Treponema pallidum-induced prostaglandin E2 secretion in skin fibroblasts leads to neuronal hyperpolarization: A cause of painless ulcers.

BACKGROUND: Primary syphilis is characterized by painless ulcerative lesions in the genitalia, the aetiology of painless remains elusive. OBJECTIVES: To investigate the role of Treponema pallidum in painless ulcer of primary syphilis, and the mechanisms underlying painless ulcers caused by T. pallidum. METHODS: An experimental rabbit model of primary syphilis was established to investigate its effects on peripheral nerve tissues. Human skin fibroblasts were used to examine the role of T. pallidum in modulating neurotransmitters associated with pain and to explore the signalling pathways related to neurotransmitter secretion by T. pallidum in vitro. RESULTS: Treponema pallidum infection did not directly lead to neuronal damage or interfere with the neuronal resting potential. Instead, it facilitated the secretion of prostaglandin E2 (PGE2) through endoplasmic reticulum stress in both rabbit and human skin fibroblasts, and upregulation of PGE2 induced the hyperpolarization of neurones. Moreover, the IRE1α/COX-2 signalling pathway was identified as the underlying mechanism by which T. pallidum induced the production of PGE2 in human skin fibroblasts. CONCLUSION: Treponema pallidum promotes PGE2 secretion in skin fibroblasts, leading to the excitation of neuronal hyperpolarization and potentially contributing to the pathogenesis of painless ulcers in syphilis.

Treponema pallidum protein Tp47 induced prostaglandin E2 to inhibit the phagocytosis in human macrophages.

BACKGROUND: During Treponema pallidum (T. pallidum) infection, the host's immune system actively engages in pursuit and elimination of T. pallidum, while T. pallidum skillfully employs various mechanisms to evade immune recognition. Macrophages exhibit incomplete clearance of T. pallidum in vitro and the underlying mechanism of how T. pallidum resists the attack of macrophage remains unclear. OBJECTIVES: To investigate the effect of T. pallidum membrane protein Tp47 on the phagocytosis of macrophages. METHODS: THP-1-derived macrophages were used to investigate the role of Tp47 in the secretion of Prostaglandin E2 (PGE2) in macrophages and the mechanism by which Tp47 induced the production of PGE2, as well as the impact of PGE2 on the macrophage's phagocytosis. RESULTS: Tp47 (1-10 µg/mL) significantly inhibited the phagocytosis of latex beads and T. pallidum in macrophages (p ≤ 0.05). PGE2 production by macrophages could be induced by Tp47, and the phagocytic function of macrophages could be restored using PGE2 antibody. Tp47 produced PGE2 by activating the PERK/NF-κB/COX-2 pathway in macrophages. Inhibitors targeting PERK, NF-κB and COX-2, respectively, reduced the level of PGE2 and restored the phagocytic function of macrophages. CONCLUSION: Tp47-induced PGE2 production via the PERK/NF-κB/COX-2 pathway contributed to macrophage phagocytosis inhibition, which potentially contributes to immune evasion during the T. pallidum infection.

Recombinant Treponema pallidum protein Tp47 promoted the phagocytosis of macrophages by activating NLRP3 inflammasome induced by PKM2-dependent glycolysis.

BACKGROUND: Glycolysis is a critical pathway in cellular glucose metabolism that provides energy and participates in immune responses. However, whether glycolysis is involved in NOD-like receptor family protein 3 (NLRP3) inflammasome activation and phagocytosis of macrophages in response to Treponema pallidum infection remains unclear. OBJECTIVES: To investigate the role of glycolysis in activating the NLRP3 inflammasome for regulating phagocytosis in macrophages in response to T. pallidum protein Tp47 and its associated mechanisms. METHODS: Interactions between activation of the NLRP3 inflammasome and phagocytosis and the role of glycolysis in Tp47-treated macrophages were investigated through experiments on peritoneal macrophages and human monocytic cell line-derived macrophages. RESULTS: Activation of phagocytosis and NLRP3 inflammasome were observed in Tp47-treated macrophages. Treatment with NLRP3 inhibitor MCC950 or si-NLRP3 attenuated Tp47-induced phagocytosis. Glycolysis and glycolytic capacity were enhanced by Tp47 stimulation in macrophages, and a change in the levels of glycolytic metabolites (phosphoenolpyruvate, citrate and lactate) was induced by Tp47 in macrophages. Inhibition of glycolysis with 2-deoxy-D-glucose, a glycolysis inhibitor, decreased the activation of NLRP3. Expression of M2 isoform of pyruvate kinase (PKM2), an enzyme catalysing a rate-limiting reaction in the glycolytic pathway, was upregulated in Tp47-stimulated macrophages. Inhibition of PKM2 with shikonin or si-PKM2 decreased glycolysis and NLRP3 activation. CONCLUSION: Tp47 promotes phagocytosis in macrophages by activating the NLRP3 inflammasome, which is induced by the enhancement of PKM2-dependent glycolysis.

