Integrating somatic mutation profiles with structural deep clustering network for metabolic stratification in pancreatic cancer: a comprehensive analysis of prognostic and genomic landscapes.

Pancreatic cancer is a globally recognized highly aggressive malignancy, posing a significant threat to human health and characterized by pronounced heterogeneity. In recent years, researchers have uncovered that the development and progression of cancer are often attributed to the accumulation of somatic mutations within cells. However, cancer somatic mutation data exhibit characteristics such as high dimensionality and sparsity, which pose new challenges in utilizing these data effectively. In this study, we propagated the discrete somatic mutation data of pancreatic cancer through a network propagation model based on protein-protein interaction networks. This resulted in smoothed somatic mutation profile data that incorporate protein network information. Based on this smoothed mutation profile data, we obtained the activity levels of different metabolic pathways in pancreatic cancer patients. Subsequently, using the activity levels of various metabolic pathways in cancer patients, we employed a deep clustering algorithm to establish biologically and clinically relevant metabolic subtypes of pancreatic cancer. Our study holds scientific significance in classifying pancreatic cancer based on somatic mutation data and may provide a crucial theoretical basis for the diagnosis and immunotherapy of pancreatic cancer patients.

Machine learning-based prediction of diabetic patients using blood routine data.

Diabetes stands as one of the most prevalent chronic diseases globally. The conventional methods for diagnosing diabetes are frequently overlooked until individuals manifest noticeable symptoms of the condition. This study aimed to address this gap by collecting comprehensive datasets, including 1000 instances of blood routine data from diabetes patients and an equivalent dataset from healthy individuals. To differentiate diabetes patients from their healthy counterparts, a computational framework was established, encompassing eXtreme Gradient Boosting (XGBoost), random forest, support vector machine, and elastic net algorithms. Notably, the XGBoost model emerged as the most effective, exhibiting superior predictive results with an area under the receiver operating characteristic curve (AUC) of 99.90% in the training set and 98.51% in the testing set. Moreover, the model showcased commendable performance during external validation, achieving an overall accuracy of 81.54%. The probability generated by the model serves as a risk score for diabetes susceptibility. Further interpretability was achieved through the utilization of the Shapley additive explanations (SHAP) algorithm, identifying pivotal indicators such as mean corpuscular hemoglobin concentration (MCHC), lymphocyte ratio (LY%), standard deviation of red blood cell distribution width (RDW-SD), and mean corpuscular hemoglobin (MCH). This enhances our understanding of the predictive mechanisms underlying diabetes. To facilitate the application in clinical and real-life settings, a nomogram was created based on the logistic regression algorithm, which can provide a preliminary assessment of the likelihood of an individual having diabetes. Overall, this research contributes valuable insights into the predictive modeling of diabetes, offering potential applications in clinical practice for more effective and timely diagnoses.

Unlocking the link: how hippocampal glutathione-glutamate coupling predicts cognitive impairment in multiple sclerosis patients.

Cognitive impairment is a common symptom of multiple sclerosis and profoundly impacts quality of life. Glutathione (GSH) and glutamate (Glu) are tightly linked in the brain, participating in cognitive function. However, GSH-Glu couplings in cognitive brain regions and their relationship with cognitive impairment in relapsing-remitting multiple sclerosis (RRMS) remains unclear. Forty-one RRMS patients and 43 healthy controls underwent magnetic resonance spectroscopy to measure GSH and Glu levels in the posterior cingulate cortex, medial prefrontal cortex and left hippocampus. Neuropsychological tests were used to evaluate the cognitive function. The Glu/GSH ratio was used to indicate the coupling between GSH and Glu and was tested as a predictor of cognitive performance. The results show that RRMS patients exhibited reduced hippocampal GSH and Glu levels, which were found to be significant predictors of worse verbal and visuospatial memory, respectively. Moreover, GSH levels were dissociated from Glu levels in the left hippocampus of RRMS patients. Hippocampal Glu/GSH ratio is significantly correlated with processing speed and has a greater predictive effect. Here we show the hippocampal Glu/GSH ratio could serve as a new potential marker for characterizing cognitive impairment in RRMS, providing a new direction for clinical detection of cognitive impairment.

