Economic burden attributable to hospital-acquired infections among tumor patients from a large regional cancer center in Southern China.

BACKGROUND: To evaluate the economic loss of hospital-acquired infections (HAIs) among tumor patients so as to help policymakers to allocate health care resources and address the issue. METHODS: We conducted a retrospective, 1:1 matched case-control study in a large region cancer hospital between January 1 and December 31, 2022. The economic burden was estimated as the median of the 1:1 pair differences of various hospitalization fees and hospital length of stay (LOS). RESULTS: In this study of 329 matched pairs, the patients with HAIs incurred higher hospitalization cost (ie, $16,927) and experienced longer hospital LOS (ie, 22 days), compared to the non-HAI groups. The extra hospitalization cost and the prolonged hospital LOS caused by HAIs were $4,919 and 9 days, respectively. Accordingly, the direct nonmedical economic loss attributable to HAI was approximately $478 to 835 per case. Furthermore, the increment of hospitalization costs varied by sites of infection, types of tumors, and stratum of age. CONCLUSIONS: HAIs lead to the increment of direct economic burden and hospital LOS in tumor patients. Our findings highlight the importance of implementing effective infection control measures in hospitals to reduce the financial burden on tumor patients.

BECN1 promotes radiation-induced G2/M arrest through regulation CDK1 activity: a potential role for autophagy in G2/M checkpoint.

Authophagy and G2/M arrest are two important mechanistic responses of cells to ionizing radiation (IR), in particular the IR-induced fibrosis. However, what interplayer and how it links the autophagy and the G2/M arrest remains elusive. Here, we demonstrate that the autophagy-related protein BECN1 plays a critical role in ionizing radiation-induced G2/M arrest. The treatment of cells with autophagy inhibitor 3-methyladenine (3-MA) at 0-12 h but not 12 h postirradiation significantly sensitized them to IR, indicating a radio-protective role of autophagy in the early response of cells to radiation. 3-MA and BECN1 disruption inactivated the G2/M checkpoint following IR by abrogating the IR-induced phosphorylation of phosphatase CDC25C and its target CDK1, a key mediator of the G2/M transition in coordination with CCNB1. Irradiation increased the nuclear translocation of BECN1, and this process was inhibited by 3-MA. We confirmed that BECN1 interacts with CDC25C and CHK2, and which is mediated the amino acids 89-155 and 151-224 of BECN1, respectively. Importantly, BECN1 deficiency disrupted the interaction of CHK2 with CDC25C and the dissociation of CDC25C from CDK1 in response to irradiation, resulting in the dephosphorylation of CDK1 and overexpression of CDK1. In summary, IR induces the translocation of BECN1 to the nucleus, where it mediates the interaction between CDC25C and CHK2, resulting in the phosphorylation of CDC25C and its dissociation from CDK1. Consequently, the mitosis-promoting complex CDK1/CCNB1 is inactivated, resulting in the arrest of cells at the G2/M transition. Our findings demonstrated that BECN1 plays a role in promotion of radiation-induced G2/M arrest through regulation of CDK1 activity. Whether such functions of BECN1 in G2/M arrest is dependent or independent on its autophagy-related roles is necessary to further identify.

PRKCSH Alternative Splicing Involves in Silica-Induced Expression of Epithelial-Mesenchymal Transition Markers and Cell Proliferation.

BACKGROUND: Mounting evidence suggests that alternative splicing is one of the ways for cells to adapt to environmental stress insults. The aim of this study was firstly to examine the effect of silica on the alternative splicing of lung fibrosis-associated genes. METHODS: Microarray analysis was used to construct the alternative splicing profile. Functional experiments were conducted using Cell Counting Kit-8, cell cycle, apoptosis, and epithelial-mesenchymal transition (EMT) analyses. Alternative splicing variants were verified by quantitative real-time polymerase chain reaction (qRT-PCR) polymerase chain reaction method. RESULTS: A total of 1850 genes that have alternative splices in response to silica insult were identified. PCDHB11, MALAT1, MT2A, RP11-126D17.1, and RP11-415I12.2 are the top 5 upregulated genes with occurrence of alternative splice, whereas NDE1, RNPEPL1, TREML2, CSF2RB, and PRKCSH are the top 5 downregulated genes with occurrence of alternative splice. Bioinformatic analysis showed these genes with the occurrence of alternative splice mainly are associated with EMT pathway, N-Glycan biosynthesis, and leukocyte transendothelial migration. Further study indicated that PRKCSH-2 knockdown promotes A549 cell proliferation potential by partially promoting EMT signals. CONCLUSIONS: Significant changes in alternative splicing of silicosis-associated genes occur in patients with silicosis in silica conditions. Our study provides basic founding for further investigation into the detail molecular mechanisms underlying silica-induced silicosis.

Suppression of LINC00460 mediated the sensitization of HCT116 cells to ionizing radiation by inhibiting epithelial-mesenchymal transition.

