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Background As the world’s population ages, hip replacement, a routine treatment for arthritis, has become more common. However, after surgery, rehabilitation has some limited effectiveness with postoperative complications and persistent impairments. This study aimed to explore the effect of a self-efficacy-enhancing intervention program following hip replacement on patients’ rehabilitation outcomes (self-efficacy, functional exercise compliance, hip function, activity and social participation, anxiety and depression, and quality of life). Methods A prospective randomized controlled trial with a repeated-measures, two-group design was conducted in a grade A general hospital in Guangdong Province, China. A total of 150 participants with a unilateral total hip replacement were recruited via convenience sampling. Participants were randomly assigned to either the self-efficacy enhancing intervention group ( n  = 76) or the control group ( n  = 74). The intervention encompassed a face-to-face education before discharge and four telephone-based follow-ups in six months after surgery. Researchers collected baseline data on one to three days after surgery, and outcomes data were collected one, three, and six months after surgery. Results Average age (deviation) in intervention and control group were 58 (10.32) and 59 (10.82), respectively. After six months, intervention group scored 86.83 ± 5.89 in rehabilitation self-efficacy, significantly higher than control group (72.16 ± 6.52, t  = -10.820, p  < 0.001) and their hip function has turned to “excellent” (90.52 ± 4.03), while that of the latter was limited to a “middle” level (78.47 ± 7.57). Statistically significant differences were found in secondary outcomes ( p  < 0.001). The advantage of intervention in improving quality of life was seen in the long term rather than in the early postoperative period. Conclusions The self-efficacy-enhancing intervention performed by nurses induced better exercise compliance and physical, psychological, and social functions after hip replacement compared with routine care. We recommend such interventions to be combined with routine care soon after hip replacement. Further research should focus on the social participation of patients with hip replacement. Trial registration Retrospectively registered at Chinese Clinical Trial Registry (31/01/2020, No. ChiCTR2000029422, http://www.chictr.org.cn/index.aspx ).

Array Comparative Genomic Hybridization (a-CGH) is a powerful molecular cytogenetic tool to detect genomic imbalances and study disease mechanism and pathogenesis. We report our experience with the clinical implementation of this high resolution human genome analysis, referred to as Chromosomal Microarray Analysis (CMA). CMA was performed clinically on 2513 postnatal samples from patients referred with a variety of clinical phenotypes. The initial 775 samples were studied using CMA array version 4 and the remaining 1738 samples were analyzed with CMA version 5 containing expanded genomic coverage. Overall, CMA identified clinically relevant genomic imbalances in 8.5% of patients: 7.6% using V4 and 8.9% using V5. Among 117 cases referred for additional investigation of a known cytogenetically detectable rearrangement, CMA identified the majority (92.5%) of the genomic imbalances. Importantly, abnormal CMA findings were observed in 5.2% of patients (98/1872) with normal karyotypes/FISH results, and V5, with expanded genomic coverage, enabled a higher detection rate in this category than V4. For cases without cytogenetic results available, 8.0% (42/524) abnormal CMA results were detected; again, V5 demonstrated an increased ability to detect abnormality. Improved diagnostic potential of CMA is illustrated by 90 cases identified with 51 cryptic microdeletions and 39 predicted apparent reciprocal microduplications in 13 specific chromosomal regions associated with 11 known genomic disorders. In addition, CMA identified copy number variations (CNVs) of uncertain significance in 262 probands; however, parental studies usually facilitated clinical interpretation. Of these, 217 were interpreted as familial variants and 11 were determined to be de novo; the remaining 34 await parental studies to resolve the clinical significance. This large set of clinical results demonstrates the significantly improved sensitivity of CMA for the detection of clinically relevant genomic imbalances and highlights the need for comprehensive genetic counseling to facilitate accurate clinical correlation and interpretation.

Purpose: This study was designed to evaluate the feasibility of using a targeted array-CGH strategy for prenatal diagnosis of genomic imbalances in a clinical setting of current pregnancies. Methods: Women undergoing prenatal diagnosis were counseled and offered array-CGH (BCM V4.0) in addition to routine chromosome analysis. Array-CGH was performed with DNA directly from amniotic fluid cells with whole genome amplification, on chorionic villus samples with amplification as necessary, and on cultured cells without amplification. Results: Ninety-eight pregnancies (56 amniotic fluid and 42 CVS specimens) were studied with complete concordance between karyotype and array results, including 5 positive cases with chromosomal abnormalities. There was complete concordance of array results for direct and cultured cell analysis in 57 cases tested by both methods. In 12 cases, the array detected copy number variation requiring testing of parental samples for optimal interpretation. Array-CGH results were available in an average of 6 and 16 days for direct and cultured cells, respectively. Patient acceptance of array-CGH testing was 74%. Conclusion: This study demonstrates the feasibility of using array-CGH for prenatal diagnosis, including reliance on direct analysis without culturing cells. Use of array-CGH should increase the detection of abnormalities relative to the risk, and is an option for an enhanced level of screening for chromosomal abnormalities in high risk pregnancies.

