Introduction In recent years, cold snare polypectomy (CSP) has increasingly been used over hot snare polypectomy (HSP) for the removal of colorectal polyps (4 – 10 mm in size). However, the optimal technique (CSP vs. HSP), in terms of complete polyp resection and complications, is uncertain. Our aim was to compare incomplete resection rate (IRR) of polyps and complications using CSP vs. HSP. Methods Randomized controlled studies (RCTs) comparing CSP and HSP for removal of 4 – 10 mm colorectal polyps were considered. Studies were included in the analysis if they obtained biopsy specimens from the resection margin to confirm the absence of residual tissue and reported complications. IRR and complication rate were the outcome measures. Pooled rates were reported as Odds Ratios (OR) or risk difference with 95 % Confidence Interval (CI). Results In total, three RCTs were included in the final analysis. A total of 1051 patients with 1485 polyps were randomized to either HSP group (n = 741 polyps) or CSP group (n = 744 polyps). The overall IRR did not differ between the two groups (HSP vs. CSP: 2.4 % vs. 4.7 %; OR 0.51, 95 %CI 0.13 – 1.99, P = 0.33, I 2 = 73 %). The HSP group had a lower rate of overall complications compared to the CSP group (3.7 % vs. 6.6 %; OR 0.53, 95 % CI 0.3 – 0.94, P = 0.03, I 2 = 0 %). Polyp retrieval rates were not different between the two groups (99 % vs. 98.1 %). Conclusion Our results suggest that HSP and CSP techniques can be effectively used for the complete removal of 4 – 10 mm colorectal polyps; however, HSP has a lower incidence of overall complications.

No single biomarker successfully differentiates PNES from ES; in fact, PNES is only diagnosed via the negation of ES. Clinical assessment and rigorous investigation of psychosocial variables specific to PNES remain critical, and subtyping of PNES is warranted. Future investigational and clinical imperatives are discussed.

Schizophrenia (SCZ) is a chronic debilitating neuropsychiatric disorder with multiple risk factors involving numerous complex genetic influences. We examined and updated a master list of clinically relevant and susceptibility genes associated with SCZ reported in the literature and genomic databases dedicated to gene discovery for characterization of SCZ genes. We used the commercially available GeneAnalytics computer-based gene analysis program and integrated genomic databases to create a molecular profile of the updated list of 608 SCZ genes to model their impact in select categories (tissues and cells, diseases, pathways, biological processes, molecular functions, phenotypes and compounds) using specialized GeneAnalytics algorithms. Genes for schizophrenia were predominantly expressed in the cerebellum, cerebral cortex, medulla oblongata, thalamus and hypothalamus. Psychiatric/behavioral disorders incorporating SCZ genes included ADHD, bipolar disorder, autism spectrum disorder and alcohol dependence as well as cancer, Alzheimer's and Parkinson's disease, sleep disturbances and inflammation. Function based analysis of major biological pathways and mechanisms associated with SCZ genes identified glutaminergic receptors (e.g., GRIA1, GRIN2, GRIK4, GRM5), serotonergic receptors (e.g., HTR2A, HTR2C), GABAergic receptors (e.g., GABRA1, GABRB2), dopaminergic receptors (e.g., DRD1, DRD2), calcium-related channels (e.g., CACNA1H, CACNA1B), solute transporters (e.g., SLC1A1, SLC6A2) and for neurodevelopment (e.g., ADCY1, MEF2C, NOTCH2, SHANK3). Biological mechanisms involving synaptic transmission, regulation of membrane potential and transmembrane ion transport were identified as leading molecular functions associated with SCZ genes. Our approach to interrogate SCZ genes and their interactions at various levels has increased our knowledge and insight into the disease process possibly opening new avenues for therapeutic intervention.

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Few studies have been conducted to evaluate the analgesic effects of AAs. The collective findings of multiple studies evaluating olanzapine in pain syndromes suggest a high, yet preliminary level of evidence of efficacy, warranting prospective studies in various pain syndrome contexts. Pharmacological mechanisms of AA action are elaborated, and the findings of this review are discussed. Risk and benefits of using AAs in chronic pain are described, and investigational implications and future directions are explored.