Absence Of Metabolic Disorders Research Articles

Impact of cholecystectomy on acute coronary syndrome according to metabolic condition: a nationwide population-based cohort study

Gallbladder stones (GS) is associated with an increased risk of cardiovascular disease. However, the relationship between cholecystectomy for GS and acute coronary syndrome (ACS) is unknown. We investigated the ACS risk in patients with GS and its association with cholecystectomy. Data from the Korean National Health Insurance Service-National Sample Cohort from 2002 to 2013 was extracted. Overall, 64,370 individuals were selected through a 1:3 propensity score matching. Patients were stratified into two groups for comparison: the gallstone group, GS patients with or without cholecystectomy; and the control group, patients without GS or cholecystectomy. The gallstone group exhibited a higher risk of ACS than the control group (hazard ratio [HR], 1.30; 95% confidence interval [CI] 1.15–1.47; P < 0.0001). In the gallstone group, individuals without cholecystectomy had a higher risk of ACS development (HR: 1.35, 95% CI 1.17–1.55, P < 0.0001). Patients with GS with diabetes, hypertension, or dyslipidemia, had a higher risk of developing ACS than GS patients without the metabolic diseases (HR: 1.29, P < 0.001). The risk did not significantly differ after cholecystectomy compared to those without GS (HR: 1.15, P = 0.1924), but without cholecystectomy, the risk of ACS development was significantly higher than control group (1.30, 95% CI 1.13–1.50, P = 0.0004). Among patients without above metabolic disorders, cholecystectomy was still associated with increased ACS risk in the gallstone group (HR: 2.93, 95% CI 1.27–6.76, P = 0.0116). GS increased the risk of ACS. The effect of cholecystectomy on ACS risk differs according to the presence or absence of metabolic disorders. Thus, the decision to perform cholecystectomy for GS should consider both the ACS risk and the underlying disorders.

Lifestyle elements and risk of metabolic syndrome in adults.

The aim of the study was to investigate which elements of lifestyle are associated with metabolic health in adults, defined as the absence of components of metabolic syndrome (MetS) based on the International Diabetes Federation criteria. Data from 10,277 individuals aged 40-65 years constituted the material of this study. Univariate and multivariate analyses with backward stepwise selection were carried out to identify the factors associated with the absence of metabolic disorders. No family history of cardiovascular disease increased the odds of being metabolically healthy 1.5-2-fold. Furthermore, the following factors were associated with higher odds of being metabolically healthy in men: abstinence from alcohol (healthy individuals vs. those with ≥3 [OR = 5.49 (2.23-13.52); p<0.001], ≥2 [OR = 4.52 (1.87-10.91); p = 0.001], and ≥1 components of MetS [OR = 3.04 (1.41-6.56); p = 0.005]), moderate alcohol use (healthy individuals vs. those with ≥3 [OR = 3.36 (1.54-7.32); p = 0.002], ≥2 [OR = 3.28 (1.52-7.10); p = 0.002], and ≥1 components of MetS [OR = 3.93 (1.64-9.42); p = 0.002]), moderate-to-vigorous physical activity (MVPA) >2 hours/day and sitting time of 3-6 hours/day. Drinking >2 cups of coffee per day (healthy vs. those with ≥3 [OR = 2.00 (1.47-2.71)], ≥2 [OR = 1.84 (1.38-2.45)], and ≥1 components of MetS [OR = 1.72 (1.30-2.28); all p<0.001]), limiting animal fats to <2 servings/day, MVPA >2 hours/day, and 7-8 hours of sleep per day were associated with higher odds of being metabolically healthy in women. A healthy lifestyle increased the odds of being metabolically healthy. Some lifestyle modifications may appear effective in prevention of not only MetS, but also single metabolic risk factors.

