Reliability of self-measured objective functional impairment using the timed up and go test in patients with diseases of the spine.

BACKGROUND: Accurate assessment of a patient's functional status is crucial for determining the need for treatment and evaluating outcomes. Objective functional impairment (OFI) measures, alongside patient-reported outcome measures (PROMs), have been proposed for spine diseases. The Timed-Up and Go (TUG) test, typically administered by healthcare professionals, is a well-studied OFI measure. This study investigates whether patient self-measurement of TUG is similarly reliable. METHODS: In a prospective, observational study, patients with spinal diseases underwent two TUG assessments: one measured by a healthcare professional and one self-measured by the patient. Interrater reliability was assessed using the intraclass correlation coefficient (ICC) with a two-way random-effects model, considered excellent between 0.75 - 1.00. Paired t-tests directly compared both measurements. The impact of variables such as age, sex, disease type, symptom severity (via PROMs), comorbidities, and frailty on reliability was also analysed. RESULTS: Seventy-four patients were included, with a mean age of 62.9 years (SD 17.8); 29 (39.2%) were female. The majority (64.9%) were treated for degenerative disc disease. The lumbo-sacral region was most affected (71.6%), and 47.3% had previous surgeries. Patient self-measurement reliability was excellent (ICC 0.8740, p < 0.001), and the difference between healthcare professional (19.3 ± 9.4 s) and patient measurements (18.4 ± 9.7 s) was insignificant (p = 0.116). Interrater reliability remained high in patients > 65 years (ICC 0.8584, p < 0.001), patients with ASA grades 3&4 (ICC 0.7066, p < 0.001), patients considered frail (ICC 0.8799, p < 0.001), and in patients not using any walking aid (ICC 0.8012, p < 0.001). High symptom severity still showed strong reliability (ICC 0.8279, p < 0.001 for Oswestry Disability Index > 40; ICC 0.8607, p = 0.011 for Neck Disability Index > 40). CONCLUSIONS: Patients with spine diseases can reliably self-measure OFI using the TUG test. The interrater reliability between self-measurements and those by healthcare professionals was excellent across all conditions. These findings could optimize patient assessments, especially in resource-limited settings.

LncRNA TUG1 regulates mir-34a-5p / SIRT6 to participate in benzene-induced hematotoxicity through PI3K / AKT /mTOR signaling pathway.

LncRNA TUG1 plays pivotal roles in various diseases. However, its exact roles in benzene - induced hematotoxicity remain unclear. Herein, we aimed to investigate the role and mechanism of TUG1 in hematoxic injuries caused by benzene. In the current study, TUG1 was found dramatically decreased in WBCs of benzene exposure workers and negatively correlated with benzene exposure duration and urine SPMA. In vitro assays demonstrated that TUG1 overexpression attenuated 1,4-BQ-caused suppression of cell viability and proliferation, and promotion of ROS generation and apoptosis via PI3K/AKT/mTOR pathway. Bioinformatic prediction and molecular assay validated miR-34a-5p was negatively regulated by TUG1. The miR-34a-5p was upregulated in 1,4-BQ treated cells and downregulated in TUG1 overexpression cells. Moreover, miR-34a-5p upregulation partially reversed the protective effects of TUG1 overexpression on 1,4-BQ - caused cytotoxicity. Furthermore, SIRT6 was a downstream target gene of miR-34a-5p, whose expression was reduced in miR-34a-5p upregulation cells and elevated in TUG1 overexpression cells. Upregulated SIRT6 could counteract accelerated cytotoxicity mediated by miR-34a-5p upregulation after 1,4-BQ treatment. Taken together, our study revealed that the critical role of the TUG1/miR-34a-5p/SIRT6 axis in benzene-caused hematotoxicity, and provided scientific basis for further understanding the epigenetic regulatory mechanisms underlying benzene hematotoxicity.

Carpal Tunnel Syndrome in Elite Female Tug-of-War Athletes: Prevalence and Risk Factor Analysis.

