Waste detection in Pomerania: non-profit project for detecting waste in environment

Waste pollution is one of the most significant environmental issues in the modern world. The importance of recycling is well known, either for economic or ecological reasons, and the industry demands high efficiency. Our team conducted comprehensive research on Artificial Intelligence usage in waste detection and classification to fight the world's waste pollution problem. As a result an open-source framework that enables the detection and classification of litter was developed. The final pipeline consists of two neural networks: one that detects litter and a second responsible for litter classification. Waste is classified into seven categories: bio, glass, metal and plastic, non-recyclable, other, paper and unknown. Our approach achieves up to 70% of average precision in waste detection and around 75% of classification accuracy on the test dataset. The code used in the studies is publicly available online.Comment: Litter detection, Waste detection, Object detectio

Treatment goal attainment for secondary prevention in coronary patients with or without diabetes mellitus : Polish multicenter study POLASPIRE

Introduction: Cardiovascular disease is still a leading cause of death in Poland and across Europe. The aim of this study was to assess the attainment of the main treatment goals for secondary cardiovascular prevention in coronary patients with or without diabetes mellitus (DM) in Poland. Material and methods: The study group included 1026 patients (65.5 ±9 y.o.; males: 72%) included at least 6 months after the index hospitalisation for myocardial infarction, unstable angina, elective percutaneous coronary intervention or coronary artery bypass surgery. The target and treatment goals were defined according to the 2016 European Society of Cardiology guidelines on cardiovascular prevention. Results: Patients with DM (n = 332; 32%) were slightly older compared to non-diabetic (n = 694) individuals (67.2 ±7 vs. 64.6 ±9 years old; p < 0.0001). The DM goal was achieved in 196 patients (60%). The rate of primary (LDL: 51% vs. 35%; p < 0.0001) and secondary (non-HDL: 56% vs. 48%; p < 0.02) goal attainment was higher in DM(+) compared to DM(–) patients. The rate of target blood pressure was lower in DM(+) than in normoglycemic patients (52% vs. 61% at < 140/90 mm Hg, p < 0.01. As expected, goal achievement of normal weight (9.5% vs. 19%; p < 0.0001) and waist circumference (7% vs. 15%; p < 0.001) was lower in diabetic patients and the rate of regular physical activity was similar (DM+ 12% vs. DM– 14%; p = ns). Finally, there was no difference in active smokers (DM+ 23% vs. DM– 22%; p = ns). Conclusions: Great majority of Polish patients in secondary prevention do not achieve treatment goals. Although lipid goals attainment is better in DM and the rate of smokers is similar, the management of all risk factors needs to be improved

TRPV4 mediates cell damage induced by hyperphysiological compression and regulates COX2/PGE2 in intervertebral discs

Background Aberrant mechanical loading of the spine causes intervertebral disc (IVD) degeneration and low back pain. Current therapies do not target the mediators of the underlying mechanosensing and mechanotransduction pathways, as these are poorly understood. This study investigated the role of the mechanosensitive transient receptor potential vanilloid 4 (TRPV4) ion channel in dynamic compression of bovine nucleus pulposus (NP) cells in vitro and mouse IVDs in vivo. Methods Degenerative changes and the expression of the inflammatory mediator cyclooxygenase 2 (COX2) were examined histologically in the IVDs of mouse tails that were dynamically compressed at a short repetitive hyperphysiological regime (vs sham). Bovine NP cells embedded in an agarose-collagen hydrogel were dynamically compressed at a hyperphysiological regime in the presence or absence of the selective TRPV4 antagonist GSK2193874. Lactate dehydrogenase (LDH) and prostaglandin E2 (PGE2) release, as well as phosphorylation of mitogen-activated protein kinases (MAPKs), were analyzed. Degenerative changes and COX2 expression were further evaluated in the IVDs of trpv4-deficient mice (vs wild-type; WT). Results Dynamic compression caused IVD degeneration in vivo as previously shown but did not affect COX2 expression. Dynamic compression significantly augmented LDH and PGE2 releases in vitro, which were significantly reduced by TRPV4 inhibition. Moreover, TRPV4 inhibition during dynamic compression increased the activation of the extracellular signal-regulated kinases 1/2 (ERK) MAPK pathway by 3.13-fold compared to non-compressed samples. Trpv4-deficient mice displayed mild IVD degeneration and decreased COX2 expression compared to WT mice. Conclusions TRPV4 therefore regulates COX2/PGE2 and mediates cell damage induced by hyperphysiological dynamic compression, possibly via ERK. Targeted TRPV4 inhibition or knockdown might thus constitute promising therapeutic approaches to treat patients suffering from IVD pathologies caused by aberrant mechanical stress

