P21 Design and operation of a human breath freshness panel

Objective  Practical treatment of halitosis requires tongue cleaning since volatile sulphur compounds (VSC) seems mainly to be from the tongue coating. From this point of view, mechanical tools such as tongue brushes or scrapers have been developed. However, approaches by chemical tongue cleaning have not been reported. Thus we developed tablets containing protease from kiwifruits, which could resolve tongue coating, and assessed the effects of the protease tablet to control tongue coating.
Methods  Crossover studies and double blind experiments were designed using volunteers with informed consent. The trial was done twice per volunteer, that is, they had a tablet with or without the addition of protease from kiwifruits (test and placebo) with intervening washout periods of at least 2 weeks. The degree of change in tongue coating was evaluated visually using a tongue coating score which consisted of an area component (0–3) and a thickness component (0–3). An image analyzer was also used to measure the changing in actual area of coating.
Results  The average value of the tongue coating scores after taking a test tablet (11.4 ± 5.2) was significantly smaller ( P  < 0.01) than before taking the tablet (18.8 ± 7.0). Image analyzer measurements also showed significant reduction ( P  < 0.01) of tongue coating by taking test tablet. On the other hand, a placebo tablet showed no significant effects in both analyses.
Conclusions  This study indicated that taking protease tablets could reduce tongue coating. We are planning further clinical trials that can show reduced VSC concentrations in mouth air with decreasing tongue coating.     

Longitudinal dynamics of infection and serum antibody in A. actinomycetemcomitans periodontitis

OBJECTS: This report describes one of the first prospective studies delineating the relationship between infection, host antibody responses and disease exacerbations and remissions in a distinct subset of periodontitis patients infected with A. actinomycetemcomitans. DESIGN: The design of this longitudinal study included visits for each patient approximately every 2 months for up to 3 years. SUBJECTS AND METHODS: Subjects (n = 51) included 16 adult periodontitis (AP) and 11 early-onset periodontitis (EOP) patients with elevated serum IgG antibody to A. actinomycetemcomitans and infection with this microorganism, 12 AP patients with normal levels of anti-Aa antibody, and 12 normal subjects. MEASUREMENT OUTCOMES: Clinical parameters included a gingival index, plaque index, bleeding on probing, pocket depth, and attachment level. Disease activity was defined as loss of attachment during the monitoring intervals. Serum IgG, IgM and IgA antibody to A. actinomycetemcomitans Y4 (serotype b) was quantit-ated using an ELISA. Subgingival plaque samples were examined for A. actinomycetemcomitans using colony immunobiotting. Human serum IgG antibody specificities to outer membrane antigens (OMA) of A. actinomycetemcomitans Y4 were determined using Western immunoblotting. RESULTS: A. actinomycetemcomitans-infected AP patients had a higher frequency of teeth infected when compared to the EOP patients. However, the EOP patients exhibited a trend for higher levels of A. actinomycetemcomitans in those teeth that were infected. Active disease patients demonstrated a significantly greater frequency of infected sites, as well as significant elevations in the proportions of A. octinomycetemcomitans. Both EOP and AP groups showed significantly elevated IgG, IgM and IgA antibody to A. actinomycetemcornitans when compared to a periodontally normal group. The level of IgG antibody was significantly elevated in A. actinomycetemcomitans-positive patients with active disease, while IgA antibody was decreased in a number of the active group patients. Plaque samples derived from active sites showed a clear and significant increase in A. actinomycetemcomitans that occurred from 2–6 months prior to the identification of disease activity. Approximately 70% of the active disease patients showed an increase in IgG antibody level by 2–4 months prior to disease activity. Studies of the antigen reactivity patterns of serum IgG indicated that antibody to antigens of 65, 58, 48, 29 and 24 kDa were more frequent in patients who showed active disease, while those patients with the greatest frequency of active disease appeared to show a general decrease in the recognition of the A. actinomycetemcomitans OMA. CONCLUSIONS: It appears that A. actinomycetemcomitans infection relates to a particular type of disease with accompanying antibody responses that reflect periods of active disease. The dynamics of A. actinomycetemcomitans infection and the level and specificity of systemic antibody responses to this pathogen support an important contribution of the immune response to managing this infection.     

