Effect of obstructive sleep apnoea on retinal microvascular function: a randomised controlled trial

Graefe's Archive for Clinical and Experimental Ophthalmology - Retinal microvascular endothelial dysfunction is thought to be of importance in the development of ocular vascular diseases....     

Percutaneous Transhepatic Cholangiodrainage as Rescue Therapy for Symptomatic Biliary Leakage Without Biliary Tract Dilation After Major Surgery

Symptomatic biliary leakage following major upper abdominal surgery is a severe complication resulting in increased morbidity and mortality. Treatment options usually include either endoscopic intervention or surgical revision. These options may be burdened by a high perioperative risk for the patient (e.g., patients with severe disease) or simply may not be possible (e.g., nonpreserved gastroduodenal passage). In the past, percutaneous transhepatic cholangiodrainage did only seem to be a viable option for patients with dilated bile ducts. Here, we present our experience in a consecutive series of patients with symptomatic biliary leakage following major upper abdominal surgery and without dilation of the biliary system that underwent percutaneous transhepatic cholangiodrainage. Percutaneous transhepatic cholangiodrainage was feasible in 15 of 18 patients (83.3%). The procedure was technically not possible in three patients (16.7%). In 10 of the 15 patients (66.6%) with feasible percutaneous transhepatic cholangiodrainage, biliary leakage was definitely controlled without the need for surgical revision. Depending on the experience with the interventional procedure, percutaneous transhepatic cholangiodrainage should be considered as an alternative for treatment of symptomatic biliary leakage instead of immediate reoperation. Presented at the Digestive Disease Week 2005 (DDW), Chicago, IL, May 14–19, 2005 (poster presentation).     

Genome sequence based, comparative analysis of the fluorescent amplified fragment length polymorphisms (FAFLP) of tubercle bacilli from seals provides molecular evidence for a new species within the Mycobacterium tuberculosis complex.

Tuberculosis in seals is caused by a member of the Mycobacterium tuberculosis complex referred to as the 'seal bacillus'. Fluorescent amplified-fragment length polymorphism (FAFLP) analysis was applied to isolates from four Australian and six Argentinean seals and compared with FAFLP pattern for standard strains belonging to the M. tuberculosis complex. The FAFLP profiles derived from EcoRI/MseI restricted fragments of blind coded DNA samples differentiated the seal bacillus from other members of the M. tuberculosis complex. According to the phylogenetic analysis performed using FAFLP data, seal bacilli appear to have diverged significantly from other members of the M. tuberculosis complex. We describe the suitability of a panel of 19 highly polymorphic markers for rapid identification and comparative genomic analyses of the seal bacillus strains. It is likely that these bacilli got separated from the M. tuberculosis lineage as a result of different insertion deletion events occurring on a genome wide scale. Our analysis reveals that the seal bacillus and M. bovis are genetically related and therefore, might have originated from a common ancestor. Our data additionally support the hypothesis that seal bacillus occupies a unique taxonomic position within the M. tuberculosis complex.     

Sparing of the flexor carpi ulnaris in ulnar neuropathy at the elbow

A common misconception attributes sparing of the flexor carpi ulnaris (FCU) in ulnar neuropathy at the elbow (UNE) to its innervating branch arising "at or above the elbow." We examined the relationship of FCU branches to the medial epicondyle (ME) and humeroulnar aponeurotic arcade (HUA) in 30 cadaver elbows. In only three did the first FCU branch arise at or proximal to the ME. In 36 UNE cases with fibrillations in the first dorsal interosseous, the FCU was normal in 10, mildly abnormal in 11, and severely abnormal in 15. FCU involvement correlated with the severity of the neuropathy and with whether compression was retroepicondylar or at the HUA. We conclude that sparing of the FCU in UNE is unrelated to the level of origin of its innervating branch, but rather is related to the internal neural topography and to the severity and level of compression.     

Toxicity and adaptive immune response to intracellular transgenes delivered by helper-dependent vs. first generation adenoviral vectors

The host immune response to intracellular transgenes delivered by helper-dependent (HDV) vs. first generation (FGV) adenoviral vectors has been relatively unstudied. Previous studies showed short-term correction of bovine and murine argininosuccinate synthetase (ASS) deficiency after first generation adenoviral-mediated liver gene therapy. To determine whether the host adaptive immune response against the intracellular transgene human ASS (hASS) contributed to loss of gene expression in this setting, the same vector (FGV-CAG-hASS) was injected into Rag-/- (immunodeficient) mice. As in wild-type C57BL/6 (B6) mice, Rag-/- mice also showed significant loss of hASS expression and vector by week 4 post-injection, with concomitant elevation of liver enzymes and disruption of liver architecture. Therefore, direct toxicity due to vector rather than adaptive immune response against hASS primarily accounted for loss of expression with FGVs. In contrast to hASS, beta-galactosidase is strongly immunogenic and activates the host adaptive immune response. Loss of transgene expression was observed in B6 mice with either a FGV or a HDV expressing beta-galactosidase. However, the drop in gene expression observed with the HDV was primarily due to the adaptive immune response, since both beta-galactosidase expression and vector genome were sustained in immunodeficient mice treated with HDV. As expected, with weakly immunogenic hASS, vector genome and hASS expression were sustained with a HDV in spite of ubiquitous expression of the transgene. Therefore, viral gene expression is a primary determinant of intermediate and chronic toxicities at day 3 and week 4 post-injection. However, even in the absence of viral gene expression, strongly immunogenic intracellular transgenes can stimulate clearance of transduced hepatocytes.     

Chromatin interactions in differentiating keratinocytes reveal novel atopic dermatitis– and psoriasis-associated genes

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Salsola pollen as a predominant cause of respiratory allergies in Kuwait.

BACKGROUND: Respiratory allergies are common in Kuwait, and the role of certain allergens has been previously documented. OBJECTIVE: To evaluate the results of skin prick tests to a range of allergens that were considered relevant to the vegetation surveys and aerobiological studies performed in Kuwait. METHOD: New patients attending our center during August 2002 to February 2003 with asthma or allergic rhinitis underwent skin prick tests to a battery of allergens. RESULTS: A total of 451 patients aged 5 to 60 years (mean age, 29.5 years) were tested. Of these patients, 403 (89.4%) had a positive test result to at least one allergen and were considered allergic. A total of 76.7% of the allergic patients had a positive reaction to Salsola pollen, with a mean wheal diameter of 8.25 mm (median, 8 mm). Chenopodium album was positive in 57.6% and Bermuda grass was positive in 38.2% of the allergic cases. Indoor allergens seemed to play a lesser role than pollens: Dermatophagoides pteronyssinus was positive in only 37.5%, and American and German cockroaches were positive in 33.2% and 22.3%, respectively. All the allergens other than Salsola elicited a mean wheal diameter of less than 6.25 mm (median, < or = 6 mm). CONCLUSIONS: Indoor allergens seem to play a lesser role in respiratory allergies in Kuwait. Most allergic patients become sensitized to pollens; the strongest and most frequent reaction is from Salsola pollen. Salsola imbricata is found growing extensively in most areas of the country, flowering mainly in autumn, when the most common pollen is of the Chenopod-Amaranth type and when most patients with seasonal allergic rhinitis become symptomatic.