Tiesuolalogistiikka

Tämän opinnäytetyön tilaajana toimii YIT Rakennus Oy. Opinnäytetyö on kehittämisprojekti, jonka tavoitteena on tuottaa tilaajalle visuaalinen hallintajärjestelmä tiesuolan materiaalivirtojen seuraamiseen. Työn lähteenä on käytetty Liikenneviraston julkaisemaa materiaalia teiden kunnossapidosta sekä YIT:n eri työmaiden tuottama dataa teiden kunnossapidosta. Kehittämisprojektin lähtötietoina käytetään olemassa olevaa dataa tiesuolasta, lisäksi projektissa kartoitetaan uusia tapoja hyödyntää olemassa olevaa dataa, yhdenmukaistetaan eri työmaiden käytäntöjä kerätä dataa sekä tuodaan mahdollisuus koko organisaatiolle hyödyntää kerättyä dataa. Työssä kerrotaan myös yleisten teiden kunnossapidosta, teiden hoitoluokista, liukkaudentorjunnasta suolaamalla sekä tiesuolan varastoinnista, kuljetuksesta sekä materiaalivirtojen hallinnasta yleisesti. Työn tuloksena on syntynyt uusi hallintajärjestelmä tiesuolan materiaalivirtojen hallintaan sekä uusia toimintatapaehdotuksia liukkaudentorjuntamateriaalien hallinnasta kerättävään dataan.This Bachelor´s thesis was commissioned by YIT Construction Ltd. The purpose of the thesis was to develop a visual control system to follow the materials flow of the ice-control salt. Another aim was to explore new ways to utilize the existing data, standardize the practice of different construction sites to collect data and provide the organization with the possibility to utilize the collected data. The sources used in the thesis were the existing data and studies on the topic including the material published by Finnish Transport Agency and the data provided by YIT´s various construction sites on road maintenance. This thesis also discusses general road maintenance, road maintenance classes, antiskid treatment through ice-control salt, storage of ice-control salt, transportation and general material flow management. As a result of the thesis a new management system for the management of road salt material flows was produced. The thesis also includes suggestions for the control of ice-control salt material

<i>cis</i>-UCA does not ameliorate colitis in IL-10^−/− mice.

<p>129Sv/EV IL-10^−/− mice were injected subcutaneously along the dorsal axis every 2 days for 24 days with either 5 or 50 µg <i>cis</i>-UCA, or vehicle (PBS) (n = 5–8). Mice were weighed every second day. <i>cis</i>-UCA had no effect on colonic histological score (A), weight/length ratio (B), MPO levels (C), or IL-17A levels (D). <i>cis</i>-UCA (50 µg) did reduce levels of colonic IFNγ in IL-10^−/− mice as compared with PBS or <i>cis</i>-UCA (5 µg) treated (E). *: p<0.05 UCA (50 µg) compared with PBS or UCA (5 µg).</p

<i>cis</i>-UCA (50 µg) ameliorates dextran sodium sulfate (DSS)-induced disease in 129Sv/Ev mice.

