Vagal neuropathy: evaluation with CT and MR imaging

The vagus nerve, as a result of its protracted course from the brain stem to the abdomen, can present a difficult imaging problem when it is compromised by a clinically occult lesion. The clinical and radiologic records of 48 patients with suspected vagus nerve dysfunction were reviewed to derive an efficient and effective approach to imaging this patient population. An imaging algorithm is proposed in which vagal neuropathies are divided both clinically and radiologically into proximal and distal categories. Proximal vagal lesions are part of a cranial neuropathy complex and have associated oropharyngeal signs and symptoms (e.g., abnormal gag reflex, uvular deviation). Distal vagal lesions occur as an isolated paralysis of the vagus nerve with no symptoms or signs referable to the oropharynx. Either computed tomography (CT) or magnetic resonance imaging can be used to diagnose proximal or distal lesions. However, CT will be insensitive in the detection of the more cephalic proximal lesions, especially those in the brain stem, basal cisterns, and skull base.     

Mortality in Dutch hospitals: Trends in time,place and cause of death after admission for myocardial infarction and stroke. An observational study

Background  

Patterns in time, place and cause of death can have an important impact on calculated hospital mortality rates. Objective is to quantify these patterns following myocardial infarction and stroke admissions in Dutch hospitals during the period 1996–2003, and to compare trends in the commonly used 30-day in-hospital mortality rates with other types of mortality rates which use more extensive follow-up in time and place of death.     

Investigation of acute lower gastrointestinal bleeding with 16‐ and 64‐slice multidetector CT†

We evaluated the usefulness of 16‐ and 64‐slice multidetector CT (MDCT) in the detection of a bleeding site in acute lower gastrointestinal tract (GIT) haemorrhage by conducting a retrospective study of cases of presumed acute lower GIT haemorrhage imaged with CT in two teaching hospitals in an 11‐month period. The patients underwent contrast enhanced CT using either a 16 or 64 MDCT. No oral contrast was used. One hundred milliliters of non‐ionic intravenous contrast agent was injected at 4.5 mL/s, followed by a 60 mL saline flush at 4 mL/s through a dual head injector. Images were acquired in arterial phase with or without non‐contrast and portal phase imaging with 16 × 1.5 mm or 64 × 0.625 mm collimation. Active bleeding was diagnosed by the presence of iodinated contrast extravasation into the bowel lumen on arterial phase images with attenuation greater than and distinct from the normal mucosal enhancement or focal pooling of increased attenuation contrast material within a bowel segment on portal‐venous images. Further management and final diagnosis was recorded. Fourteen patients and 15 studies were reviewed. CT detected and localized a presumed bleeding site or potential causative pathology in 12 (80%) of the patients. Seven of these were supported by other investigations or surgery, while five were not demonstrated by other modalities. Eight patients had mesenteric angiography, of which only four corroborated the site of bleeding. CT did not detect the bleeding site in three patients, of which two required further investigation and definitive treatment. We propose that MDCT serves a useful role as the initial rapid investigation to triage patients presenting with lower GIT bleeding for further investigation and management.     

Intravascular local gene transfer mediated by protein- coated metallic stent

Objective To assess the feasibility, efficiency and selectivity of adenovirus- mediated ge ne transfer to local arterial wall by protein- coated metallic stent. Methods A replication- defective recombinant adenovirus carrying the Lac Z reporter gene for nuclear- specific β- galactosidase (Ad- βgal) was used in this study. Th e coating for metallic stent was made by immersing it in a gelatin solution cont aining crosslinker. The coated stents were mounted on a 4. 0 or3. 0mmpe rcutaneous transluminal coronary angioplasty (PTCA) balloon and submersed into a high- titer Ad- βgal viral stock (2×10(10)pfu/ml) for 3 min, and then im planted into the carotid arteries in 4 mini- swines and into the left anterior d escending branch of the coronary artery in 2 mini- swines via 8F large lumen gui ding catheters. The animals were sacrificed7 (n=4), 14 (n=1) and 21 (n=1) days after implantation, respectively. The β- galactosidase expression was as sessed by X- gal staining. Results The results showed that the expression of transgene was detected in all animal. In 1 of carotid artery with an intact intima, the β- gal expression was l imited to endothelial cells. In vessels with denuded endothelium, gene expressi on was found in the sub- intima, media and adventitia. The transfection efficie ncy of medial smooth muscle cells was 38. 6%. In 2 animals sacrificed 7 days af ter transfection, a microscopic examination of X- gal- stained samples did not s how evidence oftransfection in remote organs and arterial segments adjacent to the treated arterial site.Conclusions Adenovirus- mediated arterial gene transfer to endothelial, smooth muscle cells and adventitia by protein- coated metallic stent is feasible. The transfection efficiency is higher. The coated stent may act as a good carrier of adenovirus - mediated gene transfer and have a potential to prevent restenosis following PT CA.     

Molecular basis of the brindled mouse mutant (Mo(br)): a murine model of Menkes disease

The brindled mouse mutant (Mo(br)) is the closest animal model of the human genetic copper deficiency, Menkes disease, which is presumed to be due to a mutation at the X-linked mottled locus (Mo). The mutant mice are hypopigmented and die at around 15 days after birth, but can be saved by treatment with copper before the 10th postnatal day. Menkes disease has been shown to be due to mutations of the gene ATP7A which encodes P-type ATPase (referred to here as MNK). MNK is likely to function in copper efflux from cells, but the full range of its biological activity is not fully understood. The nature of the mutation in the brindled mouse is of importance in our understanding of the role of MNK and for devising treatment strategies for Menkes disease. Here we show that the brindled mouse has a deletion of two amino acids in a highly conserved, but functionally uncharacterized, region of Mnk. Comparison with the Ca ATPases suggests this region may be involved in conformational changes associated with the E1/E2 transition fundamental to the action of P-type ATPases. We also describe the first Western blot data for Mnk in tissues, and these show normal levels of Mnk in mutant and brindled kidneys but none in liver. In the kidney, immunohistochemistry demonstrated Mnk in the proximal and distal tubules, the distribution is identical in mutant and normal. This distribution is consistent with Mnk being involved in copper resorption from the urine.