Miracle-dz/UniFAR-FTUs huggingface dataset:
Soft Tissue Knee Injury With Concomitant Osteochondral Fracture Is Associated With Higher Degree of Acute Joint Inflammation

Background: Osteochondral fractures are often seen on magnetic resonance imaging (MRI) of acutely injured knees, but their existence has gained little interest because of a lack of knowledge of their relation to treatment options and outcome. It is not clear whether acute phase synovial fluid (SF) concentrations of cartilage and bone markers and proinflammatory cytokines are different between traumatically injured knees with or without osteochondral fracture. Hypothesis: Acutely injured knees with an osteochondral fracture, particularly fractures with disrupted cortical bone, have higher concentrations of bone markers and cytokines than do knees without an osteochondral fracture. Study Design: Cross-sectional study; Level of evidence, 3. Methods: Synovial fluid (hemarthrosis) was aspirated (median 1 day after injury) and 1.5-T MRI was performed (median 8 days after injury) in the acutely injured knee of 98 individuals (26% women; mean age, 23 years). As visualized on MRI, 39% knees had an osteochondral fracture with disrupted cortical bone, 30% had an osteochondral fracture with intact cortical bone, and 32% did not have an osteochondral fracture. Concentrations of sulfated glycosaminoglycan, ARGS aggrecan, cartilage oligomeric matrix protein, osteocalcin, secreted protein acidic and rich in cysteine (SPARC), osteopontin and proinflammatory cytokines (interleukin [IL]–1β, IL-6, IL-8, and tumor necrosis factor [TNF]–α) were analyzed. Results: After adjusting for days between injury and SF aspiration, age at injury, and sex, knees with any osteochondral fracture (with or without disrupted cortical bone) had significantly higher SF concentrations of TNF-α (median [interquartile range (IQR)] = 9 [7-12] pg/mL vs 7 [5-14] pg/mL; P = . 013), whereas knees with an osteochondral fracture with disrupted cortical bone had significantly higher SF concentrations (medians [IQRs]) of SPARC (492 [328-754] ng/mL vs 407 [140-685] ng/mL; P = .030), IL-8 (278 [148-628] pg/mL vs 138 [67-413] pg/mL; P = .028), and TNF-α (11 [7-15] pg/mL vs 7 [5-14] pg/mL; P = .004) compared with knees without an osteochondral fracture. Conclusion: In acutely injured knees with hemarthrosis, a concomitant osteochondral fracture with disrupted cortical bone is associated with a higher degree of joint inflammation.
The productivity limit of manufacturing blood cell therapy in scalable stirred bioreactors

Manufacture of red blood cells (RBCs) from progenitors has been proposed as a method to reduce reliance on donors. Such a process would need to be extremely efficient for economic viability given a relatively low value product and high (2 × 1012) cell dose. Therefore, the aim of these studies was to define the productivity of an industry standard stirred‐tank bioreactor and determine engineering limitations of commercial red blood cells production. Cord blood derived CD34+ cells were cultured under erythroid differentiation conditions in a stirred micro‐bioreactor (Ambr™). Enucleated cells of 80% purity could be created under optimal physical conditions: pH 7.5, 50% oxygen, without gas‐sparging (which damaged cells) and with mechanical agitation (which directly increased enucleation). O2 consumption was low (~5 × 10–8 μg/cell.h) theoretically enabling erythroblast densities in excess of 5 × 108/ml in commercial bioreactors and sub‐10 l/unit production volumes. The bioreactor process achieved a 24% and 42% reduction in media volume and culture time, respectively, relative to unoptimized flask processing. However, media exchange limited productivity to 1 unit of erythroblasts per 500 l of media. Systematic replacement of media constituents, as well as screening for inhibitory levels of ammonia, lactate and key cytokines did not identify a reason for this limitation. We conclude that the properties of erythroblasts are such that the conventional constraints on cell manufacturing efficiency, such as mass transfer and metabolic demand, should not prevent high intensity production; furthermore, this could be achieved in industry standard equipment. However, identification and removal of an inhibitory mediator is required to enable these economies to be realized. Copyright © 2016 The Authors Journal of Tissue Engineering and Regenerative Medicine Published by John Wiley & Sons Ltd.
Tracking Hydrocarbon Plume Transport and Biodegradation at Deepwater Horizon

