Metronidazole-induced encephalopathy in a patient with infectious colitis: a case report

<p>Abstract</p> <p>Introduction</p> <p>Encephalopathy is a rare disease caused by adverse effects of antibiotic drugs such as metronidazole. The incidence of metronidazole-induced encephalopathy is unknown, although several previous studies have addressed metronidazole neurotoxicity. Here, we report the case of a patient with reversible cerebellar dysfunction on magnetic resonance imaging, induced by prolonged administration of metronidazole for the treatment of infectious colitis.</p> <p>Case presentation</p> <p>A 71-year-old Asian man, admitted to our hospital with hematochezia, underwent Hartmann's operation for the treatment of colorectal cancer three years ago. He was diagnosed with an infectious colitis by colonoscopy. After taking metronidazole, he showed drowsiness and slow response to verbal commands. Brain magnetic resonance imaging showed obvious bilateral symmetric hyperintensities within his dentate nucleus, tectal region of the cerebellum, and splenium of corpus callosum in T2-weighted images and fluid attenuated inversion recovery images. Our patient's clinical presentation and magnetic resonance images were thought to be most consistent with metronidazole toxicity. Therefore, we discontinued metronidazole, and his cerebellar syndrome resolved. Follow-up magnetic resonance imaging examinations showed complete resolution of previously noted signal changes.</p> <p>Conclusion</p> <p>Metronidazole may produce neurologic side effects such as cerebellar syndrome, and encephalopathy in rare cases. We show that metronidazole-induced encephalopathy can be reversed after cessation of the drug. Consequently, careful consideration should be given to patients presenting with complaints of neurologic disorder after the initiation of metronidazole therapy.</p

Solvothermal Synthesis and Characterization of Chalcopyrite CuInSe2 Nanoparticles

The ternary I-III-VI2 semiconductor of CuInSe2 nanoparticles with controllable size was synthesized via a simple solvothermal method by the reaction of elemental selenium powder and CuCl as well as InCl3 directly in the presence of anhydrous ethylenediamine as solvent. X-ray diffraction patterns and scanning electron microscopy characterization confirmed that CuInSe2 nanoparticles with high purity were obtained at different temperatures by varying solvothermal time, and the optimal temperature for preparing CuInSe2 nanoparticles was found to be between 180 and 220 °C. Indium selenide was detected as the intermediate state at the initial stage during the formation of pure ternary compound, and the formation of copper-related binary phase was completely deterred in that the more stable complex [Cu(C2H8N2)2]+ was produced by the strong N-chelation of ethylenediamine with Cu+. These CuInSe2 nanoparticles possess a band gap of 1.05 eV calculated from UV–vis spectrum, and maybe can be applicable to the solar cell devices

The overmethylated genes in Helicobacter pylori-infected gastric mucosa are demethylated in gastric cancers

<p>Abstract</p> <p>Background</p> <p>The transitional-CpG sites between weakly methylated genes and densely methylated retroelements are overmethylated in the gastric mucosa infected with <it>Helicobacter pylori </it>(<it>H. pylori</it>) and they are undermethylated in the gastric cancers depending on the level of loss of heterozygosity (LOH) events. This study delineated the transitional-CpG methylation patterns of CpG-island-containing and -lacking genes in view of the retroelements.</p> <p>Methods</p> <p>The transitional-CpG sites of eight CpG-island-containing genes and six CpG-island-lacking genes were semi-quantitatively examined by performing radioisotope-labelling methylation-specific PCR under stringent conditions. The level of LOH in the gastric cancers was estimated using the 40 microsatellite markers on eight cancer-associated chromosomes. Each gene was scored as overmethylated or undermethylated based on an intermediate level of transitional-CpG methylation common in the <it>H. pylori</it>-negative gastric mucosa.</p> <p>Results</p> <p>The eight CpG-island genes examined were overmethylated depending on the proximity to the nearest retroelement in the <it>H. pylori</it>-positive gastric mucosa. The six CpG-island-lacking genes were similarly methylated in the <it>H. pylori</it>-positive and -negative gastric mucosa. In the gastric cancers, long transitional-CpG segments of the CpG-island genes distant from the retroelements remained overmethylated, whereas the overmethylation of short transitional-CpG segments close to the retroelements was not significant. Both the CpG-island-containing and -lacking genes tended to be decreasingly methylated in a LOH-level-dependent manner.</p> <p>Conclusions</p> <p>The overmethylated genes under the influence of retroelement methylation in the <it>H. pylori</it>-infected stomach are demethylated in the gastric cancers influenced by LOH.</p

Relation between Seebeck Coefficient and Lattice Parameters of (Ca2-ySryCoO3)(x)CoO2

The effect of dopant content on the Seebeck coefficient of the Sr2+-doped (Ca2- Sr CoO3) CoO2 ( = 0 to 0.4) system was investigated. This system can be described as a misfit layered structure of (CoO2) and (Ca2- Sr CoO3) layers, which have different lattice parameters denoted by (1) and (2), respectively. Due to the solubility limit of Sr in (Ca2CoO3) CoO2, systematic investigations were available only up to = 0.2. Nevertheless, the structural uniqueness enabled partially quantitative analysis of the correlation between the crystal structure and Seebeck coefficient of the system. Substitution of Sr for Ca leads to lattice expansion which accompanies an anisotropic change of the lattice parameters. Among the lattice parameters considered, the increase in the lattice parameter (2) of the insulating layer was larger than the change of any other lattice parameter, which induced in-plane stress in the conducting layer. As a result, as the (1)/ (2) misfit ratio of (Ca2- Sr CoO3) CoO2 is decreased, the Seebeck coefficient also decreases. Practical guidance for selecting dopants to enhance thermoelectric performance is proposed.close5

FOXA2 is a sensitive and specific marker for small cell neuroendocrine carcinoma of the prostate

The median survival of patients with small cell neuroendocrine carcinoma is significantly shorter than that of patients with classic acinar-type adenocarcinoma. Small cell neuroendocrine carcinoma is traditionally diagnosed based on histologic features because expression of current immunohistochemical markers is inconsistent. This is a challenging diagnosis even for expert pathologists and particularly so for pathologists who do not specialize in prostate cancer. New biomarkers to aid in the diagnosis of small cell neuroendocrine carcinoma are therefore urgently needed. We discovered that FOXA2, a pioneer transcription factor, is frequently and specifically expressed in small cell neuroendocrine carcinoma compared with prostate adenocarcinoma from published mRNA-sequencing data of a wide range of human prostate cancers. We verified the expression of FOXA2 in human prostate cancer cell lines and xenografts, patient biopsy specimens, tissue microarrays of prostate cancers with lymph node metastasis, primary small cell neuroendocrine carcinoma, and metastatic treatment-related small cell neuroendocrine carcinoma and cases from a rapid autopsy program. FOXA2 expression was present in NCI-H660 and PC3 neuroendocrine cell lines, but not in LNCAP and CWR22 adenocarcinoma cell lines. Of the human prostate cancer specimens, 20 of 235 specimens (8.5%) showed diagnostic histologic features of small cell neuroendocrine carcinoma as judged histologically. Fifteen of 20 small cell neuroendocrine carcinoma tissues (75%) showed strong expression of FOXA2 (staining intensity 2 or 3). FOXA2 expression was also detected in 9 of 215 prostate cancer tissues (4.2%) that were histologically defined as adenocarcinoma. Our findings demonstrate that FOXA2 is a sensitive and specific molecular marker that may be extremely valuable in the pathologic diagnosis of small cell neuroendocrine carcinoma