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Background Exposure to microbes early in life has long-lasting effects on microbial community structure and function of the microbiome. However, in commercial poultry settings chicks are reared as a single-age cohort with no exposure to adult birds which can have profound effects on microbiota development and subsequent pathogen challenge. Microbiota manipulation is a proven and promising strategy to help reduce pathogen load and transmission within broiler flocks. However, administration of microbiota transplant products in a hatchery setting may prove challenging. Effective administration strategies are dependent on key factors, such as; the age of chicks receiving interventions and mode of delivery. This study aimed to assess these two aspects to provide supporting evidence towards microbiome manipulation strategies for use in commercial hatcheries. Results Manipulation of the microbiota between 4 and 72 h of hatch markedly reduced faecal shedding and colonisation with the foodborne pathogen Salmonella enterica serovar Typhimurium (ST4/74). Administration of transplant material via spray or gel drop delivery systems had minimal effect on the protection conferred with fewer birds in transplant groups shown to shed ST4/74 in the faeces compared to PBS-gavaged control birds. Analysis of the microbiome following transplantation demonstrated that all transplant groups had higher diversity and species richness than non-transplant groups during the first week of life and the early stages of infection with ST47/4.The relative abundance of the bacterium Faecalibacterium prausnitzii was significantly higher in CMT groups compared to PBS controls. The presence of F. prausnitzii was also shown to increase in PBS-challenged birds compared to unchallenged birds potentially indicating a role of this bacterium in limiting Salmonella infections. Conclusions This study demonstrated that administration of microbiome transplants, using methods that would align with hatchery practices, effectively reduced colonisation and shedding of Salmonella in chickens. Age of chicks at microbiome administration had limited effect on the diversity and composition of the microbiome and conferred protection against Salmonella infections. Traditional hatchery delivery systems, such as spray or gel-drop, are sufficient to transfer donor material, alter the microbiome and confer protection against Salmonella. This study helps highlight the opportunity for use of microbiome modification methods within the hatchery.

Pseudomonas aeruginosa undergoes diversification during infection of the cystic fibrosis (CF) lung. Understanding these changes requires model systems that capture the complexity of the CF lung environment. We previously identified loss-of-function mutations in the two-component regulatory system sensor kinase gene pmrB, in P. aeruginosa from CF and from experimental infection of mice. Here, we demonstrate that whilst such mutations lower in vitro MICs for multiple antimicrobial classes, this is not reflected in increased antibiotic susceptibility in vivo. Loss of PmrB impairs aminoarabinose modification of lipopolysaccharide, increasing the negative charge of the outer membrane and promoting uptake of cationic antimicrobials. However, in vivo, this can be offset by increased membrane binding of other positively charged molecules present in lungs. The polyamine spermidine readily coats the surface of PmrB-deficient P. aeruginosa, reducing susceptibility to antibiotics that rely on charge differences to bind the outer membrane and increasing biofilm formation. Spermidine is elevated in lungs during P. aeruginosa infection in mice and during episodes of antimicrobial treatment in people with CF. These findings highlight the need to study antimicrobial resistance under clinically relevant environmental conditions. Microbial mutations carrying fitness costs in vitro may be advantageous during infection, where host resources can be utilised.

BackgroundExposure to microbes early in life has long-lasting effects on microbial community structure and function of the microbiome. However, in commercial poultry settings chicks are reared as a single-age cohort with no exposure to adult birds which can have profound effects on microbiota development and subsequent pathogen challenge. Microbiota manipulation is a proven and promising strategy to help reduce pathogen load and transmission within broiler flocks.ResultsManipulation of the microbiota between 4 and 72 hours of hatch markedly reduces faecal shedding and colonisation with the foodborne pathogen Salmonella enterica serovar Typhimurium (ST4/74). Administration route has minimal effect on the protection conferred with fewer birds in transplant groups shown to shed ST4/74 in the faeces compared to PBS-gavaged control birds. Analysis of the microbiome following transplantation demonstrated that the relative abundance of the anti-inflammatory bacterium Faecalibacterium prausnitzii was significantly higher in CMT groups compared to PBS controls. The presence of F. prausnitzii was also shown to increase in PBS-challenged birds compared to unchallenged birds potentially indicating a role of this bacterium in limiting Salmonella infections.ConclusionsThis study highlights the efficacy of using microbiome transplants as a means to reduce colonisation and shedding of Salmonella in chickens. Effective protection can be conferred during the first few days of a chick’s life regardless of time point and traditional hatchery delivery systems are sufficient to alter the microbiome and transfer donor material. Early microbiota intervention in chickens is a promising route of pathogen control in broiler flocks in the fight to control food-borne outbreaks in the human population.