Fano resonance in molecular junctions of spin crossover complexes.

In this paper, we introduce a novel molecular switch paradigm that integrates spin crossover complexes with the Fano resonance effect. Specifically, by performing density-functional theory calculations, the feasibility of achieving Fano resonance using spin crossover complexes is demonstrated in our designed molecular junctions using the complex {Fe[H2B(pz)2]2[Bp(bipy)]} [pz = 1-pyrazolyl, Bp(bipy) = bis(phenylethynyl)(2,2'-bipyridine)]. It is further revealed that the Fano resonance, particularly the Fano dip, is most prominent in the junction with cobalt tips among all the schemes, together with the spin-filtering effect. Most importantly, this junction of cobalt tips is able to exhibit three distinct conductance states, which are controlled by the modulation of Fano resonance due to the spin-state transition of the complex and the applied gate voltage. Such a molecular switch paradigm holds potential for applications in logic gates, memory units, sensors, thermoelectrics, and beyond.

iNP_ESM: Neuropeptide Identification Based on Evolutionary Scale Modeling and Unified Representation Embedding Features.

Neuropeptides are biomolecules with crucial physiological functions. Accurate identification of neuropeptides is essential for understanding nervous system regulatory mechanisms. However, traditional analysis methods are expensive and laborious, and the development of effective machine learning models continues to be a subject of current research. Hence, in this research, we constructed an SVM-based machine learning neuropeptide predictor, iNP_ESM, by integrating protein language models Evolutionary Scale Modeling (ESM) and Unified Representation (UniRep) for the first time. Our model utilized feature fusion and feature selection strategies to improve prediction accuracy during optimization. In addition, we validated the effectiveness of the optimization strategy with UMAP (Uniform Manifold Approximation and Projection) visualization. iNP_ESM outperforms existing models on a variety of machine learning evaluation metrics, with an accuracy of up to 0.937 in cross-validation and 0.928 in independent testing, demonstrating optimal neuropeptide recognition capabilities. We anticipate improved neuropeptide data in the future, and we believe that the iNP_ESM model will have broader applications in the research and clinical treatment of neurological diseases.

Discovery of 4-methyl-3-(pyridin-2-ylamino)benzamide derivatives as C-Abl inhibitors with potential neuroprotective effect.

C-Abl is involved in various biological processes and plays an important role in neurodegenerative diseases, especially Parkinson's disease (PD). Previous studies have found that nilotinib shows a neuroprotective effect in cell and animal models of PD by inhibiting the activation of c-Abl. But the low blood-brain barrier permeability and potential toxicity limit the further use of nilotinib in PD. Based on molecular modeling studies, a series of 4-methyl-3-(pyridin-2-ylamino)benzamide derivatives were designed and synthesized. In particular, compound 9a exhibited significant inhibitory activity against c-Abl and a potent neuroprotective effect against MPP+-induced SH-SY5Y cell death. Moreover, 9a not only displayed lower cell toxicity compared with nilotinib, but also showed higher oral bioavailability and proper permeability of the blood-brain barrier. This paper provides 4-methyl-3-(pyridin-2-ylamino)benzamide derivatives as a new scaffold for c-Abl inhibitor with potential neuroprotective effect.

Electrostatic shape control of a charged molecular membrane from ribbon to scroll.