Tp47 promoted the phagocytosis of HMC3 cells though autophagy induced by endoplamic reticlum stress.

BACKGROUND: Central nervous system damage is an essential clinical feature that occurs in the early or late stages of syphilis infection. The abnormal enhancement of microglial phagocytosis can cause damage to the nervous system. However, the contribution of abnormally enhanced microglial phagocytosis to the pathogenesis of Treponema pallidum subsp. pallidum (T. pallidum) infection remains unknown. OBJECTIVES: In this study, we sought to determine the role of recombinant T. pallidum Tp47 in promoting microglia phagocytosis and its associated mechanisms. METHODS: Microglial HMC3 cells were used to investigate the effect of the Tp47 on phagocytosis and the roles of autophagy and endoplasmic reticulum stress in Tp47-induced phagocytosis. RESULTS: HMC3 cells exhibited obvious phagocytosis when stimulated with Tp47. The levels of P62 degradation, Beclin1 expression and the LC3II/LC3I ratio were significantly elevated, and the fusion of autophagosomes and lysosomes was promoted in Tp47-stimulated HMC3 cells. Treatment with the autophagy inhibitors 3-MA and Baf A1 inhibited Tp47-induced phagocytosis. Meanwhile, the endoplasmic reticulum stress markers PERK, IRE1α, GRP78, ATF4 and XBP1s were upregulated in Tp47-stimulated HMC3 cells. In addition, we found that TUDCA could inhibit Tp47-induced expression of IRE1α but not PERK or ATF4. 4-PBA inhibited TP47-induced PERK and ATF4 protein expression but did not inhibit IRE1α expression. Attenuation of endoplasmic reticulum stress by administration of TUDCA and 4-PBA abrogated Tp47-mediated autophagy. CONCLUSIONS: These results suggested that Tp47 activated autophagy through two key pathways associated with endoplasmic reticulum stress, PERK/ATF4 and IRE1/XBP1, to promote phagocytosis in HMC3 cells. These findings provided a basis for the understanding of the pathophysiology of neurological disorders that occur during the course of syphilis.

Autophagy promotes phagocytosis and clearance of Treponema pallidum via the NLRP3 inflammasome in macrophages.

BACKGROUND: Elucidating the mechanism of the macrophage phagocytic response will improve our knowledge of host defence against Treponema pallidum. OBJECTIVE: To explore whether autophagy promotes T. pallidum phagocytosis and clearance via the NLRP3 inflammasome in macrophages. METHODS: The interactions between autophagy and phagocytosis and the role of NLRP3 in these processes in T. pallidum-treated macrophages were investigated through experiments using human monocytic cell line (THP-1)-derived macrophages. Treponema pallidum clearance after phagocytosis was evaluated by inoculating rabbits with macrophage-treponeme mixtures. RESULTS: Activation of autophagy and phagocytosis in T. pallidum-treated macrophages occurred in a dose- and time-dependent manner. The percentage of spirochete-positive macrophages (22.34% vs. 70.93%, P < 0.001) and spirochete internalization (MFI: 9.62 vs. 20.33, P < 0.001) were notably reduced by silencing Beclin1. Inoculation of macrophage-treponeme mixtures into rabbits showed a 3.00-day delay in lesion development (17.55 ± 3.73 vs. 14.55 ± 1.99 days) and decreased lesion numbers [11 (36.7%) vs. 20 (66.7%) of 30; χ2  = 5.406, P = 0.020] in the control compared with the si-Beclin1 group. Furthermore, silencing NLRP3 decreased the mRNA and protein levels of Beclin-1 and LC3B [mRNA: 49.86% and 43.02%; protein: 22.31% and 24.24%, respectively, differing significantly from the control group (P < 0.001)] and reduced the percentage of spirochete-positive macrophages (30.29% vs. 70.53%, P < 0.001) and spirochete internalization (MFI: 9.82 vs. 19.33, P < 0.001). CONCLUSION: Treponema pallidum induces autophagy in macrophages to promote phagocytosis and clearance. The NLRP3 inflammasome modulates autophagy and phagocytosis in vitro. These data may be useful for understanding the host-pathogen relationship and establish the groundwork for strategies to combat syphilis.

