Study of charged particle activation analysis (II): Determination of boron concentration in human blood samples.

Boron Neutron Capture Therapy (BNCT) is a radiotherapy for the treatment of intractable cancer. In BNCT precise determination of 10B concentration in whole blood sample before neutron irradiation of the patient, as well as accurate neutron dosimetry, is crucial for control of the neutron irradiation time. For this purpose ICP-AES and neutron induced prompt γ-ray analysis are generally used. In Ibaraki Neutron Medical Research Center (iNMRC), an intense proton beam will be accelerated up to 8 MeV, which can also be used for Charged Particle Activation Analysis (CPAA). Thus, in this study, we apply the CPAA utilizing the proton beam to non-destructive and accurate determination of 10B concentration in whole blood sample. A CPAA experiment is performed by utilizing an 8 MeV proton beam from the tandem accelerator of Nuclear Science Research Institute in Japan Atomic Energy Agency. The 478 keV γ-ray of 7Be produced by the 10B(p, α)7Be reaction is used to quantify the 10B in human blood. The 478 keV γ-ray intensity is normalized by the intensities of the 847 keV and 1238 keV γ-rays of 56Co originating from Fe in blood. The normalization methods were found to be linear in the range of 3.27 µg 10B/g to 322 µg 10B/g with correlation coefficients of better than 0.9999.

Expression of human cathelicidin peptide LL-37 in inflammatory bowel disease.

Cathelicidin peptide LL-37 plays an important role in the early host response against invading pathogens via its broad-spectrum anti-microbial activity. In this study, we investigated LL-37 expression in the inflamed mucosa of inflammatory bowel disease (IBD) patients. Furthermore, the regulatory mechanism of LL-37 induction was investigated in human colonic subepithelial myofibroblasts (SEMFs). LL-37 mRNA expression and protein secretion were analysed using real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. Intracellular signalling pathways were analysed using immunoblotting and specific small interference RNA (siRNA). The expression of LL-37 mRNA was increased significantly in the inflamed mucosa of ulcerative colitis and Crohn's disease. The Toll-like receptor (TLR)-3 ligand, polyinosinic-polycytidylic acid (poly(I:C), induced LL-37 mRNA expression and stimulated LL-37 secretion in colonic SEMFs. The transfection of siRNAs specific for intracellular signalling proteins [Toll/IL-1R domain-containing adaptor-inducing interferon (IFN) (TRIF), tumour necrosis factor receptor-associated factor (TRAF)6, transforming growth factor ß-activated kinase (TAK)1] suppressed the poly(I:C)-induced LL-37 mRNA expression significantly. Poly(I:C)-induced phosphorylation of mitogen-activated protein kinases (MAPKs) and activated nuclear factor kappa B (NF-κB) and activating factor protein (AP)-1. siRNAs specific for NF-κB and c-Jun inhibited poly(I:C)-induced LL-37 mRNA expression. LL-37 suppressed lipopolysaccharide (LPS)-induced interleukin (IL)-6 and IL-8 expression significantly in colonic SEMFs. The expression of LL-37 was up-regulated in the inflamed mucosa of IBD patients. LL-37 was induced by TLR-3 stimulation and exhibited an anti-microbial effect via interaction with lipopolysaccharide (LPS).

[A case of rhinofacial entomophthoromycosis in Soudano-Sahelian tropical climate in Burkina Faso]. / Un cas d'entomophthoromycose rhinofaciale en climat tropical soudano-sahélien au Burkina Faso.