Bilayers of amphiphiles can organize into spherical vesicles, nanotubes, planar, undulating, and helical nanoribbons, and scroll-like cochleates. These bilayer-related architectures interconvert under suitable conditions. Here, a charged, chiral amphiphile (palmitoyl-lysine, C16-K1) is used to elucidate the pathway for planar nanoribbon to cochleate transition induced by salt (NaCl) concentration. In situ small- and wide-angle X-ray scattering (SAXS/WAXS), atomic force and cryogenic transmission electron microscopies (AFM and cryo-TEM) tracked these transformations over angstrom to micrometer length scales. AFM reveals that the large length (L) to width (W) ratio nanoribbons (L/W > 10) convert to sheets (L/W → 1) before rolling into cochleates. A theoretical model based on electrostatic and surface energies shows that the nanoribbons convert to sheets via a first-order transition, at a critical Debye length, with 2 shallow minima of the order of thermal energy at L/W >> 1 and at L/W = 1. SAXS shows that interbilayer spacing (D) in the cochleates scales linearly with the Debye length, and ranges from 13 to 35 nm for NaCl concentrations from 100 to 5 mM. Theoretical arguments that include electrostatic and elastic energies explain the membrane rolling and the bilayer separation-Debye length relationship. These models suggest that the salt-induced ribbon to cochleate transition should be common to all charged bilayers possessing an intrinsic curvature, which in the present case originates from molecular chirality. Our studies show how electrostatic interactions can be tuned to attain and control cochleate structures, which have potential for encapsulating, and releasing macromolecules in a size-selective manner.

ß-Catenin/LEF-1 transcription complex is responsible for the transcriptional activation of LINC01278.

BACKGROUND: Our previous study shows that LINC01278 inhibits the malignant proliferation and invasion of papillary thyroid carcinoma (PTC) cells by regulating the miR-376c-3p/DNM3 axis. However, the regulation mechanism of LINC01278 expression in PTC cells is still unclear. METHODS: The luciferase reporter and ChIP assays were used to confirm the binding of LEF-1 to the putative promoter site of LINC01278 gene. The RNA immunoprecipitation and RNA pulldown were used to determine the enrichment of LINC01278 in ß-catenin protein. The proteasome inhibitors (MG132) was used for detecting the ß-catenin ubiquitination-proteasome degradation. Wnt/ß-catenin specific agonists (LiCI), inhibitors (WiKI4) and TOP/FOP-flash reporter assay were used for detecting the activation of Wnt/ß-catenin signal. Western blot was used to detected the expression of target proteins. RESULTS: The online PROMO algorithm determines a putative LEF-1 binding site on LINC01278 promoter, the LEF-1 binds to the putative promoter site of LINC01278 gene, and ß-catenin enhances the binding of LEF-1 to the LINC01278 gene promoter. Furthermore, LINC01278 negatively regulated the protein accumulation of ß-catenin in the cytoplasm, into nucleus, and ultimately inhibited the transcription of downstream target genes activated by Wnt/ß-catenin signal. The results of RNA immunoprecipitation and RNA pulldown proved the direct binding of LINC01278 to ß-catenin protein. In addition, the combination of LINC01278 and ß-catenin promotes the ß-catenin ubiquitination-proteasome degradation. CONCLUSION: In summary, we found the transcriptional activation of LINC01278 by the ß-catenin/LEF-1 transcription factor, and the negative feedback regulation of LINC01278 onß-catenin signal.

Comparative Transcriptomic and Proteomic Analyses Prove that IFN-λ1 is a More Potent Inducer of ISGs than IFN-α against Porcine Epidemic Diarrhea Virus in Porcine Intestinal Epithelial Cells.

Type III interferon (IFN-λ) is currently considered to be largely nonredundant to type I interferon (IFN-α) in antivirus infection, especially in epithelial cells. Previous studies reported that, compared with IFN-α, IFN-λ exhibited stronger induction of interferon-stimulated genes (ISGs) at the transcriptional level in intestinal epithelial cells and stronger inhibition of porcine epidemic diarrhea virus (PEDV). In this study, the different mechanisms of ISG upregulation induced by IFN-α and IFN-λ1 were compared at the mRNA and protein levels in the porcine intestinal epithelial cell model (IPEC-J2). It was proved that IFN-λ1 consistently exhibited stronger stimulation effects at both levels. At the mRNA level, 132 genes were significantly upregulated upon IFN-λ1 stimulation, while 42 genes upon IFN-α stimulation. At the protein level, 47 proteins were significantly upregulated upon IFN-λ1 stimulation, but only 8 proteins were upregulated upon IFN-α stimulation. The shared upregulated genes/proteins by IFN-λ1 in both transcriptional and translational omics, especially the regulation factors of ISG15, were involved in the JAK-STAT signaling pathway. Compared to IFN-α, IFN-λ1 could induce more consistent upregulation of the key ISGs (ISG15, USP18, OASL, and RSAD2) at 3-24 h postinduction as measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) validation. It was further confirmed through functional analysis that ISG15 and RSAD2 could inhibit PEDV infection in dose-dependent manners. This study provided solid evidence that IFN-λ1 could induce a more unique and higher ISG expression level, which exhibited anti-PEDV effects on porcine intestinal epithelial cells.

