Eye Movement Control in the Argus II Retinal-Prosthesis Enables Reduced Head Movement and Better Localization Precision.

Purpose: Visual scanning by sighted individuals is done using eye and head movements. In contrast, scanning using the Argus II is solely done by head movement, since eye movements can introduce localization errors. Here, we tested if a scanning mode utilizing eye movements increases visual stability and reduces head movements in Argus II users. Methods: Eye positions were measured in real-time and were used to shift the region of interest (ROI) that is sent to the implant within the wide field of view (FOV) of the scene camera. Participants were able to use combined eye-head scanning: shifting the camera by moving their head and shifting the ROI within the FOV by eye movement. Eight blind individuals implanted with the Argus II retinal prosthesis participated in the study. A white target appeared on a touchscreen monitor and the participants were instructed to report the location of the target by touching the monitor. We compared the spread of the responses, the time to complete the task, and the amount of head movements between combined eye-head and head-only scanning. Results: All participants benefited from the combined eye-head scanning mode. Better precision (i.e., narrower spread of the perceived location) was observed in six out of eight participants. Seven of eight participants were able to adopt a scanning strategy that enabled them to perform the task with significantly less head movement. Conclusions: Integrating an eye tracker into the Argus II is feasible, reduces head movements in a seated localization task, and improves pointing precision.

Interaction of obesity and inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a chronic inflammatory condition of unknown etiology that is thought to result from a combination of genetic, immunologic and environmental factors. The incidence of IBD has been increasing in recent decades, especially in developing and developed nations, and this is hypothesized to be in part related to the change in dietary and lifestyle factors associated with modernization. The prevalence of obesity has risen in parallel with the rise in IBD, suggesting a possible shared environmental link between these two conditions. Studies have shown that obesity impacts disease development and response to therapy in patients with IBD and other autoimmune conditions. The observation that adipose tissue produces pro-inflammatory adipokines provides a potential mechanism for the observed epidemiologic links between obesity and IBD, and this has developed into an active area of investigative inquiry. Additionally, emerging evidence highlights a role for the intestinal microbiota in the development of both obesity and IBD, representing another potential mechanistic connection between the two conditions. In this review we discuss the epidemiology of obesity and IBD, possible pathophysiologic links, and the clinical impact of obesity on IBD disease course and implications for management.

Increased body mass index is associated with earlier time to loss of response to infliximab in patients with inflammatory bowel disease.

BACKGROUND: Obesity is an emerging problem in the care of inflammatory bowel disease (IBD) patients and has been associated with a diminished response to adalimumab. Whether obesity influences the response to infliximab (IFX) is not known. METHODS: A retrospective cohort of 124 subjects with IBD initiating IFX, naive to biologic therapy, was identified. Subjects were stratified according to their weight and body mass index (BMI). The primary outcome was the first occurrence of an IBD flare defined as dose escalation of IFX, corticosteroid use, discontinuation of IFX, hospitalization, or surgery. Multivariable logistic regression was performed considering body mass and BMI as categorical and continuous variables. RESULTS: Obese (BMI > 30 kg/m) patients with Crohn's disease were more likely to have an IBD flare than nonobese patients (adjusted hazard ratio [HR]: 3.03, P < 0.001); overweight (BMI > 25 kg/m) patients with ulcerative colitis trended toward a similar observation (HR: 9.68, P = 0.06). When considered as continuous variables, increasing mass and BMI were associated with earlier IBD flare in both Crohn's disease (adjusted HR: 1.06 per unit increase in BMI [P = 0.02] and 1.02 per kg increase in body mass [P = 0.02]) and ulcerative colitis (adjusted HR: 1.3 per unit increase in BMI [P = 0.01] and 1.11 per kg increase in body mass [P = 0.004]). CONCLUSIONS: Increased body weight is associated with an earlier time to loss of response to IFX in Crohn's disease and ulcerative colitis, a novel finding given that IFX is the only antitumor necrosis factor agent whose dosing reflects increased body weight.

An association between microscopic colitis and celiac disease.

BACKGROUND & AIMS: Microscopic colitis has been associated with celiac disease. We aimed to determine the extent and significance of this relationship. METHODS: A prospectively maintained database of celiac disease patients, seen between 1981 and 2006, was analyzed. Standardized morbidity ratios (SMR) were calculated using a general population study of microscopic colitis as the reference group. Statistical analysis was conducted using the Student t test, Pearson chi(2) test, or Fisher exact test. RESULTS: Microscopic colitis was found in 44 of 1009 patients (4.3%); this represented a 70-fold increased risk for individuals with celiac disease to have microscopic colitis, compared with the general population (SMR, 72.39; 95% confidence interval [CI], 52.52-95.36). The celiac disease patients with microscopic colitis were older (P = .0001) and had more severe villous atrophy (P = .002) than the celiac disease patients without microscopic colitis. Microscopic colitis was diagnosed after celiac disease in 64% of the patients, simultaneously in 25%, and before celiac disease in 11% (P = .0001). Pancolitis predominated, though 16% had colitis limited to the right colon. Steroid or immunosuppressant therapies were required in 66% of the celiac disease patients with microscopic colitis and given as maintenance therapy to 50% of these patients. Follow-up biopsies revealed that the colitis persisted in 57% of the patients with celiac disease and microscopic colitis, despite improved diarrhea symptoms; the diarrhea resolved in most of the patients. CONCLUSIONS: Microscopic colitis is more common in patients with celiac disease than in the general population. Patients with celiac disease and microscopic colitis have more severe villous atrophy and frequently require steroids or immunosuppressant therapies to control diarrhea.

Anemia in celiac disease is multifactorial in etiology.

Anemia in celiac disease (CD) has been attributed to nutritional deficiencies; however, the clinical manifestations of CD have changed with nongastrointestinal presentations predominating. We collected hematologic parameters from a cohort of patients seen at a tertiary care center for CD to assess the characteristics of anemia in this population. Hematological parameters measured 1995 was analyzed. Ferritin levels were compared with population controls (NHANES III). Iron deficiency was common, occurring in 33% of men and 19% of women (P < 0.001). Folate deficiency was seen in approximately 12% of the total sample and B12 deficiency in approximately 5%. Anemia was present in approximately 20% of the cohort. Among the anemic patients, ferritin was less than the 10th percentile in 45%, between the 10th and 50th percentile in 39% and greater than the 50th percentile in 13%. Ferritin > 50th percentile was more common in anemic men (24%) than in anemic women (9%; P > 0.20). Macrocytic anemia with concurrent B12 or folate deficiency was rare (3%). Elevated ESR was observed in patients with ferritin < 10th percentile and >50th. A gluten-free diet resulted in increased serum ferritin in iron-deficient patients, and decreased ferritin levels in those with high ferritin (r(2) = 0.46, P < 0.001). Although anemia is still a common presentation of celiac disease, nutritional deficiencies alone do not explain this phenomenon in all cases; inflammation appears to contribute as evidenced by the presence of anemia of chronic disease in some individuals.