Low-artifact intravascular devices: MR imaging evaluation

Flow-phantom magnetic resonance (MR) imaging, with use of both spin-echo (SE) and gradient-echo (GRE) techniques at 1.5 T, was performed on the percutaneous Greenfield (beta-III titanium alloy [TMA wire]), Amplatz (MP32-N alloy), and Simon nitinol filters and TMA wire facsimiles of the bird's nest, Gunther, new retrievable, and Amplatz vena caval filters. SE imaging allowed detection of thrombi as small as 5 X 5 mm trapped within the percutaneous Greenfield, Simon nitinol, and TMA-wire facsimile filters; with the MP32-N Amplatz filter, a larger volume of thrombus (10 X 20-mm clots) was necessary for clot detection. GRE imaging allowed detection of intraluminal tilting of the percutaneous Greenfield and facsimile Amplatz (TMA-wire) filters. GRE imaging was useful for demonstrating postfilter turbulence due to clots, which was greatest for the Amplatz filter. Imaging of facsimile vascular devices made of tantalum or TMA wire did not cause the severe "black-hole" MR artifacts typical of the stainless-steel devices. SE and GRE imaging were very useful for determining caval patency in two patients with previously placed Mobin-Uddin filters. Noninvasive MR evaluation of blood vessels in the presence of a variety of low-artifact intravascular devices appears feasible.     

Revisiting Ocular Allergy: Evaluating Symptoms,Benzalkonium Chloride and Efficacy of Topical Ketotifen 0.025%

ABSTRACT

This interesting study raises a scientific issue for revisiting three important elements on diagnosis, use of preservatives and selection of the appropriate topical treatment. Itchy feeling can be encountered in other ophthalmic conditions misdiagnosed as allergy, benzalkonium chloride is responsible for surface toxicity resulting in reduced efficacy and tolerability of topical allergy medications and it should be avoided on the management of ocular allergy. Unpreserved ketotifen 0,025% has been shown to be the least toxic formulation being the optimum option for efficacy and tolerability on the management of ocular allergy.     

Cervical radiculopathy: prospective evaluation with surface coil MR imaging, CT with metrizamide, and metrizamide myelography

A prospective study was undertaken to compare the accuracy of surface coil magnetic resonance (SCMR) imaging, metrizamide myelography (MM), and computed tomography with metrizamide (CTM) in the determination of cervical radiculopathy. Surgical findings were the objective measure of accuracy. Fifty-two patients underwent all imaging studies. Studies were evaluated for disease location and type (bone vs. soft tissue). Twenty-eight patients underwent subsequent cervical surgery at 39 levels form an anterior interbody approach. Predictions made with SCMR imaging were surgically confirmed in 74% of patients, with CTM in 85%, and with MM in 67%. There was 90% agreement with surgical findings when SCMR imaging and CTM were used jointly, and 92% agreement when CTM and MM were used jointly, In general, SCMR imaging was as sensitive as CTM for identification of disease level, but not as specific for type of disease. MM was the modality least specific for disease type. The major advantage of CTM was its ability to distinguish bone from soft tissue, for which contrast material is unnecessary. SCMR imaging is a viable alternative to MM and, together with computed tomography, if needed, provides a thorough examination of the cervical region.     

In vitro synthesis and release of inhibin in response to FSH stimulation by isolated segments of seminiferous tubules from normal adult male rats

The production of inhibin by isolated segments of seminiferous tubules from adult male rats cultured in vitro was investigated using a heterologous specific radioimmunoassay. Increasing lengths of tubules (5, 10, 20 and 40 cm) maintained in culture for 4 or 5 days produced increasing amounts of inhibin in vitro. A dose-dependent increase in inhibin production was observed after stimulation with ovine follicle-stimulating hormone (FSH)-s17 (0.1-1000 ng/ml). The tubule segments remain sensitive to FSH stimulation for up to 20 days of culture despite a progressive decline in basal inhibin production, resulting in an increase in the magnitude of the response to FSH stimulation between 0-5, 5-10 and 10-20 days of culture. In the presence of the protein synthesis inhibitor, cycloheximide (50 micrograms/ml), both basal and FSH-stimulated inhibin secretion are inhibited. Testosterone (10(-8)-10(-5) M) does not affect basal inhibin production, although inhibition of the FSH-induced production of inhibin occurred at only the highest dose of testosterone used (10(-5) M). These data demonstrate that the production of inhibin by segments of seminiferous tubules from adult male rats can be used to study the control of inhibin secretion.     

