MRI of the epididymis: can the outcome of vasectomy reversal be predicted preoperatively?

OBJECTIVE: The purpose of this study is to describe the MRI findings seen with tubular ectasia of the epididymis and investigate whether MRI may predict vasal/epididymal tubular occlusion before vasectomy reversal. MATERIALS AND METHODS: First, we compared epididymal T1 signal intensity (measured as percentage change relative to ipsilateral testis) in 24 patients with sonographically established tubular ectasia compared with 22 control patients (sonographically normal epididymides). Second, in a subset of patients with tubular ectasia who subsequently underwent surgery to restore fertility (n = 10), we examined the relationship between epididymal T1 signal intensity and surgical outcome. Vasovasostomy (simple vas deferens reanastomosis with high success rate) was possible when viable sperm were detected in the vas deferens intraoperatively. When no sperm were detected, vasal/epididymal tubular occlusion was inferred and vasoepididymostomy (vas deferens to epididymal head anastomosis, a technically challenging procedure with poorer outcome) was performed. RESULTS: In tubular ectasia, we found increased epididymal T1 signal intensity (0-77%) compared with normal epididymides (-27 to 20%) (p < 0.0001). In patients with tubular ectasia who underwent surgery (n = 10), we found higher T1 epididymal signal intensity in cases of vasal/epididymal occlusion (0-70%) relative to cases in which vasal/epididymal patency was maintained (0-10%) (p = 0.01). By logistic regression, relative epididymal T1 signal intensity increase above 19.4% corresponded to greater than 90% probability of requiring vasoepididymostomy. CONCLUSION: Increased epididymal T1 signal intensity (likely due to proteinaceous material lodged within the epididymal tubules) at preoperative MRI in patients undergoing vasectomy reversal suggests vasal/epididymal tubular occlusion and requirement for vasoepididymostomy rather than vasovasostomy.

The five-vessel arch: independent origin of both vertebral arteries from the aortic arch.

An independent origin of the left vertebral artery from the aortic arch is the second most common aortic arch anomaly and occurs in 7% of otherwise healthy persons. Bilateral and independent origins of vertebral arteries are distinctly unusual. We present and illustrate such a case.

A large set of Finnish affected sibling pair families with type 2 diabetes suggests susceptibility loci on chromosomes 6, 11, and 14.

The aim of the Finland-United States Investigation of NIDDM Genetics (FUSION) study is to identify genes that predispose to type 2 diabetes or are responsible for variability in diabetes-related traits via a positional cloning and positional candidate gene approach. In a previously published genome-wide scan of 478 Finnish affected sibling pair (ASP) families (FUSION 1), the strongest linkage results were on chromosomes 20 and 11. We now report a second genome-wide scan using an independent set of 242 Finnish ASP families (FUSION 2), a detailed analysis of the combined set of 737 FUSION 1 + 2 families (495 updated FUSION 1 families), and fine mapping of the regions of chromosomes 11 and 20. The strongest FUSION 2 linkage results were on chromosomes 6 (maximum logarithm of odds score [MLS] = 2.30 at 95 cM) and 14 (MLS = 1.80 at 57 cM). For the combined FUSION 1 + 2 families, three results were particularly notable: chromosome 11 (MLS = 2.98 at 82 cM), chromosome 14 (MLS = 2.74 at 58 cM), and chromosome 6 (MLS = 2.66 at 96 cM). We obtained smaller FUSION 1 + 2 MLSs on chromosomes X (MLS = 1.27 at 152 cM) and 20p (MLS = 1.21 at 20 cM). Among the 10 regions that showed nominally significant evidence for linkage in FUSION 1, four (on chromosomes 6, 11, 14, and X) also showed evidence for linkage in FUSION 2 and stronger evidence for linkage in the combined FUSION 1 + 2 sample.

Fat composition changes in bone marrow during chemotherapy and radiation therapy.

