Spectroscopy in Nanoscopic Cavities: Models and Recent Experiments.

The ability of nanophotonic cavities to confine and store light to nanoscale dimensions has important implications for enhancing molecular, excitonic, phononic, and plasmonic optical responses. Spectroscopic signatures of processes that are ordinarily exceedingly weak such as pure absorption and Raman scattering have been brought to the single-particle limit of detection, while new emergent polaritonic states of optical matter have been realized through coupling material and photonic cavity degrees of freedom across a wide range of experimentally accessible interaction strengths. In this review, we discuss both optical and electron beam spectroscopies of cavity-coupled material systems in weak, strong, and ultrastrong coupling regimes, providing a theoretical basis for understanding the physics inherent to each while highlighting recent experimental advances and exciting future directions.

Polarization-Resolved Electron Energy Gain Nanospectroscopy With Phase-Structured Electron Beams.

Free-electron-based measurements in scanning transmission electron microscopes (STEMs) reveal valuable information on the broadband spectral responses of nanoscale systems with deeply subdiffraction limited spatial resolution. Leveraging recent advances in manipulating the spatial phase profile of the transverse electron wavefront, we theoretically describe interactions between the electron probe and optically stimulated nanophotonic targets in which the probe gains energy while simultaneously transitioning between transverse states with distinct phase profiles. Exploiting the selection rules governing such transitions, we propose phase-shaped electron energy gain nanospectroscopy for probing the 3D polarization-resolved response field of an optically excited target with nanoscale spatial resolution.

Nanometer-Scale Spatial and Spectral Mapping of Exciton Polaritons in Structured Plasmonic Cavities.

Exciton polaritons (EPs) are ubiquitous light-matter excitations under intense investigation as test beds of fundamental physics and as components for all-optical computing. Owing to their unique attributes and facile experimental tunability, EPs potentially enable strong nonlinearities, condensation, and superfluidity at room temperature. However, the diffraction limit of light and the momentum content of fast electron probes preclude the characterization of EPs in nanoscale structured cavities exhibiting energy-momentum dispersion.

Active Far-Field Control of the Thermal Near-Field Plasmon Hybridization.

The ability to control and manipulate temperature at nanoscale dimensions has the potential to impact applications including heat-assisted magnetic recording, photothermal therapies, and temperature-driven reactivity. One challenge with controlling temperature at nanometer dimensions is the need to mitigate heat diffusion, such that the temperature only changes in well-defined nanoscopic regions of the sample. Here we demonstrate the ability to use far-field laser excitation to actively shape the thermal near-field in individual gold nanorod heterodimers by resonantly pumping either the in-phase or out-of-phase hybridized dipole plasmon modes.

A novel, bedside technique to rapidly identify umbilical cord blood units with high total nucleated cell numbers.

Background: With increasing demand for umbilical cord blood units (CBUs) with total nucleated cell (TNC) counts of more than 150 × 10(7) , preshipping assessment is mandatory. Umbilical cord blood processing requires aseptic techniques and laboratories with specific air quality and cleanliness. Our aim was to establish a fast and efficient method for determining TNC counts at the obstetric ward without exposing the CBU to the environment.

Effect of Regular Yoga Practice on Respiratory Regulation and Exercise Performance.

Yoga alters spontaneous respiratory regulation and reduces hypoxic and hypercapnic ventilatory responses. Since a lower ventilatory response is associated with an improved endurance capacity during whole-body exercise, we tested whether yogic subjects (YOGA) show an increased endurance capacity compared to matched non-yogic individuals (CON) with similar physical activity levels. Resting ventilation, the ventilatory response to hypercapnia, passive leg movement and exercise, as well as endurance performance were assessed.

Discovery and Structure-Activity Relationships of the Neoseptins: A New Class of Toll-like Receptor-4 (TLR4) Agonists.