Mechanical clot dissolution: new concept

The authors present preliminary data on in vitro mechanical clot dissolution by means of a catheter with a tiny high-speed propeller enclosed in a special housing. Preweighed human blood clots were subjected to the catheter in a test tube with saline at various propeller speeds and durations of application. After filtration of the resultant slurry, the clot residue was weighed and examined histologically. Clot dissolution was found to be related to both the duration and speed of propeller rotation. No fibrin residue was seen after dissolution, although potential embolic material, composed of clumps of cellular debris as large as 208 microns in longest dimension, was found. Mechanical clot dissolution could possibly be used in any natural or synthetic blood vessel in which there is acute or subacute thrombosis, with fewer complications and lower cost than obtained with traditional methods.     

Activin C Antagonizes Activin A in Vitro and Overexpression Leads to Pathologies in Vivo

Activin A is a potent growth and differentiation factor whose synthesis and bioactivity are tightly regulated. Both follistatin binding and inhibin subunit heterodimerization block access to the activin receptor and/or receptor activation. We postulated that the activin-β_C subunit provides another mechanism regulating activin bioactivity. To test our hypothesis, we examined the biological effects of activin C and produced mice that overexpress activin-β_C. Activin C reduced activin A bioactivity in vitro; in LNCaP cells, activin C abrogated both activin A-induced Smad signaling and growth inhibition, and in LβT2 cells, activin C antagonized activin A-mediated activity of an follicle-stimulating hormone-β promoter. Transgenic mice that overexpress activin-βC exhibited disease in testis, liver, and prostate. Male infertility was caused by both reduced sperm production and impaired sperm motility. The livers of the transgenic mice were enlarged because of an imbalance between hepatocyte proliferation and apoptosis. Transgenic prostates showed evidence of hypertrophy and epithelial cell hyperplasia. Additionally, there was decreased evidence of nuclear Smad-2 localization in the testis, liver, and prostate, indicating that overexpression of activin-β_C antagonized Smad signaling in vivo. Underlying the significance of these findings, human testis, liver, and prostate cancers expressed increased activin-βC immunoreactivity. This study provides evidence that activin-β_C is an antagonist of activin A and supplies an impetus to examine its role in development and disease.     

Over-Expression of Activin-β<Subscript>C</Subscript> Is Associated with Murine and Human Prostate Disease.

Activins are members of the TGF-β superfamily and have been linked to prostate cancer. There are four mammalian activin subunits (β_A, β_B, β_C, and β_E) that dimerize to form functional proteins. The role of activin-A (β_A-β_A) has been relatively well characterized and has been shown to generally inhibit growth in the prostate. In contrast, little is known about the biological function of the β_C and β_E subunits. Previous work indicated activin-C (β_C-β_C) to be an antagonist of activin-A. This is important because resistance to activin-A growth inhibition occurs during prostate cancer progression. This paradox is not currently well understood. Hence, we hypothesize that local expression of the activin-β_C subunit antagonizes activin-A-dependent growth inhibition and represents a key factor contributing to acquired insensitivity to activin-A observed in prostate cancer progression. To test our hypothesis, we characterized the ventral prostate lobes of 9-month-old transgenic mice over-expressing activin-β_C and examined the expression of activin-β_A, activin-β_C, and the activin intracellular signaling factor, Smad-2, in human prostate diseases. Prostate epithelial cell hyperplasia, low-grade prostatic intraepithelial neoplasia (PIN) lesions, alterations in cell proliferation, and reduced Smad-2 nuclear localization were evident in mice over-expressing activin-β_C. Increased activin-β_A and -β_C subunit immunoreactive scores and decreased Smad-2 nuclear localization were also evident in human prostate cancer. This study suggests that over-expression of activin-β_C is associated with murine and human prostate pathologies. We conclude that the activin-β_C subunit may have therapeutic and/or diagnostic implications in human prostate disease.