On the role of the magnetic dipolar interaction in cold and ultracold collisions: Numerical and analytical results for NH(3Σ−^3\Sigma^-) + NH(3Σ−^3\Sigma^-)

We present a detailed analysis of the role of the magnetic dipole-dipole interaction in cold and ultracold collisions. We focus on collisions between magnetically trapped NH molecules, but the theory is general for any two paramagnetic species for which the electronic spin and its space-fixed projection are (approximately) good quantum numbers. It is shown that dipolar spin relaxation is directly associated with magnetic-dipole induced avoided crossings that occur between different adiabatic potential curves. For a given collision energy and magnetic field strength, the cross-section contributions from different scattering channels depend strongly on whether or not the corresponding avoided crossings are energetically accessible. We find that the crossings become lower in energy as the magnetic field decreases, so that higher partial-wave scattering becomes increasingly important \textit{below} a certain magnetic field strength. In addition, we derive analytical cross-section expressions for dipolar spin relaxation based on the Born approximation and distorted-wave Born approximation. The validity regions of these analytical expressions are determined by comparison with the NH + NH cross sections obtained from full coupled-channel calculations. We find that the Born approximation is accurate over a wide range of energies and field strengths, but breaks down at high energies and high magnetic fields. The analytical distorted-wave Born approximation gives more accurate results in the case of s-wave scattering, but shows some significant discrepancies for the higher partial-wave channels. We thus conclude that the Born approximation gives generally more meaningful results than the distorted-wave Born approximation at the collision energies and fields considered in this work.Comment: Accepted by Eur. Phys. J. D for publication in Special Issue on Cold Quantum Matter - Achievements and Prospects (2011

Differential metabolic effects of oral butyrate treatment in lean versus metabolic syndrome subjects

Background: Gut microbiota-derived short-chain fatty acids (SCFAs) have been associated with beneficial metabolic effects. However, the direct effect of oral butyrate on metabolic parameters in humans has never been studied. In this first in men pilot study, we thus treated both lean and metabolic syndrome male subjects with oral sodium butyrate and investigated the effect on metabolism. Methods: Healthy lean males (n = 9) and metabolic syndrome males (n = 10) were treated with oral 4 g of sodium butyrate daily for 4 weeks. Before and after treatment, insulin sensitivity was determined by a two-step hyperinsulinemic euglycemic clamp using [6,6-2H2]-glucose. Brown adipose tissue (BAT) uptake of glucose was visualized using 18F-FDG PET-CT. Fecal SCFA and bile acid concentrations as well as microbiota composition were determined before and after treatment. Results: Oral butyrate had no effect on plasma and fecal butyrate levels after treatment, but did alter other SCFAs in both plasma and feces. Moreover, only in healthy lean subjects a significant improvement was observed in both peripheral (median Rd: from 71 to 82 μmol/kg min, p < 0.05) and hepatic insulin sensitivity (EGP suppression from 75 to 82% p < 0.05). Although BAT activity was significantly higher at baseline in lean (SUVmax: 12.4 ± 1.8) compared with metabolic syndrome subjects (SUVmax: 0.3 ± 0.8, p < 0.01), no significant effect following butyrate treatment on BAT was observed in either group (SUVmax lean to 13.3 ± 2.4 versus metabolic syndrome subjects to 1.2 ± 4.1). Conclusions: Oral butyrate treatment beneficially affects glucose metabolism in lean but not metabolic syndrome subjects, presumably due to an altered SCFA handling in insulin-resistant subjects. Although preliminary, these first in men findings argue against oral butyrate supplementation as treatment for glucose regulation in human subjects with type 2 diabetes mellitus

The Buffer Gas Beam: An Intense, Cold, and Slow Source for Atoms and Molecules

Beams of atoms and molecules are stalwart tools for spectroscopy and studies of collisional processes. The supersonic expansion technique can create cold beams of many species of atoms and molecules. However, the resulting beam is typically moving at a speed of 300-600 m/s in the lab frame, and for a large class of species has insufficient flux (i.e. brightness) for important applications. In contrast, buffer gas beams can be a superior method in many cases, producing cold and relatively slow molecules in the lab frame with high brightness and great versatility. There are basic differences between supersonic and buffer gas cooled beams regarding particular technological advantages and constraints. At present, it is clear that not all of the possible variations on the buffer gas method have been studied. In this review, we will present a survey of the current state of the art in buffer gas beams, and explore some of the possible future directions that these new methods might take

EGFR, CD10 and proliferation marker Ki67 expression in ameloblastoma: possible role in local recurrence

