Citations

The primary objective of this study was to develop a risk-based readmission prediction model using the EMR data available at discharge. This model was then validated with the LACE plus score. The study cohort consisted of about 310,000 hospital admissions of patients with cardiovascular and cerebrovascular conditions. The EMR data of the patients consisted of lab results, vitals, medications, comorbidities, and admit/discharge settings. These data served as the input to an XGBoost model v1.7.6, which was then used to predict the number of days until the next readmission. Our model achieved remarkable results, with a precision score of 0.74 (±0.03), a recall score of 0.75 (±0.02), and an overall accuracy of approximately 82% (±5%). Notably, the model demonstrated a high accuracy rate of 78.39% in identifying the patients readmitted within 30 days and 80.81% accuracy for those with readmissions exceeding six months. The model was able to outperform the LACE plus score; of the people who were readmitted within 30 days, only 47.70 percent had a LACE plus score greater than 70, and, for people with greater than 6 months, only 10.09 percent had a LACE plus score less than 30. Furthermore, our analysis revealed that the patients with a higher comorbidity burden and lower-than-normal hemoglobin levels were associated with increased readmission rates. This study opens new doors to the world of differential patient care, helping both clinical decision makers and healthcare providers make more informed and effective decisions. This model is comparatively more robust and can potentially substitute the LACE plus score in cardiovascular and cerebrovascular settings for predicting the readmission risk.

Abstract Introduction Effective pain and anxiety management during the perioperative phase remains a challenge for patients undergoing surgeries and other invasive procedures. The current standard of care involves prescribing analgesics to treat these conditions; however, there has been recent interest in applying multimodal strategies that limit the use of these medications. One such modality is meditation, which has been shown to be effective in alleviating various physical and psychological symptoms in other settings. This systematic review aims to assess how current meditative practices affect perioperative pain and anxiety. Methods We conducted a systematic review of randomized controlled trials following the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines. A comprehensive literature search was conducted using PubMed MEDLINE, Embase, PsycINFO, APA PsycINFO, EBM Reviews, Scopus, and Web of Science for all available dates. Our primary outcomes of interest were patient‐reported pain and anxiety scores using the Visual Analog Scale, the Brief Pain Inventory, the Depression Anxiety Stress Scale, the State‐Trait Anxiety Inventory (STAI), and the Hospital Anxiety and Depression Scale (HADS). For the HADS and STAI scales, only the anxiety and anxiety‐state subgroups were reported, respectively. Results The literature search yielded 1746 articles. A total of 286 full‐text articles were screened, and 16 studies were included in this systematic review. A total of eight studies assessed pain scores after invasive procedures; five reported improvements in pain scores, and three reported no change after meditative practices. Ten studies assessed anxiety outcomes after invasive procedures: nine reported a decrease in overall anxiety levels as a result of meditation practices while one study reported no change in anxiety scores. Conclusion Data from this limited literature suggests that different meditation practices could be effective in alleviating pain and anxiety within the perioperative phase for patients undergoing various types of invasive procedures. Future prospective studies are needed to determine whether routine meditation in the perioperative setting is effective in mitigating perioperative pain and anxiety.

AbstractINTRODUCTIONAge‐related and Alzheimer's disease (AD) dementia–related neurodegeneration impact brain health. While morphometric measures from T1‐weighted scans are established biomarkers, they may be less sensitive to earlier changes. Neurite orientation dispersion and density imaging (NODDI), offering biologically meaningful interpretation of tissue microstructure, may be an advanced brain health biomarker.METHODSWe contrasted regional gray matter NODDI and morphometric evaluations concerning their correlation with (1) age, (2) clinical diagnosis stage, and (3) tau pathology as assessed by AV1451 positron emission tomography.RESULTSOur study hypothesizes that NODDI measures are more sensitive to aging and early AD changes than morphometric measures. One NODDI output, free water fraction (FWF), showed higher sensitivity to age‐related changes, generally better effect sizes in separating mild cognitively impaired from cognitively unimpaired participants, and stronger associations with regional tau deposition than morphometric measures.DISCUSSIONThese findings underscore NODDI's utility in capturing early neurodegenerative changes and enhancing our understanding of aging and AD.Highlights Neurite orientation dispersion and density imaging can serve as an effective brain health biomarker for aging and early Alzheimer's disease (AD). Free water fraction has higher sensitivity to normal brain aging. Free water fraction has stronger associations with early AD and regional tau deposition.

Abstract Human immune system (HIS) mice constructed in various ways are widely used for investigations of human immune responses to pathogens, transplants and immunotherapies. In HIS mice that generate T cells de novo from hematopoietic progenitors, T cell-dependent multisystem autoimmune disease occurs, most rapidly when the human T cells develop in the native NOD.Cg- Prkdcscid Il2rgtm1Wjl (NSG) mouse thymus, where negative selection is abnormal. Disease develops very late when human T cells develop in human fetal thymus grafts, where robust negative selection is observed. We demonstrate here that PD-1+CD4+ peripheral (Tph) helper-like and follicular (Tfh) helper-like T cells developing in HIS mice can induce autoimmune disease. Tfh-like cells were more prominent in HIS mice with a mouse thymus, in which the highest levels of IgG were detected in plasma, compared to those with a human thymus. While circulating IgG and IgM antibodies were autoreactive to multiple mouse antigens, in vivo depletion of B cells and antibodies did not delay the development of autoimmune disease. Conversely, adoptive transfer of enriched Tfh- or Tph-like cells induced disease and autoimmunity-associated B cell phenotypes in recipient mice containing autologous human APCs without T cells. T cells from mice with a human thymus expanded and induced disease more rapidly than those originating in a murine thymus, implicating HLA-restricted T cell-APC interactions in this process. Since Tfh, Tph, autoantibodies and LIP have all been implicated in various forms of human autoimmune disease, the observations here provide a platform for the further dissection of human autoimmune disease mechanisms and therapies.

