The POLARBEAR Fourier transform spectrometer calibrator and spectroscopic characterization of the POLARBEAR instrument.

We describe the Fourier Transform Spectrometer (FTS) used for in-field testing of the POLARBEAR receiver, an experiment located in the Atacama Desert of Chile which measures the cosmic microwave background (CMB) polarization. The POLARBEAR-FTS (PB-FTS) is a Martin-Puplett interferometer designed to couple to the Huan Tran Telescope (HTT) on which the POLARBEAR receiver is installed. The PB-FTS measured the spectral response of the POLARBEAR receiver with signal-to-noise ratio >20 for ∼69% of the focal plane detectors due to three features: a high throughput of 15.1 sr cm2, optimized optical coupling to the POLARBEAR optics using a custom designed output parabolic mirror, and a continuously modulated output polarizer. The PB-FTS parabolic mirror is designed to mimic the shape of the 2.5 m-diameter HTT primary reflector, which allows for optimum optical coupling to the POLARBEAR receiver, reducing aberrations and systematics. One polarizing grid is placed at the output of the PB-FTS and modulated via continuous rotation. This modulation allows for decomposition of the signal into different harmonics that can be used to probe potentially pernicious sources of systematic error in a polarization-sensitive instrument. The high throughput and continuous output polarizer modulation features are unique compared to other FTS calibrators used in the CMB field. In-field characterization of the POLARBEAR receiver was accomplished using the PB-FTS in April 2014. We discuss the design, construction, and operation of the PB-FTS and present the spectral characterization of the POLARBEAR receiver. We introduce future applications for the PB-FTS in the next-generation CMB experiment, the Simons Array.

New constraint on the existence of the µ+ → e+ γ decay.

The analysis of a combined data set, totaling 3.6 × 10(14) stopped muons on target, in the search for the lepton flavor violating decay µ(+) → e(+)γ is presented. The data collected by the MEG experiment at the Paul Scherrer Institut show no excess of events compared to background expectations and yield a new upper limit on the branching ratio of this decay of 5.7 × 10(-13) (90% confidence level). This represents a four times more stringent limit than the previous world best limit set by MEG.

NF-kappaB regulatory mechanisms in alveolar macrophages from patients with acute respiratory distress syndrome.

Activation of the nuclear regulatory factor NF-kappaB occurs in the lungs of patients with the acute respiratory distress syndrome (ARDS) and may contribute to the increased expression of immunoregulatory cytokines and other proinflammatory mediators in this setting. Because of the important role that NF-kappaB activation appears to play in the development of acute lung injury, we examined cytoplasmic and nuclear NF-kapppaB counterregulatory mechanisms, involving IkappaB proteins, in alveolar macrophages obtained from 7 control patients without lung injury and 11 patients with established ARDS. Cytoplasmic levels of the NF-kappaB subunits p50, p65, and c-Rel were significantly decreased in alveolar macrophages from patients with ARDS, consistent with enhanced migration of liberated NF-kappaB dimers from the cytoplasm to the nucleus. Cytoplasmic and nuclear levels of IkappaBalpha were not significantly altered in alveolar macrophages from patients with established ARDS, compared with controls. In contrast, nuclear levels of Bcl-3 were significantly decreased in patients with ARDS compared with controls (P = 0.02). No IkappaBgamma, IkappaBbeta, or p105 proteins were detected in the cytoplasm of alveolar macrophages from control patients or patients with ARDS. The presence of activated NF-kappaB in alveolar macrophages from patients with established ARDS implies the presence of an ongoing stimulus for NF-kappaB activation. In this setting, appropriate counterregulatory mechanisms to normalize nuclear levels of NF-kappaB and to suppress NF-kappaB-mediated transcription, such as increased cytoplasmic and nuclear IkappaBalpha levels or decreased Bcl-3 levels, appeared to be induced. Nevertheless, even though counterregulatory mechanisms to NF-kappaB activation are activated in lung macrophages of patients with ARDS, NF-kappaB remains activated. These results suggest that fundamental abnormalities in transcriptional mechanisms involving NF-kappaB and important in the inflammatory response occur in the lungs of patients with ARDS.

Neutrophil apoptosis in the lung after hemorrhage or endotoxemia: apoptosis and migration are independent of IL-1beta.