Diving into Deep Water The Deepwater Horizon oil spill in the Gulf of Mexico was one of the largest oil spills on record. Its setting at the bottom of the sea floor posed an unanticipated risk as substantial amounts of hydrocarbons leaked into the deepwater column. Three separate cruises identified and sampled deep underwater hydrocarbon plumes that existed in May and June, 2010—before the well head was ultimately sealed. Camilli et al. (p. 201; published online 19 August) used an automated underwater vehicle to assess the dimensions of a stabilized, diffuse underwater plume of oil that was 22 miles long and estimated the daily quantity of oil released from the well, based on the concentration and dimensions of the plume. Hazen et al. (p. 204; published online 26 August) also observed an underwater plume at the same depth and found that hydrocarbon-degrading bacteria were enriched in the plume and were breaking down some parts of the oil. Finally, Valentine et al. (p. 208; published online 16 September) found that natural gas, including propane and ethane, were also present in hydrocarbon plumes. These gases were broken down quickly by bacteria, but primed the system for biodegradation of larger hydrocarbons, including those comprising the leaking crude oil. Differences were observed in dissolved oxygen levels in the plumes (a proxy for bacterial respiration), which may reflect differences in the location of sampling or the aging of the plumes. In late June 2010, the Deepwater Horizon oil plume stretched more than 35 kilometers at a depth of 1100 meters. The Deepwater Horizon blowout is the largest offshore oil spill in history. We present results from a subsurface hydrocarbon survey using an autonomous underwater vehicle and a ship-cabled sampler. Our findings indicate the presence of a continuous plume of oil, more than 35 kilometers in length, at approximately 1100 meters depth that persisted for months without substantial biodegradation. Samples collected from within the plume reveal monoaromatic petroleum hydrocarbon concentrations in excess of 50 micrograms per liter. These data indicate that monoaromatic input to this plume was at least 5500 kilograms per day, which is more than double the total source rate of all natural seeps of the monoaromatic petroleum hydrocarbons in the northern Gulf of Mexico. Dissolved oxygen concentrations suggest that microbial respiration rates within the plume were not appreciably more than 1 micromolar oxygen per day.
Calcium-Permeable AMPA Receptor Dynamics Mediate Fear Memory Erasure

Wiping Out Memories Inhibition of fear responses can be unexpectedly reversed even when a subject is perfectly safe. This can lead to inappropriate reactions to a fear-associated trigger, such as a bright light or loud noise. This type of reaction appears to underpin posttraumatic stress disorder, but there is little understanding of when training to inhibit fear may fail or succeed. Using a combination of electrophysiology and behavioral training in mice, Clem and Huganir (p. 1108, published online 28 October) observed that fear conditioning increased synaptic transmission by calcium-permeable AMPA receptors into the part of the brain that controls emotional responses (the amygdala). This effect lasted for about a week, during which the fearful memories could be erased if the animals were trained to reduce conditioned fear responses. Postmortem brain slices showed that the fear-induced synaptic changes also reversed, except in transgenic mice with a mutant subunit of the AMPA receptor. The subunit composition of AMPA receptors at lateral amygdala synapses changes after the acquisition of associative fear. Traumatic fear memories can be inhibited by behavioral therapy for humans, or by extinction training in rodent models, but are prone to recur. Under some conditions, however, these treatments generate a permanent effect on behavior, which suggests that emotional memory erasure has occurred. The neural basis for such disparate outcomes is unknown. We found that a central component of extinction-induced erasure is the synaptic removal of calcium-permeable α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs) in the lateral amygdala. A transient up-regulation of this form of plasticity, which involves phosphorylation of the glutamate receptor 1 subunit of the AMPA receptor, defines a temporal window in which fear memory can be degraded by behavioral experience. These results reveal a molecular mechanism for fear erasure and the relative instability of recent memory.
Side effect and disease related symptom representations among HIV+ adults on antiretroviral therapy

