Preparing forest management plans using ETÇAP model: case studies of simulation and optimization

Bu makalede, Ekosistem Tabanlı Çok Amaçlı Planlama (ETÇAP) felsefesine dayalı olarak geliştirilmiş bir Karar Destek Sistemi (KDS) ile ETÇAPSimülasyon ve ETÇAPOptimizasyon modellerinin yapısı ve gerçekleştirimi ortaya konulmuştur. KDS, Coğrafi Bilgi Sistemleri (CBS) yardımı ile üretilen konumsal veriler ile diğer yardımcı verileri (hasılat tabloları, odun ürün çeşitleri tabloları, ekonomik veriler, planlama parametreleri vs) belirlenen formatta kullanabilme özelliğine sahiptir. Geleneksel simülasyon ve doğrusal programlama tekniklerini içeren ETÇAPSimülasyon ve ETÇAPOptimizasyon modelleri ile orman ekosistemlerinin uzun vadede kestirimi meşcere bazında yapılmakta ve plan çıktıları metin, tablo, grafik ve harita olarak sunulmaktadır. Geliştirilen KDS, odun üretiminin yanı sıra, su üretimi, toprak kaybı, karbon birikimi ve oksijen üretimi gibi diğer orman değerlerini de kapsayacak şekilde hazırlanmıştır. Prototip olarak geliştirilen KDS’nin kolay kullanımını sağlamak amacıyla bir arayüz programı ile desteklenmiştir.This paper presents a sound forest management decision support system including ETÇAPSimülasyon and ETÇAPOptimizasyon based on ETÇAP philosophy. The DSS uses both spatial information driven from Geographical Information Systems and other data such as empirical yield tables, forest products and planning parameters as an input to model forest management activities implementable on the ground. Both simulation and optimization modules were developed to find the best appropriate combination of management treatment options for each stand and to display performance indicators as outputs in text, graphic, table and map format. The DSS accommodates not only the wood production objective but also water production, soil protection, carbon balance and oxygen production. An interface program was developed to implement the DSS

Investigation of the effect of thymoquinone on kidney damage in isoproterenol-induced myocardial infarction in rats and cardiorenal interactions

This study aimed to determine whether thymoquinone has any protective effects on renal tissue after an isoproterenol-induced myocardial infarction (MI). Experimental groups were formed as 4 groups (n=8). Control group (C). Thymoquinone group (THQ), 20 mg/kg single dose intragastric (i.g.) daily for seven days. Isoproterenol group (ISO) was administered 100 mg/kg intraperitoneally in two doses on days 7 and 8 of the experiment. Thymoquinone+Isoproterenol group (THQ+ISO), THQ 20 mg/kg i.g. was administered once a day for seven days. In addition, two doses of ISO 100 mg/kg i.p. were administered on the seventh and eighth days. Kidney tissues were evaluated histopathologically. Kidney tissues were evaluated histopathologically. Tumour necrosis factor alpha(TNF-α) and alpha Smooth Muscle Actin(α-SMA) immunoreactivity density changes were determined by immunohistochemistry. Glutathione(GST), Glutathione S-transferases(GSTs) and Interleukin-6(IL-6) levels were evaluated by ELISA method. Isoproterenol injection caused severe histopathological changes on kidney tissue. Also TNF-α and α-SMA levels were found to be higher in groups where ISO was administered. THQ could be effective on kidney tissue to partially correct these histopathological damages, by decreasing fibrosis and inflammation. This study shows that treatment with THQ is effective in preventing kidney damage caused by ISO-induced MI. We think that THQ as a supplementary food will be effective to prevent kidney damage

Timokinon metotreksatın neden olduğu kalp hasarını azaltır: sıçanlarda histopatolojik bir çalışma

