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Journal of Functional Morphology and... Dec 2019During pregnancy, a number of biomechanical and hormonal changes occur that can alter spinal curvature, balance, and gait patterns by affecting key areas of the human... (Review)
Review
During pregnancy, a number of biomechanical and hormonal changes occur that can alter spinal curvature, balance, and gait patterns by affecting key areas of the human body. This can greatly impact quality of life (QOL) by increasing back pain and the risk of falls. These effects are likely to be the ultimate result of a number of hormonal and biomechanical changes that occur during pregnancy. Research Question and Methodology: Using the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines, this systematic review sets out to analyse all available literature relating to the biomechanics factors caused by pregnancy and assess how this might reduce QOL. Fifty papers were deemed eligible for inclusion in this review based on the PUBMED and SCOPUS databases. Results: Angles of lordosis and kyphosis of the spine are significantly increased by pregnancy, but not consistently across all studies. Back pain is significantly increased in pregnant women, although this is not significantly correlated with spinal changes. Increased movements of centre of pressure (COP) and increased stability indexes indicate postural control is reduced in pregnancy. Trunk range of motion, hip flexion, and extension are reduced, as well as decreased stride length, decreased gait velocity, and increased step width; again, not consistently. It is likely that each woman adopts unique techniques to minimise the effects, for example increasing step width to improve balance. Further research should focus on how altered limb kinematics during gait might affect QOL by influencing the human body, as well as assessing parameters in all planes to develop a wider understanding of pregnant biomechanical alterations.
PubMed: 33467386
DOI: 10.3390/jfmk4040072 -
Shock (Augusta, Ga.) Mar 2016Cells of the innate and adaptive immune systems play a critical role in the host response to sepsis. Moreover, their accessibility for sampling and their capacity to... (Review)
Review
Cells of the innate and adaptive immune systems play a critical role in the host response to sepsis. Moreover, their accessibility for sampling and their capacity to respond dynamically to an acute threat increases the possibility that leukocytes might serve as a measure of a systemic state of altered responsiveness in sepsis.The working group of the 14th Acute Dialysis Quality Initiative (ADQI) conference sought to obtain consensus on the characteristic functional and phenotypic changes in cells of the innate and adaptive immune system in the setting of sepsis. Techniques for the study of circulating leukocytes were also reviewed and the impact on cellular phenotypes and leukocyte function of nonextracorporeal treatments and extracorporeal blood purification therapies proposed for sepsis was analyzed.A large number of alterations in the expression of distinct neutrophil and monocyte surface markers have been reported in septic patients. The most consistent alteration seen in septic neutrophils is their activation of a survival program that resists apoptotic death. Reduced expression of HLA-DR is a characteristic finding on septic monocytes, but monocyte antimicrobial function does not appear to be significantly altered in sepsis. Regarding adaptive immunity, sepsis-induced apoptosis leads to lymphopenia in patients with septic shock and it involves all types of T cells (CD4, CD8, and Natural Killer) except T regulatory cells, thus favoring immunosuppression. Finally, numerous promising therapies targeting the host immune response to sepsis are under investigation. These potential treatments can have an effect on the number of immune cells, the proportion of cell subtypes, and the cell function.
Topics: Animals; Apoptosis; Humans; Immunity, Cellular; Immunity, Innate; Immunosuppression Therapy; Sepsis; T-Lymphocytes
PubMed: 26529661
DOI: 10.1097/SHK.0000000000000495 -
Gait & Posture Oct 2022Forward head posture (FHP) is a common postural deviation. An increasing number of studies have reported that people with FHP present with impaired postural control and... (Review)
Review
BACKGROUND
Forward head posture (FHP) is a common postural deviation. An increasing number of studies have reported that people with FHP present with impaired postural control and gait; however, there is conflicting evidence. A systematic review focusing on these relationships has been unavailable to date.
RESEARCH QUESTION
Is there a relationship between FHP, postural control and gait?
METHODS
This systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) statement (PROSPERO ID: CRD42021231908). Web of Science, PubMed, Scopus, and CINAHL Plus (via EBSCO) were systematically searched, and a manual search was performed using the reference lists of included studies. Eligible studies included observational studies addressing the relationship between FHP, postural control and/or gait. Quality assessment was conducted using the Joanna Briggs Institute Critical Appraisal Checklist for Cross-Sectional Studies.