Human immune system (HIS) mice constructed in various ways are widely used for investigations of human immune responses to pathogens, transplants, and immunotherapies. In HIS mice that generate T cells de novo from hematopoietic progenitors, T cell-dependent multisystem autoimmune disease occurs, most rapidly when the human T cells develop in the native NOD.Cg- Prkdc scid Il2rg tm1Wjl (NSG) mouse thymus, where negative selection is abnormal. Disease develops very late when human T cells develop in human fetal thymus grafts, where robust negative selection is observed. We demonstrate here that PD-1 + CD4 + peripheral (Tph) helper-like and follicular (Tfh) helper-like T cells developing in HIS mice can induce autoimmune disease. Tfh-like cells were more prominent in HIS mice with a mouse thymus, in which the highest levels of IgG were detected in plasma, compared to those with a human thymus. While circulating IgG and IgM antibodies were autoreactive to multiple mouse antigens, in vivo depletion of B cells and antibodies did not delay the development of autoimmune disease. Conversely, adoptive transfer of enriched Tfh- or Tph-like cells induced disease and autoimmunity-associated B cell phenotypes in recipient mice containing autologous human APCs without T cells. Tfh/Tph cells from mice with a human thymus expanded and induced disease more rapidly than those originating in a murine thymus, implicating HLA-restricted T cell-APC interactions in this process. Since Tfh, Tph, autoantibodies, and lymphopenia-induced proliferation (LIP) have all been implicated in various forms of human autoimmune disease, the observations here provide a platform for the further dissection of human autoimmune disease mechanisms and therapies.

BACKGROUND The articular origin of intraneural cysts has been previously described and well supported. Intraneural ganglion cysts most commonly occur in adults and in the common peroneal nerve arising from the anterior aspect of the superior tibiofibular joint (STFJ). OBSERVATIONS The authors report a pediatric patient who developed a tibial intraneural cyst arising from the posterior aspect of the STFJ within months after surgical treatment of a peroneal intraneural cyst from the anterior aspect of the same joint. Surgery consisted of disconnecting the articular branch of the peroneal nerve and decompression of the cyst. Three-month postoperative magnetic resonance imaging showed resolution of the peroneal intraneural cyst and anterior compartment denervation but demonstrated a clinically occult small tibial intraneural ganglion cyst arising from the STFJ with popliteus muscle atrophy. LESSONS This case underscores the importance of addressing the underlying etiology (articular synovitis) or the communication pathways (articular branches) whenever feasible to mitigate intraneural cyst recurrence. Furthermore, this report reinforces the validity of the articular theory. https://thejns.org/doi/10.3171/CASE24277

ObjectiveWe aimed to evaluate lung cancer risk in patients with rheumatoid arthritis (RA) and RA‐interstitial lung disease (ILD).MethodsWe performed a retrospective, matched cohort study of RA and RA‐ILD within the Veterans Health Administration (VA) between 2000 and 2019. Patients with RA and RA‐ILD were identified with validated administrative‐based algorithms, then matched (up to 1:10) on age, gender, and VA enrollment year to individuals without RA. Lung cancers were identified from a VA oncology database and the National Death Index. Conditional Cox regression models assessed lung cancer risk adjusting for race, ethnicity, smoking status, Agent Orange exposure, and comorbidity burden among matched individuals. Several sensitivity analyses were performed.ResultsWe matched 72,795 patients with RA with 633,937 patients without RA (mean age 63 years; 88% male). Over 4,481,323 patient‐years, 17,099 incident lung cancers occurred. RA was independently associated with an increased lung cancer risk (adjusted hazard ratio [aHR] 1.58 [95% confidence interval (CI) 1.52–1.64]), which persisted in never smokers (aHR 1.65 [95% CI 1.22–2.24]) and in those with incident RA (aHR 1.54 [95% CI 1.44–1.65]). Compared to non‐RA controls, prevalent RA‐ILD (n = 757) was more strongly associated with lung cancer risk (aHR 3.25 [95% CI 2.13–4.95]) than RA without ILD (aHR 1.57 [95% CI 1.51–1.64]). Analyses of both prevalent and incident RA‐ILD produced similar results (RA‐ILD vs non‐RA aHR 2.88 [95% CI 2.45–3.40]).ConclusionRA was associated with a >50% increased risk of lung cancer, and those with RA‐ILD represented a particularly high‐risk group with an approximate three‐fold increased risk. Increased lung cancer surveillance in RA, and especially RA‐ILD, may be a useful strategy for reducing the burden posed by the leading cause of cancer death.