The COVID-19 pandemic precipitated catastrophic job loss, unprecedented unemployment rates, and severe economic hardship in renter households. As a result, housing precarity and the risk of eviction increased and worsened during the pandemic, especially among people of color and low-income populations. This paper considers the implications of this eviction crisis for health and health inequity, and the need for eviction prevention policies during the pandemic. Eviction and housing displacement are particularly threatening to individual and public health during a pandemic. Eviction is likely to increase COVID-19 infection rates because it results in overcrowded living environments, doubling up, transiency, limited access to healthcare, and a decreased ability to comply with pandemic mitigation strategies (e.g., social distancing, self-quarantine, and hygiene practices). Indeed, recent studies suggest that eviction may increase the spread of COVID-19 and that the absence or lifting of eviction moratoria may be associated with an increased rate of COVID-19 infection and death. Eviction is also a driver of health inequity as historic trends, and recent data demonstrate that people of color are more likely to face eviction and associated comorbidities. Black people have had less confidence in their ability to pay rent and are dying at 2.1 times the rate of non-Hispanic Whites. Indigenous Americans and Hispanic/Latinx people face an infection rate almost 3 times the rate of non-Hispanic whites. Disproportionate rates of both COVID-19 and eviction in communities of color compound negative health effects make eviction prevention a critical intervention to address racial health inequity. In light of the undisputed connection between eviction and health outcomes, eviction prevention, through moratoria and other supportive measures, is a key component of pandemic control strategies to mitigate COVID-19 spread and death.

We utilized a practical, transparent approach for systematically reviewing a chemical-specific evidence base. This approach was used for a case study of ozone inhalation exposure and adverse metabolic effects (overweight/obesity, Type 1 diabetes [T1D], Type 2 diabetes [T2D], and metabolic syndrome). We followed the basic principles of systematic review. Studies were defined as "Suitable" or "Supplemental." The evidence for Suitable studies was characterized as strong or weak. An overall causality judgment for each outcome was then determined as either causal, suggestive, insufficient, or not likely. Fifteen epidemiologic and 33 toxicologic studies were Suitable for evidence synthesis. The strength of the human evidence was weak for all outcomes. The toxicologic evidence was weak for all outcomes except two: body weight, and impaired glucose tolerance/homeostasis and fasting/baseline hyperglycemia. The combined epidemiologic and toxicologic evidence was categorized as weak for overweight/obesity, T1D, and metabolic syndrome,. The association between ozone exposure and T2D was determined to be insufficient or suggestive. The streamlined approach described in this paper is transparent and focuses on key elements. As systematic review guidelines are becoming increasingly complex, it is worth exploring the extent to which related health outcomes should be combined or kept distinct, and the merits of focusing on critical elements to select studies suitable for causal inference. We recommend that systematic review results be used to target discussions around specific research needs for advancing causal determinations.

Parkinson’s disease (PD) is a neurodegenerative disease caused by the death of dopaminergic neurons in the substantia nigra pars compacta (SNpc), characterized by motor dysfunction. While PD symptoms are well treated with L-DOPA, continuous use can cause L-DOPA-induced dyskinesia (LID). We have previously demonstrated that sub-anesthetic ketamine attenuated LID development in rodents, measured by abnormal involuntary movements (AIMs), and reduced the density of maladaptive striatal dendritic mushroom spines. Microglia may play a role by phagocytosing maladaptive neuronal spines. In this exploratory study, we hypothesized that ketamine would prevent AIMs and change microglia ramified morphology – an indicator of a microglia response. Unilaterally 6-hydroxydopamine (6-OHDA)-lesioned rats were primed with daily injections of L-DOPA for 14 days, treated on days 0 and 7 for 10-hours with sub-anesthetic ketamine (i.p.), and we replicated that this attenuated LID development. We further extended our prior work by showing that while ketamine treatment did lead to an increase of striatal interleukin-6 in dyskinetic rats, indicating a modulation of an inflammatory response, it did not change microglia number or morphology in the dyskinetic striatum. Yet an increase of CD68 in the SNpc of 6-OHDA-lesioned hemispheres post-ketamine indicates increased microglia phagocytosis suggestive of a lingering microglial response to 6-OHDA injury in the SNpc pointing to possible anti-inflammatory action in the PD model in addition to anti-dyskinetic action. In conclusion, we provide further support for sub-anesthetic ketamine treatment of LID. The mechanisms of action for ketamine, specifically related to inflammation and microglia phagocytic functions, are emerging, and require further examination.

