Αρχειοθήκη ιστολογίου

Κυριακή 23 Απριλίου 2017

Duplicated internal auditory canal with inner ear malformation: Case report and literature review

Internal auditory canal anomalies are rare. Narrow internal auditory canal is believed to occur as a result of aplasia or hypoplasia of the vestibulocochlear nerve. Narrow duplication of the internal auditory canal is considered to be very rare. Narrow duplication of the internal auditory canal with inner ear malformation has been reported in only 3 cases. We present 2 cases of narrow duplication of the internal auditory canal with inner ear malformation. The first case had inner ear malformation on only one side and the second case had inner ear malformation on both sides.

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Duplicated internal auditory canal with inner ear malformation: Case report and literature review

Internal auditory canal anomalies are rare. Narrow internal auditory canal is believed to occur as a result of aplasia or hypoplasia of the vestibulocochlear nerve. Narrow duplication of the internal auditory canal is considered to be very rare. Narrow duplication of the internal auditory canal with inner ear malformation has been reported in only 3 cases. We present 2 cases of narrow duplication of the internal auditory canal with inner ear malformation. The first case had inner ear malformation on only one side and the second case had inner ear malformation on both sides.

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Endophenotyping in idiopathic adult onset cervical dystonia

Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements, postures, or both. (Albanese et al., 2013) Idiopathic adult onset cervical dystonia (IAOCD) is considered to be an autosomal dominant genetic condition due to partially penetrant gene/s.(Stojanovic et al., 1995; Waddy et al., 1991) Hence most of the cases appear to be sporadic with a positive family history in 15-25%.(Waddy et al., 1991) Several genes have been mapped for families, which include members with cervical dystonia (Almasy et al., 1997; Charlesworth et al., 2012; Fuchs et al., 2009; Fuchs et al., 2013; Leube et al., 1996; Valente et al., 2001; Xiao et al., 2012) but in several other families with cervical dystonia linkage to these known genetic loci has been excluded.

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Acute Bacterial Meningitis and Systemic Abscesses due to Streptococcus dysgalactiae subsp. equisimilis Infection

Disseminated abscesses due to group G β-hemolytic Streptococcus dysgalactiae were observed in a 57-year-old cirrhotic patient with the skin being the putative way of entry for the pathogen. S. dysgalactiae is a rare agent in human infections responsible for acute pyogenic meningitis. The mortality rate associated with S. dysgalactiae bacteraemia and meningitis may be as high as 50%, particularly in the presence of endocarditis or brain abscesses. In our patient, main sites of infections were meningitis and ventriculitis, spondylodiscitis, septic arthritis, and soft-tissue infections. In contrast, no endocarditis was evidenced. Cirrhosis-related immune suppression was considered as a pathophysiological cofactor for the condition. Fortunately, clinical status improved after long-term (3 months) antimicrobial therapy.

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The interactive role of CB1 receptors and L-type calcium channels in hippocampal long-term potentiation in rats

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Publication date: Available online 23 April 2017
Source:Brain Research Bulletin
Author(s): Hamidreza Komaki, Fargol Saadat, Siamak Shahidi, Abdolrahman Sarihi, Parisa Hasanein, Alireza Komaki
'Long-term potentiation (LTP) of synaptic responses is a widely researched model of synaptic plasticity that occurs during learning and memory. The cannabinoid system is an endogenous system that modulate this kind of synaptic plasticity. In addition, voltage dependent calcium channels is essential for induction of LTP at some synapses in the hippocampus. However, there is currently debate over the interaction between L-type calcium channels and cannabinoid system on the synaptic plasticity. In this study, we examined the effects of an acute administration of the cannabinoid antagonist AM251 following a chronic administration of the Ca2+ channel blocker verapamil on LTP induction in the hippocampal dentate gyrus(DG) of rats. Male Wistar rats were administered verapamil(10,25,50mg/kg) or saline intraperitoneally(IP) daily for 13 days(n=10/group). After this treatment period, animals were anesthetized with an IP injection of urethane; the recording and stimulating electrodes were positioned in the DG and the perforant pathway. After obtaining a steady state baseline response, a single IP injection of saline or AM251(1 or 5mg/kg) was administered. LTP was induced by high-frequency stimulation(HFS). The population spike(PS) amplitude and the slope of excitatory postsynaptic potentials(EPSP) were compared between the experimental groups. The acute administration of the CB1 antagonist AM251 increased LTP induction. The EPSP slopes and PS amplitude in the verapamil and AM251 groups differed after HFS, such that AM251 increased LTP, whereas verapamil decreased LTP induction. These findings suggest that there are functional interactions between the L-type calcium channels and cannabinoid system in this model of synaptic plasticity in the hippocampus.