Background: Tug-of-War (TOW) games involve repetitive hand movements and vigorous force, raising the risk of peripheral neuropathy in the upper extremities. The prevalence of carpal tunnel syndrome (CTS) in TOW athletes remains unclear. We hypothesize that elite female TOW athletes have a higher prevalence of CTS than the general population. Methods: Twenty-nine female TOW athletes were recruited from a national team and participated in the study. CTS was clinically diagnosed by history taking and physical examination. Nerve conduction studies (NCS) were additionally performed to confirm CTS. Results: Twelve athletes were clinically diagnosed with CTS; however, only nine were confirmed by NCS. Ten athletes were diagnosed with subclinical CTS by NCS, while seven were classified as truly-non-CTS by both clinical assessment and NCS. The prevalence of CTS and subclinical CTS among the athletes was found to be 33.3% and 37.0%, respectively, significantly higher than 2.7% in the general population by electrodiagnosis. The body weight (p = 0.025) of the athletes with CTS and subclinical CTS was significantly different from those of the athletes without CTS. Conclusions: Our observations revealed a higher prevalence of CTS among elite female TOW athletes, with body weight being a risk factor. The forceful grasping and pulling of the rope may contribute to the development of CTS.

Determination of factors affecting exercise capacity in community-dwelling elderly people.

RATIONALE: Exercise capacity declines with age. However, the effect of common geriatric symptoms, that are related to physical performance, on exercise capacity is unclear. AIMS: The study aimed to determine the impacts of sarcopenia, frailty, balance, and depression on both overall and abnormal exercise capacity. METHODS: One hundred and nineteen community-dwelling older adults over 65 years of age were included in the cross-sectional study. Sarcopenia and frailty status were determined according to the "European Working Group on Sarcopenia in Older People2" and "Fried frailty criteria", respectively. Exercise capacity, balance and depression were assessed with the 6-min walk test (6MWT), the Timed Up and Go Test (TUG) and the Geriatric Depression Scale (GDS), respectively. RESULTS: Of the participants, 5% were sarcopenic, 32.8% were frail, and 29.4% had abnormal exercise capacity (6MWT < 82% pred). According to multivariate linear regression analysis, the model consisting of sarcopenia, frailty, TUG and GDS was explained 53% of the variation in 6MWT (R = 0.73, R2 = 0.53, p < 0.001), and all variables except GDS were independent predictors of exercise capacity (p < 0.05). Sarcopenia was the strongest predictor of 6MWT (ß =-79.76, p = 0.011). The model including sarcopenia, TUG, frailty, and GDS provided 29% prediction of abnormal exercise capacity (Nagelkerke R2 = 29.7, p < 0.001), while TUG was the sole significant predictor in the model (Odd Ratio:1.32, p < 0.002), according to logistic regression analysis. CONCLUSIONS: This study indicates that changes in exercise capacity are more influenced by the presence of sarcopenia, and that poor TUG performance is the greatest risk factor for the impaired exercise capacity.

Reconstruction of deep and perforating corneal defects in dogs-A review (Part III/III): The use of corneal sutures and reporting of ocular discomfort.

The surgical reconstruction of severe corneal disease is a common and crucial component of the clinical practice of veterinary ophthalmology. The first part of the present review described procedures that utilize autogenous ocular tissues, homologous donor tissues, and heterologous donor tissues in dogs, while the second part reviewed the use of biomaterials and keratoprosthetics in this species. This third part is dedicated to the review of the use of corneal sutures including suture type and suture pattern in corneal reconstruction of small animals including dogs and cats. The review also focused on the way studies report postoperative ocular discomfort/pain and how this is treated. Lastly, the author briefly presents the simple but effective techniques available to bury corneal knots for corneal reconstructive surgery in small animal patients, such as the "tugging" and "deep-superficial-superficial-deep" methods for simple interrupted sutures, and the adaptation of the latter for simple continuous sutures.

Influence of Knee Osteoarthritis Severity, Knee Pain, and Depression on Physical Function: A Cross-Sectional Study.