Purpose: The study aimed to evaluate the effect of thymoquinone on cardiac tissue in MTX-induced cardiac toxicity in rats with various parameters. Materials and Methods: Group I (n=8) was administered intraperitoneal saline for 10 days. Intraperitoneal olive oil was applied to Group II (n=8) for 10 days. Group III (n=8) received 10 mg/kg Thymoquinone (THQ) intraperitoneally for 10 days. Group IV (n=8) was administered a single dose of 20 mg/kg Methotrexate (MTX), 500 mg/20 ml, intraperitoneally on the 1st day of the experiment. Group V (n=8) MTX: 20 mg/kg single dose intraperitoneally on the 1st day; THQ: 10mg/kg i.p. administered for 10 days. Since Methotrexate was in liquid form, no solvent was used. At the end of the experimental period, the rats were sacrificed for analysis of heart tissue. The structure of heart tissue was evaluated by hematoxylin eosin staining. Immunohistochemically, Connexin-43, HSP90, and HIF 1α antibodies were stained. Results: Group IV was found to have histopathological deterioration, which was ameliorated by THQ. In addition to this; Connexin-43 immunoreactivity was the lowest in Group IV compared to other groups: 108.5±7.4. Compared to other groups, HSP90 immunoreactivity was highest in Group IV: 103.6±10.4. Compared to other groups, HIF-1α immunoreactivity was highest in Group IV: 95.2 ±9.1. Conclusion: Thymoquinone has a positive effect on Connexin-43, one of the proteins providing conduction in intercalary discs, HSP90, one of the chaperones in the cell and HIF-1α expression against MTX toxicity. At the same time, THQ provides a significant improvement in cardiac tissue histopathologically by showing a cardioprotective effect

The diagnostic value of serum copeptin levels in an acute pulmonary embolism

Background: Acute pulmonary embolism (APE) is a common disease which is associated with high mortality and morbidity. Circulating level of copeptin, which was demonstrated to be elevated in heart failure, acute myocardial infarction and pulmonary arterial hypertension, were reported to be independent predictors of poor outcome in recent studies. The aim of the present study was to investigate the clinical utility of copeptin in the diagnosis of APE. Methods: A total of 90 consecutive patients, admitted to emergency service due to acute chest pain and/or dyspnea and who underwent pulmonary computerized tomography angiography (CTA) due to suspicion of APE, were included in this prospective study. The patients diagnosed with APE were defined as APE (+) group and the remaining individuals with normal pulmonary CTA result were defined as APE (–) group. Results: Copeptin levels (7.76 ± 4.4 vs. 3.81 ± 1.34 ng/dL; p < 0.001) were higher in the APE (+) group as compared to the APE (–) group. Copeptin was significantly positively correlated with B-type natriuretic peptide (r = 0.434, p < 0.001), D-dimer (r = 0.315, p = 0.003) and troponin I (r = 0.300, p = 0.004) and inversely correlated with arterial oxygen saturations (r = –0.533, p < 0001). When the correlation of copeptin with right ventricular dysfunction parameters was investigated, it was significantly inversely correlated with the tricuspid annular plane systolic excursion (r = –0.521, p < 0.001) and positively correlated with right to left ventricle ratio (r = 0.329, p = 0.024). Copeptin (OR 1.836, 95% CI 1.171–2.878, p = 0.008) was found as a significant independent predictor of APE in a multivariate analysis, after adjusting for other risk parameters.  Conclusions: Copeptin is a promising new biomarker, which may be used to support the need for further investigations and to improve the diagnosis of patients with APE.

Marmara Seawater Desalination by Membrane Distillation: Direct Consumption Assessment of Produced Drinking Water

Drinking water was produced from Marmara seawater by membrane distillation (MD). The best operating conditions were determined by batch experiments as: 0.45 μm PTFE, 30°C distillate temperature and temperature difference, and 270–360 L/h cross‐flow rates in feed‐distillate. Seawater desalination was carried out with 99.93% solute rejection and 17.2 L/m2h permeate flux in 66% concentration ratio by lab‐scale pilot system. Since the desalinated water contained no organic carbon, turbidity, and nitrate, it seemed to be very suitable for immediate service with quality of 7.3 pH, clear, odor‐free, 76.0 µS/cm, 47.1 mg TDS/L, <0.001 color, and 0.01 mg boron/L. The product water lacked of vital cations, especially Na+, K+, Ca2+, Mg2+ that are essentials for promoting osmotic balanced body liquid and healthy development. A holistic management approach towards satisfying specific water quality requirements in direct service of MD effluents to human consumption was proposed that jointly included in injecting into urban potable water, adding appropriate chemicals into the effluent, and mixing effluents with raw or concentrated seawater (1:250/1:1000 for Marmara seawater) or brackish natural waters under hygienic precautions

