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To explore the favorable factors that help slow the progression of disease in patients with mild Cervical Spondylotic Myelopathy (CSM). A retrospective analysis was conducted, involving the enrollment of 115 CSM patients. The categorization of patients into two groups was based on the duration of symptoms, assessments using the mJOA scale and Health Transition (HT) scores: mild-slow group and severe-rapid group. We found that the patients in both groups had similar degrees of spinal cord compression, but mild-slow group were older and had smaller C2–C7 cobb angle (Flexion) (CL(F)), C2–C7 cobb angle (Range of motion) (CL(ROM)), Transverse area (TA), Normal-TA, Compressive spinal canal area (CSCA), Normal-Spinal canal area (Normal-SCA) and lower Spinal cord increased signal intensity (ISI) Grade than the severe-rapid group. A binary logistic regression analysis showed that CL(ROM) and Normal-TA are favorable factors to help slow the progression of disease patients with mild CSM. Through ROC curves, we found that when CL(ROM) < 39.1° and Normal-TA < 80.5mm2, the progression of disease in CSM patients may be slower. Meanwhile, we obtained a prediction formula by introducing joint prediction factor: L = CL(ROM) + 2.175 * Normal-TA. And found that when L < 213.0, the disease progression of patients may be slower which was superior to calculate CL(ROM) and Normal-TA separately.

Chronic kidney disease (CKD) is a significant threat to the quality of life of the global population. Thus, slowing kidney disease progression is considered vital in the treatment of CKD patients. The study aimed to evaluate the effectiveness of a program designed to slow the progression of CKD among Type 2 diabetes mellitus patients with HT with stage 3 CKD (CKD 3) in Thailand by adopting the information-motivation-behavioral skills (IMB) model and applying technology. This study was conducted as a cluster randomized controlled trial. The program activities comprised: (i) providing disease information and teaching behaviors to slow the progression of kidney disease to patients and family members via a 2-h session; (ii) teaching practical behavioral skills for appropriate diet and exercise to patients and family members via a 2-h session; (iii) enhancing personal motivation via the Line application and motivational interviewing via telephone calls; (iv) enhancing social motivation with the support of a family member; (v) employing technology to monitor behaviors and increase patient motivation; and (vi) assessing behaviors that were not practical, exploring barriers to behavior modification, and teaching further practical behavioral skills via the Line application. The data were analyzed using percentages, means, standard deviations, chi-square tests, t-tests, and a 2-way repeated-measures analysis of variance. The results showed that after the experiment, the experimental group had significantly higher mean scores in terms of knowledge, perceived benefits, perceived severity, self-efficacy, and behaviors to slow the progression of kidney disease than the control group (P < .05). Further, the experimental group had significantly better clinical outcomes (SBP, DBP, eGFR, BUN, creatinine, albuminuria, FBS, and HbA1c) than the control group (P < .05). In summary, the findings indicate that the program improved clinical outcomes, especially kidney function, effectively slowing the progression of kidney disease.

This chapter contains sections titled: Introduction Heart failure: the facts Occupational perspective of cardiac services An overview of community cardiac care in the community Case study 1 Case study 2 Working occupationally with this client group Heart failure service perspective The potential and future of occupational therapy within this type of setting Conclusion References

Background Alzheimer’s disease (AD) pathology impairs cognitive function. Yet some individuals with high amounts of AD pathology suffer marked memory impairment, while others with the same degree of pathology burden show little impairment. Why is this? One proposed explanation is cognitive reserve i.e., factors that confer resilience against, or compensation for the effects of AD pathology. Deep NREM slow wave sleep (SWS) is recognized to enhance functions of learning and memory in healthy older adults. However, that the quality of NREM SWS (NREM slow wave activity, SWA) represents a novel cognitive reserve factor in older adults with AD pathology, thereby providing compensation against memory dysfunction otherwise caused by high AD pathology burden, remains unknown. Methods Here, we tested this hypothesis in cognitively normal older adults ( N = 62) by combining 11 C-PiB (Pittsburgh compound B) positron emission tomography (PET) scanning for the quantification of β-amyloid (Aβ) with sleep electroencephalography (EEG) recordings to quantify NREM SWA and a hippocampal-dependent face-name learning task. Results We demonstrated that NREM SWA significantly moderates the effect of Aβ status on memory function. Specifically, NREM SWA selectively supported superior memory function in individuals suffering high Aβ burden, i.e., those most in need of cognitive reserve ( B = 2.694, p = 0.019). In contrast, those without significant Aβ pathological burden, and thus without the same  need for cognitive reserve, did not similarly benefit from the presence of NREM SWA ( B = -0.115, p = 0.876). This interaction between NREM SWA and Aβ status predicting memory function was significant after correcting for age, sex, Body Mass Index, gray matter atrophy, and previously identified cognitive reserve factors, such as education and physical activity ( p = 0.042). Conclusions These findings indicate that NREM SWA is a novel cognitive reserve factor providing resilience against the memory impairment otherwise caused by high AD pathology burden. Furthermore, this cognitive reserve function of NREM SWA remained significant when accounting both for covariates, and factors previously linked to resilience, suggesting that sleep might be an independent cognitive reserve resource. Beyond such mechanistic insights are potential therapeutic implications. Unlike many other cognitive reserve factors (e.g., years of education, prior job complexity), sleep is a modifiable factor. As such, it represents an intervention possibility that may aid the preservation of cognitive function in the face of AD pathology, both present moment and longitudinally.

Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease that progressively debilitates neuronal cells that control voluntary muscle activity. Biomarkers are urgently needed to facilitate ALS diagnosis and prognosis, and as indicators of therapeutic response in clinical trials. microRNAs (miRNAs), small posttranscriptional modifiers of gene expression, are frequently altered in disease conditions. Besides their important regulatory role in variety of biological processes, miRNAs can also be released into the circulation by pathologically affected tissues and display remarkable stability in body fluids. In a mouse model of ALS that expresses mutated human superoxide dismutase 1 (SOD1-G93A) skeletal muscle is one of the tissues affected early by mutant SOD1 toxicity. To find biomarkers for ALS, we studied miRNA alterations from skeletal muscle and plasma of SOD1-G93A mice, and subsequently tested the levels of the affected miRNAs in the serum from human ALS patients. Fast-twitch and slow-twitch muscles from symptomatic SOD1-G93A mice (age 90 days) and their control littermates were first studied using miRNA microarrays and then evaluated with quantitative PCR from five age groups from neonatal to the terminal disease stage (10-120 days). Among those miRNA changed in various age/gender/muscle groups (miR-206, -1, -133a, -133b, -145, -21, -24), miR-206 was the only one consistently altered during the course of the disease pathology. In both sexes, mature miR-206 was increased in fast-twitch muscles preferably affected in the SOD1-G93A model, with highest expression towards the most severely affected animals. Importantly, miR-206 was also increased in the circulation of symptomatic animals and in a group of 12 definite ALS patients tested. We conclude that miR-206 is elevated in the circulation of symptomatic SOD1-G93A mice and possibly in human ALS patients. Although larger scale studies on ALS patients are warranted, miR-206 is a promising candidate biomarker for this motor neuron disease.

Aims/hypothesisMultiple islet autoimmunity increases risk of diabetes, but not all individuals positive for two or more islet autoantibodies progress to disease within a decade. Major islet autoantibodies recognise insulin (IAA), GAD (GADA), islet antigen-2 (IA-2A) and zinc transporter 8 (ZnT8A). Here we describe the baseline characteristics of a unique cohort of ‘slow progressors’ (n = 132) who were positive for multiple islet autoantibodies (IAA, GADA, IA-2A or ZnT8A) but did not progress to diabetes within 10 years.MethodsIndividuals were identified from five studies (BABYDIAB, Germany; Diabetes Autoimmunity Study in the Young [DAISY], USA; All Babies in Southeast Sweden [ABIS], Sweden; Bart’s Oxford Family Study [BOX], UK and the Pittsburgh Family Study, USA). Multiple islet autoantibody characteristics were determined using harmonised assays where possible. HLA class II risk was compared between slow progressors and rapid progressors (n = 348 diagnosed <5 years old from BOX) using the χ2 test.ResultsIn the first available samples with detectable multiple antibodies, the most frequent autoantibodies were GADA (92%), followed by ZnT8A (62%), IAA (59%) and IA-2A (41%). High risk HLA class II genotypes were less frequent in slow (28%) than rapid progressors (42%, p = 0.011), but only two slow progressors carried the protective HLA DQ6 allele.ConclusionNo distinguishing characteristics of slow progressors at first detection of multiple antibodies have yet been identified. Continued investigation of these individuals may provide insights into slow progression that will inform future efforts to slow or prevent progression to clinical diabetes.

To conduct a systematic review of the literature to examine the associations between slowwave sleep (SWS) disturbance and dementia. We systematically searched PubMed and Embase for cohort and case-control studies that examined SWS differences between patients with dementia and healthy controls. Study quality was assessed using the Newcastle-Ottawa Scale. In total, 19 studies (three cohort and 16 case-control) were included in analysis. Overall, one cohort study and 14 case-control studies found that reduced SWS was associated with dementia; the evidence was stronger in case-control studies than cohort studies. Study quality of studies varied; most were above average. Most studies regarding the association between SWS and dementia are cross-sectional; more longitudinal studies are needed to determine whether reduction in SWS can predict incident dementia. Future studies should include multi-night recordings and the use of standardised criteria to enhance the accuracy of recordings and facilitate comparisons between studies.