Purpose: Decreased physical function with increasing life expectancy is a public health concern worldwide. Knee osteoarthritis (KOA) is considered one of the primary illnesses causing decreased physical function. Depression affects decreased physical function and is closely related to knee pain in KOA. However, the effect of these interacting factors on physical function is not clear. Patients and Methods: We conducted a cross-sectional analysis of the baseline data of 1106 subjects of the 2009 Locomotive Syndrome and Health Outcome in Aizu Cohort Study (LOHAS). We determined the association between their Timed Up and Go test (TUG) scores and radiographic KOA, knee pain, and depression in a multivariate analysis. Results: Severe knee pain was significantly associated with decreased physical function (the odds ratio [OR] was 2.13, 95% confidence interval [CI]: 1.32-4.89), as was depression (OR 2.64, 95% CI 1.61-4.33). Only Kellgren-Lawrence (KL) grade 4 was significantly associated with decreased physical function in the radiographic KOA severity (OR 6.58, 95% CI 1.75-24.68). Conclusion: Severe knee pain and depression were significantly associated with decreased physical function, but not radiographic KOA severity except for KL grade 4. The limitations of using radiographic KOA severity alone as the indicator of assessment for physical function were suggested. When assessing decreased physical function, the clinical focus tends to be on radiographic KOA severity, but it is important to consider the patient's knee pain and psychological factors.

Assessing Variance in Male Reproductive Skew Based on Long-Term Data in Free-Ranging Rhesus Macaques.

The unequal share in male reproduction (male reproductive skew) has been reported across primate species. To explain the distribution of male reproduction within groups various skew models have been applied to primates, however the "dynamic tug-of-war" model first accounted for the specifics of primate sociality. This model assumes that an increase in the number of competing males, a high degree of female cycle synchrony and their interaction will result in a lower degree of male reproductive skew. Here, we first tested the predictors of this model in rhesus macaques (Macaca mulatta) using long-term demographic and genetic data (up to 9 groups over 22 seasons) of the Cayo Santiago population (Puerto Rico). We also tested an extended version including group size and sex ratio and their interaction with female cycle synchrony. Finally, we investigated which male attributes determine the probability to become a top sire (highest paternity share per group and season). Confirming studies, male rhesus macaques exhibited low to medium degrees of reproductive skew based on the multinomial index, M. Unlike predicted, reproductive skew was higher in groups with more males. The extended analysis suggested that reproductive skew increased with group size in more male-biased groups, but decreased with group size in female-biased groups indicating that the numbers of male and female group members matter. We detected no effect of female cycle synchrony on the variance of reproductive skew. Finally, only maternal rank predicted the probability to become a top sire as long as males resided in their natal group. Together, our results did not support predictions by the dynamic skew model in rhesus macaques, but strengthen studies suggesting that other factors in addition to male-male competition predict male reproductive output in rhesus macaques. Future skew studies should consider female choice and alternative male mating strategies.

Epitranscriptomic m6A modifications during reactivation of HIV-1 latency in CD4+ T cells.

Despite effective antiretroviral therapy reducing HIV-1 viral loads to undetectable levels, the presence of latently infected CD4+ T cells poses a major barrier to HIV-1 cure. N6-methyladenosine (m6A) modification of viral and cellular RNA has a functional role in regulating HIV-1 infection. m6A modification of HIV-1 RNA can affect its stability, translation, and splicing in cells and suppresses type-I interferon induction in macrophages. However, the function of m6A modification in regulating HIV-1 latency reactivation remains unknown. We used the Jurkat T cell line-derived HIV-1 latency model (J-Lat cells) to investigate changes in m6A levels of cellular RNA in response to latency reversal. We observed a significant increase in m6A levels of total cellular RNA upon reactivation of latent HIV-1 in J-Lat cells. This increase in m6A levels was transient and returned to steady-state levels despite continued high levels of viral gene expression in reactivated cells compared to control cells. Upregulation of m6A levels occurred without significant changes in the protein expression of m6A writers or erasers that add or remove m6A, respectively. Knockdown of m6A writers in J-Lat cells significantly reduced HIV-1 reactivation. Treatment with an m6A writer inhibitor reduced cellular RNA m6A levels, along with a reduction in HIV-1 reactivation. Furthermore, using m6A-specific sequencing, we identified cellular RNAs that are differentially m6A-modified during HIV-1 reactivation in J-Lat cells. Knockdown of identified m6A-modified RNA validates these results with an established primary CD4+ T cell model of HIV-1 latency. These results show the importance of m6A RNA modification in HIV-1 latency reversal. IMPORTANCE: RNA m6A modification is important for regulating gene expression and innate immune responses to HIV-1 infection. However, the functional significance of m6A modification during HIV-1 latency reactivation is unknown. To address this important question, in this study, we used established cellular models of HIV-1 latency, m6A-specific sequencing at single-base resolution, and functional assays. We demonstrate that HIV-1 latency reversal leads to increased levels of cellular m6A modification, correlates with cellular m6A levels, and is dependent on the catalytic activity of the m6A methyltransferase enzyme. We also identified cellular genes that are differentially m6A-modified during HIV-1 reactivation, as well as the sites of m6A within HIV-1 RNA. Our novel findings point toward a significant role for m6A modification in HIV-1 latency reversal.

