The Simons Observatory Large Aperture Telescope Receiver

The Simons Observatory (SO) Large Aperture Telescope Receiver (LATR) will be coupled to the Large Aperture Telescope located at an elevation of 5,200 m on Cerro Toco in Chile. The resulting instrument will produce arcminute-resolution millimeter-wave maps of half the sky with unprecedented precision. The LATR is the largest cryogenic millimeter-wave camera built to date with a diameter of 2.4 m and a length of 2.6 m. It cools 1200 kg of material to 4 K and 200 kg to 100 mk, the operating temperature of the bolometric detectors with bands centered around 27, 39, 93, 145, 225, and 280 GHz. Ultimately, the LATR will accommodate 13 40 cm diameter optics tubes, each with three detector wafers and a total of 62,000 detectors. The LATR design must simultaneously maintain the optical alignment of the system, control stray light, provide cryogenic isolation, limit thermal gradients, and minimize the time to cool the system from room temperature to 100 mK. The interplay between these competing factors poses unique challenges. We discuss the trade studies involved with the design, the final optimization, the construction, and ultimate performance of the system

Data from: An investigation of sepsis surveillance and emergency treatment on patient mortality outcomes: an observational cohort study

Objective. To determine the prevalence of initiating the sepsis 3-hour bundle of care and estimate effects of bundle completion on risk-adjusted mortality among ED patients screened-in by electronic surveillance. Materials and Methods. This was a multiple center observational cohort study conducted in 2016. The study population was comprised of patients screened-in by St. John Sepsis Surveillance Agent within four hours of ED arrival, had a sepsis bundle initiated, and admitted to hospital. We built multivariable logistic regression models to estimate impact of a 3-hour bundle completed within three hours of arrival on mortality outcomes. Results. Approximately 3% ED patients were screened-in by electronic surveillance within four hours of arrival and admitted to hospital. Nearly 7 in 10 (69%) patients had a bundle initiated, with most bundles completed within three hours of arrival. The fully-adjusted risk model achieved good discrimination on mortality outcomes (AUROC = .82, 95% CI = .79 to .85) and estimated 34% reduced mortality risk among patients with a bundle completed within three hours of arrival compared to non-completers. Discussion. The sepsis bundle is an effective intervention for many vulnerable patients, and likely to be completed within three hours after arrival when electronic surveillance with reliable alert notifications are integrated into clinical workflow. Beginning at triage, the platform and sepsis program enables identification and management of patients with greater precision, and increases the odds of good outcomes. Conclusion. Sepsis surveillance and clinical decision support accelerate accurate recognition and stratification of patients, and facilitate timely delivery of healthcare

Afobazole nanoparticles formulation for enhanced therapeutics

A novel nanoparticle drug composition and method of use thereof is presented herein. The nanoparticle drug composition is comprised of at least one nanoparticle carrier, formed from the conjugation of PLGA and PEG, which encapsulates a drug such as afobazole and its derivatives, in a pharmaceutically acceptable carrier. The nanoparticle drug composition may be used to treat various diseases of the central nervous system involving excessive neuronal activity and inflammation such as stroke, Alzheimer\u27s disease and anxiety

Afobazole nanoparticles formulation for enhanced therapeutics

A novel nanoparticle drug composition and method of use thereof is presented herein. The nanoparticle drug composition is comprised of at least one nanoparticle carrier, formed from the conjugation of PLGA and PEG, which encapsulates a drug such as afobazole and its derivatives, in a pharmaceutically acceptable carrier. The nanoparticle drug composition may be used to treat various diseases of the central nervous system involving excessive neuronal activity and inflammation such as stroke, Alzheimer\u27s disease and anxiety

Dryad_data_1508

Use Data for "sepsis surveillance and emergency treatment

Effect of freezing and hardening on injured versus intact cells of Listeria in ice cream mix.

Ice cream manufacturing relies on pasteurization to eliminate any Listeria contamination. However, factors such as cross-contamination levels, entrapment in polymorpholeukocytes, and product matrices may influence cellular injury. Our previous studies demonstrated a dose-dependent, random presence of heat-injured cells of Listeria in pasteurized ice cream mix. Such cells did not show any recovery within the mix itself under normal handling conditions. The present study evaluates the effect of freezing and hardening of ice cream mix on heat-injured and intact cells of Listeria. Raw ice cream mix (42% TS) samples were spiked with 4.36 ± 0.13 logs per gram of Listeria innocua (a surrogate) and subjected to pasteurization (69°C for 30min), which resulted in the random presence of heat-injured cells. To simulate the post-pasteurization contamination of mix with intact cells, 2.65 ± 0.07 logs per gram of L. innocua were spiked in the pasteurized mix samples. The mixes containing injured and intact cells were followed through aging (72h at 7°C), freezing (−4.4°C), and hardening (12 h at −40°C) steps. Direct plating on Listeria selective agars enumerated intact cells, while Listeria enrichment broth (BLEB) was used to recover heat-injured cells before plating. All trials were conducted in triplicates and data were statistically analyzed. Although no post-pasteurization survivors were observed on direct plating, the enrichment protocol revealed heatinjured cells at all of the post-pasteurization stages of processing, tested. Freezing and hardening steps thus did not appear to have any detrimental effects on heat-injured cells. Injured cells have not been associated with any outbreaks; however, it would be interesting to study their ability to recover during any handling-abuse at retail or consumer end. In case of spiked intact cells, no detrimental effect of freezing and hardening was observed. This implies that post-pasteurization contamination of mix might pose a greater risk. Results from this study emphasize a need to design stage-specific critical control points to prevent any potential Listeria outbreaks

Evaluating the recovery potential of injured cells of Listeria innocua under product temperature-abuse conditions and passage through simulated gastrointestinal fluids.