Radiation resistance is the most common challenge for improving radiotherapy. The mechanisms underlying the development of radioresistance remain poorly understood. This study aims to explore the role of LINC00460 in ionizing radiation-induced radioresistance as well as the mechanisms by which LINC00460 is regulated by radiation exposure. The expression of LINC00460 was measured. Cell proliferation and colony formation were measured in HCT116 cells after treatment by radiation. The development of epithelial-mesenchymal transition (EMT) was determined with or without knockdown LINC00460 expression using western blot analysis. Transcription activity was determined using a series of LINC00460-promoter luciferase reporter gene vectors. LINC00460 expression was significantly higher in HCT116 cells, relative to other cell types, with LINC00460 expression significantly affecting HCT116 cell proliferation. Suppression of LINC00460 inhibits EMT development in HCT116 cells via regulation of ZEB1 expression. Furthermore, LINC00460 expression was induced by irradiation via the activation of c-jun transcription factor-binding element located on the LINC00460 promoter. LINC00460 was shown to play a crucial role in EMT-associated progression of colorectal cancer, indicating that LINC00460 may be an indicator or new potential therapeutic target for colorectal cancer radiosensitization.

Impact of PM10 and meteorological factors on the incidence of hand, foot, and mouth disease in female children in Ningbo, China: a spatiotemporal and time-series study.

Hand, foot, and mouth disease (HFMD) is a viral illness that is considered a critical public health challenge worldwide. Previous studies have demonstrated that meteorological parameters are significantly related to the incidence of HFMD in children; however, few studies have focused only on female children. This study quantified the associations of HFMD incidence with meteorological parameters and PM10 (particulate matter with an aerodynamic diameter of 10 µm) among female children. Data were collected on daily HFMD cases, meteorological variables, and PM10 levels in Ningbo, China, from January 2012 to December 2016. Data were assessed using a distributed lag nonlinear model (DLNM) with Poisson distribution. A total of 59,809 female children aged 0-15 years with HFMD were enrolled. The results showed that highest relative risk (RR) of HFMD for temperature was 3 °C and the lag effect was 3 days. The highest RR for PM10 was 80 mg/m3 and the lag effect was 5 days. Spatial analysis showed that female HFMD incidence was mainly concentrated in the suburban of Ningbo city indicating that female children in this area should be more paid attention on avoiding this disease outbreak. Our findings suggest that HFMD prevention strategies should focus more attention on local meteorological parameters.

Low blood lead levels and attention-deficit hyperactivity disorder in children: a systematic review and meta-analysis.

Attention-deficit hyperactivity disorder (ADHD) of children is one of the most common neurodevelopmental diseases; the etiology remains unclear. We reviewed and meta-analyzed case-control studies to assess the effects of blood lead levels in children on ADHD symptoms. Relevant studies were identified by searching electronic databases. A meta-analysis was performed using the fixed model of Review Manager 5.3 software. Seven relevant studies were identified. The case groups exhibited significant increases in ADHD symptoms [mean difference (MD), 0.59; 95% confidence interval (CI), 0.50-0.68; p < 0.0001]. Subgroup assessment showed that even children with blood lead levels <3 µg/dL exhibited significant increases in ADHD symptoms (MD, 0.47; 95% CI, 0.39-0.56; p < 0.0001). Subgroup assessment also showed that children aged 5-12 years exhibited more significant increases in ADHD symptoms (MD, 1.35; 95% CI, 0.28-2.41; p < 0.0001) than children aged >12 years. Our findings suggest that low blood lead levels may be associated with ADHD symptoms in children. However, caution is needed when interpreting the results because among-study heterogeneity was in play. Primary interventions should focus on children with low blood lead levels.

LncRNA Uc.173 is a key molecule for the regulation of lead-induced renal tubular epithelial cell apoptosis.

Transcribed ultra-conserved region (T-UCR) transcripts are a novel class of long non-coding RNAs (lncRNAs) transcribed from ultra-conserved region which is highly conserved in human, rat, and mouse genome. LncRNA UC.173 has been found significantly down-regulated in lead-exposed population and lead-exposed animal mode, and had an inhibitory effect on lead-induced nerve cell apoptosis. We supposed that lncRNA UC.173 had an inhibitory effect on lead-induced renal tubular epithelial cell apoptosis. Thus, the aim of our study was to explore the function of lncRNA UC.173 in lead-exposed renal tubular epithelial cells. In our results, lead exposure inhibited renal tubular epithelial cells viability and promoted cell apoptosis and apoptosis-associated genes expression, but no effect on cell-cycle distribution. Lead exposure inhibited the expression of lncRNA UC.173 in renal tubular epithelial cells, and the inhibition effect was time-dependent and concentration-dependent. Up-regulation of lncRNA UC.173 had no effect on renal tubular epithelial cell viability, cell cycle and apoptosis, but significantly rescued lead-induced inhibition of renal tubular epithelial cell viability and suppressed lead-induced cell apoptosis. In summary, our experiments suggest that lncRNA UC.173 is certainly involved in the regulation of lead-induced renal tubular epithelial cell apoptosis, which may supply a new strategy to minimize lead-induced nephrotoxicity.

