Laparoscopic Sleeve Gastrectomy is a Safe and Effective Bariatric Procedure for the Lower BMI (35.0–43.0 kg/m<Superscript>2</Superscript>) Population

Background  

The laparoscopic vertical sleeve gastrectomy (LSG) is derived from the biliopancreatic diversion with duodenal switch operation (Marceau et al., Obes Surg 3:29–35, 1993; Hess and Hess, Obes Surg 8:267–82, 1998; Chu et al., Surg Endosc 16:S069, 2002). Later, LSG was advocated as the first step of a two-stage procedure for super-obese patients (Regan et al., Obes Surg 13:861–4, 2003; Cottam et al., Surg Endosc 20:859–63, 2006). However, recent support is mounting that continues to establish LSG as the definitive procedure for surgical treatment of morbid obesity. We will report our experience with the LSG as a primary bariatric procedure and evaluate if this operation is suitable as a stand-alone procedure.     

Polymorphisms in NQO1 and the clinical course of urinary bladder neoplasms

OBJECTIVE: Urinary bladder neoplasms differ considerably in biological potential, and tumor morphology alone cannot predict their clinical behaviors. Polymorphisms in xenobiotic metabolic genes reportedly modulate susceptibility to bladder neoplasms and may affect the clinical course and outcomes of the disease. This study was conducted to determine the effect of polymorphisms in the xenobiotic metabolic genes on the disease course and clinical outcomes of urinary bladder neoplasms. MATERIAL AND METHODS: Patients with urinary bladder neoplasms who had been followed up for a 5-year period were genotyped for NQO1 (R139W, P187S), NAT (rapid/slow), GSTP1 (I105V), GSTT1 and GSTM1 (non-null/null) and MTHFR (A222V, E429A) polymorphisms. RESULTS: Variant allele carriers of the NQO1 (P187S) polymorphism showed a higher risk for high-stage disease than non-carriers at diagnosis [relative risk (RR)=1.4; 95% CI 1.0-1.8). A higher risk for highly malignant disease (T2+) was also observed in variant allele carriers than non-carriers of the GSTP1 (I105V) polymorphism (RR=1.6; 95% CI 1.1-2.5). NQO1 (R139W) variant allele carrier patients with intermediate malignant disease (TaG3+T1) had shorter disease-free survival than non-carriers (p=0.05). In contrast, carriers of the variant allele for the MTHFR (A222V) polymorphism had significantly longer disease-free survival than non-carriers (p=0.02). CONCLUSIONS: Our data are consistent with the notion that NQO1 polymorphisms influence the course and clinical outcomes of urinary bladder neoplasms. However, our results need to be confirmed in a large study as most of the associations detected were only of marginal statistical significance, and would be lost on correction for multiple comparisons.     

Association of a polymorphism in the ABCB1 gene with Parkinson's disease

The ATP-binding cassette, sub-family B, member 1 (ABCB1) gene encoding the protein P-glycoprotein (P-gp) has been implicated in the pathophysiology of Parkinson's disease (PD) due to its role in regulating transport of endogenous molecules and exogenous toxins. In the present study, we analyzed the ABCB1 single nucleotide polymorphisms (SNPs) 1236C/T (exon 12), 2677G/T/A (exon 21) and 3435C/T (exon 26) in 288 Swedish PD patients and 313 control subjects and found a significant association of SNP 1236C/T with disease (p = 0.0159; χ² = 8.28), whereas the distributions of wild-type and mutated alleles were similar for 2677G/T/A and 3435C/T in patients and controls. Haplotype analysis revealed significant association of the 1236C–2677G haplotype with PD (p = 0.026; χ² = 4.955) and a trend towards association with disease of the 1236C–2677G–3435C haplotype (p = 0.072; χ² = 3.229). Altered ABCB1 and/or P-pg expression was recently shown in PD patients, and impaired drug efflux across barriers such as the gastrointestinal and nasal mucosal linings or the blood–brain barrier, might result in accumulation of drugs and/or endogenous molecules in toxic amounts, possibly contributing to disease. ABCB1 polymorphisms thus constitute an example of how genetic predisposition and environmental influences may combine to increase risk of PD.     

Motives to quit smoking and reasons to relapse differ by socioeconomic status

Objective

To investigate motives, strategies and experiences to quit smoking and reasons to relapse as a function of socioeconomic status.

Methods

A population-based study, Inter99, Denmark. Two thousand six hundred twenty-one daily smokers with a previous quit attempt completed questionnaires at baseline. Cross-sectional baseline-data (1999-2001) were analysed in adjusted regression analyses.

Results.