Long non-coding RNA TNRC6C-AS1 promotes methylation of STK4 to inhibit thyroid carcinoma cell apoptosis and autophagy via Hippo signalling pathway.

The role of long non-coding RNAs (lncRNAs) in thyroid carcinoma (TC), the most frequent endocrine malignancy, has been extensively examined. This study investigated effect of interaction among lncRNA TNRC6C-AS1, serine/threonine-protein kinase 4 (STK4) and Hippo signalling pathway on TC. Initially, lncRNA TNRC6C-AS1 expression in TC tissues was detected. To explore roles of lncRNA TNRC6C-AS1, STK4 and Hippo signalling pathway in TC progression, their expressions were altered. Interaction between lncRNA TNRC6C-AS1 and STK4, STK4 promoter methylation, or Hippo signalling pathway was verified. After that, a series of experiments were employed to evaluate in vitro ability of apoptosis, proliferation and autophagy of TC cells and in vivo tumorigenicity, and tumour growth of TC cells. lncRNA TNRC6C-AS1 was highly expressed while STK4 was poorly expressed in TC tissues. LncRNA TNRC6C-AS1 promoted the STK4 methylation and down-regulated STK4 expression, which further activated the Hippo signalling pathway. STK4 silencing was observed to promote the proliferation ability of TC cells, inhibit the apoptosis and autophagy abilities, as well as enhance the tumorigenicity and tumour growth. Moreover, the in vitro proliferation ability as well as the in vivo tumorigenicity and tumour growth of TC cells were inhibited after the blockade of Hippo signalling pathway, while the apoptosis and autophagy abilities were promoted. The results demonstrate that the lncRNA TNRC6C-AS1 increases STK4 promoter methylation to down-regulate STK4 expression, thereby promoting the development of TC through activation of Hippo signalling pathway. It highlights that lncRNA TNRC6C-AS1 may be a novel therapeutic target for the treatment of TC.

Peptidyl-Lys metalloendopeptidase (Lys-N) purified from dry fruit of Grifola frondosa demonstrates "mirror"digestion property with lysyl endopeptidase (Lys-C).

RATIONALE: Lys-N, also known as lysine-specific metalloendopeptidase, functions as the "sister" enzyme of lysyl endopeptidase (Lys-C) in proteomic research. Its digestion specificity at the N-terminal lysine residue makes it a very useful tool in proteomics analysis, especially in mass spectrometry (MS)-based de novo sequencing of proteins. METHODS: Here we present a complete production process of highly purified Lys-N from dry fruit of Grifola frondosa (maitake mushroom). The purification process includes one step of microfiltration plus one step of UF/DF (ultrafiltration used in tandem with a diafiltration method) recovery and four steps of chromatographic purification. RESULTS: The overall yield of the process was approximately 6.7 mg Lys-N protein/kg dry fruit of G. frondosa. The assay data demonstrated that the purified Lys-N exhibited high enzymatic activity and specificity. CONCLUSIONS: The novel production process provides for the first time the extraction of Lys-N from dry fruit of G. frondosa. The process is also stable and scalable, and provides an economic way of producing the enzyme in large quantities for MS-based proteomics and other biological studies.

[Machine learning-based method for interpreting the guidelines of the diagnosis and treatment of COVID-19].

