Remote monitoring of beehive activity

Colonies of the European honeybee, the most important pollinator insects, are subjected to many negative impacts of modern society, in form of pollution, pests, invading species and colony collapse disorder (CCD). The newly emerging technology of the Internet of Things (IoT), enables remote monitoring using wireless sensors inside beehives. In this paper, we present the model of the system for remote temperature monitoring on a various points inside the beehive colony using IoT devices. Measured data is transmitted to a remote server where received data streams are processed in real-time using Complex Event Processing (CEP) which enables detection of critical events and report it to the beekeeper. These data streams are compared with reference temperature patterns using machine learning algorithms, which give computers the ability to learn to detect events without being explicitly programmed. This system can significantly reduce the beekeeper reaction time and increase chances for a beehive colony overcoming certain types of anomalies with human intervention.Publishe

Benzo[a]pyrene-induced changes in carboxylesterase, acetylcholinesterase and heat shock protein 70 of Lymantria dispar (Lepidoptera: Lymantriidae) from unpolluted and polluted forests

Plant vegetation accumulates polycyclic aromatic hydrocarbons (PAHs) among which benzo[a]pyrene (B[a]P) is recognized as being very toxic, including cancerogenic. Lymantria dispar L. larvae are sensitive to changes in the environment, providing potential signs of pollutant presence. We examined the chronic effects of two concentrations of B[a] P on the activity of carboxylesterase (CaE), acetylcholinesterase (AChE) and heat shock protein 70 (Hsp70) levels in the brain tissue of two populations of L. dispar larvae, originating from unpolluted and polluted habitats. We found that the relative growth rate was significantly lower in both populations and that only larvae from polluted forests were sensitive to low B[a]P concentrations, exhibiting a significant increase in brain tissue CaE activity and Hsp70 concentration. AChE activity showed no changes in response to B[a]P exposure in either population. Examined biochemical parameters indicate that their sensitivity to chronic treatment with B[a]P was highly dependent on the pre-exposure history of L. dispar larvae, suggesting that they could be promising biomarkers of B[a]P and PAH pollution in forest ecosystem

Distinct effects of virgin coconut oil supplementation on the glucose and lipid homeostasis in non-diabetic and alloxan-induced diabetic rats

Non-diabetic and alloxan-induced diabetic rats were fed with standard laboratory food enriched with 20% virgincoconut oil for 16 weeks. In non-diabetic animals coconut oil improved insulin sensitivity and ability to controlglycaemia and decreased the serum triglycerides for almost 50% in comparison with controls. Supplementationwith coconut oil caused liver steatosis in both non-diabetic and diabetic animals. However, the severity ofsteatosis was lower in diabetic animals compared to non-diabetic animals. Coconut oil had no effects on hearthistology, ascending and abdominal aorta wall thickening and atherosclerotic plaques development neither innon-diabetic nor in diabetic animals. While alloxan treatment caused Type I diabetes in rats, supplementationwith coconut oil in combination with the alloxan unexpectedly resulted in Type II diabetes. The development ofsevere insulin resistance and deterioration in serum lipid profile implied that the use of coconut oil is contra-indicated in diabetic condition

The Protective Effects of Probiotic Bacteria on Cadmium Toxicity in Rats

One of the useful properties of probiotic bacteria is their capacity to bind different targets, thus eliminating them through feces. It is supposed that one of these targets could be cadmium, a widespread environmental toxicant that causes various disturbances in biological systems. This study examined the protective effects of probiotic supplementation against cadmium-induced toxicity in the rat. The experiment was conducted in the course of 5 weeks. Animals were divided into four groups: (1) controls, (2) probiotics treated, (3) cadmium treated, and (4) probiotics + cadmium treated. The cadmium concentration was measured in the blood, liver, kidney, and feces, as well as the blood alanine aminotransferase (ALT) and aspartate aminotransferase (AST) as biomarkers of the liver function. Histomorphological changes in the liver and kidney were also determined. Our results revealed that probiotics combined with cadmium increase this metal concentration in feces. As a result, blood, liver, and kidney Cd levels, as well as blood ALT and AST activities were lessened compared to the rat group treated with cadmium only. Besides, probiotics consumed simultaneously with cadmium attenuated histomorphological changes in the liver and kidney caused by cadmium. The rise in lactobacilli number in feces of rats treated simultaneously with cadmium and probiotics results in strong correlation with the increase of Cd concentration in their feces and the decrease of Cd concentration in their blood. We speculate that probiotics actively contribute to cadmium excretion through feces, probably, by its binding to their bacterial cell wall