Consistent findings across the three indicators of socioeconomic status (employment, school education, higher education/vocational training): smokers with low socioeconomic status were significantly more likely than smokers with high socioeconomic status to report that they wanted to quit because smoking was too expensive (OR: 1.85 (1.4-2.4), for school education) or because they had health related problems (OR: 1.75 (1.4-2.2)). When looking at previous quit attempts, smokers with low socioeconomic status were significantly more likely to report that it had been a bad experience (OR: 1.41 (1.1-1.8)) and that they had relapsed because they were more nervous/restless/depressed (OR: 1.43 (1.1-1.8)).

Conclusions.

This study shows that smokers with low socioeconomic status have other motives to quit and other reasons to relapse than smokers with high socioeconomic status. Future tobacco prevention efforts aimed at smokers with low socioeconomic status should maybe focus on current advantages of quitting smoking, using high cost of smoking and health advantages of quitting as motivating factors and by including components of mental health as relapse prevention.     

Neurodevelopmental problems in maltreated children referred with indiscriminate friendliness

We aimed to explore the extent of neurodevelopmental difficulties in severely maltreated adopted children. We recruited 34 adopted children, referred with symptoms of indiscriminate friendliness and a history of severe maltreatment in their early childhood and 32 typically developing comparison children without such a history, living in biological families. All 66 children, aged 5-12 years, underwent a detailed neuropsychiatric assessment. The overwhelming majority of the adopted/indiscriminately friendly group had a range of psychiatric diagnoses, including Attention Deficit Hyperactivity Disorder (ADHD), Post-Traumatic Stress Disorder (PTSD) and Reactive Attachment Disorder (RAD) and one third exhibited the disorganised pattern of attachment. The mean IQ was 15 points lower than the comparison group and the majority of the adopted group had suspected language disorder and/or delay. Our findings show that school-aged adopted children with a history of severe maltreatment can have very complex and sometimes disabling neuropsychiatric problems.     

Suicide attempters: biological stressmarkers and adverse life events

Risk factors for suicidal behaviour include adverse life events as well as biochemical parameters acting, e.g. within the hypothalamic–pituitary–adrenal axis and/or monoaminergic systems. The aim of the present investigation was to study stressful life events and biological stress markers among former psychiatric inpatients, who were followed up 12 years after an index suicide attempt. At the time of the index suicide attempt, and before treatment, cerebrospinal fluid (CSF) samples were taken, and 24 h (h) urine (U) was collected. 3-Methoxy-4-hydroxyphenylglycole (MHPG) in CSF and 24 h urinary samples of cortisol and noradrenaline/adrenaline (NA/A) were analysed. Data concerning stressful life events were collected retrospectively from all participants in the study through semi-structured interviews at follow-up. We found that patients who reported sexual abuse during childhood and adolescence had significantly higher levels of CSF-MHPG and U-NA/A, than those who had not. Low 24 h U-cortisol was associated with feelings of neglect during childhood and adolescence. In conclusion, this study has shown significant and discrepant biological stress-system findings in relation to some adverse life events.     

The endocannabinoids anandamide and 2-arachidonoylglycerol inhibit cholinergic contractility in the human colon

The effects of the endocannabinoids anandamide and 2-arachidonoylglycerol (2-AG) were determined on cholinergic contractility in strips of human colonic longitudinal muscle and circular muscle in vitro, in the presence of nitric oxide synthase blockade with N-nitro-l-arginine (10(-4) M). Anandamide and 2-AG inhibited longitudinal muscle and circular muscle contractile responses to acetylcholine (10(-9)-10(-4) M) in a concentration-dependent manner. This was unaltered following pretreatment with the cannabinoid CB(1) receptor-selective antagonist AM251 (10(-7) M), however in isolation AM251 elicited a significant rightward shift in the potency of acetylcholine-evoked contraction in both longitudinal muscle and circular muscle preparations. Pretreatment with an inhibitor of anandamide catabolism, arachidonoyl trifluoromethyl ketone (10(-5) M), alone caused a significant decrease in the potency of acetylcholine-evoked contraction in both longitudinal and circular muscle, but had no significant additional effect on the anandamide-induced (10(-5) M) suppression of contraction. Pretreatment with the cannabinoid CB(2) receptor inverse agonist JTE 907 (10(-6) M) neither influenced the potency of acetylcholine-evoked contraction alone nor prevented the potency shift in acetylcholine-evoked contraction in the presence of anandamide (10(-5) M). The findings of the present study indicate that the endocannabinoids anandamide and 2-arachidonoylglycerol suppress colonic cholinergic contractility via a non conventional cannabinoid or non-cannabinoid receptor-mediated pathway. Cholinergic contraction may be tonically modulated by endocannabinoids and/or products of arachidonate metabolism unrelated to endocannabinoid production. The extent of anandamide metabolism is not sufficient to influence the functional effects of its exogenous administration in human colonic tissue in vitro.