyzed using an associated program, pc-QUANL. Fifty Q-samples were selected to sort the concepts, and 53 professionals sorted the Q-samples. Six concepts were summarized, namely, the Optimistic Innovation Positive Type, Pessimistic Resistance to Technology-Driven Medicine Type, Intelligent Information Technology Centered Type, Bio-technology Centered Type, Personal Health Data Centered Type, and Customized Care Centered Type. The results could be used in the future design of consumer-centered health services. Advanced technology may accommodate the individual needs of different stakeholders and carve an ecosystem-wide suite of interacting complex adaptive systems.

[Asymmetric crying facies and vocal cord paralysis accompanied by congenital heart disease in an infant].

A female infant was admitted to the hospital due to perioral cyanosis two hours after birth. The infant was born at the gestational age of 35 weeks by cesarean section with a birth weight of 2 400 g. Physical examination revealed wry mouth to the left side while crying, small auricles, and high palatal arch; fibrolaryngoscopy suggested bilateral vocal cord paralysis; echocardiography suggested ventricular septal defect; single nucleotide polymorphism testing showed 22q11.21 microdeletion. Therefore, the infant was given a definite diagnosis of asymmetric crying facies syndrome accompanied by 22q11.21 microdeletion. After 8-month follow-up, the infant still had asymmetric crying facies with presence of growth retardation.

[Prognosis of bronchopulmonary dysplasia in preterm infants: a follow-up during infancy].

OBJECTIVE: To investigate the physical development, incidence of common respiratory diseases, and motor development during infancy in preterm infants with bronchopulmonary dysplasia (BPD). METHODS: A retrospective analysis was performed on the clinical features and infantile outcomes of preterm infants with BPD who were admitted to the neonatal intensive care unit between January 2012 and December 2015. Preterm infants without BPD were used as controls who were admitted to the neonatal intensive care unit during the same period and had similar gestational age and birth weight. Physical development, number of hospital stays, the incidences of pneumonia and wheezing, and motor development during infancy were compared between the two groups. RESULTS: Compared with the control group, BPD infants had a significantly higher incidence of extrauterine growth retardation at discharge (48% vs 41%; P<0.05); BPD infants were more susceptible to pneumonia, wheezing, eczema and rhinitis; BDP infants also had a significantly higher number of readmissions due to respiratory tract infection (P<0.05). BPD infants had a significantly smaller head circumference than the control group at corrected ages of 3, 6, and 12 months (P<0.05). BPD infants had significantly delayed gross, fine, and overall motor development than the control group at corrected ages of 6 and 9 months (P<0.05). CONCLUSIONS: Infants with BPD are susceptible to extrauterine growth retardation at discharge. Their head circumference growth is relatively slow. They are susceptible to pneumonia and wheezing during infancy. Moreover, they have delayed motor development when compared with those without BPD at corrected ages of 6 and 9 months.

[Persistent hypertension for two months in a preterm infant].

A boy aged 2 months (born at 36 weeks of gestation) was admitted due to cough and dyspnea. After admission, he was found to have persistent hypertension, proteinuria, and persistent convulsion, and imaging examination showed extensive calcification of the aorta and major branches and stenosis of local lumens of the abdominal aorta and the right renal artery with increased blood flow velocity. The boy was admitted during the neonatal period due to wet lung and pulmonary arterial hypertension and was found to have hypertension and proteinuria. High-throughput whole-exome sequencing was performed and found two compound heterozygous mutations in the ENPP1 gene from his parents, c.130C>T (p.Q44X) and c.1112A>T (p.Y371F). c.130C>T was a nonsense mutation, which could cause partial deletion of protein from 44 amino acids, and was defined as a primary pathogenic mutation. c.1112A>T was a missense mutation which had been reported as a pathogenic mutation associated with idiopathic infantile arterial calcification (IIAC). Therefore, he was diagnosed with IIAC. He was given phosphonate drugs, antihypertensive drugs, anticonvulsion treatment, and respiratory support. Blood pressure was maintained at the upper limit of normal value. There was no deterioration of arterial calcification. It is concluded that IIAC should be considered for infants with persistent hypertension and extensive vascular calcification, and imaging and genetic examinations should be performed as early as possible to make a confirmed diagnosis.

