Epithelia form intelligent, dynamic barriers between the external environment and an organism's interior. Intercellular cadherin-based adhesions adapt and respond to mechanical forces and cell density, while tight junctions flexibly control diffusion both within the plasma membrane and between adjacent cells. Epithelial integrity and homeostasis are of central importance to survival, and mechanisms have evolved to ensure these processes are maintained during growth and in response to damage. For instance, cell competition surveys the fitness of cells within epithelia and removes the less fit; extrusion or delamination can remove apoptotic or defective cells from the epithelial sheet and can restore homeostasis when an epithelial layer becomes too crowded; spindle orientation ensures two-dimensional growth in simple epithelia and controls stratification in complex epithelia; and transition to a mesenchymal phenotype enables active escape from an epithelial layer. This review will discuss these various mechanisms and consider how they are subverted in disease.
A major pathway of beta-alanine synthesis in insects is through the alpha-decarboxylation of aspartate, but the enzyme involved in the decarboxylation of aspartate has not been clearly defined in mosquitoes and characterized in any insect species. In this study, we expressed two putative mosquito glutamate decarboxylase-like enzymes of mosquitoes and critically analyzed their substrate specificity and biochemical properties. Our results provide clear biochemical evidence establishing that one of them is an aspartate decarboxylase and the other is a glutamate decarboxylase. The mosquito aspartate decarboxylase functions exclusively on the production of beta-alanine with no activity with glutamate. Likewise the mosquito glutamate decarboxylase is highly specific to glutamate with essentially no activity with aspartate. Although insect aspartate decarboxylase shares high sequence identity with glutamate decarboxylase, we are able to closely predict aspartate decarboxylase from glutamate decarboxylase based on the difference of their active site residues.
Brain fingerprinting detects concealed information stored in the brain by measuring brainwave responses. We compared P300 and P300-MERMER event-related brain potentials for error rate/accuracy and statistical confidence in four field/real-life studies. 76 tests detected presence or absence of information regarding (1) real-life events including felony crimes; (2) real crimes with substantial consequences (either a judicial outcome, i.e., evidence admitted in court, or a $100,000 reward for beating the test); (3) knowledge unique to FBI agents; and (4) knowledge unique to explosives (EOD/IED) experts. With both P300 and P300-MERMER, error rate was 0 %: determinations were 100 % accurate, no false negatives or false positives; also no indeterminates. Countermeasures had no effect. Median statistical confidence for determinations was 99.9 % with P300-MERMER and 99.6 % with P300. Brain fingerprinting methods and scientific standards for laboratory and field applications are discussed. Major differences in methods that produce different results are identified. Markedly different methods in other studies have produced over 10 times higher error rates and markedly lower statistical confidences than those of these, our previous studies, and independent replications. Data support the hypothesis that accuracy, reliability, and validity depend on following the brain fingerprinting scientific standards outlined herein.
Influenza A virus (IAV) is a leading cause of respiratory tract disease worldwide. Anti-viral CD8(+) T lymphocytes responding to IAV infection are believed to eliminate virally infected cells by direct cytolysis but may also contribute to pulmonary inflammation and tissue damage via the release of pro-inflammatory mediators following recognition of viral antigen displaying cells. We have previously demonstrated that IAV antigen expressing inflammatory cells of hematopoietic origin within the infected lung interstitium serve as antigen presenting cells (APC) for infiltrating effector CD8(+) T lymphocytes; however, the spectrum of inflammatory cell types capable of serving as APC was not determined. Here, we demonstrate that viral antigen displaying neutrophils infiltrating the IAV infected lungs are an important cell type capable of acting as APC for effector CD8(+) T lymphocytes in the infected lungs and that neutrophils expressing viral antigen as a result of direct infection by IAV exhibit the most potent APC activity. Our findings suggest that in addition to their suggested role in induction of the innate immune responses to IAV, virus clearance, and the development of pulmonary injury, neutrophils can serve as APCs to anti-viral effector CD8(+) T cells within the infected lung interstitium.
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