Hemorrhage and endotoxemia are associated with neutrophil accumulation in the lungs and the development of acute inflammatory lung injury. Because alterations in the rate of apoptosis may affect the number and function of neutrophils in the lungs, we determined the percentage of neutrophils undergoing apoptosis in the lungs of control, hemorrhaged, or endotoxemic mice. In control mice, 18.5 +/- 1.2% of pulmonary neutrophils were apoptotic. The proportion of apoptotic neutrophils in the lungs was significantly decreased 1 h after hemorrhage (6.5 +/- 1.6%, P < 0.01 compared to control) or endotoxemia (7.0 +/- 0.9%, P < 0.01 compared to control). Between 1 and 24 h after endotoxemia or hemorrhage, the proportion of apoptotic neutrophils in the lung remained significantly depressed compared to that in control, unmanipulated mice. By 48 h, the proportion of apoptotic neutrophils returned to baseline levels in the lungs of hemorrhaged (21.4 +/- 1.4%) or endotoxemic (16.4 +/- 1. 6%) mice. Lung neutrophil IL-1beta mRNA was significantly increased from that of control mice [i.e., 0.12 +/- 0.06 relative absorbance units (RAU)] 1 h after hemorrhage (5.19 +/- 0.068 RAU, P < 0.05 compared to control) or endotoxemia (8.90 +/- 1.53 RAU, P < 0.01 compared to control). In IL-1beta-deficient mice, there was no significant difference in lung neutrophil apoptosis or neutrophil entry into the lung after hemorrhage or endotoxemia compared to wild-type mice. Our results show that apoptosis among lung neutrophils is decreased for more than 24 h after hemorrhage or endotoxemia. Although IL-1beta expression is increased in lung neutrophils under these conditions, IL-1beta is not responsible for either the influx of neutrophils into the lung or the reduction of apoptosis in neutrophil populations after hemorrhage or endotoxemia.

Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation.

Endotoxemia produces elevations in catecholamine levels in the pulmonary and systemic circulation as well as rapid increases in neutrophil number and proinflammatory cytokine expression in the lungs. In the present experiments, we examined the effects of endogenous and exogenous adrenergic stimulation on endotoxin-induced lung neutrophil accumulation and activation. Levels of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, and macrophage inflammatory protein (MIP)-2 mRNAs were increased in lung neutrophils from endotoxemic mice compared with those present in lung neutrophils from control mice or in peripheral blood neutrophils from endotoxemic or control mice. Treatment with the beta-adrenergic antagonist propranolol before endotoxin administration did not affect trafficking of neutrophils to the lungs or the expression of IL-1beta, TNF-alpha, or MIP-2 by lung neutrophils. Administration of the alpha-adrenergic antagonist phentolamine before endotoxemia did not alter lung neutrophil accumulation as measured by myeloperoxidase (MPO) levels but did result in significant increases in IL-1beta, TNF-alpha, and MIP-2 mRNA expression by lung neutrophils compared with endotoxemia alone. Administration of the alpha1-adrenergic agonist phenylephrine before endotoxin did not affect trafficking of neutrophils to the lungs but was associated with significantly increased expression of TNF-alpha and MIP-2 mRNAs by lung neutrophils compared with that found after endotoxin alone. In contrast, treatment with the alpha2-adrenergic agonist UK-14304 prevented endotoxin-induced increases in lung MPO and lung neutrophil cytokine mRNA levels. The suppressive effects of UK-14304 on endotoxin-induced increases in lung MPO were not affected by administration of the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester. These data demonstrate that the initial accumulation and activation of neutrophils in the lungs after endotoxemia can be significantly diminished by alpha2-adrenergic stimulation. Therapy with alpha2-adrenergic agents may have a role in modulating inflammatory pulmonary processes associated with sepsis-induced acute lung injury.

Systemic blood loss affects NF-kappa B regulatory mechanisms in the lungs.