Herein, we report studies leading to the discovery of the neoseptins and a comprehensive examination of the structure-activity relationships (SARs) of this new class of small-molecule mouse Toll-like receptor 4 (mTLR4) agonists. The compounds in this class, which emerged from screening an α-helix mimetic library, stimulate the immune response, act by a well-defined mechanism (mouse TLR4 agonist), are easy to produce and structurally manipulate, exhibit exquisite SARs, are nontoxic, and elicit improved and qualitatively different responses compared to lipopolysaccharide, even though they share the same receptor.

COMPARISON OF METHODS TO DETECT ALLELOPATHIC EFFECTS OF SUBMERGED MACROPHYTES ON GREEN ALGAE(1).

Detecting allelopathic inhibition of phytoplankton by submerged macrophytes in an ecologically meaningful way is not easy. Multiple-approach investigations from a laboratory scale to the ecosystem level have been recommended to overcome the shortcomings of individual methods. Whether results of different methods are qualitatively or quantitatively comparable has not yet been tested.

Polymorphisms and mutations of human TMPRSS6 in iron deficiency anemia.

Male subjects with iron deficiency from the general population were examined for polymorphisms or sporadic mutations in TMPRSS6 to identify genetic risk factors for iron deficiency anemia. Three uncommon non-synonymous polymorphisms were identified, G228D, R446W, and V795I (allele frequencies 0.0074, 0.

Suppression of the hepcidin-encoding gene Hamp permits iron overload in mice lacking both hemojuvelin and matriptase-2/TMPRSS6.

Hepcidin, the master regulator of enteric iron absorption, is controlled by the opposing effects of pathways activated in response to iron excess or iron attenuation. Iron excess is regulated through a pathway involving the cell surface receptor hemojuvelin (HFE2) that stimulates expression of the hepcidin encoding gene (HAMP). Iron attenuation is countered through a pathway involving the hepatocyte-specific plasma membrane protease matriptase-2 encoded by TMPRSS6, leading to suppression of HAMP expression.

Genetic screening for low-penetrance variants in protein-coding genes.

Genetic testing holds great promise as a screening tool to identify persons at risk for a disease at the presymptomatic stage. However, the complexities of gene-disease associations, even in single-gene diseases, pose important challenges. These challenges include defining the role of screening for mutations that have low penetrance, which cause disease in only a minority of patients with the genotype.

Regulation of hepcidin and iron-overload disease.

Hepcidin, a 25-amino-acid antimicrobial peptide, is the central regulator of iron homeostasis. Hepcidin transcription is upregulated by inflammatory cytokines, iron, and bone morphogenetic proteins and is downregulated by iron deficiency, ineffective erythropoiesis, and hypoxia. The iron transporter ferroportin is the cognate receptor of hepcidin and is destroyed as a result of interaction with the peptide.

The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis.

Glucose-6-phosphate deficiency is the most prevalent enzyme deficiency, with an estimated 400 million people affected worldwide. This inherited deficiency causes neonatal hyperbilirubinemia and chronic hemolytic anemia. Although most affected individuals are asymptomatic, exposure to oxidative stressors such as certain drugs or infection, can elicit acute hemolysis.

Two BMP responsive elements, STAT, and bZIP/HNF4/COUP motifs of the hepcidin promoter are critical for BMP, SMAD1, and HJV responsiveness.

Hepcidin plays a major role in the regulation of iron homeostasis. Several bone morphogenetic proteins (BMPs) are strong inducers of hepcidin (Hamp1, HAMP) expression. Hemojuvelin, a protein critical for maintaining appropriate levels of hepcidin, acts as a coreceptor for BMP2 and BMP4, thereby providing a link between iron homeostasis and the BMP-signaling pathway.

Severe iron overload with a novel aminolevulinate synthase mutation and hepatitis C infection. A case report.

A 55 year old man with a history of chronic hepatitis C infection was found to have severe hemochromatosis: hepatic cirrhosis, cardiomyopathy, arrhythmia, hypogonadism, diabetes and bronzed skin color. After 50 phlebotomies, he underwent a combined heart and liver transplant. Genetic analyses identified a novel mutation in the iron responsive element of the ALAS2 gene.