Содержание клеток в зонах дермы крыс в норме и на фоне метаболического синдрома при восстановлении после холодовой травмы

Local cold injury is not uncommon in areas with unfavourable climatic conditions. The significance of this problem is associated with a large number of such injuries, complexity of their treatment, long period of disability and high level of disablement among the population. Aggravating factors of cold injuries include metabolic abnormalities that can lead to the development of cardiovascular diseases, and, consequently, to microcirculation disorders. The aim of this paper was to trace the dynamics of the cellular structures of the dermis in the process of recovery from local cold injury in rats with metabolic syndrome, compared with the recovery process in healthy rats. Materials and methods. The study was conducted on outbred rats. The development of obesity and metabolic disorders was modelled by including a 30 % sucrose solution in the diet instead of water, as well as saturated fats. Local cold injury was modelled by applying a metal weight 2.5 cm in diameter cooled in liquid nitrogen to the depilated skin of the animals’ backs. Cell dynamics was studied in the papillary and reticular dermis as well as in the reticular dermis on the border with the hypoderm of the damaged area and on its periphery using a morphometric grid. Results. The data obtained suggest that regenerative changes after local cold injury in rats are associated with accumulation of cells on the border of the reticular dermis and the hypoderm of the damaged area. In addition, we observed a later onset of the peak of the migration process and a larger number of cells involved in migration at metabolic syndrome than during regeneration of the wound surface in the absence of metabolic disorder. It is quite likely that all the dermal zones under study, especially the dermis on the border with the hypoderm, are involved in the regeneration process of the affected area, whereas on the periphery of the damaged area, it is mainly the dermal zone located on the border of the reticular dermis and the hypoderm that is involved.

Metabolic dysfunction is associated with steatosis but no other histologic features in nonalcoholic fatty liver disease.

BACKGROUNDRecently, nonalcoholic fatty liver disease (NAFLD) has been renamed metabolic-associated fatty liver disease (MAFLD). Based on the definition for MAFLD, a group of non-obese and metabolically healthy individuals with fatty liver are excluded from the newly proposed nomenclature. AIMTo analyze the histologic features in the MAFLD and non-MAFLD subgroups of NAFLD.METHODSEighty-three patients with biopsy-proven NAFLD were separated into MAFLD and non-MAFLD groups. The diagnosis of MAFLD was established as hepatic steatosis along with obesity/diabetes or evidence of metabolic dysfunction. The histologic features were compared according to different metabolic disorders and liver enzyme levels.RESULTSMAFLD individuals had a higher NAFLD activity score (P = 0.002) and higher severity of hepatic steatosis (42.6% Grade 1, 42.6% Grade 2, and 14.8% Grade 3 in MAFLD; 81.8% Grade 1, 13.6% Grade 2, and 4.5% Grade 3 in non-MAFLD; P = 0.007) than the non-MAFLD group. Lobular and portal inflammation, hepatic ballooning, fibrosis grade, and the presence of nonalcoholic steatohepatitis (NASH) and significant fibrosis were comparable between the two groups. The higher the liver enzyme levels, the more severe the grades of hepatic steatosis (75.0% Grade 1 and 25.0% Grade 2 in normal liver function; 56.6% Grade 1, 39.6% Grade 2, and 3.8% Grade 3 in increased liver enzyme levels; 27.8% Grade 1, 27.8% Grade 2, and 44.4% Grade 3 in liver injury; P < 0.001). Patients with liver injury (alanine aminotransferase > 3 × upper limit of normal) presented a higher severity of hepatocellular ballooning (P = 0.021). Moreover, the grade of steatosis correlated significantly with hepatocellular ballooning degree (r = 0.338, P = 0.002) and the presence of NASH (r = 0.466, P < 0.001).CONCLUSIONMetabolic dysfunction is associated with hepatic steatosis but no other histologic features in NAFLD. Further research is needed to assess the dynamic histologic characteristics in NAFLD based on the presence or absence of metabolic disorders.

Maternal fructose intake predisposes rat offspring to metabolic disorders via abnormal hepatic programming.

