Pre-existing Metabolic Diseases Research Articles

Effects of Laser Acupuncture on Metabolic Functions of Sedentary People: A Double-Blind Randomized Clinical Trial.

Background: Laser acupuncture regulates energy flow and restores body fluid metabolism. Objective: To evaluate the effects of the laser acupuncture protocol (LAP) on hepatic and renal metabolism in sedentary people. Methods: Longitudinal, double-blind, and randomized clinical trial with 29 participants, adults, both sexes, sedentary, without pre-existing metabolic diseases, subdivided into control and laser groups. Based on the STandards for Reporting Interventions in Clinical Trials of Acupuncture 2010 guidelines, 10 laser applications (660 nm ±10 nm wavelength, 100 mW power. The irradiation tip has a diameter of 5 mm, which corresponds to an area of 0.19 cm2, totaling a power density of 0.52 W/cm2 and considering the irradiation time of 90 s, the energy density applied was 47.3 J/cm2) were performed on the acupoints of metabolic functions (LR3, SP6, ST36, and LI4) and blood samples were collected for fasting glycemia, lipid profile (HDL, LDL, total cholesterol, and triglycerides), liver function (AST/GOT and ALT/GPT), and renal function (serum creatinine and urea). A repeated measures analysis of variance (ANOVA) with Bonferroni corrected post hoc comparisons was applied to compare statistical differences between groups and times, adopting p < 0.05 as the null hypothesis. Results: The laser stimulated changes in serum lipid profile values and renal and hepatic functions. There was a significant (p = 0.014) reduction in LDL ("bad" cholesterol) from 105.75 ± 32.83 pre- to 84.32 ± 18.38 mg/dL postintervention, associated with cardioprotective function. Positive significant (p = 0.035) impacts were also observed in the reduction of creatinine (0.86 ± 0.12 mg/dL to 0.75 ± 0.12 mg/dL) and the enzyme AST/GOT (33.73 ± 12.95 U/L to 20.80 ± 4.99 U/L, p = 0.002). Conclusion: LAP applied to basal metabolism acupoints promoted positive metabolic changes in the lipid profile (LDL), and in main markers of the liver (AST/GOT) and kidney (creatinine) functions, contributing to risk control of cardiovascular diseases.

Cardiac remodeling associated with chronic kidney disease is enhanced in a rat model of metabolic syndrome: Preparation of mesenchymal transition.

Cardiac alteration due to chronic kidney disease is described by tissue fibrosis. This remodeling involves myofibroblasts of various origins, including epithelial or endothelial to mesenchymal transitions. In addition, obesity and insulin resistance together or separately seem to exacerbate cardiovascular risk in chronic kidney disease (CKD). The main objective of this study was to assess if pre-existing metabolic disease exacerbates CKD-induced cardiac alterations. In addition, we hypothesised that endothelial to mesenchymal transition participates in this enhancement of cardiac fibrosis. Rats fed cafeteria type diet for 6months underwent a subtotal nephrectomy at 4months. Cardiac fibrosis was evaluated by histology and qRT-PCR. Collagens and macrophages were quantified by immunohistochemistry. Endothelial to mesenchymal transitions were assessed by qRT-PCR (CD31, VE-cadherin, α-SMA, nestin) and also by CD31 immunofluorescence staining. Rats fed with cafeteria type regimen were obese, hypertensive and insulin resistant. Cardiac fibrosis was predominant in CKD rats and was highly majored by cafeteria regimen. Collagen-1 and nestin expressions were higher in CKD rats, independently of regimen. Interestingly, in rats with CKD and cafeteria diet we found an increase of CD31 and α-SMA co-staining with suggest an implication of endothelial to mesenchymal transition during heart fibrosis. We showed that rats already obese and insulin resistant had an enhanced cardiac alteration to a subsequent renal injury. Cardiac fibrosis process could be supported by a involvement of the endothelial to mesenchymal transition phenomenon.