<p>129Sv/Ev mice were treated with 5% DSS for 7 days to induce acute colitis. Beginning on the first day of DSS administration mice were injected subcutaneously along the dorsal axis daily for 7 days with either 5 or 50 µg <i>cis</i>-UCA, or vehicle (PBS). Measurements were taken on Day 7. DSS treatment induced weight loss in mice, and this was attenuated by treatment with <i>cis</i>-UCA (50 µg). Mice receiving <i>cis-</i>UCA and DSS at the low dose (5 µg) had a transient increased weight loss compared with mice receiving the high dose of <i>cis-</i>UCA and DSS at days 1 and 2 (A). Total colonic disease activity score (DIA) was reduced by <i>cis</i>-UCA (50 µg) treatment (B). DSS treatment increased the colonic weight/length ratio, and this was prevented by treatment with <i>cis</i>-UCA (50 µg). Mice receiving the low dose of <i>cis-</i>UCA had a reduced weight/length ratio compared with PBS-treated and <i>cis-</i>UCA (50 µg) mice (C). DSS treatment increased levels of the chemokine, CXCL1, in colonic tissue, and this was attenuated by <i>cis</i>-UCA (50 µg) treatment (D). Total tissue levels of myeloperoxidase (MPO) were significantly increased in <i>cis-</i>UCA (5 µg) + DSS treated mice (E). n = 5–25 mice for all measurements. †: p<0.05 UCA (50 µg) compared with UCA (5 µg); *: p<0.05 UCA (50 µg) compared with PBS. a: p<0.01 UCA (50 µg) compared with PBS; b: p<0.01 Control UCA (5 µg) compared with control PBS, control UCA (50 µg), PBS+DSS, DSS+UCA (5 µg), and DSS+UCA (50 µg). c: p<0.05 PBS+DSS compared with control PBS, control UCA (5 µg), control UCA (50 µg), and DSS+UCA (50 µg). d: p<0.01 DSS+PBS compared with control PBS, control UCA (5 µg), control UCA (50 µg), and DSS+UCA (50 µg). e: p<0.01 DSS+UCA (5 µg) compared with control PBS, control UCA (5 µg), control UCA (50 µg), and DSS+UCA (50 µg). f: p<0.05 DSS+UCA(50 µg) compared with control PBS and control UCA (50 µg). g: p<0.05 DSS+UCA (5 µg) compared to control UCA (5 µg) and DSS+UCA (50 µg).</p

Treatment with <i>cis</i>-UCA (50 µg) maintains splenic T-regulatory cell populations.

<p>129Sv/Ev mice were given 5% DSS for 7 days and treated with <i>cis</i>-UCA (50 µg) or PBS vehicle daily. Spleens from mice were removed on day 7. Total splenocytes were stained for CD4, CD25, FoxP3 and IL-10 and analyzed via flow cytometry. Cells positive for CD4 and CD25 (A) were gated and analyzed for their expression of FoxP3 (B). DSS treated mice had reduced levels of CD4+CD25+FoxP3+ cells when cell numbers were expressed as percentage of total cells (C). cis-UCA (50 µg) treated mice had similar numbers of CD4+CD25+FoxP3+ cells as compared with control mice (D). DSS and <i>cis</i>-UCA (50 µg) treatment did not alter levels of IL-10 secreting CD4+CD25+FoxP3+ cells (D). n = 4–13 for all measurements. a; p<0.05 DSS+PBS compared to control PBS, control UCA, and DSS+UCA (50 µg).</p

Effect of <i>cis</i>-UCA and DSS on tissue cytokines.

<p>129Sv/Ev mice were treated with 5% DSS for 7 days to induce acute colitis. Beginning on the first day of DSS administration mice were injected subcutaneously along the dorsal axis daily for 7 days with 50 µg <i>cis</i>-UCA or vehicle (PBS). Colonic tissue was ultrasonicated and supernatants were analyzed for total levels of cytokines. <i>cis</i>-UCA and DSS had no significant effects on tissue levels of IL-10 (A). DSS treated mice had increased levels of IL-17, and these were further increased in mice treated with <i>cis</i>-UCA (50 µg) (B). DSS treated mice had increased levels of colonic IL-6 (C) and IL-23 (D) and these values were not altered by <i>cis</i>-UCA (50 µg) n = 5–25 for all measurements. a: p<0.01 DSS+PBS compared with control PBS, control UCA (50 µg), and DSS+UCA (50 µg). b: p<0.01 DSS+UCA (50 µg) compared with control PBS and control UCA (50 µg). c: p<0.01 DSS+PBS compared with control PBS, and control UCA (50 µg). d: p<0.01 DSS+UCA (50 µg) compared with control PBS, and control UCA (50 µg). e: p<0.01 DSS+PBS compared with control PBS, and control UCA (50 µg). f: p<0.01 DSS+UCA (50 µg) compared with control PBS, and control UCA (50 µg).</p

Weight loss and fecal occult blood in stool in response to DSS.

