NMR studies of the incommensurate helical antiferromagnet EuCo2P2 : determination of the antiferromagnetic propagation vector

Recently Ding et al. [Phys. Rev. B 95, 184404 (2017)] reported that their nuclear magnetic resonance (NMR) study on EuCo$_2$As$_2$ successfully characterized the antiferromagnetic (AFM) propagation vector of the incommensurate helix AFM state, showing that NMR is a unique tool for determination of the spin structures in incommensurate helical AFMs. Motivated by this work, we have carried out $^{153}$Eu, $^{31}$P and $^{59}$Co NMR measurements on the helical antiferromagnet EuCo$_2$P$_2$ with an AFM ordering temperature $T_{\rm N}$ = 66.5 K. An incommensurate helical AFM structure was clearly confirmed by $^{153}$Eu and $^{31}$P NMR spectra on single crystalline EuCo$_2$P$_2$ in zero magnetic field at 1.6 K and its external magnetic field dependence. Furthermore, based on $^{59}$Co NMR data in both the paramagnetic and the incommensurate AFM states, we have determined the model-independent value of the AFM propagation vector k = (0, 0, 0.73 $\pm$ 0.09)2$\pi$/$c$ where $c$ is the $c$-axis lattice parameter. The temperature dependence of k is also discussed.Comment: 8 pages, 10 figures, accepted for publication in Phys. Rev. B. arXiv admin note: substantial text overlap with arXiv:1704.0629

ウマにおけるS.fayeriの簡易検査法の開発を基盤とした寄生部位の解析（Parasitism distribution analysis of S.fayeri in the horse based on development of a rapid and simple method for the detection.）

博士（薬学）崇城大

Spontaneously Ruptured Giant Splenic Cyst with Elevated Serum Levels of CA 19-9, CA 125 and Carcinoembryonic Antigen

Splenic cyst is a relatively rare disease; however, the occurrence of complications associated with its rupture is even more rare. A 20-year-old female patient who had severe abdominal and left shoulder pain was admitted to our hospital. The patient's abdomen was hard and tender to the touch and she presented with a high fever. The patient's serum levels of the tumor markers carbohydrate antigen 19-9, cancer antigen 125 and carcinoembryonic antigen were high. Ultrasonography and computed tomography of the abdomen showed an 11-cm multilocular cystic lesion in the spleen and the presence of free intraperitoneal fluid. Peritonitis with ruptured splenic cyst was diagnosed, and the patient underwent an emergency laparotomy. The abdominal cavity was filled with purulent fluid. The cyst was localized to the spleen and had already ruptured. Total splenectomy and cyst resection were performed. The postoperative course was uneventful. The patient was discharged on day 9 following surgery. The histological findings showed the lesion to be a benign epidermoid cyst completely lined with inner stratified squamous epithelium with a capsule of connective tissue. In the immunostaining analyses, the squamous epithelium was positive for carcinoembryonic antigen. A ruptured splenic cyst causes sudden onset of severe peritonitis and elevation of serous tumor markers. An emergency operation is indicated as the treatment for a ruptured splenic cyst with peritonitis, after which a favorable outcome can be expected

Intracranial self-stimulation increases differentially in vivo hydroxylation of tyrosine but similarly in vivo hydroxylation of tryptophan in rat medial prefrontal cortex, nucleus accumbens and striatum

We have examined using microdialysis the effect of intracranial self-stimulation (ICSS) on the in vivo hydroxylation rate of tyrosine and tryptophan in the medial prefrontal cortex (mPFC), nucleus accumbens (NAC) and striatum (STR). A decarboxylase inhibitor NSD-1015 was included in the perfusate, which enabled the simultaneous measurement of 3,4-dihydroxyphenylalanine (DOPA) and 5-hydroxytryptophan (5-HTP) as an index of the in vivo hydroxylation level of tyrosine and tryptophan. When rats were exposed to 1 h of ICSS at the medial forebrain bundle (MFB), their extracellular levels of DOPA significantly increased in the mPFC, NAC and STR, but with a different magnitude and time course. The same stimulation produced a delayed increase in extracellular 5-HTP, compared to DOPA, in these brain regions. The profile of 5-HTP response demonstrated no apparent difference among the regions. These findings indicate that ICSS of the MFB can increase differentially the in vivo hydroxylation of tyrosine but similarly the in vivo hydroxylation of tryptophan in the mPFC, NAC and STR

Chronic Systemic Exposure to Low-Dose Rotenone Induced Central and Peripheral Neuropathology and Motor Deficits in Mice: Reproducible Animal Model of Parkinson's Disease

Epidemiological studies demonstrated that pesticide exposure, such as rotenone and paraquat, increases the risk of Parkinson's disease (PD). Chronic systemic exposure to rotenone, a mitochondrial complex I inhibitor, could reproduce many features of PD. However, the adoption of the models is limiting because of variability in animal sensitivity and the inability of other investigators to consistently reproduce the PD neuropathology. In addition, most of rotenone models were produced in rats. Here, we tried to establish a high-reproducible rotenone model using C57BL/6J mice. The rotenone mouse model was produced by chronic systemic exposure to a low dose of rotenone (2.5 mg/kg/day) for 4 weeks by subcutaneous implantation of rotenone-filled osmotic mini pump. The rotenone-treated mice exhibited motor deficits assessed by open field, rotarod and cylinder test and gastrointestinal dysfunction. Rotenone treatment decreased the number of dopaminergic neuronal cells in the substantia nigra pars compacta (SNpc) and lesioned nerve terminal in the striatum. In addition, we observed significant reduction of cholinergic neurons in the dorsal motor nucleus of the vagus (DMV) and the intestinal myenteric plexus. Moreover, alpha-synuclein was accumulated in neuronal soma in the SNpc, DMV and intestinal myenteric plexus in rotenone-treated mice. These data suggest that the low-dose rotenone mouse model could reproduce behavioral and central and peripheral neurodegenerative features of PD and be a useful model for investigation of PD pathogenesis

Pregabalin- and azithromycin-induced rhabdomyolysis with purpura: An unrecognized interaction: A case report

AbstractIntroductionRhabdomyolysis associated with the use of pregabalin or azithromycin has been demonstrated to be a rare but potentially life-threatening adverse event. Here, we report an extremely rare case of rhabdomyolysis with purpura in a patient who had used pregabalin and azithromycin.Presentation of caseWe present the case of a 75-year-old woman with a history of fibromyalgia who was admitted with mild limb weakness and lower abdominal purpura. She was prescribed pregabalin (75mg, twice daily) for almost 3 months to treat chronic back pain. Her medical history revealed that 3days before admission, she began experiencing acute bronchitis and was treated with a single dose of azithromycin (500mg). She had developed rapid onset severe myalgia, mild whole body edema, muscle weakness leading to gait instability, abdominal purpura and tender purpura on the lower extremities. Laboratory values included a white blood cell count of 25,400/mL and a creatinine phosphokinase (CPK) concentration of 1250 IU/L. Based on these findings and the patient’s clinical history, a diagnosis of pregabalin- and azithromycin-induced rhabdomyolysis was made.DiscussionThe long-term use of pregabalin and the initiation azithromycin therapy followed by a rapid onset of rhabdomyolysis is indicative of a drug interaction between pregabalin and azithromycin.ConclusionWe report an extremely rare case of rhabdomyolysis with purpura caused by a drug interaction between pregabalin and azithromycin. However, the mechanisms of the interactions between azithromycin on the pregabalin are still unknown