Dysfunctional Metabolisms Of T Cells In Collegiate Football Players Infected With Sars-cov2

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2) is the causative agent ofCOVID19, which caused a global pandemic. One of the pathogenic hallmarks of COVID19 is adysregulation of immune cell metabolism accompanied by excessive inflammatory cytokineresponse, particularly in adults with underlying co-morbidities. However, the impact of SARS-CoV2 on metabolic function in discrete cellular populations, such as T cells, in young, otherwisehealthy, elite-level athletes who recovered from COVID19 is currently unknown. PURPOSE: Weexamined whether NCAA Division I Football Players exhibited altered T cell metabolism afterrecovering from COVID19. METHOD: We studied 9 PCR SARS-CoV2 post-positive (COVID19+)collegiate football players following 14-day quarantine and 4 COVID19 naïve players(COVID19-). Resting T cells were isolated and stimulated overnight with either: 1) SARS-CoV2peptivator pool of S + N + M peptides (JPT peptides), 2) T cell activator beads CD3/CD28, 3)SARS-CoV2 peptides+CD3/CD28 beads, or 4) T cells alone. Following overnight stimulation, Tcell bioenergetics were characterized using the Seahorse BioAnalzyzer (Agilent) to measureextracellular acidification rates (ECAR, a measure of glycolysis) and oxygen consumption rates(OCR, a measure of mitochondrial bioenergetics). Differences between groups were analyzedusing ANOVA and Dunnett’s post hoc tests. RESULTS: The ECAR of T cells isolated fromCOVID19+ participants was 32.5% lower when activated with CD3/CD28 beads and the SARS-CoV2 peptides, than that of T cells activated with beads alone (p < 0.05), but no difference wasobserved in T cells from COVID19- controls (p > 0.05). Similarly, OCR associated with ATPproduction was also 32.7% lower in COVID19+ participants (p < 0.001) when stimulated withSARS-CoV2 peptides, but not in COVID19- participants (p > 0.05). DISCUSSION: Our data suggestthat SARS-CoV2 infection is associated with impaired T cell bioenergetics, which coulddetrimentally impact T cell effector functions. As such, SARS-CoV2 infection appears to beassociated with hallmarks of T cell exhaustion even in elite collegiate athletes, which would beexacerbated in adults with pre-existing metabolic diseases (i.e., diabetes, obesity) and other co-morbidities.

Dual contribution of the mTOR pathway and of the metabolism of amino acids in prostate cancer.

Prostate cancer is the leading cause of cancer in men, and its incidence increases with age. Among other risk factors, pre-existing metabolic diseases have been recently linked with prostate cancer, and our current knowledge recognizes prostate cancer as a condition with important metabolic anomalies as well. In malignancies, metabolic disorders are commonly associated with aberrations in mTOR, which is the master regulator of protein synthesis and energetic homeostasis. Although there are reports demonstrating the high dependency of prostate cancer cells for lipid derivatives and even for carbohydrates, the understanding regarding amino acids, and the relationship with the mTOR pathway ultimately resulting in metabolic aberrations, is still scarce. In this review, we briefly provide evidence supporting prostate cancer as a metabolic disease, and discuss what is known about mTOR signaling and prostate cancer. Next, we emphasized on the amino acids glutamine, leucine, serine, glycine, sarcosine, proline and arginine, commonly related to prostate cancer, to explore the alterations in their regulatory pathways and to link them with the associated metabolic reprogramming events seen in prostate cancer. Finally, we display potential therapeutic strategies for targeting mTOR and the referred amino acids, as experimental approaches to selectively attack prostate cancer cells.

Metabolic disorders and the risk of COVID-19

In the present review the analysis of the world literature devoted to the study of metabolic disorders in the body and the risk of COVID-19 disease. It is known that metabolic syndrome is an independent risk factor for the severe course of new coronavirus infection. This review summarizes data on the mechanisms of metabolic dysfunction in a new coronavirus infection, analyzes the results of studies that investigated the issues of associations between the course of COVID-19 and various metabolic disorders, such as hyperglycemia and diabetes mellitus, dyslipidemia, obesity, non-alcoholic fatty liver disease, their severity, potential targets of therapy, predictors of the development of a severe course of new coronavirus infection are considered. These metabolic disorders increase the impairment of the immune system and make patients more susceptible to the development of infectious diseases, in particular, to infection with a new coronavirus infection. Taking into account the obtained data, it becomes obvious the need to identify and monitor patients with pre-existing metabolic diseases, as well as their development during and after COVID-19. The information on the topic from publications based on PubMed, PubMed Central, Scopus, Google Scholar, Medscape, UpYoDate, eLIBRARY.RU data were used.

Interaction between Sars-CoV-2 structural proteins and host cellular receptors: From basic mechanisms to clinical perspectives.

Severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2) has caused a global pandemic that has affected the lives of billions of individuals. Sars-CoV-2 primarily infects human cells by binding of the viral spike protein to angiotensin-converting enzyme 2 (ACE2). In addition, novel means of viral entry are currently being investigated, including Neuropillin 1, toll-like receptors (TLRs), cluster of differentiation 147 (CD147), and integrin α5β1. Enriched expression of these proteins across metabolic regulatory organs/tissues, including the circulatory system, liver, pancreas, and intestine contributes to major clinical complications among COVID-19 patients, particularly the development of hypertension, myocardial injury, arrhythmia, acute coronary syndrome and increased coagulation in the circulatory system during and post-infection. Pre-existing metabolic disease, such as cardiovascular disease, obesity, diabetes, and non-alcoholic fatty liver disease, is associated with increased risk of hospitalization, persistent post-infection complications and worse outcomes in patients with COVID-19. This review overviews the biological features of Sars-CoV-2, highlights recent findings that delineate the pathological mechanisms of COVID-19 and the consequent clinical diseases.

Bilateral femoral neck fracture following a convulsion in the presence of chronic kidney disease. A case report.

Introduction and importanceBilateral femoral neck fractures in young adults are a rare entity. It is usually associated with pre-existing metabolic diseases, such as osteoporosis, renal osteodystrophy, or hypocalcemic seizures. Hence, it is essential in such cases to look for other associated injuries following a traumatic event. Missing associated injuries may lead to significant morbidities and poor functional outcomes.Case presentationA 37 years old male, who had chronic renal failure secondary to hypertension, and presented to the emergency room following a seizure episode, in which he developed a generalized tonic-clonic convulsion secondary to electrolyte imbalances with metabolic acidosis. As a result, he developed bilateral neck of femur fracture.Intervention and outcomeThe medical team optimized electrolytes imbalance and then the patient underwent surgical stabilization of both femur neck fracture, 1 year following the surgical fixation the patient had full range of motion of both hips with radiological evidence of complete healing of the fracture.ConclusionIn cases of fractures secondary to metabolic conditions, bilateral femoral neck fractures should be suspected and investigated; especially in young patients who develop a generalized tonic-clonic seizure. The etiology is multifactorial, and the treating surgeon should be aware of predisposing factors which may affect bone quality, thereby raising the risk of fractures even with low-energy atraumatic events. Hip preservation should always be the primary target when treating these patients.

The accentuation in post-traumatic stress disorder-like symptoms induced by diabetes in rats is not associated with a further increase in astrocyte activation in the hippocampus

Individuals with post-traumatic stress disorder (PTSD) show increased rates of several serious metabolic diseases. However, little is known about pre-existing metabolic diseases and the development of PTSD. Therefore, we aimed to evaluate the course of post-traumatic stress disorder (PTSD) development in rats with preexisting diabetes. In addition, we quantified glial fibrillary acidic protein (GFAP) in the hippocampus of the experimental animals. For this, we used male Wistar rats and divided them into two groups: saline and alloxan (150 mg/Kg, i.p.). The animals were weighed, and plasma glucose was measured after 48 h of diabetes induction by alloxan. The animals were either exposed to inescapable footshocks or not, followed by social isolation. After 14 days, the animals were re-exposed to the box, and the freezing time was evaluated for 10 min. Over the following days, the animals were tested on the open field, social interaction and forced swimming tests. In another group of animals, elevated plus maze and object recognition tests were performed. Our results demonstrated that animals with diabetes had more pronounced PTSD-like symptoms as a reduction in social interaction, an increase in immobility time in forced swimming, a reduction in permanence in the open arms of the elevated plus maze, and a deficit in the object recognition index more accentuated. However, this did not reflect astrocyte activation in the hippocampus. In conclusion, diabetes accentuates post-traumatic stress disorder-like symptoms but not astrocyte activation in the hippocampus.

Familial hypercholesterolemia and COVID-19: A menacing but treatable vasculopathic condition