Oncology patients are at high risk for development of HAPIs due to the severity of cancer diagnosis, chemotherapy, comorbidities, mobility limitation and nutrient loss related to hypermetabolism and neoplastic cachexia. From December 2021 to February 2022, three HAPIs including one deep tissue injury, one stage II, and one unstageable pressure injury (PI), occurred after admission in our acute inpatient oncology unit. Research studies support evidence-based practices that show HAPIs can be decreased significantly when bedside nurses apply a PIP bundle - a group of key elements of PIP, to high-risk patients. Various evidence also found a chart audit can promote compliance to the implementation of the PIP bundle. The aim of this project was to reduce HAPIs among our inpatient oncology patients through implementation of an evidence-based PIP bundle and use of chart audits to promote PIP bundle compliance. A PIP bundle was applied to patients at high risk for HAPI development. The PIP bundle consisted of ten key elements - skin assessment, risk assessment using the Braden Scale, support surface, activity management, nutrition management, patient and family education, moisture and incontinent management, reposition, documentation of intervention, and a chart audit. A chart audit form was used to ensure compliance with implementation of the PIP bundle. HAPIs incidences reduced PIs from Pre-Implementation 2.1 per 1,000 patient-day to 0.7 Post-Implementation 0.7 per 1,000 patient-day. The overall rates of compliance increased consistently from 91% in May, 92% in June, to 99% in July. Compliance was higher for applying Mapilax and a specialty bed than repositioning among high risk PI oncology patients. Repositioning only reached a high of an 80% compliance in June the second month after implementation of the PIP bundle related to float-in nurses assigned. This is attributed to some floated-in nursing staff who were not included in the education of the implementation of the PIP bundle upon arriving on the unit for the day. Implementation of an evidence-based PIP bundle resulted in a considerable decrease in HAPIs on our unit. A chart audit for compliance use of the PIP bundle was vital to ensure consistency of our practice. Incorporating the mix of the PIP bundle and the chart audit into practice resulted in a significant decrease in HAPIs.

By analyzing genomic copy-number differences using high-resolution mouse whole-genome BAC arrays, we uncover substantial differences in regional DNA content between inbred strains of mice. The identification of these apparently common segmental polymorphisms suggests that these differences can contribute to genetic variability and pathologic susceptibility.

Although radiation can directly induce DNA damage and is a known human and animal carcinogen, the number of genetic changes in radiation-induced tumors, and the pathways responsible for generating them, are unknown. We have used high-density BAC arrays covering >95% of the mouse genome for analysis of genomic patterns of aberrations in spontaneous and radiation-induced mouse lymphomas. The majority of radiation-induced tumors exhibit one of three ‘signatures’ based on gene copy number changes. Some exhibit extensive scrambling of the genome, with very high numbers of recurrent gains and losses. Two other signatures are characterized by excess gains but relatively few losses, or vice versa . Changes in spontaneous tumors often involve whole chromosomes, whereas radiation-induced tumors exhibit a high frequency of localized deletion/amplification events. The number of copy number abnormalities does not correlate with the latency or pathology of the tumors. We propose that specific early events following radiation exposure induce changes in ‘caretaker’ genes that control specific downstream pathways involved in DNA damage repair. The nature of these early events may determine the overall genomic signature observed in the resulting tumor.

To explore and compare the clinical control of three atomized inhalation budesonide (BUD) regimens for Chinese preschool children with recurrent wheezing using Test for Respiratory and Asthma Control (TRACK) scores. A total of 474 preschool children with positive Modified Asthma Predictive Index (mAPI) were randomly assigned to a daily group (initially given inhaled BUD 1 mg once a day and assessed every 4 weeks; if symptom were well controlled for 12 weeks, the dose was reduced to 25–50% of the previous dose until afinal dose of 0.25 mg once a day, maintained until 52 weeks), an intermittent high-dose group (1 mg twice daily for 7 days starting early during a predefined respiratory tract illness) and an intermittent medium-dose group (0.5 mg twice daily as soon as they contacted allergens or experienced nasal congestion, a runny nose, cough or other suspicious respiratory symptoms and continuing until symptoms were reduced or risk factors were absent for 3 days) for 52 weeks of treatment. The TRACK questionnaire was administered every 4 weeks. When TRACK scores were ≥ 80, symptoms were considered to be controlled. The average TRACK scores of the three groups after treatment were significantly higher than those before treatment (P < 0.001). There were no significant differences in the average TRACK scores and control rate after treatment at every 4 weeks in the three groups (P > 0.05). Te number of systemic glucocorticoid courses, urgent care visits for wheezing, and wheezing episodes before and after treatment were significantly different within each of the three groups (P < 0.001), but not among the three groups (P > 0.05). In clinical treatment of children, one of the three treatment options can be selected according to the specific situation case of mAPI- positive recurrent wheezing children.