The anemia of ageing is not associated with increased plasma hepcidin levels.

It has been proposed that the anemia of ageing may be caused, at least in part, by elevated hepcidin levels, representing a response to increased IL-6 levels. Using a recently developed immunoassay, we have measured the plasma hepcidin levels of eight patients with the anemia of ageing and sex- and age-matched controls, and found that the levels of hepcidin were not increased in patients with the anemia of ageing. In contrast, patients with the anemia of inflammation have higher hepcidin levels than sex- and age-matched controls.

The serine protease TMPRSS6 is required to sense iron deficiency.

Hepcidin, a liver-derived protein that restricts enteric iron absorption, is the key regulator of body iron content. Several proteins induce expression of the hepcidin-encoding gene Hamp in response to infection or high levels of iron. However, mechanism(s) of Hamp suppression during iron depletion are poorly understood.

Glucose-6-phosphate dehydrogenase deficiency: a historical perspective.

Glucose-6-phosphate dehydrogenase deficiency serves as a prototype of the many human enzyme deficiencies that are now known. Since its discovery more than 50 years ago, the high prevalence of the defect and the easy accessibility of the cells that manifest it have made it a favorite tool of biochemists, epidemiologists, geneticists, and molecular biologists as well as clinicians. In this brief historical review, we trace the discovery of this defect, its clinical manifestations, detection, population genetics, and molecular biology.

A new case of human atransferrinemia with a previously undescribed mutation in the transferrin gene.

Hereditary atransferrinemia is a very rare disorder characterized by microcytic anemia and iron overload. It has been reported in only 10 patients in 8 families. The molecular basis of atransferrinemia has been determined in only 3 human cases.

Screening for hemochromatosis by measuring ferritin levels: a more effective approach.

Because the penetrance of HFE hemochromatosis is low, traditional population screening measuring the transferrin saturation is unlikely to be cost-effective because the majority of subjects detected neither have clinical disease nor are likely to develop it. Three independent studies show that only patients with serum ferritin concentrations more than 1000 microg/L are at risk for cirrhosis, one of the main morbidities of hemochromatosis. Among 29,699 white subjects participating in the Scripps/Kaiser hemochromatosis study, only 59 had serum ferritin levels more than 1000 microg/L; 24 had homozygous mutant or compound heterozygous mutant HFE genotypes.

Chronic non-spherocytic hemolytic anemia associated with severe neurological disease due to gamma-glutamylcysteine synthetase deficiency in a patient of Moroccan origin.

A previously undescribed mutation of hereditary gamma-glutamylcysteine synthetase (GCS) deficiency was found in a 5 year old boy of Moroccan origin. He presented with chronic haemolytic anaemia, delayed psychomotor development and progressive motor sensitive neuropathy of lower extremities. The parents were third degree relatives.

Glucose-6-phosphate dehydrogenase deficiency and antimalarial drug development.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is relatively common in populations exposed to malaria. This deficiency appears to provide some protection from this infection, but it can also cause hemolysis after administration of some antimalarial drugs, especially primaquine. The risk of drug-induced G6PD deficiency-related hemolysis depends on a number of factors including the G6PD variant, the drug and drug dosage schedule, patient status, and disease factors.

Congenital Gaucher disease with nonimmune hydrops/erythroblastosis, infantile arterial calcification, and neonatal hepatitis/fibrosis. Clinicopathologic report with enzymatic and genetic analysis.

The findings in a stillborn female fetus of 31 weeks' gestation with congenital Gaucher disease, nonimmune hydrops/erythroblastosis, infantile arterial calcification, and neonatal hepatitis/fibrosis are presented, the first report of this complete constellation. Prior reports describe two similar patients. One lacked the hepatocellular features of giant cell hepatitis although manifesting hepatic fibrosis; the second lacked hepatic pathology.