We describe a rhinofacial entomophthoramycosis case in a sexagenarian (65 years old) housewife. She was immunocompetent and resident of Burkina Faso. She consulted both the service of dermatology and the service of stomatology of the Teaching Hospital of Bobo-Dioulasso in February 2016 for a diffuse facial tumefaction evolving over six months. This tumefaction was associated with headaches and a left nasal obstruction. Histological examination of the lesion showed an important and polymorphic inflammatory reaction. Also, a filamentous fungus with wide non-septated hyphae and right-angled fungal branching, consistent with mucormycosis was isolated. Mycological diagnosis based on fungal culture with Sabouraud medium without any antibiotic and cyclohexemide after incubation at 27°C and at 30°C was negative. Furthermore, it was not possible to amplify the DNA extracted from biopsy. Antifungal therapy based on the administration of fluconazole per os at 800mg/day was started allowing clinical improvement. This is the first case of a rhinofacial entomophtharomycosis documented in Bobo-Dioulasso. Rhinofacial entomophthoromycosis is largely unknown, even in tropical regions such as Burkina Faso. This lack of knowledge results in a delay in the diagnosis, and subsequently a bad prognosis. It is therefore urgent to improve knowledge on this disease to guide diagnostic steps, prognosis of outcome, and antifungal therapy.

[Multiple sites extrapodal actinomycetoma: Favorable outcome to treatment with a combination of cotrimoxazole and NSAI]. / Mycétome actinomycosique extrapodal plurifocal : bonne réponse au traitement par l'association cotrimoxazole et AINS.

Mycetoma is a bacteriological or fungal infectious disease affecting the skin and/or soft tissues, which can be complicated by bone involvement. The most common feature is a tumor of the foot, but extrapodal localizations have been described. We report one case of a 47-year-old man who presented with tumefaction of a leg with multiple skin fistulae. Histopathological examination permitted to confirm the diagnosis of actinomycetoma and TDM showed the degree of bone and soft tissues involvement. Our case was characterized by the very inflammatory aspect of the tumor, its localization to the leg without foot involvement, the modest functional signs compared to the importance of radiological bone involvements, the deep destruction of the fibula while the tibia was apparently intact and the good response to treatment. In spite of its characteristic features, diagnosis of mycetoma is still late in our country, often with bone and/or articular spread. Priority may be given to measures for reduction of mycetoma diagnosis lateness.

[Cryptococcosis: a potential aetiology of facial ulceration]. / La cryptococcose: une étiologie potentielle d'ulcération faciale.

UNLABELLED: Cutaneous cryptococcosis is an uncommon aetiology of chronic facial ulceration but which may be associated to a potentially lethal focus of cryptococcosis. OBSERVATION: A 35-year-old AIDS patient under antiretroviral therapy, presented with a chronic facial ulceration. Histopathological examination of a biopsy of the facial ulceration showed an inflammatory granuloma and masses of yeasts. Mycological culture of the cerebrospinal fluid revealed Cryptococcus neoformans. The diagnosis of AIDS-related cutaneous cryptococcosis of the face and cryptococcal meningitis was concluded. DISCUSSION: Cryptococcosis should be thought as a potential aetiology of a chronic facial ulceration in an AIDS patient. Screening of other foci of the cryptococcosis such as that of the central nervous system is mandatory. Mycological examinations are of great interest for the diagnosis in rare resources setting.

Seroprevalence of latent Toxoplasma gondii infection among HIV-infected pregnant women in Bobo-Dioulasso, Burkina Faso.

The deficit of cellular immunity, as found in HIV infected individuals, may lead to the reactivation of latent Toxoplasma gondii cysts, with as consequence, the occurrence of toxoplasmosis and an eventual vertical transmission of the disease during pregnancy. The present study was designed for determining the occurrence of latent Toxoplasma gondii among HIV-infected pregnant women during the first trimester in Bobo-Dioulasso. Thus, 348 pregnant women aged from 17 to 47 years (average age of 6.64 ± 4.75 yaers) were enrolled. The specific anti-Toxoplasma gondii IgG and IgM antibodies were quantified from whole blood specimens using the high-sensitivity direct agglutination and the enzyme linked fluorescent assays, respectively, the IgG avidity test being used for the dating of the primary infection. The results revealed that the seroprevalence of Toxoplasma gondii latent infection was 34.7%. It was significantly higher in HIV-infected women compared with uninfected ones (68,7%; CI 95%: 43,6%-88,9%) versus (33,1%; CI 95%: 28, 2%-38,3%). In addition, all the occurrences of the high IgG avidity were closely linked with the presence of IgM. These results underlined the need for the clinical follow-up of the maternal HIV diseases including the toxoplasmosis during the pregnancy since; the newborns are still exposed to vertical transmission of Toxoplasma infection in endemic areas like Burkina Faso.

