ZASTOSOWANIE WYŁADOWANIA ELEKTRYCZNEGO DO OZONOWANIA GLEBY

In this study, influence of ozone treatment on physical properties of soil was investigated. We used a quartz container for ozone treatment of soil. The amount of soil used for treatment was 100 g. Treating time was 90 minutes. Flow rate of ozone gas was 1.5 L/min. We measured characteristics of soil such as inorganic nutrient (NO3-N, NO2-N, and NH4-N), pH(H2O), fungi, DNA of soil, and exchangeable bases (Ca, K, Fe, and Al) before and after ozone treatment.W niniejszym opracowaniu, opisano badania wpływu obróbki ozonem na własności fizyczne gleby. Do ozonowania gleby wykorzystaliśmy pojemnik kwarcowy. Ilość gleby poddanej działaniu ozonu wynosiła 100g, a czas oddziaływania 90 minut. Przepływ ozonu wyniósł 1.5l/min. Mierzono właściwości gleby, takie jak nieorganiczne składniki odżywcze (NO3-N, NO2-N i NH4-N), pH(H2O), grzyby, DNA w glebie i zasady wymienne (Ca, K, Fe i Al) przed i po poddaniu jej działaniu ozonu

ZASTOSOWANIE WYŁADOWANIA ELEKTRYCZNEGO DO OZONOWANIA GLEBY

In this study, influence of ozone treatment on physical properties of soil was investigated. We used a quartz container for ozone treatment of soil. The amount of soil used for treatment was 100 g. Treating time was 90 minutes. Flow rate of ozone gas was 1.5 L/min. We measured characteristics of soil such as inorganic nutrient (NO3-N, NO2-N, and NH4-N), pH(H2O), fungi, DNA of soil, and exchangeable bases (Ca, K, Fe, and Al) before and after ozone treatment.W niniejszym opracowaniu, opisano badania wpływu obróbki ozonem na własności fizyczne gleby. Do ozonowania gleby wykorzystaliśmy pojemnik kwarcowy. Ilość gleby poddanej działaniu ozonu wynosiła 100g, a czas oddziaływania 90 minut. Przepływ ozonu wyniósł 1.5l/min. Mierzono właściwości gleby, takie jak nieorganiczne składniki odżywcze (NO3-N, NO2-N i NH4-N), pH(H2O), grzyby, DNA w glebie i zasady wymienne (Ca, K, Fe i Al) przed i po poddaniu jej działaniu ozonu

Scalp Microbiome and Sebum Composition in Japanese Male Individuals with and without Androgenetic Alopecia

The skin microbiome and sebum may be associated with inflammation-related diseases of the scalp. To assess the pathogenesis and progression of androgenetic alopecia (AGA), we analyzed the composition of sebum and the bacterial and fungal microbiomes of the scalps of 118 Japanese male individuals with and without AGA, then discussed their roles in the pathogenesis of AGA. Sebum triglyceride and palmitic acid contents were higher in the AGA group than in the non-AGA group. Malassezia restricta, a lipophilic fungus that consumes palmitic acid, was abundant on the scalps of patients with AGA. Cutibacterium, Corynebacterium, and Staphylococcus were the most common genera in both groups, and patients with AGA exhibited scalp dysbiosis (increased abundance of Cutibacterium and decreased abundance of Corynebacterium). Our findings suggest that both sebum and the bacterial and fungal microbiomes of the scalp may be involved in the development of AGA

A Case of Krukenberg Tumor Metastasized from Colon Cancer Subsequent to Synchronous Multiple Liver Metastasis

A 34-year-old woman with synchronous, multiple liver metastases of stage IV, T4N2M0H2P0 descending colon cancer was referred to our hospital. The lesion was considered unresectable because of insufficient estimated future remnant liver volume resulting from invasion of three hepatic veins and the hepatic hilum, and she underwent laparoscopic left hemicolectomy. The patient underwent 14 courses of mFOLFOX6 (5-flurouracil, leucovorin and oxaliplatin) and 21 cetuximab administrations as first-line chemotherapy, which allowed her to maintain a complete response for 6 months despite adverse reactions such as mild neutropenia and thrombocytopenia. However, abdominal computed tomography (CT) revealed a large ovarian mass 6 months after chemotherapy cessation. A bilateral adnexectomy at another hospital revealed involvement of both ovaries, and immunohistochemistry revealed that the tumor was CK7− and CK20+, compatible with a colon cancer origin. The ovarian lesions were histologically diagnosed as Krukenberg tumor metastasized from the colon cancer. This case highlights the possibility of metastatic tumor development from colon cancer

A New Therapeutic Modality for Acute Myocardial Infarction: Nanoparticle-Mediated Delivery of Pitavastatin Induces Cardioprotection from Ischemia-Reperfusion Injury via Activation of PI3K/Akt Pathway and Anti-Inflammation in a Rat Model.