SARS-CoV-2 infection continues to cause increased morbidity and mortality, and due to the slow pace of vaccination COVID-19 will probably remain a global burden to health systems for a long time. Unfortunately, the necessary prevention and treatment strategies of COVID-19 have led to restriction measures that are hampering the routine care of common chronic metabolic conditions like hypercholesterolemia. It is of particular concern that during the acute phase of COVID-19, the control of pre-existing metabolic diseases tends to get worse which again increases the risk for complications and a poor outcome in these patients. A significant contributor to these complications is endothelial dysfunction which is associated with COVID-19. This Commentary will discuss the impact of COVID-19 on endothelial function particularly in patients with familial hypercholesterolemia (FH), a metabolic inherited disease known to in itself adversely affect endothelial function. There should be no hesitation to continue with statin therapy in severe hypercholesterolemic patients with COVID-19. We argue that in FH patients with COVID-19 the clinicians need even consider intensifying statin therapy as well as the addition of other lipid-lowering agents, such as proprotein convertase subtilisin/kexin type 9(PCSK9) inhibitors. In contrast to statins, the PCSK9 inhibitors lower lipoprotein(a) [Lp(a)] level, and, accordingly, these latter drugs need to be considered particularly in FH patients with an elevated level of Lp(a). This call applies to the in-hospital stay and also beyond. When considering that the vasculopathic effects of COVID-19 may persist, a long-term follow-up of individualized therapies in FH patients is warranted.

Characterization in mice of the resident mesenchymal niche maintaining AT2 stem cell proliferation in homeostasis and disease.

Resident mesenchymal cells (rMCs defined as Cd31Neg Cd45Neg EpcamNeg ) control the proliferation and differentiation of alveolar epithelial type 2 (AT2) stem cells in vitro. The identity of these rMCs is still elusive. Among them, Axin2Pos mesenchymal alveolar niche cells (MANCs), which are expressing Fgf7, have been previously described. We propose that an additional population of rMCs, expressing Fgf10 (called rMC-Sca1Pos Fgf10Pos ) are equally important to maintain AT2 stem cell proliferation. The alveolosphere model, based on the AT2-rMC co-culture in growth factor-reduced Matrigel, was used to test the efficiency of different rMC subpopulations isolated by FACS from adult murine lung to sustain the proliferation and differentiation of AT2 stem cells. We demonstrate that rMC-Sca1Pos Fgf10Pos cells are efficient to promote the proliferation and differentiation of AT2 stem cells. Co-staining of adult lung for Fgf10 mRNA and Sftpc protein respectively, indicate that 28% of Fgf10Pos cells are located close to AT2 cells. Co-ISH for Fgf7 and Fgf10 indicate that these two populations do not significantly overlap. Gene arrays comparing rMC-Sca1Pos Axin2Pos and rMC-Sca1Pos Fgf10Pos support that these two cell subsets express differential markers. In addition, rMC function is decreased in obese ob/ob mutant compared to WT mice with a much stronger loss of function in males compared to females. In conclusion, rMC-Sca1Pos Fgf10Pos cells play important role in supporting AT2 stem cells proliferation and differentiation. This result sheds a new light on the subpopulations of rMCs contributing to the AT2 stem cell niche in homeostasis and in the context of pre-existing metabolic diseases.

The excess insulin requirement in severe COVID-19 compared to non-COVID-19 viral pneumonitis is related to the severity of respiratory failure and pre-existing diabetes.

IntroductionSevere COVID‐19 has been anecdotally associated with high insulin requirements. It has been proposed that this may be driven by a direct diabetogenic effect of the virus that is unique to SARS‐CoV‐2, but evidence to support this is limited. To explore this, we compared insulin requirements in patients with severe COVID‐19 and non‐COVID‐19 viral pneumonitis.MethodsThis is a retrospective cohort study of patients with severe COVID‐19 admitted to our intensive care unit between March and June 2020. A historical control cohort of non‐COVID‐19 viral pneumonitis patients was identified from routinely collected audit data.ResultsInsulin requirements were similar in patients with COVID‐19 and non‐COVID‐19 viral pneumonitis after adjustment for pre‐existing diabetes and severity of respiratory failure.ConclusionsIn this single‐centre study, we could not find evidence of a unique diabetogenic effect of COVID‐19. We suggest that high insulin requirements in this disease relate to its propensity to cause severe respiratory failure in patients with pre‐existing metabolic disease.

Type 2 diabetes induced microbiome dysbiosis is associated with therapy resistance in pancreatic adenocarcinoma

Resistance to therapy is one of the major factors that contribute to dismal survival statistics in pancreatic cancer. While there are many tumor intrinsic and tumor microenvironment driven factors that contribute to therapy resistance, whether pre-existing metabolic diseases like type 2 diabetes (T2D) contribute to this has remained understudied. It is well accepted that hyperglycemia associated with type 2 diabetes changes the gut microbiome. Further, hyperglycemia also enriches for a “stem-like” population within the tumor. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to gemcitabine/paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group. Additionally, we also observed an increase in the CD133+ tumor cells population in the T2D model. These observations indicated that in an animal model for T2D, microbial dysbiosis is associated with increased resistance to chemotherapeutic compounds.

