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Acute and chronic wounds have varying etiologies and are an economic burden to healthcare systems around the world. The advanced wound care market is expected to exceed $22 billion by 2024. Wound care professionals rely heavily on images and image documentation for proper diagnosis and treatment. Unfortunately lack of expertise can lead to improper diagnosis of wound etiology and inaccurate wound management and documentation. Fully automatic segmentation of wound areas in natural images is an important part of the diagnosis and care protocol since it is crucial to measure the area of the wound and provide quantitative parameters in the treatment. Various deep learning models have gained success in image analysis including semantic segmentation. This manuscript proposes a novel convolutional framework based on MobileNetV2 and connected component labelling to segment wound regions from natural images. The advantage of this model is its lightweight and less compute-intensive architecture. The performance is not compromised and is comparable to deeper neural networks. We build an annotated wound image dataset consisting of 1109 foot ulcer images from 889 patients to train and test the deep learning models. We demonstrate the effectiveness and mobility of our method by conducting comprehensive experiments and analyses on various segmentation neural networks. The full implementation is available at https://github.com/uwm-bigdata/wound-segmentation .

The neutrophil-to-lymphocyte ratio (NLR) in peripheral blood reflects the balance between systemic inflammation and immunity and is emerging as a prognostic biomarker in many diseases, but its predictive role for mortality in the general population has not been investigated. We analyzed 1999–2014 National Health and Nutrition Examination Survey mortality-linked data, followed up until 2015. In participants aged > 30 with measurements of differential white blood cell counts, NLR was calculated and categorized into quartiles. Associations of increased NLR with overall or cause-specific mortality were assessed with Cox proportional hazard regression models, adjusted for potential confounders. Increased NLR was associated with overall mortality (hazard ratio [HR] 1.14, 95% confidence interval [CI] 1.10–1.17, per quartile NLR) and mortality due to heart disease (1.17, 1.06–1.29), chronic lower respiratory disease (1.24, 1.04–1.47), influenza/pneumonia (1.26, 1.03–1.54) and kidney disease (1.26, 1.03–1.54). NLR was associated with cancer mortality only in the first follow-up year (HR 1.48, 95% CI 1.11–1.98). The association with chronic lower respiratory disease mortality was stronger in individuals with prevalent lung diseases (HR 1.46, 95% CI 1.14–1.88, P interaction  = 0.01), while NLR showed positive associations with mortality from heart disease (1.21, 1.07–1.38) and cerebrovascular disease (1.30, 1.04–1.63) only among individuals without these conditions at baseline. NLR is associated with mortality overall and due to certain causes in the general population. Associations over short follow-up intervals and among individuals with conditions at baseline suggest effects of disordered inflammation and immunity on progression of those conditions, while other associations may reflect contributions to disease etiology.

Most irreversible blindness results from retinal disease. To advance our understanding of the etiology of blinding diseases, we used single-cell RNA-sequencing (scRNA-seq) to analyze the transcriptomes of ~85,000 cells from the fovea and peripheral retina of seven adult human donors. Utilizing computational methods, we identified 58 cell types within 6 classes: photoreceptor, horizontal, bipolar, amacrine, retinal ganglion and non-neuronal cells. Nearly all types are shared between the two retinal regions, but there are notable differences in gene expression and proportions between foveal and peripheral cohorts of shared types. We then used the human retinal atlas to map expression of 636 genes implicated as causes of or risk factors for blinding diseases. Many are expressed in striking cell class-, type-, or region-specific patterns. Finally, we compared gene expression signatures of cell types between human and the cynomolgus macaque monkey, Macaca fascicularis . We show that over 90% of human types correspond transcriptomically to those previously identified in macaque, and that expression of disease-related genes is largely conserved between the two species. These results validate the use of the macaque for modeling blinding disease, and provide a foundation for investigating molecular mechanisms underlying visual processing.

