Relationship between Spinal Range of Motion and Functional Tests in University Students: The Role of Demographic Factors.

Spinal disorders are some of the most prevalent health concerns, especially among students. Based on student demographics, this cross-sectional study evaluated the correlation between functional tests (FTs) and spinal range of motion (ROM). This study included 206 students (age = 19.85 ± 1.80 years) from the Vasile Alecsandri University of Bacau. Participants' assessments were conducted using the following tests: (i) Ott, (ii) Schober, (iii) Stibor, (iv) finger-to-floor distance, (v) lateral flexion of the cervical and lumbar spine, and (vi) flexion of the cervical spine. Correlation analyses were evaluated using the Spearman correlation coefficient analysis. The results indicated a very strong relationship between lateral flexion of the lumbar spine on the left (LFLSL) and right (LFLSR) for all departments (r = 0.85 to 0.97, p < 0.05). There was a stronger relationship between FT results and spinal ROM for physical-education-department students compared to students from other departments (n = 17, r = -0.38 to 0.93, p < 0.05). There was no statistically significant correlation between FTs and spinal ROM based on age (p > 0.05). The study results provide evidence of the primary risk factors that predispose students to postural deviations. Practitioners and physiotherapists can utilize these values as a reference for potential therapeutic interventions.

Effects of Myofascial Release Techniques on Joint Range of Motion of Athletes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Although myofascial release techniques (MRTs) are commonly used to improve athletes' range of motion (ROM), the effectiveness of MRTs may vary depending on the specific method performed. This systematic review and meta-analysis aimed to evaluate the effects of MRTs on the ROM performance of athletes. (2) Methods: The electronic databases of Cochrane Library, PubMed, Scopus, and Web of Science were searched to identify relevant articles published up to June 2023. This study utilized the PRISMA guidelines, and four databases were searched. The methodological quality of the studies was assessed using the PEDro scale, and the certainty of evidence was reported using the GRADE scale. The overall effect size was calculated using the robust variance estimator, and subgroup analyses were conducted using the Hotelling Zhang test. (3) Ten studies met the inclusion criteria. The overall effect size results indicated that the myofascial release intervention had a moderate effect on ROM performance in athletes when compared to the active or passive control groups. (4) Conclusions: Alternative MRTs, such as myofascial trigger point therapy, can further improve the ROM performance of athletes. Gender, duration of intervention, and joint type may have a moderating effect on the effectiveness of MRTs.

The Relationship between Magnetic Resonance Imaging and Functional Tests Assessment in Patients with Lumbar Disk Hernia.

Although magnetic resonance imaging (MRI) findings are the gold standard for diagnosing herniated discs, there are many limitations to accessing MRI scanning devices in practice. This study aimed to evaluate the relationship between functional tests (the visual analog scale (VAS), the SLUMP test, the Sciatica Bothersomeness Index (SBI), the Oswestry Disability Index (ODI), and the LASEGUE test and MRI findings (LSA, IVDH L4-L5, IVDH L5-S1, DHS L4-L5, and DHS L5-S1) in patients diagnosed with disc herniation. Seventy-eight patients who met the inclusion criteria participated in the study. Radiologists and neurologists evaluated patients with disc herniation. After the disc hernia diagnosis, the patients were referred to a physical therapist for conservative management of the disk hernia. The physical therapists assessed the pain level and performed functional tests on patients. All statistical analyses were performed using R (Core Team) software. The correlation between the measured variables was conducted using the Pearson and Spearman tests. The study results indicated statistically significant correlations between DHS L4-L5 vertebral level and functional tests (VAS: r = 0.49, p = 0.00; SBI: r = 0.44, p = 0.00; ODI: r = 0.49, p = 0.00; LASEGUE: r = -0.48, p = 0.00; SLUMP: r = 0.50, p = 0.00). In conclusion, physiotherapists may prefer functional tests to diagnose the herniated disc, and these functional tests may contribute to performing evidence-based assessments.

Validity, Reliability, and Sensitivity of Mobile Applications to Assess Change of Direction Speed.

