Revealing nature's beauty through crafting structural color-coated fabrics with bioinspired modification of MXene.

In recent years, there has been a notable shift towards the use of structural colors in textile dyeing, replacing traditional chemical dyes. This change is primarily attributed to the increasing popularity of structural colors due to their eco-friendly characteristics. In thus study, SiO2 particles underwent modification with PDA and Ti3C2Tx (MXene) to establish a core-shell structure, resulting in MSiO2/PDA@MXene photonic crystals characterized by electrostatic assembly and hydrogen bonding. These crystals comprise a SiO2 core encased in black PDA@MXene shells. The PDA@MXene shell works by absorbing scattered light indiscriminately, thereby intensifying the vividness of the structural colors. Adjusting the size of the MSiO2/PDA@MXene microspheres enables the generation of diverse structural colors. Then, chitosan-coated cotton fabrics were decorated using photonic crystals of MSiO2/PDA@MXene. Coating cotton fabric with chitosan introduced positively charged groups onto its surface, which enabled electrostatic interaction with photonic crystals. The prepared fabrics also showed excellent antioxidant property, further enhancing their appeal for outdoor applications. These structural colors offer a sustainable substitute for conventional textile dyes, meeting the increasing need for environmentally conscious practices within the textile sector.

The schizophrenia risk gene C4 induces pathological synaptic loss by impairing AMPAR trafficking.

Neuroimmune interactions play a significant role in regulating synaptic plasticity in both the healthy and diseased brain. The complement pathway, an extracellular proteolytic cascade, exemplifies these interactions. Its activation triggers microglia-dependent synaptic elimination via the complement receptor 3 (CR3). Current models of pathological complement activity in the brain propose that accelerated synaptic loss resulting from overexpression of C4 (C4-OE), a gene associated with schizophrenia, follows this pathway. Here, we report that C4-mediated cortical hypoconnectivity is CR3-independent. Instead, C4-OE triggers impaired GluR1 trafficking through an intracellular mechanism involving the endosomal protein SNX27, resulting in pathological synaptic loss. Moreover, C4 circuit alterations in the prefrontal cortex, a brain region associated with neuropsychiatric disorders, were rescued by increasing neuronal levels of SNX27, which we identify as an interacting partner of this neuroimmune protein. Our results link excessive complement activity to an intracellular endo-lysosomal trafficking pathway altering synaptic plasticity.

Hallux Valgus Bunion Splint: Surgical Dressing Technique.

BACKGROUND: Hallux valgus is a common condition with a complex etiology resulting in numerous treatment options. Recurrence of the deformity can occur following correction. Surgical technique and possibly also postoperative care play a role in reducing recurrence rates. This article highlights a postoperative surgical dressing technique which allows for semirigid support during the immediate postoperative period. METHODS: A wooden tongue depressor placed along the medial border of the hallux comprises the primary support for the dressing. The rigidity of the tongue depressor allows for the hallux to be drawn toward the depressor, encouraging neutral alignment of the hallux. Dressings are removed 2 weeks postoperatively, with new dressings applied in similar fashion and maintained in place until 6 weeks postoperatively. RESULTS: Based upon our observations, our surgical dressing technique provides sufficient support following hallux valgus correction surgery while being straightforward to replicate without the need for frequent dressing changes. The dressing materials are of negligible cost and are typically readily available. No associated wound complications have been observed. CONCLUSIONS: We present an easily replicable and affordable option for postoperative hallux valgus correction surgical dressings. LEVELS OF EVIDENCE: Level V: Expert Opinion.

C4 induces pathological synaptic loss by impairing AMPAR trafficking.

During development, activation of the complement pathway, an extracellular proteolytic cascade, results in microglia-dependent synaptic elimination via complement receptor 3 (CR3). Here, we report that decreased connectivity caused by overexpression of C4 (C4-OE), a schizophrenia-associated gene, is CR3 independent. Instead, C4-OE triggers GluR1 degradation through an intracellular mechanism involving endosomal trafficking protein SNX27, resulting in pathological synaptic loss. Moreover, the connectivity deficits associated with C4-OE were rescued by increasing levels of SNX27, linking excessive complement activity to an intracellular endolysosomal recycling pathway affecting synapses.

ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome.

Unlike many other hematologic malignancies, Richter syndrome (RS), an aggressive B cell lymphoma originating from indolent chronic lymphocytic leukemia, is responsive to PD-1 blockade. To discover the determinants of response, we analyze single-cell transcriptome data generated from 17 bone marrow samples longitudinally collected from 6 patients with RS. Response is associated with intermediate exhausted CD8 effector/effector memory T cells marked by high expression of the transcription factor ZNF683, determined to be evolving from stem-like memory cells and divergent from terminally exhausted cells. This signature overlaps with that of tumor-infiltrating populations from anti-PD-1 responsive solid tumors. ZNF683 is found to directly target key T cell genes (TCF7, LMO2, CD69) and impact pathways of T cell cytotoxicity and activation. Analysis of pre-treatment peripheral blood from 10 independent patients with RS treated with anti-PD-1, as well as patients with solid tumors treated with anti-PD-1, supports an association of ZNF683high T cells with response.

Intraduodenal nutrient infusion differentially alters intestinal nutrient sensing, appetite, and satiety responses in lean and obese subjects.

BACKGROUND: Intestinal nutrient sensing regulates food intake and energy metabolism by acting locally and relaying nutritional status to the brain. It is unclear whether these mechanisms are altered in obese humans. OBJECTIVES: We aimed to investigate differences in duodenal nutrient sensing in humans with or without obesity and the effects of transiently blocking vagal transmission on nutrient sensing, hunger, and appetite. METHODS: In a single-blinded, randomized, cross-over design, subjects with or without obesity (n = 14 and n = 11, respectively) were infused intraduodenally with saline or a combination of glucose and oleic acid for 90 min (glucose load: 22.5 g, 1 kcal/min; oleic acid load: 10 g, 1 kcal/min) in the presence or absence of local anesthetic (benzocaine). Blood was sampled at 10-min intervals (120-240 min) and 15-min intervals until termination of the study for measurements of gut hormones, insulin, leptin, and C-peptide. Hunger and satiety sensations were scored using the visual analog scale, and hepatic glucose production and glucose oxidation rates were measured. RESULTS: Duodenal nutrient infusion in lean subjects led to a 65% drop in acyl ghrelin release and robustly increased cholecystokinin 8 (CCK-8) release (65%; P = 0.023); benzocaine infusion delayed this response (2-factor repeated-measures analysis of variance, P = 0.0065). In contrast, subjects with obesity had significantly blunted response to nutrient infusion, and no further effects were observed with benzocaine. Additionally, significant delays were observed in peptide YY (3-36), pancreatic polypeptide, glucose inhibitory peptide, and glucagon-like peptide 1 (7-36) response. No significant interactions were found between body mass index (BMI) or baseline hormone levels and areas under the curve for hormones except CCK-8 (BMI, P = 0.018; baseline CCK, P = 0.013). Nutrient-induced hunger and satiety sensations were impeded by benzocaine only in the lean cohort. Hunger and satiety sensations in subjects with obesity were not responsive to nutrient entry into the duodenum, and no additional effects were observed by blocking neural signaling. CONCLUSION: Nutrient-induced gut hormone release and response to transient vagal blockade are significantly blunted in subjects with obesity. This trial was registered at clinicaltrials.org as NCT02537314.

Hedgehog signaling via its ligand DHH acts as cell fate determinant during skeletal muscle regeneration.

Successful muscle regeneration relies on the interplay of multiple cell populations. However, the signals required for this coordinated intercellular crosstalk remain largely unknown. Here, we describe how the Hedgehog (Hh) signaling pathway controls the fate of fibro/adipogenic progenitors (FAPs), the cellular origin of intramuscular fat (IMAT) and fibrotic scar tissue. Using conditional mutagenesis and pharmacological Hh modulators in vivo and in vitro, we identify DHH as the key ligand that acts as a potent adipogenic brake by preventing the adipogenic differentiation of FAPs. Hh signaling also impacts muscle regeneration, albeit indirectly through induction of myogenic factors in FAPs. Our results also indicate that ectopic and sustained Hh activation forces FAPs to adopt a fibrogenic fate resulting in widespread fibrosis. In this work, we reveal crucial post-developmental functions of Hh signaling in balancing tissue regeneration and fatty fibrosis. Moreover, they provide the exciting possibility that mis-regulation of the Hh pathway with age and disease could be a major driver of pathological IMAT formation.