Although much attention has been generated in popular media regarding the deleterious effects of pediatric mild traumatic brain injury (pmTBI), a paucity of empirical evidence exists regarding the natural course of biological recovery. Fifty pmTBI patients (12–18 years old) were consecutively recruited from Emergency Departments and seen approximately 1 week and 4 months post‐injury in this prospective cohort study. Data from 53 sex‐ and age‐matched healthy controls (HC) were also collected. Functional magnetic resonance imaging was obtained during proactive response inhibition and at rest, in conjunction with independent measures of resting cerebral blood flow. High temporal resolution imaging enabled separate modeling of neural responses for preparation and execution of proactive response inhibition. A priori predictions of failed inhibitory responses (i.e., hyperactivation) were observed in motor circuitry (pmTBI>HC) and sensory areas sub‐acutely and at 4 months post‐injury. Paradoxically, pmTBI demonstrated hypoactivation (HC>pmTBI) during target processing, along with decreased activation within prefrontal cognitive control areas. Functional connectivity within motor circuitry at rest suggested that deficits were limited to engagement during the inhibitory task, whereas normal resting cerebral perfusion ruled out deficits in basal perfusion. In conclusion, current results suggest blood oxygen‐level dependent deficits during inhibitory control may exceed commonly held beliefs about physiological recovery following pmTBI, potentially lasting up to 4 months post‐injury.

Background Trichloroethylene (TCE) was negative for developmental toxicity after inhalation and oral gavage exposure of pregnant rats but fetal cardiac defects were reported following drinking water exposure throughout gestation. Because of the deficiencies in this latter study, we performed another drinking water study to evaluate whether TCE causes heart defects. Methods Groups of 25 mated Sprague Dawley rats consumed water containing 0, 0.25, 1.5, 500, or 1,000 ppm TCE from gestational day 1–21. TCE concentrations were measured at daily formulation, when placed into water bottles each day and when water bottles were removed from cages. Four additional mated rats per group were used for plasma measurements. At termination, fetal hearts were carefully dissected fresh and examined. Results All TCE concentrations were >90% of target when initially placed in water bottles and when bottles were placed on cages. All dams survived with no clinical signs. Rats in the two higher dose groups consumed less water/day than other groups but showed no changes in maternal or fetal weights. The only fetal cardiac observation was small (

The rates of microbial and abiotic iron oxidation were determined in a variety of cold (T = 9–12 °C), circumneutral (pH = 5.5–9.0) environments in the Swiss Alps. These habitats include iron–bicarb...

Counties: Butler, Carter, Howell, Oregon, and Ripley.||"This present study is the the seventeenth in continuation of a project begun by the English Department of the University of Missouri in 1928, that of finding and recording the origin of the names of places in Missouri. I count it a rare privilege to have a small share in this worthy work. I have chosen tor my portion a group of the southern border counties consisting or Carter, Howell, Oregon, Hipley, and Butler. The last four are a part of the first tier or counties next to the Missouri-Arkansas boundary; Carter lies just north of Oregon, and because of its position, might be considered in either the first or second row from the state line. I prefer to name this study Place Names in Five Southern Border Counties of Missouri."--Introduction.

Childhood cancer survivors are at increased risk for treatment‐related late effects; data are lacking on how coronavirus disease 2019 (COVID‐19) infection impacts this cohort. We assessed COVID‐19‐related symptoms, severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) IgG seroprevalence, and rate of COVID‐19‐related hospitalization among 321 asymptomatic survivors of childhood cancer or transplantation seen for routine long‐term follow‐up between May and September 2020 in a New York City tertiary cancer center. While 10.9% (n = 35) reported possible COVID‐19‐related symptoms, 7.8% (n = 20) of those tested had positive SARS‐CoV‐2 IgG, and one patient (0.3%) required COVID‐19‐related hospitalization. This report suggests that childhood cancer survivors appear to be at relatively low risk for COVID‐19 complications.

OBJECTIVE: This article reviews childhood cancers and the treatments that affect bone integrity. Interventions related to exercise, hormone replacement, vitamin D and calcium supplementation, and bisphosphonate use are addressed. DATA SOURCES: Literature was reviewed related to childhood cancers, treatment and side effects, assessment, and management to optimize bone health. CONCLUSIONS: Cure rates of childhood cancer have dramatically improved due to new therapeutic advances allowing children diagnosed with cancer to live longer. Unfortunately, the cost of cure can be the increased development of chronic health issues. Since many children receive their treatment including antineoplastic agents, radiation, surgery, and corticosteroid therapy during time of active skeletal maturation and growth, their bone health may be negatively impacted. The development of bone mass can be impaired, bone density may be decreased, fractures may occur, growth may be restricted and there may be poor bone repair. Review of the data indicates that more research is needed to understand what is necessary for optimal bone health in the pediatric population in general, specifically for the child affected by cancer. IMPLICATIONS FOR NURSING PRACTICE: Nurses are integral to the development of comprehensive understanding of the bone health needs of the pediatric oncology patient population and educating the patient and family about the importance of bone health. Children and young adults survivors would benefit from collaborative care between all their health care providers. Steps to improve bone health before diagnosis, on treatment and through to survivorship remain to be addressed by future research.