Are nontreponemal tests suitable for monitoring syphilis treatment efficacy? Evidence from rabbit infection models.

OBJECTIVES: We aimed to characterize kinetics of non-treponamal antibody titres during the natural course of syphilis and explore their roles in monitoring syphilis treatment efficacy. METHODS: Sixty New Zealand white male rabbits were challenged with Nichols or Amoy Treponema pallidum strains, and the rapid plasma reagin (RPR) test was performed to quantify non-treponemal antibody titres during the infection course. Viable T. pallidum in the challenged rabbits was assessed with rabbit infectivity tests. RESULTS: The RPR titres of the Nichols or Amoy strain between no benzathine penicillin G (BPG) and BPG treatment subgroups displayed a similar trend: first ascending and then descending. Compared with baseline, the proportions of fourfold decline in RPR titres in the Nichols or Amoy group presented a similar result on days 30, 60 and 180 between the no BPG and BPG treatment subgroups (0%, 0/5; 80%, 4/5; 100%, 5/5; vs. 0%, 0/5; 80%, 4/5; 100%, 5/5; p 0.999; 0%, 0/5; 80%, 4/5; 80%, 4/5; vs. 40%, 2/5; 100%, 5/5; 100%, 5/5; p 0.098, respectively). Compared with the maximum baseline titre, the proportion of fourfold decline in PRR titre also showed a similar result in the two groups on days 30, 60 and 180 between the no BPG and the BPG treatment subgroups (0%, 0/5; 100%, 5/5; 100%, 5/5, vs. 40%, 2/5; 100%, 5/5; 100%, 5/5; p 0.129; 0%, 0/5; 100%, 5/5; 100%, 5/5, vs. 80%, 4/5; 100%, 5/5; 100%, 5/5; p 0.091, respectively. Moreover, regardless of whether the RPR titres presented a fourfold decline, viable T. pallidum could be detected in untreated rabbits' lymph nodes at 30, 60 and 180 days post infection, while viable T. pallidum was not detected in any of the treated rabbits' lymph nodes. CONCLUSIONS: The RPR titre increased and then decreased (even became negative) during the natural course of syphilis, similar to that seen after BPG treatment. The RPR tetre is thus a questionable indicator of syphilis treatment efficacy.

Recombinant Treponema pallidum protein Tp0136 promotes fibroblast migration by modulating MCP-1/CCR2 through TLR4.

BACKGROUND: Chancre self-healing is an important clinical feature in the early stages of syphilis infection. Wound healing may involve an important mechanism by the migration of fibroblasts filling the injured lesion. However, the specific mechanism underlying this process is still unknown. OBJECTIVES: We aimed to analyse the role of Tp0136 in the migration of fibroblasts and the related mechanism. METHODS: The migration ability of fibroblasts was detected by a wound-healing assay. RT-PCR and ELISA detected the expression of MCP-1, IL-6 and MMP-9. TLR4 expression was detected by RT-PCR. The protein levels of CCR2 and relevant signalling pathway molecules were measured by Western blotting. RESULTS: Tp0136 significantly promoted fibroblast migration. Subsequently, the levels of MCP-1 and its receptor CCR2 were increased in this process. The migration of fibroblasts was significantly inhibited by an anti-MCP-1 neutralizing antibody or CCR2 inhibitors. Furthermore, studies demonstrated that Tp0136 could activate the ERK/JNK/PI3K/NF-κB signalling pathways through TLR4 activity and that signalling pathways inhibitors could weaken MCP-1 secretion and fibroblast migration. CONCLUSIONS: These findings demonstrate that Tp0136 promotes the migration of fibroblasts by inducing MCP-1/CCR2 expression through signalling involving the TLR4, ERK, JNK, PI3K and NF-κB signalling pathways, which could contribute to the mechanism of chancre self-healing in syphilis.

