Argentine ant extract induces an osm-9 dependent chemotaxis response in C. elegans.

Many ant species are equipped with chemical defenses, although how these compounds impact nervous system function is unclear. Here, we examined the utility of Caenorhabditis elegans chemotaxis assays for investigating how ant chemical defense compounds are detected by heterospecific nervous systems. We found that C. elegans respond to extracts from the invasive Argentine Ant ( Linepithema humile ) and the osm-9 ion channel is required for this response. Divergent strains varied in their response to L. humile extracts, suggesting genetic variation underlying chemotactic responses. These experiments were conducted by an undergraduate laboratory course, highlighting how C. elegans chemotaxis assays in a classroom setting can provide genuine research experiences and reveal new insights into interspecies interactions.

Albino Xenopus laevis tadpoles prefer dark environments compared to wild type.

Tadpoles display preferences for different environments but the sensory modalities that govern these choices are not well understood. Here, we examined light preferences and associated sensory mechanisms of albino and wild-type Xenopus laevis tadpoles. We found that albino tadpoles spent more time in darker environments compared to the wild type, although they showed no differences in overall activity. This preference persisted when the tadpoles had their optic nerve severed or pineal glands removed, suggesting these sensory systems alone are not necessary for phototaxis. These experiments were conducted by an undergraduate laboratory course, highlighting how X. laevis tadpole behavior assays in a classroom setting can reveal new insights into animal behavior.

Post-sepsis immunosuppression depends on NKT cell regulation of mTOR/IFN-γ in NK cells.

As treatment of the early, inflammatory phase of sepsis improves, post-sepsis immunosuppression and secondary infection have increased in importance. How early inflammation drives immunosuppression remains unclear. Although IFN-γ typically helps microbial clearance, we found that increased plasma IFN-γ in early clinical sepsis was associated with the later development of secondary Candida infection. Consistent with this observation, we found that exogenous IFN-γ suppressed macrophage phagocytosis of zymosan in vivo, and antibody blockade of IFN-γ after endotoxemia improved survival of secondary candidemia. Transcriptomic analysis of innate lymphocytes during endotoxemia suggested that NKT cells drove IFN-γ production by NK cells via mTORC1. Activation of invariant NKT (iNKT) cells with glycolipid antigen drove immunosuppression. Deletion of iNKT cells in Cd1d-/- mice or inhibition of mTOR by rapamycin reduced immunosuppression and susceptibility to secondary Candida infection. Thus, although rapamycin is typically an immunosuppressive medication, in the context of sepsis, rapamycin has the opposite effect. These results implicated an NKT cell/mTOR/IFN-γ axis in immunosuppression following endotoxemia or sepsis. In summary, in vivo iNKT cells activated mTORC1 in NK cells to produce IFN-γ, which worsened macrophage phagocytosis, clearance of secondary Candida infection, and mortality.

mTORC2/Akt activation in adipocytes is required for adipose tissue inflammation in tuberculosis.

BACKGROUND: Mycobacterium tuberculosis has co-evolved with the human host, adapting to exploit the immune system for persistence and transmission. While immunity to tuberculosis (TB) has been intensively studied in the lung and lymphoid system, little is known about the participation of adipose tissues and non-immune cells in the host-pathogen interaction during this systemic disease. METHODS: C57BL/6J mice were aerosol infected with M. tuberculosis Erdman and presence of the bacteria and the fitness of the white and brown adipose tissues, liver and skeletal muscle were studied compared to uninfected mice. FINDINGS: M. tuberculosis infection in mice stimulated immune cell infiltration in visceral, and brown adipose tissue. Despite the absence of detectable bacterial dissemination to fat tissues, adipocytes produced localized pro-inflammatory signals that disrupted adipocyte lipid metabolism, resulting in adipocyte hypertrophy. Paradoxically, this resulted in increased insulin sensitivity and systemic glucose tolerance. Adipose tissue inflammation and enhanced glucose tolerance also developed in obese mice after aerosol M. tuberculosis infection. We found that infection induced adipose tissue Akt signaling, while inhibition of the Akt activator mTORC2 in adipocytes reversed TB-associated adipose tissue inflammation and cell hypertrophy. INTERPRETATION: Our study reveals a systemic response to aerosol M. tuberculosis infection that regulates adipose tissue lipid homeostasis through mTORC2/Akt signaling in adipocytes. Adipose tissue inflammation in TB is not simply a passive infiltration with leukocytes but requires the mechanistic participation of adipocyte signals.

Spinal clearance in unconscious children following traumatic brain injury.

Spinal clearance in unconscious children following traumatic brain injury is an area of controversy. The risk of significant injury in this high-risk group needs to be balanced against that of prolonged spinal immobilization and all its implications. No national or international guideline exists to aid clinicians faced with such a scenario. This article reviews traumatic spinal injury in children looking at prevalence, risk factors, anatomical considerations, and radiological investigation. Spinal immobilization is discussed along with the use of appropriate and targeted radiological investigations to aid clearance.

Perioperative management of the severely obese patient: a selective pathophysiological review.

PURPOSE: Obesity is widespread, yet it is often understood primarily as a disorder of body structure. This article provides anesthesiologists with a synopsis of recent research into the complex pathophysiology of obesity. It emphasizes the importance of this information for the perioperative planning and management of this patient group and for reviewing some of the major perioperative challenges. PRINCIPAL FINDINGS: Obesity is a multisystem chronic pro-inflammatory disorder associated with increased morbidity and mortality. Adipocytes are far more than storage vessels for lipids. They secrete a large number of physiologically active substances called adipokines that lead to inflammation, vascular and cardiac remodelling, airway inflammation, and altered microvascular flow patterns. They contribute to linked abnormalities, such as insulin resistance and the metabolic syndrome, and they attract and activate inflammatory cells such as macrophages. These changes can lead ultimately to organ dysfunction, especially cardiovascular and pulmonary issues. In the respiratory system, anesthesiologists should be familiar not just with screening tools for obstructive sleep apnea but also with obesity hypoventilation syndrome, which is less well appreciated and carries a significant outcome disadvantage. Perioperative management is challenging. It is centred around cardiorespiratory and metabolic optimization, minimizing adverse effects of both pain and systemic opioids, effective use of regional anesthesia, and an emphasis on mobilization and nutrition - given the prevalence of micronutrient deficiencies in the severely obese. There is a risk of incorrect drug dosing in obesity, which requires an understanding of the appropriate dosing weights for perioperative medications. CONCLUSION: The literature clearly highlights the complexity of severe obesity as a multisystem disease, and anesthesiologists caring for these patients perioperatively must have a sound understanding of the changes in order to offer the highest quality care to these patients.