A causal relationship between right paraduodenal hernia and superior mesenteric artery syndrome: a case report

<p>Abstract</p> <p>Introduction</p> <p>Cases of right paraduodenal hernia and superior mesenteric artery syndrome have been reported separately, but their occurrence in combination has not been reported.</p> <p>Case presentation</p> <p>A 46-year-old Japanese man who had never undergone laparotomy was admitted to our hospital due to an acute abdomen. An enhanced multidetector-row computed tomography scan of our patient showed a cluster of small intestines with ischemic change in his right lateral abdominal cavity. Emergency surgery was subsequently performed, and strangulation of the distal jejunum along with incidental right paraduodenal hernia was found. His necrotic ileum was resected, and the jejunum encapsulated by the sac was repaired manually without reduction.</p> <p>Three days after the operation, however, our patient developed vomiting. An upper gastrointestinal series revealed a straight line cut-off sign on the third portion of his duodenum. A second enhanced multidetector-row computed tomography scan showed that he had a lower aortomesenteric angle and a shorter aortomesenteric distance compared to his condition before his right paraduodenal hernia was surgically repaired. We strongly suspected that the right paraduodenal hernia repair may have induced superior mesenteric artery syndrome. On the 21st post-operative day, duodenojejunostomy was performed because conservative management had failed.</p> <p>Conclusions</p> <p>In this case, enhanced multidetector-row computed tomography, which permits reconstructed multiplanar imaging, helped us to visually identify these diseases easily. It is important to recognize that surgical repair of a right paraduodenal hernia may cause superior mesenteric artery syndrome.</p

The impact of maternal separation on adult mouse behaviour and on the total neuron number in the mouse hippocampus

The maternal separation paradigm has been applied to C57BL/6J mice as an animal developmental model for understanding structural deficits leading to abnormal behaviour. A maternal separation (MS) model was used on postnatal day (PND) 9, where the pups were removed from their mother for 24 h (MS24). When the pups were 10 weeks old, the level of anxiety and fear was measured with two behavioural tests; an open field test and an elevated plus maze test. The Barnes platform maze was used to test spatial learning, and memory by using acquisition trials followed by reverse trial sessions. The MS24 mice spent more time in the open arms of the elevated plus maze compared to controls, but no other treatment differences were found in the emotional behavioural tests. However, in the reverse trial for the Barnes maze test there was a significant difference in the frequency of visits to the old goal, the number of errors made by the MS24 mice compared to controls and in total distance moved. The mice were subsequently sacrificed and the total number of neurons estimated in the hippocampus using the optical fractionator. We found a significant loss of neurons in the dentate gyrus in MS mice compared to controls. Apparently a single maternal separation can impact the number of neurons in mouse hippocampus either by a decrease of neurogenesis or as an increase in neuron apoptosis. This study is the first to assess the result of maternal separation combining behaviour and stereology

The TLR9 agonist MGN1703 triggers a potent type I interferon response in the sigmoid colon

Toll-like receptor 9 (TLR9) agonists are being developed for treatment of colorectal and other cancers, yet the impact of these drugs on human intestines remains unknown. This, together with the fact that there are additional potential indications for TLR9 agonist therapy (e.g., autoimmune and infectious diseases), led us to investigate the impact of MGN1703 (Lefitolimod) on intestinal homeostasis and viral persistence in HIV-positive individuals. Colonic sigmoid biopsies were collected (baseline and week four) from 11 HIV+ individuals on suppressive antiretroviral therapy, who received MGN1703 (60 mg s.c.) twice weekly for 4 weeks in a single-arm, phase 1b/2a study. Within sigmoid mucosa, global transcriptomic analyses revealed 248 modulated genes (false discovery rate<0.05) including many type I interferon (IFN)-stimulated genes. MGN1703 increased the frequencies of cells exhibiting MX1 (P=0.001) and ISG15 (P=0.014) protein expression. No changes were observed in neutrophil infiltration (myeloperoxidase; P=0.97). No systematic effect on fecal microbiota structure was observed (analysis of similarity Global R=-0.105; P=0.929). TLR9 expression at baseline was inversely proportional to the change in integrated HIV DNA during MGN1703 treatment (P=0.020). In conclusion, MGN1703 induced a potent type I IFN response, without a concomitant general inflammatory response, in the intestines