Sliding and pressure evaluation on conventional and V-shaped seats of reclining wheelchairs for stroke patients with flaccid hemiplegia: a crossover trial

<p>Abstract</p> <p>Background</p> <p>Reclining wheelchairs are commonly used to transport elderly stroke patients in Taiwan. However, there is concern that the patient's body in the wheelchair often slides forward when they return to a seated position, increasing the sitting pressure. Therefore, a novel reclining wheelchair with an ergonomic "V-Seat" was designed to prevent forward sliding and pressure sores. The use of these reclining chairs by stroke patients has not yet been studied. Thus, we investigated the effects of V-shaped and conventional seats in reclining wheelchairs on the extent of forward sliding and on the sitting pressure of stroke patients with flaccid hemiplegia and of able-bodied elders.</p> <p>Methods</p> <p>We recruited 13 able-bodied elders and 11 stroke patients with flaccid hemiplegia and performed 5 reclining cycles in both types of wheelchair. The amount of sliding along the backrest (BS) plane and the seat (SS) plane, the mean sitting pressure (MP), and the sacral peak pressure (SPP) of the subjects were recorded. We used the Wilcoxon signed-rank test to compare the BS, SS, MP, and SPP in wheelchairs with conventional and V-shaped seats, and we used the Wilcoxon rank sum test to compare the differences in BS and SS between stroke patients and able-bodied elders in both types of reclining wheelchair.</p> <p>Results</p> <p>The BS, SS, and SPP of stroke patients were significantly lower in the wheelchairs with V-shaped seats than in conventional wheelchairs in most comparisons; however, the BS of able-bodied elders was higher in V-shaped seats than in conventional seats. The SS and SPP of stroke patients were significantly higher than those of able-bodied elders in both types of reclining wheelchair, and the BS of stroke patients was significantly higher than that of able-bodied elders only in conventional reclining wheelchairs.</p> <p>Conclusions</p> <p>The use of V-shaped seats in reclining wheelchairs can help reduce the forward sliding and sacral peak pressure of stroke patients with flaccid hemiplegia. The back displacement of able-bodied subjects when using both conventional and V-shape seats in reclining positions differs from the back displacement of stroke patients with flaccid hemiplegia when using such seats. These results are of paramount value and should be considered when prescribing the use of reclining wheelchairs to subjects with flaccid hemiplegia.</p

First-principles method of propagation of tightly bound excitons: exciton band structure of LiF and verification with inelastic x-ray scattering

We propose a simple first-principles method to describe propagation of tightly bound excitons. By viewing the exciton as a composite object (an effective Frenkel exciton in Wannier orbitals), we define an exciton kinetic kernel to encapsulate the exciton propagation and decay for all binding energy. Applied to prototypical LiF, our approach produces three exciton bands, which we verified quantitatively via inelastic x-ray scattering. The proposed real-space picture is computationally inexpensive and thus enables study of the full exciton dynamics, even in the presence of surfaces and impurity scattering. It also provides intuitive understanding to facilitate practical exciton engineering in semiconductors, strongly correlated oxides, and their nanostructures.Comment: 5 pages, 4 figures. Accepted by PR

PreFallKD: Pre-Impact Fall Detection via CNN-ViT Knowledge Distillation

Fall accidents are critical issues in an aging and aged society. Recently, many researchers developed pre-impact fall detection systems using deep learning to support wearable-based fall protection systems for preventing severe injuries. However, most works only employed simple neural network models instead of complex models considering the usability in resource-constrained mobile devices and strict latency requirements. In this work, we propose a novel pre-impact fall detection via CNN-ViT knowledge distillation, namely PreFallKD, to strike a balance between detection performance and computational complexity. The proposed PreFallKD transfers the detection knowledge from the pre-trained teacher model (vision transformer) to the student model (lightweight convolutional neural networks). Additionally, we apply data augmentation techniques to tackle issues of data imbalance. We conduct the experiment on the KFall public dataset and compare PreFallKD with other state-of-the-art models. The experiment results show that PreFallKD could boost the student model during the testing phase and achieves reliable F1-score (92.66%) and lead time (551.3 ms)

Effects of epidural compression on stellate neurons and thalamocortical afferent fibers in the rat primary somatosensory cortex

A number of neurological disorders such as epidural hematoma can cause compression of cerebral cortex. We here tested the hypothesis that sustained compression of primary somatosensory cortex may affect stellate neurons and thalamocortical afferent (TCA) fibers. A rat model with barrel cortex subjected to bead epidural compression was used. Golgi‑Cox staining analyses showed the shrinkage of dendritic arbors and the stripping of dendritic spines of stellate neurons for at least 3 months post‑lesion. Anterograde tracing analyses exhibited a progressive decline of TCA fiber density in barrel field for 6 months post‑lesion. Due to the abrupt decrease of TCA fiber density at 3 days after compression, we further used electron microscopy to investigate the ultrastructure of TCA fibers at this time. Some TCA fiber terminal profiles with dissolved or darkened mitochondria and fewer synaptic vesicles were distorted and broken. Furthermore, the disruption of mitochondria and myelin sheath was observed in some myelinated TCA fibers. In addition, expressions of oxidative markers 3‑nitrotyrosine and 4‑hydroxynonenal were elevated in barrel field post‑lesion. Treatment of antioxidant ascorbic acid or apocynin was able to reverse the increase of oxidative stress and the decline of TCA fiber density, rather than the shrinkage of dendrites and the stripping of dendritic spines of stellate neurons post‑lesion. Together, these results indicate that sustained epidural compression of primary somatosensory cortex affects the TCA fibers and the dendrites of stellate neurons for a prolonged period. In addition, oxidative stress is responsible for the reduction of TCA fiber density in barrels rather than the shrinkage of dendrites and the stripping of dendritic spines of stellate neurons