Recombinant Treponema pallidum protein Tp47 induces angiogenesis by modulating the matrix metalloproteinase/tissue inhibitor of metalloproteinase balance in endothelial cells.

BACKGROUND: Although angiogenesis is an obvious pathological manifestation in the pathogenesis of syphilis, little is known about the underlying mechanisms of angiogenesis induced by reactions to Treponema pallidum antigens. OBJECTIVE: In this study, we sought to determine the role of recombinant T. pallidum Tp47 in promoting angiogenesis in endothelial cells and the related mechanism. METHODS: Evaluation of the pro-angiogenic activity of recombinant T. pallidum Tp47 in human umbilical vein endothelial cells (HUVECs) was assessed, and the balance of matrix metalloproteinase (MMP)/tissue inhibitor of metalloproteinase (TIMP) and the mechanisms underlying the involvement of Akt/mTOR/S6 pathways in this process were explored. RESULTS: Under stimulation by Tp47, HUVECs exhibited obvious proliferation, migration and tube formation. In addition, the apparent promotion of angiogenesis by Tp47 was observed using a zebrafish embryo model. During angiogenesis, the levels of MMP-1 and MMP-10 were significantly elevated, whereas those of TIMP-1 and TIMP-2 did not change. In addition, after transfection with siRNAMMP-1 and siRNAMMP-10, migration and tube formation were significantly inhibited. Akt/mTOR/S6 signalling was found to be involved in upregulating MMP-1 and MMP-10 expression, and the sequential blockade of steps in the pathways effectively prevented Tp47-induced angiogenesis. CONCLUSION: The results reveal the underlying mechanism of angiogenesis promoted by Tp47, namely, upregulating MMP-1 and MMP-10 expression to disrupt the MMP/TIMP balance through the Akt/mTOR/S6 pathway. These findings contribute to our understanding of the pathophysiology of syphilis.

Analysis of serum metabolite profiles in syphilis patients by untargeted metabolomics.

BACKGROUND: Global metabolomics analysis can provide substantial information on energy metabolism, physiology, possible diagnostic biomarkers and intervention strategies for pathogens. OBJECTIVE: To gain a better understanding of the mechanisms of syphilis and analysis of serum metabolite profiles in syphilis patients. METHODS: We conducted an untargeted metabolomics analysis of serum from 20 syphilis patients and 20 healthy controls. RESULTS: A total of 2890 molecular features were extracted from each sample, and the peak intensity of each feature was obtained. Distinct differential metabolites were identified by principal component analysis, partial least squares-discriminant analysis and hierarchical clustering analysis. Furthermore, five metabolites were identified as significantly different by Student's t-test, including trimethylamine N-oxide, l-arginine, lysoPC(18:0), betaine and acetylcarnitine. KEGG analysis showed that these differential metabolites were in various pathways, including Chagas disease, fatty acid biosynthesis, primary bile acid biosynthesis, Salmonella infection, ABC transporters, glycerophospholipid metabolism and choline metabolism. Among them, trimethylamine N-oxide was 3.922 times in patients with syphilis than healthy controls. CONCLUSION: Trimethylamine N-oxide may be used as an indicator to distinguish between syphilis patients and healthy controls. The changes in these metabolites suggest that Treponema pallidum affects the normal metabolic activity of host cells, providing some clues for elucidating the pathogenesis of T. pallidum.

Using the "Hill-Sachs interval to glenoid track width ratio" for prediction of recurrent instability after arthroscopic Bankart repair.