Genetic Profiling of Breast Cancer with and Without Preexisting Metabolic Disease

Breast cancer is the most commonly diagnosed cancer and the leading cause of cancer death among women. Various mechanisms are involved in the initiation and progression of breast cancer. Metabolic dysregulation has been associated with increasing breast cancer incidence and mortality. However, little is known about how metabolic disease regulates the development and progression of breast cancer at the molecular level. Here, using a hybridization capture-based panel including 124 cancer-associated genes, we performed targeted next-generation sequencing of tumor tissues and matched blood samples from 20 postmenopausal patients with primary breast cancer, in which 6 cases suffered from preexisting metabolic disorders including hypertension, type 2 diabetes, and coronary heart disease. We took only the protein-altering variants and identified 170 somatic mutations of 59 genes. Among these, 40 mutated genes were found in the metabolic disease group, and 33 mutated genes were found in the non–metabolic disease group. Importantly, nonsynonymous mutations of 26 genes (MSH3, BRAF, MLH3, MTOR, DDR2, ALK, etc.) were uniquely present in the metabolic disease group. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were performed to investigate biological functions and key pathways of somatic mutations. TP53, PIK3CA, and PTEN were the top three commonly mutated genes at a higher frequency compared with the Cancer Genome Atlas (TCGA) data, and several novel but infrequent mutations in other genes were also found. Although further studies are required to validate these variants, our results are the first to suggest a specific molecular profile of breast cancer with preexisting metabolic disease.

Protection from chronic stress- and depressive symptom-induced vascular endothelial dysfunction in female rats is abolished by preexisting metabolic disease.

While it is known that chronic stress and clinical depression are powerful predictors of poor cardiovascular outcomes, recent clinical evidence has identified correlations between the development of metabolic disease and depressive symptoms, creating a combined condition of severely elevated cardiovascular disease risk. In this study, we used the obese Zucker rat (OZRs) and the unpredictable chronic mild stress (UCMS) model to determine the impact of preexisting metabolic disease on the relationship between chronic stress/depressive symptoms and vascular function. Additionally, we determined the impact of metabolic syndrome on sex-based protection from chronic stress/depressive effects on vascular function in female lean Zucker rats (LZRs). In general, vasodilator reactivity was attenuated under control conditions in OZRs compared with LZRs. Although still impaired, conduit arterial and resistance arteriolar dilator reactivity under control conditions in female OZRs was superior to that in male or ovariectomized (OVX) female OZRs, largely because of better maintenance of vascular nitric oxide and prostacyclin levels. However, imposition of metabolic syndrome in combination with UCMS in OZRs further impaired dilator reactivity in both vessel subtypes to a similarly severe extent and abolished any protective effect in female rats compared with male or OVX female rats. The loss of vascular protection in female OZRs with UCMS was reflected in vasodilator metabolite levels, which closely matched those in male and OVX female OZRs subjected to UCMS. These results suggest that presentation of metabolic disease in combination with depressive symptoms can overwhelm the vasoprotection identified in female rats and, thereby, may reflect a severe impairment to normal endothelial function. NEW & NOTEWORTHY This study addresses the protection from chronic stress- and depression-induced vascular dysfunction identified in female compared with male or ovariectomized female rats. We determined the impact of preexisting metabolic disease, a frequent comorbidity of clinical depression in humans, on that vascular protection. With preexisting metabolic syndrome, female rats lost all protection from chronic stress/depressive symptoms and became phenotypically similar to male and ovariectomized female rats, with comparably poor vasoactive dilator metabolite profiles.

