Surface plasmon polaritons are a central concept in nanoplasmonics and have been exploited to develop ultrasensitive chemical detection platforms, as well as imaging and spectroscopic techniques at ...the nanoscale. Surface plasmons can decay to form highly energetic (or hot) electrons in a process that is usually thought to be parasitic for applications, because it limits the lifetime and propagation length of surface plasmons and therefore has an adverse influence on the functionality of nanoplasmonic devices. Recently, however, it has been shown that hot electrons produced by surface plasmon decay can be harnessed to produce useful work in photodetection, catalysis and solar energy conversion. Nevertheless, the surface-plasmon-to-hot-electron conversion efficiency has been below 1% in all cases. Here we show that adiabatic focusing of surface plasmons on a Schottky diode-terminated tapered tip of nanoscale dimensions allows for a plasmon-to-hot-electron conversion efficiency of ∼30%. We further demonstrate that, with such high efficiency, hot electrons can be used for a new nanoscopy technique based on an atomic force microscopy set-up. We show that this hot-electron nanoscopy preserves the chemical sensitivity of the scanned surface and has a spatial resolution below 50 nm, with margins for improvement.
COVID-19 pandemic and chaos theory Postavaru, O.; Anton, S.R.; Toma, A.
Mathematics and computers in simulation,
03/2021, Letnik:
181
Journal Article
Recenzirano
Odprti dostop
The dynamics of COVID-19 is investigated with regard to complex contributions of the omitted factors. For this purpose, we use a fractional order SEIR model which allows us to calculate the number of ...infections considering the chaotic contributions into susceptible, exposed, infectious and removed number of individuals. We check our model on Wuhan, China-2019 and South Korea underlying the importance of the chaotic contribution, and then we extend it to Italy and the USA. Results are of great guiding significance to promote evidence-based decisions and policy.
The detection of a few molecules in a highly diluted solution is of paramount interest in fields including biomedicine, safety and eco-pollution in relation to rare and dangerous chemicals. ...Nanosensors based on plasmonics are promising devices in this regard, in that they combine the features of high sensitivity, label-free detection and miniaturization. However, plasmonic-based nanosensors, in common with general sensors with sensitive areas on the scale of nanometres, cannot be used directly to detect molecules dissolved in femto- or attomolar solutions. In other words, they are diffusion-limited and their detection times become impractical at such concentrations. In this Article, we demonstrate, by combining super-hydrophobic artificial surfaces and nanoplasmonic structures, that few molecules can be localized and detected even at attomolar (10-18 mol l-1 ) concentration. Moreover, the detection can be combined with fluorescence and Raman spectroscopy, such that the chemical signature of the molecules can be clearly determined.
Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney disease (CKD). Here we show that recessive mutations in FAT1 cause a distinct renal disease entity in four families with a ...combination of SRNS, tubular ectasia, haematuria and facultative neurological involvement. Loss of FAT1 results in decreased cell adhesion and migration in fibroblasts and podocytes and the decreased migration is partially reversed by a RAC1/CDC42 activator. Podocyte-specific deletion of Fat1 in mice induces abnormal glomerular filtration barrier development, leading to podocyte foot process effacement. Knockdown of Fat1 in renal tubular cells reduces migration, decreases active RAC1 and CDC42, and induces defects in lumen formation. Knockdown of fat1 in zebrafish causes pronephric cysts, which is partially rescued by RAC1/CDC42 activators, confirming a role of the two small GTPases in the pathogenesis. These findings provide new insights into the pathogenesis of SRNS and tubulopathy, linking FAT1 and RAC1/CDC42 to podocyte and tubular cell function.