Neurobiochemical, Peptidomic, and Bioinformatic Approaches to Characterize Tauopathy Peptidome Biomarker Candidates in Experimental Mouse Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) is a multidimensional damage, and currently, no FDA-approved medicine is available. Multiple pathways in the cell are triggered through a head injury (e.g., calpain and caspase activation), which truncate tau and generate variable fragment sizes (MW 400-45,000 K). In this study, we used an open-head TBI mouse model generated by controlled cortical impact (CCI) and collected ipsilateral (IC) and contralateral (CC) mice htau brain cortices at one (D1) three (D3), and seven (D7) days post-injury. We implemented immunological (antibody-based detection) and peptidomic approaches (nano-reversed-phase liquid chromatography/tandem mass spectrometry) to investigate proteolytic tau peptidome (low molecular weight (LMW) < 10 K)) and pathological phosphorylation sites (high-molecular-weight (HMW); > 10 K) derived from CCI-TBI animal models. Our immunoblotting analysis verified tau hyperphosphorylation, HMW, and HMW breakdown products (HMW-BDP) formation of tau (e.g., pSer202, pThr181, pThr231, pSer396, and pSer404), following CCI-TBI. Peptidomic data revealed unique sequences of injury-dependent proteolytic peptides generated from human tau protein. Among the N-terminal tau peptides, EIPEGTTAEEAGIGDTPSLEDEAAGHVTQA (a.a. 96-125) and AQPHTEIPEGTTAEEAGIGDTPSLEDEAAGHVTQARM (a.a. 91-127). Examples of tau C-terminal peptides identified include NVSSTGSIDMVDSPQLATLADEVSASLAKQGL (a.a. 410-441) and QLATLADEVSASLAKQGL (a.a. 424-441). Our peptidomic bioinformatic tools showed the association of proteases, such as CAPN1, CAPN2, and CTSL; CASP1, MMP7, and MMP9; and ELANE, GZMA, and MEP1A, in CCI-TBI tau peptidome. In clinical trials for novel TBI treatments, it might be useful to monitor a subset of tau peptidome as targets for biomarker utility and use them for a "theranostic" approach.

Evolutionary history of transformation from chronic lymphocytic leukemia to Richter syndrome.

Richter syndrome (RS) arising from chronic lymphocytic leukemia (CLL) exemplifies an aggressive malignancy that develops from an indolent neoplasm. To decipher the genetics underlying this transformation, we computationally deconvoluted admixtures of CLL and RS cells from 52 patients with RS, evaluating paired CLL-RS whole-exome sequencing data. We discovered RS-specific somatic driver mutations (including IRF2BP2, SRSF1, B2M, DNMT3A and CCND3), recurrent copy-number alterations beyond del(9p21)(CDKN2A/B), whole-genome duplication and chromothripsis, which were confirmed in 45 independent RS cases and in an external set of RS whole genomes. Through unsupervised clustering, clonally related RS was largely distinct from diffuse large B cell lymphoma. We distinguished pathways that were dysregulated in RS versus CLL, and detected clonal evolution of transformation at single-cell resolution, identifying intermediate cell states. Our study defines distinct molecular subtypes of RS and highlights cell-free DNA analysis as a potential tool for early diagnosis and monitoring.

A Guide to Examining Intramuscular Fat Formation and its Cellular Origin in Skeletal Muscle.

