Pre-screening for bariatric surgery patients: comparative effectiveness of transnasal endoscopy versus esophagogastroduodenoscopy.

BACKGROUND: Endoscopic evaluation is frequently performed before bariatric surgery to identify foregut pathology that may alter procedure selection. Transnasal endoscopy (TNE) is an alternative to esophagogastroduodenoscopy (EGD). The objective of this study was to compare TNE to EGD. METHODS: Patients who underwent TNE or EGD before bariatric surgery from January 2012 through April 2019 were reviewed. Statistical analyses included Chi-square, Wilcoxon two-sample, and Fisher's exact tests. A p value < 0.05 was considered significant. RESULTS: Three hundred and forty-five patients underwent preoperative screening (63% EGD, 37% TNE) before bariatric surgery. Mean age and preoperative body mass index in the TNE and EGD groups were 46.2 ± 12.4 vs 45.5 ± 11.6 years (p = 0.58) and 46.5 ± 7.1 vs. 45.5 ± 6.1 kg/m2 (p = 0.25), respectively. Three TNEs were aborted, resulting in a success rate of 98%. Of patients who underwent EGD, 1 (0.5%) visited the emergency department (ED), and 7 (3%) called the nurse with post-procedure concerns. There were no ED visits or nurse calls from patients who underwent TNE. The median total time in the procedure room was 77 (57-97) min for EGD vs. 26 (8-33) min for TNE (p < 0.001). One patient who underwent TNE required subsequent EGD. Mean charge per patient for EGD and TNE was $5034.70 and $1464.00, respectively. CONCLUSIONS: TNE was associated with less post-procedure care, shorter procedure time and fewer charges compared to EGD. TNE could be considered an initial screening tool for patients undergoing bariatric surgery, while EGD could be used selectively in patients with abnormal TNE findings.

Heat therapy improves glucose tolerance and adipose tissue insulin signaling in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is associated with high rates of obesity and metabolic dysfunction. Repeated passive heat exposure (termed heat therapy) is a novel lifestyle intervention for improving health in obese women with PCOS. The purpose of this study was to examine changes in metabolic function in obese women with PCOS following heat therapy. Eighteen age- and BMI-matched obese women with PCOS (age: 27 ± 1 yr, BMI: 41.3 ± 1.1 kg/m-2) were assigned to heat therapy (HT) or time control (CON). HT participants underwent 30 one-hour hot tub sessions over 8-10 wk, while CON participants completed all testing but did not undergo heat therapy. Before (Pre), at the mid-point (Mid), and following (Post) 8-10 wk of heat therapy, metabolic health was assessed using a 2-h oral glucose tolerance test, a subcutaneous abdominal fat biopsy (Pre-Post only), and other blood markers relating to metabolic function. HT participants exhibited improved fasting glucose (Pre: 105 ± 3, Post: 89 ± 5mg/dl; P = 0.001), glucose area under the curve (AUC) (Pre: 18,698 ± 1,045, Post: 16,987 ± 1,017 mg·dl-1·min-1; P = 0.028) and insulin AUC (Pre: 126,924 ± 11,730, Post: 91,233 ± 14,429 IU l-1·min-1; P = 0.012). Adipocyte insulin signaling (p-AKT at Ser-473 with 1.2 nM insulin) increased in HT (Pre: 0.29 ± 0.14, Post: 0.93 ± 0.29 AU; P = 0.021). Additionally, serum testosterone declined in HT participants (Pre: 51 ± 7, Post: 34 ± 4 ng/dl; P = 0.033). No parameters changed over time in CON, and no change in BMI was observed in either group. HT substantially improved metabolic risk profile in obese women with PCOS. HT also reduced androgen excess and may improve PCOS symptomology.

Meta-inflammation and cardiometabolic disease in obesity: Can heat therapy help?

