Design and development of a low temperature, inductance based high frequency ac susceptometer

We report on the development of an induction based low temperature high frequency ac susceptometer capable of measuring at frequencies up to 3.5 MHz and at temperatures between 2 K and 300 K. Careful balancing of the detection coils and calibration have allowed a sample magnetic moment resolution of $5\times10^{-10} Am^2$ at 1 MHz. We will discuss the design and characterization of the susceptometer, and explain the calibration process. We also include some example measurements on the spin ice material CdEr$_2$S$_4$ and iron oxide based nanoparticles to illustrate functionality

Bilateral testicular self-castration due to cannabis abuse: a case report

<p>Abstract</p> <p>Introduction</p> <p>The self-mutilating patient is an unusual psychiatric presentation in the emergency room. Nonetheless, serious underlying psychiatric pathology and drug abuse are important background risk factors. A careful stepwise approach in the emergency room is essential, although the prognosis, follow-up, and eventual rehabilitation can be problematic.</p> <p>We present a unique and original case of bilateral self-castration caused by cannabis abuse.</p> <p>Case Presentation</p> <p>We report a case of a 40-year-old Berber man, who was presented to our emergency room with externalization of both testes using his long fingernails, associated with hemodynamic shock. After stabilization of his state, our patient was admitted to the operating room where hemostasis was achieved.</p> <p>Conclusion</p> <p>The clinical characteristics of self-mutilation are manifold and there is a lack of agreement about its etiology. The complex behavior associated with drug abuse may be one cause of self-mutilation. Dysfunction of the inhibitory brain circuitry caused by substance abuse could explain why this cannabis-addicted patient lost control and self-mutilated. To the best of our knowledge, this is the first case report which presents an association between self-castration and cannabis abuse.</p

Giant primary adrenal hydatid cyst presenting with arterial hypertension: a case report and review of the literature

<p>Abstract</p> <p>Introduction</p> <p>A primary hydatid cyst of the adrenal gland is still an exceptional localization. The adrenal gland is an uncommon site even in Morocco, where echinococcal disease is endemic.</p> <p>Case presentation</p> <p>We report the case of a 64-year-old Moroccan man who presented with the unusual symptom of arterial hypertension associated with left flank pain. Computed tomography showed a cystic mass of his left adrenal gland with daughter cysts filing the lesion (Type III). Despite his negative serology tests, the diagnosis of a hydatid cyst was confirmed on surgical examination. Our patient underwent surgical excision of his left adrenal gland with normalization of blood pressure. No recurrence has occurred after 36 months of follow-up.</p> <p>Conclusion</p> <p>There are two remarkable characteristics of this case report; the first is the unusual location of the cyst, the second is the association of an adrenal hydatid cyst with arterial hypertension, which has rarely been reported in the literature.</p

Identification of a strong enhancer element upstream from the pregenomic RNA start site of the duck hepatitis B virus genome.

The genome of the duck hepatitis B virus (DHBV) contains an enhancer element. This sequence, of 192 bp, is located in the 3'-terminal coding region of the DNA polymerase gene (nucleotides 2159 to 2351), upstream from the pregenomic RNA start site. This enhancer potentiates a marked increased activity from the heterologous thymidine kinase promoter in an orientation-independent manner and at a proximal, as well as a distal, location. The DHBV enhancer activates transcription in a relatively cell-type-independent manner. Sequence homologies with the nuclear factor EF-C binding site are located in the DHBV enhancer. By using the HepG2 nuclear extracts and the DHBV enhancer as probes, a complex was observed in mobility shift assays

Binding of Nuclear Factors to Functional Domains of the Duck Hepatitis B Virus Enhancer

International audienceWe have analyzed the structures, relative organization, and activities of binding sites for nuclear factors in the duck hepatitis B virus (duck HBV) enhancer. DNase I footprinting analysis and mobility shift assays demonstrate that this enhancer of 192 bp contains at least three binding sites for transcription factors: one for hepatocyte-adipocyte C/EBP, a second for the liver-specific transactivator hepatocyte nuclear factor 1 HNF-1, and a third for a factor, called F3, which binds to a DNA sequence bearing some resemblance to that for the ubiquitous factor EF-C. Analysis of transcriptional activity reveals that oligonucleotides corresponding to the individual binding sites, inserted upstream from a heterologous promoter, display very weak enhancer activity, whereas the enhancer encompassing these three sites displays very high activity. Analysis of duck HBV enhancer mutants indicates that the deletion of any of these sites leads to a modification of transcriptional enhancer activity. The hepatocyte nuclear factor 1 binding site is crucial, since an internal deletion of 14 bp abolishes the activity. The C/EBP site can act as repressor, and the F3 site is required for full activity. Comparative analysis reveals that the nuclear factors are similar to those bound to the human HBV enhancer but that the organization of their binding sites in the duck HBV enhancer is different

Hepatitis B virus X protein transactivates the long terminal repeats of human immunodeficiency virus types 1 and 2

The X gene product of the hepatitis B virus (HBV) has been expressed transiently in HepG2 cells, and the 17-kilodalton protein has been detected by Western (immuno-) blot analysis. Cotransfection of the X gene with the long terminal repeat of human immunodeficiency virus type 1 or 2 results in a stimulation of long terminal repeat-directed expression that is higher than the X-induced stimulation of the HBV enhancer linked to either autologous promoter or to the heterologous simian virus 40 promoter. A frameshift mutation abolished this transactivation. In vitro nuclear transcription assays revealed that HBV X acts at the transcriptional level. The carboxy terminus of the HBV X protein does not seem to be necessary for its transactivating activity, as demonstrated by using HBV X protein deletion mutants