INTRODUCTION: The glenoid track concept was used to confirm the engaging Hill-Sachs lesion (HSL) as a risk factor for recurrent instability following arthroscopic Bankart repair (ABR). However, the post-operative condition of soft tissue in vivo was not comparable to that designed in the intact condition in vitro in the original study of the glenoid track concept. Herein, the possibility of engagement may be underestimated. HYPOTHESIS: A threshold of the Hill-Sachs interval to glenoid track width ratio (H/G ratio) that is related to recurrent instability after ABR could be found, in order to adjust the original glenoid track concept. PATIENTS AND METHODS: Patients who underwent ABR with minimum 24-months follow-up were reviewed retrospectively. The primary outcome was evaluated with the recurrent instability. The H/G ratio of individual patients was used to calculate the sensitivity, specificity, and a receiver operating characteristic (ROC) curve, which aimed to establish a H/G ratio threshold related to recurrent instability after ABR. RESULTS: From June 2005 to December 2013, 160 patients with a mean age of 27.7years were enrolled. The mean follow-up period was 77.2 months. The ROC curve indicated that H/G ratio≥0.7 had the sensitivity and specificity of 0.74 and 0.71, respectively, in predicting recurrent instability. On univariate logistic regression analysis, the H/G ratio≥0.7 was a significant predictor of higher risk for recurrent instability (p<0.001). DISCUSSION: H/G ratio seems to be a reliable parameter for predicting recurrent instability. H/G ratio≥0.7 may be considered as a positive predictor for recurrent instability after ABR. LEVEL OF EVIDENCE: Level IV: retrospective diagnostic study.

Risk factors and outcome of levofloxacin-resistant Elizabethkingia meningoseptica bacteraemia in adult patients in Taiwan.

Elizabethkingia meningoseptica is an emerging nosocomial pathogen associated with high mortality and inherently resistant to many antimicrobial agents. Levofloxacin has been considered as a therapeutic agent based on in vitro susceptibility. We aim to investigate the risk factors and outcomes for levofloxacin-resistant E. meningoseptica bacteraemia. Adult patients with E. meningoseptica bacteraemia were identified retrospectively in a medical centre in Taiwan from January 2011 to July 2015. These strains were identified by the Vitek2 automated system or matrix-assisted laser desorption-ionization time-of-flight mass spectrometry. We compared clinical features and outcomes of patients with levofloxacin-resistant (MIC >2 µg/mL) and levofloxacin-susceptible (MIC ≤2 µg/mL) E. meningoseptica bacteraemia. A total of 93 patients were identified, including 51 (54.8%) with levofloxacin-resistant E. meningoseptica bacteraemia. The APACHE II score (OR, 1.08; 95% CI, 1.02-1.14; p = 0.008) was the only independent risk factor for levofloxacin-resistant E. meningoseptica bacteraemia. The 14-day mortality for patients with levofloxacin-resistant E. meningoseptica bacteraemia (attributable mortality: 30.7%) was significantly higher than that for patients with the levofloxacin-susceptible strain (56.9% versus 26.2%, p = 0.003). In the multivariate analysis of risk factors for mortality, appropriate definite antibiotic use was the only factor associated with 14-day survival (OR, 0.11; 95% CI, 0.02-0.55, p = 0.007). The levofloxacin-resistant strain was borderline significantly associated with mortality (OR, 3.09; 95% CI, 0.88-10.91, p = 0.079). The early identification of levofloxacin resistance in E. meningoseptica isolates is important to tackle this multi-drug resistance pathogen.

Factors associated with syphilis infection: a comprehensive analysis based on a case-control study.

This study aimed to comprehensively evaluate factors that influence the likelihood of syphilis infection from risk-taking behaviours and medical conditions. A retrospective case-control study was conducted by enrolling 664 syphilis inpatients (excluding 11 congenital syphilis patients) and 800 sex- and age-matched controls. Medical histories, clinical data and patient interview data were collected and subjected to logistic regression analyses. The prevalence of syphilis in the study population was 3·9% (675/17,304). By univariate analysis, syphilis infection was associated with migration between cities, marital status, smoking, reproductive history, hypertension, elevated blood urea nitrogen (BUN) and infection with hepatitis B virus (HBV) (P < 0·05). A high rate of syphilis-HBV co-infection was observed in HIV-negative patients and further research revealed an association between syphilis and specific HBV serological reactivity. Syphilis was also associated with the frequency, duration and status of tobacco use. Multivariate analysis indicated that syphilis infection was independently associated with migration between cities [adjusted odds ratio (aOR) 1·368, 95% confidence interval (CI) 1·048-1·785], current smoking (aOR 1·607, 95% CI 1·177-2·195), elevated BUN (aOR 1·782, 95% CI 1·188-2·673) and some serological patterns of HBV infection. To prevent the spread of infectious diseases, inpatients and blood donors should be tested for HIV, syphilis, HBV and HCV simultaneously.