Reportedly, 300 million people worldwide are affected by the consumption of arsenic contaminated groundwater. India prominently figures amongst them and the state of Bihar has shown an upsurge in cases affected by arsenic poisoning. Escalated arsenic content in blood, leaves 1 in every 100 human being highly vulnerable to being affected by the disease. Uncontrolled intake may lead to skin, kidney, liver, bladder, or lung related cancer but even indirect forms of cancer are showing up on a regular basis with abnormal arsenic levels as the probable cause. But despite the apparent relation, the etiology has not been understood clearly. Blood samples of 2000 confirmed cancer patients were collected from pathology department of our institute. For cross-sectional design, 200 blood samples of subjects free from cancer from arsenic free pockets of Patna urban agglomeration, were collected. Blood arsenic levels in carcinoma patients as compared to sarcomas, lymphomas and leukemia were found to be higher. The geospatial map correlates the blood arsenic with cancer types and the demographic area of Gangetic plains. Most of the cancer patients with high blood arsenic concentration were from the districts near the river Ganges. The raised blood arsenic concentration in the 2000 cancer patients strongly correlates the relationship of arsenic with cancer especially the carcinoma type which is more vulnerable. The average arsenic concentration in blood of the cancer patients in the Gangetic plains denotes the significant role of arsenic which is present in endemic proportions. Thus, the study significantly correlates and advocates a strong relation of the deleterious element with the disease. It also underlines the need to address the problem by deciphering the root cause of the elevated cancer incidences in the Gangetic basin of Bihar and its association with arsenic poisoning.

Aberrant mechanical factor is one of the etiologies of the intervertebral disc (IVD) degeneration (IVDD). However, the exact molecular mechanism of spinal mechanical loading stress-induced IVDD has yet to be elucidated due to a lack of an ideal and stable IVDD animal model. The present study aimed to establish a stable IVDD mouse model and evaluated the effect of aberrant spinal mechanical loading on the pathogenesis of IVDD. Eight-week-old male mice were treated with lumbar spine instability (LSI) surgery to induce IVDD. The progression of IVDD was evaluated by μCT and Safranin O/Fast green staining analysis. The metabolism of extracellular matrix, ingrowth of sensory nerves, pyroptosis in IVDs tissues were determined by immunohistological or real-time PCR analysis. The apoptosis of IVD cells was tested by TUNEL assay. IVDD modeling was successfully produced by LSI surgery, with substantial reductions in IVD height, BS/TV, Tb.N. and lower IVD score. LSI administration led to the histologic change of disc degeneration, disruption of the matrix metabolism, promotion of apoptosis of IVD cells and invasion of sensory nerves into annulus fibrosus, as well as induction of pyroptosis. Moreover, LSI surgery activated Wnt signaling in IVD tissues. Mechanical instability caused by LSI surgery accelerates the disc matrix degradation, nerve invasion, pyroptosis, and eventually lead to IVDD, which provided an alternative mouse IVDD model.

Ancestral environmental exposures to a variety of factors and toxicants have been shown to promote the epigenetic transgenerational inheritance of adult onset disease. One of the most widely used agricultural pesticides worldwide is the herbicide glyphosate (N-(phosphonomethyl)glycine), commonly known as Roundup. There are an increasing number of conflicting reports regarding the direct exposure toxicity (risk) of glyphosate, but no rigorous investigations on the generational actions. The current study using a transient exposure of gestating F0 generation female rats found negligible impacts of glyphosate on the directly exposed F0 generation, or F1 generation offspring pathology. In contrast, dramatic increases in pathologies in the F2 generation grand-offspring, and F3 transgenerational great-grand-offspring were observed. The transgenerational pathologies observed include prostate disease, obesity, kidney disease, ovarian disease, and parturition (birth) abnormalities. Epigenetic analysis of the F1, F2 and F3 generation sperm identified differential DNA methylation regions (DMRs). A number of DMR associated genes were identified and previously shown to be involved in pathologies. Therefore, we propose glyphosate can induce the transgenerational inheritance of disease and germline (e.g. sperm) epimutations. Observations suggest the generational toxicology of glyphosate needs to be considered in the disease etiology of future generations.

Ovarian carcinoma is caused by multiple factors, but its etiology associated with microbes and infection is unknown. Using 16S rRNA high-throughput sequencing methods, the diversity and composition of the microbiota from ovarian cancer tissues (25 samples) and normal distal fallopian tube tissues (25 samples) were analyzed. High-throughput sequencing showed that the diversity and richness indexes were significantly decreased in ovarian cancer tissues compared to tissues from normal distal fallopian tubes. The ratio of the two phyla for Proteobacteria / Firmicutes was notably increased in ovarian cancer, which revealed that microbial composition change might be associated with the process of ovarian cancer development. In addition, transcriptome-sequencing (RNA-seq) analyses suggested that the transcriptional profiles were statistically different between ovarian carcinoma and normal distal fallopian tubes. Moreover, a set of genes including 84 different inflammation-associated or immune-associated genes, which had been named as the human antibacterial-response genes were also modulated expression. Therefore, we hypothesize that the microbial composition change, as a novel risk factor, may be involving the initiation and progression of ovarian cancer via influencing and regulating the local immune microenvironment of fallopian tubes except for regular pathways.

Ulcerative colitis (UC) is a chronic immune-mediated disorder, whose etiology is not fully understood and for which no effective treatment is available. Recently, research has focused on the dysbiosis of gut microbiome in UC. However, the results so far remain inconsistent and insufficient to understand the microbial component in UC pathogenesis. In this study, we determine specific changes in the gut microbial profile in Polish UC patients compared to healthy subjects for the first time. Using 16S rRNA gene-based analysis we have described the intestinal microbial community in a group of 20 individuals (10 UC patients and 10 controls). Our results after multiple hypothesis testing correction demonstrated substantially lower gut microbiome diversity in UC cases compared to the controls and considerable differences at the phylum level, as well as among 13 bacterial families and 20 bacterial genera ( p  < 0.05). UC samples were more abundant in Proteobacteria (8.42%), Actinobacteria (6.89%) and Candidate Division TM7 (2.88%) than those of healthy volunteers (2.57%, 2.29% and 0.012%, respectively). On the other hand, Bacteroidetes and Verrucomicrobia were presented at a lower level in UC relative to the controls (14% and 0% vs 27.97% and 4.47%, respectively). In conclusion, our results show a reduced gut microbial diversity in Polish UC patients, a reduction of taxa with an anti-inflammatory impact and an increased abundance of potentially pathogenic bacteria.

Studying respiratory illness-specific microbial signatures and their interaction with other micro-residents could provide a better understanding of lung microbial ecology. Each respiratory illness has a specific disease etiology, however, so far no study has revealed disease—specific microbial markers. The present study was designed to determine disease-specific microbial features and their interactions with other residents in chronic obstructive pulmonary diseases (stable and exacerbated), sarcoidosis, and interstitial lung diseases. Broncho-alveolar lavage samples (n = 43) were analyzed by SSU rRNA gene sequencing to study the alveolar microbiome in these diseases. A predominance of Proteobacteria followed by Firmicutes, Bacteroidetes, Actinobacteria, and Fusobacteria was observed in all the disease subsets. Shannon diversity was significantly higher in stable COPD when compared to exacerbated chronic obstructive pulmonary disease (ECOPD) ( p  = 0.0061), and ILD patient samples ( p  = 0.037). The lung microbiome of the patients with stable COPD was more diverse in comparison to ECOPD and ILD patients ( p  < 0.001). Lefse analysis identified 40 disease—differentiating microbial features (LDA score (log10) > 4). Species network analysis indicated a significant correlation ( p  < 0.05) of diseases specific microbial signature with other lung microbiome members. The current study strengthens the proposed hypothesis that each respiratory illness has unique microbial signatures. These microbial signatures could be used as diagnostic markers to differentiate among various respiratory illnesses.

East Asia has experienced an excessive increase in myopia in the past decades with more than 80% of the younger generation now affected. Environmental and genetic factors are both assumed to contribute in the development of refractive errors, but the etiology is unknown. The environmental factor argued to be of greatest importance in preventing myopia is high levels of daylight exposure. If true, myopia prevalence would be higher in adolescents living in high latitude countries with fewer daylight hours in the autumn-winter. We examined the prevalence of refractive errors in a representative sample of 16–19-year-old Norwegian Caucasians (n = 393, 41.2% males) in a representative region of Norway (60° latitude North). At this latitude, autumn-winter is 50 days longer than summer. Using gold-standard methods of cycloplegic autorefraction and ocular biometry, the overall prevalence of myopia [spherical equivalent refraction (SER) ≤−0.50 D] was 13%, considerably lower than in East Asians. Hyperopia (SER ≥ + 0.50 D), astigmatism (≥1.00 DC) and anisometropia (≥1.00 D) were found in 57%, 9% and 4%. Norwegian adolescents seem to defy the world-wide trend of increasing myopia. This suggests that there is a need to explore why daylight exposure during a relatively short summer outweighs that of the longer autumn-winter.