It is becoming increasingly clear that the community of microorganisms living in the mammalian gut (the gut microbiota) exerts a significant influence on brain function. Evidence suggests that the microbiota plays a role in anxiety and anxiety-like behavior in animal models. Several studies have demonstrated reduced anxiety-like behavior with administration of probiotics (live bacteria with known health benefits), but less work has been done to investigate the potential anxiolytic effects of prebiotics (dietary substances that promote probiotics already residing in the gut). Prebiotics have several advantages over probiotics as an intervention against anxiety. We tested the effects of a diet containing prebiotics on anxiety-like symptoms in male Fischer 344 rats, including behavior in the open field test, corticosterone levels, and the weights of the adrenals, spleen, and thymus. One group of animals consumed the prebiotic diet for approximately 4 weeks and underwent behavioral testing during adolescence; another group consumed the diet for 6 weeks and underwent testing during adulthood. Animals who consumed the prebiotic diet displayed anxiolytic-like behavior in the open field test regardless of age, spending more time in the aversive open center of the field compared to controls. These animals also exhibited reduced relative adrenal and spleen weight. Interestingly, relative adrenal weight was inversely correlated with time spent in the center of the field during the open field test in adult rats. These results suggest an anxiolytic effect of dietary prebiotics. Further investigation is required to determine what changes in the microbiota, metabolome, and brain may have accompanied this anxiolytic effect.
Severe, repeated or chronic stress produces negative health outcomes including disruptions of the sleep/wake cycle and gut microbial dysbiosis. Diets rich in prebiotics and glycoproteins impact the gut microbiota and may increase gut microbial species that reduce the impact of stress. This experiment tested the hypothesis that consumption of dietary prebiotics, lactoferrin (Lf) and milk fat globule membrane (MFGM) will reduce the negative physiological impacts of stress. Male F344 rats, postnatal day (PND) 24, received a diet with prebiotics, Lf and MFGM (test) or a calorically matched control diet. Fecal samples were collected on PND 35/70/91 for 16S rRNA sequencing to examine microbial composition and, in a subset of rats; Lactobacillus rhamnosus was measured using selective culture. On PND 59, biotelemetry devices were implanted to record sleep/wake electroencephalographic (EEG). Rats were exposed to an acute stressor (100, 1.5 mA, tail shocks) on PND 87 and recordings continued until PND 94. Test diet, compared to control diet, increased fecal Lactobacillus rhamnosus colony forming units (CFU), facilitated non-rapid eye movement (NREM) sleep consolidation (PND 71/72) and enhanced rapid eye movement (REM) sleep rebound after stressor exposure (PND 87). Rats fed control diet had stress-induced reductions in alpha diversity and diurnal amplitude of temperature, which were attenuated by the test diet (PND 91). Stepwise multiple regression analysis revealed a significant linear relationship between early-life Deferribacteres (PND 35) and longer NREM sleep episodes (PND 71/72). A diet containing prebiotics, Lf and MFGM enhanced sleep quality, which was related to changes in gut bacteria and modulated the impact of stress on sleep, diurnal rhythms and the gut microbiota.
Hip-knee coupling is a well-documented phenomenon, and interventions to one joint can alter biomechanics at the other. The purpose of this study was to investigate if knee surgery is associated with later onset of femoroacetabular impingement syndrome (FAIS).
The purpose of this study was to analyze the relationship between the intra-articular inflammatory response and any associated systemic inflammatory response following knee injury requiring operative management. Patients undergoing primary knee arthroscopy provided synovial fluid, blood, and urine samples immediately prior to surgery. Samples were analyzed using a multiplex magnetic bead immunoassay for the concentrations of cytokines and growth factors that have been shown to be associated with post-injury inflammation. One hundred and fifty-one patients undergoing arthroscopic management of meniscus, ACL, and focal chondral lesions were included in the analysis. After correction for multiple tests, there were no statistically significant correlations between synovial fluid biomarkers and biomarkers in plasma or urine for any of the intra-articular pathologies assessed. This analysis suggests that the most accurate measurement of the post-injury inflammatory response must be sampled from the intra-articular space. In the post-traumatic knee, there is no substitute for synovial fluid biomarker analysis.