Measurement of Organic Chemical Refractive Indexes Using an Optical Time-Domain Reflectometer

In this investigation, we propose and experimentally demonstrate a method for measuring the refractive index (RI) of liquid organic chemicals. The scheme is based on a single-mode fiber (SMF) sensor and an optical time-domain reflectometer (OTDR). Here, due to the different reflectance (R) between the SMF and organic liquid chemicals, the reflected power level of the backscattering light (BSL) measured by the OTDR would be different. Therefore, we can measure the RI of chemical under test via the measured BSL level. The proposed RI sensor is simple and easy to manipulate, with stable detected signals, and has the potential to be a valuable tool for use in biological and chemical applications

AMP-Activated Protein Kinase Activation during Cardioplegia-Induced Hypoxia/Reoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress

Cardioplegic-induced H/R injury results in cardiomyocytic apoptosis. AMPK has been shown to reduce ER stress and the unfolded protein response (UPR). Whether AMPK activation can attenuate cardiomyocytic apoptosis after cardioplegia-induced H/R injury is unknown. Cardiomyocytes were exposed to simulated ischemia by incubation in a hypoxic chamber with intermittent cold cardioplegia solution infusion at 20-minute intervals and subsequently reoxygenated in a normoxic environment. Various doses of AMPK activators (AICAR or metformin) were given 2 days before H/R injury. The cardiomyocytes were harvested after reoxygenation for subsequent examination. With both AMPK activators, the antiapoptotic genes of ER stress and UPR, the subsequent production of proapoptotic proteins was attenuated, and the antiapoptotic proteins were elevated. The activity of the apoptotic effectors of ER stress was also reduced with AMPK activation. Moreover, TUNEL staining showed that AMPK activation significantly reduced the percentage of apoptotic cardiomyocytes after cardioplegia-induced H/R injury. Our results revealed that AMPK activation during cardioplegia-induced H/R injury attenuates cardiomyocytic apoptosis, via enhancement of antiapoptotic and reduction of proapoptotic responses, resulting from lessening ER stress and the UPR. AMPK activation may serve as a future pharmacological target to reduce H/R injury in the clinical setting

An Improvement of the Triangular Inequality Elimination Algorithm for Vector Quantization

Abstract: This study proposes an improvement of the triangular inequality elimination (TIE) algorithm for vector quantization (VQ). More than 26% additional computation saving is achieved. The proposed approach uses dynamic and intersection (DI) rules to recursively compensate and enhance the TIE algorithm. The dynamic rule changes the reference codeword dynamically and reaches the smallest candidate group. The intersection rule removes redundant codewords from these candidate groups. The DI-TIE approach avoids the over-reliance on continuity of input signal. The VQ-based line spectral pair (LSP) quantization in ITU-T G.729 standard and some standard test images are used to test the contribution of the DI-TIE. Experimental results confirm that the DI rules in the TIE algorithm have an excellent performance. Moreover, in comparison with the quasi-binary search (QBS) approach, both the QBS and the DI-TIE methods are independent on the continuity of input signal. Nevertheless, the DI-TIE approach proposed in the paper is superior to the QBS method in the computation saving issue

HPV infection and p53 inactivation in pterygium

PurposeOur recent report indicated that tumor suppressor gene (p53) mutations and protein aberrant expression were detected in pterygium. Inactivation of p53 by Human papillomavirus (HPV) 16/18 E6 plays a crucial role in cervical tumorigenesis. In this study, we further speculate that p53 inactivation may be linked with HPV infection in pterygium pathogenesis. To investigate the involvement of HPV 16/18 E6 in p53 inactivation in pterygium, the association between HPV 16 or HPV 18 infection, the HPV E6 oncoprotein, and p53 protein expression was analyzed in this study.MethodsHPV 16/18 infection was detected by nested-polymerase chain reaction (nested-PCR), the p53 mutation was detected by direct sequencing, and the p53 and the HPV 16/18 E6 proteins were studied using immunohistochemistry on 129 pterygial specimens and 20 normal conjunctivas.ResultsThe HPV 16/18 was detected in 24% of the pterygium tissues (31 of 129) but not in the normal conjunctiva, and the HPV16/18 E6 oncoprotein was detected in 48.3% of HPV 16/18 DNA-positive pterygium tissues (15 of 31). In addition, p53 protein negative expression in pterygium was correlated with HPV16/18 E6 oncoprotein expression but not with a p53 mutation.ConclusionsHPV 16/18 E6 contributes to HPV-mediated pterygium pathogenesis as it is partly involved in p53 inactivation and is expressed in HPV DNA-positive pterygium

The nucleolar protein NIFK promotes cancer progression via CK1α/β-catenin in metastasis and Ki-67-dependent cell proliferation.

Nucleolar protein interacting with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein. However, its precise function in cancer remains largely uninvestigated. Here we show the clinical significance and metastatic mechanism of NIFK in lung cancer. NIFK expression is clinically associated with poor prognosis and metastasis. Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, invasion in vitro and metastasis in vivo via downregulation of casein kinase 1α (CK1α), a suppressor of pro-metastatic TCF4/β-catenin signaling. Inversely, CK1α is upregulated upon NIFK knockdown. The silencing of CK1α expression in NIFK-silenced cells restores TCF4/β-catenin transcriptional activity, cell migration, and metastasis. Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1 (CK1α) that is negatively regulated by NIFK. Our results demonstrate the prognostic value of NIFK, and suggest that NIFK is required for lung cancer progression via the RUNX1-dependent CK1α repression, which activates TCF4/β-catenin signaling in metastasis and the Ki-67-dependent regulation in cell proliferation