Aversive side effects from medical treatments can seem as challenging a coping demand as the health condition being treated. A clear framework for understanding how individuals taking treatment differentially understand and approach side effects from treatment and symptoms of disease is needed. Guided by Leventhal's Self Regulation Model, the present study investigates how cognitive and emotional representations of physical problems relate to quality of life (QOL) and adherence to care outcomes in the context of HIV treatment. A sample of 109 HIV + adults on highly active antiretroviral treatment (HAART) were interviewed using self- and interviewer-administered measures of side effect and disease-symptom representations, health-related QOL, and adherence to HAART. Results suggest that (1) side effects of disease are as important as symptoms of illness in their relationships with QOL, (2) studying an individual physical complaint in depth explains such symptoms' associations with QOL better than aggregate symptom and side effect checklists alone, and (3) the Self Regulation Model offers a useful framework from which to evaluate and intervene upon side effect and symptom related experiences. Findings offer guidance for research and clinical practice.
Symbiotic Bacterium Modifies Aphid Body Color

Turncoat Aphids Aphid color has consequences for the fate of the wearer: Coccinellid beetles prefer to eat red ones and parasitoid wasps attack green ones. What might happen if aphids could change color and outwit their predators? Tsuchida et al. (p. 1102) have found that a subpopulation of the pea aphid can do this, but not without help from a previously unknown species of bacterium that lives intimately with the aphid as an endosymbiont and makes red aphids turn green. The bacterium interferes with host pigment biosynthesis—itself borrowed from fungi long ago in evolution—to stimulate blue-green pigment production as the aphid larva matures, turning the red nymph into a green adult. The ecological consequences of this about-turn of color have yet to be tested, but other studies have shown a variety of effects on aphid behavior mediated by endosymbionts in response to adaptation to different food plants, temperature tolerance, and predator avoidance. Infection with a symbiotic bacterium leads to a spectacular phenotypic change in its host, making red aphids turn green. Color variation within populations of the pea aphid influences relative susceptibility to predators and parasites. We have discovered that infection with a facultative endosymbiont of the genus Rickettsiella changes the insects’ body color from red to green in natural populations. Approximately 8% of pea aphids collected in Western Europe carried the Rickettsiella infection. The infection increased amounts of blue-green polycyclic quinones, whereas it had less of an effect on yellow-red carotenoid pigments. The effect of the endosymbiont on body color is expected to influence prey-predator interactions, as well as interactions with other endosymbionts.
The 1μg short Synacthen test in chronic fatigue syndrome

Many studies suggest mild hypocortisolism in chronic fatigue syndrome (CFS), usually assumed to be due to reduced suprahypothalamic drive to the hypothalamo‐pituitary‐adrenal (HPA) axis. We wished to explore further the state of the HPA axis in CFS using the 1 μg low dose short Synacthen test.
Structural Basis of Biological N2O Generation by Bacterial Nitric Oxide Reductase

Dissecting Nitric Oxide Reductase Bacterial breakdown of nitrogen compounds in soil and the oceans provides the largest emission source of the greenhouse gas, nitrous oxide (N2O). A key enzyme in this process is nitric oxide reductase (NOR), which catalyzes the reduction of nitric oxide (NO) to N2O. Hino et al. (p. 1666, published online 25 November; see the Perspective by Moënne-Loccoz and Fee) now describe the crystal structure of NOR from Pseudomonas aeruginosa. Consistent with their evolutionary relatedness, the transmembrane region topology and arrangement of metal centers in NOR are similar to those in cytochrome oxidases, key enzymes in aerobic respiration. A structural comparison gives insight into the features that allow conversion between nitric oxide and oxygen reduction. Nitric oxide reductase (NOR) is an iron-containing enzyme that catalyzes the reduction of nitric oxide (NO) to generate a major greenhouse gas, nitrous oxide (N2O). Here, we report the crystal structure of NOR from Pseudomonas aeruginosa at 2.7 angstrom resolution. The structure reveals details of the catalytic binuclear center. The non-heme iron (FeB) is coordinated by three His and one Glu ligands, but a His-Tyr covalent linkage common in cytochrome oxidases (COX) is absent. This structural characteristic is crucial for NOR reaction. Although the overall structure of NOR is closely related to COX, neither the D- nor K-proton pathway, which connect the COX active center to the intracellular space, was observed. Protons required for the NOR reaction are probably provided from the extracellular side.
Glenoid Bone Loss in the Setting of an Anterior Labroligamentous Periosteal Sleeve Avulsion Tear