RESULTS
Nineteen studies were selected for this review. Consistent evidence supported that people with FHP had significant alterations in limits of stability (n = 3), performance-based balance (n = 3), and cervical proprioception (n = 4). Controversial evidence existed for a relationship of FHP with static balance (n = 4) and postural stability control (n = 4). Limited evidence existed to support an alteration in gait and vestibular function. Three studies on induced FHP consistently identified no reduced postural control.
SIGNIFICANCE
Current evidence supports an association between FHP and a detrimental alteration in limits of stability, performance-based balance, and cervical proprioception. Instead of simply indicating impaired overall balance, the findings of this review indicate that a reduction in specific aspects of the postural control requires to be clarified in clinical evaluation for individuals with FHP, which would facilitate the planning and application of appropriate interventions to prevent dysfunctions and disability.
Topics: Humans; Posture; Cross-Sectional Studies; Postural Balance; Gait; Neck
PubMed: 36274469
DOI: 10.1016/j.gaitpost.2022.10.008 -
Beneficial Microbes Mar 2019The gut microbiota contributes to host energy metabolism, and altered gut microbiota has been associated with obesity-related metabolic disorders. We previously reported... (Clinical Trial)
Clinical Trial Randomized Controlled Trial
The gut microbiota contributes to host energy metabolism, and altered gut microbiota has been associated with obesity-related metabolic disorders. We previously reported that a probiotic alone or together with a prebiotic controls body fat mass in healthy overweight or obese individuals in a randomised, double-blind, placebo controlled clinical study (ClinicalTrials.gov NCT01978691). We now aimed to investigate whether changes in the gut microbiota may be associated with the observed clinical benefits. Faecal and plasma samples were obtained from a protocol compliant subset (n=134) of participants from a larger clinical study where participants were randomised (1:1:1:1) into four groups: (1) placebo, 12 g/d microcrystalline cellulose; (2) Litesse® Ultra™ polydextrose (LU), 12 g/day; (3) Bifidobacterium animalis subsp. lactis 420™ (B420), 10 cfu/d in 12 g microcrystalline cellulose; (4) LU+B420, 1010 cfu/d of B420 in 12 g/d LU for 6 months of intervention. The faecal microbiota composition and metabolites were assessed as exploratory outcomes at baseline, 2, 4, 6 months, and +1 month post-intervention and correlated to obesity-related clinical outcomes. Lactobacillus and Akkermansia were more abundant with B420 at the end of the intervention. LU+B420 increased Akkermansia, Christensenellaceae and Methanobrevibacter, while Paraprevotella was reduced. Christensenellaceae was consistently increased in the LU and LU+B420 groups across the intervention time points, and correlated negatively to waist-hip ratio and energy intake at baseline, and waist-area body fat mass after 6 months treatment with LU+B420. Functional metagenome predictions indicated alterations in pathways related to cellular processes and metabolism. Plasma bile acids glycocholic acid, glycoursodeoxycholic acid, and taurohyodeoxycholic acid and tauroursodeoxycholic acid were reduced in LU+B420 compared to Placebo. Consumption of B420 and its combination with LU resulted in alterations of the gut microbiota and its metabolism, and may support improved gut barrier function and obesity-related markers.
Topics: Adult; Aged; Bacteria; Body Fat Distribution; Double-Blind Method; Feces; Female; Gastrointestinal Microbiome; Humans; Male; Metabolomics; Metagenomics; Microbiota; Middle Aged; Obesity; Overweight; Placebos; Probiotics; Synbiotics; Treatment Outcome
PubMed: 30525950
DOI: 10.3920/BM2018.0028 -
Cell Aug 2014Acquisition of the intestinal microbiota begins at birth, and a stable microbial community develops from a succession of key organisms. Disruption of the microbiota...
