The Effects of Different Substrates on the Quality of Seedlings and Yield in Organic Production of Lettuce

An experiment was conducted under glasshouse condition. Lettuce were sown in 5 different substrate: 100% earthworm; 60% earthworm + 40% potting soil; 85% earthwarm + 15% potting soil; 100% potting soil; certified organic substrate from the market (mix of white and black peat). The quality parameters of seedlings were noted: number of days from sowing to emergence, development of first leaf, total number of emerged plants. During vegetation are recorded dates about dynamics of growth. On the harvested yield were counted number of marketable and damaged leafs, diameter and height of head were determined and total weight of heads. Recorded results show that best substrate for production of seedlings of organic lettuce are mix of 60% earthwarm + 40% potting soil and commercial mix of white and black peats

Olympic Soul Searching A look into Chicago's Olympic City Image Potential for 2016

This study investigates what the Olympics could bring to the Chicago community, along with what Chicago could bring to the Olympic Movement. Particular attention is dedicated to popular culture, our area of interest, which has minimal Olympic research associated to it. Past Olympic Cities possess a plethora of characteristics unique only to them, but also hold Olympic legacy requirements. As a 2016 applicant city, Chicago must look deeply into its current image, along with how it fits an Olympic City image, in order to evaluate its potential in finding its Olympic soul. The research method concentrates on desk studies and expert interviews involving the Olympics, the city of Chicago and destination image. The interviewees include individuals within organizations that play a pivotal role in formulating Chicago‘s image, either directly or indirectly, and its 2016 Olympic possibility. Upon completion of an Olympic City Model and a current Chicago Image Portrayal Model, results indicate that Chicago has the necessary steps and requirements in place and could be ready for hosting the 2016 Olympics, adding its own distinctive touch to the Olympic legacy.Tourism and Hospitality Managemen

The Pt(S-pr-thiosal)2 and BCL1 Leukemia Lymphoma: Antitumor Activity In Vitro and In Vivo

B cell malignancies are, despite the development of targeted therapy in a certain percentage of the patients still a chronic disease with relapses, requiring multiple lines of therapy. Regimens that include platinum-based drugs provide high response rates in different B cell lymphomas, high-risk chronic lymphocytic leukemia (CLL), and devastating complication of CLL, Richter’s syndrome. The aim of this study was to explore the potential antitumor activity of previously synthetized platinum(IV) complex with alkyl derivatives of thyosalicilc acid, PtCl2(S-pr-thiosal)2, toward murine BCL1 cells and to delineate possible mechanisms of action. The PtCl2(S-pr-thiosal)2 reduced the viability of BCL1 cells in vitro but also reduced the growth of metastases in the leukemia lymphoma model in BALB/c mice. PtCl2(S-pr-thiosal)2 induced apoptosis, inhibited proliferation of BCL1 cells, and induced cell cycle disturbance. Treatment of BCL1 cells with PtCl2(S-pr-thiosal)2 inhibited expression of cyclin D3 and cyclin E and enhanced expression of cyclin-dependent kinase inhibitors p16, p21, and p27 resulting in cell cycle arrest in the G1 phase, reduced the percentage of BCL1 cells in the S phase, and decreased expression of Ki-67. PtCl2(S-pr-thiosal)2 treatment reduced expression of phosphorylated STAT3 and downstream-regulated molecules associated with cancer stemness and proliferation, NANOG, cyclin D3, and c-Myc, and expression of phosphorylated NFκB in vitro and in vivo. In conclusion, PtCl2(S-pr-thiosal)2 reduces STAT3 and NFκB phosphorylation resulting in inhibition of BCL1 cell proliferation and the triggering of apoptotic cell death

Type 2 Diabetic Patients with Ischemic Stroke: Decreased Insulin Sensitivity and Decreases in Antioxidant Enzyme Activity Are Related to Different Stroke Subtypes