Background: Glenoid bone loss is a factor that has been inversely associated with the success of shoulder instability repair. Recently, patients with an anterior labroligamentous periosteal sleeve avulsion (ALPSA) lesion have also been identified as having a higher failure rate after surgical repair. Purpose: To determine differences in the amount of glenoid bone loss and to compare demographic factors of instability in patients with and without ALPSA tears. Study Design: Case-control study; Level of evidence, 3. Methods: Over a 3-year period, all patients (N = 83) who were treated for anterior shoulder instability at a single institution were reviewed retrospectively. A total of 39 (47%) were identified as having an ALPSA lesion and 44 (53%) as having no ALPSA tear. Glenoid bone loss was determined in 2 ways: (1) radiographically by 3-dimensional computed tomography (3D CT) (humeral head digitally subtracted by 3 blinded observers) and (2) with arthroscopic techniques at the time of surgery. Demographic data such as the time from the initial instability event to advanced imaging and surgery were noted. These data were then analyzed with the Student t test to determine any significant differences between the 2 groups. Results: The patients with an ALPSA lesion had more preoperative instability events than those without (8.2 vs 3.6, respectively; P = .04). The mean glenoid bone loss measured by 3D CT was 12.7% (range, 0%-22.3%) for those with ALPSA tears versus 6.25% (range, 0%-23.1%) for those without (P = .002). The mean duration of total instability for those with ALPSA tears was 42.9 months versus 46.3 months for those without (P = .95). Lastly, the mean bone loss based on arthroscopic measures was 11.4% for patients with ALPSA tears and 4.3% for those without ALPSA tears (P = .017). From the existing magnetic resonance imaging/arthrography scans reviewed, 82% of patients could be correctly identified as having an ALPSA lesion. Conclusion: Patients with anterior shoulder instability who have an ALPSA lesion have nearly twice the amount of glenoid bone loss as those with a standard Bankart tear (no ALPSA lesion). Patients with ALPSA lesions had statistically more instability events, and this may be an additional factor in either developing an ALPSA lesion or glenoid bone loss or both.
Motor Control by Sensory Cortex

By a Whisker Every student learns that the sensory cortex is used for processing sensation and the motor cortex is used for perceiving movement. However, in the real world, this may not always be so neatly arranged. Matyas et al. (p. 1240) have found that sensory and motor fields are specialized for different types of movement, such that in mice the motor cortex controlled the forward movement (protraction) of their whiskers and the sensory cortex controlled backwards movements (retraction) of whiskers. So if a whisker hits an object, then a reasonable first reaction might be a motor command for retraction. Similarly, the motor cortex stimulates protraction for more active exploration. Hence, the sensory cortex is also motor and the motor cortex is also sensory. In an ecological context, these combined reactions offer a repertoire useful for a mouse seeking food and shelter in a complex environment. Mouse whisker movements are controlled by both the sensory and motor cortex. Classical studies of mammalian movement control define a prominent role for the primary motor cortex. Investigating the mouse whisker system, we found an additional and equally direct pathway for cortical motor control driven by the primary somatosensory cortex. Whereas activity in primary motor cortex directly evokes exploratory whisker protraction, primary somatosensory cortex directly drives whisker retraction, providing a rapid negative feedback signal for sensorimotor integration. Motor control by sensory cortex suggests the need to reevaluate the functional organization of cortical maps.
Stereological Quantification of Immune-Competent Cells in Baseline Biopsy Specimens From Achilles Tendons

