Possible participation of isolated epicardial cell clusters in the formation of chick embryonic epicardium

The embryonic epicardium is formed by the spreading of cells derived from the extracardiac proepicardial organ over the myocardial surface after transfer to the dorsal side of the myocardium via a bridge of villous projections. Using whole-heart immunostaining for keratin, we found that the chronology and pattern of epicardial formation in the chick was basically identical to that reported previously in the quail. However, discrete epicardial islands were observed on the ventrolateral surface of the atrioventricular canal as well as in two previously reported areas. Closer examination by scanning electron microscopy demonstrated the presence of isolated, sparsely distributed epicardial cell clusters on both the dorsal and ventral surfaces of the myocardium. These cells showed a surface morphology similar to that of the epicardial cells at the advancing edge of the spreading epicardial sheet and possessed numerous well-developed filopodia, suggesting active motility. These clusters are probably seeded onto the myocardium by vesicular transport from proepicardial villi, and our findings suggest that the resulting small, localised patches of epicardial cells might accelerate, supplement and tune the epicardial formation mediated by radial spreading of the epicardial sheet in the chick embryonic heart.     

Case report of periodontal disease with periodic neutropenia

A case of periodic neutropenia with specific symptoms of gingiva and alveolar bone loss in primary dentition is reported. The patient was a boy, and it was followed between the ages of 3- and 9 years-old. At the period of neutropenia he was suffered from recurrent redness, swelling and bleeding of the gingiva, and also with cold-like symptoms with fever. Although the cause of these symptoms was not definite at first, even in medical exploration, we could diagnose this disease as periodic neutropenia by the process of dental therapy. By alveolar bone resorption, pocket formation and severe tooth mobility, the patient had lost more than half of his primary teeth at the end of 2 years after the initial examination. However throughout this period we motivated and instructed the patient and his mother how to brush his teeth. His oral hygiene was improved in the mixed and permanent dentition stages. Then there was no evidence of bone resorption around the teeth of the permanent dentition stage, but recurrent gingival symptoms are continuing now. The specific feature of this case is found in the gingival findings. There was no ulceration of the oral mucosa, but a bright red jelly-like appearance was found periodically in the area of the marginal and attached gingiva. The junction between the reddened attached gingiva and the alveolar mucosa was well-defined. The serial examination of peripheral blood in this case revealed the cycle of neutropenia as 16 to 21 days. During this examination, and at the almost time of neutropenia of this patient, hyperplasia of monocytes and lymphocytes occurred. In this situation there was no clinical signs except for gingival redness. However at other times, generally marked signs were recurrent. This may have occurred due to the lack of both neutrophils and monocytes. From the above results we think that periodic neutropenia may be diagnosed first in the dental clinic by the distinctive redness in the gingival area as one specific sign of this disease. We also think that plaque control procedures may retain the teeth.     

Horizontal transmission of foot‐and‐mouth disease virus O/JPN/2010 among different animal species by direct contact

Foot‐and‐mouth disease (FMD) is highly contagious and easily transmitted among species of cloven‐hoofed animals. To investigate the transmission of FMD virus (FMDV) among different animal species, experimental infections using the O/JPN/2010 strain were performed in cows, goats and pigs. One cow or two goats/pigs were housed with a different species of inoculated animals, and clinical observations, virus shedding and antibody responses were analysed daily. Whilst all cows and goats were infected horizontally by contact with inoculated pigs, transmission from cows to goats/pigs and from goats to cows/pigs was not observed in all in‐contact animals. In particular, no pigs were infected horizontally by contact with inoculated goats. Comparison with our previous study on experimental infections among animals of the same species indicates that horizontal transmission occurred more easily between animals of the same species than between those of the different species. These findings will be useful for establishing and performing species‐specific countermeasures in farms and regions where multiple species of animals coexist in potential future outbreaks.     

A male case with CDKL5-associated encephalopathy manifesting transient methylmalonic acidemia

Mutations in the X-linked gene CDKL5 cause early-onset epileptic encephalopathy and severe developmental delay. Because this disorder predominantly affects females, the full clinical spectrum of male patients remains elusive. We herein report a 16-year-old boy, who suffered from intractable seizures 20 days after birth. Serial electroencephalograms detected recurrent focal epileptiform discharges from age 4 months, which evolved to hypsarrhythmia later in infancy. Mass-spectrometric analyses revealed increase in urinary excretion of methylmalonic acid without perturbed concentrations of propionic acid, homocystein and methionine. Whole-exome sequencing identified a de novo, truncating mutation in CDKL5 (NM_003159.2:c.419dupA, p.Asn140Lysfs*8). Targeted sequencing excluded concomitant mutations in methylmalonic academia-associated genes. No methylmalonic acidemia has been reported in children with CDKL5 disorder. Extensive analyses on organic acid metabolism for males with CDKL5 mutations will gain more insight into their biochemical profiles in infancy.     

Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis

Lyme arthritis results from colonization of joints by Borrelia burgdorferi and the ensuing host response. Using gene array-based differential analysis of B. burgdorferi gene expression and quantitative reverse trancription-polymerase chain reaction, we identified two paralogous spirochete genes, bmpA and bmpB, that are preferentially up-regulated in mouse joints compared with other organs. Transfer of affinity-purified antibodies against either BmpA or BmpB into B. burgdorferi-infected mice selectively reduced spirochete numbers and inflammation in the joints. B. burgdorferi lacking bmpA/B were therefore generated to further explore the role of these proteins in the pathogenesis of Lyme disease. B. burgdorferi lacking bmpA/B were infectious in mice, but unable to persist in the joints, and they failed to induce severe arthritis. Complementation of the mutant spirochetes with a wild-type copy of the bmpA and bmpB genes partially restored the original phenotype. These data delineate a role for differentially produced B. burgdorferi antigens in spirochete colonization of mouse joints, and suggest new strategies for the treatment of Lyme arthritis.     

Rapid detection of the hepatitis B virus YMDD mutant using TaqMan-minor groove binder probes

BACKGROUND: TaqMan-minor groove binder (MGB) probes were used in a real-time PCR-based assay for the rapid and accurate detection of hepatitis B virus (HBV) YMDD mutants. METHODS: TaqMan-MGB probes were designed to distinguish between wild-type (YMDD) and mutant (YVDD and YIDD) strains of HBV. The detection limit and sensitivity of the assay were determined using a dilution series of a mixture of wild-type and mutant plasmids. Serum samples collected from four patients with chronic mutant HBV infections during lamivudine therapy were analyzed using this method. RESULTS: The detection limit for YVDD and YIDD was 10 and 50 copies, respectively, whereas the sensitivity was 10% within a mixed virus population. In the clinical samples, mutant strains of HBV could be detected at levels <2.6 log copies/ml of HBV DNA. While 15 of the 21 samples tested by this method were positive for the YMDD mutant, direct sequencing and a reverse hybridization line probe assay (INNO-LiPA HBV DR v2) detected the mutant strain in only 11 and 9 samples, respectively. Moreover, the data for 6 samples analyzed by TA cloning were fully consistent with our TaqMan PCR results. CONCLUSIONS: We successfully established a sensitive and accurate assay for the YMDD mutant of HBV. This method may be useful for monitoring patients treated with lamivudine.     

Voxel-based analysis of age and gender effects on striatal [123I] FP-CIT binding in healthy Japanese adults

Annals of Nuclear Medicine - Although previous studies have investigated age and gender effects on striatal subregional dopamine transporter (DaT) binding, these studies were mostly based on a...     

Guide for medical professionals (i.e. dermatologists) for the management of Rhododenol‐induced leukoderma

Because some users develop depigmentation after the use of melanogenesis‐inhibiting products containing the quasi‐drug ingredient Rhododenol, Japanese Dermatological Association (JDA) established a Special Committee on the Safety of Cosmetics Containing Rhododenol on July 17, 2013 and management guide for dermatologists has been updated on the website in order to delineate the diagnostic criteria for Rhododenol‐induced leukoderma and provides a broad guide for standard treatment based on current knowledge. This guide is produced on the basis of the guide (version 7) updated on June 20, 2014 in the website. Rhododenol‐induced leukoderma refers to depigmentation of varying severity that develops after the use of cosmetics containing Rhododenol, mainly at the site of use. In most cases, repigmentation of part or all the affected area is evident after discontinuation. Histopathologically cellular infiltration around the hair follicles and melanophages are present in most cases. The number of melanocytes in the lesion is declined but not totally absent in most cases. Rhododenol itself is a good substrate for tyrosinase, resulting in the formation of Rhododenol metabolites (e.g., Rhododenol quinone). Melanocytes are damaged by Rhododenol metabolites during the subsequent metabolic process. The continued use of cosmetics containing Rhododenol thus induces tyrosinase activity‐dependent cytotoxicity in melanocytes in the epidermis at application sites, resulting in decreasing the amount of melanin produced by melanocytes; the addition of some other factor to this process is believed to subsequently cause the decrease or disappearance of melanocytes themselves from the epidermis.     

伯氏疏螺旋体膜蛋白OspC研究进展

莱姆病是由伯氏疏螺旋体引起,即莱姆病螺旋体引起的多系统感染性疾病。伯氏疏螺旋体本身并不具有生物活性,不能分泌毒力因子,其唯一的致毒因子为外膜脂蛋白。其中,外膜脂蛋白C(O spC)相对于外膜蛋白A(O spA)以及鞭毛蛋白来说,其分子量较大。并且,最重要的一点是O spC在宿主体内能引起早期免疫反应;同时O spC抗原性强,免疫O spC后可以检测出,血清中抗体的浓度明显上升。因此,本文对目前国内外对O spC的研究进行了综述。