The outbreak of pneumonia caused by novel coronavirus (COVID-19) at the end of 2019 was a major public health emergency in human history. In a short period of time, Chinese medical workers have experienced the gradual understanding, evidence accumulation and clinical practice of the unknown virus. So far, National Health Commission of the People's Republic of China has issued seven trial versions of the "Guidelines for the Diagnosis and Treatment of COVID-19". However, it is difficult for clinicians and laymen to quickly and accurately distinguish the similarities and differences among the different versions and locate the key points of the new version. This paper reports a computer-aided intelligent analysis method based on machine learning, which can automatically analyze the similarities and differences of different treatment plans, present the focus of the new version to doctors, reduce the difficulty in interpreting the "diagnosis and treatment plan" for the professional, and help the general public better understand the professional knowledge of medicine. Experimental results show that this method can achieve the topic prediction and matching of the new version of the program text through unsupervised learning of the previous versions of the program topic with an accuracy of 100%. It enables the computer interpretation of "diagnosis and treatment plan" automatically and intelligently.

ETFDH Mutations and Flavin Adenine Dinucleotide Homeostasis Disturbance Are Essential for Developing Riboflavin-Responsive Multiple Acyl-Coenzyme A Dehydrogenation Deficiency.

OBJECTIVE: Riboflavin-responsive multiple acyl-coenzyme A dehydrogenation deficiency (RR-MADD) is an inherited fatty acid metabolism disorder mainly caused by genetic defects in electron transfer flavoprotein-ubiquinone oxidoreductase (ETF:QO). The variant ETF:QO protein folding deficiency, which can be corrected by therapeutic dosage of riboflavin supplement, has been identified in HEK-293 cells and is believed to be the molecular mechanism of this disease. To verify this hypothesis in vivo, we generated Etfdh (h)A84T knockin (KI) mice. METHODS: Tissues from these mice as well as muscle biopsies and fibroblasts from 7 RR-MADD patients were used to examine the flavin adenine dinucleotide (FAD) concentration and ETF:QO protein amount. RESULTS: All of the homozygous KI mice (Etfdh (h)A84T/(h)A84T , KI/KI) were initially normal. After being given a high-fat and vitamin B2 -deficient (HF-B2 D) diet for 5 weeks, they developed weight loss, movement ability defects, lipid storage in muscle and liver, and elevated serum acyl-carnitine levels, which are clinically and biochemically similar to RR-MADD patients. Both ETF:QO protein and FAD concentrations were significantly decreased in tissues of HF-B2 D-KI/KI mice and in cultured fibroblasts from RR-MADD patients. After riboflavin treatment, ETF:QO protein increased in proportion to elevated FAD concentrations, but not related to mRNA levels. These results were further confirmed in cultured fibroblasts from RR-MADD patients. INTERPRETATION: For the first time, we successfully developed a RR-MADD mice model and confirmed that FAD homeostasis disturbances played a crucial role on the pathomechanism of RR-MADD in this mouse model and culture cells from patients. Supplementation of riboflavin may stabilize variant ETF:QO protein by rebuilding FAD homeostasis. Ann Neurol 2018;84:667-681.

Electrostatic Origin of Element Selectivity during Rare Earth Adsorption.

Rare earths, which are fundamental components of modern technologies, are often extracted from aqueous solutions using surfactants at oil-water interfaces. Heavier lanthanides are more easily extracted, even though all lanthanides are chemically very similar. Using x-ray fluorescence measurements and theoretical arguments, we show that there is a sharp bulk-concentration-dependent transition in the interfacial adsorption of cations from aqueous solutions containing Er^{3+} or Nd^{3+} in contact with a floating monolayer. The threshold bulk concentration of erbium (Z=68) is an order of magnitude lower than that of neodymium (Z=60), and erbium is preferentially adsorbed when the solution contains both ions. This implies that elemental selectivity during separation originates at the surfactant interface. Electrostatic effects arising from the interface dielectric mismatch, ionic correlations, and sizes of the ions explain the sharp adsorption curve and selectivity.

Influence of punch geometry (head-flat diameter) and tooling type ('B' or 'D') on the physical-mechanical properties of formulation tablets.