GPR40 agonist ameliorates neurodegeneration and motor impairment by regulating NLRP3 inflammasome in Parkinson's disease animal models.

Parkinson's disease (PD) is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra (SN) and accumulation of intracellular α-synuclein (ɑ-syn) aggregates known as Lewy bodies and Lewy neurites. Levels of polyunsaturated fatty acids (PUFAs) have previously been shown to be reduced in the SN of PD patients. G protein-coupled receptor 40 (GPR40) serves as a receptor for PUFAs, playing a role in neurodevelopment and neurogenesis. Additionally, GPR40 has been implicated in several neuropathological conditions, such as apoptosis and inflammation, suggesting its potential as a therapeutic target in PD. In this study, we investigated the neuroprotective effects of the GPR40 agonist, TUG469 in PD models. Our results demonstrated that TUG469 reduces the neurotoxicity induced by 6-OHDA in SH-SY5Y cells. In 6-OHDA-induced PD model mice, TUG469 treatment improved motor impairment, preserved dopaminergic fibers and cell bodies in the striatum (ST) or SN, and attenuated 6-OHDA-induced microgliosis and astrogliosis in the brain. Furthermore, in a PD model involving the injection of mouse ɑ-syn fibrils into the brain (mPFFs-PD model), TUG469 treatment reduced the levels of pSer129 ɑ-syn, and decreased microgliosis and astrogliosis. Our investigation also revealed that TUG469 modulates inflammasome activation, apoptosis, and autophagy in the 6-OHDA-PD model, as evidenced by the results of RNA-seq and western blotting analyses. In summary, our findings highlight the neuroprotective effects of GPR40 agonists on dopaminergic neurons and their potential as therapeutic agents for PD. These results underscore the importance of targeting GPR40 in PD treatment, particularly in mitigating neuroinflammation and preserving neuronal integrity.

Does the Timed-Up-and-Go Test Predict Length of Stay After Total Hip Arthroplasty? A Retrospective Study.

Background: The prevalence of ambulatory total hip arthroplasty (THA) is rising, but it is not appropriate for all patients. Preoperative patient selection considers medical and social factors but overlooks patients' prior level of physical function. Purpose: The aim of this study was to evaluate if preoperative physical function, measured by the Timed-Up-and-Go (TUG) test, is associated with length of stay (LOS) in patients who underwent primary THA. Methods: A retrospective study was performed using 396 patients who underwent primary THA within a 2-month period at a single institution. Regression analysis evaluated the relationship between preoperative TUG scores and hospital LOS. Receiver-operating characteristic (ROC) curves were generated to identify a cutoff TUG score associated with LOS longer than 24 hours. Results: Univariate regression analysis of those discharged in less than 24 hours and those discharged in more than 24 hours found lower TUG scores (10.7 vs 13.7, respectively) were associated with patient discharge within 24 hours. Multivariate regression analysis showed a higher TUG score (adjusted odds ratio [aOR]: 0.91, 95% confidence interval [CI]: 0.84-0.99) was associated with decreased odds of discharge within 24 hours. Receiver-operating characteristic curve analysis was performed on the entire study cohort and the ambulatory surgery group and identified TUG scores of 10.3 and 10.5 seconds, respectively, associated with LOS of less than 24 hours (OR full cohort: 3.02, 95% CI: 1.94-4.71; OR ambulatory surgery: 2.97, 95% CI: 1.90-4.60). Sensitivity and specificity were not sufficient to support the use of these cutoff scores alone in predicting LOS. Conclusion: Although we were unable to establish a cutoff TUG score in patients who underwent primary THA that could determine LOS of more than 24 hours, the preoperative TUG score may be useful as a tool to aid in identifying patients who may require a longer hospital LOS. Further study is needed.

Exosomal lncRNA TUG1 derived from BMSC ameliorate collagen-induced arthritis via BLIMP1-mediated Th17/Treg balance.

