Plasma Cholecystokinin Levels after Vertical Banded Gastroplasty: Effects of an Acidified Meal

Background: Although cholecystokinin (CCK) is involved in the short-term regulation of satiety, it has not been investigated in obese patients subjected to bariatric restrictive operations. Methods: 8 morbidly obese patients (BMI 49.1 ± 6.9), 7F and 1M, were investigated before and after vertical banded gastroplasty (VBG). 6 healthy lean volunteers served as the control group. CCK was determined (RIA) after an overnight fast and after the administration of an acidified (pH 3) liquid meal. Blood samples were taken 45 min before the meal, 5 min after it and then every 30 min for 3 hours. Results: There were no differences between groups in basal CCK levels. However, the peak of CCK after the meal was significantly higher (P <0.01) in obese patients after VBG (24.9 ± 18 pmol/l) than before VBG (9.8 ± 6.7 pmol/l) and when compared with the control group (8.0 ± 6.3 pmol/l).The time needed to reach the peak was longer in healthy volunteers (105 ± 24.9 min) than in obese patients before VBG (45 ± 40 min) and after VBG (7.5± 12 min) (P<0.01). Conclusions: VBG increases the peak of CCK secretion and shortens the time to reach it. These changes could contribute to the satiety effects of gastric restrictive operations.     

Lipoprotein(a)-associated atherothrombotic risk in hemodialysis patients

BACKGROUND: Hemodialysis patients show a considerably higher risk of atherothrombotic disease than the general population. We investigated both lipoprotein(a) [Lp(a)] plasma levels and apolipoprotein(a) [apo(a)] phenotypes in relation to occurrence of atherothrombotic events in hemodialysis patients compared with subjects showing a normal kidney function. Methods: Lp(a) levels and apo(a) isoforms were determined in 118 hemodialysis patients, including 59 with prior atherothrombotic events, and in 182 subjects with normal creatinine clearance, including 82 who experienced a prior atherothrombotic event. Results: Lp(a) levels in hemodialysis patients (median; 20 mg/dl) were higher (p < 0.01) than in age- and sex-matched subjects with normal renal function without a history of atherothrombosis (11.3 mg/dl). Among hemodialysis patients, median Lp(a) levels were higher in subjects with than in those without prior atherothrombosis (34 vs. 15 mg/dl, p < 0.05). In hemodialysis patients and in subjects without nephropathy, the percentage of low-molecular-weight apo(a) phenotypes were significantly higher in patients with than in those without a history of prior atherothrombotic events (56.9% vs. 33.9%, p < 0.05; 62.2% vs. 25%, p < 0.00001,respectively). Stepwise regression analysis indicated that the presence of at least one apo(a) isoform of low molecular weight was an independent predictor of atherothrombosis in hemodialysis patients (p < 0.05). Conclusions: Elevated Lp(a) plasma levels appear to be associated with atherothrombosis, independent of their origin due to genetic factors or related to the impaired kidney function. Low-molecular-weight apo(a) isoforms are reliable genetic markers of atherothrombosis both in patients with impaired kidney function and in subjects without nephropathy.     

Robotic aortic valve replacement: case report

We have developed a technique that enables robotic aortic valve replacement with port access via a small right anterior thoracotomy and minimally invasive aortic cross clamping. The procedure is performed under video guidance with all the annular sutures placed with the robot. In the case we report, the patient's postoperative course was extremely simple and pain was minimal. We believe that this is the first reported aortic valve replacement using robotic technology and that it opens a new field of application for robotic assisted surgery.     

Suicide rates in five-year age-bands after the age of 60 years: the international landscape†

Background: There is paucity of studies examining suicide rates in narrow five-year age-bands after the age of 60 years. This study examined suicide rates in eight five-year age-bands between the age of 60 and 99 years because this will allow more precise comparison between the young old (60–79 years) and the oldest old (80+ years) age groups.

Methods: Data on the number of suicides (International Classification of Diseases – ICD-10 codes, X60-84) in each of the eight five-year age-bands between the age-bands 60–64 years and 95–99 years in both gender for as many years as possible from 2000 were ascertained from three sources: colleagues with access to national data, national statisics office websites and email contact with the national statistics offices. The population size for the corresponding years and age-bands was estimated for each country using data provided by the United Nations website.

Results: In men, suicide rates continued to increase for each of the seven five-year age-bands from 60–64 years to 90–94 years age-band, and then declined slightly for the 95–99 year age-band. In women, suicide rates continued to increase for each of the six five-year age-bands from 60–64 years to 85–89 years age-bands, and then declined slightly for the 90–94 years and 95–99 years age-bands.

Conclusions: The overall global suicide rates for each of the eight five-year age-bands are sufficiently large for them to constitute a public health concern. This is especially important given the ongoing rise in the elderly population size and the paucity of data on risk and protective factors for suicide in the five-year age-bands after the age of 60 years.     

