Sonoluminescing air bubbles rectify argon

The dynamics of single bubble sonoluminescence (SBSL) strongly depends on the percentage of inert gas within the bubble. We propose a theory for this dependence, based on a combination of principles from sonochemistry and hydrodynamic stability. The nitrogen and oxygen dissociation and subsequent reaction to water soluble gases implies that strongly forced air bubbles eventually consist of pure argon. Thus it is the partial argon (or any other inert gas) pressure which is relevant for stability. The theory provides quantitative explanations for many aspects of SBSL.Comment: 4 page

Dynamic MAIT cell response with progressively enhanced innateness during acute HIV-1 infection.

Mucosa-associated invariant T (MAIT) cell loss in chronic HIV-1 infection is a significant insult to antimicrobial immune defenses. Here we investigate the response of MAIT cells during acute HIV-1 infection utilizing the RV217 cohort with paired longitudinal pre- and post-infection samples. MAIT cells are activated and expand in blood and mucosa coincident with peak HIV-1 viremia, in a manner associated with emerging microbial translocation. This is followed by a phase with elevated function as viral replication is controlled to a set-point level, and later by their functional decline at the onset of chronic infection. Interestingly, enhanced innate-like pathways and characteristics develop progressively in MAIT cells during infection, in parallel with TCR repertoire alterations. These findings delineate the dynamic MAIT cell response to acute HIV-1 infection, and show how the MAIT compartment initially responds and expands with enhanced function, followed by progressive reprogramming away from TCR-dependent antibacterial responses towards innate-like functionality

Occurrence of malignant neoplasia in patients with primary hyperparathyroidism

Introduction The association between primary hyperparathyroidism (1HPT) and cancer is debated. The present study was aimed to investigate the occurrence of neoplasia in 1HPT. Patients and methods All consecutive patients (n = 1750) referred to our \u201cOsteoporosis and Metabolic Disease\u201d outpatients clinic for osteoporosis or hypercalcemia were eligible for the study. The exclusion criteria were: the finding of osteoporosis and/or altered calcium-phosphorous metabolism in the context of investigations for malignancy, the presence of diseases known to influence the cancer risk and the heavy smoking habit. Eventually, 1606 patients (1407 females, 199 males) were enrolled. In all patients calcium-phosphorous metabolism, PTH and vitamin D levels were measured and the occurrence of cancer during the 10 years prior the study inclusion was recorded. Results One-hundred-sixty-three patients had 1HPT while 1443 had not. Patients with and without 1HPT were comparable for age and gender. In 1HPT patients the occurrence of all, breast, kidney and skin cancer was significantly higher (21.5%, 12.2%, 2.5%, 1.8%, respectively) than in patients without 1HPT (12.4%, 6.9%, 0.3%, 0.3%, p < 0.05 for all comparisons). The 1HPT presence was significantly associated with the occurrence of all neoplasia and of breast, skin and kidney neoplasia (odds ratio, 95% confidence interval, p value: 1.93, 1.27\u20132.92, 0.002; 1.93, 1.11\u20133.35, 0.002; 9.18, 2.16\u201338.8, 0.003; 8.23, 1.71\u201339.5, 0.008, respectively), after adjusting for age, gender (as appropriate), smoking habit and vitamin D levels. Conclusion During the 10 years prior the diagnosis of 1HPT, the occurrence of all, breast, skin and kidney neoplasia is increased

Energy metabolism and ketogenic diets: What about the skeletal health? a narrative review and a prospective vision for planning clinical trials on this issue

The existence of a common mesenchymal cell progenitor shared by bone, skeletal muscle, and adipocytes cell progenitors, makes the role of the skeleton in energy metabolism no longer surprising. Thus, bone fragility could also be seen as a consequence of a “poor” quality in nutrition. Ketogenic diet was originally proven to be effective in epilepsy, and long-term follow-up studies on epileptic children undergoing a ketogenic diet reported an increased incidence of bone fractures and decreased bone mineral density. However, the causes of such negative impacts on bone health have to be better defined. In these subjects, the concomitant use of antiepileptic drugs and the reduced mobilization may partly explain the negative effects on bone health, but little is known about the effects of diet itself, and/or generic alterations in vitamin D and/or impaired growth factor production. Despite these remarks, clinical studies were adequately designed to investigate bone health are scarce and bone health related aspects are not included among the various metabolic pathologies positively influenced by ketogenic diets. Here, we provide not only a narrative review on this issue, but also practical advice to design and implement clinical studies on ketogenic nutritional regimens and bone health outcomes. Perspectives on ketogenic regimens, microbiota, microRNAs, and bone health are also included

Trends in alcohol use among Hawai‘i adolescents

It is important to review trends in youth alcohol use over time in order to effectively tailor prevention programs to address those trends. This article reviews data on alcohol use behaviors from the Centers for Disease Control and Prevention\u27s Youth Risk Behavior Survey in Hawai‘i from 1993 to 2007. Five alcohol use indicators were examined and stratified by grade level, from 9th grade through 12th grade. Significant drops in nearly all indicators are seen among 9th through 11th graders, but not among 12th graders. This suggests that Hawai‘i youth are responding well to anti-alcohol messaging as young teens, but a different approach may be needed to target older teens