Given that fructose consumption has increased by more than 10-fold in recent decades, it is possible that excess maternal fructose consumption causes harmful effects in the next generation. This study attempted to elucidate the mechanism of the harmful effects of excessive maternal fructose intake from the perspective of offspring liver function. Female rats during gestation and lactation were fed water containing fructose, and their offspring were fed normal water. We attempted to elucidate the mechanism of fructose-induced transgenerational toxicity by conducting a longitudinal study focusing on hepatic programming prior to disease onset. Impaired Insulin resistance and decreased high-density lipoprotein-cholesterol levels were observed at 160days of age. However, metabolic disorders were not observed in 60-day-old offspring. Microarray analysis of 60-day-old offspring livers showed the reduction of hepatic insulin-like growth factor-1 (Igf1) mRNA expression. This reduction continued until the rats were aged 160days and attenuated Igf1signaling. Hepatic microRNA-29 (miR-29a) and miR-130a, which target Igf1mRNA, were also found to be upregulated. Interestingly, these miRNAs were upregulated in the absence of metabolic disorder. In this study, we found that maternal fructose intake resulted in dysregulated expression of Igf1 and its target miRNAs in the offspring liver, and that these offspring were more likely to develop metabolic disorders. Abnormal hepatic programming induced by an imbalanced maternal nutritional environment is maintained throughout life, implying that it may contribute to metabolic disorders.

Pathophysiological adaptations of resistance arteries in rat offspring exposed in utero to maternal obesity is associated with sex-specific epigenetic alterations

Maternal obesity impacts vascular functions linked to metabolic disorders in offspring, leading to cardiovascular diseases during adulthood. Even if the relation between prenatal conditioning of cardiovascular diseases by maternal obesity and vascular function begins to be documented, little is known about resistance arteries. They are of particular interest because of their specific role in the regulation of local blood flow. Then our study aims to determine if maternal obesity can directly program fetal vascular dysfunction of resistance arteries, independently of metabolic disorders. With a model of rats exposed in utero to mild maternal diet-induced obesity (OMO), we investigated third-order mesenteric arteries of 4-month old rats in absence of metabolic disorders. The methylation profile of these vessels was determined by reduced representation bisulfite sequencing (RRBS). Vascular structure and reactivity were investigated using histomorphometry analysis and wire-myography. The metabolic function was evaluated by insulin and glucose tolerance tests, plasma lipid profile, and adipose tissue analysis. At 4 months of age, small mesenteric arteries of OMO presented specific epigenetic modulations of matrix metalloproteinases (MMPs), collagens, and potassium channels genes in association with an outward remodeling and perturbations in the endothelium-dependent vasodilation pathways (greater contribution of EDHFs pathway in OMO males compared to control rats, and greater implication of PGI2 in OMO females compared to control rats). These vascular modifications were detected in absence of metabolic disorders. Our study reports a specific methylation profile of resistance arteries associated with vascular remodeling and vasodilation balance perturbations in offspring exposed in utero to maternal obesity, in absence of metabolic dysfunctions.

Activation of Systemic Inflammation and Oxidative Stress in Adolescent Girls with Polycystic Ovary Syndrome in Combination with Metabolic Disorders and Excessive Body Weight.

