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Introduction: Isolated patellar tendon (PT) or anterior cruciate ligament (ACL) ruptures are common injuries, yet the co-occurrence of both presents a rare challenge for clinicians. The objectives of the study are to document diagnostic and therapeutic approaches, outcomes, and complications of combined PT and ACL injuries and to develop an algorithm to guide clinicians in decision-making. Methods: The systematic review und metanalysis was conducted according to the PRISMA guidelines. Studies reporting on simultaneous PT and ACL ruptures were included. Meta-analysis was performed to compare different diagnostic modalities and treatment strategies. Results: Thirty-six studies reporting on 56 Patients were included. 88% of patients had a concomitant injury (apart from PT and ACL) to the ipsilateral knee. Part of the diagnosis was missed in 23% of the cases. Performance of MRI significantly reduced the risk of missing a part of the injury (5% with MRI vs 69% without MRI, p < 0.001). Surgical treatment was used only for the PT in 21% of the cases and for the PT and ACL in 77% of the cases (48% one-stage, 52% two-stage surgical treatment). Conclusion: Combined ACL and PT rupture is rare, and recognizing its full extent is crucial for successful management. Performing an MRI in PT rupture from high-energy trauma and diagnostic arthroscopy/arthrotomy when MRI is not done is essential. PT ruptures should be treated surgically. For ACL rupture, conservative and operative treatment, one- or two-stage surgery are possible based on the patient's profile and concomitant injuries. Based on the limited available literature, this systematic review provides a diagnostic and therapeutic algorithm to assist in clinical decision-making. [ABSTRACT FROM AUTHOR]

Pain is a multidimensional experience, potentially rendering unidimensional pain scales inappropriate for assessment. Prior research highlighted their inadequacy as reliable indicators of analgesic requirement. This systematic review aimed to compare multidimensional with unidimensional pain scales in assessing analgesic requirements in the emergency department (ED). Embase, Medline, CINAHL, and PubMed Central were searched to identify ED studies utilizing both unidimensional and multidimensional pain scales. Primary outcome was desire for analgesia. Secondary outcomes were amount of administered analgesia and patient satisfaction. Two independent reviewers screened, assessed quality, and extracted data of eligible studies. We assessed risk of bias with the ROBINS-I tool and provide a descriptive summary. Out of 845 publications, none met primary outcome criteria. Three studies analyzed secondary outcomes. One study compared the multidimensional Defense and Veterans Pain Rating Scale (DVPRS) to the unidimensional Numerical Rating Scale (NRS) for opioid administration. DVPRS identified more patients with moderate instead of severe pain compared to the NRS. Therefore, the DVPRS might lead to a potential reduction in opioid administration for individuals who do not require it. Two studies assessing patient satisfaction favored the short forms (SF) of the Brief Pain Inventory (BPI) and McGill Pain Questionnaire (MPQ) over the Visual Analogue Scale (VAS) and the NRS. Limited heterogenous literature suggests that in the ED, a multidimensional pain scale (DVPRS), may better discriminate moderate and severe pain compared to a unidimensional pain scale (NRS). This potentially impacts analgesia, particularly when analgesic interventions rely on pain scores. Patients might prefer multidimensional pain scales (BPI-SF, MPQ-SF) over NRS or VAS for assessing their pain experience. [ABSTRACT FROM AUTHOR]

Background: Cardiorespiratory fitness (CRF) is a potent health marker, the improvement of which is associated with a reduced incidence of non-communicable diseases and all-cause mortality. Identifying metabolic signatures associated with CRF could reveal how CRF fosters human health and lead to the development of novel health-monitoring strategies. Objective: This article systematically reviewed reported associations between CRF and metabolites measured in human tissues and body fluids. Methods: PubMed, EMBASE, and Web of Science were searched from database inception to 3 June, 2021. Metabolomics studies reporting metabolites associated with CRF, measured by means of cardiopulmonary exercise test, were deemed eligible. Backward and forward citation tracking on eligible records were used to complement the results of database searching. Risk of bias at the study level was assessed using QUADOMICS. Results: Twenty-two studies were included and 667 metabolites, measured in plasma (n = 619), serum (n = 18), skeletal muscle (n = 16), urine (n = 11), or sweat (n = 3), were identified. Lipids were the metabolites most commonly positively (n = 174) and negatively (n = 274) associated with CRF. Specific circulating glycerophospholipids (n = 85) and cholesterol esters (n = 17) were positively associated with CRF, while circulating glycerolipids (n = 152), glycerophospholipids (n = 42), acylcarnitines (n = 14), and ceramides (n = 12) were negatively associated with CRF. Interestingly, muscle acylcarnitines were positively correlated with CRF (n = 15). Conclusions: Cardiorespiratory fitness was associated with circulating and muscle lipidome composition. Causality of the revealed associations at the molecular species level remains to be investigated further. Finally, included studies were heterogeneous in terms of participants' characteristics and analytical and statistical approaches. PROSPERO Registration Number: CRD42020214375. [ABSTRACT FROM AUTHOR]