Defining non-functioning adrenal adenomas on the basis of the occurrence of hypocortisolism after adrenalectomy

Background In patients with adrenal incidentalomas (AI), there is uncertainty on how to rule out hypercortisolism. The occurrence of post-surgical (unilateral adrenalectomy) hypocortisolism (PSH) has been proposed as a proof of the presence of a pre-surgical hypercortisolism in AI patients. The aim of this study was to define the thresholds of cortisol level after 1 mg overnight dexamethasone suppression test (F-1mgDST), urinary free cortisol (UFC), midnight serum cortisol (MSC) and adrenocorticotroph hormone (ACTH) able to predict the absence of PSH in AI patients undergoing surgery. Methods In 60 patients who underwent AI excision, cortisol secretion was assessed by low-dose corticotropin stimulation test or insulin tolerance test, when needed. We searched for the lowest pre-surgical value of F-1mgDST, UFC and MSC and the highest value for ACTH in AI patients with PSH as indexes of normal cortisol secretion. Results the lowest values of F-1mgDST, UFC and MSC and the highest value for ACTH in PSH patients were 1.2 \ub5g/dL (33 nmol/L), 10.4 \ub5g/24h (29 nmol/24h), 1.2 \ub5g/dL (33 nmol/L) and 26.9 pg/ml (6 pmol/L), respectively, but only F-1mgDST &lt;1.2 \ub5g/dL (33 nmol/L) was able to predict the absence of PSH. Among AI patients with F-1mgDST &lt;1.2 \ub5g/dL (33 nmol/L) no subjects had diabetes mellitus and/or metabolic syndrome and these subjects tended to have a better metabolic profile than those with F-1mgDST 651.2 \ub5g/dL (33nmol/L) Conclusion in AI patients a F-1mgDST &lt;1.2 \u3bcg/dL (33 nmol/L) rules out PSH and could be used to exclude hypercortisolism in AI patients

Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility

Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of bone fragility fractures compared to nondiabetic subjects. This increased fracture risk may occur despite normal or even increased values of bone mineral density (BMD), and poor bone quality is suggested to contribute to skeletal fragility in this population. These concepts explain why the only evaluation of BMD could not be considered an adequate tool for evaluating the risk of fracture in the individual T2DM patient. Unfortunately, nowadays, the bone quality could not be reliably evaluated in the routine clinical practice. On the other hand, getting further insight on the pathogenesis of T2DM-related bone fragility could consent to ameliorate both the detection of the patients at risk for fracture and their appropriate treatment. The pathophysiological mechanisms underlying the increased risk of fragility fractures in a T2DM population are complex. Indeed, in T2DM, bone health is negatively affected by several factors, such as inflammatory cytokines, muscle-derived hormones, incretins, hydrogen sulfide (H2S) production and cortisol secretion, peripheral activation, and sensitivity. All these factors may alter bone formation and resorption, collagen formation, and bone marrow adiposity, ultimately leading to reduced bone strength. Additional factors such as hypoglycemia and the consequent increased propensity for falls and the direct effects on bone and mineral metabolism of certain antidiabetic medications may contribute to the increased fracture risk in this population. The purpose of this review is to summarize the literature evidence that faces the pathophysiological mechanisms underlying bone fragility in T2DM patients

Pathophysiology and Management of Type 2 Diabetes Mellitus Bone Fragility

Individuals with type 2 diabetes mellitus (T2DM) have an increased risk of bone fragility fractures compared to nondiabetic subjects. This increased fracture risk may occur despite normal or even increased values of bone mineral density (BMD), and poor bone quality is suggested to contribute to skeletal fragility in this population. These concepts explain why the only evaluation of BMD could not be considered an adequate tool for evaluating the risk of fracture in the individual T2DM patient. Unfortunately, nowadays, the bone quality could not be reliably evaluated in the routine clinical practice. On the other hand, getting further insight on the pathogenesis of T2DM-related bone fragility could consent to ameliorate both the detection of the patients at risk for fracture and their appropriate treatment. The pathophysiological mechanisms underlying the increased risk of fragility fractures in a T2DM population are complex. Indeed, in T2DM, bone health is negatively affected by several factors, such as inflammatory cytokines, muscle-derived hormones, incretins, hydrogen sulfide (H2S) production and cortisol secretion, peripheral activation, and sensitivity. All these factors may alter bone formation and resorption, collagen formation, and bone marrow adiposity, ultimately leading to reduced bone strength. Additional factors such as hypoglycemia and the consequent increased propensity for falls and the direct effects on bone and mineral metabolism of certain antidiabetic medications may contribute to the increased fracture risk in this population. The purpose of this review is to summarize the literature evidence that faces the pathophysiological mechanisms underlying bone fragility in T2DM patients

Bubble Shape Oscillations and the Onset of Sonoluminescence

An air bubble trapped in water by an oscillating acoustic field undergoes either radial or nonspherical pulsations depending on the strength of the forcing pressure. Two different instability mechanisms (the Rayleigh--Taylor instability and parametric instability) cause deviations from sphericity. Distinguishing these mechanisms allows explanation of many features of recent experiments on sonoluminescence, and suggests methods for finding sonoluminescence in different parameter regimes.Comment: Phys. Rev. Lett., in pres