Objective Immunogenic cell death (ICD) has emerged as a promising strategy to activate the adaptive immune response, modulate the tumor microenvironment (TME) and enhance the efficacy of immune therapy. However, the relationship between ICD and TME reprogramming in hepatocellular carcinoma (HCC) remains poorly understood. Methods Transcriptional profiles and clinical spectrum of 486 HCC patients were obtained from TCGA and GEO databases. We utilized consensus clustering analysis to construct two distinct molecular subtypes and established an ICD-based scoring system (named ICD score) via WGCNA and LASSO Cox regression to predict the prognosis of the HCC cohort. Then we employed CIBERSORT and ESTIMATE methods to analyze the immune landscape of ICD score in HCC. Subsequently, the immunophenoscore (IPS) and tumor immune dysfunction and rejection (TIDE) analyses were performed to determine whether the ICD score could influence the immune therapeutic effect. Based on the ICD scoring system, a novel nomogram was generated to provide a numerical probability of HCC patients’ overall survival (OS). Results We identified two independent ICD clusters (cluster A/B), and cluster B possessed a worse prognosis and higher immune cell infiltration. Using ICD scoring system, the HCC patients were divided into high- and low-ICD-score groups. Through integrative analyses, the high-ICD cohort owned advanced TNM stage, high pathologic grade and increased suppressive immune cell enrichment. We developed a nomogram containing the ICD score, demonstrating a high predictive accuracy with a C-index of 0.703. We further discovered that PSMD2 and PSMD14 could serve as ICD-associated prognostic biomarkers and therapeutic targets in HCC. Conclusion The ICD score exhibits a high degree of reliability for predicting prognosis and may provide valuable guidance for the selection of immunotherapy for HCC patients. This novel scoring system enables the estimation of clinical immunotherapy response for HCC patients, offering new opportunities for personalized immunotherapy.

BackgroundCircular RNAs (circRNAs) play a significant role in the initiation and progression of various cancers, including hepatocellular carcinoma (HCC). Circular syntaxin 6 (circSTX6, also known as hsa_circ_0007905) has been identified as a microRNA (miRNA) sponge in pancreatic adenocarcinoma. However, its full range of functions in terms of protein scaffold and translation remain largely unexplored in the context of HCC.MethodsThe expression of circSTX6 and its encoded protein was examined in HCC tumour tissues. N6-methyladenosine (m6A) on circSTX6 was verified and quantified by methylated RNA immunoprecipitation (Me-RIP), RIP and dual luciferase reporter assays. The biological functions of circSTX6 and its encoded protein in HCC were clarified by in vitro and in vivo experiments. Mechanistically, the interaction between circSTX6 and heterogeneous nuclear ribonucleoprotein D (HNRNPD) was investigated by RNA pull-down, RIP and fluorescence in situ hybridization (FISH)/IF. The regulatory effects of circSTX6 and HNRNPD on activating transcription factor 3 (ATF3) mRNA were determined by mRNA stability and RIP assays. Furthermore, the presence of circSTX6-encoded protein was verified by mass spectrometry.ResultsCircSTX6 and its encoded 144 amino acid polypeptide, circSTX6-144aa, were highly expressed in HCC tumour tissues and served as independent risk factors for overall survival in HCC patients. The expression of circSTX6 was regulated by METTL14 in an m6A-dependent manner. Functionally, circSTX6 accelerated HCC proliferation and tumourigenicity and reinforced tumour metastasis in vitro and in vivo. Mechanistically, circSTX6 acted as a sponge for HNRNPD protein, facilitating its binding to ATF3 mRNA, consequently promoting ATF3 mRNA decay. Meanwhile, circSTX6-144aa promoted HCC proliferation, migration and invasion independent of circSTX6 itself.ConclusionCollectively, our study reveals that m6A-modified circSTX6 drives malignancy in HCC through the HNRNPD/ATF3 axis, while its encoded circSTX6-144aa contributes to HCC progression independent of circSTX6. CirSTX6 and its encoded protein hold promise as potential biomarkers and therapeutic targets in HCC.