Preoperative computerized tomography-guided blue dye localization for metastatic lymphadenopathy and peritoneal tumor implants during laparoscopic surgery: Two case reports.

RATIONALE: Computerized tomography (CT)-guided blue dye localization has been widely discussed for preoperative localization of pulmonary nodules. However, few studies have investigated this technique for intra-abdominal lesions. Although preoperative localization is not commonly required in laparotomy, it may assume importance with advancements in the field of laparoscopic surgery. PATIENT CONCERNS: Herein, we report the cases of 2 patients diagnosed with colon cancer who underwent hemicolectomy with extended lymphadenectomy and subsequent chemotherapy. DIAGNOSES: Follow-up CT scans showed newly developed metastatic lymphadenopathy and peritoneal tumor implants. INTERVENTIONS: Considering the difficulty in identification of and access to the target lesions during laparoscopic surgery, preoperative CT-guided blue dye localization was performed in both cases. OUTCOMES: All the target lesions were identified by the dye marker and removed successfully. The pathologic results revealed adenocarcinoma. LESSONS: We established the following strategy for preoperative CT-guided dye localization of intra-abdominal lesions:Intra-abdominal lesions that are hard to identify due to their size or morphology, and difficult to approach due to their location or surrounding structures, maybe the candidates for this procedure, especially in cases of laparoscopic surgery.Operators should adjust their localization planning based on the surgery method, cutting path, and location of port sites. The target dye marker should be clearly visible in the presumed intra-operative field of view.A second dye marker should be made to ensure surgical success when the target dye marker is obscured by the surrounding structures in the presumed intra-operative field of view.

Successful Transarterial Embolization of Uterine Arteriovenous Malformation: Report of Three Cases.

Uterine arteriovenous malformations (AVMs) are relatively rare disorders that can cause life-threatening vaginal bleeding. We describe three childbearing-age females, who had abdominal pain and heavy vaginal bleeding, and were diagnosed as uterine AVM by color Doppler and angiography. The patients received successful superselective transarterial embolization (TAE) with N-butyl cyanoacrylate (NBCA). Three years after treatment, one of them was admitted to our hospital for vaginal delivery at 39 weeks of gestation, and the baby was healthy.

Privacy preserving index for encrypted electronic medical records.

With the development of electronic systems, privacy has become an important security issue in real-life. In medical systems, privacy of patients' electronic medical records (EMRs) must be fully protected. However, to combine the efficiency and privacy, privacy preserving index is introduced to preserve the privacy, where the EMR can be efficiently accessed by this patient or specific doctor. In the literature, Goh first proposed a secure index scheme with keyword search over encrypted data based on a well-known primitive, Bloom filter. In this paper, we propose a new privacy preserving index scheme, called position index (P-index), with keyword search over the encrypted data. The proposed index scheme is semantically secure against the adaptive chosen keyword attack, and it also provides flexible space, lower false positive rate, and search privacy. Moreover, it does not rely on pairing, a complicate computation, and thus can search over encrypted electronic medical records from the cloud server efficiently.

Characterization of Ca2+ signalling in postnatal mouse retinal ganglion cells: involvement of OPA1 in Ca2+ clearance.