The presented study assessed the influence of punch geometry (head-flat [HF] diameter) and tooling type ('B' or 'D') on the physical-mechanical properties of tablets prepared by direct-compression of two guaifenesin (25% or 40% w/w) formulations. Tablets of both formulations were prepared on instrumented, single-layer, rotary tablet press using 10 mm, flat-faced, 'B' or 'D'-type tooling with different HF diameters, and compression forces (CF) ranging from 5 to 25 kN with 5 kN increments. The tablets were evaluated for dimensions, weight variation, tensile strength (TS), friability, and capping index. In general, tablets prepared using 'D' tooling showed a significantly (p < 0.05) higher TS compared to those prepared using 'B' tooling, likely due to higher dwell-times associated with 'D' tooling. Formulations containing 25% w/w guaifenesin showed a significantly (p < 0.05) higher TS compared to those containing 40% w/w guaifenesin, at given compression CF, punch geometry, or tooling type. This could be due to the higher ratio of Prosolv® SMCC contributing to the compressibility. For both formulations compressed using 'B' tooling, differences in TS profiles were observed between different HF tooling. The TS of these tablets increased significantly with increasing HF diameter. For formulations compressed using 'D' tooling, this trend was observed only up to a CF of 15 kN, beyond which the TS plateaued, possibly due to work-hardening of the formulation at higher CF. These formulations also exhibited capping at CF above 15 kN and with higher HF diameters. The study showed a significant influence of punch geometry and tooling type on the physical properties of tablets.

Altered hippocampal GABA and glutamate levels and uncoupling from functional connectivity in multiple sclerosis.

There is growing evidence for dysfunctional glutamatergic excitation and/or gamma-aminobutyric acid (GABA)ergic inhibition in patients with multiple sclerosis (MS). Cognitive impairment may occur during the early stages of MS and hippocampal abnormalities have been suggested as biomarkers. However, researchers have not clearly determined whether changes in hippocampal GABA and glutamate (Glu) levels are associated with cognitive impairment and aberrant neural activity in patients with MS. We used magnetic resonance spectroscopy to measure GABA+ and Glu levels in the left hippocampal region of 29 patients with relapsing-remitting MS and 29 healthy controls (HCs). Resting-state functional connectivity (FC) with the hippocampus was also examined. Compared to HCs, patients exhibited significantly lower GABA+ and Glu levels, which were associated with verbal and visuospatial memory deficits, respectively. Patients also showed decreased FC strengths between the hippocampus and several cortical regions, which are located within the default mode network. Moreover, hippocampal GABA+ levels and Glu/GABA+ ratios correlated with the FC strengths in HCs but not in patients with MS. This study describes a novel method for investigating the complex relationships among excitatory/inhibitory neurotransmitters, brain connectivity and cognition in health and disease. Strategies that modulate Glu and GABA neurotransmission may represent new therapeutic treatments for patients with MS.

MicroRNA-125b Affects Vascular Smooth Muscle Cell Function by Targeting Serum Response Factor.

BACKGROUND/AIMS: Increasing evidence links microRNAs to the pathogenesis of peripheral vascular disease. We recently found microRNA-125b (miR-125b) to be one of the most significantly down­regulated microRNAs in human arteries with arteriosclerosis obliterans (ASO) of the lower extremities. However, its function in the process of ASO remains unclear. This study aimed to investigate the expression, regulatory mechanisms, and functions of miR-125b in the process of ASO. METHODS: Using the tissue explants adherent method, vascular smooth muscle cells (VSMCs) were prepared for this study. A rat carotid artery balloon injury model was constructed to simulate the development of vascular neointima, and a lentiviral transduction system was used to overexpress serum response factor (SRF) or miR-125b. Quantitative real­time PCR (qRT­PCR) was used to detect the expression levels of miR­125b and SRF mRNA. Western blotting was performed to determine the expression levels of SRF and Ki67. In situ hybridization analysis was used to analyze the location and expression levels of miR-125b. CCK-8 and EdU assays were used to assess cell proliferation, and transwell and wound closure assays were performed to measure cell migration. Flow cytometry was used to evaluate cell apoptosis, and a dual-luciferase reporter assay was conducted to examine the effects of miR­125b on SRF. Immunohistochemistry and immunofluorescence analyses were performed to analyze the location and expression levels of SRF and Ki67. RESULTS: miR-125b expression was decreased in ASO arteries and platelet-derived growth factor (PDGF)-BB-stimulated VSMCs. miR-125b suppressed VSMC proliferation and migration but promoted VSMC apoptosis. SRF was determined to be a direct target of miR-125b. Exogenous miR-125b expression modulated SRF expression and inhibited vascular neointimal formation in balloon-injured rat carotid arteries. CONCLUSIONS: These findings demonstrate a specific role of the miR-125b/SRF pathway in regulating VSMC function and suggest that modulating miR-125b levels might be a novel approach for treating ASO.