Levels of F2-isoprostanes, F4-neuroprostanes, and total nitrate/nitrite in plasma and cerebrospinal fluid of patients with traumatic brain injury.

Several events occurring during the secondary damage of traumatic brain injury (TBI) can cause oxidative stress. F(2)-isoprostanes (F(2)-IsoPs) and F(4)-neuroprostanes (F(4)-NPs) are specific lipid peroxidation markers generated from arachidonic acid and docosahexaenoic acid, respectively. In this study, we evaluated oxidative stress in patients with moderate and severe TBI. Since sedatives are routinely used to treat TBI patients and propofol has been considered an antioxidant, TBI patients were randomly treated with propofol or midazolam for 72 h postoperation. We postoperatively collected cerebrospinal fluid (CSF) and plasma from 15 TBI patients for 6-10 d and a single specimen of CSF or plasma from 11 controls. Compared with the controls, the TBI patients exhibited elevated levels of F(2)-IsoPs and F(4)-NPs in CSF throughout the postsurgery period regardless of the sedative used. Compared with the group of patients who received midazolam, those who received propofol exhibited markedly augmented levels of plasma F(2)-IsoPs, which were associated with higher F(4)-NPs levels and lower total nitrate/nitrite levels in CSF early in the postsurgery period. Furthermore, the higher CSF F(2)-IsoPs levels correlated with 6-month and 12-month worse outcomes, which were graded according to the Glasgow Outcome Scale. The results demonstrate enhanced oxidative damage in the brain of TBI patients and the association of higher CSF levels of F(2)-IsoPs with a poor outcome. Moreover, propofol treatment might promote lipid peroxidation in the circulation, despite possibly suppressing nitric oxide or peroxynitrite levels in CSF, because of the increased loading of the lipid components from the propofol infusion.

Photocatalytic reduction of CO2with SiC recovered from silicon sludge wastes.

In the present study, silicon carbide (SiC) recovered from silicon sludge wastes is used as catalysts for photocatalytic reduction of CO2. By X-ray diffraction, it is clear that the main components in the silicon sludge wastes are silicon and SiC. The grain size of the SiC separated from the sludge waste is in the range of 10-20 µm in diameter (observed by scanning electron microscopy). By solid state nuclear magnetic resonance, it is found that α-SiC is the main crystallite in the purified SiC. The α-SiC has the band-gap of 3.0 eV. To yield C1-C2chemicals from photocatalytic reduction of CO2, hydrogen is provided by simultaneous photocatalytic splitting of H2O. Under the light (253-2000 nm) illumination, 12.03 and 1.22 µmol/h g cat of formic and acetic acids, respectively, can be yielded.

Prevention of orofacial injury via the use of mouthguards among young male rugby players.

The purpose of this study was to examine factors hindering the use of mouthguards and the incidence of orofacial injury among young male rugby players. 69 high school rugby players (Group 1) and 431 medical student rugby players (Group 2) participated in this study. Participants in Group 1 used custom-made mouthguards fabricated according to a standardized method, whereas participants in Group 2 used custom-made or over-the-counter mouthguards of their choice. The factors associated with orofacial injury were assessed by logistic regression analysis, while factors hindering mouthguard use were assessed by multinomial logistic regression analysis. All data were obtained from a questionnaire developed by the Japanese Academy of Sports Dentistry. We found that breathing problems were the main factor contributing to the reduced frequency of mouthguard use. In both groups, a significant negative association was observed between the frequency of mouthguard use and the risk of orofacial injury. The group using standardized custom-made mouthguards reported fewer complaints about breathing problems and a higher frequency of mouthguard use. The results of this study suggest that increasing the frequency of mouthguard use would reduce the risk of orofacial injury among young male rugby players. We also conclude that users of custom-made mouthguards complain less frequently of breathing difficulties.