The purpose of this study was to evaluate the association between timing of nerve repair and the ability to perform a primary nerve repair versus a bridge repair requiring the use of allograft, autograft, or a conduit in lacerated upper extremity peripheral nerve injuries.This is a retrospective case-control study of patients who underwent upper extremity nerve repair for lacerated peripheral nerves identified by Current Procedural Terminology codes. Timing of injury and surgery, as well as other information such as demographic information, mechanism of injury, site of injury, and type of nerve repair, was recorded. The odds of a patient requiring bridge repair based on the duration of time between injury and surgery was evaluated using logistic regression.A total of 403 nerves in 335 patients (mean age 35.87 ± 15.33 years) were included. In all, 241 nerves were primarily repaired and 162 required bridge repair. Patients requiring bridge repair had a greater duration between injury and surgery compared with patients who underwent primary repair. Furthermore, the nerves requiring bridge repair were associated with a greater gap compared with the nerves repaired primarily. Based on logistic regression, each 1-day increase in duration between injury and surgery was associated with a 3% increase in the odds of requiring bridge repair.There is no defined critical window to achieve a primary nerve repair following injury. This study demonstrated that nerve injuries requiring bridge repair were associated with a significantly greater delay to surgery.
Stressor exposure can produce disruptions in sleep that may contribute to altered behavioral phenotypes. Prebiotics can selectively promote the expansion of microbial species in the mammalian gut that may increase stress robustness. Previous studies showed that a prebiotic blend of polydextrose (PDX) and galactooligosaccharides (GOS) increase Bifidobacterium spp. and Lactobacillus spp. in fecal samples. In this study, we hypothesized that an experimental diet would modulate the sleep cycle and protect sleep architecture following stress. Male F344 rats, postnatal day 24 (P24), were placed on either a diet containing a prebiotic blend of PDX and GOS with bioactive whey protein fractions (TEST) or a control diet. Fecal samples were collected and telemetry devices were implanted to examine differences in sleep across development. Rats were exposed to an acute stressor on P87 to examine the effects of the TEST diet on stress-induced disruptions of sleep. Rats fed the TEST diet, when compared with rats fed the control diet, had equal weight gain and greater NREM sleep consolidation in early adulthood. Rats fed the TEST diet also displayed enhanced REM rebound after stress. These results demonstrate that the selected dietary factors can increase NREM sleep consolidation and protect against REM sleep disruptions. Future research will examine if other functional outcomes, such as cognitive processes, may be associated with these changes in sleep parameters.
Regular physical activity produces resistance to the negative health consequences of stressor exposure. One way that exercise may confer stress resistance is by reducing the impact of stress on diurnal rhythms and sleep; disruptions of which contribute to stress-related disease including mood disorders. Given the link between diurnal rhythm disruptions and stress-related disorders and that exercise both promotes stress resistance and is a powerful non-photic biological entrainment cue, we tested if wheel running could reduce stress-induced disruptions of sleep/wake behavior and diurnal rhythms. Adult, male F344 rats with or without access to running wheels were instrumented for biotelemetric recording of diurnal rhythms of locomotor activity, heart rate, core body temperature (CBT), and sleep (i.e. REM, NREM, and WAKE) in the presence of a 12 h light/dark cycle. Following 6 weeks of sedentary or exercise conditions, rats were exposed to an acute stressor known to disrupt diurnal rhythms and produce behaviors associated with mood disorders. Prior to stressor exposure, exercise rats had higher CBT, more locomotor activity during the dark cycle, and greater %REM during the light cycle relative to sedentary rats. NREM and REM sleep were consolidated immediately following peak running to a greater extent in exercise, compared to sedentary rats. In response to stressor exposure, exercise rats expressed higher stress-induced hyperthermia than sedentary rats. Stressor exposure disrupted diurnal rhythms in sedentary rats; and wheel running reduced these effects. Improvements in sleep and reduced diurnal rhythm disruptions following stress could contribute to the health promoting and stress protective effects of exercise.
