Effective capture of radioactive organic iodides from nuclear waste remains a significant challenge due to the drawbacks of current adsorbents such as low uptake capacity, high cost, and non-recyclability. We report here a general approach to overcome this challenge by creating radioactive organic iodide molecular traps through functionalization of metal-organic framework materials with tertiary amine-binding sites. The molecular trap exhibits a high CH3I saturation uptake capacity of 71 wt% at 150 °C, which is more than 340% higher than the industrial adsorbent Ag0@MOR under identical conditions. These functionalized metal-organic frameworks also serve as good adsorbents at low temperatures. Furthermore, the resulting adsorbent can be recycled multiple times without loss of capacity, making recyclability a reality. In combination with its chemical and thermal stability, high capture efficiency and low cost, the adsorbent demonstrates promise for industrial radioactive organic iodides capture from nuclear waste. The capture mechanism was investigated by experimental and theoretical methods.

IntroductionJejunal diverticula are rare and are usually asymptomatic. However, they may cause chronic non-specific symptoms or rarely lead to an acute presentation.Case presentationWe report the case of an 82-year-old Caucasian woman presenting with a one-day history of generalized abdominal pain, with three episodes of vomiting. An abdominal X-ray displayed multiple dilated loops of the small bowel. A subsequent computed tomography scan of the abdomen and pelvis revealed a thickening of the duodenum and dilatation of the proximal jejunum. Multiple small bowel diverticula were identified with surrounding pockets of free air adjacent to the jejunal diverticula suggestive of a small bowel perforation. Our patient underwent a laparotomy, which identified multiple jejunal diverticula with two pinhole jejunal perforations and associated fecal contamination. The perforations were repaired with primary closure and extensive washout was performed.ConclusionJejunal diverticulosis in the elderly can lead to significant morbidity and mortality and so should be suspected in those presenting with crampy abdominal pain and altered bowel habits.

Abstract

Background

Osteoporosis, a disease of decreased bone mineral density represents a significant and growing burden in the western world. Aging population structure and therapeutic use of glucocorticoids have contributed in no small way to the increase in the incidence of this disease. Despite substantial investigative efforts over the last number of years the exact molecular mechanism underpinning the initiation and progression of osteoporosis remain to be elucidated. This has meant that no significant advances in therapeutic strategies have emerged, with joint replacement surgery being the mainstay of treatment.

Methods

In this study we have used an integrated genomics profiling and computational biology based strategy to identify the key osteoblast genes and gene clusters whose expression is altered in response to dexamethasone exposure. Primary human osteoblasts were exposed to dexamethasone in vitro and microarray based transcriptome profiling completed.

Results

These studies identified approximately 500 osteoblast genes whose expression was altered. Functional characterization of the transcriptome identified developmental networks as being reactivated with 106 development associated genes found to be differentially regulated. Pathway reconstruction revealed coordinate alteration of members of the WNT signaling pathway, including frizzled-2, frizzled-7, DKK1 and WNT5B, whose differential expression in this setting was confirmed by real time PCR.

Conclusion

The WNT pathway is a key regulator of skeletogenesis as well as differentiation of bone cells. Reactivation of this pathway may lead to altered osteoblast activity resulting in decreased bone mineral density, the pathological hallmark of osteoporosis. The data herein lend weight to the hypothesis that alterations in developmental pathways drive the initiation and progression of osteoporosis.