Background: Coeliac disease may be regarded as refractory disease (RCD) when symptoms persist or recur despite strict adherence to a gluten-free diet. RCD may be subdivided into types I and II with a ...phenotypically normal and aberrant intraepithelial T-cell population, respectively. RCD I seems to respond well to azathioprine/prednisone therapy. RCD II is usually resistant to any known therapy and transition into enteropathy-associated T-cell lymphoma (EATL) is common. Aim: To provide further insight into RCD and the development of EATL, by reporting on long-term survival and risk of transition of RCD into EATL in a large cohort of patients with complicated coeliac disease. Design and Methods: Retrospective comparison of responses to therapy in four groups of patients with complicated coeliac disease: 43, RCD I; 50, RCD II (total), of whom 26 with RCD II developed EATL after a period of refractoriness to a gluten-free diet (secondary EATL) and 13 were EATL patients without preceding history of complicated coeliac disease (de novo EATL). Results: No coeliac-disease-related mortality was recognised in the RCD I group. The overall 5-year survival in the RCD I group it was 96%; in the RCD II (total) group was 58%; and in the RCD II group after developing EATL it was only 8%. The 2-year survival in the de novo EATL group was 20% versus 15% in secondary EATL group (p = 0.63). Twenty-eight (56%) of the 50 patients with RCD II died, 23 (46%) due to EATL, 4 due to a progressive refractory state with emaciation and 1 from neurocoeliac disease. Conclusion: Remarkably, no patient with RCD I developed RCD II or EATL within the mean follow-up period of 5 years (range 2–15 years). A total of 52% of the RCD II patients developed EATL within 4–6 years after the diagnosis of RCD II. More aggressive and targeted therapies seem necessary in RCD II and EATL.
Kidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old ...embryos. Gene expression profiles between these two developmental stages identify cxcl12a and myca as candidates involved in the repair process. Zebrafish embryos with cxcl12a, cxcr4b, or myca deficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout, Cxcl12 and Myc gene deletions suppress mitochondrial metabolism and glycolysis, and delay the recovery after ischemia/reperfusion injury. Probing these observations in zebrafish reveal that inhibition of glycolysis slows fast migrating cells and delays the repair after injury, but does not affect the slow cell movements during kidney development. Our findings demonstrate that Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis.
MicroRNAs (miR), as important epigenetic control factors, reportedly regulate wound repair. However, our insufficient knowledge of clinically relevant miRs hinders their potential therapeutic use. ...For this, we performed paired small and long RNA-sequencing and integrative omics analysis in human tissue samples, including matched skin and acute wounds collected at each healing stage and chronic nonhealing venous ulcers (VUs). On the basis of the findings, we developed a compendium (
https://www.xulandenlab.com/humanwounds-mirna-mrna
), which will be an open, comprehensive resource to broadly aid wound healing research. With this first clinical, wound-centric resource of miRs and mRNAs, we identified 17 pathologically relevant miRs that exhibited abnormal VU expression and displayed their targets enriched explicitly in the VU gene signature. Intermeshing regulatory networks controlled by these miRs revealed their high cooperativity in contributing to chronic wound pathology characterized by persistent inflammation and proliferative phase initiation failure. Furthermore, we demonstrated that miR-34a, miR-424, and miR-516, upregulated in VU, cooperatively suppressed keratinocyte migration and growth while promoting inflammatory response. By combining miR expression patterns with their specific target gene expression context, we identified miRs highly relevant to VU pathology. Our study opens the possibility of developing innovative wound treatment that targets pathologically relevant cooperating miRs to attain higher therapeutic efficacy and specificity.
Developing organisms need to adapt to environmental variations as well as to rapid changes in substrate availability and energy demands imposed by fast-growing tissues and organs. Little is known ...about the adjustments that kidneys undergo in response to these challenges. We performed single-cell RNA sequencing of zebrafish pronephric duct cells to understand how the developing kidney responds to changes in filtered substrates and intrinsic energy requirements. We found high levels of glucose transporters early in development and increased expression of monocarboxylate transporters at later times. This indicates that the zebrafish embryonic kidney displays a high glucose transporting capacity during early development, which is replaced by the ability to absorb monocarboxylates and amino acids at later stages. This change in transport capacity was accompanied by the upregulation of mitochondrial carriers, indicating a switch to increased oxidative phosphorylation to meet the increasing energy demand of a developing kidney.
The zebrafish embryonic kidney has high levels of glucose transporters during early development, which are replaced by monocarboxylate and amino acid transporters later on. Inhibition of Na
-glucose cotransporter-dependent glucose transport by sotagliflozin also increased
expression, supporting the idea that the glucose transport capacity is dynamically adjusted during zebrafish pronephros development. Concurrent upregulation of mitochondrial SCL25 transporters at later stages supports the idea that the pronephros adjusts to changing substrate supplies and/or energy demands during embryonic development.
