Development of a Method for Measuring the Ozone Concentration in the Atmosphere Using Passive Method
1. Introduction Passive method is widely used for measuring air pollutant for one day to several weeks. This method can be used easily and doesn’t need electricity, but expensive devices are needed for measuring substances, so this is not suitable for high school students for measuring or investigating. Then, we focused on the reaction, in which Indigo, the blue pigment, is discolored by ozone, and we built up a hypothesis, that indigo is suitable for measuring ozone concentration. 2. Experimental Section We soaked a 10 mm×20 mm filter paper in an indigo solution, including hosphoric acid. Then, they were dried in an automatic oven. 5.5 cm×10 cm PTFE sheet was fold in two and five sheets of indigo filters were fixed inside (passive sampler). The passive samplers were fixed on a stand and exposed to ozone in the atmosphere. After a few days, we collected the samplers and put each indigo filter and 4.0 mL of ion-exchange water into sample tubes. Then we shook this and extracted the color pigment. We had the average value of 600 nm from the five sheets as a measure value. 3. Results and Discussion The total amount of ozone for one to seven days measured in the experiment was directly proportional to the amount of ozone measured by Osaka Prefecture. We found that we can measure ozone in atmosphere using our method. Passive method has an advantage: it can be carried out easily. We employed this trait and measured ozone concentration at 23 points simultaneously in the north of Osaka for 48 hours. We made the map of ozone concentration by marking on a blank map. The map we made was just like the map published by Osaka Prefecture. We expect that this method will be useful in measuring ozone, where measuring devices are not available. 4. Conclusion We succeeded developing new method for measuring ozone in the atmosphere by passive method using indigo, the blue pigment.
Up the Creek
After an annual swimming rally in the Nahoon river, concerns were raised after several swimmers fell ill, complaining of possible symptoms of mild E.coli infection. Research was hence conducted to determine the following: \r \r \r The Nahoon River is safe for recreational activity in terms of faecal-coliforms and E.coli \r \r \r Whether the amount of rainfall affects these levels. \r \r \r If faecal pollution is present, to determine the possible point sources of the pollution \r \r \r To devise a method that needs no assistance from a laboratory, and could be done in a home environment at low cost. \r \r \r \r Procedures \r Colilert-18, (the reagent) contains nutrients which react to faecal-coliforms and E.coli in the sample. It causes samples to change colour when contamination is present. A dilution method (used by the Kowie Catchment Campaign) was used to test the severity of the contamination. The dilution levels were as follows: 1, 1/10, 1/100 and 1/1000. A control test was also performed. One Colilert capsule was divided among the five samples, which were incubated in a household stove at 37ºC for 18 hours. A sample was collected every four days and after heavy rainfall. \r The results were rated on a severity scale of 0-4, where a two was considered unsafe for recreational activity. If the undiluted sample remained clear, it was ra ted 0, if all the samples changed colour, it was rated as a four. The same rating system was used when fluorescing samples to test for E.coli. The daily rainfall level was compared to the levels of faecal-coliforms and E.coli. \r Conclusion \r As it has high levels of faecal coliforms and E.coli, the Nahoon River is not safe for recreational activity on a daily basis. \r Heavy rainfall causes the levels of E.coli and faecal coliforms to rise. \r The major source of the contamination is a stream entering the river from a newly developed settlement, and not a leaking sewer. \r This experiment has developed cost-effective home environment testing method which could be used in researching other rivers, marine environments, recreational waters and even drinking water by community researc
Expression of TRPV5 in Astrocytes: Implications for Ischemic Stroke
Elevation of intracellular calcium secondary to increased calcium influx along with increased gliosis are implicated in the pathogenesis of focal ischemic stroke. In astrocytes, which play a major role in maintaining homeostasis in brain ischemia, the identities of the ion channels responsible for increased calcium influx during ischemia is relatively unknown although several Ca2+-permeable transient receptor potential (TRP) channels have been identified to have contributing roles. The transient receptor potential vanilloid 5 (TRPV5) channel is a Ca2+-permeable cationic channel expressed primarily in kidney epithelial cells and at low levels in the brain, but the exact localization and role this channel plays in the brain has not been explored. To investigate the possible role TRPV5 plays in astrocytic calcium influx in ischemia, we examined the functional expression of TRPV5 in astrocytes subjected to hypoxia-ischemia in vitro and in rat models of ischemic stroke in vivo. We hypothesize that TRPV5 contributes to increased calcium influx in ischemia. By treating astrocytes with culture conditions without glucose and with low oxygen levels, we found that TRPV5 is upregulated with increasing durations of simulated hypoxia-ischemia in vitro. Similarly, rat models of ischemic stroke with middle cerebral artery occlusion also show TRPV5 upregulation in reactive astrocytes, suggesting a possible role of TRPV5 in reactive gliosis in vivo. Microfluorimetric intracellular calcium imaging using Fura-2 on primary cultured astrocytes show a voltage-independent increase in astrocytic calcium influx after hypoxia-ischemia in vitro that is selective for extracellular Ca2+ concentration and is reduced by inhibition of TRPV5 with ruthenium red. Electrophysiology measurements using the whole-cell patch clamp technique on primary cultured astrocytes reveal a non-selective cation current similar to that of TRPV5 that is inhibited by Mg2+, another inhibitor of TRPV5. Preliminary results on astrocyte cell viability during hypoxia-ischemia with TRPV5 inhibition by ruthenium red also suggest that inhibition of TRPV5 could enhance astrocyte survival and reactive gliosis in vitro, indicating a beneficial role in blocking non-selective Ca2+ entry via TRPV5 into astrocytes. Since TRPV5 is highly selective for Ca2+ and an important channel for Ca2+ absorption in various epithelial cells, TRPV5 upregulation may contribute significantly to elevated Ca2+ influx in astrocytes in hypoxia-ischemia. Also, Ca2+ influx has been demonstrated to play a crucial role in reactive gliosis, further suggesting that TRPV5 upregulation is involved in reactive gliosis. We propose that TRPV5 is involved in ischemia-induced calcium influx in astrocytes, and might participate in the pathogenesis of focal ischemic stroke.