Laboratorial characteristics of patients with diarrhoea suffering from egg white allergy

BACKGROUND: Egg allergy is associated with diarrhoeal symptoms. However, the mechanism underlying allergic diarrhoea remains unclear. OBJECTIVE: To determine whether egg white-specific IgE antibodies coexist with egg white-specific IgG antibodies in patients with egg allergy featuring diarrhoeal symptoms, and whether there is any relationship between these two antibody types. METHODS: A total of 89 patients with egg allergy featuring diarrhoeal symptoms (average age, 23.2 years; range, 1-78 years), all of whom tested positive for egg white-specific IgG, were enrolled in this study. The concentration of total IgE, egg white-specific IgE and number of eosinophils in the serum were determined. RESULTS: Among the 89 egg white allergic patients tested, 49 (55.1%) patients showed high reactivity to egg white-specific IgG, 48 (53.9%) patients had elevated serum total IgE levels, and 25 (28.1%) patients had elevated absolute eosinophil numbers. Out of the 89 egg white allergic patients, 25 showed elevated egg white-specific IgE antibody levels. Of the 25 patients who were positive for egg white-specific IgE antibody, 21 presented high sensitive reaction to egg white-specific IgG, three presented moderate sensitive reaction to egg white-specific IgG, and one presented mild sensitive reaction to egg white-specific IgG. A moderate correlation between egg white-specific IgG and egg white-specific IgE, egg white-specific IgG and absolute eosinophil number was found in the egg white allergic patients (r = 0.438, P = 0.000; r = 0.322, P = 0.002). Egg white-specific IgE levels varied in different age groups; the egg white-specific IgE concentration of younger patients (age ≤ 18 years, mean rank 54.29) was significantly higher than that of the adult patients (age > 18 years, mean rank 34.61) (Z = −3.629, P = 0.000). CONCLUSION: Egg white-specific IgE antibody could coexist with egg white-specific IgG antibody in patients suffering from egg white allergy. Aberrant changes in the concentration of egg white-specific IgE antibody were associated with the presence of egg white-specific IgG antibody

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Photocatalytic splitting of seawater effected by (Ni-ZnO)@C nanoreactors.

Novel photocatalysts i.e., metallic nickel and zinc oxide nanoparticles embedded in the carbon-shell ((Ni-ZnO)@C) have been used for photocatalytic splitting of seawater to generate H2. The (Ni-ZnO)@C core-shell nanoparticles having the Zn/Ni ratios of 0-3 were prepared by carbonization of Ni(2+)- and Zn(2+)-ß-cyclodextrin at 673 K for 2 h. To increase the collision frequency of water and photoactive sites within the carbon-shell, Ni and ZnO are partially etched from the (Ni-ZnO)@C core-shell to form yolk-shell nanoparticles with a H2SO4 solution (2N). By X-ray diffraction spectroscopy, mainly Ni and ZnO crystallites are observed in the core- and yolk-shell nanoparticles. The sizes of the Ni and ZnO in the (Ni-ZnO)@C nanoreactors are between 7 and 23 nm in diameters determined by TEM and small angel scattering spectroscopy. Under a 5-h UV-Vis light irradiation, 5.01 µmol/hgcat of H2 are yielded from photocatalytic splitting of seawater effected by (Ni-ZnO)@C nanoreactors.

Mouthguard and sports drinks on tooth surface pH.

The influence of sports drinks and mouthguards on the pH level of tooth surface was examined. A custom-made mouthguard was fabricated for each subject. The pH level was measured by electric pH meter with sensitivity of 0.01 up to 30 min. Sports drinks (pH=3.75) containing 9.4% sugar were used in this study. Measurements were performed on a cohort of 23 female subjects without a mouthguard (control), wearing a mouthguard only (MG), wearing a mouthguard after 30 ml sports drink intake (SD+MG), wearing a mouthguard during a 5-min jogging exercise (MG+EX) and wearing a mouthguard during jogging after sports drink intake (SD+MG+EX). For 7 male subjects, the same measurements were performed while a sports drink was taken over the mouthguard (MG+SD, MD+EX+SD). MG showed statistically higher pH level than control (p<0.05). SD+MG exhibited a significant decrease in pH level, and SD+MG+EX exhibited even below the critical level of pH 5.5 in some subjects. When sports drinks were taken over the mouthguard, no significant differences in pH level were observed among the different conditions.Within the limitations of this study, it was suggested that wearing a mouthguard during exercise is in itself not a possible risk factor for dental caries, while wearing a mouthguard after consuming sports drinks is.