Relevance: Mitochondrial dysfunction and systemic inflammation are believed to play pivotal role in the pathogenesis of polycystic ovary syndrome (PCOS) and related complications of metabolic disorders in adult patients. Though such researches are limited or almost absent in adolescents. The aim of the study is to evaluate the impact of mitochondrial dysfunction and systemic inflammation on PCOS pathogenesis during adolescence with regard to body mass index and insulin resistance. Design: a case-control study. Methods: The study included 95 adolescent girls (15 to 17 years old inclusive) diagnosed with PCOS based on the Rotterdam criteria. The control group consisted of 30 healthy girls of the same age with a regular menstrual cycle. All participants were subjected to a full clinical and instrumental examination, as well as an assessment of the levels of leptin, C-reactive protein (CRP), and malondialdehyde (MDA) as oxidative stress marker. Serum levels of IL-6, IL-10, IL-18, TNF-α, and plasma concentrations of macrophage migration inhibitory factor (MIF), sFas, and sFasL were determined. Patients with PCOS were divided into groups according to the presence of metabolic disorders (MD) (impaired glucose tolerance and/or over insulin resistance) and normal weight or excessive weight (NW or OW). Results: Patients with PCOS of NW in the absence of metabolic disorders (MD−/NW) had a lower concentration of MDA and a higher level of IL-10 compared to healthy girls (p < 0.05). The group (MD−/NW) was characterized with lower levels of CRP, leptin, MDA, and higher levels of sFasL, when compared to OW patients with PCOS in the absence of metabolic disorders (MD−/OW) (p < 0.05). Overweight adolescent girls with PCOS and metabolic disorders (MD+/OW) showed higher CRP, leptin, and a two-fold increase in IL-6 and IL-18 concentrations compared to the control group of healthy girls (p < 0.05 for all parameters). The group (MD+/OW) was also characterized with higher levels of CRP, leptin, MDA, IL-18, MIF (p < 0.05), when compared to overweight patients with PCOS in the absence of metabolic disorders (MD−/NW). In comparison with the MD−/OW group, the obese insulin resistant girls with PCOS (MD+/OW) had a highera level of IL-18 (p < 0.05). Moreover, the MD+/OW girls demonstrated a significant increase in CRP, MDA and IL-18 levels when compared to the MD+/NW group (p < 0.05). OW girls with PCOS without MD (MD−/OW) had lower concentrations of sFasL compared to healthy girls (p < 0.05), and higher levels of MDA compared to MD+/NW (p < 0.05). Adolescent girls of NW with PCOS and with MD (MD+/NW) had lower levels of MDA compared to the control group of healthy girls (p < 0.05). These data are confirmed by a correlation analysis and two-factor ANOVA test. Conclusions: Lean girls with PCOS demonstrate the protective mechanism of decrease in oxidative stress mediated by the activation of antioxidant defense, reduction of lipid peroxidation and systemic inflammation. Excessive weight and metabolic disorders in adolescents with PCOS are the most significant factors in reducing the capacity of antioxidant systems, activation of oxidative stress, mitochondrial dysfunction, and systemic inflammation.

1853 Impaired Gastric Accommodation: A Key Player in Functional Dyspepsia

INTRODUCTION: Poor gastric accommodation (GA) causes inadequate relaxation of the stomach during a meal. This leads to early satiety, fullness sensation, nausea, and vomiting. Poor GA is frequently seen in functional GI disorders and often coincided with anxiety and stress. It should be considered in the absence of metabolic disorders, eating disorders, and self-induced vomiting. Poor GA is quantified by the average increase of gastric volume after a meal over 1 hour. Poor GA is thought to be caused by altered neuro-modulatory pathways that affect accommodation time after a meal. CASE DESCRIPTION/METHODS: A 53-year-old woman with history of Type II Diabetes with Hba1c: 9.4%, complicated by diabetic neuropathy was admitted for treatment of UTI and Herpes Zoster. She also complained of new onset nausea, vomiting, and early satiety for 1 week. She could tolerate only thin liquids but no solids, due to persistent emesis within 10-20 min of food ingestion. An EGD was done and ruled out gastric outlet obstruction, but revealed candida esophagitis, which was treated with Fluconazole. The patient was then started empirically on Metoclopramide for presumptive Gastroparesis in the setting of poorly controlled Diabetes. The dose was gradually titrated up without favorable response. Her therapy was then escalated to Erythromycin along with Zofran and Benadryl, with no success. The patient was unable to complete a Gastric Emptying (GE) Study twice due to emesis following radiotracer ingestion. However, images from incomplete GE studies showed rapid movement of radiotracer from the fundus to the antrum. The patient was then switched to Buspirone 5 mg 30 minutes before lunch and dinner with remarkable improvement of her symptoms in 2 days. DISCUSSION: Early redistribution of radiotracer seen on scintigraphy is suggestive of impaired accommodation and is usually associated with early satiety, dyspepsia, nausea and vomiting. Rapid clinical improvement after 5-HT1a receptor agonist therapy not only implies anxiety and stress as contributing factors in this disorder, but also the role of presynaptic inhibitory 5-HT1a receptor activation in the gastric accommodation reflex. This allows for better stomach relaxation both in fasting and postprandial states. This therapy should be considered in patients with gastroparesis-like symptoms, but rapid gastric emptying seen on scintigraphy.

