The Prediction of Dry Weight for Chronic Hemodialysis Athletes Using a Machine Learning Approach: Sports Health Implications / La predicción del peso seco para atletas en hemodiálisis crónica mediante un enfoque de aprendizaje automático: implicaciones para la salud deportiva

This study seeks to evaluate the ability of machine learning methods to predict the dry weight of chronic hemodialysis athletes. The researcher has reached out to kidney patients who have had to give up sports and athletic careers due to chronic hemodialysis. This paper explores the development of medical prediction algorithms that combine image analysis with numerical data, which is widely used in the field of medicine. This deep learning method is widely employed to enhance the treatment of athletes who have kidney conditions. Regular hemodialysis is crucial for maintaining the health of athletes who have kidney disease. Accurately predicting dry weight is a crucial step in the process of performing hemodialysis. In this context, dry weight refers to the optimal moisture level at which excess water is effectively eliminated from the patient (athletes) through ultrafiltration during hemodialysis. In order to accurately determine the optimal amount of hemodialysis, predicting the correct dry weight is crucial. However, this task is quite challenging and often yields inaccurate results due to the extensive data analysis required by experienced nephrologists. This paper presents a deep learning methodology utilising the Artificial Neural Network (ANN) approach to efficiently address these issues. The proposed method aims to predict dry weight rapidly by analysing image values and clinical data from X-ray images obtained during routine check-ups. The current study has several theoretical and practical implications. This study contributes to the existing literature on chronic hemodialysis and the dry weight of athletes, offering valuable insights to sports health organisations. By doing so, these organisations can effectively prepare to proactively evaluate the atypical health conditions of athletes.(AU)

Post-intensive care syndrome and health-related quality of life in long-term survivors of intensive care unit.

OBJECTIVE: The objective of this study was to provide preliminary data for improving the health-related quality of life of long-term intensive care unit survivors by identifying the relationship between health-related quality of life and post-intensive care syndrome. METHODS: Using a descriptive correlation research design, data from patients who visited the outpatient department for continuous treatment after discharge from the intensive care unit were analysed. Post-intensive care syndrome was measured by physical, cognitive, and mental problems. Data were collected from 1st August to 31st December, 2019, and 121 intensive care unit survivors participated in the study. RESULTS: Health-related quality of life showed a negative correlation with physical, mental, and cognitive problems. The factors associated with health-related quality of life were physical and mental problems, education level, sedatives and neuromuscular relaxants, and marital status. CONCLUSIONS: To improve the health-related quality of life of intensive care unit survivors, post-intensive care syndrome prevention is important, and a systematic strategy is required through a long-term longitudinal trace study. In addition, intensive care unit nurses and other healthcare professionals need to provide early interventions to reduce post-intensive care syndrome.

Correlates of Successful Aging in South Korean Older Adults: A Meta-Analytic Review.

The purpose of this study was to examine the factors contributing to achieving successful aging (SA) among the Korean older population and identified the strength of each factor's contribution to SA. We extensively searched 4 Korean and 3 English online databases, extracting a total of 64 studies for the analysis. Finally, 42 associated factors and 347 correlation coefficients were found, which were then categorized into 5 domains: functional, psychological, familial, social, and demographic. The psychological domain had the highest effect size. This was followed, in descending order, by the social, functional and familial, and demographic domains. Importantly, the familial domain, which has not been explored in many existing SA models, emerged as a notable predictor. This study is meaningful in terms of understanding one of the minority older populations more deeply and providing stronger evidence for developing evidence-based intervention programs for Korean older adults.

Corrigendum to "Effect of Inhalation of Aromatherapy Oil on Patients with Perennial Allergic Rhinitis: A Randomized Controlled Trial".

[This corrects the article DOI: 10.1155/2016/7896081.].

Effect of Inhalation of Aromatherapy Oil on Patients with Perennial Allergic Rhinitis: A Randomized Controlled Trial.

