Relationships between trunk muscle activation and thoraco-lumbar kinematics in non-specific chronic low back pain subgroups during a forward bending task.

Background: Trunk muscle activity and thoraco-lumbar kinematics can discriminate between non-specific chronic low back pain (NSCLBP) subgroups and healthy controls. However, research commonly focuses on lumbar kinematics, with limited understanding of relationships between kinematics and muscle activity across clinical subgroups. Similarly, the thoracic spine, whilst intuitively associated with NSCLBP, has received less attention and potential relationships between spinal regions and muscle activity requires exploration.

Increased phosphorylation of HexM improves lysosomal uptake and potential for managing GM2 gangliosidoses.

Tay-Sachs and Sandhoff diseases are genetic disorders resulting from mutations in or , which code for the α- and β-subunits of the heterodimer β-hexosaminidase A (HexA), respectively. Loss of HexA activity results in the accumulation of GM2 ganglioside (GM2) in neuronal lysosomes, culminating in neurodegeneration and death, often by age 4. Previously, we combined critical features of the α- and β-subunits of HexA into a single subunit to create a homodimeric enzyme known as HexM.

Effect of Lung Volume Recruitment on Pulmonary Function in Progressive Childhood-Onset Neuromuscular Disease: A Systematic Review.

Objectives: The focus of this systematic review was to consider whether lung volume recruitment (LVR) has an effect on pulmonary function test parameters in individuals with progressive childhood-onset neuromuscular diseases. The review was registered on PROSPERO (No. CRD42019119541).

Comparison of intra subject repeatability of quantitative fluoroscopy and static radiography in the measurement of lumbar intervertebral flexion translation.

Low back pain patients are sometimes offered fusion surgery if intervertebral translation, measured from static, end of range radiographs exceeds 3 mm. However, it is essential to know the measurement error of such methods, if selection for back surgery is going to be informed by them. Fifty-five healthy male (34) and female (21) pain free participants aged 21-80 years received quantitative fluoroscopic (QF) imaging both actively during standing and passively in the lateral decubitus position.

Investigating differences in trunk muscle activity in non-specific chronic low back pain subgroups and no-low back pain controls during functional tasks: a case-control study.

Background: Trunk muscle dysfunction is often regarded as a key feature of non-specific chronic low back pain (NSCLBP) despite being poorly understood and variable with increases, decreases and no change in muscle activity reported. Differences in thoraco-lumbar kinematics have been observed in motor control impairment NSCLBP subgroups (Flexion Pattern, Active Extension Pattern) during static postures and dynamic activities. However, potential differences in muscle activity during functional tasks has not been established in these subgroups to date.

Comparison of gait, functional activities, and patient-reported outcome measures in patients with knee osteoarthritis and healthy adults using 3D motion analysis and activity monitoring: an exploratory case-control analysis.

Objective: To examine functional performance differences using kinematic and kinetic analysis between participants with and without knee osteoarthritis (OA) to determine which outcomes best characterize persons with and without knee OA.

Methods: Participants with unilateral moderate knee OA (Kellgren-Lawrence grades 2 or 3) and controls without knee pain were matched for age, gender, and body mass index. Primary outcomes included temporal parameters, joint rotations and moments, and ground reaction forces assessed via 3D motion capture during walking and ascending/descending stairs.

Intrasubject repeatability of in vivo intervertebral motion parameters using quantitative fluoroscopy.

Purpose: In vivo quantification of intervertebral motion through imaging has progressed to a point where biomarkers for low back pain are emerging. This makes possible deeper study of the condition's biometrics. However, the measurement of change over time involves error.

Synthesis and Activity of a Novel Autotaxin Inhibitor-Icodextrin Conjugate.

Autotaxin is an extracellular phospholipase D that catalyzes the hydrolysis of lysophosphatidyl choline (LPC) to generate the bioactive lipid lysophosphatidic acid (LPA). Autotaxin has been implicated in many pathological processes relevant to cancer. Intraperitoneal administration of an autotaxin inhibitor may benefit patients with ovarian cancer; however, low molecular mass compounds are known to be rapidly cleared from the peritoneal cavity.