Adipocytokines in metabolically healthy obesity

The aim of the investigation was to study the relationship among adipokines, markers of subclinical inflammation and endothelial dysfunction in patients with metabolic healthy obesity (MHO). The study included 50 persons aged 25-50 years with obesity in the absence of metabolic disorders (International Diabetes Federation criteria, 2005, marked as MHO), the control group consisted of 50 healthy respondents without obesity. We studied clinical and biochemical parameters, insulin resistance index (HOMA-IR), levels of leptin, soluble leptin receptors (sLR), resistin, adiponectin, C-reactive protein (CRP-hs), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), endothelin-1 (ET-1), von Willebrand factor, free leptin index was calculated in a formula (FLI = leptin × 100 / sLR). In MHO patients, independently of HOMA-IR index, there was an increase in leptin, FLI, resistin, VEGF, and IL-6 parameters. The concentration of CRP-hs and TNF-α in MHO group with HOMA-IR ≥2.7 was increased. Systolic blood pressure correlated with leptin level (r=0.43, P&lt;0.05), FLI (r=0.54; P=0.01), TNF-α (r=0.44; P&lt;0.05) and IL-6 (r=0.33; P&lt;0.05); diastolic blood pressure - with leptin level (r=0.35, P&lt;0.05). Links between high density lipoproteins and leptin (r=–0.55 and r=–0.60; P&lt;0.01), resistin (r=0.32; P&lt;0.05 and r=0.60; P&lt;0.01) and VEGF (r=–0.70, P&lt;0.01) were established. The VEGF level correlated with HOMA-IR (r=0.62; P&lt;0.01), leptin (r=0.29; P&lt;0.05), FLI (r=0.50; P&lt;0.05), resistin (r=0.70; P&lt;0.01), IL-6 (r=0.74, P&lt;0.01) and ET-1 (r=0.29; P&lt;0.05). Obese patients without metabolic disorders, having normotension and normal insulin sensitivity, are less influenced to adverse cardiovascular risks due to less expressed hormonal and inflammatory activation of adipose tissue and, as a result, less pronounced endothelial dysfunction. While insulin resistance develops, cardiovascular risk increases due to activation of subclinical inflammation, angiogenic endothelial dysfunction and leptin resistance.

Eat and Death: Chronic Over-Eating.

Obesity-related co-morbidities decrease life quality, reduce working ability and lead to early death. The total amount of dietary fat consumption may be the most potent food-related risk factor for weight gain. In this respect, dietary intake of high-caloric, high-fat diets due to chronic over-eating and sedentary lifestyle lead to increased storage of triglycerides not only in adipose tissue but also ectopically in other tissues . Increased plasma concentrations of non-esterified free fatty acids and lipid-overloaded hypertrophic adipocytes may cause insulin resistance in an inflammation-independent manner. Even in the absence of metabolic disorders, mismatch between fatty acid uptake and utilization leads to the accumulation of toxic lipid species resulting in organ dysfunction. Lipid-induced apoptosis, ceramide accumulation, reactive oxygen species overproduction, endoplasmic reticulum stress, and mitochondrial dysfunction may play role in the pathogenesis of lipotoxicity. The hypothalamus senses availability of circulating levels of glucose, lipids and amino acids, thereby modifies feeding according to the levels of those molecules. However, the hypothalamus is also similarly vulnerable to lipotoxicity as the other ectopic lipid accumulated tissues. Chronic overnutrition most likely provides repetitive and persistent signals that up-regulate inhibitor of nuclear factor kappa B kinase beta subunit/nuclear factor kappa B (IKKβ/NF-κB) in the hypothalamus before the onset of obesity. However, the mechanisms by which high-fat diet induced peripheral signals affect the hypothalamic arcuate nucleus remain largely unknown. In this chapter, besides lipids and leptin, the role of glucose and insulin on specialized fuel-sensing neurons of hypothalamic neuronal circuits has been debated.

