Intelligent Thermochromic Heating E-Textile for Personalized Temperature Control in Healthcare.

Heating electronic textiles (e-textiles) are widely used for thermal comfort and energy conservation, but prolonged heating raises concerns about heat-related illnesses, especially in the elderly. Despite advancements, achieving universal user satisfaction remains difficult due to diverse thermal needs. This paper introduces an intelligent thermochromic heating e-textile with an artificial intelligence (AI)-based temperature control system for optimized personal comfort and color indicators for elderly caregivers.

The burden of psychiatric morbidity in Multiple Sclerosis, AQP4-antibody NMOSD and MOGAD before and after neurological diagnosis.

Background: Psychiatric comorbidities are common in Multiple Sclerosis (MS) and are increasingly recognised in Aquaporin-4-Antibody Neuromyelitis Optica Spectrum Disorders (AQP4-Ab NMOSD) and Myelin Oligodendrocyte Glycoprotein-Antibody Associated Disease (MOGAD). However, it is unclear if these psychiatric comorbidities predate neurological diagnosis or classical neurological symptoms that are conventionally used to establish the onset of these central nervous system inflammatory demyelinating diseases. We sought to: (1) assess the frequency and incidence of psychiatrist-diagnosed psychiatric disorders before and after formal MS, AQP4-Ab NMOSD, and MOGAD diagnosis, and (2) identify potential factors associated with the presence of pre-existing psychiatric morbidity and depression severity at the first clinical visit for MS patients.

A comparison of multiple sclerosis disease characteristics across three genetically diverse Asian racial groups in Singapore.

Studies in Western populations have shown that Black and Hispanic patients have an earlier age of Multiple Sclerosis (MS) onset and a more severe disease course characterised by faster disability accrual compared to Whites. It is yet unclear whether MS disease characteristics and clinical course differ amongst Asian racial groups. Singapore is uniquely poised to investigate this as its multi-racial population comprises three genetically diverse Asian racial groups-Chinese, Malay and South Asian.

Longitudinally extensive transverse myelopathy in spinal cord infarction.

Spinal cord infarction may present as longitudinally extensive myelopathy, similar to inflammatory myelitis such as neuromyelitis optica. Magnetic resonance imaging features such as diffusion-weighted imaging/apparent diffusion coefficient showing restricted diffusion and lack of contrast enhancement are helpful in the diagnosis of spinal cord infarction and differentiating them from inflammatory myelitis.

Dexamethasone suppression test versus selective ovarian and adrenal vein catheterization in identifying virilizing tumors in postmenopausal hyperandrogenism - a systematic review and meta-analysis.

Objective: The diagnostic accuracy of tests in identifying virilizing tumors in postmenopausal hyperandrogenism is limited. This systematic review compares the dexamethasone suppression test against selective ovarian and adrenal vein sampling of androgens in distinguishing neoplastic from non-neoplastic causes of postmenopausal hyperandrogenism.

Methods: Diagnostic test accuracy studies on these index tests in postmenopausal women were selected based on pre-established criteria.

Gonadotropin-Releasing Hormone Analogue Stimulation Test Versus Venous Sampling in Postmenopausal Hyperandrogenism.

Postmenopausal hyperandrogenism can be due to excessive androgen secretion from adrenal or ovarian virilizing tumors or nonneoplastic conditions. The etiology of postmenopausal hyperandrogenism can be difficult to discern because of limited accuracy of current diagnostic tests. This systematic review compares the diagnostic accuracy of the gonadotropin-releasing hormone (GnRH) analogue stimulation test against selective ovarian and adrenal vein sampling of androgens in distinguishing neoplastic from nonneoplastic causes of postmenopausal hyperandrogenism.

Phenotypic bases of NOTCH2NLC GGC expansion positive neuronal intranuclear inclusion disease in a Southeast Asian cohort.

Neuronal intranuclear inclusion disease (NIID) is a neurodegenerative disorder associated with GGC repeats of >60 to 500 copies in the 5'-untranslated region of NOTCH2NLC. The clinical and genetic characterization of NIID outside of East Asia remains unknown. We identified twelve patients who underwent genetic testing using long-read sequencing or repeat primed polymerase chain reaction.