<p>n = 6 for Ct and Sh groups; n = 9 for ICR groups. Values are given as Mean ± SEM. Experiments were performed 2x with n = 3 in each of the control and sham groups, and 3x with an n = 3 for the ICR groups. (A) Animal weight from day of surgery (Day 0) to DSS treatment (Day 9–13). Mice in the ICR-D group showed significant weight loss by day 15. *p<0.05 compared with Ct, Ct-D, Sh, and Sh-D. (B) Animal weight from day of surgery (Day 0) to DSS treatment (Day 24–28). There were no significant changes in body weight over the course of the experiment. (C,D) Kaplan-Meier curves demonstrating time to occult blood positive stools. Significance was determined using the log-rank test for equality in survivor analysis. ICR mice showed a significantly earlier onset of occult blood positive stools compared with Ct-D and Sh-D groups in both the early DSS group (C) and in the late DSS group (D).</p

Serum cytokine levels.

<p>Ct-D groups had increased levels of IL-1β, CXCL1, IL-6, TNFα, and IFNγ compared with Ct, ICR, and ICR-D. Results are representative of 6 independent experiments. * p ≤ 0.05 relative to Ct, ICR, and ICR-D.</p

Timeline of experiments in two separate cohorts of ICR mice.

<p>All mice were placed on a liquid diet one day prior to surgery. Following ICR, mice remained on a liquid diet for 2 days, and then were placed back on chow diet. In Group 1, DSS was administered between days 9 and 13 post-op, followed by water for 2 days. Mice were sacrificed on Day 16 and tissues removed for analysis. In Group 2, DSS was administered between days 24 and 28 post-op, followed by water for 2 days. Mice were then scarified on day 31 and tissues removed for analysis.</p

Weight loss and fecal occult blood in stool in response to DSS.

<p>n = 6 for Ct and Sh groups; n = 9 for ICR groups. Values are given as Mean ± SEM. Experiments were performed 2x with n = 3 in each of the control and sham groups, and 3x with an n = 3 for the ICR groups. (A) Animal weight from day of surgery (Day 0) to DSS treatment (Day 9–13). Mice in the ICR-D group showed significant weight loss by day 15. *p<0.05 compared with Ct, Ct-D, Sh, and Sh-D. (B) Animal weight from day of surgery (Day 0) to DSS treatment (Day 24–28). There were no significant changes in body weight over the course of the experiment. (C,D) Kaplan-Meier curves demonstrating time to occult blood positive stools. Significance was determined using the log-rank test for equality in survivor analysis. ICR mice showed a significantly earlier onset of occult blood positive stools compared with Ct-D and Sh-D groups in both the early DSS group (C) and in the late DSS group (D).</p

Phenotypic characterization of mice.

<p>(A) Tissue weight to length ratios in the ileum. ICR and ICR-D mice had increased weight/length in the neo-terminal ileum at day 16 post-op (early DSS) compared with control and sham mice. This was maintained through day 31 (late DSS). DSS treatment did not induce any further increases in weight/length ratio. *p<0.05compared with Ct, Ct-D, Sh, and Sh-D. (B) MPO levels in ileum. Ileal MPO was increased at day 16 in the ICR and ICR-D mice (Group 1—early DSS) but had returned to control levels by day 31 (Group 2- late DSS). DSS did not induce any changes in MPO levels. *p<0.05 compared with Ct, Ct-D, Sh, and Sh-D. (C) Tissue weight to length ratio in the colon. DSS treatment increased weight/length ratios in control and sham groups. ICR and ICR-D mice had increased weight/length ratios at day 31 post-op (late DSS) compared with controls and sham mice. *p<0.05 compared with Ct and Sh. (D) MPO levels in colon. DSS treatment increased MPO levels in control (Ct-D) and sham (Sh-D) groups. In the ICR mice, MPO was increased at day 16 (Group 1 –early DSS) compared with controls and sham mice. MPO decreased by day 31 (Group 2- late DSS) and was not increased by DSS treatment in the ICR mice. *p<0.01 compared with C and Sh. #p<0.05 compared with Ct and Sh. (E) 16s gene copy number in terminal ileum. There was a significant increase in bacterial load in the ICR groups by day 31 (Group 2 –late DSS). * p≤0.05 relative to Ct and Sh.</p