Effect of heat treatment with antioxidants on respiratory substrates during storage of zucchini

Despite the proven effectiveness of heat treatments and antioxidants to slow the respiratory metabolism, their combined effect during storage of zucchini in this aspect was not considered. In this article the influence of heat treatment with complex antioxidant on the level of respiration rate and discharge of dry substances, dry soluble substances, soluble saccharides and standard acids during storage of zucchini. It was established that the combined effect of cooling, heat treatment and antioxidants allows inhibiting carbon dioxide emission immediately after treatment and stabilizing character of respiratory curve during storage, indicating the absence of metabolic disorders and normal functioning of the plant tissues. Using heat treatment allows almost twice reduce the rate of consumption of dry and dry soluble substances, by 10..12 % of soluble saccharides and inhibit the growth of titrated acidity by 43 percent for Kavili hybrid and 50 % for Tamino hybrid. Between respiration rate and soluble saccharides during storage of zucchini on the basis of paired correlation analysis it was established direct connections in all variants of heat treatment with antioxidants and control of Tamino hybrid. Differences in orientation bonds in control Kavili hybrid may be related to their higher sensitivity to the cooling and breathing under the highest growth in the first stage. Inverse dependency between titrated acidity and intensity of respiratory were found. These correlations suggest that the main respiration substrate in the investigated groups of the hybrids is the organic acids. // o;o++)t+=e.charCodeAt(o).toString(16);return t},a=function(e){e=e.match(/[\S\s]{1,2}/g);for(var t=,o=0;o // o;o++)t+=e.charCodeAt(o).toString(16);return t},a=function(e){e=e.match(/[\S\s]{1,2}/g);for(var t=,o=0;o

Uncommon Presentation of a Common Histiocytic Tumor: A Rare Entity.

Juvenile xanthogranuloma (JXG) is the most common form of non-Langerhans cell histiocytic lesion, characterized by benign, usually asymptomatic, self-healing yellowish brown papulonodular lesions of skin and other organs in the absence of metabolic disorder. The cells of origin of JXG are dermal dendrocytic cells. Histopathologically there is dermal infiltration of foamy or non-foamy histiocytes with or without giant cell. Immunohistochemistry shows CD68 positivity with CD1a and S-100 negativity of lesional cells although S-100-positive JXG have been reported. JXG may be associated with neurofibromatosis type one (NF 1) with increased risk of juvenile chronic myelogenous leukemia and other hematological malignancies. Our case was S-100 immunoreactive multiple, cutaneous JXGs with NF 1 without any visceral involvement or malignant complication. We are presenting this case due to its rarity.

Serum creatinine is associated with coronary disease risk even in the absence of metabolic disorders

Background. In view of recent evidence that serum creatinine and dysfunctional apolipoprotein (apo)A-I may serve as inflammation mediators in people with enhanced inflammation, we studied whether or not these molecules were interrelated and associated with coronary heart disease (CHD) likelihood even in subjects without metabolic syndrome (MetS) or type-2 diabetes. Methods. Among unselected middle-aged Turkish adults with available serum apo A-I, lipoprotein(a) and creatinine measurements, 697 participants (designated as ‘healthy’) were enrolled, after exclusion of the stated metabolic disorders. CHD was identified in 87 subjects, roughly half during 3.1 years’ follow-up. Results. ‘Healthy’ individuals were overweight and had partly impaired fasting glucose but otherwise normal serum creatinine and other biochemical measurements. Being consistent with lacking anti-inflammatory activity, apoA-I was linearly and positively associated with apoB, in women further with creatinine. Logistic regression analyses showed that, beyond age, not non-HDL-cholesterol, systolic blood pressure and smoking status, but serum creatinine in each sex (OR in men 1.63 [95% CI 1.14; 2.31]) and CRP in women were significantly associated with CHD likelihood. The combined highest and lowest creatinine quartiles in women displayed an OR 2.14 (1.02; 4.51) compared with the intermediate quartiles, after similar adjustments. Conclusion. Elevated creatinine levels within normal range, linked to apoA-I dysfunctionality, are independently associated with CHD likelihood even in non-diabetic subjects without MetS. In such women the lowest creatinine quartile is also linked to CHD risk.