BACKGROUND: Aberrant differentiation of Th17 cells has been identified as a critical factor in the development of rheumatoid arthritis (RA). BLIMP1 plays a key role in regulating plasma cell differentiation, T helper cell differentiation and Treg cell differentiation. Treatment with exosome injection or bone marrow mesenchymal stem cell (BMSC) transplantation reduce joint damage in RA. But the precise regulatory mechanisms remain unclear. METHODS: We injected BMSC-derived exosomes into RA mice, and then performed histological analysis on mouse ankle joints. We cultured CD4+ T cells in vitro, then added exosomes with or without si-TUG1 and induced the differentiation of Th17 cells and Treg cells, and then we used flow cytometry to detect the ratio of Th17 cells and Treg cells. Furthermore, we injected exosomes into sh-NC or sh-BLIMP1-treated RA mice, and then performed histological analysis on the ankle joints. RESULT: The results of our study demonstrate that exosome treatment decreased the proportion of differentiated Th17 cells, while increasing the proportion of Treg cells. And we observed that the Exo si-TUG1 group had an increased proportion of Th17 cells and a decreased proportion of Treg cells. We observed an increase in BLIMP1 expression in both the peripheral blood of mice and in CD4+ T cells cultured in vitro in the Exo group. Conversely, the Exo si-TUG1 group showed a decrease in BLIMP1 expression. Notably, inhibiting BLIMP1 expression led to the reversal of the therapeutic effects of exosomes. CONCLUSION: Our findings suggest that BMSC-derived exosomes promote the expression of BLIMP1 through Lnc TUG1-carrying exosomes, which may modulate the balance between Th17 cells and Treg cells. This mechanism ultimately alleviates damage caused by RA, suggesting that BMSC-derived exosomes enriched in Lnc TUG1 hold promise as a potential therapeutic approach for treating RA.

Role of long noncoding RNAs in the regulation of alternative splicing in glioblastoma.

Glioblastoma multiforme (GBM) is a highly severe primary brain tumor. Despite extensive research, effective treatments remain elusive. Long noncoding RNAs (lncRNAs) play a significant role in both cancer and normal biology. They influence alternative splicing (AS), which is crucial in cancer. Advances in lncRNA-specific microarrays and next-generation sequencing have enhanced understanding of AS. Abnormal AS contributes to cancer invasion, metastasis, apoptosis, therapeutic resistance, and tumor development, including glioma. lncRNA-mediated AS affects several cellular signaling pathways, promoting or suppressing cancer malignancy. This review discusses the lncRNAs regulating AS in glioblastoma and their mechanisms.

The role of LncRNA TUG1 in DNA damage and malignant transformation induced by Helicobacter pylori and N-methyl-N'-nitro-N-nitrosoguanidine on human esophageal epithelial cells.

N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG) and Helicobacter pylori might synergistically promote the malignant transformation of human esophageal epithelial cells (HEECs) through inducing DNA double-strand breaks (DSBs) and inhibition of PAXX protein expression. The long noncoding RNA (lncRNA) TUG1 is associated with multiple cancers, and its overexpression can promote cancer by interfering with the functions of oncogenes. LncRNA TUG1 is also associated with DNA methyltransferase 1 (DNMT1) and the epithelial signaling pathway of H. pylori infection. To explore the role of LncRNA TUG1 in the malignant transformation of HEECs induced by H.pylori + MNNG, a stable strain of HEECs with LncRNA TUG1 knockdown (LncRNA TUG1-KD) was constructed using RNA interference technology with lentivirus as a vector. Set up negative controls LncRNA TUG1-NC (null carrier lentivirus was selected to transfect HEECs) and block controls (normal HEECs without exposure). H. pylori + MNNG were added to the LncRNA TUG1-KD and LncRNA TUG1-NC groups for 6 h and then passaged until their malignant transformation. From each group, cells in the early, intermediate, and late stages of malignant transformation were used for the alkaline comet assay and determination of protein expression, including γ-H2AX and PAXX, by western blotting assay to assess DNA damage and repair processes. Clone formation assay in soft agar and nude mouse xenograft model was used to assess malignancy. This study suggests that H. pylori + MNNG promotes the malignant transformation of HEECs by inducing DNA DSBs and inhibiting PAXX expression, and this effect may be alleviated by LncRNA TUG1 knockdown. It elucidates the pathogenesis of EC from the perspective of the combined effect of epigenetic and environmental carcinogens, offering new insights for the comprehensive prevention and treatment of EC.