Can different seating aids influence a sitting posture in healthy individuals and does gender matter?

This study determined differences in spinal-pelvic kinematics sitting on (i) mat (ii) block and (iii) novel 10º forward inclined wedge (Buttafly) in a same-subject repeated measures cross-over design in 60 healthy individuals (34 females). Repeated measures ANOVA revealed statistically significant differences between sitting conditions and lumbar and pelvic sagittal angles. Both, the inclined wedge and the block seating aids reduced overall flexion, but the inclined wedge had a greater influence in the lumbar region whilst the block induced the greatest change in the pelvis.

Non-specific chronic low back pain: differences in spinal kinematics in subgroups during functional tasks.

Purpose: A multidimensional classification approach suggests that motor control impairment subgroups exist in non-specific chronic low back pain (NSCLBP). Differences in sitting lumbar posture have been identified between two such subgroups [flexion pattern (FP) and active extension pattern (AEP)] and healthy individuals; however, functional spinal movement has not been explored. This study will evaluate whether NSCLBP subgroups exhibit regional spinal kinematic differences, compared to healthy individuals, during functional tasks.

Hyaluronidase 2 Deficiency Causes Increased Mesenchymal Cells, Congenital Heart Defects, and Heart Failure.

Background: Hyaluronan (HA) is required for endothelial-to-mesenchymal transition and normal heart development in the mouse. Heart abnormalities in hyaluronidase 2 (HYAL2)-deficient ( ) mice and humans suggested removal of HA is also important for normal heart development. We have performed longitudinal studies of heart structure and function in mice to determine when, and how, HYAL2 deficiency leads to these abnormalities.

Hyaluronidase 2 (HYAL2) is expressed in endothelial cells, as well as some specialized epithelial cells, and is required for normal hyaluronan catabolism.

Hyaluronidase 2 (HYAL2) is a membrane-anchored protein that is proposed to initiate the degradation of hyaluronan (HA) in the extracellular matrix. The distribution of HYAL2 in tissues, and of HA in tissues lacking HYAL2, is largely unexplored despite the importance of HA metabolism in several disease processes. Herein, we use immunoblot and histochemical analyses to detect HYAL2 and HA in mouse tissues, as well as agarose gel electrophoresis to examine the size of HA.

Growth arrest in the ribosomopathy, Bowen-Conradi syndrome, is due to dramatically reduced cell proliferation and a defect in mitotic progression.

Bowen-Conradi syndrome (BCS) is a ribosomopathy characterized by severe developmental delay and growth failure that typically leads to death by one year of age. It is caused by a c.257A>G, p.

Long-term correction of Sandhoff disease following intravenous delivery of rAAV9 to mouse neonates.

G(M2) gangliosidoses are severe neurodegenerative disorders resulting from a deficiency in β-hexosaminidase A activity and lacking effective therapies. Using a Sandhoff disease (SD) mouse model (Hexb(-/-)) of the G(M2) gangliosidoses, we tested the potential of systemically delivered adeno-associated virus 9 (AAV9) expressing Hexb cDNA to correct the neurological phenotype. Neonatal or adult SD and normal mice were intravenously injected with AAV9-HexB or -LacZ and monitored for serum β-hexosaminidase activity, motor function, and survival.

Mutation of EMG1 causing Bowen-Conradi syndrome results in reduced cell proliferation rates concomitant with G2/M arrest and 18S rRNA processing delay.

Bowen-Conradi syndrome (BCS) is a lethal autosomal recessive disorder caused by a D86G substitution in the protein, Essential for Mitotic Growth 1 (EMG1). EMG1 is essential for 18S rRNA maturation and 40S ribosome biogenesis in yeast, but no studies of its role in ribosome biogenesis have been done in mammals. To assess the effect of the EMG1 mutation on cell growth and ribosomal biogenesis in humans, we employed BCS patient cells.

Garden and landscape-scale correlates of moths of differing conservation status: significant effects of urbanization and habitat diversity.

Moths are abundant and ubiquitous in vegetated terrestrial environments and are pollinators, important herbivores of wild plants, and food for birds, bats and rodents. In recent years, many once abundant and widespread species have shown sharp declines that have been cited by some as indicative of a widespread insect biodiversity crisis. Likely causes of these declines include agricultural intensification, light pollution, climate change, and urbanization; however, the real underlying cause(s) is still open to conjecture.

Murine hyaluronidase 2 deficiency results in extracellular hyaluronan accumulation and severe cardiopulmonary dysfunction.

Hyaluronidase (HYAL) 2 is a membrane-anchored protein that is proposed to hydrolyze hyaluronan (HA) to smaller fragments that are internalized for breakdown. Initial studies of a Hyal2 knock-out (KO) mouse revealed a mild phenotype with high serum HA, supporting a role for HYAL2 in HA breakdown. We now describe a severe cardiac phenotype, deemed acute, in 54% of Hyal2 KO mice on an outbred background; Hyal2 KO mice without the severe cardiac phenotype were designated non-acute.

Hyaluronidase 1 and β-hexosaminidase have redundant functions in hyaluronan and chondroitin sulfate degradation.

Hyaluronan (HA), a member of the glycosaminoglycan (GAG) family, is a critical component of the extracellular matrix. A model for HA degradation that invokes the activity of both hyaluronidases and exoglycosidases has been advanced. However, no in vivo studies have been done to determine the extent to which these enzymes contribute to HA breakdown.

The C. elegans hyaluronidase: a developmentally significant enzyme with chondroitin-degrading activity at both acidic and neutral pH.

Mammalian hyaluronidases degrade hyaluronan and some structurally related glycosaminoglycans. We generated a deletion mutant in the Caenorhabditis elegans orthologue of mammalian hyaluronidase, hya-1. Mutant animals are viable and grossly normal, but exhibit defects in vulval morphogenesis and egg-laying and showed increased staining with alcian blue, consistent with an accumulation of glycosaminoglycan.

Hyaluronidase 3 (HYAL3) knockout mice do not display evidence of hyaluronan accumulation.

Hyaluronidases are endoglycosidases that initiate the breakdown of hyaluronan (HA), an abundant component of the vertebrate extracellular matrix. In humans, six paralogous genes encoding hyaluronidase-like sequences have been identified on human chromosomes 3p21.3 (HYAL2-HYAL1-HYAL3) and 7q31.

A mouse model of human mucopolysaccharidosis IX exhibits osteoarthritis.

Hyaluronidases are endoglycosidases that hydrolyze hyaluronan (HA), an abundant component of the extracellular matrix of vertebrate connective tissues. Six human hyaluronidase-related genes have been identified to date. Mutations in one of these genes cause a deficiency of hyaluronidase 1 (HYAL1) resulting in a lysosomal storage disorder, mucopolysaccharidosis (MPS) IX.

Mouse Hyal3 encodes a 45- to 56-kDa glycoprotein whose overexpression increases hyaluronidase 1 activity in cultured cells.

Hyaluronidases are enzymes that mediate the breakdown of hyaluronan (HA), a large polysaccharide abundant in the extracellular matrix of vertebrate tissues. Six genes have been predicted to encode hyaluronidases in humans, but the protein products of only SPAM1, HYAL1, and HYAL2 have been characterized. We have now expressed the mouse Hyal3 gene product, hyaluronidase 3 (Hyal3), in Baby Hamster Kidney (BHK) cells and demonstrated the presence of multiple forms of Hyal3 ranging from approximately 45 to 56 kDa in expression lysates.

Human growth factor receptor bound 14 binds the activated insulin receptor and alters the insulin-stimulated tyrosine phosphorylation levels of multiple proteins.

To identify proteins interacting in the insulin-signaling pathway that might define new pathways or regulate existing ones, we have employed the yeast two-hybrid system. In a two-hybrid screen of a human liver cDNA library, we identified the human growth factor receptor bound 14 (hGrb14) adaptor protein as a partner of the activated insulin receptor. Additional analysis of the insulin receptor--hGrb14 interaction in the yeast two-hybrid system revealed that the SH2 domain of hGrb14 was not the sole region involved in binding the activated insulin receptor.