Laboratorial characteristics of patients with diarrhoea suffering from egg white allergy.

BACKGROUND: Egg allergy is associated with diarrhoeal symptoms. However, the mechanism underlying allergic diarrhoea remains unclear. OBJECTIVE: To determine whether egg white-specific IgE antibodies coexist with egg white-specific IgG antibodies in patients with egg allergy featuring diarrhoeal symptoms, and whether there is any relationship between these two antibody types. METHODS: A total of 89 patients with egg allergy featuring diarrhoeal symptoms (average age, 23.2 years; range, 1-78 years), all of whom tested positive for egg white-specific IgG, were enrolled in this study. The concentration of total IgE, egg white-specific IgE and number of eosinophils in the serum were determined. RESULTS: Among the 89 egg white allergic patients tested, 49 (55.1%) patients showed high reactivity to egg white-specific IgG, 48 (53.9%) patients had elevated serum total IgE levels, and 25 (28.1%) patients had elevated absolute eosinophil numbers. Out of the 89 egg white allergic patients, 25 showed elevated egg white-specific IgE antibody levels. Of the 25 patients who were positive for egg white-specific IgE antibody, 21 presented high sensitive reaction to egg white-specific IgG, three presented moderate sensitive reaction to egg white-specific IgG, and one presented mild sensitive reaction to egg white-specific IgG. A moderate correlation between egg white-specific IgG and egg white-specific IgE, egg white-specific IgG and absolute eosinophil number was found in the egg white allergic patients (r=0.438, P=0.000; r=0.322, P=0.002). Egg white-specific IgE levels varied in different age groups; the egg white-specific IgE concentration of younger patients (age≤18 years, mean rank 54.29) was significantly higher than that of the adult patients (age>18 years, mean rank 34.61) (Z=-3.629, P=0.000). CONCLUSION: Egg white-specific IgE antibody could coexist with egg white-specific IgG antibody in patients suffering from egg white allergy. Aberrant changes in the concentration of egg white-specific IgE antibody were associated with the presence of egg white-specific IgG antibody.

Ruptured symptomatic internal carotid artery dorsal wall aneurysm with rapid configurational change. Clinical experience and management outcome: an original article.

BACKGROUND: Aneurysms located at non-branching sites, protruding from the dorsal wall of the supraclinoid internal carotid artery (ICA) with rapid configurational changes, were retrospectively reviewed in effort to identify and characterize these high-risk aneurysms. METHODS: A total of 447 patients with 491 intracranial aneurysms were treated from March 2005 to August 2008, and of these, eight patients had ICA dorsal wall aneurysms. Four of them suffered subarachnoid hemorrhage (SAH), and all had aneurysms undergoing rapid configuration changes during the treatment course. Digital subtraction cerebral angiography (DSA) performed soon after the SAH events. Data analyzed were patient age, sex, Hunt and Kosnik grade, time interval from first DSA to second DSA, aneurysm treatment, and modified Rankin scale score after treatment for 3 months. Success or failure of therapeutic management was examined among the patients. RESULTS: Digital subtraction cerebral angiography showed only lesions with small bulges in the dorsal walls of the ICAs. However, the patients underwent DSA again for re-bleeding or for post-treatment follow-up, confirming the SAH source. ICA dorsal wall aneurysms with rapid growth and configurational changes were found on subsequent DSA studies. CONCLUSIONS: Among the four patients, ICA dorsal wall aneurysms underwent rapid growth with configurational change from a blister type to a saccular type despite different management. ICA trapping including the lesion segment can be considered as the first treatment option if the balloon occlusion test (BOT) is successful. If a BOT is not tolerated by the patient, extracranial-intracranial bypass revascularization surgery with endovascular ICA occlusion is another treatment option.