Androgen receptor deficiency-induced TUG1 in suppressing ferroptosis to promote benign prostatic hyperplasia through the miR-188-3p/GPX4 signal pathway.

Benign prostatic hyperplasia (BPH), characterized by the non-malignant enlargement of the prostate, exhibits a pronounced association with inflammation resulting from androgen receptor (AR) deficiency. Ferroptosis, a cell death mechanism triggered by iron-dependent lipid peroxidation and closely linked to inflammation, has yet to be fully understood in the context of BPH. Using RNA sequencing, we observed a significant elevation of taurine-upregulated gene 1 (TUG1) long noncoding RNA (lncRNA) in BPH tissues compared to normal prostate tissue. High levels of TUG1 exhibited a discernible correlation with both prostate volume and the extent of inflammatory infiltration in BPH patients. The suppression of TUG1 not only led to a reduction in prostate size but also ameliorated AR-deficiency-induced prostatic hyperplasia. Mechanistically, a decrease in AR in prostate luminal cells prompted macrophage aggregation and the release of IL-1ß, subsequently fostering the transcription of TUG1 via MYC. Induced TUG1, through competitive binding with miR-188-3p, facilitated the expression of GPX4, thereby diminishing intracellular ROS levels and impeding ferroptosis in prostate luminal cells. Notably, the ferroptosis inducer JKE-1674 alleviated inflammation-induced prostatic hyperplasia in vivo. Together, these findings suggest that AR deficiency crucially inhibits ferroptosis, promoting BPH via the TUG1/miR-188-3p/GPX4 signaling axis, and making ferroptosis induction a promising therapeutic strategy for BPH patients with AR deficiency.

Suppression of the lncRNA TUG1 alleviates neuropathic pain in rats with chronic contractile injury via the miR-29b-3p/HMGB1 axis.

INTRODUCTION: The present research focused on the function of lncRNA taurine upregulated 1 (TUG1) in a rat neuropathic pain (NP) model constructed by chronic contractile injury (CCI). MATERIAL AND METHODS: Construction of the NP rat model was performed by CCI surgery. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were applied to examine the NP behavior. RT-qPCR was established to explore the levels of TUG1, microRNA (miR)-29b-3p, and HMGB1. ELISA was carried out to evaluate the concentrations of interleukin (IL)-6, IL-1ß, tumor necrosis factor α (TNF-α), IL-4, and IL-6. The underlying mechanisms of TUG1 were explored by RNA-binding protein immunoprecipitation (RIP) and dual-luciferase reporter (DLR) assay. RESULTS: TUG1 and HMGB1 were statistically elevated in the tissue of CCI rats, while miR-29b-3p was reduced. TUG1 competitively binds to miR-29b-3p to upregulate HMGB1 levels. Suppression of TUG1 persistently decreased PWL and PWT along with increased frequency of paw-lifting, whereas this alleviation was typically rescued by the abrogated miR-29b-3p. Analogously, knockdown of TUG1 inhibited CCI-induced overproduction of IL-6, IL-1ß, and TNF-α, and reduction of IL-4 and IL-6, but this inhibition was partially abrogated by the reduction of miR-29b-3p. CONCLUSIONS: Suppression TUG1 can alleviate NP hypersensitivity and neuroinflammation in CCI rats by competitively binding miR-29b-3p to weaken HMGB1.

UMATUG: A dataset of inertial signals of older and young adults using a gerontologic simulator collected during instrumented Timed Up and Go (iTUG) tests.

Timed Up and Go (TUG) test is one of the most popular clinical tools aimed at the assessment of functional mobility and fall risk in older adults. The automation of the analysis of TUG movements is of great medical interest not only to speed up the test but also to maximize the information inferred from the subjects under study. In this context, this article describes a dataset collected from a cohort of 69 experimental subjects (including 30 adults over 60 years), during the execution of several repetitions of the TUG test. In particular, the dataset includes the measurements gathered with four wearables devices embedding four sensors (accelerometer, gyroscope magnetometer and barometer) located on four body locations (waist, wrist, ankle and chest). As a particularity, the dataset also includes the same measurements recorded when the young subjects repeat the test while wearing a commercial geriatric simulator, consisting of a set of weighted vests and other elements intended to replicate the limitations caused by aging. Thus, the generated dataset also enables the investigation into the potential of such tools to emulate the actual dynamics of older individuals.