Serum High-Mobility Group Box 1 and Heme Oxygenase-1 as Biomarkers in COVID-19 Patients at Hospital Admission

The careful monitoring of patients with mild/moderate COVID-19 is of particular importance because of the rapid progression of complications associated with COVID-19. For prognostic reasons and for the economic management of health care resources, additional biomarkers need to be identified, and their monitoring can conceivably be performed in the early stages of the disease. In this retrospective cross-sectional study, we found that serum concentrations of high-mobility group box 1 (HMGB1) and heme oxygenase-1 (HO-1), at the time of hospital admission, could be useful biomarkers for COVID-19 management. The study included 160 randomly selected recovered patients with mild to moderate COVID-19 on admission. Compared with healthy controls, serum HMGB1 and HO-1 levels increased by 487.6 pg/mL versus 43.1 pg/mL and 1497.7 pg/mL versus 756.1 pg/mL, respectively. Serum HO-1 correlated significantly with serum HMGB1, oxidative stress parameters (malondialdehyde (MDA), the phosphatidylcholine/lysophosphatidylcholine ratio (PC/LPC), the ratio of reduced and oxidative glutathione (GSH/GSSG)), and anti-inflammatory acute phase proteins (ferritin, haptoglobin). Increased heme catabolism/hemolysis were not detected. We hypothesize that the increase in HO-1 in the early phase of COVID-19 disease is likely to have a survival benefit by providing protection against oxidative stress and inflammation, whereas the level of HMGB1 increase reflects the activity of the innate immune system and represents levels within which the disease can be kept under control

The effect of long-term high-dose coconut oil supplementation on rat sliver and serum lipids

We investigated the effect of long-term high-dose virgin coconut oil (VCO) supplementation on rat liver and serum lipid status. Animals were divided into two groups with 8 of them in each: normally fed (Control group) and the group fed with coconut oil at a concentration of 20% in food (VCO group). The experiment lasted for four months. On the last day of the experiment animals were killed, and blood and liver tissue were collected. In serum we measured the levels of total cholesterol (TC), high-density lipoproteins (HDL), non-HDL lipoproteins, triglycerides (TG), aspartate aminotransferase (9\.ST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). We also measured both liver and serum levels of high mobility group protein B 1 (HMGB 1) and haptoglobin (HP), as ,.vell as the liver level of NF-KB p65/ p-NF-KB p65 transcription factor, together with the histopathology analysis on liver slices and liver Comet assay. The results show that coconut oil do not change serum TC and HDL, but reduces non-HDL and TG levels (10% and 50%, respectively) comparing to control. As a result, atherogenic index of serum (AI) is strongly reduced in VCO group versus control. As for the liver status, results show that coconut supplementation increases AST, ALT and ALP levels in VCO group (50%, 30% and 60%, respectively) comparing to control. This effect is caused by the accumulation of coconut oil fat in liver, as confirmed by the histopathology showing signs of mild nonalcoholic steatohepatitis in VCO group, followed with the increased %of DNA in comet tail. The liver inflammation in VCO group is further demonstrated with the liver HP, HMGBl and p-NF-KB p65 level increase, and increase in nuclear level ofNF­kB p65, but not accompanying serum HP and HMGBl increase. In conclusion, our results show that coconut oil supplementation, despite causing mild and localized steatohepatitis, also lowers serum atherogcnic index, a predictor of cardiovascular risk

The effect of long-term high-dose coconut oil supplementation on rat sliver and serum lipids