<p>Abstract</p> <p>Background</p> <p>Ameloblastoma is an odontogenic neoplasm characterized by local invasiveness and tendency towards recurrence.</p> <p>Aims</p> <p>Studying the role played by EGFR, CD10 and Ki67 in the recurrence of ameloblastoma.</p> <p>Methods</p> <p>This study was carried out on 22 retrospective cases of mandibular ameloblastoma from the period from Jan 2002 to Jan 2008 with follow up period until Jan 2011 (3 to 8 years follow up peroid). Archival materials were obtained from pathology department, Mansoura university. Paraffin sections of tumor tissue from all cases were submitted for routine H&E stains and immunohistochemistry using EGFR, CD10 and Ki67 monoclonal antibodies. Statistical analysis using of clinical data for all patients, tumor type, EGFR, CD10 and Ki67 expression in relation to recurrence were evaluated.</p> <p>Results</p> <p>Among the 22 cases, 10 cases were males and 12 were females with sex ratio 1:1.2. Age ranged from 34 to 59 years old with a mean age 44.18 year. Five cases showed local recurrence within studied period and proved by biopsy. No statistically significant relation was found between local recurrence and patient age, tumor size, tumor type, EGFR expression. There was a significant relation between CD10 expression as well as Ki67 labelling index and recurrence (P value = 0.003, 0.000 respectively).</p> <p>Conclusion</p> <p>Evaluation of CD10 and Ki67 status together with conventional histological evaluation can help in providing more information about the biologic behavior of the tumor, while EGFR could be a target of an expanding class of anticancer therapies.</p> <p>Since ameloblastomas are EGFR-positive tumors, anti-EGFR agents could be considered to reduce the size of large tumors and to treat unresectable tumors that are in close proximity to vital structures.</p> <p>Virtual Slides</p> <p>The virtual slide(s) for this article can be found here:</p> <p><url>http://www.diagnosticpathology.diagnomx.eu/vs/1902106905645651</url></p

Oral functioning after open versus closed treatment of unilateral condylar neck or base fractures: A two-centre controlled clinical trial

Background: Oral functioning and rehabilitation in patients after condylar trauma can be measured by objective functional outcomes and patient-reported outcomes. The similarities or differences between these outcomes may contribute to the decision if open treatment (OT) or closed treatment (CT) will obtain the most advantageous results. Objectives: The aim of this study was to compare OT versus CT for unilateral condylar mandibular neck or base fractures in a two-centre controlled clinical trial by objective functional outcomes and patient-reported outcomes measured at 6 weeks and 6 months follow-up. Additionally, these outcomes were compared within each group. Methods: Patients were enrolled between January 2017 and November 2019. In one centre, patients received OT by extra-oral open reduction and internal fixation. In another centre, patients received CT by maxillomandibular fixation. Objective measurements included the mixing ability test (MAT) and mandibular active range of motion (ROM). Patient-reported outcomes included the mandibular function impairment questionnaire (MFIQ) and visual analogue scale (VAS) for pain. Independent t-tests and Mann–Whitney U-tests were used to determine differences between the treatment groups at 6 weeks and 6 months follow-up. Paired t-tests and Wilcoxon signed rank tests were used to determine differences within each group. Results: Thirty-three patients were enrolled. No differences were found between the groups treated with OT or CT for MAT, ROM, MFIQ and VAS. Both groups showed functional improvement. Conclusion: Good objective functional outcomes and patient-reported outcomes were achieved with both OT and CT in patients with unilateral condylar mandibular neck or base fractures

The vitamin D metabolites 25(OH)D and 1,25(OH)2D are not related to either glucose metabolism or insulin action in obese women

Aim: Vitamin D deficiency has been proposed to be involved in obesity-induced metabolic disease. However, data on the relationship between 25-hydroxycholecalciferol (25(OH)D) and insulin resistance have been inconsistent, and few studies have investigated the active vitamin D metabolite, 1,25-dihydroxycholecalciferol (1,25(OH)2D). This study aimed to determine the relationship between circulating levels of both 25(OH)D and 1,25(OH)2D and direct measures of glucose metabolism and insulin action in obese women. Methods: Serum levels of 25(OH)D and 1,25(OH)2D, and glucose metabolism and tissue-specific insulin action, as assessed in the basal state and during a two-step euglycaemic-hyperinsulinaemic clamp study with [6,6-2H2]glucose infusion, were measured in 37 morbidly obese women (age: 43±10 years; body mass index: 44±6kg/m2). Results: Sixteen subjects had circulating 25(OH)D levels<50nmol/L, consistent with vitamin D deficiency, and 21 had normal 25(OH)D levels. There were no differences in either baseline characteristics or parameters of glucose metabolism and insulin action between the groups. Serum 25(OH)D, but not 1,25(OH)2D, was negatively correlated with both body mass index (r =-0.42, P =0.01) and total body fat (r =-0.46, P <0.01). Neither 25(OH)D nor 1,25(OH)2D levels were related to any measured metabolic parameters, including fasting glucose, fasting insulin, basal endogenous glucose production, and hepatic, adipose-tissue and skeletal muscle insulin sensitivity. Conclusion: Obesity was associated with lower levels of circulating 25(OH)D, but not with the hormonally active metabolite 1,25(OH)2D. Neither 25(OH)D nor 1,25(OH)2D were related to glucose metabolism and tissue-specific insulin sensitivity in obese women, suggesting that vitamin D does not play a major role in obesity-related insulin resistance

Methods for quantifying adipose tissue insulin resistance in overweight/obese humans