Fibro-adipogenic progenitors (FAPs) are mesenchymal stromal cells that play a crucial role during skeletal muscle homeostasis and regeneration. FAPs build and maintain the extracellular matrix that acts as a molecular myofiber scaffold. In addition, FAPs are indispensable for myofiber regeneration as they secrete a multitude of beneficial factors sensed by the muscle stem cells (MuSCs). In diseased states, however, FAPs are the cellular origin of intramuscular fat and fibrotic scar tissue. This fatty fibrosis is a hallmark of sarcopenia and neuromuscular diseases, such as Duchenne Muscular Dystrophy. One significant barrier in determining why and how FAPs differentiate into intramuscular fat is effective preservation and subsequent visualization of adipocytes, especially in frozen tissue sections. Conventional methods of skeletal muscle tissue processing, such as snap-freezing, do not properly preserve the morphology of individual adipocytes, thereby preventing accurate visualization and quantification. To overcome this hurdle, a rigorous protocol was developed that preserves adipocyte morphology in skeletal muscle sections allowing visualization, imaging, and quantification of intramuscular fat. The protocol also outlines how to process a portion of muscle tissue for RT-qPCR, enabling users to confirm observed changes in fat formation by viewing differences in the expression of adipogenic genes. Additionally, it can be adapted to visualize adipocytes by whole-mount immunofluorescence of muscle samples. Finally, this protocol outlines how to perform genetic lineage tracing of Pdgfrα-expressing FAPs to study the adipogenic conversion of FAPs. This protocol consistently yields high-resolution and morphologically accurate immunofluorescent images of adipocytes, along with confirmation by RT-qPCR, allowing for robust, rigorous, and reproducible visualization and quantification of intramuscular fat. Together, the analysis pipeline described here is the first step to improving our understanding of how FAPs differentiate into intramuscular fat, and provides a framework to validate novel interventions to prevent fat formation.

A Window Into the Tired Brain: Neurophysiological Dynamics of Visuospatial Working Memory Under Fatigue.

OBJECTIVE: We examine the spatiotemporal dynamics of neural activity and its correlates in heart rate and its variability (HR/HRV) during a fatiguing visuospatial working memory task. BACKGROUND: The neural and physiological drivers of fatigue are complex, coupled, and poorly understood. Investigations that combine the fidelity of neural indices and the field-readiness of physiological measures can facilitate measurements of fatigue states in operational settings. METHOD: Sixteen healthy adults, balanced by sex, completed a 60-minute fatiguing visuospatial working memory task. Changes in task performance, subjective measures of effort and fatigue, cerebral hemodynamics, and HR/HRV were analyzed. Peak brain activation, functional and effective connections within relevant brain networks were contrasted against spectral and temporal features of HR/HRV. RESULTS: Task performance elicited increased neural activation in regions responsible for maintaining working memory capacity. With the onset of time-on-task effects, resource utilization was seen to increase beyond task-relevant networks. Over time, functional connections in the prefrontal cortex were seen to weaken, with changes in the causal relationships between key regions known to drive working memory. HR/HRV indices were seen to closely follow activity in the prefrontal cortex. CONCLUSION: This investigation provided a window into the neurophysiological underpinnings of working memory under the time-on-task effect. HR/HRV was largely shown to mirror changes in cortical networks responsible for working memory, therefore supporting the possibility of unobtrusive state recognition under ecologically valid conditions. APPLICATIONS: Findings here can inform the development of a fieldable index for cognitive fatigue.

Botulinum Injection Into the Proximal Intestinal Wall of Diet-Induced Obese Mice Leads to Weight Loss and Improves Glucose and Fat Tolerance.

Botulinum neurotoxin (available commercially as BOTOX) has been used successfully for treatment of several neuromuscular disorders, including blepharospasm, dystonia, spasticity, and cerebral palsy in children. Our data demonstrate that injection of Botox into the proximal intestinal wall of diet-induced obese (DIO) mice induces weight loss and reduces food intake. This was associated with amelioration of hyperglycemia, hyperlipidemia, and significant improvement of glucose tolerance without alteration of energy expenditure. We also observed accelerated gastrointestinal transit and significant reductions in glucose and lipid absorption, which may account, at least in part, for the observed weight loss and robust metabolic benefits, although possible systemic effects occurring as a consequence of central and/or peripheral signaling cannot be ignored. The observed metabolic benefits were found to be largely independent of weight loss, as demonstrated by pair-feeding experiments. Effects lasted ∼8 weeks, for as long as the half-life of Botox as reported in prior rodent studies. These results have valuable clinical implications. If the observed effects are translatable in humans, this approach could lay the foundation for therapeutic approaches geared toward robust and sustained weight loss, mimicking some of the benefits of bariatric operations without its cost and complications.