The nuclear regulatory factor (NF)-kappa B is activated in the lungs of patients with acute respiratory distress syndrome (ARDS). In experimental models of acute lung injury, activation of NF-kappa B contributes to the increased expression of immunoregulatory cytokines and other proinflammatory mediators in the lungs. Because of the important role that NF-kappa B activation appears to play in the development of acute lung injury, we examined cytoplasmic and nuclear NF-kappa B counterregulatory mechanisms in lung mononuclear cells, using a murine model in which inflammatory lung injury develops after blood loss. Sustained activation of NF-kappa B was present in lung mononuclear cells over the 4-h period after blood loss. The activation of NF-kappa B after hemorrhage was accompanied by alterations in levels of the NF-kappa B regulatory proteins I kappa B alpha and Bcl-3. Cytoplasmic and nuclear I kappa B alpha were increased and nuclear Bcl-3 was decreased during the first hour after blood loss, but, by 4 h posthemorrhage, cytoplasmic and nuclear I kappa B alpha levels were decreased and nuclear levels of Bcl-3 were increased. Inhibition of xanthine oxidase activity in otherwise unmanipulated unhemorrhaged mice resulted in increased levels of I kappa B alpha and decreased amounts of Bcl-3 in nuclear extracts from lung mononuclear cells. No changes in the levels of nuclear I kappa B alpha or Bcl-3 occurred after hemorrhage when xanthine oxidase activity was inhibited. These results demonstrate that blood loss, at least partly through xanthine oxidase-dependent mechanisms, produces alterations in the levels of both I kappa B alpha and Bcl-3 in lung mononuclear cell populations. The effects of hemorrhage on proteins that regulate activation of NF-kappa B may contribute to the frequent development of inflammatory lung injury in this setting.

Hemorrhage increases cytokine expression in lung mononuclear cells in mice: involvement of catecholamines in nuclear factor-kappaB regulation and cytokine expression.

The expression of proinflammatory and immunoregulatory cytokines rapidly increases in the lungs after hemorrhage, and such alterations contribute to the frequent development of acute inflammatory lung injury in this setting. Blood loss also produces elevations in catecholamine concentrations in the pulmonary and systemic circulation. In the present experiments, we used alpha- and beta-adrenergic receptor blockade to examine in vivo interactions between hemorrhage-induced adrenergic stimulation and pulmonary cytokine expression. Treatment of mice with the alpha-adrenergic receptor antagonist phentolamine prevented not only the elevation in mRNA levels of IL-1beta, TNF-alpha, and TGF-beta1, the increase in IL-1beta protein, but also the activation of nuclear factor (NF)-KB and cyclic AMP response element binding protein, which occurred in lung cells of untreated animals during the first hour after hemorrhage. In contrast, treatment before hemorrhage with the beta-adrenergic receptor antagonist propranolol was associated with increases in mRNA levels for IL-1beta, TNF-alpha, and TGF-beta1, which were greater than those present in untreated hemorrhaged mice, and did not prevent hemorrhage-associated increases in lung IL-1beta protein. Treatment with propranolol prevented hemorrhage-induced phosphorylation of cyclic AMP response element binding protein, but increased hemorrhage-associated activation of NF-KB. These results demonstrate that hemorrhage initially increases pulmonary cytokine expression through alpha- but not beta-adrenergic stimulation, and suggest that such alpha-adrenergic-mediated effects occur through activation of the transcriptional regulatory factor NF-kappaB.

An anatomical and biochemical study of the pituitary proopiomelanocortin systems in the polypteriform fish Calamoichthys calabaricus.

Immunohistochemical and biochemical analyses were performed on the pituitary Proopiomelanocortin (POMC) systems of the polypteriform fish Calamoichthys calabaricus. Immunohistochemical staining of the pituitary revealed a clustering of ACTH immunopositive cells within the rostral pars distalis. alpha-Melanocyte stimulating hormone (alpha-MSH)-related and beta-endorphin-related immunoreactivity were found colocalized in epithelial cells of the pars intermedia. Biochemical analyses included Sephadex G-50 column chromatography, reversed-phase HPLC, and cation exchange chromatography. These analyses revealed the presence of immunoreactive forms of ACTH which stimulated glucocorticoid release when tested on isolated Bufo marinus adrenocortical tissue. Three forms of alpha-MSH were detected, and the major form had the same HPLC chromatographic properties as synthetic monoacetylated alpha-MSH. Finally, five forms of beta-endorphin were detected, and all of these forms were N-acetylated. Based on these observations, it appears that N-acetylation is a major post-translational processing event within the melanotropic cells of C. calabaricus. Given the position of Order Cladistia in the phylogeny of actinopterygian fish, it appears that N-acetylation of POMC-related products is an ancestral trait of osteichthyean fish.