应激干预对抑郁症患者皮电和心率的影响

目的：了解放松训练和静坐两种干预方式对抗心算对抑郁症患者皮电和心率的影响，以及正常人、单纯抑郁症患者和伴焦虑症状的抑郁症患者在皮电和心率上的差异。方法：选择2006—06／09在河北医科大学第一附属医院精神卫生科门诊及住院的单纯抑郁症和伴焦虑症状的抑郁症患者各24例作为单纯抑郁症组和伴焦虑抑郁症组，均符合中国精神障碍分类与诊断标准，每组男女各12例，年龄17—50岁。选择同期院内医护人员及患者家属24人作为对照组，男女各12人，年龄19-47岁。所有对象对实验均知情同意。以心算为应激源，放松训练和静坐为干预手段，记录被试在基线期、干预期、应激期及恢复期的皮电和心率。结果：抑郁症患者48例及健康对照者24人全部进人结果分析。①在基线期，伴焦虑抑郁组心率明显高于单纯抑郁症组和对照组，皮电明显低于另外两组（P〈0．01），单纯抑郁症组和对照组皮电和心率比较，差异均不明显（P〉0．05）。②在干预期，被试的皮电升高，心率下降，放松训练的效果明显好于静坐，尤其对伴焦虑症状的抑郁症患者效果最好，静坐会加重伴焦虑症状的抑郁症患者的紧张状态。③在应激期，放松训练有效的对抗心算引起的皮电下降以及心率的升高，效果明显好于静坐组。④恢复期放松训练和静坐时的皮电、心率指标基本都恢复到静息状态。结论：①静息状态下伴焦虑症状的抑郁症患者的交感神经功能亢进，兴奋性高于单纯抑郁症患者和正常人。②放松训练可以缓解交感神经的紧张程度，并能够较静坐更好的对抗应激引起的交感神经活动增强。③静坐对单纯抑郁症患者和正常人有放松作用，但可引起伴焦虑症状的抑郁症患者更多的紧张情绪。     

JMH variants: serologic, clinical, and biochemical analyses in two cases

BACKGROUND: JMH is a high-frequency red cell blood group antigen that resides on a 76- to 80-kDa glycosylphosphatidylinositol-linked protein also known as CDw108. Antibodies with JMH specificity are often autoimmune and are usually, if not always, clinically benign. Some individuals with JMH-variant antigen produce alloantibodies to JMH, but little evidence concerning their clinical significance is available. This article reports on two patients who express a JMH-variant antigen and produced alloanti-JMH. STUDY DESIGN AND METHODS: Murine monoclonal antibodies and human antibodies to JMH were used in hemagglutination, radioimmunoassay, and Western blot testing of red cells from two JMH- variant patients; antiserum from one of these patients was also used in biochemical studies. In addition, in vivo survival of JMH-positive red cells was studied in the same patient. RESULTS: Biochemically, both examples of red cells with the JMH-variant phenotype expressed a JMH protein with a molecular weight similar to that of the normal JMH protein. For both patients, family studies suggested an autosomal recessive pattern of inheritance. Survival study demonstrated reduced in vivo red cell survival in one patient. CONCLUSION: JMH-variant phenotypes express a protein of normal molecular weight and are inherited in an autosomal recessive pattern. Furthermore, individuals with this phenotype can produce clinically significant antibodies.     

Creutzfeldt--Jakob Disease in Recipients of Human Growth Hormone in the United Kingdom: A Clinical and Radiographic Study

In the past 3 years there have been five further cases, in additionto one case reported in 1985, of Creutzfeldt-Jakob disease inrecipients of human growth hormone in the United Kingdom. Theclinical findings of two of these cases are described, demonstratinga typical presentation with a predominantly cerebellar syndromeat onset which is not commonly a presenting feature of sporadicCreutzfeldt-Jakob disease. In one case a ^99mTc hexamethylpropylenaminesingle photon emission tomographic scan showed marked impairmentof tracer uptake in the basal ganglia and cerebral cortex ata time when the clinical picture was predominantly cerebellar.This technique may be useful in early diagnosis. In the othercase post mortem examination of the brain showed prominent amyloiddeposition in the cerebellum, which has not been described previouslyin pituitary-hormone related Creutzfeldt-Jakob disease. Thepreviously published cases of growth hormone-related Creutzfeldt-Jakobdisease are reviewed and reasons for the particular clinicalpattern seen are discussed.     