Highly unstable heterogeneous representations in VIP interneurons of the anterior cingulate cortex.

A hallmark of the anterior cingulate cortex (ACC) is its functional heterogeneity. Functional and imaging studies revealed its importance in the encoding of anxiety-related and social stimuli, but it is unknown how microcircuits within the ACC encode these distinct stimuli. One type of inhibitory interneuron, which is positive for vasoactive intestinal peptide (VIP), is known to modulate the activity of pyramidal cells in local microcircuits, but it is unknown whether VIP cells in the ACC (VIPACC) are engaged by particular contexts or stimuli. Additionally, recent studies demonstrated that neuronal representations in other cortical areas can change over time at the level of the individual neuron. However, it is not known whether stimulus representations in the ACC remain stable over time. Using in vivo Ca2+ imaging and miniscopes in freely behaving mice to monitor neuronal activity with cellular resolution, we identified individual VIPACC that preferentially activated to distinct stimuli across diverse tasks. Importantly, although the population-level activity of the VIPACC remained stable across trials, the stimulus-selectivity of individual interneurons changed rapidly. These findings demonstrate marked functional heterogeneity and instability within interneuron populations in the ACC. This work contributes to our understanding of how the cortex encodes information across diverse contexts and provides insight into the complexity of neural processes involved in anxiety and social behavior.

Preoperative hematocrit and platelet count are associated with blood loss during spinal fusion for children with neuromuscular scoliosis.

AIM: To assess the relationship of preoperative hematology laboratory results with intraoperative estimated blood loss and transfusion volumes during posterior spinal fusion for pediatric neuromuscular scoliosis. METHODS: Retrospective chart review of 179 children with neuromuscular scoliosis undergoing spinal fusion at a tertiary children's hospital between 2012 and 2017. The main outcome measure was estimated blood loss. Secondary outcomes were volumes of packed red blood cells, fresh frozen plasma, and platelets transfused intraoperatively. Independent variables were preoperative blood counts, coagulation studies, and demographic and surgical characteristics. Relationships between estimated blood loss, transfusion volumes, and independent variables were assessed using bivariable analyses. Classification and Regression Trees were used to identify variables most strongly correlated with outcomes. RESULTS: In bivariable analyses, increased estimated blood loss was significantly associated with higher preoperative hematocrit and lower preoperative platelet count but not with abnormal coagulation studies. Preoperative laboratory results were not associated with intraoperative transfusion volumes. In Classification and Regression Trees analysis, binary splits associated with the largest increase in estimated blood loss were hematocrit ≥44% vs. <44% and platelets ≥308 vs. <308 × 109/L. CONCLUSIONS: Preoperative blood counts may identify patients at risk of increased bleeding, though do not predict intraoperative transfusion requirements. Abnormal coagulation studies often prompted preoperative intervention but were not associated with increased intraoperative bleeding or transfusion needs.

Hospital Volumes of Inpatient Pediatric Surgery in the United States.

BACKGROUND: Perioperative outcomes of children depend on the skill and expertise in managing pediatric patients, as well as integration of surgical, anesthesiology, and medical teams. We compared the types of pediatric patients and inpatient surgical procedures performed in low- versus higher-volume hospitals throughout the United States. METHODS: Retrospective analysis of 323,258 hospitalizations with an operation for children age 0 to 17 years in 2857 hospitals included in the Agency for Healthcare Research and Quality (AHRQ) Kids' Inpatient Database (KID) 2016. Hospitals were categorized by their volume of annual inpatient surgical procedures. Specific surgeries were distinguished with the AHRQ Clinical Classification System. We assessed complex chronic conditions (CCCs) using Feudtner and Colleagues' system. RESULTS: The median annual volume of pediatric inpatient surgeries across US hospitals was 8 (interquartile range [IQR], 3-29). The median volume of inpatient surgeries for children with a CCC was 4 (IQR, 1-13). Low-volume hospitals performed significantly fewer types of surgeries (median 2 vs 131 types of surgeries in hospitals with 1-24 vs ≥2000 volumes). Appendectomy and fixation of bone fracture were among the most common surgeries in low-volume hospitals. As the volume of surgical procedures increased from 1 to 24 to ≥2000, the percentage of older children ages 11 to 17 years decreased (70.9%-32.0% [P < .001]) and the percentage of children with a CCC increased (11.2%-60.0% [P < .001]). CONCLUSIONS: Thousands of US hospitals performed inpatient surgeries on few pediatric patients, including those with CCCs who have the highest risk of perioperative morbidity and mortality. Evaluation of perioperative decision making, workflows, and pediatric clinicians in low- and higher-volume hospitals is warranted.