Background: Limited data exist on the presence and function of immune-competent cells in chronic tendinopathic tendons and their potential role in inflammation and tissue healing as well as in predicting long-term outcome. Purpose: To quantify subtypes of immune-competent cells in biopsy specimens from nonruptured chronic tendinopathic Achilles tendons and healthy control tendons. In addition, to examine whether findings in baseline cell biopsy specimens can predict the long-term presence of Achilles tendon symptoms. Study Design: Cross-sectional and case-control study; Level of evidence, 3. Methods: Fifty patients with nonruptured chronic Achilles tendinopathy and 15 healthy participants were included. At time of inclusion, an ultrasound examination was performed immediately before an ultrasound-guided Achilles tendon biopsy specimen was obtained. Tissue samples were evaluated immunohistochemically by quantifying the presence of macrophages (CD68-PGM1+, CD68-KP1+), hemosiderophages (Perls blue), T lymphocytes (CD2+, CD3+, CD4+, CD7+, CD8+), B lymphocytes (CD20+), natural killer cells (CD56+), mast cells (NaSDCl+), Schwann cells (S100+), and endothelial cells (CD34+) using a stereological technique. A follow-up examination was conducted more than 4 years (range, 4-9 years) after the biopsy procedure to evaluate the long-term presence of Achilles tendon symptoms. Results: Macrophages, T lymphocytes, mast cells, and natural killer cells were observed in the majority (range, 52%-96%) of biopsy specimens from nonruptured chronic tendinopathic Achilles tendons. CD68-KP1+ macrophages (0.29% vs 0; P = .005) and CD34+ endothelial cells (3% vs 0.97%; P = .04) were significantly more numerous in tendinopathic tendons compared with healthy tendons. The presence of iron+ hemosiderophages was more frequently observed in biopsy specimens obtained from the group who was asymptomatic at follow-up compared with the symptomatic group (42% vs 5%; P = .02). Conclusion: This study provides evidence for the presence of immune-competent cells in the majority of biopsy specimens from nonruptured chronic tendinopathic Achilles tendons. Macrophages and endothelial cells were significantly more numerous in tendinopathic tendons than in healthy tendons. The presence of iron+ hemosiderophages in baseline biopsy specimens was associated with a good prognosis. Clinical Relevance: New insight into the role of immune-competent cells in chronic Achilles tendinopathy.
Does Decreased Meniscal Thickness Affect Surgical Outcomes After Medial Meniscectomy?

Background: There have been no clinical studies regarding the effect of decreased meniscal thickness on outcomes after meniscectomy. Purpose: To examine the postoperative outcomes of partial meniscectomy with or without horizontal resection compared with the outcomes of subtotal meniscectomy and to evaluate the influence of decreased thickness of the medial meniscus on outcomes after partial meniscectomy. Study Design: Cohort study; Level of evidence, 3. Methods: A total of 312 patients who underwent medial meniscectomy were retrospectively reviewed. Patients were divided into 3 groups: group A (n = 84) included patients with partial meniscectomy with vertical resection, group B (n = 140) consisted of those with partial meniscectomy with horizontal resection, and group C (n = 88) included those with subtotal meniscectomy. Clinical function was evaluated by use of the Lysholm knee scoring scale, International Knee Documentation Committee (IKDC) subjective knee evaluation form, and Tapper and Hoover grading system. Radiologic evaluation was performed with the IKDC radiographic assessment scale as well as with measurements of the medial compartment height at the tibiofemoral joint. Preoperative values and postoperative values measured 5 years after operation were assessed. Results: Functional outcomes in group C were inferior to those in groups A and B according to the Lysholm knee score (mean ± SD for group A = 96.1 ± 4.7, group B = 94.9 ± 5.2, group C = 84.8 ± 11.4; P < .001), IKDC subjective score (group A = 92.1 ± 6.5, group B = 91.3 ± 8.8, group C = 81 ± 11.4; P < .001), and Tapper and Hoover grading system (P = .003). There was no significant difference in scores between groups A and B. With regard to radiologic evaluation, the IKDC radiographic grade for group C was worse than the grades for groups A and B (P < .001); there was no significant difference between groups A and B. However, the postoperative joint space on the affected side was higher for group A (4.7 ± 0.6 mm) than for groups B (4.3 ± 0.5 mm; P < .001) and C (3.7 ± 0.8 mm; P < .001). The joint space was higher in group B than in group C (P < .001). Conclusion: Despite joint space narrowing, decreases in meniscal thickness after partial meniscectomy for horizontal tear had no additional adverse effect on 5-year functional and radiographic outcomes compared with conventional partial meniscectomy preserving whole meniscal thickness. In treating horizontal tears of the meniscus, partial meniscectomy with complete resection of the unstable leaf was an effective method in a 5-year follow-up study.