PURPOSE: To quantify changes in bone marrow fat fraction and determine associations with peripheral blood cell counts. METHODS AND MATERIALS: In this prospective study, 19 patients received either highly myelotoxic treatment (radiation therapy plus cisplatin, 5-fluorouracil mitomycin C [FU/MMC], or cisplatin/5-FU/cetuximab) or less myelotoxic treatment (capecitabine-radiation therapy or no concurrent chemotherapy). Patients underwent MR imaging and venipuncture at baseline, midtreatment, and posttreatment visits. We performed mixed effects modeling of the mean proton density fat fraction (PDFF[%]) by linear time, treatment, and vertebral column region (lumbar [L]4-sacral [S]2 vs thoracic [T]10-L3 vs cervical[C]3-T9), while controlling for cumulative mean dose and other confounders. Spearman rank correlations were performed by white blood cell (WBC) counts versus the differences in PDFF(%) before and after treatment. RESULTS: Cumulative mean dose was associated with a 0.43% per Gy (P=.004) increase in PDFF(%). In the highly myelotoxic group, we observed significant changes in PDFF(%) per visit within L4-S2 (10.1%, P<.001) and within T10-L3 (3.93%, P=.01), relative to the reference C3-T9. In the less myelotoxic group, we did not observe significant changes in PDFF(%) per visit according to region. Within L4-S2, we observed a significant difference between treatment groups in the change in PDFF(%) per visit (5.36%, P=.04). Rank correlations of the inverse log differences in WBC versus the differences in PDFF(%) overall and within T10-S2 ranged from 0.69 to 0.78 (P<.05). Rank correlations of the inverse log differences in absolute neutrophil counts versus the differences in PDFF(%) overall and within L4-S2 ranged from 0.79 to 0.81 (P<.05). CONCLUSIONS: Magnetic resonance imaging fat quantification is sensitive to marrow composition changes that result from chemoradiation therapy. These changes are associated with peripheral blood cell counts. This study supports a rationale for bone marrow-sparing treatment planning to reduce the risk of hematologic toxicity.

Transcranial sonothrombolysis using high-intensity focused ultrasound: impact of increasing output power on clot fragmentation.

BACKGROUND: The primary goal of this study was to investigate the relationship between increasing output power levels and clot fragmentation during high-intensity focused ultrasound (HIFU)-induced thrombolysis. METHODS: A HIFU headsystem, designed for brain applications in humans, was used for this project. A human calvarium was mounted inside the water-filled hemispheric transducer. Artificial thrombi were placed inside the skull and located at the natural focus point of the transducer. Clots were exposed to a range of acoustic output power levels from 0 to 400 W. The other HIFU operating parameters remained constant. To assess clot fragmentation, three filters of different mesh pore sizes were used. To assess sonothrombolysis efficacy, the clot weight loss was measured. RESULTS: No evidence of increasing clot fragmentation was found with increasing acoustic intensities in the majority of the study groups of less than 400 W. Increasing clot lysis could be observed with increasing acoustic output powers. CONCLUSION: Transcranial sonothrombolysis could be achieved in vitro within seconds in the absence of tPA and without producing relevant clot fragmentation, using acoustic output powers of <400 W.

White Paper Report of the RAD-AID Conference on International Radiology for Developing Countries: identifying challenges, opportunities, and strategies for imaging services in the developing world.

The RAD-AID Conference on International Radiology for Developing Countries was an assembly of individuals and organizations interested in improving access to medical imaging services in developing countries where the availability of radiology has been inadequate for both patient care and public health programs. The purpose of the meeting was to discuss data, experiences, and models pertaining to radiology in the developing world and to evaluate potential opportunities for future collaboration. Conference participants included radiologists, technologists, faculty members of academic medical institutions, and leadership of nongovernmental organizations involved in international health care and social entrepreneurship. Four main themes from the conference are presented in this white paper as important factors for the implementation and optimization of radiology in the developing world: (1) ensuring the economic sustainability of radiologic services through financial and administrative training support of health care personnel; (2) designing, testing, and deploying clinical strategies adapted for regions with limited resources; (3) structuring and improving the role of American radiology residents interested in global health service projects; and (4) implementing information technology models to support digital imaging in the developing world.

Identification of a protein, G0S2, that lacks Bcl-2 homology domains and interacts with and antagonizes Bcl-2.

The Bcl-2 family of proteins consists of both antiapoptotic and proapoptotic factors, which share sequence homology within conserved regions known as Bcl-2 homology domains. Interactions between Bcl-2 family members, as well as with other proteins, regulate apoptosis through control of mitochondrial membrane permeability and release of cytochrome c. Here we identify a novel regulator of apoptosis that lacks Bcl-2 homology domains but acts by binding Bcl-2 and modulating its antiapoptotic activity. To identify regulators of apoptosis, we performed expression profiling in human primary fibroblasts treated with tumor necrosis factor-alpha (TNF-alpha), a potent inflammatory cytokine that can regulate apoptosis and functions, at least in part, by inducing expression of specific genes through NF-kappaB. We found that the gene undergoing maximal transcriptional induction following TNF-alpha treatment was G(0)-G(1) switch gene 2 (G0S2), the activation of which also required NF-kappaB. We show that G0S2 encodes a mitochondrial protein that specifically interacts with Bcl-2 and promotes apoptosis by preventing the formation of protective Bcl-2/Bax heterodimers. We further show that ectopic expression of G0S2 induces apoptosis in diverse human cancer cell lines in which endogenous G0S2 is normally epigenetically silenced. Our results reveal a novel proapoptotic factor that is induced by TNF-alpha through NF-kappaB and that interacts with and antagonizes Bcl-2.