Shikonin induces glioma cell necroptosis in vitro by ROS overproduction and promoting RIP1/RIP3 necrosome formation.

Necroptosis is a type of programmed necrosis regulated by receptor interacting protein kinase 1 (RIP1) and RIP3. Necroptosis is found to be accompanied by an overproduction of reactive oxygen species (ROS), but the role of ROS in regulation of necroptosis remains elusive. In this study, we investigated how shikonin, a necroptosis inducer for cancer cells, regulated the signaling leading to necroptosis in glinoma cells in vitro. Treatment with shikonin (2-10 µmol/L) dose-dependently triggered necrosis and induced overproduction of intracellular ROS in rat C6 and human SHG-44, U87 and U251 glioma cell lines. Moreover, shikonin treatment dose-dependently upregulated the levels of RIP1 and RIP3 and reinforced their interaction in the glioma cells. Pretreatment with the specific RIP1 inhibitor Nec-1 (100 µmol/L) or the specific RIP3 inhibitor GSK-872 (5 µmol/L) not only prevented shikonin-induced glioma cell necrosis but also significantly mitigated the levels of intracellular ROS and mitochondrial superoxide. Mitigation of ROS with MnTBAP (40 µmol/L), which was a cleaner of mitochondrial superoxide, attenuated shikonin-induced glioma cell necrosis, whereas increasing ROS levels with rotenone, which improved the mitochondrial generation of superoxide, significantly augmented shikonin-caused glioma cell necrosis. Furthermore, pretreatment with MnTBAP prevented the shikonin-induced upregulation of RIP1 and RIP3 expression and their interaction while pretreatment with rotenone reinforced these effects. These findings suggest that ROS is not only an executioner of shikonin-induced glioma cell necrosis but also a regulator of RIP1 and RIP3 expression and necrosome assembly.

[Retracted] Knockdown of SNHG16 suppresses the proliferation and induces the apoptosis of leukemia cells via miR­193a­5p/CDK8.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the colony formation assay data shown in Fig. 7A on p. 1183 were strikingly similar to data appearing in different form in the following article written by different authors at different research institutes that had already been published prior to its date of submission: Lou L, Chen G, Zhong B and Liu F: Lycium barbarum polysaccharide induced apoptosis and inhibited proliferation in infantile hemangioma endothelial cells via down­regulation of PI3K/AKT signaling pathway. Biosci Rep 39: BSR20191182, 2019. In addition, possible anomalies were noted regarding the appearance of the western blots in the paper. Owing to the fact that the contentious data in the above article had already been published prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 46: 1175­1185, 2020; DOI: 10.3892/ijmm.2020.4671].

Sevoflurane Exposure Induces Neuronal Cell Ferroptosis Initiated by Increase of Intracellular Hydrogen Peroxide in the Developing Brain via ER Stress ATF3 Activation.

Neuronal cell death is acknowledged as the primary pathological basis underlying developmental neurotoxicity in response to sevoflurane exposure, but the exact mechanism remains unclear. Ferroptosis is a form of programmed cell death characterized by iron-dependent lipid peroxidation that is driven by hydrogen peroxide (H2O2) and ferrous iron through the Fenton reaction and participates in the pathogenesis of multiple neurological diseases. As stress response factor, activating transcription factor 3 (ATF3) can be activated by the PERK/ATF4 pathway during endoplasmic reticulum (ER) stress, followed by increased intracellular H2O2, which is involved in regulation of apoptosis, autophagy, and ferroptosis. Here, we investigated whether ferroptosis and ATF3 activation were implicated in sevoflurane-induced neuronal cell death in the developing brain. The results showed that sevoflurane exposure induced neuronal death as a result of iron-dependent lipid peroxidation damage secondary to H2O2 accumulation and ferrous iron increase, which was consistent with the criteria for ferroptosis. Furthermore, we observed that increases in iron and H2O2 induced by sevoflurane exposure were associated with the upregulation and nuclear translocation of ATF3 in response to ER stress. Knockdown of ATF3 expression alleviated iron-dependent lipid peroxidation, which prevented sevoflurane-induced neuronal ferroptosis. Mechanistically, ATF3 promoted sevoflurane-induced H2O2 accumulation by activating NOX4 and suppressing catalase, GPX4, and SLC7A11 expression. Additionally, an increase in H2O2 was accompanied by the upregulation of TFR and TF and downregulation of FPN, which linked iron overload to ferroptosis induced by sevoflurane. Taken together, our results demonstrated that ER stress-mediated ATF3 activation contributed to sevoflurane-induced neuronal ferroptosis via H2O2 accumulation and the resultant iron overload.

