Comparison of respiratory triggering and gating techniques for the removal of respiratory artifacts in MR imaging

Respiratory movement degrades magnetic resonance (MR) images of the chest and abdomen by increasing noise through the production of "ghost" artifacts and by decreasing edge sharpness in moving structures. Respiratory gating, which limits data acquisition to end-expiration, is successful in restoring edge sharpness and reducing ghosts but increases imaging time two to three times, which limits its use to sequences with short repetition times (TRs). To overcome this limitation, an alternative technique, respiratory triggering, was developed, which triggers the acquisition of an MR section at a fixed point on the respiratory cycle. This technique restores edge sharpness and reduces ghosts, but unlike gating, it can be used to produce an image at any phase of the respiratory cycle. Triggering requires long TRs since the TR is limited to the respiratory period (TP) or one-half of TP, depending on whether the same section is triggered once or twice during a single respiratory cycle. Gating and triggering were evaluated and compared for single-section and multi-section imaging of both volunteers and patients. The authors conclude that when a chest or abdominal survey is required, triggering takes less time than gating if TRs are required that exceed one-fifth of TP.     

Bifid origin of the left vertebral artery

Two patients demonstrating a bifid origin of the left vertebral artery are described. The embryologic origin of this anomaly is reviewed together with diagnostic and therapeutic implications, emphasizing the importance of knowledge and recognition of the anomaly. It is suggested that this anomaly is not as rare as previously thought.     

Subacute and chronic bone infections: diagnosis using In-111, Ga-67 and Tc-99m MDP bone scintigraphy, and radiography

The usefulness of indium-111 white blood cell scintigraphy in the diagnosis of subacute or chronic bone infection was examined in 21 orthopedic patients. In-111 WBC imaging was compared with gallium-67 and technetium-99m methylene diphosphonate skeletal scintigraphy and bone radiography, all studies being performed within 1 week. In-111 WBC scintigraphy showed no definite advantage over Ga-67 scintigraphy in the identification of chronic bone infection. The two tests had the same sensitivity (80%) and similar specificity (In-111 WBC 75%, Ga-67 83%; difference not significant). Bone radiography had a sensitivity of 60% and a specificity of 67%. A negative Tc-99m MDP bone scintigram ruled out infection (sensitivity 100%), but because of low specificity (25%), final evaluation required performance of Ga-67 or In-111 WBC scintigraphy.     

High expression of Lewis<Superscript>y/b</Superscript>antigens is associated with decreased survival in lymph node negative breast carcinomas

Introduction  

There is sufficient evidence that blood group related Lewis antigens are tumour-associated molecules. The Lewis^y and Lewis^b antigens are complex carbohydrates that are over-expressed by breast, lung, colon and ovarian cancers. The SC101 mAb is a unique Lewis^y/b binding antibody that binds to native and extended Lewis^y and Lewis^b haptens, displaying no cross reactivity with H type 1, H type 2, Lewis^x or normal blood group antigens.     

Germline mutations of the MEN1 gene in familial multiple endocrine neoplasia type 1 and related states

Familial multiple endocrine neoplasia type 1 (FMEN1) is an autosomal dominant trait characterized by tumors of the parathyroids, gastro- intestinal endocrine tissue, anterior pituitary and other tissues. We recently cloned the MEN1 gene and confirmed its identity by finding mutations in FMEN1. We have now extended our mutation analysis to 34 more unrelated FMEN1 probands and to two related states, sporadic MEN1 and familial hyperparathyroidism. There was a high prevalence of heterozygous germline MEN1 mutations in sporadic MEN1 (8/11 cases) and in FMEN1 (47/50 probands). One case of sporadic MEN1 was proven to be a new MEN1 mutation. Eight different mutations were observed more than once in FMEN1. Forty different mutations (32 FMEN1 and eight sporadic MEN1) were distributed across the MEN1 gene. Most predicted loss of function of the encoded menin protein, supporting the prediction that MEN1 is a tumor suppressor gene. No MEN1 germline mutation was found in five probands with familial hyperparathyroidism, suggesting that familial hyperparathyroidism often is caused by mutation in another gene or gene(s).      

Relationship of acute lung inflammatory injury to Fas/FasL system

There is mounting evidence that apoptosis plays a significant role in tissue damage during acute lung injury. To evaluate the role of the apoptosis mediators Fas and FasL in acute lung injury, Fas (lpr)- or FasL (gld)-deficient and wild-type mice were challenged with intrapulmonary deposition of IgG immune complexes. Lung injury parameters ((125)I-albumin leak, accumulation of myeloperoxidase, and wet lung weights) were measured and found to be consistently reduced in both lpr and gld mice. In wild-type mice, lung injury was associated with a marked increase in Fas protein in lung. Inflamed lungs of wild-type mice showed striking evidence of activated caspase-3, which was much diminished in inflamed lungs from lpr mice. Intratracheal administration of a monoclonal Fas-activating antibody (Jo2) in wild-type mice induced MIP-2 and KC production in bronchoalveolar lavage fluids, and a murine alveolar macrophage cell line (MH-S) showed significantly increased MIP-2 production after incubation with this antibody. Bronchoalveolar lavage fluid content of MIP-2 and KC was substantially reduced in lpr mice after lung injury when compared to levels in wild-type mice. These data suggest that the Fas/FasL system regulates the acute lung inflammatory response by positively affecting CXC-chemokine production, ultimately leading to enhanced neutrophil influx and tissue damage.