[Biochemical studies of the cerebral ischemia in the rat--changes in cerebral free amino acids, catecholamines and uric acid].

Changes in cerebral free amino acids, catecholamines and uric acid levels were explored for up to 7 days after cerebral ischemia in the rat. Fifty male Sprague-Dawley rats were subjected to occlusion of the middle cerebral artery on the olfactory tract, under halothane anesthesia. The animals were decapitated at 2, 4, 6, 12, 24 hours and 2, 3, 5, 7 days after the surgery, respectively. The brains were rapidly removed. The cerebral hemispheres were divided into right and left halves, and homogenized in sulfosalicylic acid solution. Free amino acids were analyzed by colormetric method. Cathecholamines and uric acid were analyzed by high-performance liquid chromatography. Each parameters were measured both on the ischemic and contralateral hemispheres. The time course of changes in each parameters were observed by means of the ratio, which is the value of ischemic side divided by that of contralateral side. Free amino acids Dicarboxylic group; Decreases in glutamate and increases in glutamine suggest one aspect of detoxication of ammonia within the ischemia tissue. Monocarboxylic group; GABA, glycine, alanine were increased in early ischemic state, and gradually lowered to the normal values. These suggest the impairment of tricarboxylic acid (TCA) cycle in the ischemic tissues, since these amino acids are closely related to TCA cycle. Essential amino acids, except for tryptophan, were increased until the end of study. These increases suggest the utilization of essential amino acids for protein synthesis might be disturbed in the ischemic tissues. Catecholamines and precursors; Norepinephrine and dopamine were lowered gradually. On the other hand, phenylalanine and tyrosine were increased during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

[Carotid dissecting aneurysm due to blunt (rubbing) injury of the Kendo protector].

A case of dissecting aneurysm of the cervical internal carotid artery due to rare mechanism by non-penetrating injury is described. A 45-year-old right-handed man had complaints of the right lateral neck pain during exercise of KENDO wearing a tight headneck protector. Following sudden dysarthria and left hemiplegia, he developed loss of consciousness and generalized convulsion. Five hours after admission, he became alert and had no neurological deficits. Four days after these episodes, he loss visual acuity of the right eye, and a few days later he showed left hemiplegia, hypotension, hypersomnia and right-sides Horner's syndrome. Right retrograde brachial angiography revealed so-called "string sign" in the right extracranial internal carotid artery and delayed circulation in the right cerebral hemisphere. He was diagnosed as having traumatic dissecting aneurysm due to blunt (rubbing) injury. He was treated with STA-MCA anastomosis 3 weeks after the accident. Usually, carotid dissecting aneurysm due to blunt injury is produced by hyperextension and contralateral rotation of the neck or direct blow to the neck, but our case shows a possible mechanism of rubbing injury such as simple anteroposterior flexion under tight neck fixation.

[Changes in regional cerebral catecholamines following middle cerebral artery occlusion in the rat].

Ischemic brain injury affects the content and metabolism of brain monomines. Our aim was to know the time course of changes in regional cerebral catecholamines during focal cerebral ischemia, and whether focal cerebral ischemia may affect the metabolism of catecholamines in distant area of the brain. Methods Fifty-five rats were subjected to occlusion of the middle cerebral artery (MCA) on the olfactory tract, under halothane anesthesia. Fourteen animals were sham-operated group. Animals were decapitated at 1/2, 1,2,3,6,12 and 24 hours post-occlusion (PO), respectively. The brains were removed, and the brain structures dissected out include bilateral corpus striatum, cerebral cortex (MCA territory) and cerebellar hemisphere. Catecholamines were extracted by alumina procedure, and determined by high-performance liquid chromatography with electrochemical detection. Results Dopamine (DA) contents, in ipsilateral corpus striatum and cerebral cortex to the ischemia, decreased at 1 hour PO, and reached, at 6 hours PO, to 40% of control value in corpus striatum and 30% in cerebral cortex, respectively. After 6 hours PO, DA remained low. Norepinephrine (NE) content in the ipsilateral corpus striatum gradually reduced and reached to 60% of control value at 24 hours PO. NE in the ipsilateral cerebral cortex decreased to 50% of control at 1 hour PO, and thereafter remained reduced. In the contralateral corpus striatum and cerebral cortex, either DA or NE showed no significant changes, except 1/2 hour PO. NE contents in bilateral cerebral cortex showed a transient increase at 1/2 hour PO. Cerebellar NE content, bilaterally, reduced slowly to 70% of control at 24 hours PO.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral infarction in rats using homologous blood emboli: development of a new experimental model.