Epithelial expression of interleukin-37b in inflammatory bowel disease.

Interleukin (IL)-37 is a member of the IL-1 cytokine family. We investigated IL-37b expression in the inflamed mucosa of inflammatory bowel disease (IBD) patients. Furthermore, we analysed IL-37b expression in human colonic epithelial cells. The human colonic epithelial cell line T84 and human colonic subepithelial myofibroblasts (SEMFs) were used. IL-37b expression in the IBD mucosa was evaluated by immunohistochemistry. IL-37b mRNA and protein expression were determined by real time-polymerase chain reaction (PCR) and Western blotting, respectively. IL-37b was not detected in the normal colonic mucosa. In the inflamed mucosa of IBD patients, epithelial IL-37b expression was increased markedly. In ulcerative colitis (UC) and Crohn's disease (CD) patients, IL-37b expression was enhanced in the affected mucosa. In the intestinal epithelial cell line T84, the expression of IL-37b mRNA and protein was enhanced by tumour necrosis factor (TNF)-α. This IL-37b induction by TNF-α was mediated by nuclear factor (NF)-κB and activator protein (AP)-1 activation. Furthermore, IL-37b inhibited TNF-α-induced interferon-γ-inducible protein (IP)-10 expression significantly in human colonic SEMFs. Epithelial IL-37b expression was increased in IBD patients, especially UC patients. IL-37b may be involved in the pathophysiology of IBD as an anti-inflammatory cytokine and an inhibitor of both innate and acquired immune responses.

[Retrospective study of cases of neuromeningeal cryptococcosis at the University Hospital of Bobo Dioulasso since accessibility to antiretroviral in Burkina Faso]. / Étude rétrospective des cas de cryptococcose neuroméningée au centre hospitalier universitaire de Bobo Dioulasso depuis l'accessibilité aux antirétroviraux au Burkina Faso.

AIMS OF THE STUDY: To study the prevalence of neuromeningeal cryptococcosis since the availability of antiretroviral drugs and to determine the epidemiological profiles, clinical and biological treatment of neuromeningeal cryptococcosis cases diagnosed in the service of parasitology and mycology of university hospital center of Bobo-Dioulasso from 2002 to 2010. PATIENTS, MATERIAL AND METHODS: We included all patients diagnosed with neuromeningeal cryptococcosis for which the presence of the fungi was observed on microscopic examination of cerebrospinal fluid after staining with Indian ink. Data were collected from the registers of the clinical service and from the laboratory of the university hospital center of Bobo Dioulasso. RESULTS: The prevalence of neuromeningeal cryptococcosis was 1.8% (61/5129). A decrease in the prevalence was observed from 2002 to 2010 (3.1%, to 0.2%). This decrease occurred even though the number of patients treated with antiretroviral drugs increase. Headaches were the predominant clinical signs (81.9%). The CD4 median count was 56/mm(3). All patients were successfully treated with fluconazole in relay to amphotericin B intravenous. Lethality rate is 27.8%. CONCLUSION: The overall prevalence of 1.8% of neuromeningeal cryptococcosis observed in this study was lower than that in previous studies in the same laboratory in 2001. The arrival of antiretroviral drugs could have contributed to the decline in the prevalence of neuromeningeal cryptococcosis in this study.

[Mansonelliasis identified by a cervicovaginal smear at the university hospital center of Bobo-Dioulasso (Burkina Faso)]. / Frottis cervicovaginal révélant une mansonellose au centre hospitalier universitaire de Bobo-Dioulasso, Burkina Faso

INTRODUCTION: Mansonella perstans is a genus of filaria that is often asymptomatic or responsible for unspecific symptoms. M. perstans microfilariae are uncommon on cervicovaginal smears. CASE: We report the case of a woman with pruritis and eosinophilia. Microfilariae of M. perstans were observed on both cervicovaginal and blood smears. The patient was successfully treated with a combined single dose of 400 mg of albendazole and ivermectin (150 µg/kg). CONCLUSION: We described here an atypical and rare localization of M. perstans. The routine examination of cervicovaginal smears of women admitted to Bobo-Dioulasso Hospital for screening of cervical neoplasia should allow us to determine the frequency of this parasitosis and propose appropriate treatment.