Sedentary behavior contributes to increased atherosclerotic risk in adults. Whether or not this can be extended to pediatric populations is unclear. This systematic review assessed associations of sedentary behavior with large artery structure and function in pediatric populations. MEDLINE, EMBASE, CENTRAL, and Web of Science were searched from the earliest available date to 31st of December 2018. Analyses of associations of sedentary behavior with large artery structure or function in a pediatric (sub-)population were included, adhering to the PRISMA guidelines. The protocol was published in advance on PROSPERO (CRD42018112996). Study quality and quality of evidence were analyzed using NHLBI Study Quality assessment tools and GRADE. Six observational studies found no association of exposure and outcome variables, and one had contradicting results. One intervention found reduced flow-mediated dilation after 3 h of uninterrupted sitting. Exposure and outcome measures were highly heterogeneous. Study quality was low to moderate. Quality of evidence was very low or low in the observational studies and high in the intervention.Conclusion: In pediatric populations, current evidence is limited and of low quality about how acute effects of sedentary behavior translate into early vascular aging and the long-term development of vascular dysfunction and atherosclerotic risk. Future studies should emphasize a careful choice of the adequate type and measurement site of a biomarker for large artery structure and function as well as conduct a detailed assessment of sedentary behavior patterns.Trial registration: PROSPERO Registration Number: CRD42018112996What is known: • An independent association of sedentary behavior and biomarkers of large artery structure and function has been demonstrated in adults. • In children, sedentary behavior is directly associated with classical cardiovascular risk factors like elevated blood glucose levels, insulin resistance, high blood pressure, obesity, and elevated blood lipids.What is new: • Currently, only few studies of low quality in children and adolescents provide limited evidence about how acute effects of sedentary behavior translate into early vascular aging and the long-term development of atherosclerosis. • The type and measurement site of vascular biomarker need to be chosen carefully, and a detailed assessment of sedentary behavior patterns is important to minimize the methodological bias. [ABSTRACT FROM AUTHOR]

The molecular networks that control endoplasmic reticulum (ER) redox conditions in mammalian cells are incompletely understood. Here, we show that after reductive challenge the ER steady-state disulphide content is restored on a time scale of seconds. Both the oxidase Ero1α and the oxidoreductase protein disulphide isomerase (PDI) strongly contribute to the rapid recovery kinetics, but experiments in ERO1-deficient cells indicate the existence of parallel pathways for disulphide generation. We find PDI to be the main substrate of Ero1α, and mixed-disulphide complexes of Ero1 primarily form with PDI, to a lesser extent with the PDI-family members ERp57 and ERp72, but are not detectable with another homologue TMX3. We also show for the first time that the oxidation level of PDIs and glutathione is precisely regulated. Apparently, this is achieved neither through ER import of thiols nor by transport of disulphides to the Golgi apparatus. Instead, our data suggest that a dynamic equilibrium between Ero1- and glutathione disulphide-mediated oxidation of PDIs constitutes an important element of ER redox homeostasis. [ABSTRACT FROM AUTHOR]

Oxidative maturation of secretory and membrane proteins in the endoplasmic reticulum (ER) is powered by Ero1 oxidases. To prevent cellular hyperoxidation, Ero1 activity can be regulated by intramolecular disulphide switches. Here, we determine the redox-driven shutdown mechanism of Ero1α, the housekeeping Ero1 enzyme in human cells. We show that functional silencing of Ero1α in cells arises from the formation of a disulphide bond—identified by mass spectrometry—between the active-site Cys94 (connected to Cys99 in the active enzyme) and Cys131. Competition between substrate thiols and Cys131 creates a feedback loop where activation of Ero1α is linked to the availability of its substrate, reduced protein disulphide isomerase (PDI). Overexpression of Ero1α-Cys131Ala or the isoform Ero1β, which does not have an equivalent disulphide switch, leads to augmented ER oxidation. These data reveal a novel regulatory feedback system where PDI emerges as a central regulator of ER redox homoeostasis. [ABSTRACT FROM AUTHOR]