Ice cream handling and serving conditions on the consumer side may result in temperature abuse before consumption. Under some extreme conditions, even the sporadic presence of injured bacterial cells might pose a health risk due to the possibility of recovery of those cells. We conducted this investigation to evaluate the potential of injured cells of Listeria innocua to recover under ice cream temperature abuse conditions and on exposure to simulated gastrointestinal (GI) fluids. Ice cream mix samples (42% total solids), spiked with 4 log10 cfu/g of Listeria innocua, were thermally treated at 69°C for 30 min. Potential heat-injured cells were recovered in buffered Listeria broth (BLEB), followed by isolation on Listeria-specific modified Oxford agar (MOX). The ice cream mix samples, containing potentially injured cells of Listeria innocua, were followed through overnight aging (7°C), freezing (−3.3°C), and overnight hardening (−40°C) steps to obtain the final ice cream samples. To simulate temperature abuse conditions, the samples were held for 12 h at 4.4°C, followed by 30 min at room temperature (22°C); this treatment was considered the first cycle of temperature abuse. To generate a worst-case scenario, the samples were exposed to 3 such consecutive temperature abuse cycles. At the end of each cycle, direct plating was done on MOX to recover viable cells, and BLEB enrichment verified the presence of potential injured cells. In addition, the ice cream samples, containing potential injured cells, were passed through simulated GI fluids. As a first step, samples were mixed (1:1) with simulated gastric fluids (pH 1.0 and 2.0 before mixing) and held at 37°C in a shaker incubator. Samples drawn at 15, 30, and 60 min were analyzed for viable and potential injured cells. To study the effect of sequential transit through simulated intestinal fluid, a mixture of ice cream and gastric fluid (1:1) from the gastric fluid experiment above was added to simulated intestinal fluid (pH 6.8) and held at 37°C. Samples were analyzed at 30 and 360 min for viable and potential injured cells. Three trials were conducted and the samples collected in duplicates. The temperature abuse or GI fluid exposure studies did not result in the recovery of potential injured cells of Listeria innocua in the ice cream samples under the conditions tested. Exposure to gastric fluids, however, did not eliminate the potential injured cells. Further studies are necessary to understand the exact risk implications of these findings

Recovery potential of heat-injured cells of Listeria under ice cream temperature abuse conditions versus simulated gastrointestinal fluids

Serving practices in nursing homes may result in temperature abuse of ice cream before consumption. Presence of even low numbers of injured cells may pose a risk, due to their potential to recover, especially to immunocompromised patients. This investigation was conducted to evaluate injured cell recovery under temperature abuse conditions and on exposure to gastrointestinal (GI) fluids. Based on our previous studies, ice cream mix samples (42% TS), spiked with 4.54 log cfu/gram of Listeria innocua, were lab pasteurized (69°C for 30 min). Heat-injured cells were recovered in BLEB, followed by isolation on MOX. The ice cream mix samples, containing injured cells, were followed through overnight aging (7°C), freezing (−4°C), and overnight hardening (−40°C) steps. To simulate serving practices, the samples were held for 12 h at 4.4°C, followed by 30 min holding at room temperature (22°C), identified as the first cycle of temperature abuse. In all, the samples were exposed to 3 such consecutive cycles. At the end of each cycle, direct plating was done on MOX to detect any intact cells. Parallelly, the ice cream samples, containing injured cells, were mixed (1:1) with simulated gastric fluids (pH 1.0 and 2.0) and were held at 37°C in a shaker incubator. Samples were drawn at 15, 30, and 60 min intervals. For studying the effect of sequential transit through a simulated intestinal fluid, 2 mL of gastric fluid + ice cream (1:1) from gastric fluid experiments were added to 50 mL of simulated intestinal fluid (pH 6.8) and held at 37°C, as above. Samples were drawn at 30, and 360 min intervals. To ascertain the recovery of any injured cells, samples were direct plated on MOX. Experiments were conducted in replicates of 3 and counts were compared for differences. The temperature abuse or GI fluid exposure studies did not result in any recovery of injured cells in the ice cream samples. However, it was also observed that the injured cells were not eliminated during exposure to gastric fluid. Further studies are necessary to understand the exact implications of these findings

Role of Nutritional Factors in Pathogenesis of Cancer

Diet and nutrition are crucial factors throughout the complete life course in the promotion and upholding of good health. It has always been accepted that our defencelessness to infection and disease was influenced by diet and environmental as well as genetic factors. Nutrition is coming to the front position as a principle modifiable determinant of chronic disease, with scientific confirmation with time more supporting the view that alterations in diet have strong effects, equally positive as well as negative, on health throughout life. For the most part notably, nutritional adjustments may not only influence present health but also determine whether or not an individual will develop chronic non-communicable diseases like cancer. Diet is a blend of protective, mutagenic, and carcinogenic agents; the majority of them are metabolized by the enzymes of biotransformation process. Genetic polymorphisms that alter protein expression or else the function of these enzymes can change the risk of developing cancer. The scientific community has identified numerous naturally occurring materials in plant food with the power to resolve possible carcinogens. A few of these nutrients and natural phytochemicals look for toxins and usher them from the body before they can cause cell damage that may lead to cancer. Others give the impression to make it easier for the body to make repairs at the cellular level. At a standstill, others may help bring to an end cancer cells from reproducing. Even after a cell begins to experience damage that can lead to cancer, what you eat and drink, and how you live can still help short-circuit the cancer process. It is thought that a diet containing defensive micronutrients as well as carcinogens and mutagens may adapt the risk of cancer development, particularly in genetically susceptible individuals