Distinctive binding properties of human monoclonal LGI1 autoantibodies determine pathogenic mechanisms.

Autoantibodies against leucine-rich glioma inactivated 1 (LGI1) are found in patients with limbic encephalitis and focal seizures. Here, we generate patient-derived monoclonal antibodies (mAbs) against LGI1. We explore their sequences and binding characteristics, plus their pathogenic potential using transfected HEK293T cells, rodent neuronal preparations, and behavioural and electrophysiological assessments in vivo after mAb injections into the rodent hippocampus.

Identifying patients with neuronal intranuclear inclusion disease in Singapore using characteristic diffusion-weighted MR images.

Purpose: Adult-onset neuronal intranuclear inclusion disease (NIID) is a rare neurodegenerative disorder described mainly in the Japanese population, with characteristic DWI abnormalities at the junction between gray and white matter. We identify possible cases of NIID in the picture archive and communication system (PACS) of a tertiary neurological referral hospital in Singapore and describe their radiological features.

Methods: The neuroradiology imaging database was reviewed using keyword search of radiological reports to identify patients who had "subcortical U fibre" abnormalities on DWI.

A retrospective review of a tertiary Hospital's isolation and de-isolation policy for suspected pulmonary tuberculosis.

Background: Effective protocols for the isolation and de-isolation of patients with suspected pulmonary tuberculosis (PTB) are essential determinants of health-care costs. Early de-isolation needs to be balanced with the need to prevent nosocomial transmission of PTB. The aim of our study was to evaluate the efficiency of our hospital's current protocol for isolating and de-isolating patients with suspected PTB, in particular assessing the timeliness to de-isolation of patients with AFB smear negative respiratory samples.

Proteasome inhibition promotes Parkin-Ubc13 interaction and lysine 63-linked ubiquitination.

Disruption of the ubiquitin-proteasome system, which normally identifies and degrades unwanted intracellular proteins, is thought to underlie neurodegeneration. Supporting this, mutations of Parkin, a ubiquitin ligase, are associated with autosomal recessive parkinsonism. Remarkably, Parkin can protect neurons against a wide spectrum of stress, including those that promote proteasome dysfunction.

Parkin pathway activation mitigates glioma cell proliferation and predicts patient survival.

Mutations in the parkin gene, which encodes a ubiquitin ligase, are a major genetic cause of parkinsonism. Interestingly, parkin also plays a role in cancer as a putative tumor suppressor, and the gene is frequently targeted by deletion and inactivation in human malignant tumors. Here, we investigated a potential tumor suppressor role for parkin in gliomas.

Parkin enhances the expression of cyclin-dependent kinase 6 and negatively regulates the proliferation of breast cancer cells.

Although mutations in the parkin gene are frequently associated with familial Parkinsonism, emerging evidence suggests that parkin also plays a role in cancers as a putative tumor suppressor. Supporting this, we show here that parkin expression is dramatically reduced in several breast cancer-derived cell lines as well as in primary breast cancer tissues. Importantly, we found that ectopic parkin expression in parkin-deficient breast cancer cells mitigates their proliferation rate both in vitro and in vivo, as well as reduces the capacity of these cells to migrate.

Protein misfolding and aggregation in Parkinson's disease.

Protein aggregation as a result of misfolding is a common theme underlying neurodegenerative diseases. In Parkinson's disease (PD), research on protein misfolding and aggregation has taken center stage following the association of alpha-synuclein gene mutations with familial forms of the disease, and importantly, the identification of the protein as a major component of Lewy bodies, a pathological hallmark of PD. Fueling this excitement is the subsequent identification of another PD-linked gene, parkin, as a ubiquitin ligase associated with the proteasome, a major intracellular protein degradation machinery that destroys unwanted, albeit mainly soluble, proteins.

Autophagy-mediated clearance of aggresomes is not a universal phenomenon.

