Diet and nutrition against inflammatory bowel disease: Trick or treat(ment)?

Even if the relationships between nutrition and inflammatory bowel disease (IBD) remain underexplored, the current literature is providing, day by day, much more evidence on the effects of various diets in both prevention and treatment of such illnesses. Wrong dietary habits, together with other environmental factors such as pollution, breastfeeding, smoke, and/or antibiotics, are among the theoretical pathogenetic causes of IBD, whose multifactorial aetiology has been already confirmed. While some of these risk factors are potentially reversible, some others cannot be avoided, and efficient treatments become necessary to prevent IBD spread or recurrence. Furthermore, the drugs currently available for treatment of such disease provide low-to-no effect against the symptoms, making the illnesses still strongly disabling. Whether nutrition and specific diets will prove to effectively interrupt the course of IBD has still to be clarified and, in this sense, further research concerning the applications of such dietary interventions is still needed.     

The effects of preservation on microvascular vein grafts in rats

Segments 15 mm in length were excised from the femoral veins of rats and preserved by refrigeration at 4 C in lactated Ringer's solution for periods up to 21 days. The findings show that veins can be preserved for up to seven days and successfully grafted to recipients. Although there was some success in preserving vein segments for more than seven days, a high rate of thrombosis occurred after implantation in the recipients. It is generally accepted that damaged endothelium causes thrombosis. The light and electron microscopic observations in this study, however, suggest that the condition of the endothelium may not be the only important factor in the patency of small vessels. A thickened and prominent elastic lamina may also play a role in keeping the lumen open.     

Mydriasis in giant-cell arteritis

A previously healthy 60-year-old woman developed headache, cervical pain, bilateral mydriasis (right greater than left), and bilateral conjunctival injection as the sole manifestations of acute giant-cell arteritis.     

Novel heteroplasmic mtDNA mutation in a family with heterogeneous clinical presentations.

The protean manifestations of a novel maternally inherited point mutation of the mitochondrial genome are reported. The proband showed isolated, spastic paraparesis. A brother, who had suffered from a multisystem progressive disorder, ultimately died of cardiomyopathy. Another brother is healthy. The proband's mother showed truncal ataxia, dysarthria, severe hearing loss, mental regression, ptosis, ophthalmoparesis, distal cyclones, and diabetes mellitus. A muscle biopsy performed in the proband failed to show the morphological abnormalities typical of mitochondrial disorders; the activities of respiratory chain complexes were normal. However, complex I and IV activities were low in the muscle homogenate of the affected mother and brother. Sequence analysis of mtDNA showed a heteroplasmic mutation of the tRNA(Ile) gene (G4284A). The mutation load was approximately 55%, 80%, and 90% in the muscle mtDNA of the proband, his mother, and his affected brother, respectively. Mutation was undetected in the healthy brother, as well as in 100 control samples. Several cybrid clones containing homoplasmic mutant mtDNA from the proband showed significant reductions of complex IV activity and maximum oxygen consumption rate, compared with homoplasmic wild-type clones derived from the same subject.