This study aimed to investigate the effects of aromatherapy oil inhalation on symptoms, quality of life, sleep quality, and fatigue level among adults with perennial allergic rhinitis (PAR). Fifty-four men and women aged between 20 and 60 were randomized to inhale aromatherapy oil containing essential oil from sandalwood, geranium, and Ravensara or almond oil (the placebo) for 5 minutes twice daily for 7 days. PAR symptoms determined by Total Nasal Symptom Score (TNSS), the Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ), sleep quality by Verran Synder-Halpern (VSH) scale, and fatigue level by Chalder Fatigue Scale (CFS) were assessed before and after intervention period. Compared with the placebo, the experimental group showed significant improvement in TNSS, especially in nasal obstruction. The aromatherapy group also showed significantly higher improvements in total score of RQLQ and CFS. These findings indicate that inhalation of certain aromatherapy oil helps relieve PAR symptoms, improve rhinitis-specific quality of life, and reduce fatigue in patients with PAR. In conclusion, inhalation of aromatherapy essential oil may have potential as an effective intervention to alleviate PAR.

T-cell immunoglobulin and mucin domain 3 genetic polymorphisms are associated with rheumatoid arthritis independent of a shared epitope status.

The aim of this study was to investigate T-cell immunoglobulin and mucin domain 3 (TIM3) genetic polymorphisms and rheumatoid arthritis (RA) according to the shared epitope (SE) status. Six single nucleotide polymorphisms (SNPs: rs11742259 [C/T], rs10515746 [C/A], rs35960726 [A/G], rs1036199 [A/C], rs4704846 [A/G], and rs11134551 [A/G]) in the TIM3 gene from 366 RA patients and 389 healthy controls were investigated using the real-time polymerase chain reaction method. Associations between these SNPs and clinical manifestations (including SE status) were investigated using the SPSS program and Haploview. Polymorphisms of rs35690726 (AG+ GG vs AA: 8.2% vs 1.8%, p(c) < 0.001) were significantly associated with RA with or without SE (p(c) < 0.001 or p(c) = 0.009, respectively). Polymorphisms of rs11742259 (p(c) = 0.003) and rs1036199 (p(c) = 0.012) were significantly different in RA patients with SE, but not in those without SE. In haplotype analysis with a permutation test for the first 4 SNPs (rs11742259, rs10515746, rs35690726, and, rs1036199), CCAA, CCGA, CCGC, and CAAA haplotypes were significantly associated with RA. The clinical characteristics of RA patients were not significantly associated with any TIM3 polymorphism. TIM3 genetic polymorphisms may have a role in the development of RA regardless of a shared epitope status.

The virtual histology intravascular ultrasound appearance of newly placed drug-eluting stents.

Intravascular ultrasound (IVUS) is used before and after intervention and at follow-up to assess the quality of the acute result as well as the long-term effects of stent implantation. Virtual histology (VH) IVUS classifies tissue into fibrous and fibrofatty plaque, dense calcium, and necrotic core. Although most interventional procedures include stent implantation, VH IVUS classification of stent metal has not been validated. In this study, the VH IVUS appearance of acutely implanted stents was assessed in 27 patients (30 lesions). Most stent struts (80%) appeared white (misclassified as "calcium") surrounded by red (misclassified as "necrotic core"); 2% appeared just white, and 17% were not detectable (compared with grayscale IVUS because of the software-imposed gray medial stripe). The rate of "white surrounded by red" was similar over the lengths of the stents; however, undetectable struts were mostly at the distal edges (31%). Quantitatively, including the struts within the regions of interest increased the amount of "calcium" from 0.23 +/- 0.35 to 1.07 +/- 0.66 mm(2) (p <0.0001) and the amount of "necrotic core" from 0.59 +/- 0.65 to 1.31 +/- 0.87 mm(2) (p <0.0001). Most important, because this appearance occurs acutely, it is an artifact, and the red appearance should not be interpreted as peristrut inflammation or necrotic core when it is seen at follow-up. In conclusion, acutely implanted stents have an appearance that can be misclassified by VH IVUS as "calcium with or without necrotic core." It is important not to overinterpret VH IVUS studies of chronically implanted stents when this appearance is observed at follow-up. A separate classification for stent struts is necessary to avoid these misconceptions and misclassifications.

Cardiovascular and hematopoietic defects associated with Notch1 activation in embryonic Tie2-expressing populations.