Nomogram for Predicting the Risk of Complications in Hospitalized Children With Peripheral Intravenous Catheters.

OBJECTIVE: The aim of the study is to identify the hospitalized children at risk of peripheral intravenous catheter (PIVC) complications by severity prediction. METHODS: The study included the data of 301 hospitalized children with PIVC complications in 2 tertiary teaching hospitals. A researcher-designed tool was used to collect risk factors associated with PIVC complications. Predictors of PIVC complications at univariate analysis and multivariable logistic regression analysis by backward stepwise. A nomogram was constructed based on the results of the final multivariable model, making it possible to estimate the probability of developing complications. RESULTS: A total of 182 participants (60.5%) had a moderate injury from PIVC complications. Multivariable logistic regression analysis indicated that the vascular condition, limb immobilization, needle adjustment in venipuncture, infusion length, infusion speed, and insertion site were independent predictors. The nomogram for assessing the severity of PIVC complications indicated good predictive accuracy (area under the curve = 0.79) and good discrimination (concordance index = 0.779). Decision curve analysis demonstrated that the nomogram was a good clinical value with a wide range of threshold probabilities (4%-100%). CONCLUSIONS: The risk prediction model has good predictive performance, and the nomogram provides an easy-to-use visualization to identify the severity of PIVC complications and guide timely nursing care management.

SIRT1 activated by AROS sensitizes glioma cells to ferroptosis via induction of NAD+ depletion-dependent activation of ATF3.

Ferroptosis is a type of programmed cell death resulting from iron overload-dependent lipid peroxidation, and could be promoted by activating transcription factor 3 (ATF3). SIRT1 is an enzyme accounting for removing acetylated lysine residues from target proteins by consuming NAD+, but its role remains elusive in ferroptosis and activating ATF3. In this study, we found SIRT1 was activated during the process of RSL3-induced glioma cell ferroptosis. Moreover, the glioma cell death was aggravated by SIRT1 activator SRT2183, but suppressed by SIRT inhibitor EX527 or when SIRT1 was silenced with siRNA. These indicated SIRT1 sensitized glioma cells to ferroptosis. Furthermore, we found SIRT1 promoted RSL3-induced expressional upregulation and nuclear translocation of ATF3. Silence of ATF3 with siRNA attenuated RSL3-induced increases of ferrous iron and lipid peroxidation, downregulation of SLC7A11 and GPX4 and depletion of cysteine and GSH. Thus, SIRT1 promoted glioma cell ferroptosis by inducting ATF3 activation. Mechanistically, ATF3 activation was reinforced when RSL3-induced decline of NAD+ was aggravated by FK866 that could inhibit NAD + synthesis via salvage pathway, but suppressed when intracellular NAD+ was maintained at higher level by supplement of exogenous NAD+. Notably, the NAD + decline caused by RSL3 was enhanced when SIRT1 was further activated by SRT2183, but attenuated when SIRT1 activation was inhibited by EX527. These indicated SIRT1 promoted ATF3 activation via consumption of NAD+. Finally, we found RSL3 activated SIRT1 by inducing reactive oxygen species-dependent upregulation of AROS. Together, our study revealed SIRT1 activated by AROS sensitizes glioma cells to ferroptosis via activation of ATF3-dependent inhibition of SLC7A11 and GPX4.