Traumatic subclavian arterial rupture: a case report and review of literature

ABSTRACT: Subclavian artery injuries represent an uncommon complication of blunt chest trauma, this structure being protected by subclavius muscle, the clavicle, the first rib, and the deep cervical fascia as well as the costo-coracoid ligament, a clavi-coraco-axillary fascia portion. Subclavian artery injury appears early after trauma, and arterial rupture may cause life-treatening haemorrages, pseudo-aneurysm formation and compression of brachial plexus. These clinical eveniences must be carefully worked out by accurate physical examination of the upper limb: skin color, temperature, sensation as well as radial pulse and hand motility represent the key points of physical examination in this setting. The presence of large hematomas and pulsatile palpable mass in supraclavicular region should raise the suspicion of serious vascular injury. Since the first reports of endovascular treatment for traumatic vascular injuries in the 90's, an increasing number of vascular lesions have been treated this way. We report a case of traumatic subclavian arterial rupture after blunt chest trauma due to a 4 meters fall, treated by endovascular stent grafting, providing a complete review of the past twenty years' literature.     

Direct Control of Brown Adipose Tissue Thermogenesis by Central Nervous System Glucagon-Like Peptide-1 Receptor Signaling

We studied interscapular brown adipose tissue (iBAT) activity in wild-type (WT) and glucagon-like peptide 1 receptor (GLP-1R)–deficient mice after the administration of the proglucagon-derived peptides (PGDPs) glucagon-like peptide (GLP-1), glucagon (GCG), and oxyntomodulin (OXM) directly into the brain. Intracerebroventricular injection of PGDPs reduces body weight and increases iBAT thermogenesis. This was independent of changes in feeding and insulin responsiveness but correlated with increased activity of sympathetic fibers innervating brown adipose tissue (BAT). Despite being a GCG receptor agonist, OXM requires GLP-1R activation to induce iBAT thermogenesis. The increase in thermogenesis in WT mice correlates with increased expression of genes upregulated by adrenergic signaling and required for iBAT thermogenesis, including PGC1a and UCP-1. In spite of the increase in iBAT thermogenesis induced by GLP-1R activation in WT mice, Glp1r^−/− mice exhibit a normal response to cold exposure, demonstrating that endogenous GLP-1R signaling is not essential for appropriate thermogenic response after cold exposure. Our data suggest that the increase in BAT thermogenesis may be an additional mechanism whereby pharmacological GLP-1R activation controls energy balance.The increasing incidence of type 2 diabetes (T2D) and obesity worldwide has prompted the need for new therapies. Agonism of the receptor for glucagon-like peptide-1 (GLP-1) is currently one of the most successfully and widely used therapies for T2D. GLP-1 is a product of proglucagon that also gives rise to glucagon (GCG) and oxyntomodulin (OXM) (1). Both GLP-1 and its receptor (GLP-1R) are expressed in peripheral tissues and in areas of the central nervous system (CNS) involved in the control of energy balance. Treatment with GLP-1R agonists improves glycemic control and reduces body weight in diabetic humans (2). Studies in animals have demonstrated that CNS–GLP-1R signaling contributes to the body weight–reducing effect of these agonists (3).GCG is produced in the α cells of the pancreatic islets and is involved in the maintenance of euglycemia. Although its exogenous administration induces body weight loss associated with anorexia and increased energy expenditure (4), GCG has been traditionally dismissed as a potential drug target because of its diabetogenic effects. However, recent preclinical data have shown that simultaneous activation of both GLP-1R and GCG receptor (GCGR) leads to greater efficacy in both glycemic control and weight loss than the activation of GLP-1R alone (5,6).OXM can bind to and activate both GLP-1R and GCGR (7), and studies with rodents (8,9) and humans (10) suggest that it may be efficacious in treating obesity and diabetes. OXM regulates feeding, at least in part, through GLP-1R (7,11). There is evidence that OXM action in the CNS reduces body weight by increasing energy expenditure (12). This may involve activation of brown adipose tissue (BAT) metabolism, since intracerebroventricular (ICV) administration of OXM reduces the weight of interscapular BAT (iBAT) pads and increases body temperature in rats (12). The relative contribution of GLP-1R and GCGR to this process has never been investigated; however, it is known that GCG regulates iBAT activity, and this may be, at least in part, centrally mediated (13). The contribution of GLP-1R to the control of energy expenditure, and more specifically to BAT metabolism, remains largely unknown.The sympathetic nervous system (SNS) is essential for control of BAT metabolism by the CNS (14) and is involved in the CNS–GLP-1R control of lipid metabolism in white adipose tissue (WAT) (15). This, in addition to the evidence that GCG may increase BAT thermogenesis through actions in the CNS (13), led us to hypothesize that the action(s) of GCGR and GLP-1R in the brain controls BAT thermogenesis through the SNS. Here, we show that central administration of both GCGR and GLP-1R agonists increased SNS activity to iBAT and induced thermogenesis. Thus, we propose that CNS–GLP-1R may contribute to the control of energy balance by regulating BAT thermogenesis. The existence of functional BAT in adult humans has now been determined (16–18), and effort needs to be directed toward a better understanding of the regulation of this tissue as a target for antiobesity therapeutics. The increase in BAT metabolism described here may contribute to the weight loss induced by GCGR and GLP-1R agonists in both animal models and humans.