Notch signaling is critical for the development and maintenance of the cardiovasculature, with loss-of-function studies defining roles of Notch1 in the endothelial/hematopoietic lineages. No in vivo studies have addressed complementary gain-of-function strategies within these tissues to define consequences of Notch activation. We developed a transgenic model of Cre recombinase-mediated activation of a constitutively active mouse Notch1 allele (N1ICD(+)) and studied transgene activation in Tie2-expressing lineages. The in vivo phenotype was compared to effects of Notch1 activation on endothelial tubulogenesis, paracrine regulation of smooth muscle cell proliferation, and hematopoiesis. N1ICD(+) embryos showed midgestation lethality with defects in angiogenic remodeling of embryonic and yolk sac vasculature, cardiac development, smooth muscle cell investment of vessels, and hematopoietic differentiation. Angiogenic defects corresponded with impaired endothelial tubulogenesis in vitro following Notch1 activation and paracrine inhibition of smooth muscle cells when grown with Notch1-activated endothelial cells. Flow cytometric analysis of hematopoietic and endothelial precursor populations demonstrated a significant loss of CD71(+)/Ter119(+) populations with an active N1ICD(+) allele and a corresponding increase in c-Kit(+)/CD71 and Flk1(+) populations, suggesting a developmental block during the transition between c-Kit- and Ter119-expressing erythroblasts. Cardiovascular lineages are sensitive to an imbalance in Notch signaling, with aberrant activation reflecting a vascular phenotype comparable to a loss-of-function Notch1 mutation.

Korean older adults' perceptions of the aging process.

This qualitative study was conducted to describe Korean older adults' perceptions of the aging process. A total of 18 Korean older adults were interviewed, and a grounded theory approach was used to analyze the interview data. The participants were found to perceive aging as a process of Generating, Expressing, and Transforming of Growing Futility. The degree to which they perceived their Growing Futility depended on the actions and interactions of a set of conditional structures. This study revealed five patterns of Korean older adults' perception of the aging process. These findings allow for the possibility of a more refined theoretical development for the aging process, especially when a comparative study becomes available through cross-cultural qualitative research.

Clinical implications of matrix metalloproteinase-1, -3, -7, -9, -12, and plasminogen activator inhibitor-1 gene polymorphisms in colorectal cancer.

BACKGROUND AND AIM: Overexpression of matrix metalloproteinase (MMP)-1, -3, -7, -9, and plasminogen activator inhibitor-1 (PAI-1) are implicated in the invasion and metastasis of colorectal cancer, while MMP-12 provides a protective role against colorectal cancer. The promoter and exon polymorphisms of their genes, which are known to affect the transcription of these genes, were assessed to correlate with colorectal cancer susceptibility. METHODS: MMP1, 3, 7, 9, 12 and PAI1 were assayed in 185 colorectal cancer patients and 304 healthy controls using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) analysis. Respective genotypes and haplotypes were compared between the population groups and also between clinicopathological characteristics in the colorectal cancer patients. RESULTS: The homozygous MMP1-1,607 dupG genotype was significantly more frequent in colorectal cancer patients than in healthy controls. The frequency of MMP1-1,607 dupG homozygotes was also greater in patients of less than or equal to 50 years of age, and in patients with 10 or more metastatic lymph nodes, compared with those of older age or with fewer lymph nodes. The frequency of MMP9-1,562 C homozygotes was significantly greater in colorectal cancer patients than in healthy controls. However, the genotype and allele frequencies of MMP3-1,171dupA, MMP7-181A > G, MMP12-82A > G, MMP9-90(CA)(14-27), and R279Q did not differ between the population groups or clinicopathological parameters. The MMP7-181A-MMP1-1,607dupG-MMP3-1,171A-MMP12-82A and MMP9-1,562C-90(CA)(20)+ 279Q haplotypes were significantly more frequent in colorectal cancer patients than in healthy controls. The genotype and allele frequencies of PAI1-675 G were similar between patients and healthy controls, but the frequency of PAI1-675 G homozygotes was significantly greater in patents over 50 years of age. CONCLUSIONS: MMP1-1,607 dupG and MMP9-1,562 C homozygotes demonstrated an increased risk of colorectal cancer regardless of ethnic differences, whereas other MMP and PAI1 polymorphisms did not. Nevertheless, specific MMP haplotypes on 11q22.1-23.3 and 20q12-13 seem to be implicated in susceptibility to colorectal cancer.