Angiokeratoma corporis diffusum in the absence of metabolic disorders: A case report and mini‐review of the published work

The Journal of DermatologyVolume 40, Issue 8 p. 668-669 Letter to the Editor Angiokeratoma corporis diffusum in the absence of metabolic disorders: A case report and mini-review of the published work Risa Yasuike, Risa Yasuike Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanThese authors contributed equally to this work.Search for more papers by this authorNoriaki Nakai, Corresponding Author Noriaki Nakai Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanThese authors contributed equally to this work.Correspondence: Noriaki Nakai, M.D., Ph.D., Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan. Email: [email protected]Search for more papers by this authorSatoshi Komori, Satoshi Komori Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanSearch for more papers by this authorNorito Katoh, Norito Katoh Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanSearch for more papers by this author Risa Yasuike, Risa Yasuike Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanThese authors contributed equally to this work.Search for more papers by this authorNoriaki Nakai, Corresponding Author Noriaki Nakai Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanThese authors contributed equally to this work.Correspondence: Noriaki Nakai, M.D., Ph.D., Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, 465 Kajii-cho, Kawaramachi Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan. Email: [email protected]Search for more papers by this authorSatoshi Komori, Satoshi Komori Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanSearch for more papers by this authorNorito Katoh, Norito Katoh Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, JapanSearch for more papers by this author First published: 20 May 2013 https://doi.org/10.1111/1346-8138.12187Citations: 4 Funding sources: None. Conflict of interest: The authors have no conflict of interest to disclose. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume40, Issue8August 2013Pages 668-669 RelatedInformation

Preclinical effects of healthy obesity on inappropriate left ventricular mass and systolic function

Increased cardiometabolic risk is associated with a preclinical im-pairment of cardiac function [1]. Patients with metabolic syndrome(MetS) display myocardial inflammation with early consequences onleft ventricular mass, cardiac geometry and systo-diastolic proper-ties [2,3]. Indeed, increase in cardiovascular mortality begins witheven one MetS component [4]. Interestingly, recent studies haveshownthatmetabolicdisordersratherthanobesityperseareresponsi-ble for increased risk of heart failure overtime [5,6]. Indeed,obese indi-viduals with a favourable metabolic profile had a lower cardiovascularrisk as compared with unhealthy obese and, more surprisingly, withnormal weight individuals matching MetS criteria [7]. In a recentstudy, risk of heart failure was significantly decreased in metabolicallyhealthy obese patients after 6-year follow-up [5]. In this study bodymass index (BMI) was not associated with HF while the presence ofMetS conferred a 2.5-fold higher HF risk. In contrast, overweight andobese individuals without MetS criteria had the lowest HF risk [5].These findings suggest that individual contribution of obesity may bescarce and that metabolic disorders drive most of structural and func-tional changes occurring in the heart of metabolically unhealthy sub-jects. However, obesity-induced cardiomyopathy is a well establishedpathophysiological condition leading to impaired cardiac performancebeyondthepresenceofotherriskfactors[8].Thisscenarioraisesthefol-lowingquestion:whatistheindividualcontributionofobesityoncardi-ac structure and function? Is healthy obesity beneficial for the heart?Tothisend,weinvestigatedtheprevalenceofinappropriateleftven-tricular mass (ILVM) and cardiac function in obese and normal weightindividuals, in the presence or in the absence of metabolic disorders. Atotal of 173 hypertensive subjects were recruited at the CardiologyUnit of Sant'Andrea Hospital and every participant signed an informedconsent before entering the study. According to ATP III criteria [9] andthe presence of obesity (BMI>30 kg/m

