Post-flood--infectious diseases in Mozambique

INTRODUCTION: The types of medical care required during a disaster are determined by variables such as the cycle and nature of the disaster. Following a flood, there exists the potential for transmission of water-borne diseases and for increased levels of endemic illnesses such as vector-borne diseases. Therefore, consideration of the situation of infectious diseases must be addressed when providing relief. The Japan Disaster Relief (JDR) Medical Team was sent to Mozambique where a flood disaster occurred during January to March 2000. The team operated in the Hokwe area of the State of Gaza, in the mid-south of Mozambique where damage was the greatest. METHODS: An epidemiological study was conducted. Information was collected from medical records by abstracting data at local medical facilities, interviewing in habitants and evacuees, and conducting analyses of water. RESULTS: A total of 2,611 patients received medical care during the nine days. Infectious diseases were detected in 85% of all of patients, predominantly malaria, respiratory infectious diseases, and diarrhea. There was no outbreak of cholera or dysentery. Self-reports of the level of health decreased among the flood victims after the event. The incidence of malaria increased by four to five times over non-disaster periods, and the quality of drinking water deteriorated after the event. CONCLUSIONS: Both the number of patients and the incidence of endemic infectious diseases, such as malaria and diarrhea, increased following the flood. Also, there was a heightening of risk factors for infectious diseases such as an increase in population, deterioration of physical strength due to the shortage of food and the temporary living conditions for safety purposes, and turbid degeneration of drinking water. These findings support the hypotheses that there exists the potential for the increased transmission of water borne diseases and that there occurs increased levels of endemic illnesses during the post-flood period.     

The evaluation of early embryonic neurogenesis after exposure to the genotoxic agent 5-bromo-2'-deoxyuridine in mice

Developmental neurotoxicity (DNT) is an important issue in children's health. Neurogenesis occurs throughout the early fetal to the postnatal period. The proliferation of embryonic stem cells can be a target for toxicants, especially genotoxic compounds. 5-Bromo-2'-deoxyuridine (BrdU), a thymidine analogue, has been used as a marker for proliferating cells. However, we reported that prenatal BrdU exposure induced behavioral abnormalities such as hyperactivity in rat and mouse offspring. In this study, to further clarify the toxic effect of BrdU on the early neurogenesis and to examine the usefulness of the evaluation of this process in DNT, C57BL/6 mice were exposed to 100 mg/kg of BrdU once on gestational day (GD) 9 or 11, and serial sections from a wide variety of areas of the embryonic brains 24 h after the exposure were examined. BrdU exposure on GD11 induced cell death in some specific areas, such as the neocortex and striatum, but not in the substantia nigra, raphe and pons, even though BrdU was incorporated into those cells. BrdU decreased the number of cells positive for phosphorylated histone 3 (phospho-histone 3), a marker for proliferating cells at metaphase of mitosis, in the cortex, mammillary body and cerebellum, suggesting that BrdU affected the proliferation of neural stem cells. Exposure on GD9 did not induce cell death in the fetal brain. These results indicate that BrdU actually impaired the early neurogenesis, supporting the postnatal results, and demonstrated that embryonic neurogenesis has heterogeneous sensitivity to the genotoxic agents BrdU that differs according to the area and developmental stage. The evaluation of events in early neurogenesis such as the proliferation of neural stem cells shortly after chemical exposure will be one of the valuable endpoints for studying postnatal neurodevelopmental disorders.     

Which Has Superior Acid-Suppressive Effect, 10 Mg Omeprazole Once Daily or 20 Mg Famotidine Twice Daily? Effects of Single or Repeated Administration in Japanese <Emphasis Type="Italic">Helicobacter Pylori</Emphasis>-Negative CYP2C19 Extensive Metabolizers

Low-dose omeprazole is superior to full-dose famotidine in maintenance therapy for gastroesophageal reflux disease, whereas “on-demand” famotidine is more effective for relief of episodes of heartburn. To explain this apparent discrepancy, intragastric pH was measured for 24-hr seven times in eight Japanese Helicobacter pylori-negative cytochrome P450 2C19 extensive metabolizers; on Days 1, 8, and 15 of repeated administration of 10 mg of omeprazole once daily and of 20 mg of famotidine twice daily and before medication. During repeated administration of omeprazole, mean intragastric pH and % time that intragastric pH > 4.0 were significantly higher and became greater. With famotidine, although these parameters were significantly higher, the degrees became smaller. Consequently, acid-suppressive effect was in the order; omeprazole < famotidine on Day 1, omeprazole≈famotidine on Day 8, and omeprazole >famotidine on Day 15. This discrepancy possibly results from the “potentiation” of acid-suppressive effect of omeprazole and the “tolerance” phenomenon in respect to famotidine.     

Determination of total cefozopran concentrations in human peritoneal fluid by HPLC with cefepime as an internal standard: Comparative pharmacokinetics in the fluid and plasma

A simple, rapid and precise HPLC method using ultrafiltration to remove protein was developed to determine total cefozopran concentrations in human peritoneal fluid in the same manner as in human plasma, irrespective of the amount of protein. The recovery of cefozopran after ultrafiltration in peritoneal fluid was higher than that in plasma, because the protein content in peritoneal fluid was lower than that in plasma. Furthermore, it was found that an internal standard with a similar protein-binding ratio to cefozopran could revise the cefozopran loss by ultrafiltration in plasma and peritoneal fluid samples irrespective of the amount of protein. Therefore, it was concluded that cefepime may be used as an internal standard. Cefozopran and cefepime were detected by measuring their ultraviolet absorbances at 235 nm. The calibration curve obtained for cefozopran in peritoneal fluid was linear from 0.2 to 200 μg/ml. The intraday and interday precisions were less than 5.77% (CV), and the accuracy was between 96.3% and 108% above 0.2 μg/ml. The lower limit of detection was 0.05 μg/ml in peritoneal fluid, which was the same as that in plasma. The assay has been applied to therapeutic drug monitoring of cefozopran in both plasma and peritoneal fluid and has contributed to peritoneal pharmacokinetic studies in patients.     

Oxidative stress in neurodegeneration in dentatorubral-pallidoluysian atrophy

Dentatorubral-pallidoluysian atrophy (DRPLA) is one of the CAG-repeat diseases, and is classified into juvenile and early adult types showing progressive myoclonus epilepsy (PME) in addition to late adult type. We immunohistochemically examined accumulation of oxidative products and expression of superoxide dismutase (SOD) in autopsy cases of DRPLA. Oxidative products to nucleosides, 8-hydroxy-2'-deoxyguanosine and 8-hydroxyguanosine, were accumulated in the lenticulate nucleus predominantly in DRPLA cases having PME. Neuronal accumulation of 4-hydroxy nonenal, a reactive lipid aldehyde, was found in the hippocampus, globus pallidus and cerebellar dentate nucleus in adult DRPLA cases and controls. Cytoplasmic immunoreactivity for Cu/ZnSOD was reduced in the external segment of globus pallidus, dentate nucleus and cerebellar cortex in DRPLA cases. Mitochondrial immunoreactivity for MnSOD was reduced in the lenticulate nucleus and cerebellum in DRPLA cases having PME. Some DRPLA cases showed reduced immunoreactivity for MnSOD in the cerebral cortex. Coexistence of reduced SOD expression and polyglutamine was observed in a few cases. It has been discussed in Huntington's disease that expanded polyglutamine can lead to oxidative neurodegeneration. It is likely that oxidative stress can be involved in DRPLA, although relationship with expanded polyglutamine remains to be elusive.