310 Role of Polyunsaturated Fatty Acids Consumption on Development of NAFLD in Hispanic USA Population

Background and Aims: Fructose overconsumption inWestern diet is linked to non-alcoholic fatty liver disease (NAFLD). In animal models fructose overconsumption leads to chronic metabolic low-grade inflammation and was also linked to cardiovascular disease (CVD) as well as development of type-II-Diabetes (T2DM). Until now, the impact of fructose overconsumption is often studied in overweight, T2DM or NAFLD patients, but is not as well described in healthy subjects. To test our hypothesis that fructose overconsumption may impact on the gut-liver axis by increasing intestinal permeability, bacterial translocation, and consecutively metabolic inflammation as important mechanisms in the pathogenesis of NAFLD, CVD and T2DM, we examined the impact of a high oral fructose challenge (150g/ day for 4 weeks) on intestinal permeability and inflammation. Methods: Ten healthy volunteers were enrolled (m:f=5:5; median[range] age=24.5[21-37] [years]; p=n.s.). Intestinal permeability was assessed by sucrose-lactulose-mannitol (SLM) test using high performance liquid chromatography of urine collected over 5 hours. Interleukin-6 (IL-6) was assessed by ELISA. C-reactive Protein (CRP) and Fibronectin were assessed using nephelometry. Results: After the oral fructose challenge changes in energymetabolism reflected by increased BMI (mean±SD 21.11±2.68 vs 21.51±2.77 [kg/m^2]; p<0.001) as well as fasting glucose levels (mean±SD 83.2±8.37 vs 88.4±5.48 [mg/dL]; p=0.035) were observed. Gastroduodenal permeability, reflected by recovered sucrose (median[range] 0.075[0-0.1] vs 0.089[0-0.1] [mmol/L]; p=0.68) as well as small intestinal permeability reflected by lactulose/mannitolratio (mean±SD 0.021±0.006 vs 0.019±0.008 [%]; p=0.622) remained stable. In line, inflammatory parameters CRP (median[range] 0.5[0-3] vs 0[0-1] [mg/dL]; p=0.066) and Fibronectin (mean±SD 35.3±8.63 vs 35.3±7.73 [mg/dL]; p=1.0) remained unchanged. IL-6 was below the detection limit prior and after fructose challenge, suggesting a high oral fructose challenge does not affect intestinal permeability in healthy young volunteers. Conclusion: Healthy young volunteers are capable of handling fructose overconsumption (150g/day for 4 weeks) on top of their normal diet without any increase in intestinal permeability or inflammation. This further supports the hypothesis that fructose overconsumption may act as hepatotoxin as a second hit in pre-existing metabolic diseases and/or on top of genetically predisposing backgrounds such as PNPLA3 genotype. Acknowledgements: The research leading to these results has received funding from the Medical Scientific Fund of the Mayor of the City of Vienna (grant number 12040).

The Management of Metabolically Unhealthy Obesity

Increasing rates of obesity are related to increasing incidence of metabolic diseases such as type 2 diabetes, hypertension and cardiovascular disease. The need to prevent and treat obesity is an obvious way to reduce its incidence and to reduce the complications associated with metabolic diseases. To reduce the risk of cardiovascular disease in obese adults, it is important not only to lose weight but to manage preexisting metabolic disease. Therefore, a systematic and organized approach is needed for the management of obesity with metabolic disease. (J Korean Diabetes 2013;15:24-29)

Deep and Superficial Fat Ratio in Dietary and Surgically Induced Weight Loss Patients

Architecture of abdominal fat above and below Scarpa's fascia is morphologically different. Little information is available about the relative distribution patterns of deep and superficial fat layers in massive weight loss (MWL) patients. This study aimed to evaluate the relative distribution patterns of deep and superficial abdominal fat layers in two groups of MWL patients presenting for abdominoplasty: (1) MWL via nutritional management and (2) MWL via bariatric surgery. All MWL patients with stable body weight for a minimum of 24months presenting for abdominal body contouring at Lausanne University Hospital, Department of Plastic Surgery between July 2008 and June 2009 were included. Patients with preexisting metabolic diseases were excluded. Patients with nutritional deficiencies were deferred until corrected. Nineteen consecutive patients were included in the study, 7 post-bariatric patients and 12 patients after dietary-induced weight loss (5 were males and 14 were females; average age 45.5years, range 36-64years), with an average weight loss of 48kg (57kg post-bariatric, 28kg dietary induced) and a mean body mass index of 29.2kg/m(2) (range 24.0-40.7) at the time of abdominoplasty. Morphologic evaluation yielded a relative distribution of deep to superficial fat layers of 42 to 58% in the post-bariatric group versus 31 to 69% (p < 0.05) in the nutritionally induced group. These data show that the morphologic distribution patterns of deep and superficial abdominal fat layers differ with regards to mode of weight loss.

Cardiac screening examination of the fetus: guidelines for performing the ‘basic’ and ‘extended basic’ cardiac scan

Cardiac screening examination of the fetus: guidelines for performing the ‘basic’ and ‘extended basic’ cardiac scan