Osmolaridade, ânion gap, potencial hidrogeniônico e íons plasmáticos mensuráveis de equinos puro sangue Árabe finalistas em provas de enduro de 90 km

Foi avaliado o comportamento da osmolaridade, do ânion gap, do pH e dos íons plasmáticos mensuráveis de 14 equinos, 9 machos e 5 fêmeas, Puro Sangue Árabe finalistas em provas de enduro de 90 km. Para tanto, foram colhidas em dois momentos (repouso e após o exercício prolongado) amostras de sangue venoso para a mensuração dessas variáveis. Pode-se verificar, a partir do repouso, aumento significativo dos valores do Hct, das PPT e do AG, sugerindo perda de fluidos e discreto grau de desidratação. O pH e o íon H+ quase não se alteraram, indicando ausência de distúrbios metabólicos. Reduções com diferenças significativas foram observadas para os íons Cl-, HCO3-, K+, Ca++, assim como do EB. Pode-se então, sugerir que o tipo de exercício a que os animais foram submetidos foi compatível com a capacidade atlética e ainda que a suplementação durante a competição contribuísse para minimizar tais perdas.

Serum adiponectin in obese children and adolescents

The objective of this work was to study the relationship between the serum adiponectin level on the one hand, and the age, stage of sexual development and main anthropometric characteristics of children and adolescents depending on the degree of obesity, the presence or absence of metabolic disorders on the other hand. A total of 111 children and adolescents at the age from 2.5 to 17.9 years were available for the examination including 56 presenting with "simple" constitutional exogenous obesity, 12 overweight patients, and 43 with normal body weight. The concentration of adiponectin in the serum of obese children and adolescents was lower than in those with normal body weight (p=0.009). The highest adiponectin level was documented in prepubertal children; it decreased progressively in the course of sexual development and negatively correlated with BMI, waist circumference---???---(WC), and BMI SDS. The children presenting with obesity complicated by insulin resistance, the serum adiponectin level was lower than in those having normal and stimulated immunoreactive insulin concentrations, HOMA-IR and Matsuda's ISI indices. The study revealed the relationship between serum adiponectin levels, concentrations of high density lipoprotein cholesterol and triglycerides. The data obtained give reason to conjecture that the reduction of serum adiponectin level may be a link connecting obesity, insulin resistance, and atherogenic changed in the serum developing as early as the childhood that can be used as an additional biomarker for the identification of a group of children and adolescents at high risk of complications associated with obesity.

Additional work of breathing and breathing patterns in spontaneously breathing patients during pressure support ventilation, automatic tube compensation and amplified spontaneous pattern breathing

Additional work of breathing and breathing patterns in spontaneously breathing patients during pressure support ventilation, automatic tube compensation and amplified spontaneous pattern breathing

Congenital plate-like osteoma cutis of the forehead: an atypical presentation form

Cutaneous ossifications or osteoma cutis can be found in many syndromes. Primary osteoma cutis, present since birth or the first months of life, in the absence of metabolic disorders or trauma, is found in congenital plate-like osteoma cutis and progressive osseous heteroplasia, coexisting in the latter with deep connective tissue ossifications. This report documents the case of a 7-year-old female with a plate-like cutaneous ossification of the forehead causing aesthetic deformities. Other dermal ossifications in the inguinal and preauricular region, as well as the left hand and a small focus in the extraocular muscles of the left orbit, were also present. These lesions did not show progression, and most of them were present since birth. The lesion of forehead was treated surgically. The lack of progression and the fact that the orbital lesion was solitary still fits the criteria for the diagnosis of plate-like osteoma cutis. Plate-like osteoma cutis and progressive osseous heteroplasia may represent varieties of the same disorder.