Acquisition of the intestinal microbiota begins at birth, and a stable microbial community develops from a succession of key organisms. Disruption of the microbiota during maturation by low-dose antibiotic exposure can alter host metabolism and adiposity. We now show that low-dose penicillin (LDP), delivered from birth, induces metabolic alterations and affects ileal expression of genes involved in immunity. LDP that is limited to early life transiently perturbs the microbiota, which is sufficient to induce sustained effects on body composition, indicating that microbiota interactions in infancy may be critical determinants of long-term host metabolic effects. In addition, LDP enhances the effect of high-fat diet induced obesity. The growth promotion phenotype is transferrable to germ-free hosts by LDP-selected microbiota, showing that the altered microbiota, not antibiotics per se, play a causal role. These studies characterize important variables in early-life microbe-host metabolic interaction and identify several taxa consistently linked with metabolic alterations. PAPERCLIP:
Topics: Animals; Anti-Bacterial Agents; Bacteria; Disease Models, Animal; Female; Intestinal Mucosa; Intestines; Male; Mice; Mice, Inbred C57BL; Microbiota; Obesity; Penicillins
PubMed: 25126780
DOI: 10.1016/j.cell.2014.05.052 -
Frontiers in Psychiatry 2022The current epistemology of autism as a phenotype derives from the consistency of historical accounts and decades of work within the tradition of descriptive... (Review)
Review
The current epistemology of autism as a phenotype derives from the consistency of historical accounts and decades of work within the tradition of descriptive epidemiology, culminating in current categorical descriptions within DSM and ICD nosologies and the concept of "prototypical autism." The demonstrated high heritability of this phenotype has led to an essentialist theory of autism as a biological entity and the concerted search within the developmental brain and genetic science for discrete biological markers. This search has not revealed simple markers explaining autistic outcomes and has led to moves towards a more dimensional account. This article proposes an alternative transactional approach. It proposes to understand autistic states as an emergent property within a complex developmental system; as the neurodivergent brain, and mind and body, encounter their social and physical environment within early development. Key evidence in support of this approach comes from random allocation intervention trials based on such transactional development theory, both in the infancy pre-diagnostic prodrome and the early post-diagnostic period. In replicated evidence, these intervention trials show that a targeted alteration in the quality of social transactional environment available for the child leads to significant, predictable, and sustained alterations in the outcome dimensional autistic phenotype over time; and further, in one prodromal trial, to a significant reduction in later categorical classification status. The inference from this evidence is that the prototypical autistic phenotype is to a degree malleable with a changed experienced social environment and that it is emergent from its constituent traits. Such a transactional approach enlarges our notion of the phenotype and brings the study of autism within mainstream individual difference developmental science. It challenges essentialist views, for instance as to intrinsic autistic "social avoidance" or theory of mind empathy deficits, integrates dimensional and categorical perspectives, and is consistent with the lived experience of autistic people and their advocacy for improved understanding within a social model.
PubMed: 36304560
DOI: 10.3389/fpsyt.2022.988755 -
Frontiers in Cellular and Infection... 2023Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has infected a substantial portion of the world's population, and novel consequences of COVID-19 on the... (Meta-Analysis)
Meta-Analysis
INTRODUCTION
Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has infected a substantial portion of the world's population, and novel consequences of COVID-19 on the human body are continuously being uncovered. The human microbiome plays an essential role in host health and well-being, and multiple studies targeting specific populations have reported altered microbiomes in patients infected with SARS-CoV-2. Given the global scale and massive incidence of COVID on the global population, determining whether the effects of COVID-19 on the human microbiome are consistent and generalizable across populations is essential.
METHODS
We performed a synthesis of human microbiome responses to COVID-19. We collected 16S rRNA gene amplicon sequence data from 11 studies sampling the oral and nasopharyngeal or gut microbiome of COVID-19-infected and uninfected subjects. Our synthesis included 1,159 respiratory (oral and nasopharyngeal) microbiome samples and 267 gut microbiome samples from patients in 11 cities across four countries.
RESULTS
Our reanalyses revealed communitywide alterations in the respiratory and gut microbiomes across human populations. We found significant overall reductions in the gut microbial diversity of COVID-19-infected patients, but not in the respiratory microbiome. Furthermore, we found more consistent community shifts in the gut microbiomes of infected patients than in the respiratory microbiomes, although the microbiomes in both sites exhibited higher host-to-host variation in infected patients. In respiratory microbiomes, COVID-19 infection resulted in an increase in the relative abundance of potentially pathogenic bacteria, including .
DISCUSSION
Our findings shed light on the impact of COVID-19 on the human-associated microbiome across populations, and highlight the need for further research into the relationship between long-term effects of COVID-19 and altered microbiota.