Characterization of Phenolic Plant Exudates by Nuclear Magnetic Resonance Spectroscopy.

The class of plant exudates that contain the phenol functionality, termed phenolics, is defined, surveyed, and characterized by solid-state 13C NMR spectroscopy and by solution-state 1H NMR spectroscopy. Materials in this group are identified by the phenolic 13C resonance (from the ipso carbon of ArOH) at δ 145-160 (δ 160-167 for ArOR). The resonance patterns define several subclasses based on the collective similarity of their 13C spectra, specifically, aloetics from the genus Aloe, guaiacs from the genus Guaiacum and other eurosid and conifer genera, xanthics from the genus Garcinia, and kinos from the genus Eucalyptus and many other genera. Phenolic exudates often are mixed with terpenoid materials (the building block of exudates known as resins) and carbohydrates (the building block of exudates known as gums) to form hybrid subgroups such as guaiac gums, guaiac resins, and kino resins. There are numerous phenolic exudates not affiliated with any of these groups, both as pure phenolics and as hybrids (phenolic resins, phenolic gum resins, and phenolic waxes).

Tracking POPs in Global Air from the First 10 Years of the GAPS Network (2005 to 2014).

The Global Atmospheric Passive Sampling (GAPS) network, initiated in 2005 across 55 global sites, supports the global monitoring plan (GMP) of the Stockholm Convention on Persistent Organic Pollutants (POPs) by providing information on POP concentrations in air on a global scale. These data inform assessments of the long-range transport potential of POPs and the effectiveness evaluation of chemical regulation efforts, by observing changes in concentrations over time. Currently, measurements spanning 5-10 sampling years are available for 40 sites from the GAPS Network. This study was the first time that POP concentrations in air were reported on a global scale for an extended time period and the first to evaluate worldwide trends with an internally consistent sample set. For consistency between sampling years, site- and sample specific sampling rates were calculated with a new, public online model, which accounts for the effects of wind speed variability. Concentrations for legacy POPs in air between 2005 and 2014 show different trends for different organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs). The POPs discussed in this study were chosen due to being the most frequently detected, with detection at the majority of sites. PCB, endosulfan, and hexachlorocyclohexane (HCH) concentrations in air are decreasing at most sites. The global trends reflect global sources and recycling of HCH, ongoing emissions from old stockpiles for PCBs, and recent use restrictions for endosulfan. These chlorinated OCPs continue to present exposure threat to humans and ecosystems worldwide. Concentrations of other OCPs, such as chlordanes, heptachlor and dieldrin, are steady and/or declining slowly at the majority of sites, reflecting a transition from primary to secondary sources (i.e., re-emission from reservoirs where these POPs have accumulated historically) which now control ambient air burdens.

Identifying risk factors for missed compartment syndrome in patients with tibia shaft fractures: An analysis of the national trauma data bank.