Modic type 2 changes are fibroinflammatory changes with complement system involvement adjacent to degenerated vertebral endplates

Background Vertebral endplate signal intensity changes visualized by magnetic resonance imaging termed Modic changes (MC) are highly prevalent in low back pain patients. Interconvertibility between the three MC subtypes (MC1, MC2, MC3) suggests different pathological stages. Histologically, granulation tissue, fibrosis, and bone marrow edema are signs of inflammation in MC1 and MC2. However, different inflammatory infiltrates and amount of fatty marrow suggest distinct inflammatory processes in MC2. Aims The aims of this study were to investigate (i) the degree of bony (BEP) and cartilage endplate (CEP) degeneration in MC2, (ii) to identify inflammatory MC2 pathomechanisms, and (iii) to show that these marrow changes correlate with severity of endplate degeneration. Methods Pairs of axial biopsies (n = 58) spanning the entire vertebral body including both CEPs were collected from human cadaveric vertebrae with MC2. From one biopsy, the bone marrow directly adjacent to the CEP was analyzed with mass spectrometry. Differentially expressed proteins (DEPs) between MC2 and control were identified and bioinformatic enrichment analysis was performed. The other biopsy was processed for paraffin histology and BEP/CEP degenerations were scored. Endplate scores were correlated with DEPs. Results Endplates from MC2 were significantly more degenerated. Proteomic analysis revealed an activated complement system, increased expression of extracellular matrix proteins, angiogenic, and neurogenic factors in MC2 marrow. Endplate scores correlated with upregulated complement and neurogenic proteins. Discussion The inflammatory pathomechanisms in MC2 comprises activation of the complement system. Concurrent inflammation, fibrosis, angiogenesis, and neurogenesis indicate that MC2 is a chronic inflammation. Correlation of endplate damage with complement and neurogenic proteins suggest that complement system activation and neoinnervation may be linked to endplate damage. The endplate-near marrow is the pathomechanistic site, because MC2 occur at locations with more endplate degeneration. Conclusion MC2 are fibroinflammatory changes with complement system involvement which occur adjacent to damaged endplates

Secondary prevention of coronary artery disease in Poland : results from the POLASPIRE survey

Background: The highest priority in preventive cardiology is given to patients with established coronary artery disease (CAD). The aim of the study was to assess the current implementation of the guidelines for secondary prevention in everyday clinical practice by evaluating control of the main risk factors and the cardioprotective medication prescription rates in patients following hospitalization for CAD. Methods: Fourteen departments of cardiology participated in the study. Patients (aged <= 80 years) hospitalized due an acute coronary syndrome or for a myocardial revascularization procedure were recruited and interviewed 6-18 months after the hospitalization. Results: Overall, 947 patients were examined 6-18 months after lwspitalization. The proportion of patients with high blood pressure (>= 140/90 mmHg) was 42%, with high low-density lipoprotein cholesterol (LDL-C >= 1.8 mmol/L) 62%, and with high fasting glucose (>= 7.0 mmol/L) 22%, 17% of participants were smokers and 42% were obese. The proportion of atients taking an antiplatelet agent 6-18 months after hospitalization was 93%, beta-blacker 89%, angiotensin converting enzyme inhibitor or sartan 86%, and a lipid-lowering drug 90%. Only 2.3% patients had controlled all the five main risk factors well (non-smoking, blood pressure < 140190 mmHg, LDL-C < 1.8 mmoIlL and glucose < 7.0 mmoilL, body mass index < 25 kg/m(2)), while 179% had 1 out of 5, 40.9% had 2 out of 5, and 29% had 3 out of 5 risk factors uncontrolled. Conclusions: The documented multicenter survey provides evidence that there is considerable potential for further reductions of cardiovascular risk in CAD patients in Poland. A revision of the state funded cardiac prevention programs seems rational

Secondary prevention of coronary artery disease in Poland. Results from the POLASPIRE survey