We investigated the effect of long-term high-dose virgin coconut oil (VCO) supplementation on rat liver and serum lipid status. Animals were divided into two groups with 8 of them in each: normally fed (Control group) and the group fed with coconut oil at a concentration of 20% in food (VCO group). The experiment lasted for four months. On the last day of the experiment animals were killed, and blood and liver tissue were collected. In serum we measured the levels of total cholesterol (TC), high-density lipoproteins (HDL), non-HDL lipoproteins, triglycerides (TG), aspartate aminotransferase (9\.ST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). We also measured both liver and serum levels of high mobility group protein B 1 (HMGB 1) and haptoglobin (HP), as ,.vell as the liver level of NF-KB p65/ p-NF-KB p65 transcription factor, together with the histopathology analysis on liver slices and liver Comet assay. The results show that coconut oil do not change serum TC and HDL, but reduces non-HDL and TG levels (10% and 50%, respectively) comparing to control. As a result, atherogenic index of serum (AI) is strongly reduced in VCO group versus control. As for the liver status, results show that coconut supplementation increases AST, ALT and ALP levels in VCO group (50%, 30% and 60%, respectively) comparing to control. This effect is caused by the accumulation of coconut oil fat in liver, as confirmed by the histopathology showing signs of mild nonalcoholic steatohepatitis in VCO group, followed with the increased %of DNA in comet tail. The liver inflammation in VCO group is further demonstrated with the liver HP, HMGBl and p-NF-KB p65 level increase, and increase in nuclear level ofNF­kB p65, but not accompanying serum HP and HMGBl increase. In conclusion, our results show that coconut oil supplementation, despite causing mild and localized steatohepatitis, also lowers serum atherogcnic index, a predictor of cardiovascular risk

Supplementary data for the article: Đurašević, S.; Stojković, M.; Sopta, J.; Pavlović, S.; Borković-Mitić, S.; Ivanović, A.; Jasnić, N.; Tosti, T.; Đurović, S.; Đorđević, J.; Todorović, Z. The Effects of Meldonium on the Acute Ischemia/Reperfusion Liver Injury in Rats. Sci Rep 2021, 11 (1), 1305. https://doi.org/10.1038/s41598-020-80011-y.

Supplementary material for: [https://doi.org/10.1038/s41598-020-80011-y]Related to published version: [https://cherry.chem.bg.ac.rs/handle/123456789/4458

The effects of meldonium on the renal acute ischemia/reperfusion injury in rats

Acute renal ischemia/reperfusion (I/R) injury is a clinical condition that is challenging to treat. Meldonium is an anti-ischemic agent that shifts energy production from fatty acid oxidation to less oxygen-consuming glycolysis. Thus, in this study we investigated the effects of a four-week meldonium pre-treatment (300 mg/kg b.m./day) on acute renal I/R in male rats (Wistar strain). Our results showed that meldonium decreased animal body mass gain, food and water intake, and carnitine, glucose, and lactic acid kidney content. In kidneys of animals subjected to I/R, meldonium increased phosphorylation of mitogen-activated protein kinase p38 and protein kinase B, and increased the expression of nuclear factor erythroid 2-related factor 2 and haeme oxygenase 1, causing manganese superoxide dismutase expression and activity to increase, as well as lipid peroxidation, cooper-zinc superoxide dismutase, glutathione peroxidase, and glutathione reductase activities to decrease. By decreasing the kidney Bax/Bcl2 expression ratio and kidney and serum high mobility group box 1 protein content, meldonium reduced apoptotic and necrotic events in I/R, as confirmed by kidney histology. Meldonium increased adrenal noradrenaline content and serum, adrenal, hepatic, and renal ascorbic/dehydroascorbic acid ratio, which caused complex changes in renal lipidomics. Taken together, our results have confirmed that meldonium pretreatment protects against I/R-induced oxidative stress and apoptosis/necrosis

The Effects of a Meldonium Pre-Treatment on the Course of the Faecal-Induced Sepsis in Rats

Sepsis is a life-threatening condition caused by the dysregulated and overwhelming response to infection, accompanied by an exaggerated pro-inflammatory state and lipid metabolism disturbance leading to sequential organ failure. Meldonium is an anti-ischemic and anti-inflammatory agent which negatively interferes with lipid metabolism by shifting energy production from fatty acid oxidation to glycolysis, as a less oxygen-demanding pathway. Thus, we investigated the effects of a four-week meldonium pre-treatment on faecal-induced sepsis in Sprague-Dawley male rats. Surprisingly, under septic conditions, meldonium increased animal mortality rate compared with the meldonium non-treated group. However, analysis of the tissue oxidative status did not provide support for the detrimental effects of meldonium, nor did the analysis of the tissue inflammatory status showing anti-inflammatory, anti-apoptotic, and anti-necrotic effects of meldonium. After performing tissue lipidomic analysis, we concluded that the potential cause of the meldonium harmful effect is to be found in the overall decreased lipid metabolism. The present study underlines the importance of uninterrupted energy production in sepsis, closely drawing attention to the possible harmful effects of lipid-mobilization impairment caused by certain therapeutics. This could lead to the much-needed revision of the existing guidelines in the clinical treatment of sepsis while paving the way for discovering new therapeutic approaches