LncRNA MIR31HG overexpression serves as poor prognostic biomarker and promotes cells proliferation in lung adenocarcinoma.

MIR31HG, as the host gene of miR-31, has been suggested to involve in various cancer developments. However, little is known about the clinical significance and biological function of MIR31HG in lung adenocarcinoma. In our study, we found MIR31HG was highly expressed in lung adenocarcinoma tissues and cell lines, and associated with clinical staging, N classification, M classification and differentiated degree. Survival analysis showed MIR31HG high-expression was an independent unfavorable prognostic factor for lung adenocarcinoma patients. Loss-of-function studies suggested down-regulation of MIR31HG inhibited lung adenocarcinoma cells proliferation and blocked cell-cycle, but has no effect on cell apoptosis. There was no correlation between MIR31HG and miR-31 expression in lung adenocarcinoma tissues, down-regulation of MIR31HG had no effect on the expression of miR-31 in lung adenocarcinoma cells. In conclusion, MIR31HG high-expression is an independent unfavorable prognostic factor for lung adenocarcinoma patients, and serves an oncogenic role to modulate lung adenocarcinoma cells proliferation and cell-cycle.

"What do you know?"--knowledge among village doctors of lead poisoning in children in rural China.

BACKGROUND: This study evaluates the extent of village doctors' knowledge of lead poisoning in children in rural China and assesses the characteristics associated with possessing accurate knowledge. METHODS: A cross-sectional, questionnaire-based survey of 297 village doctors in Fenghuang County, Hunan Province, China was conducted. All village doctors were interviewed face-to-face using a "What do you know" test questionnaire focusing on prevention strategies and lead sources in rural children. RESULTS: A total of 287 (96.6%) village doctors completed the survey in full. Most village doctors had an appropriate degree of general knowledge of lead poisoning; however, they had relatively poor knowledge of lead sources and prevention measures. Village doctors with an undergraduate level education scored an average of 2.7 points higher than those who had a junior college level education (p = 0.033). Village doctors with an annual income ≤ 10,000 RMB yuan scored 1.03 points lower than those whose income was >10,001 RMB yuan. Ethnic Han village doctors scored 1.12 points higher, on average, than ethnic Tujia village doctors (p = 0.027). CONCLUSIONS: This study identified important gaps in knowledge concerning lead poisoning in children among a rural population of village doctors. There is a clear need for multifaceted interventions that target village doctors to improve their knowledge regarding lead poisoning in children. The "What do you know" questionnaire is a new tool to evaluate lead poisoning knowledge and education projects.

Probiotics for the Treatment of Atopic Dermatitis in Children: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Objective: Atopic dermatitis (AD) is a prevalent, burdensome, and psychologically important pediatric concern. Probiotics have been suggested as a treatment for AD. Some reports have explored this topic; however, the utility of probiotics for AD remains to be firmly established. Methods: To assess the effects of probiotics on AD in children, the PubMed/Medline, Cochrane Library Scopus, and OVID databases were searched for reports published in the English language. Results: Thirteen studies were identified. Significantly higher SCORAD values favoring probiotics over controls were observed (mean difference [MD], -3.07; 95% confidence interval [CI], -6.12 to -0.03; P < 0.001). The reported efficacy of probiotics in children < 1 year old was -1.03 (95%CI, -7.05 to 4.99) and that in children 1-18 years old was -4.50 (95%CI, -7.45 to -1.54; P < 0.001). Subgroup analyses showed that in Europe, SCORAD revealed no effect of probiotics, whereas significantly lower SCORAD values were reported in Asia (MD, -5.39; 95%CI, -8.91 to -1.87). Lactobacillus rhamnosus GG (MD, 3.29; 95%CI, -0.30 to 6.88; P = 0.07) and Lactobacillus plantarum (MD, -0.70; 95%CI, -2.30 to 0.90; P = 0.39) showed no significant effect on SCORAD values in children with AD. However, Lactobacillus fermentum (MD, -11.42; 95%CI, -13.81 to -9.04), Lactobacillus salivarius (MD, -7.21; 95%CI, -9.63 to -4.78), and a mixture of different strains (MD, -3.52; 95%CI, -5.61 to -1.44) showed significant effects on SCORAD values in children with AD. Conclusions: Our meta-analysis indicated that the research to date has not robustly shown that probiotics are beneficial for children with AD. However, caution is needed when generalizing our results, as the populations evaluated were heterogeneous. Randomized controlled trials with larger samples and greater power are necessary to identify the species, dose, and treatment duration of probiotics that are most efficacious for treating AD in children.