Using transcutaneous carbon dioxide monitor (TOSCA 500) to detect respiratory failure in patients with amyotrophic lateral sclerosis: A validation study

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative condition, respiratory failure being the commonest cause of death. Quality of life and survival can be improved by supporting respiratory function with non-invasive ventilation. Transcutaneous carbon dioxide monitoring is a non-invasive method of measuring arterial carbon dioxide levels enabling simple and efficient screening for respiratory failure. The aim of this study was to validate the accuracy of carbon dioxide level recorded transcutaneously with a TOSCA 500 monitor. It is a prospective, observational study of 40 consecutive patients with ALS, recruited from a specialist ALS clinic. The partial pressure of carbon dioxide (PCO(2)) in each patient was determined by both transcutaneous monitoring and by an arterialized ear lobe capillary blood sample. The carbon dioxide (CO(2)) levels obtained with these two methods were compared by Bland-Altman analysis. The results showed that the mean difference between arterialized and transcutaneous readings was - 0.083 kPa (SD 0.318). The Bland-Altman limits of agreement ranged from 0.553 to - 0.719 kPa. The difference was ?0.5 kPa, with a maximum recorded difference of 0.95 kPa. In conclusion, non-invasive carbon dioxide monitoring using a TOSCA monitor is a useful clinical tool in neurology practice. Users should be aware of the possibility of occasional inaccurate readings. A clinically unexpected or incompatible reading should be verified with a blood gas analysis, especially when a decision to provide ventilatory support is required.     

FcR gamma-chain is essential for both surface expression and function of human Fc gamma RI (CD64) in vivo

Most Ig receptors exist as hetero-oligomeric complexes with separate ligand binding (alpha) and signal transducing (beta, gamma, or zeta) subunits. For Fc gamma RIIIa and Fc epsilon RI, association with the FcR gamma-chain is essential for surface expression. However, the human high affinity IgG receptor, hFc gamma RI, was found to be surface- expressed by itself in transient transfection models. We have now analyzed the integrity of hFc gamma RI expression in more detail in stable transfectants. In vitro we noted that, in the absence of FcR gamma-chain, surface expression of hFc gamma RI rapidly declined to background levels, in both IIA1.6 B cells and NIH3T3 fibroblasts. The effect of FcR gamma-chain on hFc gamma RI surface expression in vivo was evaluated by using two newly generated transgenic mouse lines, selectively expressing hFc gamma RI on myeloid cells. These transgenic mice were crossed with FcR gamma-chain-deficient mice. Analysis of blood monocytes and peritoneal macrophages showed that surface expression of hFc gamma RI was reduced by approximately 80%. The remaining approximately 20% of receptors were still capable of binding IgG-opsonized RBC, suggesting FcR gamma-chain not to be critical for hFc gamma RI ligand-binding capacity. Importantly, however, hFc gamma RI signaling capacity was lost in FcR gamma-chain-deficient cells. No phagocytosis could be observed using either ligand sensitized (EA- IgG2a) or CD64-targeted erythrocytes (using a bispecific antibody) in both hFc gamma RI transgenic lines. This documents the FcR gamma-chain to be indispensable for both surface membrane expression and function of human Fc gamma RI in vivo.     

Potential therapeutic target for malignant paragangliomas: ATP synthase on the surface of paraganglioma cells

F1FoATP synthase (ATP synthase) is a ubiquitous enzyme complex in eukaryotes. In general it is localized to the mitochondrial inner membrane and serves as the last step in the mitochondrial oxidative phosphorylation of ADP to ATP, utilizing a proton gradient across the inner mitochondrial membrane built by the complexes of the electron transfer chain. However some cell types, including tumors, carry ATP synthase on the cell surface. It was suggested that cell surface ATP synthase helps tumor cells thriving on glycolysis to survive their high acid generation. Angiostatin, aurovertin, resveratrol, and antibodies against the α and β subunits of ATP synthase were shown to bind and selectively inhibit cell surface ATP synthase, promoting tumor cell death. Here we show that ATP synthase β (ATP5B) is present on the cell surface of mouse pheochromocytoma cells as well as tumor cells of human SDHB-derived paragangliomas (PGLs), while being virtually absent on chromaffin primary cells from bovine adrenal medulla by confocal microscopy. The cell surface location of ATP5B was verified in the tissue of an SDHB-derived PGL by immunoelectron microscopy. Treatment of mouse pheochromocytoma cells with resveratrol as well as ATP5B antibody led to statistically significant proliferation inhibition. Our data suggest that PGLs carry ATP synthase on their surface that promotes cell survival or proliferation. Thus, cell surface ATP synthase may present a novel therapeutic target in treating metastatic or inoperable PGLs.