Asymmetric electrolytes near structured dielectric interfaces.

The ion distribution of electrolytes near interfaces with dielectric contrast has important consequences for electrochemical processes and many other applications. To date, most studies of such systems have focused on geometrically simple interfaces, for which dielectric effects are analytically solvable or computationally tractable. However, all real surfaces display nontrivial structure at the nanoscale and have, in particular, a nonuniform local curvature. Using a recently developed, highly efficient computational method, we investigate the effect of surface geometry on ion distribution and interface polarization. We consider an asymmetric 2:1 electrolyte bounded by a sinusoidally deformed solid surface. We demonstrate that even when the surface is neutral, the electrolyte acquires a nonuniform ion density profile near the surface. This profile is asymmetric and leads to an effective charging of the surface. We furthermore show that the induced charge is modulated by the local curvature. The effective charge is opposite in sign to the multivalent ions and is larger in concave regions of the surface.

Surface Polarization Effects on Ion-Containing Emulsions.

Surface polarization in ion-containing heterogeneous dielectric media such as cell media and emulsions is determined by and determines the positions of the ions. We compute the surface polarization self-consistently as the ions move and analyze their effects on the interactions between electro-neutral, ion-containing droplets using coarse-grained molecular dynamics simulations based on the true energy functional. For water droplets immersed in oil, the interdroplet interaction is attractive, and the surface polarization makes the major contribution. By contrast, for oil droplets in water, the ion-surface induced charge interaction is repulsive and counteracts the attraction between the ions, leading to a small attractive interaction between the droplets. This research improves our understanding of self-assembly in mixed phases such as metal extraction for recovering rare earth elements and nuclear waste as well as water purification.

A Carbon Nanoparticle Lymphatic Tracer Protected Parathyroid Glands During Radical Thyroidectomy for Papillary Thyroid Non-Microcarcinoma.

The study assessed the role of an activated carbon nanoparticle lymphatic tracer in reducing unintentional damage to the parathyroid glands during thyroidectomy for papillary thyroid non-microcarcinoma diagnosed intraoperatively by cryosections. A total of 103 patients with papillary thyroid non-microcarcinomas diagnosed by intraoperative cryosection were randomly assigned to receive routine radical thyroidectomy or radical thyroidectomy following administration of activated carbon nanoparticle lymphatic tracer to the contralateral thyroid, at the department of Thyroid Surgery, Sun Yat-sen Memorial Hospital (Guangzhou, China), between January 2012 and May 2013. The success of level VI lymphadenectomy and postoperative parathyroid function were compared. Administration of the activated carbon nanoparticle lymphatic tracer did not affect the frequency of recovered lymph nodes containing metastases; however, it did significantly reduce the incidence of permanent and transient hypoparathyroidism from 2 to 0 and 18 to 6, and reduced the mean recovery time for transient hypoparathyroidism from 57.0 days to 22.3 days. Administration of activated carbon nanoparticles to the contralateral thyroid after intraoperative cryosections did not contribute to lymphadenectomy for papillary thyroid non-microcarcinoma, but significantly protected parathyroid functions. This approach could decrease the morbidity of radical thyroidectomy and the occurrence of hypoparathyroidism.