This study aimed to assess the validity, reliability, and sensitivity of mobile applications for assessing change-of-direction speed (CODS) performance. Thirty college athletes performed two Illinois CODS tests during one session. Assessments were carried out simultaneously using six devices (the CODTimer app, Seconds Count app, StopwatchCamera app, two analog stopwatches, and timing gates). Validity analyses included Pearson's product-moment correlation analysis, a linear regression model, and Bland-Altman plots. Reliability analyses included the intraclass correlation coefficient (ICC), the coefficient of variation (CV%), and the paired-sample t test. Sensitivity analyses included the typical error and smallest worthwhile change (SWC). The results showed that validity, reliability, and sensitivity values were higher for the CODTimer app (r = 0.99, R2 = 0.99, mean bias = -0.03 ± 0.10, CV% = 3.21, ICC = 0.89, SWC rating: good, p = 0.84) and the Seconds Count app (r = 0.99, R2 = 0.99, mean bias = -0.03 ± 0.08, CV% = 3.28, ICC = 0.88, SWC rating: good, p = 0.84) relative to the StopwatchCamera app (r = 0.98, R2 = 0.97, mean bias = -0.11 ± 0.22, CV% = 3.43, ICC = 0.86, SWC rating: marginal, p = 0.10), Analog Stopwatch 1 (r = 0.98, R2 = 0.96, mean bias = -0.09 ± 0.42, CV% = 2.95, ICC = 0.90, SWC rating: good, p = 0.91), and Analog Stopwatch 2 (r = 0.99, R2 = 0.97, mean bias = -0.12 ± 0.88, CV% = 3.51, ICC = 0.87, SWC rating: marginal, p = 0.96). In conclusion, compared to timing gates, the CODTimer app and Seconds Count app provided lower measurement bias and higher sensitivity for assessing CODS performance.

Biosensing of glucose in flow injection analysis system based on glucose oxidase-quantum dot modified pencil graphite electrode.

A novel amperometric glucose biosensor was proposed in flow injection analysis (FIA) system using glucose oxidase (GOD) and Quantum dot (ZnS-CdS) modified Pencil Graphite Electrode (PGE). After ZnS-CdS film was electrochemically deposited onto PGE surface, GOD was immobilized on the surface of ZnS-CdS/PGE through crosslinking with chitosan (CT). A pair of well-defined reversible redox peak of GOD was observed at GOD/CT/ZnS-CdS/PGE based on enzyme electrode by direct electron transfer between the protein and electrode. Further, obtained GOD/CT/ZnS-CdS/PGE offers a disposable, low cost, selective and sensitive electrochemical biosensing of glucose in FIA system based on the decrease of the electrocatalytic response of the reduced form of GOD to dissolved oxygen. Under optimum conditions (flow rate, 1.3mL min(-1); transmission tubing length, 10cm; injection volume, 100µL; and constant applied potential, -500mV vs. Ag/AgCl), the proposed method displayed a linear response to glucose in the range of 0.01-1.0mM with detection limit of 3.0µM. The results obtained from this study would provide the basis for further development of the biosensing using PGE based FIA systems.

Type II collagen antibody response is enriched in the synovial fluid of rheumatoid joints and directed to the same major epitopes as in collagen induced arthritis in primates and mice.

INTRODUCTION: Antibodies towards type II collagen (CII) are detected in patients with rheumatoid arthritis (RA) and in non-human primates and rodents with collagen induced arthritis (CIA). We have previously shown that antibodies specific for several CII-epitopes are pathogenic using monoclonal antibodies from arthritic mice, although the role of different anti-CII epitopes has not been investigated in detail in other species. We therefore performed an inter-species comparative study of the autoantibody response to CII in patients with RA versus monkeys and mice with CIA. METHODS: Analysis of the full epitope repertoire along the disease course of CIA was performed using a library of CII triple-helical peptides. The antibody responses to the major CII epitopes were analyzed in sera and synovial fluid from RA patients, and in sera from rhesus monkeys (Macaca mulatta), common marmosets (Callithrix jacchus) and mice. RESULTS: Many CII epitopes including the major C1, U1, and J1 were associated with established CIA and arginine residues played an important role in the anti-CII antibody interactions. The major epitopes were also recognized in RA patients, both in sera and even more pronounced in synovial fluid: 77% of the patients had antibodies to the U1 epitope. The anti-CII immune response was not restricted to the anti-citrulline protein antibodies (ACPA) positive RA group. CONCLUSION: CII conformational dependent antibody responses are common in RA and are likely to originate from rheumatoid joints but did not show a correlation with ACPA response. Importantly, the fine specificity of the anti-CII response is similar with CIA in monkeys and rodents where the recognized epitopes are conserved and have a major pathogenic role. Thus, anti-CII antibodies may both contribute to, as well as be the consequence of, local joint inflammation.

Epitope-specific antibody response is controlled by immunoglobulin V(H) polymorphisms.

Autoantibody formation is essential for the development of certain autoimmune diseases like rheumatoid arthritis (RA). Anti-type II collagen (CII) antibodies are found in RA patients; they interact with cartilage in vivo and are often highly pathogenic in the mouse. Autoreactivity to CII is directed to multiple epitopes and conserved between mice and humans. We have previously mapped the antibody response to CII in a heterogeneous stock cohort of mice, with a strong association with the IgH locus. We positioned the genetic polymorphisms and determined the structural requirements controlling antibody recognition of one of the major CII epitopes. Polymorphisms at positions S31R and W33T of the associated variable heavy chain (VH) allele were identified and confirmed by gene sequencing. The Fab fragment binding the J1 epitope was crystallized, and site-directed mutagenesis confirmed the importance of those two variants for antigen recognition. Back mutation to germline sequence provided evidence for a preexisting recognition of the J1 epitope. These data demonstrate a genetic association of epitope-specific antibody responses with specific VH alleles, and it highlights the importance of germline-encoded antibodies in the pathogenesis of antibody-mediated autoimmune diseases.

Crystal structure of an arthritogenic anticollagen immune complex.

OBJECTIVE: In rheumatoid arthritis, joint inflammation and cartilage destruction are mediated by autoantibodies directed to various self antigens. Type II collagen (CII)-specific antibodies are likely to play a role in this process and have been shown to induce experimental arthritis in susceptible animals. The purpose of this study was to reveal how arthritogenic autoantibodies recognize native CII in its triple-helical conformation. METHODS: Site-directed mutagenesis and crystallographic studies were performed to reveal crucial contact points between the CII antibody and the triple-helical CII peptide. RESULTS: The crystal structure of a pathogenic autoantibody bound to a major triple-helical epitope present on CII was determined, allowing a first and detailed description of the interactions within an arthritogenic complex that is frequently occurring in both mice and humans with autoimmune arthritis. The crystal structure emphasizes the role of arginine residues located in a commonly recognized motif on CII and reveals that germline-encoded elements are involved in the interaction with the epitope. CONCLUSION: The crystal structure of an arthritogenic antibody binding a triple-helical epitope on CII indicates a crucial role of germline-encoded and arginine residues as the target structures.

A leukotriene A4 hydrolase-related aminopeptidase from yeast undergoes induced fit upon inhibitor binding.

Vertebrate leukotriene A(4) hydrolases are bifunctional zinc metalloenzymes with an epoxide hydrolase and an aminopeptidase activity. In contrast, highly homologous enzymes from lower organisms only have the aminopeptidase activity. From sequence comparisons, it is not clear why this difference occurs. In order to obtain more information on the evolutionary relationship between these enzymes and their activities, the structure of a closely related leucine aminopeptidase from Saccharomyces cerevisiae that only shows a very low epoxide hydrolase activity was determined. To investigate the molecular architecture of the active site, the structures of both the native protein and the protein in complex with the aminopeptidase inhibitor bestatin were solved. These structures show a more spacious active site, and the protected cavity in which the labile substrate leukotriene A(4) is bound in the human enzyme is partially obstructed and in other parts is more solvent accessible. Furthermore, the enzyme undergoes induced fit upon binding of the inhibitor bestatin, leading to a movement of the C-terminal domain. The main triggers for the domain movement are a conformational change of Tyr312 and a subtle change in backbone conformation of the PYGAMEN fingerprint region for peptide substrate recognition. This leads to a change in the hydrogen-bonding network pulling the C-terminal domain into a different position. Inasmuch as bestatin is a structural analogue of a leucyl dipeptide and may be regarded as a transition state mimic, our results imply that the enzyme undergoes induced fit during substrate binding and turnover.

Antibodies to citrullinated proteins: molecular interactions and arthritogenicity.

The discovery of antibodies specific for citrullinated protein epitopes [anti-citrullinated protein antibodies (ACPAs)] is a hallmark for the diagnosis and prognosis of rheumatoid arthritis (RA) and will also be a useful tool for understanding the fundamental pathologic processes. There are several essential questions pertaining to ACPA that remain to be explored, such as understanding the early specificity of the underlying T-cell recognition, whether the production of ACPA is a primary or secondary process, and in the event of such antibodies being arthritogenic, whether they could possibly regulate the disease development. To answer these questions, animal models are needed, but unfortunately ACPA is not a prominent feature of any of the classical animal models of RA. However, we showed recently that ACPA can be isolated from animals susceptible to collagen-induced arthritis that are specific for citrullinated type II collagen (CII). The citrulline specificity could be visualized, and the specificity is determined primarily by a direct interaction with citrulline. We also demonstrated that these antibodies are specific for the citrullinated epitopes and are pathogenic in vivo. A new hypothesis to explain how inflammation in RA can be directed to cartilaginous joints and be self-perpetuating is suggested, which involves recognition of post-translational modifications (glycosylation and citrullination) on CII by T and B cells that can have both arthritogenic and regulatory consequences.

New insights into DNA-binding behavior of Wilms tumor protein (WT1)--a dual study.

Wilms Tumor suppressor protein (WT1) is a transcription factor that is involved in a variety of developmental functions during organ development. It is also implicated in the pathology of several different cancer forms. The protein contains four C(2)H(2)-type zinc fingers and it specifically binds GC-rich sequences in the promoter regions of its target genes, which are either up or down regulated. Two properties make WT1 a more unusual transcription factor - an unconventional amino acid composition for zinc finger 1, and the insertion of a tri-peptide KTS in some of the splice isoforms of WT1. Using six WT1 constructs in which zinc fingers are systematically deleted, a dual study based on a bacterial 1-hybrid system and surface plasmon resonance measurements is performed. The experiments show that the effect of zinc finger 1 is not significant in terms of overall DNA-binding kinetics, however it influences both the specificity of target recognition and stability of interaction in presence of KTS. The KTS insertion, however, only mildly retards binding affinity, mainly by affecting the on-rate. We suggest that the insertion disturbs zinc finger 4 from its binding frame, thus weakening the rate of target recognition. Finally, for the construct in which both zinc fingers 1 and 4 were deleted, the two middle fingers 2-3 still could function as a 'minimal DNA-recognition domain' for WT1, however the formation of a stable protein-DNA complex is impaired since the overall affinity was dramatically reduced mainly since the off-rate was severely affected.

Structure and pathogenicity of antibodies specific for citrullinated collagen type II in experimental arthritis.

Antibodies to citrulline-modified proteins have a high diagnostic value in rheumatoid arthritis (RA). However, their biological role in disease development is still unclear. To obtain insight into this question, a panel of mouse monoclonal antibodies was generated against a major triple helical collagen type II (CII) epitope (position 359-369; ARGLTGRPGDA) with or without arginines modified by citrullination. These antibodies bind cartilage and synovial tissue, and mediate arthritis in mice. Detection of citrullinated CII from RA patients' synovial fluid demonstrates that cartilage-derived CII is indeed citrullinated in vivo. The structure determination of a Fab fragment of one of these antibodies in complex with a citrullinated peptide showed a surprising beta-turn conformation of the peptide and provided information on citrulline recognition. Based on these findings, we propose that autoimmunity to CII, leading to the production of antibodies specific for both native and citrullinated CII, is an important pathogenic factor in the development of RA.

The crystal structure of the pathogenic collagen type II-specific mouse monoclonal antibody CIIC1 Fab: structure to function analysis.

Monoclonal anti-collagen type II antibody CIIC1 is an arthritogenic autoantibody, which induces arthritis in mice. We crystallized and solved the structure of CIIC1 Fab molecule. Analysis of structure revealed an interaction between the CDR regions of one Fab to the CH1 domain of another Fab, which resembles an antibody-antigen interaction. ELISA experiments confirmed the cross-reactivity of both the full CIIC1 antibody and a single chain Fv fragment to other anti-collagen antibodies which are of different isotypes and epitope specificity. The rheumatoid factor like reactivity of CIIC1 antibody together with its collagen type II specificity may explain the pathogenicity of this antibody.