There is an unmet need to develop an innovative cardioprotective modality for acute myocardial infarction (AMI), for which the effectiveness of interventional reperfusion therapy is hampered by myocardial ischemia-reperfusion (IR) injury. Pretreatment with statins before ischemia is shown to reduce MI size in animals. However, no benefit was found in animals and patients with AMI when administered at the time of reperfusion, suggesting insufficient drug targeting into the IR myocardium. Here we tested the hypothesis that nanoparticle-mediated targeting of pitavastatin protects the heart from IR injury.In a rat IR model, poly(lactic acid/glycolic acid) (PLGA) nanoparticle incorporating FITC accumulated in the IR myocardium through enhanced vascular permeability, and in CD11b-positive leukocytes in the IR myocardium and peripheral blood after intravenous treatment. Intravenous treatment with PLGA nanoparticle containing pitavastatin (Pitavastatin-NP, 1 mg/kg) at reperfusion reduced MI size after 24 hours and ameliorated left ventricular dysfunction 4-week after reperfusion; by contrast, pitavastatin alone (as high as 10 mg/kg) showed no therapeutic effects. The therapeutic effects of Pitavastatin-NP were blunted by a PI3K inhibitor wortmannin, but not by a mitochondrial permeability transition pore inhibitor cyclosporine A. Pitavastatin-NP induced phosphorylation of Akt and GSK3β, and inhibited inflammation and cardiomyocyte apoptosis in the IR myocardium.Nanoparticle-mediated targeting of pitavastatin induced cardioprotection from IR injury by activation of PI3K/Akt pathway and inhibition of inflammation and cardiomyocyte death in this model. This strategy can be developed as an innovative cardioprotective modality that may advance currently unsatisfactory reperfusion therapy for AMI

Effects of Pitavastatin-NP on cell death after IR.

<p><b>(A)</b>, Effects of Pitavastatin-NP at the time of reperfusion after pretreatment with Cyclosporine A (CsA) (10 mg/kg) every 12 hours starting 36 hours before ischemia on MI size. N = 7 per group. Data are compared using one-way ANOVA followed by Bonferroni’s multiple comparison tests. <b>(B)</b>, Effects of Pitavastatin-NP at the time of reperfusion after pretreatment with CsA (10 mg/kg) every 12 hours starting 36 hours before ischemia on cytosolic cytochrome C in IR myocardium 30 minutes after reperfusion. N = 4 per group. Data are compared using one-way ANOVA followed by Bonferroni’s multiple comparison tests. <b>(C)</b>, Effects of Pitavastatin-NP at the time of reperfusion after pretreatment with Cyclosporine A (CsA) (10 mg/kg) every 12 hours starting 36 hours before ischemia on mitochondrial cytochrome C in IR myocardium 30 minutes after reperfusion. Data are mean±SEM (n = 4 per group). Data are compared using one-way ANOVA followed by Bonferroni’s multiple comparison tests. <b>(D)</b>, Representative photomicrographs of cross-sections from IR myocardium stained with ED-1 in AAR. Scale bar: 20 μm. <b>(E),</b> Effects of Pitavastatin-NP at the time of reperfusion after pretreatment with CsA (10 mg/kg) every 12 hours starting 36 hours before ischemia on ED-1-positive leukocyte (monocytes) infiltration in IR myocardium 24-hour after reperfusion. N = 7 per group. Data are compared using one-way ANOVA followed by Dunnett’s multiple comparison tests.</p

Effects of Pitavastatin-NP on MI size.

<p><b>(A)</b>, Representative stereomicrographs of heart sections double-stained with Evans blue and TTC 24 hours after reperfusion. Scale bar: 5 mm. <b>(B),</b> Effects of Pitavastatin-NP and pitavastatin alone on MI size at the time of reperfusion. N = 6–10 per group. Data are compared using one-way ANOVA followed by Bonferroni’s multiple comparison tests. <b>(C)</b>, Quantification of Area at risk in the group treated with pitavastatin-NP or pitavastatin alone. Data are mean are (n = 6–10 per group) Data are compared using one-way ANOVA followed by Bonferroni’s multiple comparison tests.</p

Leukocyte counts and Plasma biomarker profile 24 hours after IR.

<p>Data are expressed as the mean ± SEM (N = 6 each).</p><p>*<i>P</i><0.05 versus vehicle group. IR: ischemia-reperfusion.</p><p>Leukocyte counts and Plasma biomarker profile 24 hours after IR.</p