HIV-induced malnutrition is highly prevalent in different parts of the world particularly in sub-Saharan Africa. The food intervention package is one of the strategies that targets malnutrition among ...HIV-infected people through nutritional evaluation, counseling and care. However, little is known concerning the outcomes of intervention in such patients in treatment program. Therefore, this study aimed to assess nutritional treatment outcomes and its predictors among adult HIV-positive undernourished individuals in Ethiopia.
Facility based retrospective cohort study was deployed in Adult Antiretroviral therapy clinic of Hawassa University Comprehensive Specialized Hospital. Data of 419 patients were extracted from the food by prescription registration book and patient cards using structured questionnaires. Statistical significance was assessed using Cox-proportional Hazard model by determining hazard ratios and 95% confidence interval.
The proportion of adult HIV patients who recovered from malnutrition after they were enrolled in the food by prescription therapy was 53.0%. The variables found to have an association with good nutritional treatment outcomes of food by prescription in the final model are being female (Adjusted Hazard Ratio (AHR) = 3.38, 95% CI: 2.15, 5.32), secondary education (AHR = 2.16, 95% CI: 1.11, 4.18), tertiary education (AHR = 3.75, 95% CI: 1.66, 8.48), SAM (AHR = 0.20; 95% CI: 0.12, 0.35), and HAART (AHR = 2.70, 95% CI: 1.50, 4.86). Having Severe Acute Malnutrition (SAM) at baseline nutritional assessment (AHR = 3.42, 95% CI; 2.81, 5.15), taking ART for more than 12 months (AHR = 0.26, 95% CI: 0.13, 0.84) and starting HAART immediately after testing positive (AHR = 0.26, 95% CI: 0.13, 0.84) are significantly associated with nutritional treatment failure.
Fifty-three percent of HIV patients recovered from malnutrition after they were enrolled in the food by prescription therapy.
Nephronophthisis (NPH), an autosomal recessive ciliopathy, results from mutations in more than 20 different genes (NPHPs). These gene products form protein complexes that regulate trafficking within ...the cilium, a microtubular structure that plays a crucial role in developmental processes. Several NPHPs, including NPHP2/Inversin, have been linked to extraciliary functions. In addition to defining a specific segment of primary cilia (Inversin compartment), NPHP2 participates in planar cell polarity (PCP) signaling along with Dishevelled and Vangl family members.
We used the mutant zebrafish line invssa36157, containing a stop codon at amino acid 314, to characterize tissue-specific functions of zebrafish Nphp2. The invssa36157 line exhibits mild ciliopathy phenotypes and increased glomerular and cloaca cyst formation. These mutants showed enhanced susceptibility to the simultaneous depletion of the nphp1/nphp2/nphp8 module, known to be involved in the cytoskeletal organization of epithelial cells. Notably, simultaneous depletion of zebrafish nphp1 and vangl2 led to a pronounced increase in cloaca malformations in the invssa36157 mutant embryos. Time-lapse imaging showed that the pronephric cells correctly migrated towards the ectodermal cells in these embryos, but failed to form the cloaca opening. Despite these abnormal developments, cellular fate does not seem to be affected in nphp1 and vangl2 MO-depleted invssa36157 mutants, as shown by in situ hybridizations for markers of pronephros and ectodermal cell development. However, significantly reduced apoptotic activity was observed in this double knockdown model, signifying the role of apoptosis in cloacal morphogenesis. Our findings underscore the critical interplay of nphp1, nphp2/Inversin, and vangl2 in orchestrating normal cloaca formation in zebrafish, shedding light on the complex molecular mechanisms underlying ciliopathy-associated phenotypes.
•nphp genes depletion causes cysts and cloaca malformation in zebrafish.•invssa36157 zebrafish exhibit mild ciliopathy phenotypes.•nphp1 and vangl2 depletion worsens cloaca malformation.•nphp1 and vangl2 knockdown impairs cell rearrangement in invssa36157 mutants.•Cell fate unaffected but altered apoptosis may contribute to cloaca defects.
PDF