Heat shock protein 70 alters the endosome-lysosomal localization of huntingtin.

Huntington's disease is caused by CAG trinucleotide expansions in the gene encoding huntingtin. N- terminal fragments of huntingtin with polyglutamine produce aggregates in the endosome-lysosomal system, where proteolytic fragments of huntingtin is generated. Heat shock protein 70 (HSP70) prevents the formation of protein aggregates, but the effect of HSP70 on the huntingtin in the endosome-lysosomal system is unknown. This study was to determine whether HSP70 alters the distribution of huntingtin in endosome-lysosomal system. HSP70 expressing stable cells (NIH/3T3 or cerebral hybrid cell line A1) were generated, and mutant [(CAG)(100)] huntingtin was transiently overexpressed. Analysis of subcellular distribution by immunocytochemistry or proteolysis cleavage by Western blotting was performed. 18 CAG repeat wild type [WT; (CAG)(18)] huntingtin was used as a control. Cells with huntingtin showed patterns of endosome-lysosomal accumulation, from a "dispersed vacuole (DV)" type into a coalescent "perinuclear vacuole (PV)" type over time. In WT huntingtin, HSP70 increased the cells with the PV types that enhanced the proteolytic cleavage of huntingtin. However, HSP70 reduced cells of the DV and PV types expressing mutant huntingtin, that result in less proteolysis than that of control. In addition, intranuclear inclusions were formed only in mutant cells, which was not affected by HSP70. These results suggest that HSP70 alters the distribution of huntingtin in the endosome- lysosomal system, and that this contributes to huntingtin proteolysis.

Ovalbumin modified by gamma irradiation alters its immunological functions and allergic responses.

It is well known that gamma (gamma)-ray irradiation results in the alteration of biological function of bioactive materials such as proteins, saccharides and lipids. In this study the effect of gamma-irradiation on the chemical and immunological property of an allergen, ovalbumin (OVA), was investigated. Irradiation of more than 10 kGy resulted in the alteration of the structure of OVA. However, OVA treated with 10 kGy irradiation (10 kGy-OVA), but not 100 kGy-OVA, fully maintained immunological reactivity to a monoclonal antibody specific to the intact allergen (clone 14). Mice immunized with 10 kGy- as well as 100 kGy-OVA showed significantly lower antibody response to the allergen than those with intact OVA in a gamma-ray dosage-dependent manner. Especially immunization of both 10 kGy- and 100 kGy-OVA induced a significant decrease of OVA-specific IgE. Splenocytes of mice immunized with irradiated OVA showed a significant reduction in OVA-specific T cell proliferation and the secretion of Th1-type (IFN-gamma and IL-2) and Th2-type cytokines (IL-4 and IL-6). The expression of T cell activation markers such as CD25 and CD44 was also down-regulated in T cells of mice immunized with irradiated OVAs. These results suggest that gamma-ray irradiation of OVA suppress humoral and cellular immune responses specific to the allergen OVA, and the modification method with gamma-irradiation may be available for the control of allergy.

Association of TNFA promoter region haplotype in Behçet's Disease.

Although the etiology of Behçet's Disease (BD; MIM 109650) remains to be clearly elucidated, levels of tumor necrosis factor alpha (TNF-alpha) have been reported to be significantly elevated in BD patients, and TNF-alpha blockers have been demonstrated to exhibit some degree of therapeutic efficacy for a certain subset of BD sufferers. In this study, we have conducted an analysis of the TNFA haplotypes in the promoter response element that affect the binding affinity of specific transcription factors, in order to characterize their association with the clinical features of BD. Six polymorphisms in the promoter region of TNFA were genotyped in 254 BD patients and 344 control subjects, via the PCR-RFLP technique. TNFA -1031*C, -863*A and -308*G alleles were associated with an increased risk of BD (p=0.030, OR=1.4; p=0.008, OR=1.5; p=0.010, OR=1.8, respectively). The sole TNFA haplotype -1031C-863A-857C-376G-308G-238G, was associated with a 1.6 fold increase in the risk of BD, whereas the TNFA haplotype -1031T-863C-857C-376G-308A-238G was associated with a 0.6 decreased risk of BD. The TNFA -1031*C, -863*A, -857*C and -308*G alleles were significantly associated with BD. The findings of this study, collectively, indicate that TNFA haplotypes in the promoter response elements may exert significant influence on susceptibility to BD.