PURPOSE: The regulation of Ca(2+) entry and removal is a fine-tuned process which remains not well understood in mouse retinal ganglion cells (RGCs). The latter are known to be sensitive to dysfunctions of mitochondria, organelles playing a pivotal role in Ca(2+) reuptake. METHODS: We first described the Ca(2+) signals of RGCs in response to varied drugs with Fura-2 imaging, and secondly tested the role of optic atrophy 1 or OPA1, the gene responsible for Autosomal Dominant Optic Atrophy, on mitochondrial ability to capture intracellular Ca(2+) in cells transfected with the OPA1 small interfering ribonucleic acids (siRNAs). RESULTS: In control RGCs, K(+)-evoked [Ca(2+)](i) increase was blocked by the Ca(2+) channel antagonists (Ni(2+)+ Cd(2+)) and GABA(A) receptor agonist muscimol-induced [Ca(2+)](i) responses were attenuated by the GABA(A) receptor antagonists, picrotoxin and gabazine. We also prove the presence of NMDA and AMPA/Kainate (glutamate receptor agonists) responsive receptors in this model. Application of cyclopiazonic acid, an inhibitor of Ca(2+)-ATPase pumps of the intracellular Ca(2+) stores, induced an increase in [Ca(2+)](i) while ryanodine or caffeine had no effect on resting [Ca(2+)](i). Spontaneous Ca(2+) oscillations in contacting neurons highlighted the importance of cross-talks between RGCs during maturation. The mitochondrial respiration uncoupler, carbonyl cyanide 3-chlorophenylhydrazone (CCCP), induced robust raises of intracellular Ca(2+) after K(+) application, with a more pronounced effect in cells silenced for OPA1, which could lead to cell death. CONCLUSIONS: Our results indicate an important role of OPA1 in mitochondrial dependent Ca(2+) homeostasis and cell survival in RGCs, suggesting a possible patho-physiological mechanism involved in inherited optic neuropathies.

[A murine model of transitory optic neuropathy based on small interference RNA-induced OPA1 silencing in vivo (gene mutation associated with Kjer's disease)]. / Modèle murin de neuropathie optique transitoire par inhibition in vivo de l'expression d'OPA1 (gène impliqué dans la maladie de Kjer).

PURPOSE: Developing a murine model of OPA1 linked optic neuropathy. METHODS: Intravitreal injections (in adult C57BL/6J mice) of small interference RNA (siRNA) specific to OPA1 were performed in the left eye. The right eye served as control, injected with nonspecific siRNA (siRNA scramble). Visual evoked potentials and flash electroretinograms were performed 5 and 12 days after injection. Three months after injection, microscopy of optic nerve sections was performed. RESULTS: The electrophysiological tests showed a significant reduction in the VEP when the siRNA OPA1-injected eye was stimulated, compared with the control eye injected with siRNA scramble. The electroretinogram was normal in both eyes: no significant difference between the right and the left eye was found. Three months after injection, no measurable axonal degeneration was found in either eye. CONCLUSION: The reduced expression of OPA1 based on RNA silencing in adult mice could induce reversible dysfunction of retinal ganglion cells.

Expression of the Opa1 mitochondrial protein in retinal ganglion cells: its downregulation causes aggregation of the mitochondrial network.

PURPOSE: Mutations in the mitochondrial dynamin-related GTPase OPA1 cause autosomal dominant optic atrophy (ADOA), but the pathophysiology of this disease is unknown. As a first step in functional studies, this study was conducted to evaluate the expression of Opa1 in whole retina and in isolated retinal ganglion cells (RGCs) and to test the effects of Opa1 downregulation in cultured RGCs. METHODS: Opa1 mRNA isoforms from total retina and from RGCs freshly isolated by immunopanning were determined by RT-PCR. Protein expression was examined by immunohistochemistry and Western blot with antibodies against Opa1 and cytochrome c, and the mitochondrial network was visualized with a mitochondrial marker. Short interfering (si)RNA targeting OPA1 mRNAs were transfected to cultured RGCs and mitochondrial network phenotypes were followed for 15 days, in comparison with those of cerebellar granule cells (CGCs). RESULTS: Opa1 expression did not predominate in rat postnatal RGCs as found by immunohistochemistry and Western blot analysis. The pattern of mRNA isoforms was similar in whole retina and RGCs. After a few days in culture, isolated RGCs showed fine mitochondrial punctiform structures in the soma and neurites that colocalized with cytochrome c and Opa1. Opa1 knockdown in RGCs induced mitochondrial network aggregation at a higher rate than in CGCs. CONCLUSIONS: Results suggest that the level of expression and the mRNA isoforms do not underlie the vulnerability of RGCs to OPA1 mutations. However, aggregation of the mitochondrial network induced by the downregulation of Opa1 appears more frequent in RGCs than in control CGCs.