OBJECTIVES: Acute compartment syndrome (CS) is a common complication of tibia shaft fractures (TSFs), and occurs when the pressure inside a myofascial compartment rises and impairs tissue perfusion. If treatment is delayed due to a missed diagnosis, amputation or permanent loss of function can result. This study aims to determine the incidence, clinical associations, and risk factors for missed CS following surgical stabilization of tibia shaft fractures (TSFs) using data from the National Trauma Data Bank (NTDB). METHODS: NTDB data files from 2007 to 2016 were accessed to collect information on patients undergoing surgical fixation of TSFs. Patients with an Injury Severity Score (ISS) > 15 or inferred Gustilo-Anderson IIIB/IIIC fractures were excluded to create a more homogenous sample of lower-grade TSFs. Compartment syndrome that was originally missed leading to late intervention was the main outcome under investigation. Bivariate tests were used to assess the relationships between missed CS and the preoperative variables. If a variable and a complication had an association with a P ≤ 0.2, it was included in a multivariate logistic regression model. RESULTS: A total of 184,612 patients met our inclusion criteria, and 1,269 patients (0.76%) had a missed CS diagnosis. Bivariate analysis demonstrated that male gender had a significant positive association with a missed CS diagnosis, while older age had a significant negative association (odds ratio [OR] = 2.17, 0.99; P < 0.001). Multivariate analysis revealed that male gender was the most significant independent risk factor for a missed diagnosis of compartment syndrome (OR = 1.84, P < 0.00001), followed by alcoholism, penetrating trauma, and smoking (OR = 1.51, 1.46, 1.43; P < 0.02). The only significant protective factor was open fracture (OR = 0.70, P < 0.0001). CONCLUSIONS: Our research identified several significant risk factors for missed CS after TSF, as well as positive and negative associations. Male gender, age, and lifestyle choices such as alcohol use and smoking conferred increased risks. These variables may assist physicians in identifying at-risk patients who may benefit from increased monitoring, and potentially prevent the high morbidity associated with this condition.

Neural Signatures of Handgrip Fatigue in Type 1 Diabetic Men and Women.

Type 1 diabetes (T1D) is associated with reduced muscular strength and greater muscle fatigability. Along with changes in muscular mechanisms, T1D is also linked to structural changes in the brain. How the neurophysiological mechanisms underlying muscle fatigue is altered with T1D and sex related differences of these mechanisms are still not well investigated. The aim of this study was to determine the impact of T1D on the neural correlates of handgrip fatigue and examine sex and T1D related differences in neuromuscular performance parameters, neural activation and functional connectivity patterns between the motor regions of the brain. Forty-two adults, balanced by condition (healthy vs T1D) and sex (male vs female), and performed submaximal isometric handgrip contractions until voluntary exhaustion. Initial strength, endurance time, strength loss, force variability, and complexity measures were collected. Additionally, hemodynamic responses from motor-function related cortical regions, using functional near-infrared spectroscopy (fNIRS), were obtained. Overall, females exhibited lower initial strength (p < 0.0001), and greater strength loss (p = 0.023) than males. While initial strength was significantly lower in the T1D group (p = 0.012) compared to the healthy group, endurance times and strength loss were comparable between the two groups. Force complexity, measured as approximate entropy, was found to be lower throughout the experiment for the T1D group (p = 0.0378), indicating lower online motor adaptability. Although, T1D and healthy groups fatigued similarly, only the T1D group exhibited increased neural activation in the left (p = 0.095) and right (p = 0.072) supplementary motor areas (SMA) over time. A sex × condition × fatigue interaction effect (p = 0.044) showed that while increased activation was observed in both T1D females and healthy males from the Early to Middle phase, this was not observed in healthy females or T1D males. These findings demonstrate that T1D adults had lower adaptability to fatigue which they compensated for by increasing neural effort. This study highlights the importance of examining both neural and motor performance signatures when investigating the impact of chronic conditions on neuromuscular fatigue. Additionally, the findings have implications for developing intervention strategies for training, rehabilitation, and ergonomics considerations for individuals with chronic conditions.

Transient Brachial Plexopathy After Fixation of a Clavicle Fracture Nonunion: A Case Report.

CASE: A 54-year-old man presented with a comminuted left midclavicle fracture that progressed to a symptomatic nonunion after nonsurgical management. Nonunion open reduction and internal fixation (ORIF) was performed, but a left brachial plexopathy developed 48 hours postoperatively. Imaging failed to demonstrate an emergent cause. The patient was monitored and completely recovered, with occasional neuralgia and mildly limited forward elevation of the shoulder. CONCLUSION: Development of a brachial plexopathy 48 hours after routine clavicle nonunion ORIF using plate fixation is an unusual complication. Future studies are needed to determine if this "wait-and-see" approach can be generalized to similar cases.