[Impact of clinical nurses' power and empowerment on job satisfaction and organizational commitment].

PURPOSE: This study was performed to analyze effects of the power and empowerment on job satisfaction and organizational commitment. This study was based on the Kanter's theory of organizational empowerment. METHOD: A predictive, non-experimental design was used to test the model in a sample of 688 nurses working in 7 university hospitals that have over 500 beds in Seoul, Kyunggi and Kangwon provinces. The data were collected from December, 2003 to January, 2004. It was analyzed with descriptive statistics and Pearson correlation of SPSS and with path analysis of LISREL. RESULT: The formal and informal power had direct effects on empowerment. Formal power also had direct effects on informal power. Empowerment had direct effects on job satisfaction and organizational commitment. Organizational commitment had direct effects on job satisfaction. There was positive effects in all of the variables. CONCLUSION: The positive changes show on personal behaviors and attitudes when the nurses who have formal and informal power are empowered. These findings would be important resource to nurse administrators for clinical implication.

Start codon polymorphisms in the vitamin D receptor and colorectal cancer risk.

The expression of the nuclear vitamin D receptor (VDR), which is involved in regulating cell growth and proliferation, may contribute to the development of colorectal cancer. Polymorphisms in the VDR gene (OMIM 601769) may influence the expression or function of the VDR protein. A population-based, case-control study of VDR start codon, intron, and exon polymorphisms, haplotypes for these polymorphisms, and the relationships between these polymorphisms and clinicopathological parameters in 190 colorectal cancer patients and 318 controls was conducted. The start codon variant VDR 27823*C/*C genotype was associated with an increased risk for colorectal cancer, while the 27823*T/*T genotype was associated with a decreased risk. In addition, the VDR 61888*G/*G genotype was associated with reduced colorectal cancer risk. The intron 8 60880G>A and exon 9 61968T>C polymorphisms were not associated with colorectal cancer risk. The VDR 27823*C-60890*G-61888*T-61968*T haplotype was associated with an increased risk of colorectal cancer, whereas the VDR 27823*T-60890*G-61888*G-61968*T haplotype was associated with a decreased risk of colorectal cancer. Moreover, the 27823*C/*C genotype was more frequently identified in patients with preoperative serum carcinoembryonic antigen (CEA) levels over 6ng/mL. These results suggest that the VDR start codon 27823*C allele may be linked to high risk for colorectal cancer, especially in a subset of colorectal cancers showing specific biological behaviors.

Cooperative actions of Tra2alpha with 9G8 and SRp30c in the RNA splicing of the gonadotropin-releasing hormone gene transcript.

In earlier studies, we demonstrated that excision of the first intron (intron A) from the gonadotropin-releasing hormone (GnRH) transcript is highly cell type- and developmental stage-specific. The removal of GnRH intron A requires exonic splicing enhancers on exons 3 and 4 (ESE3 and ESE4, respectively). Tra2alpha,a serine/arginine-rich (SR)-like protein, specifically binds to ESE4, although it requires additional nuclear co-factors for efficient removal of this intron. In the present study, we demonstrate the cooperative action of multiple SR proteins in the regulation of GnRH pre-mRNA splicing. SRp30c specifically binds to both ESE3 and ESE4, whereas 9G8 binds to an element in exon 3 and strongly enhances the excision of GnRH intron A in the presence of minimal amount of other nuclear components. Interestingly, Tra2alpha can interact with either 9G8 or SRp30c, whereas no interaction between 9G8 and SRp30c is observed. Tra2alpha has an additive effect on the RNA binding of these proteins. Overexpression or knock-down of these three proteins in cultured cells further suggests their essential role in intron A excision activities, and their presence in GnRH neurons of the mouse preoptic area further strengthens this possibility. Together, these results indicate that interaction of Tra2alpha with 9G8 and SRp30c appears to be crucial for ESE-dependent GnRH pre-mRNA splicing, allowing efficient generation of mature mRNA in GnRH-producing cells.