Topics: Humans; COVID-19; SARS-CoV-2; RNA, Ribosomal, 16S; Microbiota; Gastrointestinal Microbiome
PubMed: 37600938
DOI: 10.3389/fcimb.2023.1211348 -
Obstetrical & Gynecological Survey Oct 2015Several different bodies of evidence support a link between infection and altered brain development. Maternal infections, such as influenza and human immunodeficiency... (Review)
Review
Several different bodies of evidence support a link between infection and altered brain development. Maternal infections, such as influenza and human immunodeficiency virus, have been linked to the development of autism spectrum disorders, differences in cognitive test scores, and bipolar disorder; an association that has been shown in both epidemiologic and retrospective studies. Several viral, bacterial, and parasitic illnesses are associated with alterations in fetal brain structural anomalies including brain calcifications and hydrocephalus. The process of infection can activate inflammatory pathways causing the release of various proinflammatory biomarkers and histological changes consistent with an infectious intrauterine environment (chorioamnionitis) or umbilical cord (funisitis). Elevations in inflammatory cytokines are correlated with cerebral palsy, schizophrenias, and autism. Animal studies indicate that the balance of proinflammatory and anti-inflammatory cytokines is critical to the effect prenatal inflammation plays in neurodevelopment. Finally, chorioamnionitis is associated with cerebral palsy and other abnormal neurodevelopmental outcomes. In conclusion, a plethora of evidence supports, albeit with various degrees of certainty, the theory that maternal infection and inflammation that occur during critical periods of fetal development could theoretically alter brain structure and function in a time-sensitive manner.
Topics: Animals; Brain; Brain Diseases; Female; Fetal Development; Humans; Pregnancy; Pregnancy Complications, Infectious
PubMed: 26490164
DOI: 10.1097/OGX.0000000000000236 -
Comprehensive Physiology Oct 2014In patients with impaired inspiratory muscle function or altered respiratory system mechanics, an imbalance between load and capacity can arise. The ventilatory control... (Review)
Review
In patients with impaired inspiratory muscle function or altered respiratory system mechanics, an imbalance between load and capacity can arise. The ventilatory control system normally compensates for this by increasing drive to maintain adequate alveolar ventilation levels, thereby keeping arterial CO2 within its normal range. To reduce work of breathing, a pattern of reduced tidal volume and increased respiratory rate occurs. This pattern itself may eventually reduce effective ventilation by increasing dead space ventilation. However, the impact of sleep on breathing and its role in the development of diurnal respiratory failure is often overlooked in this process. Sleep not only reduces respiratory drive, but also diminishes chemoresponsiveness to hypoxia and hypercapnia creating an environment where significant alterations in oxygenation and CO2 can occur. Acute increases in CO2 load especially during rapid eye movement sleep can initiate the process of bicarbonate retention which further depresses ventilatory responsiveness to CO2. Treatment of hypoventilation needs to be directed toward factors underlying its development. Nocturnal noninvasive positive pressure therapy is the most widely used and reliable strategy currently available to manage hypoventilation syndromes. Although this may not consistently alter respiratory muscle strength or the mechanical properties of the respiratory system, it does appear to reset chemosensitivity by reducing bicarbonate, resulting in a more appropriate ventilatory response to CO2 during wakefulness. Not only is diurnal hypoventilation reduced with noninvasive ventilation, but quality of life, functional capacity and survival are also improved. However, close attention to how therapy is set up and used are key factors in achieving clinical benefits.
Topics: Animals; Humans; Hypoventilation; Oxygen Inhalation Therapy; Respiration; Sleep Apnea Syndromes
PubMed: 25428856
DOI: 10.1002/cphy.c140008 -
Proceedings of the National Academy of... Sep 2023Protein synthesis is a fundamental cellular process in neurons that is essential for synaptic plasticity and memory consolidation. Here, we describe our investigations...
Protein synthesis is a fundamental cellular process in neurons that is essential for synaptic plasticity and memory consolidation. Here, we describe our investigations of a neuron- and muscle-specific translation factor, ukaryotic longation actor (eEF1A2), which when mutated in patients results in autism, epilepsy, and intellectual disability. We characterize three patient mutations, G70S, E122K, and D252H, and demonstrate that all three mutations decrease de novo protein synthesis and elongation rates in HEK293 cells. In mouse cortical neurons, the mutations not only decrease de novo protein synthesis but also alter neuronal morphology, regardless of endogenous levels of eEF1A2, indicating that the mutations act via a toxic gain of function. We also show that eEF1A2 mutant proteins display increased tRNA binding and decreased actin-bundling activity, suggesting that these mutations disrupt neuronal function by decreasing tRNA availability and altering the actin cytoskeleton. More broadly, our findings are consistent with the idea that eEF1A2 acts as a bridge between translation and the actin cytoskeleton, which is essential for proper neuron development and function.
Topics: Animals; Humans; Mice; Actins; Autistic Disorder; Epilepsy; HEK293 Cells; Mutation; Peptide Elongation Factor 1
PubMed: 37695913
DOI: 10.1073/pnas.2307704120