A reproducible model of thromboembolism in the rat was developed and the temporal relationship between hydrogen clearance, regional cerebral blood flow (rCBF) and power spectral-analyzed electroencephalographic (EEG) activity explored for up to four hours postinsult. Sixteen rats were subjected to right internal carotid artery homologous blood embolization after electrocautery of the pterygopalatine artery. Four rats were subjected to sham operation. Cerebral angiography before and for up to four hours postinsult was used to verify the distal migration and fragmentation of the emboli. Preembolic mean rCBF was 62 +/- 9 ml . 100g-1 . min-1 and 65 +/- 12 ml . 100g-1 . min-1 in the embolized and contralateral sides, respectively. Based upon the distribution of the emboli at sacrifice, the experimental group of 12 rats fell into three subgroups: unilateral proximal embolism, n = 8; unilateral peripheral embolism, n = 3; and bilateral proximal embolism, n = 1. In unilateral proximal embolism the mean rCBF in the embolized hemisphere ranged between 10 and 20 ml . 100g-1 . min-1 and correlated well with changes in EEG power spectra. In unilateral peripheral embolism, the mean rCBF in the embolized hemisphere fell significantly 30 min postembolism. It returned progressively towards preembolic values as the embolic clots migrated distally and fragmented. Despite the restoration of rCBF, recovery of EEG activity appeared to be delayed. Our results did not show luxury perfusion after embolic insults. The time course for the reopening of the embolized artery and the delay in recovery of neuronal function (i.e., EEG activity) relative to the restoration of rCBF are discussed.

[Aneurysm of peripheral cerebral arteries with developmental anomaly of the anterior cerebral artery].

We report a 71-year-old woman who was initially admitted because of a ruptured internal carotid aneurysm, and found to have an aneurysm of the terminal portion (A5 portion) of pericallosal artery. Both of the aneurysms were surgically treated at one stage operation. A saccular aneurysm of the pericallosal artery was verified at operation. Right internal carotid angiography disclosed that medial part of the right anterior cerebral hemisphere was supplied by the right callosomarginal artery, and that unpaired pericallosal artery made a trifurcation at A5 portion, where the saccular aneurysm arose. According to Baptista's classification, anomaly of the anterior cerebral artery (ACA) in this patient was bihemispheric ACA type. Distal ACA aneurysms almost always locate at or near the genu of corpus callosum, either in pericallosal-callosomarginal or in pericallosal-frontopolar junction. In reviewing the literature, we were able to find 14 cases, including ours, of aneurysms located beyond either pericallosal-callosomarginal junction or the genu of corpus callosum. Also the possible role of hemodynamic stress caused by vascular anomaly for aneurysm formation are discussed.

[Cranial hemihypertrophy in Klippel-Trenaunay syndrome (author's transl)].

Klippel-Trenaunay Syndrome with hemicranial hypertrophy and macrodactyly is reported. The patient was a 3-year-old Japanese woman with an extensive nevus flammeus which extended over the right side of the neck, axilla, upper arm, and leg. Her right extremities were longer and thicker than left, and showed apparent macrodactyly in the right hand. Her skin of right side body was irregular, rough surface and was pigmented prominently. Hyperthermia was present in the hypertrophic limbs, but hyperhidrosis was none. She had moderate mental retardation, delayed speech. Her hemicranial hypertrophy (same side as hypertrophic limbs) was examined by CT scan. Her right lateral ventricle was dilatated and cortical sulci was well demonstrated. Her right hemicranial volume was enlarged but rt-cerebral hemisphere was atrophic, and her infratentorial structures were symmetrical. Presented case, Klippel-Trenaunay Syndrome with hemicranial hypertrophy, suggested the embryological theory affecting on trilaminar disc in embryonal stage as the genesis of this rare syndrome.