Background/Objectives:Insulin resistance of adipose tissue is an important feature of obesity-related metabolic disease. However, assessment of lipolysis in humans requires labor-intensive and expensive methods, and there is limited validation of simplified measurement methods. We aimed to validate simplified methods for the quantification of adipose tissue insulin resistance against the assessment of insulin sensitivity of lipolysis suppression during hyperinsulinemic-euglycemic clamp studies.Subjects/Methods:We assessed the insulin-mediated suppression of lipolysis by tracer-dilution of [1,1,2,3,3-2 H 5]glycerol during hyperinsulinemic-euglycemic clamp studies in 125 overweight or obese adults (85 men, 40 women; age 50±11 years; body mass index 38±7 kg m2). Seven indices of adipose tissue insulin resistance were validated against the reference measurement method.Results:Low-dose insulin infusion resulted in suppression of the glycerol rate of appearance ranging from 4% (most resistant) to 85% (most sensitive), indicating a good range of adipose tissue insulin sensitivity in the study population. The reference method correlated with (1) insulin-mediated suppression of plasma glycerol concentrations (r=0.960, P<0.001), (2) suppression of plasma non-esterified fatty acid (NEFA) concentrations (r=0.899, P<0.001), (3) the Adipose tissue Insulin Resistance (Adipo-IR) index (fasting plasma insulin-NEFA product; r=0.526, P<0.001), (4) the fasting plasma insulin-glycerol product (r=0.467, P<0.001), (5) the Adipose Tissue Insulin Resistance Index (fasting plasma insulin-basal lipolysis product; r=0.460, P<0.001), (6) the Quantitative Insulin Sensitivity Check Index (QUICKI)-NEFA index (r=0.621, P<0.001), and (7) the QUICKI-glycerol index (r=0.671, P<0.001). Bland-Altman plots showed no systematic errors for the suppression indices but proportional errors for all fasting indices. Receiver-operator characteristic curves confirmed that all indices were able to detect adipose tissue insulin resistance (area under the curve ≥0.801, P<0.001).Conclusions:Adipose tissue insulin sensitivity (that is, the antilipolytic action of insulin) can be reliably quantified in overweight and obese humans by simplified index methods. The sensitivity and specificity of the Adipo-IR index and the fasting plasma insulin-glycerol product, combined with their simplicity and acceptable agreement, suggest that these may be most useful in clinical practice

Insulin resistance in obesity can be reliably identified from fasting plasma insulin

Insulin resistance is the major contributor to cardiometabolic complications of obesity. We aimed to (1) establish cutoff points for insulin resistance from euglycemic hyperinsulinemic clamps (EHCs), (2) identify insulin-resistant obese subjects and (3) predict insulin resistance from routinely measured variables. We assembled data from non-obese (n=112) and obese (n=100) men who underwent two-step EHCs using [6,6-(2)H2]glucose as tracer (insulin infusion dose 20 and 60 mU m(-2) min(-1), respectively). Reference ranges for hepatic and peripheral insulin sensitivity were calculated from healthy non-obese men. Based on these reference values, obese men with preserved insulin sensitivity or insulin resistance were identified. Cutoff points for insulin-mediated suppression of endogenous glucose production (EGP) and insulin-stimulated glucose disappearance rate (Rd) were 46.5% and 37.3 μmol kg(-)(1) min(-)(1), respectively. Most obese men (78%) had EGP suppression within the reference range, whereas only 12% of obese men had Rd within the reference range. Obese men with Rd 74 pmol l(-1). Most obese men have hepatic insulin sensitivity within the range of non-obese controls, but below-normal peripheral insulin sensitivity, that is, insulin resistance. Fasting insulin (>74 pmol l(-1) with current insulin immunoassay) may be used for identification of insulin-resistant (or metabolically unhealthy) obese men in research and clinical setting

Taming molecular beams

Contains fulltext : 98803.pdf (preprint version ) (Open Access

The pathophysiology of human obstructive cholestasis is mimicked in cholestatic Gold Syrian hamsters

Obstructive cholestasis causes liver injury via accumulation of toxic bile acids (BAs). Therapeutic options for cholestatic liver disease are limited, partially because the available murine disease models lack translational value. Profiling of time-related changes following bile duct ligation (BDL) in Gold Syrian hamsters revealed a biochemical response similar to cholestatic patients in terms of BA pool composition, alterations in hepatocyte BA transport and signaling, suppression of BA production, and adapted BA metabolism. Hamsters tolerated cholestasis well for up to 28days and progressed relatively slowly to fibrotic liver injury. Hepatocellular necrosis was absent, which coincided with preserved intrahepatic energy levels and only mild oxidative stress. The histological response to cholestasis in hamsters was similar to the changes seen in 17 patients with prolonged obstructive cholestasis caused by cholangiocarcinoma. Hamsters moreover upregulated hepatic fibroblast growth factor 15 (Fgf15) expression in response to BDL, which is a cytoprotective adaptation to cholestasis that hitherto had only been documented in cholestatic human livers. Hamster models should therefore be added to the repertoire of animal models used to study the pathophysiology of cholestatic liver diseas