We analyzed (a) insulin sensitivity (IS) and (b) glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD) antioxidant enzyme activity in type 2 diabetic (T2D) patients with atherothrombotic infarction (ATI) (group A), lacunar infarction (LI) (B), or without stroke (C) and in nondiabetics with ATI (D), LI (E), or without stroke (F). ATI and LI were confirmed by brain imaging IS levels were determined by minimal model (Si index), and the enzyme activity by spectrophotometry. In T2D patients, Si was lower in A and B versus C (1.14 ± 0.58, 1.00 ± 0.26 versus 3.14 ± 0.62 min −1 /mU/l × 10 4 , < 0.001) and in nondiabetics in D and E versus F (3.38 ± 0.77, 3.03 ± 0.72 versus 6.03 ± 1.69 min −1 /mU/l × 10 4 , < 0.001). Also, GSH-Px and GR activities were lower in A and B versus C (GSH-Px: 21.96 ± 3.56, 22.51 ± 1.23 versus 25.12 ± 1.67; GR: 44.37 ± 3.58, 43.50 ± 2.39 versus 48.58 ± 3.67 U/gHb; < 0.001) and in D and E versus F (GSH-Px: 24.75 ± 3.02, 25.57 ± 1.92 versus 28.56 ± 3.91; GR: 48.27 ± 6.81, 49.17 ± 6.24 versus 53.67 ± 3.96 U/gHb; < 0.001). Decreases in Si and GR were significantly related to both ATI and LI in T2D. Our results showed that decreased IS and impaired antioxidant enzymes activity influence ischemic stroke subtypes in T2D. The influence of insulin resistance might be exerted on the level of glutathione-dependent antioxidant enzymes

Type 2 Diabetic Patients with Ischemic Stroke: Decreased Insulin Sensitivity and Decreases in Antioxidant Enzyme Activity Are Related to Different Stroke Subtypes

We analyzed (a) insulin sensitivity (IS) and (b) glutathione peroxidase (GSH-Px), glutathione reductase (GR), and superoxide dismutase (SOD) antioxidant enzyme activity in type 2 diabetic (T2D) patients with atherothrombotic infarction (ATI) (group A), lacunar infarction (LI) (B), or without stroke (C) and in nondiabetics with ATI (D), LI (E), or without stroke (F). ATI and LI were confirmed by brain imaging IS levels were determined by minimal model (Si index), and the enzyme activity by spectrophotometry. In T2D patients, Si was lower in A and B versus C (1.14±0.58, 1.00±0.26 versus 3.14±0.62 min−1/mU/l × 104, P<0.001) and in nondiabetics in D and E versus F (3.38±0.77, 3.03±0.72 versus 6.03±1.69 min−1/mU/l × 104, P<0.001). Also, GSH-Px and GR activities were lower in A and B versus C (GSH-Px: 21.96±3.56,  22.51±1.23 versus 25.12±1.67; GR: 44.37±3.58,  43.50±2.39 versus 48.58±3.67 U/gHb; P<0.001) and in D and E versus F (GSH-Px: 24.75±3.02,  25.57±1.92 versus 28.56±3.91; GR: 48.27±6.81,  49.17±6.24 versus 53.67±3.96 U/gHb; P<0.001). Decreases in Si and GR were significantly related to both ATI and LI in T2D. Our results showed that decreased IS and impaired antioxidant enzymes activity influence ischemic stroke subtypes in T2D. The influence of insulin resistance might be exerted on the level of glutathione-dependent antioxidant enzymes

Decreased Insulin Sensitivity and Impaired Fibrinolytic Activity in Type 2 Diabetes Patients and Nondiabetics with Ischemic Stroke

We analyzed (a) insulin sensitivity (IS), (b) plasma insulin (PI), and (c) plasminogen activator inhibitor-1 (PAI-1) in type 2 diabetes (T2D) patients with (group A) and without (group B) atherothrombotic ischemic stroke (ATIS), nondiabetics with ATIS (group C), and healthy controls (group D). IS was determined by minimal model (Si). Si was lower in A versus B (1.18±0.67 versus 2.82±0.61 min−1/mU/L × 104; P<0.001) and in C versus D (3.18±0.93 versus 6.13±1.69 min−1/mU/L × 104; P<0.001). PI and PAI-1 were higher in A versus B (PI: 19.61±4.08 versus 14.91±1.66 mU/L; P<0.001, PAI-1: 7.75±1.04 versus 4.57±0.72 mU/L; P<0.001) and in C versus D (PI: 15.14±2.20 versus 7.58±2.05 mU/L; P<0.001, PAI-1: 4.78±0.98 versus 3.49±1.04 mU/L; P<0.001). Si correlated with PAI-1 in T2D patients and nondiabetics, albeit stronger in T2D. Binary logistic regression identified insulin, PAI-1, and Si as independent predictors for ATIS in T2D patients and nondiabetics. The results imply that insulin resistance and fasting hyperinsulinemia might exert their atherogenic impact through the impaired fibrinolysis