The fates of trichothecene mycotoxins, nivalenol and fusarenon-X, in mice

In order to investigate the comparative fates of nivalenol (NIV) and 4-acetyl derivative of NIV (fusarenon-X, FX) in mice, ³H-FX or ³H-NIV was given p.o. to mice. Radioactivity was excreted mainly via the urine in mice given ³H-FX, but mainly via the feces in mice given ³H-NIV. The plasma radioactivity reached a peak at 30 or 60 min after the administration of ³H-FX or ³H-NIV, respectively. The plasma peak level was 5 times higher, and the area under curve (AUC) was 10 times higher, in ³H-FX-administered than ³H-NIV-administered mice. These findings clearly demonstrate that FX is absorbed from the gastrointestinal tract more rapidly and efficiently than NIV. The HPLC profile of radioactivity of acetonitrile extracts of urine and feces indicated that FX is rapidly metabolized to NIV after being absorbed from the gastrointestinal tract. In vitro incubation of tissue homogenates with ³H-FX demonstrated that the liver and kidney are the organs responsible for the FX-to-NIV conversion. Thus this study demonstrated that the higher oral toxicity of FX than NIV that has been observed in mice and rats is due to the efficient absorption of FX than NIV from the gastrointestinal tract, followed by its rapid conversion to NIV by the liver and kidney.     

Development of early apopotosis and changes in lymphocyte subsets in lymphoid organs of mice orally inoculated with nivalenol

Development of early apoptosis and changes in lymphocyte subsets were examined in lymphoid organs of female BALB/c mice after oral administration of 15 mg/kg b.w. of nivalenol (NIV), the major type B trichothecene mycotoxin, by FACS analysis. Judging from the results of viable cell count and apoptotic cell index, NIV attacked Peyer's patches first and thymus most severely. In thymus, selective damage in CD4(+)CD8(+) cells was observed at 12 and 24 h after inoculation (HAI), following the peak of apoptosis at 9 HAI. CD4(+) cells were clearly suppressed at 3 HAI in Peyer's patches, at and after 9 HAI in mesenteric lymph nodes, and 3 to 12 HAI in spleen, respectively. CD8(+) cells were also suppressed at 24 HAI in mesenteric lymph nodes and at 12 HAI in spleen, respectively. As to changes in B cell subsets, IgG(+) cells significantly decreased from 3 to 12 HAI and all B cell subsets at 24 HAI in mesenteric lymph nodes. In spleen, IgM(+) cells were suppressed at 9 HAI. On the other hand, in Peyer's patches, following clear decrease in the numbers of pan-T and pan-B cells and viable cells at 3 HAI, all B cell subsets, especially IgA(+) cells, showed a significant increase in their numbers at 9 HAI, and the numbers of IgA(+) and IgM(+) cells remained higher values than controls thereafter. Taken together, in the course of recovery from NIV-induced prominent damage in Peyer's patches at 3 HAI, interaction of NIV with Peyer's patches might result in in vivo stimulation of interleukin production at this site and result in increased proliferation and differentiation of IgA-secreting B cells at and after 9 HAI.     

Viral hepatitis infections among dialysis patients: Thailand registry report

BACKGROUND: Patients on dialysis are at high risk of acquiring viral hepatitis infections. However, there were only few data from Thailand. The aim of the present study was to assess the prevalence, incidence and associated risk factors of viral hepatitis infections among dialysis patients. METHODS: A retrospective study was conducted to evaluate 5179 medical records of dialysis patients from the Thailand Renal Replacement Therapy Registry. RESULTS: In 2002, the seroprevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections were 6.3% (n = 2454) and 4.8% (n = 2167), respectively. HBV and HCV seroprevalence became 6.5% (n = 2585) and 4.3% (n = 2399) in 2003. The incidence of HBV and HCV infections were 1.5 and 2.4 cases per 1000 patient-years, respectively. Logistic regression analysis showed that age and gender were significant risk factors for HBV infection, but not for HCV infection. CONCLUSION: In Thailand, it was not uncommon for dialysis patients to acquire viral hepatitis infections. However, our prevalence is similar to reports from some other South-East Asian countries.     

Predetermining glenoid dimensions using the scapular dimensions

European Journal of Orthopaedic Surgery & Traumatology - Variations of morphology of the glenoid cavity have been previously reported. These influence the surgical reconstruction or...     

Management of alveolar clefts

The management of alveolar clefts has changed through the years as medical knowledge has improved. An alveolar cleft is the result of abnormal primary palate formation during weeks 4 to 12 of gestation. The rationale for its closure includes 1) stabilizing the maxillary arch, 2) permitting support for tooth eruption, 3) eliminating oronasal fistulae, and 4) providing improved esthetic results. Methods for closure of the alveolar cleft have been solidified during the last century with the use of bone grafting. Secondary bone grafting is now the preferred method of treatment, because early grafting has proven detrimental to midfacial growth. Various materials for bone grafting have been proposed, including iliac crest, cranium, tibia, rib, and mandibular symphysis. Regardless of the timing and materials used, the main principles in approaching alveolar clefts have been well described. They include 1) appropriate flap design, 2) wide exposure, 3) nasal floor reconstruction, 4) closure of oronasal fistula, 5) packing bony defect with cancellous bone, and 6) coverage of bone graft with gingival mucoperiosteal flaps. Certain alveolar clefts are difficult to manage by grafting alone, and orthodontic preparation may be required. Complications of alveolar bone grafts include donor site morbidity as well as graft exposure and loss.     

Placental and milk transmission of trichothecene mycotoxins, nivalenol and fusarenon-X, in mice.

In order to investigate the transfer of nivalenol (NIV) and fusarenon-X (FX) from pregnant to fetal mice and from lactating to suckling mice, (3)H-NIV or (3)H-FX was given p.o. to pregnant or lactating mice. Radioactivity was detected in the whole fetal tissues as well as the fetal liver and kidney, the levels being comparable to those of the maternal tissues. Radioactivity was also detected in the milk, and liver and kidney tissues taken from suckling mice of both (3)H-NIV or (3)H-FX administered dams. HPLC analysis of fetal tissue homogenates from non-labeled FX- or NIV-administered pregnant mice revealed transmission of NIV to fetuses after administration of either toxin. In mice given the non-labeled FX, major and minor peaks of NIV and FX on HPLC were noted in suckling pup tissue homogenates. The results demonstrate that NIV transfers in unchanged form to fetal or suckling mice via placenta or milk, respectively, and that FX does so mainly after being metabolized to NIV in maternal body.