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Inhibition of Allogeneic Cytotoxic T Cell (CD8+) Proliferation Via Polymer-Induced Treg (CD4+) Cells

Publication date: Available online 23 April 2017
Source:Acta Biomaterialia
Author(s): Ning Kang, Wendy M. Toyofuku, Xining Yang, Mark D. Scott
T cell-mediated immune rejection remains a barrier to successful transplantation. Polymer-based bioengineering of cells may provide an effective means of preventing allorecognition and the proliferation of cytotoxic (CD8+) T lymphocytes (CTL). Using MHC-disparate murine splenocytes modified with succinimidyl valerate activated methoxypoly(ethylene glycol) [SVA-mPEG] polymers, the effects of leukocyte immunocamouflage on CD8+ and CD4+ alloproliferation and T regulatory (Treg) cell induction were assessed in a mixed lymphocyte reaction (MLR) model. Polymer-grafting effectively camouflaged multiple leukocyte markers (MHC class I and II, TCR and CD3) essential for effective allorecognition. Consequent to the polymer-induced immunocamouflage of the cell membrane, both CD8+ and CD4+ T cell alloproliferation were significantly inhibited in a polymer dose-dependent manner. The loss of alloproliferation correlated with the induction of Treg cells (CD4+CD25+Foxp3+). The Tregs, surprisingly, arose primarily via differentiation of naive, non-proliferating, CD4+ cells. Of biologic importance, the polymer-induced Treg were functional and exhibited potent immunosuppressive activity on allogeneic CTL proliferation. These results suggest that immunocamouflage-mediated attenuation of alloantigen-TCR recognition can prevent the tissue destructive allogeneic CD8+ T cell response, both directly and indirectly, through the generation/differentiation of functional Tregs. Immunocamouflage induced tolerance could be clinically valuable in attenuating T cell-mediated transplant rejection and in the treatment of autoimmune diseases.Statement of significanceWhile our previous studies have demonstrated that polymer-grafting to MHC disparate leukocytes inhibits CD4+ cell proliferation, the effects of PEGylation of on the alloproliferation of CD8+ cytotoxic T cells (CTL) was not examined. As shown here, PEGylation of allogeneic leukocytes prevents the generation of the CTL response responsible for acute rejection. The loss of CTL proliferation is consequent to the polymer-based attenuation of allorecognition and the induction of T regulatory cells (Tregs). Interestingly, the Tregs are primarily generated via the differentiation of non-proliferating naive T cells. Importantly, the Tregs are functional and effectively induce a tolerogenic environment when transferred to an alloresponsive environment. The use of polymer-modified leukocytes provides a unique approach to effectively maximize the biologic production of functional Tregs both in vitro and in vivo. By using this approach it may be possible to attenuate unwanted alloresponses (e.g., graft rejection) or to While our previous studies have demonstrated that polymer-grafting to MHC disparate leukocytes inhibits CD4+ cell proliferation, the effects of PEGylation of on the alloproliferation of CD8+ cytotoxic T cells (CTL) was not examined. As shown here, PEGylation of allogeneic leukocytes prevents the generation of the CTL response responsible for acute rejection. The loss of CTL proliferation is consequent to the polymer-based attenuation of allorecognition and the induction of T regulatory cells (Tregs). Interestingly, the Tregs are primarily generated via the differentiation of non-proliferating naive T cells. Importantly, the Tregs are functional and effectively induce a tolerogenic environment when transferred to an alloresponsive environment. The use of polymer-modified leukocytes provides a unique approach to effectively maximize the biologic production of functional Tregs both in vitro and in vivo. By using this approach it may be possible to attenuate unwanted alloresponses (e.g., graft rejection) or to

Graphical abstract

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Fifty Shades of Grey project: 115 new articles

You may have noticed that some links in Radiopaedia are grey (dead) rather than blue (active). They indicate a link to a not-yet-existing article; as soon as it is written that article turns blue and is correctly linked. 

Over the last month or so we challenged our editors to write 5 new articles each hence turning many grey links blue. 

At the end of this project, it's not just fifty grey-shaded links that changed colour. Collectively a staggering 115 new articles were created by our editors. A special note of appreciation goes to Craig Hacking who contributed 54 new articles alone, Frank Gaillard (11), Andrew Murphy (10), and Vincent Tatco (7).

Here are just a few: 

We hope to have inspired our fellow radiology-minded professionals to also contribute new articles. So next time you see a grey link and realise that article is yet to be written, feel free to fade away some grey links yourself.

Have a look at our instructions if you don't know where to start. Our community is there to help and expand whatever you start out with.



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