Obesity and associated metabolic dysfunction have reached epidemic proportions worldwide. The current theory linking metabolic disease and obesity involves ischemic adipose tissue initiating an inflammatory cascade that results in systemic insulin resistance and may eventually lead to type II diabetes mellitus. Diabetes and associated metabolic dysfunction increase the risk of developing cardiovascular disease and fatal cardiovascular events. By targeting key steps in this process, ischemia and inflammation, this cascade may be prevented or reversed and thus metabolic and cardiovascular health may be preserved in obesity. Regular heat exposure (termed 'heat therapy') offers potential to improve cardiometabolic health in obese individuals through a variety of mechanisms that include but are not limited to heat shock proteins, hypoxia-inducible factor 1α, and hemodynamic effects. The purpose of this review is to highlight the cardiometabolic decline in obese individuals stemming from adipose tissue dysfunction, and examine the ways in which heat therapy and associated cellular and systemic adaptations can intersect with this decline in function to improve or restore cardiovascular and metabolic health.

Expression of GABA(B) receptor in the avian auditory brainstem: ontogeny, afferent deprivation, and ultrastructure.

Nucleus magnocellularis (NM), nucleus angularis (NA), and nucleus laminaris (NL), second- and third-order auditory neurons in the avian brainstem, receive GABAergic input primarily from the superior olivary nucleus (SON). Previous studies have demonstrated that both GABA(A) and GABA(B) receptors (GABA(B)Rs) influence physiological properties of NM neurons. We characterized the distribution of GABA(B)R expression in these nuclei during development and after deafferentation of the excitatory auditory nerve (nVIII) inputs. We used a polyclonal antibody raised against rat GABA(B)Rs in the auditory brainstem during developmental periods that are thought to precede and include synaptogenesis of GABAergic inputs. As early as embryonic day (E)14, dense labeling is observed in NA, NM, NL, and SON. At earlier ages immunoreactivity is present in somas as diffuse staining with few puncta. By E21, when the structure and function of the auditory nuclei are known to be mature, GABA(B) immunoreactivity is characterized by dense punctate labeling in NM, NL, and a subset of NA neurons, but label is sparse in the SON. Removal of the cochlea and nVIII neurons in posthatch chicks resulted in only a small decrease in immunoreactivity after survival times of 14 or 28 days, suggesting that a major proportion of GABA(B)Rs may be expressed postsynaptically or on GABAergic terminals. We confirmed this interpretation with immunogold TEM, where expression at postsynaptic membrane sites is clearly observed. The characterization of GABA(B)R distribution enriches our understanding of the full complement of inhibitory influences on central auditory processing in this well-studied neuronal circuit.

Avian superior olivary nucleus provides divergent inhibitory input to parallel auditory pathways.

The avian auditory brainstem displays parallel processing, a fundamental feature of vertebrate sensory systems. Nuclei specialized for temporal processing are largely separate from those processing other aspects of sound. One possible exception to this parallel organization is the inhibitory input provided by the superior olivary nucleus (SON) to nucleus angularis (NA), nucleus magnocellularis (NM), and nucleus laminaris (NL) and contralateral SON (SONc). We sought to determine whether single SON neurons project to multiple targets or separate neuronal populations project independently to individual target nuclei. We introduced two different fluorescent tracer molecules into pairs of target nuclei and quantified the extent to which retrogradely labeled SON neurons were double labeled. A large proportion of double-labeled SON somata were observed in all cases in which injections were made into any pair of ipsilateral targets (NA and NM, NA and NL, or NM and NL), suggesting that many individual SON neurons project to multiple targets. In contrast, when injections involved the SONc and any or all of the ipsilateral targets, double labeling was rare, suggesting that contralateral and ipsilateral targets are innervated by distinct populations of SON neurons arising largely from regionally segregated areas of SON. Therefore, at the earliest stages of auditory processing, there is interaction between pathways specialized to process temporal cues and those that process other acoustic features. We present a conceptual model that incorporates these results and suggest that SON circuitry, in part, functions to offset interaural intensity differences in interaural time difference processing.