Aggresomes are juxtanuclear inclusion bodies that have been proposed to act as staging grounds for the disposal of protein aggregates via the autophagic route. To examine whether the composition of an aggresome influences its clearance by autophagy, we ectopically expressed a variety of aggregation-prone proteins in cultured cells to generate aggresomes that differ in their protein content. We found that whereas aggresomes generated in cells expressing mutant huntingtin or mutant tau, or co-expressing synphilin-1 and alpha-synuclein, are amenable to clearance by autophagy, those produced in AIMP2 (p38)- or mutant desmin-expressing cells are apparently resistant to autophagic clearance.

Role of the ubiquitin proteasome system in Parkinson's disease.

Parkinson's disease (PD) is the most common neurodegenerative movement disorder. Although a subject of intense research, the etiology of PD remains poorly understood. Recently, several lines of evidence have implicated an intimate link between aberrations in the ubiquitin proteasome system (UPS) and PD pathogenesis.

Lysine 63-linked ubiquitination promotes the formation and autophagic clearance of protein inclusions associated with neurodegenerative diseases.

Although ubiquitin-enriched protein inclusions represent an almost invariant feature of neurodegenerative diseases, the mechanism underlying their biogenesis remains unclear. In particular, whether the topology of ubiquitin linkages influences the dynamics of inclusions is not well explored. Here, we report that lysine 48 (K48)- and lysine 63 (K63)-linked polyubiquitination, as well as monoubiquitin modification contribute to the biogenesis of inclusions.

Relative sensitivity of parkin and other cysteine-containing enzymes to stress-induced solubility alterations.

Loss of parkin function is a predominant cause of familial Parkinsonism. Emerging evidence also suggests that parkin expression variability may confer a risk for sporadic Parkinson disease. We have recently demonstrated that a wide variety of Parkinson disease-linked stressors, including dopamine (DA), induce parkin solubility alterations and promote its aggregation within the cell, a phenomenon that may underlie the progressive susceptibility of the brain to degeneration.

Cellular expression, localization and interactions of the product of the human MOST-1 gene associated with breast and prostate cancers.

We previously isolated and characterized the novel human gene MOST-1 (C8orf17) that is ubiquitously expressed in all cancer cell lines tested but differentially expressed in normal adult tissues. MOST-1 maps to chromosome region 8q24.2 whose amplification is frequently associated with breast and prostate cancers.

Parkin blushed by PINK1.

Mutations in the PTEN-induced putative kinase 1 (PINK1) are a common cause of autosomal recessive Parkinson's disease. In a recent issue of Nature, two independent reports by and show that loss of Drosophila PINK1 leads to defects in mitochondrial function resulting in male sterility, apoptotic muscle degeneration, and minor loss of dopamine neurons that is rescued by overexpression of the ubiquitin E3 ligase, parkin. Thus, PINK1 and parkin appear to function in a common pathway suggesting a convergence of the two genes most commonly associated with autosomal recessive PD.

Alterations in the solubility and intracellular localization of parkin by several familial Parkinson's disease-linked point mutations.

Mutations in the parkin gene, which encodes a ubiquitin ligase, are currently recognized as the main contributor to familial forms of Parkinson's disease (PD). A simple assumption about the effects of PD-linked mutations in parkin is that they impair or ablate the enzyme activity. However, a number of recent studies, including ours, have indicated that many disease-linked point mutants of parkin retain substantial catalytic activity.

Parkin mediates nonclassical, proteasomal-independent ubiquitination of synphilin-1: implications for Lewy body formation.

It is widely accepted that the familial Parkinson's disease (PD)-linked gene product, parkin, functions as a ubiquitin ligase involved in protein turnover via the ubiquitin-proteasome system. Substrates ubiquitinated by parkin are hence thought to be destined for proteasomal degradation. Because we demonstrated previously that parkin interacts with and ubiquitinates synphilin-1, we initially expected synphilin-1 degradation to be enhanced in the presence of parkin.

The 350-fold compacted Fugu parkin gene is structurally and functionally similar to human Parkin.

Mutations in the human parkin gene (huParkin) are the predominant genetic cause of familial parkinsonism. The huParkin locus, spanning about 1.4 Mb, is one of the largest in the human genome.