Bone marrow transplantation ameliorates pathology in interleukin-10 knockout colitic mice.

The authors have previously reported the derivation of colonic subepithelial myofibroblasts (SEMFs) in both humans and mice from bone marrow (BM). In the pathogenesis of inflammatory bowel disease (IBD), such as Crohn's disease and ulcerative colitis, colonic SEMFs mediate several types of inflammatory response. In the present study, interleukin (IL)-10-/- mice were used as a model of IBD to investigate the involvement of BM-derived cells in the inflamed mucosa. Male whole BM [either C57/BL10 (wild type: WT) or IL-10-/- donor mice] was used to perform bone marrow transplantation (BMT) into both WT and IL-10-/- female mice. Tissue samples were evaluated by immunohistochemistry for alpha-smooth muscle actin expression and by in situ hybridization using a Y-chromosome-specific probe to track the donor-derived colonic SEMFs. The mucosal expression of mRNA for pro-inflammatory cytokines was analysed by reverse transcriptase-polymerase chain reaction (RT-PCR). In addition, mRNA expression of matrix metalloproteinase (MMP)-7 and osteopontin in the inflamed mucosa was assessed using in situ hybridization. Body weights and histological scores showed that IL-10-/- mice that received WT BM had an improved course of colitis, decreased mucosal pro-inflammatory mRNA expression, and up to 30% of their SEMFs were of BM origin. Conversely, IL-10-/- mice receiving IL-10-/- BM progressed to extensive colitis, and Y probe analysis revealed that up to 45% of colonic SEMFs were of BM origin. WT mice receiving IL-10-/- or WT BM had no signs of colonic inflammation. The expression of MMP-7 and osteopontin was up-regulated in the inflamed mucosa. In conclusion, IL-10-/- mice displayed ameliorated disease activity after WT BMT, whilst colitis was not induced in WT mice by IL-10-/- BMT. The contribution of BM-derived cells to colonic SEMFs was significantly increased in the inflamed mucosa compared with non-inflamed mucosa.

Increased expression of interleukin 17 in inflammatory bowel disease.

BACKGROUND AND AIM: Interleukin (IL) 17 is a cytokine which exerts strong proinflammatory activities. In this study we evaluated changes in IL-17 expression in the inflamed mucosa and in the serum of patients with inflammatory bowel disease (IBD). METHODS: Tissue samples were obtained endoscopically or surgically from patients with ulcerative colitis (UC) (n=20), Crohn's disease (CD) (n=20), infectious colitis (n=5), ischaemic colitis (n=8), and normal colorectal tissues (n=15). IL-17 expression was evaluated by a standard immunohistochemical procedure. Serum IL-17 levels were determined by ELISA. IL-17 mRNA expression was analysed by reverse transcriptase-polymerase chain reaction. RESULTS: IL-17 expression was not detected in samples from normal colonic mucosa, infectious colitis, or ischaemic colitis. In the inflamed mucosa of active UC and CD patients, IL-17 expression was clearly detectable in CD3(+) T cells or CD68(+) monocytes/macrophages. The average number of IL-17(+) cells was significantly increased in active UC and CD patients compared with inactive patients. IL-17 mRNA expression was not detected in normal mucosa but was detectable in the mucosa from active UC and CD patients. IL-17 was not detected in the sera from normal individuals, infectious colitis, or ischaemic colitis patients but IL-17 levels were significantly elevated in IBD patients. CONCLUSIONS: IL-17 expression in the mucosa and serum was increased in IBD patients. It is likely that IL-17 expression in IBD may be associated with altered immune and inflammatory responses in the intestinal mucosa.