Background: The highest priority in preventive cardiology is given to patients with established coronary artery disease (CAD). The aim of the study was to assess the current implementation of the guidelines for secondary prevention in everyday clinical practice by evaluating control of the main risk factors and the cardioprotective medication prescription rates in patients following hospitalization for CAD.Methods: Fourteen departments of cardiology participated in the study. Patients (aged ≤ 80 years) hospitalized due an acute coronary syndrome or for a myocardial revascularization procedure were recruited and interviewed 6–18 months after the hospitalization.Results: Overall, 947 patients were examined 6–18 months after hospitalization. The proportion of patientswith high blood pressure (≥ 140/90 mmHg) was 42%, with high low-density lipoprotein cholesterol (LDL-C ≥ 1.8 mmol/L) 62%, and with high fasting glucose (≥ 7.0 mmol/L) 22%, 17% of participants were smokers and 42% were obese. The proportion of patients taking an antiplatelet agent 6–18 months after hospitalization was 93%, beta-blocker 89%, angiotensin converting enzyme inhibitor or sartan 86%, and a lipid-lowering drug 90%. Only 2.3% patients had controlled all the five main risk factors well (non-smoking, blood pressure &lt; 140/90 mmHg, LDL-C &lt; 1.8 mmol/L and glucose &lt; 7.0 mmol/L, body mass index &lt; 25 kg/m2), while 17.9% had 1 out of 5, 40.9% had 2 out of 5, and 29% had 3 out of 5 risk factors uncontrolled.Conclusions: The documented multicenter survey provides evidence that there is considerable potential for further reductions of cardiovascular risk in CAD patients in Poland. A revision of the state funded cardiac prevention programs seems rational

Extracellular vimentin is sufficient to promote cell attachment, spreading, and motility by a mechanism involving N-acetyl glucosamine-containing structures

Vimentin intermediate !laments form part of the cytoskeleton of mesenchymal cells, but under pathological conditions often associatedwith in ammation, vimentin !laments depolymerize as the result of phosphorylation or citrullination, and vimentin oligomers are secreted or released into the extracellular environment. In the extracellular space, vimentin can bind surfaces of cells and the extracellular matrix, and the interaction between extracellular vimentin and cells can trigger changes in cellular functions, such as activation of !broblasts to a !brotic phenotype. The mechanism by which extracellular vimentin binds external cell membranes and whether vimentin alone can act as an adhesive anchor for cells is largely uncharacterized. Here, we show that various cell types (normal and vimentin null !broblasts, mesenchymal stem cells, and A549 lung carcinoma cells) attach to and spread on polyacrylamide hydrogel substrates covalently linked to vimentin. Using traction force microscopy and spheroid expansion assays, we characterize how different cell types respond to extracellular vimentin. Cell attachment to and spreading on vimentin-coated surfaces is inhibited by hyaluronic acid degrading enzymes, hyaluronic acid synthase inhibitors, soluble heparin or N-acetyl glucosamine, all of which are treatments that have little or no effect on the same cell types binding to collagen-coated hydrogels. These studies highlight the effectiveness of substratebound vimentin as a ligand for cells and suggest that carbohydrate structures, including the glycocalyx and glycosylated cell surface proteins that contain N-acetyl glucosamine, form a novel class of adhesion receptors for extracellular vimentin that can either directly support cell adhesion to a substrate or !ne-tune the glycocalyx adhesive properties

Smoking cessation in patients with established coronary artery disease: data from the POLASPIRE survey

Background: Smoking cessation in patients with coronary artery disease (CAD) is related to decreased risk of cardiovascular events. Aims: To evaluate factors related to persistent smoking in patients with established coronary artery disease. Methods: Patients aged 80 years or younger and hospitalized for acute coronary syndrome or a myocardial revascularization procedure were interviewed 6 to 18 months after the recruiting event. Medical history, smoking behavior, and exposure to environmental smoke were assessed during the interview. Self­­reported smoking status was validated by carbon monoxide in exhaled air measurement. Persistent smoking was defined as smoking at the time of interview among those who smoked during the month prior to the recruiting event. Results: We analyzed the data of 1034 patients, including 764 (73.9%) who reported smoking at any time in the past and 296 (28.6%) who smoked within 1 month before the recruiting hospitalization. At the time of the interview, the overall smoking rate was 17.2%, whereas 54.7% of patients were persistent smokers. Secondhand smoke exposure and duration of smoking were associated with lower likelihood whereas older age, high socioeconomic status, cardiac rehabilitation following a cardiovascular event, and consultation with a cardiologist were associated with higher likelihood of smoking cessation. Conclusions: Over half of all smokers hospitalized for CAD are still smoking 6 to 18 months after discharge. Older age, secondhand smoking, low socioeconomic status, lack of consultation with a cardiologist, and cardiac rehabilitation following hospitalization were related to persistent smoking. Our findings may help develop strategies aimed at assisting smoking cessation in patients with CAD

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio