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Long-term monitoring studies on the transition of different land cover units to barren areas are crucial to gain a better understanding of the potential challenges and threats that land surface ecosystems face. This study utilized the Moderate Resolution Imaging Spectroradiometer (MODIS) land cover products (MCD12C1) to conduct geospatial analysis based on the maximum extent (MaxE) concept, to assess the spatiotemporal changes in barren areas from 2001 to 2022, at global and continental scales. The MaxE area includes all the pixels across the entire period of observations where the barren land cover class was at least once present. The relative expansion or reduction of the barren areas can be directly assessed with MaxE, as any annual change observed in the barren distribution is comparable over the entire dataset. The global barren areas without any land change (UA) during this period were equivalent to 12.8% (18,875,284 km2) of the global land surface area. Interannual land cover changes to barren areas occurred in an additional area of 3,438,959 km2 (2.3% of the global area). Globally, barren areas show a gradual reduction from 2001 (91.1% of MaxE) to 2012 (86.8%), followed by annual fluctuations until 2022 (88.1%). These areas were mainly interchanging between open shrublands and grasslands. A relatively high transition between barren areas and permanent snow and ice is found in Europe and North America. The results show a 3.7% decrease in global barren areas from 2001 to 2022. Areas that are predominantly not barren account for 30.6% of the transitional areas (TAs), meaning that these areas experienced short-term or very recent transitions from other land cover classes to barren. Emerging barren areas hotspots were mainly found in the Mangystau region (Kazakhstan), Tibetan plateau, northern Greenland, and the Atlas Mountains (Morocco, Tunisia).

Ant colony optimization (ACO) has proven its adaptation capabilities on optimization problems with dynamic environments. In this work, the dynamic traveling salesman problem (DTSP) is used as the base problem to generate dynamic test cases. Two types of dynamic changes for the DTSP are considered: (1) node changes and (2) weight changes. In the experiments, ACO algorithms are systematically compared in different DTSP test cases. Statistical tests are performed using the arithmetic mean and standard deviation of ACO algorithms, which is the standard method of comparing ACO algorithms. To complement the comparisons, the quantiles of the distribution are also used to measure the peak-, average-, and bad-case performance of ACO algorithms. The experimental results demonstrate some advantages of using quantiles for evaluating the performance of ACO algorithms in some DTSP test cases.

It is well-established that both volume conduction and the choice of recording reference (montage) affect the correlation measures obtained from scalp EEG, both in the time and frequency domains. As a result, a number of correlation measures have been proposed aiming to reduce these effects. In our previous work, we have showed that scalp-EEG based functional brain networks in patients with epilepsy exhibit clear periodic patterns at different time scales and that these patterns are strongly correlated to seizure onset, particularly at shorter time scales (around 3 and 5 h), which has important clinical implications. In the present work, we use the same long-duration clinical scalp EEG data (multiple days) to investigate the extent to which the aforementioned results are affected by the choice of reference choice and correlation measure, by considering several widely used montages as well as correlation metrics that are differentially sensitive to the effects of volume conduction. Specifically, we compare two standard and commonly used linear correlation measures, cross-correlation in the time domain, and coherence in the frequency domain, with measures that account for zero-lag correlations: corrected cross-correlation, imaginary coherence, phase lag index, and weighted phase lag index. We show that the graphs constructed with corrected cross-correlation and WPLI are more stable across different choices of reference. Also, we demonstrate that all the examined correlation measures revealed similar periodic patterns in the obtained graph measures when the bipolar and common reference (Cz) montage were used. This includes circadian-related periodicities (e.g., a clear increase in connectivity during sleep periods as compared to awake periods), as well as periodicities at shorter time scales (around 3 and 5 h). On the other hand, these results were affected to a large degree when the average reference montage was used in combination with standard cross-correlation, coherence, imaginary coherence, and PLI, which is likely due to the low number of electrodes and inadequate electrode coverage of the scalp. Finally, we demonstrate that the correlation between seizure onset and the brain network periodicities is preserved when corrected cross-correlation and WPLI were used for all the examined montages. This suggests that, even in the standard clinical setting of EEG recording in epilepsy where only a limited number of scalp EEG measurements are available, graph-theoretic quantification of periodic patterns using appropriate montage, and correlation measures corrected for volume conduction provides useful insights into seizure onset.

Background: Complement factor H-related protein 5 (CFHR5) nephropathy is an inherited renal disease characterized by microscopic and synpharyngitic macroscopic haematuria, C3 glomerulonephritis and renal failure. It is caused by an internal duplication of exons 2-3 within the CFHR5 gene resulting in dysregulation of the alternative complement pathway. The clinical characteristics and outcomes of transplanted patients with this rare familial nephropathy remain unknown., Methods: This is a retrospective case series study of 17 kidney transplant patients with the established founder mutation, followed-up over a span of 30 years., Results: The mean (±SD) age of patients at the time of the study and at transplantation was 58.6 ± 9.9 and 46.7 ± 8.8 years, respectively. The 10- and 15-year patient survival rates were 100 and 77.8%, respectively. Proteinuria was present in 33.3% and microscopic haematuria in 58.3% of patients with a functional graft. Serum complement levels were normal in all. 'Confirmed' and 'likely' recurrence of CFHR5 nephropathy were 16.6 and 52.9%, respectively; however, 76.5% of patients had a functional graft after a median of 120 months post-transplantation. Total recurrence was not associated with graft loss (P = 0.171), but was associated with the presence of microscopic haematuria (P = 0.001) and proteinuria (P = 0.018). Graft loss was associated with the presence of proteinuria (P = 0.025)., Conclusions: We describe for the first time the clinical characteristics and outcome of patients with CFHR5 nephropathy post-transplantation. Despite the recurrence of CFHR5 nephropathy, we provide evidence for a long-term favourable outcome and support the continued provision of kidney transplantation as a renal replacement option in patients with CFHR5 nephropathy., (© The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.)

Functional hypothalamic amenorrhoea (FHA) is a neuroendocrine disorder caused by an energy deficit and characterized by low leptin levels. Based on this, previous studies have suggested that leptin administration may play a crucial role in FHA treatment. However, FHA is also associated with abnormal psychosocial and dietary behaviour that needs to be addressed. In this context, this systematic review examined the efficacy of leptin treatment, non-pharmacological therapy and nutritional interventions in FHA. PubMed, Medline and Cochrane Library databases were searched in order to find relevant papers, including randomized controlled trials, clinical trials, prospective studies and case reports. The effects of different treatments on reproductive function, hormonal status and bone markers were recorded. Studies regarding other forms of treatment were excluded. In total, 111 papers were retrieved. After the removal of 29 duplicate papers, the abstracts and titles of 82 papers were examined. Subsequently, 53 papers were excluded based on title, and seven papers were omitted based on abstract. The remaining 11 papers were used: three based on leptin treatment, three regarding non-pharmacological treatment and five regarding dietary intervention. This literature review indicates that all of these treatment strategies improved reproductive function and hormonal status significantly, although conclusive results could not be drawn on bone markers. While leptin may be a promising new treatment, social aspects of FHA should also be addressed. As a result, a multifaceted therapeutic approach should be applied to treat affected women., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Thin-basement-membrane nephropathy (TBMN) and Alport syndrome (AS) are progressive collagen IV nephropathies caused by mutations in COL4A3/A4/A5 genes. These nephropathies invariably present with microscopic hematuria and frequently progress to proteinuria and CKD or ESRD during long-term follow-up. Nonetheless, the exact molecular mechanisms by which these mutations exert their deleterious effects on the glomerulus remain elusive. We hypothesized that defective trafficking of the COL4A3 chain causes a strong intracellular effect on the cell responsible for COL4A3 expression, the podocyte. To this end, we overexpressed normal and mutant COL4A3 chains (G1334E mutation) in human undifferentiated podocytes and tested their effects in various intracellular pathways using a microarray approach. COL4A3 overexpression in the podocyte caused chain retention in the endoplasmic reticulum (ER) that was associated with activation of unfolded protein response (UPR)-related markers of ER stress. Notably, the overexpression of normal or mutant COL4A3 chains differentially activated the UPR pathway. Similar results were observed in a novel knockin mouse carrying the Col4a3-G1332E mutation, which produced a phenotype consistent with AS, and in biopsy specimens from patients with TBMN carrying a heterozygous COL4A3-G1334E mutation. These results suggest that ER stress arising from defective localization of collagen IV chains in human podocytes contributes to the pathogenesis of TBMN and AS through activation of the UPR, a finding that may pave the way for novel therapeutic interventions for a variety of collagenopathies.

Clear cell renal cell carcinoma (ccRCC) is the predominant subtype of renal cell carcinoma (RCC). It is one of the most therapy-resistant carcinomas, responding very poorly or not at all to radiotherapy, hormonal therapy and chemotherapy. A more comprehensive understanding of the deregulated pathways in ccRCC can lead to the development of new therapies and prognostic markers. We performed a meta- analysis of 5 publicly available gene expression datasets and identified a list of co- deregulated genes, for which we performed extensive bioinformatic analysis coupled with experimental validation on the mRNA level. Gene ontology enrichment showed that many proteins are involved in response to hypoxia/oxygen levels and positive regulation of the VEGFR signaling pathway. KEGG analysis revealed that metabolic pathways are mostly altered in ccRCC. Similarly, Ingenuity Pathway Analysis showed that the antigen presentation, inositol metabolism, pentose phosphate, glycolysis/gluconeogenesis and fructose/mannose metabolism pathways are altered in the disease. Cellular growth, proliferation and carbohydrate metabolism, were among the top molecular and cellular functions of the co-deregulated genes. qRT-PCR validated the deregulated expression of several genes in Caki-2 and ACHN cell lines and in a cohort of ccRCC tissues. NNMT and NR3C1 increased expression was evident in ccRCC biopsies from patients using immunohistochemistry. ROC curves evaluated the diagnostic performance of the top deregulated genes in each dataset. We show that metabolic pathways are mostly deregulated in ccRCC and we highlight those being most responsible in its formation. We suggest that these genes are candidate predictive markers of the disease.