Gait analysis and geriatric syndromes: An association among elderly patients attending a teaching hospital of Delhi.

Background: Gait abnormalities are prevalent, affecting a substantial portion of the elderly population, and leading to mobility limitations, reduced quality of life, falls, hospitalizations, and premature death. Objectives: The study aims to assess gait patterns among individuals aged 75 years and above attending the geriatric OPD of a tertiary care hospital in New Delhi and evaluate their association with various geriatric syndromes. Materials and Methods: This cross-sectional study, conducted at a tertiary care hospital in Delhi, from May 2019 to November 2021, involved 100 participants aged 75 and above. It encompassed a thorough assessment protocol covering demographics, health history, clinical and functional evaluations, depression, cognition, balance, frailty, urinary incontinence, polypharmacy, nutrition, comorbidities, and gait analysis. Results: In this study of elderly individuals, the mean age was 78.56 years, and the mean BMI was 23.11. The participants had an average of 1.74 comorbidities, with hypertension being the most prevalent (62%), followed by diabetes (25%), chronic obstructive airway disease (COAD) (11%), and coronary artery disease (15%). Geriatric assessments revealed varying proportions of frailty (34%), polypharmacy (40%), and urinary incontinence (9%). The mean scores for activities of daily living, instrumental activities of daily living, nutritional status, cognitive function, Timed Up and Go Test, and depression scale were also reported. Various gait parameters demonstrated significant correlations with these geriatric factors, including frailty, comorbidities, BMI, and mobility scores. Conclusion: The study identified significant associations between gait patterns and various geriatric syndromes, emphasizing the importance of gait analysis in assessing the health and mobility of elderly individuals.

The role of EZH2 and its regulatory lncRNAs as a serum-based biomarker in Alzheimer's disease.

BACKGROUND: Long noncoding RNAs (lncRNAs) have become a hot topic in the human nervous system. Moreover, circulating lncRNAs have been suggested as possible biomarkers for central nervous system processes and neurodegenerative diseases. The present research aimed to highlight the role of plasma lncRNAs TUG1, FEZF1-AS1, and EZH2 gene as diagnostic biomarkers in Alzheimer's disease (AD). METHODS: Plasma samples for the study were provided by 100 AD patients and 100 matched controls. Real-time quantitative reverse transcriptase PCR was used to determine the plasma level of the aforementioned lncRNAs. Furthermore, the plasma level of EZH2 protein in the participants' blood was determined using the ELISA technique. RESULTS: In contrast to controls, down-regulation of the EZH2 gene and protein was reported in the plasma of patients with AD. Additionally, plasma samples from AD patients showed up-and-down-regulation of the lncRNAs TUG1 and FEZF1-AS1, respectively. CONCLUSION: Our new findings suggest that the EZH2 gene, plasma lncRNA TUG1, and FEZF1-AS1 may contribute, as valuable biomarkers, to AD diagnosis.

Distinct binding hotspots for natural and synthetic agonists of FFA4 from in silico approaches.

FFA4 has gained interest in recent years since its deorphanization in 2005 and the characterization of the Free Fatty Acids receptors family for their therapeutic potential in metabolic disorders. The expression of FFA4 (also known as GPR120) in numerous organs throughout the human body makes this receptor a highly potent target, particularly in fat sensing and diet preference. This offers an attractive approach to tackle obesity and related metabolic diseases. Recent cryo-EM structures of the receptor have provided valuable information for a potential active state although the previous studies of FFA4 presented diverging information. We performed molecular docking and molecular dynamics simulations of four agonist ligands, TUG-891, Linoleic acid, α-Linolenic acid, and Oleic acid, based on a homology model. Our simulations, which accumulated a total of 2 µs of simulation, highlighted two binding hotspots at Arg992.64 and Lys293 (ECL3). The results indicate that the residues are located in separate areas of the binding pocket and interact with various types of ligands, implying different potential active states of FFA4 and a highly adaptable binding intra-receptor pocket. This article proposes additional structural characteristics and mechanisms for agonist binding that complement the experimental structures.