Microscopic colitis is a common cause of chronic, nonbloody diarrhea. Microscopic colitis is more common in women than men and usually affects patients in their sixth and seventh decade. This article reviews the etiology and medical management of microscopic colitis. The etiology of microscopic colitis is unknown, but it is associated with autoimmune disorders, such as celiac disease, polyarthritis, and thyroid disorders. Smoking has been identified as a risk factor of microscopic colitis. Exposure to medications, such as non-steroidal anti-inflammatory drugs, proton pump inhibitors, and selective serotonin reuptake inhibitors, is suspected to play a role in microscopic colitis, although their direct causal relationship has not been proven. Multiple medications, including corticosteroids, anti-diarrheals, cholestyramine, bismuth, 5-aminosalicylates, and immunomodulators, have been used to treat microscopic colitis with variable response rates. Budesonide is effective in inducing and maintaining clinical remission but relapse rate is as high as 82% when budesonide is discontinued. There is limited data on management of steroid-dependent microscopic colitis or refractory microscopic colitis. Immunomodulators seem to have low response rate 0%-56% for patients with refractory microscopic colitis. Response rate 66%-100% was observed for use of anti-tumor necrosis factor (TNF) therapy for refractory microscopic colitis. Anti-TNF and diverting ileostomy may be an option in severe or refractory microscopic colitis.

A hallmark of productive infection by DNA viruses is the coupling of viral late gene expression to genome replication. Here we report the identification of open reading frame 30 (ORF30) and ORF34 as viral trans factors crucial for activating late gene transcription following viral DNA replication during lytic infection of murine gammaherpesvirus 68 (MHV-68). The mutant virus lacking either ORF30 or ORF34 underwent normal DNA replication but failed to express viral late gene transcripts, leading to nonproductive infection. In a reporter assay system, ORF30 and ORF34 were required for MHV-68 to activate the viral late gene promoters. Furthermore, studies using chromatin immunoprecipitation assays showed that the recruitment of RNA polymerase II to the viral late promoters during lytic infection was significantly reduced in the absence of ORF30 or ORF34. Together, the results suggest that ORF30 and ORF34 may play an important role in the assembly of the transcription initiation complex at the late gene promoters. Our discovery of the viral mutants that uncouple late gene transcription from DNA replication lays an important foundation to dissect the mechanism of this critical step of gene expression regulation.

Addition of FISH and mutation analyses to cytology analysis significantly increased the level of sensitivity with which we detected malignancy in biliary strictures, with 100% specificity. These techniques can be performed using standard brush samples collected during endoscopic retrograde cholangiopancreatography, with mutations detected in free DNA in supernatant fluid of samples. The tests are complementary and therefore should be used sequentially in the diagnostic evaluation of biliary strictures.

Upper gastrointestinal bleeding from peptic ulcer disease is not a new clinical problem. Yet, the approach to management continues to evolve with the accumulation of data and well designed studies on the subject.

Background: Racial–ethnic inequity in type 1 diabetes technology use is well documented and contributes to disparities in glycemic and long-term outcomes. However, solutions to address technology inequity remain sparse and lack stakeholder input. Methods: We employed user-centered design principles to conduct workshop sessions with multidisciplinary panels of stakeholders, building off of our prior study highlighting patient-identified barriers and proposed solutions. Stakeholders were convened to review our prior findings and co-create interventions to increase technology use among underserved populations with type 1 diabetes. Stakeholders included type 1 diabetes patients who had recently onboarded to technology; endocrinology and primary care physicians; nurses; diabetes educators; psychologists; and community health workers. Sessions were recorded and analyzed iteratively by multiple coders for common themes. Results: We convened 7 virtual 2-h workshops for 32 stakeholders from 11 states in the United States. Patients and providers confirmed prior published studies highlighting patient barriers and generated new ideas by co-creating solutions. Common themes of proposed interventions included (1) prioritizing more equitable systems of offering technology, (2) using visual and hands-on approaches to increase accessibility of technology and education, (3) including peer and family support systems more, and (4) assisting with insurance navigation and social needs. Discussion: Our study furthers the field by providing stakeholder-endorsed intervention ideas that propose feasible changes at the patient, provider, and system levels to reduce inequity in diabetes technology use in type 1 diabetes. Multidisciplinary stakeholder engagement in disparities research offers unique insight that is impactful and acceptable to the target population.