Abstract Study Objectives Sleep disturbances and genetic variants have been identified as risk factors for Alzheimer’s disease (AD). Our goal was to assess whether genome-wide polygenic risk scores (PRS) for AD associate with sleep phenotypes in young adults, decades before typical AD symptom onset. Methods We computed whole-genome PRS for AD and extensively phenotyped sleep under different sleep conditions, including baseline sleep, recovery sleep following sleep deprivation, and extended sleep opportunity, in a carefully selected homogenous sample of 363 healthy young men (22.1 years ± 2.7) devoid of sleep and cognitive disorders. Results AD PRS was associated with more slow-wave energy, that is, the cumulated power in the 0.5–4 Hz EEG band, a marker of sleep need, during habitual sleep and following sleep loss, and potentially with larger slow-wave sleep rebound following sleep deprivation. Furthermore, higher AD PRS was correlated with higher habitual daytime sleepiness. Conclusions These results imply that sleep features may be associated with AD liability in young adults, when current AD biomarkers are typically negative, and support the notion that quantifying sleep alterations may be useful in assessing the risk for developing AD.

Background Inflammatory markers may provide insights into the underlying mechanisms of slow coronary flow (SCF), including subclinical atherosclerosis and endothelial dysfunction. Interleukin-34 (IL-34), known for its role in immuno-inflammatory diseases, might hold significance in SCF. We aimed to explore the potential association between IL-34 and SCF in patients undergoing diagnostic elective coronary angiography. Methods This observational, cross-sectional study enrolled 256 participants: 124 with SCF and 132 with normal coronary flow (NCF). All participants had undergone outpatient coronary angiography for suspected coronary artery disease. SCF assessment employed the TIMI frame count (TFC) for quantifying coronary flow rate. Results SCF patients exhibited significantly elevated TFC in all three major coronary arteries compared to controls ( p  < 0.05). IL-34 displayed a noteworthy positive correlation with average TFC [for all participants: r = 0.514, p  < 0.001; for SCF patients: r = 0.526, p  < 0.001; for normal controls: r = -0.288, p  > 0.05]. Similarly, high-sensitivity C-reactive protein (hsCRP) showed a significant and positive relationship with average TFC [for all participants: r = 0.504, p  < 0.001; for SCF patients: r = 0.558, p  < 0.001; for normal controls: r = -0.148, p  > 0.05]. SCF patients presented coronary arteries of larger size compared to controls. Conclusion Mean coronary diameter and IL-34 emerged as independent predictors of SCF. Additionally, hsCRP, mean coronary diameter, and IL-34 exhibited a positive correlation with mean TFC values. IL-34 appears to be a more effective indicator than hsCRP in SCF patients.

Background Soluble amyloid-beta oligomers (Aβo) begin to accumulate in the human brain one to two decades before a clinical diagnosis of Alzheimer’s disease (AD). The literature supports that soluble Aβo are implicated in synapse and neuronal losses in the brain regions such as the hippocampus. This region importantly contributes to explicit memory, the first type of memory affected in AD. During AD preclinical and prodromal stages, people are also experiencing wake/sleep alterations such as insomnia (e.g., difficulty initiating sleep, decreased sleep duration), excessive daytime sleepiness, and sleep schedule modifications. In addition, changes in electroencephalographic (EEG) activity during wake and sleep have been reported in AD patients and animal models. However, the specific contribution of Aβo to wake/sleep alterations is poorly understood and was investigated in the present study. Methods Chronic hippocampal injections of soluble Aβo were conducted in male rats and combined with EEG recording to determine the progressive impact of Aβ pathology specifically on wake/sleep architecture and EEG activity. Bilateral injections were conducted for 6 consecutive days, and EEG acquisition was done before, during, and after Aβo injections. Immunohistochemistry was used to assess neuron numbers in the hippocampal dentate gyrus (DG). Results Aβo injections did not affect the time spent in wakefulness, slow wave sleep (SWS), and paradoxical sleep but altered EEG activity during wake and SWS. More precisely, Aβo increased slow-wave activity (SWA; 0.5–5 Hz) and low-beta activity (16–20 Hz) during wake and decreased theta (5–9 Hz) and alpha (9–12 Hz) activities during SWS. Moreover, the theta activity/SWA ratio during wake and SWS was decreased by Aβo. These effects were significant only after 6 days of Aβo injections and were found with alterations in neuron counts in the DG. Conclusions We found multiple modifications of the wake and SWS EEG following Aβo delivery to the hippocampus. These findings expose a specific EEG signature of Aβ pathology and can serve the development of non-invasive and cost-effective markers for the early diagnosis of AD or other amyloid-related diseases.