Imaging protein aggregates in Parkinson’s Disease serum using aptamer-assisted single-molecule pull-down

The formation of soluble α-synuclein (α-syn) and amyloid-β (Aβ) aggregates is associated with the development of Parkinson’s disease (PD). Current methods mainly focus on the measurement of the aggregate concentration and are unable to determine their heterogeneous size and shape, which potentially also change during the development of PD due to increased protein aggregation. In this work, we introduce aptamer-assisted single-molecule pull-down (APSiMPull) combined with super-resolution fluorescence imaging of α-syn and Aβ aggregates in human serum from early PD patients and age-matched controls. Our diffraction-limited imaging results indicate that the proportion of α-syn aggregates (α-syn/(α-syn+Aβ)) can be used to distinguish PD and control groups with an area under the curve (AUC) of 0.85. Further, super resolution fluorescence imaging reveals that PD serums have a higher portion of larger and rounder α-syn aggregates than controls. Little difference was observed for Aβ aggregates. Combining these two metrics, we constructed a new biomarker and achieved an AUC of 0.90. The combination of the aggregate number and morphology provides a new approach to early PD diagnosis

Soluble amyloid beta-containing aggregates are present throughout the brain at early stages of Alzheimer's disease.

Protein aggregation likely plays a key role in the initiation and spreading of Alzheimer's disease pathology through the brain. Soluble aggregates of amyloid beta are believed to play a key role in this process. However, the aggregates present in humans are still poorly characterized due to a lack of suitable methods required for characterizing the low concentration of heterogeneous aggregates present. We have used a variety of biophysical methods to characterize the aggregates present in human Alzheimer's disease brains at Braak stage III. We find soluble amyloid beta-containing aggregates in all regions of the brain up to 200 nm in length, capable of causing an inflammatory response. Rather than aggregates spreading through the brain as disease progresses, it appears that aggregation occurs all over the brain and that different brain regions are at earlier or later stages of the same process, with the later stages causing increased inflammation

Different soluble aggregates of Aβ42 can give rise to cellular toxicity through different mechanisms.

Protein aggregation is a complex process resulting in the formation of heterogeneous mixtures of aggregate populations that are closely linked to neurodegenerative conditions, such as Alzheimer's disease. Here, we find that soluble aggregates formed at different stages of the aggregation process of amyloid beta (Aβ42) induce the disruption of lipid bilayers and an inflammatory response to different extents. Further, by using gradient ultracentrifugation assay, we show that the smaller aggregates are those most potent at inducing membrane permeability and most effectively inhibited by antibodies binding to the C-terminal region of Aβ42. By contrast, we find that the larger soluble aggregates are those most effective at causing an inflammatory response in microglia cells and more effectively inhibited by antibodies targeting the N-terminal region of Aβ42. These findings suggest that different toxic mechanisms driven by different soluble aggregated species of Aβ42 may contribute to the onset and progression of Alzheimer's disease.This study is supported by the Marie-Curie Individual Fellowship programme (S.D.), EPSRC Studentship (D.C.W.), Boehringer Ingelheim Fonds (P.F.), Studienstiftung des deutschen Volkes (P.F.), Senior Research Fellowship from the Alzheimer's Society, Grant Number 317, AS-SF-16-003, UK (F.A.A), Swiss National Fondation for Science and Darwin College grant number P2ELP2_162116 and P300P2_171219 (F.S.R.), Borysiewicz Biomedical Fellowship from the University of Cambridge(P.S), the UK Biotechnology and Biochemical Sciences Research Council (C.M.D.); the Wellcome Trust (C.M.D) the Cambridge Centre for Misfolding Diseases (P.F., F.A.A., P.S., C.M.D., and M.V.) and the European Research Council Grant Number 669237 (D.K.) and the Royal Society (D.K.)