Interleukin-1beta and tumor necrosis factor-alpha induce chemokine and matrix metalloproteinase gene expression in human colonic subepithelial myofibroblasts.

BACKGROUND: Colonic subepithelial myofibroblasts may play a role in the inflammatory responses and in extracellular matrix (ECM) metabolism. In this study, we investigated the effects of interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha on chemokine (IL-8 and monocyte chemoattractant protein (MCP)-1) and ECM turnover (proliferation of subepithelial myofibroblasts, and secretion of ECM and matrix metalloproteinases (MMPs)) in colonic subepithelial myofibroblasts. METHODS: Human colonic subepithelial myofibroblasts were isolated using the method described by Mahida et al. Chemokine and MMP expressions were determined by ELISA and Northern blotting. Nuclear factor (NF)-kappaB and NF-IL6 DNA binding activities were evaluated by electrophoretic gel mobility shift assays (EMSA). RESULTS: IL-1beta and TNF-alpha did not affect the proliferation of subepithelial myofibroblasts, but stimulated the secretion of types I and IV collagens weakly. Unstimulated subepithelial myofibroblasts secreted a large amount of MMP-2, but a small amount of IL-8, MCP-1 and MMP-1. IL-1beta and TNF-alpha both induced a dose- and time-dependent increase in IL-8, MCP-1 and MMP-1 secretion, and weakly stimulated MMP-2 secretion. IL-1beta and TNF-alpha both rapidly evoked NF-kappaB DNA-binding activity. The inhibition of NF-kappaB activation markedly blocked both IL-1beta- and TNF-alpha-induced IL-8 and MCP-1 mRNA expression, but did not affect MMP-1 mRNA expression. CONCLUSIONS: These observations indicate that chemokine secretion and ECM metabolism are collectively regulated by the proinflammatory cytokines, IL-1beta and TNF-alpha, in colonic subepithelial myofibroblasts. Thus, colonic subepithelial myofibroblasts may play an important role in the pathophysiology of inflammation in the colon.

Cooperation of interleukin-17 and interferon-gamma on chemokine secretion in human fetal intestinal epithelial cells.

Interleukin (IL)-17 is a newly identified T cell-derived cytokine that can regulate the functions of a variety of cell types. In this study, we investigated the effects of IL-17 and interferon (IFN)-gamma on chemokine secretion in human fetal intestinal epithelial cells. IL-8 and monocyte chemoattractant protein (MCP)-1 secretion by the human fetal intestinal epithelial cell line, intestine-407, was evaluated by ELISA and Northern blot. The expression of IL-17 receptor (R) was analysed by a binding assay using [(125)I]-labelled IL-17. The activation of nuclear factor-kappa B (NF-kappa B), NF-IL6 and AP-1 was assessed by an electrophoretic gel mobility shift assay (EMSA). IL-17 induced a dose-dependent increase in IL-8 and MCP-1 secretion. The inducing effects of IL-17 on IL-8 and MCP-1 mRNA abundance reached a maximum as early as 3 h, and then gradually decreased. IL-17 and IFN-gamma synergistically increased IL-8 and MCP-1 secretion and mRNA abundance. IFN-gamma induced a weak increase in IL-17 R mRNA abundance, and incubation with IFN-gamma for 24 h enhanced [(125)I]-labelled IL-17-binding by 2.4-fold. IL-17 rapidly induced the phosphorylation and degradation of I kappa B alpha molecules, and the combination of IL-17 and IFN-gamma induced a marked increase in NF-kappa B DNA-binding activity as early as 1.5 h after the stimulation. Furthermore, this combination induced an increase in NF-IL-6 and AP-1 DNA-binding activity. In conclusion, it becomes clear that IL-17 is an inducer of IL-8 and MCP-1 secretion by human fetal intestinal epithelial cells. The combination of IL-17 with IFN-gamma synergistically enhanced chemokine secretion. These effects of IL-17 and IFN-gamma might play an important role in the inflammatory responses in the intestinal mucosa.