IFN-gamma/IRF-1-induced p27kip1 down-regulates telomerase activity and human telomerase reverse transcriptase expression in human cervical cancer.

Telomerase activation is regulated by the expression of human telomerase reverse transcriptase (hTERT) and is a key step in the development of human cancers. Interferon-gamma (IFN-gamma) signaling induces growth arrest in many tumors through multiple regulatory mechanisms. The p27 tumor suppressor protein inhibits the formation of tumors through the induction of cell cycle arrest and/or apoptosis. We demonstrate here that p27Kip1 inhibits hTERT mRNA expression and telomerase activity through post-transcriptional up-regulation by IFN-gamma/IRF-1 signaling. The ectopic expression of p27 suppressed hTERT expression and telomerase activity in human cervical cancer cell lines, HeLa and HT3. Furthermore, hTERT promoter activity of mouse embryonic fibroblasts (MEFs) deficient in p27 (p27-/- MEFs) was significantly higher than that of wild-type MEFs. Overexpression of p27 suppressed hTERT promoter activity and telomerase activity of p27-/- MEFs. In addition p27 down-regulated E7 protein expression and in transiently transfected HeLa cells, E7 increased hTERT promoter activity. In conclusion, we propose that inhibition of the hTERT expression and telomerase activity may be a novel tumor suppressor function of p27.

Thymosin {beta}(10) inhibits angiogenesis and tumor growth by interfering with Ras function.

Thymosin beta(10) is a monomeric actin sequestering protein that regulates actin dynamics. Previously, we and others have shown that thymosin beta(10) acts as an actin-mediated tumor suppressor. In this study, we show that thymosin beta(10) is not only a cytoskeletal regulator, but that it also acts as a potent inhibitor of angiogenesis and tumor growth by its interaction with Ras. We found that overexpressed thymosin beta(10) significantly inhibited vascular endothelial growth factor-induced endothelial cell proliferation, migration, invasion, and tube formation in vitro. Vessel sprouting was also inhibited ex vivo. We further show that thymosin beta(10) directly interacted with Ras. This interaction resulted in inhibition of the Ras downstream mitogen-activated protein kinase/extracellular signal-regulated kinase kinase signaling pathway, leading to decreased vascular endothelial growth factor production. Thymosin beta(10) injected into a xenograft model of human ovarian cancer in nude mice markedly inhibited tumor growth and reduced tumor vascularity. In contrast, a related thymosin family member, thymosin beta(4), did not bind to Ras and showed positive effects on angiogenesis. These findings show that the inhibition of Ras signal transduction by thymosin beta(10) results in antiangiogenic and antitumor effects, suggesting that thymosin beta(10) may be valuable in anticancer therapy.

Association of MICA polymorphism with HLA-B51 and disease severity in Korean patients with Behcet's disease.

The HLA-B51 allele is known to be associated with Behcet's disease (BD) in many ethnic group. However, it has not yet been clarified whether the HLA-B51 gene itself is the pathogenic gene related to BD or whether it is some other gene in linkage disequlibrium with HLA-B51. Recently, the Triplet repeat (GCT/AGC) polymorphism in transmembrane region of the MHC class I chain-related A (MICA) gene was identified. To investigate the association of MICA with BD, we studied the MICA polymorphism in 108 Korean BD patients and 204 healthy controls in relation to the presence of HLA-B51 and clinical manifestations. The triplet repeat polymorphism was determined by polymerase chain reaction (PCR)-denaturing polyacrylamide gel electrophoresis (PAGE). The phenotype frequency of the MICA*A6 allele (relative risk, RR=2.15, p=0.002) and HLA-B51(RR=1.87, p=0.022) were significantly increased in the Korean patients with BD. A strong linkage disequilibrium was observed between the MICA*A6 and HLA-B51 in both the patients with BD and control subjects. Stratification analysis showed that MICA*A6 homozygosity was strongly associated with BD in the HLA-B51-negative population, and HLA-B51 was also associated with MICA*A6-negative population. In conclusion, MICA*A6 rather than HLA-B51 was strongly associated with Korean patients with BD, and the MICA*A6 allele is a useful susceptibility marker of BD, especially in the HLA-B5-negative