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Since the establishment of the first global refinery in 1856, crude oil has remained one of the most lucrative natural resources worldwide. However, during the extraction process from reservoirs, crude oil gets contaminated with sediments, water, and other impurities. The presence of pressure, shear forces, and surface-active compounds in crude oil leads to the formation of unwanted oil/water emulsions. These emulsions can take the form of water-in-oil (W/O) emulsions, where water droplets disperse continuously in crude oil, or oil-in-water (O/W) emulsions, where crude oil droplets are suspended in water. To prevent the spread of water and inorganic salts, these emulsions need to be treated and eliminated. In existing literature, different demulsification procedures have shown varying outcomes in effectively treating oil/water emulsions. The observed discrepancies have been attributed to various factors such as temperature, salinity, pH, droplet size, and emulsifier concentrations. It is crucial to identify the most effective demulsification approach for oil/water separation while adhering to environmental regulations and minimizing costs for the petroleum sector. Therefore, this study aims to explore and review recent advancements in two popular demulsification techniques: chemical demulsification and magnetic nanoparticles-based (MNP) demulsification. The advantages and disadvantages of each technique are assessed, with the magnetic approach emerging as the most promising due to its desirable efficiency and compliance with environmental and economic concerns. The findings of this report are expected to have a significant impact on the overall process of separating oil and water, benefiting the oil and gas industry, as well as other relevant sectors in achieving the circular economy., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Advanced prostate cancers are treated with therapies targeting the androgen receptor (AR) signaling pathway. While many tumors initially respond to AR inhibition, nearly all develop resistance. It is critical to understand how prostate tumor cells respond to AR inhibition in order to exploit therapy-induced phenotypes prior to the outgrowth of treatment-resistant disease. Here, we comprehensively characterize the effects of AR blockade on prostate cancer metabolism using transcriptomics, metabolomics, and bioenergetics approaches. The metabolic response to AR inhibition is defined by reduced glycolysis, robust elongation of mitochondria, and increased reliance on mitochondrial oxidative metabolism. We establish DRP1 activity and MYC signaling as mediators of AR-blockade-induced metabolic phenotypes. Rescuing DRP1 phosphorylation after AR inhibition restores mitochondrial fission, while rescuing MYC restores glycolytic activity and prevents sensitivity to complex I inhibition. Our study provides insight into the regulation of treatment-induced metabolic phenotypes and vulnerabilities in prostate cancer., Competing Interests: Declaration of interests P.C.B. sits on the scientific advisory boards of Sage Bionetworks, BioSymetrics, Inc., and Intersect Diagnostics, Inc., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)

Prostate-specific membrane antigen (PSMA) is an important cell surface target in prostate cancer. There are limited data on the heterogeneity of PSMA tissue expression in metastatic castration-resistant prostate cancer (mCRPC). Furthermore, the mechanisms regulating PSMA expression (encoded by the FOLH1 gene) are not well understood. Here, we demonstrate that PSMA expression is heterogeneous across different metastatic sites and molecular subtypes of mCRPC. In a rapid autopsy cohort in which multiple metastatic sites per patient were sampled, we found that 13 of 52 (25%) cases had no detectable PSMA and 23 of 52 (44%) cases showed heterogeneous PSMA expression across individual metastases, with 33 (63%) cases harboring at least 1 PSMA-negative site. PSMA-negative tumors displayed distinct transcriptional profiles with expression of druggable targets such as MUC1. Loss of PSMA was associated with epigenetic changes of the FOLH1 locus, including gain of CpG methylation and loss of histone 3 lysine 27 (H3K27) acetylation. Treatment with histone deacetylase (HDAC) inhibitors reversed this epigenetic repression and restored PSMA expression in vitro and in vivo. Collectively, these data provide insights into the expression patterns and regulation of PSMA in mCRPC and suggest that epigenetic therapies - in particular, HDAC inhibitors - can be used to augment PSMA levels.

Basal cell carcinoma (BCC) of the prostate is a rare tumor. Compared with the more common acinar adenocarcinoma (AAC) of the prostate, BCCs show features of basal cell differentiation and are thought to be biologically distinct from AAC. The spectrum of molecular alterations of BCC has not been comprehensively described, and genomic studies are lacking. Herein, whole genome sequencing was performed on archival formalin-fixed, paraffin-embedded specimens of two cases with BCC. Prostatic BCCs were characterized by an overall low copy number and mutational burden. Recurrent copy number loss of chromosome 16 was observed. In addition, putative driver gene alterations in KIT, DENND3, PTPRU, MGA, and CYLD were identified. Mechanistically, depletion of the CYLD protein resulted in increased proliferation of prostatic basal cells in vitro. Collectively, these studies show that prostatic BCC displays distinct genomic alterations from AAC and highlight a potential role for loss of chromosome 16 in the pathogenesis of this rare tumor type., (Copyright © 2023 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.)

RNA Polymerase I (Pol I) synthesizes rRNA, which is the first and rate-limiting step in ribosome biogenesis. Factors governing the stability of the polymerase complex are not known. Previous studies characterizing Pol I inhibitor BMH-21 revealed a transcriptional stress-dependent pathway for degradation of the largest subunit of Pol I, RPA194. To identify the E3 ligase(s) involved, we conducted a cell-based RNAi screen for ubiquitin pathway genes. We establish Skp-Cullin-F-box protein complex F-box protein FBXL14 as an E3 ligase for RPA194. We show that FBXL14 binds to RPA194 and mediates RPA194 ubiquitination and degradation in cancer cells treated with BMH-21. Mutation analysis in yeast identified lysines 1150, 1153, and 1156 on Rpa190 relevant for the protein degradation. These results reveal the regulated turnover of Pol I, showing that the stability of the catalytic subunit is controlled by the F-box protein FBXL14 in response to transcription stress., Competing Interests: Conflict of interest M. L., H. L., A. B., and W. F. hold patents or patent applications on Pol I inhibitors, which are managed by the Johns Hopkins University. All other authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Anaplastic lymphoma kinase (ALK) is a tyrosine kinase with genomic and expression changes in many solid tumors. ALK inhibition is first line therapy for lung cancers with ALK alterations, and an effective therapy in other tumor types, but has not been well-studied in prostate cancer. Here, we aim to delineate the role of ALK genomic and expression changes in primary and metastatic prostate cancer. We determined ALK expression by immunohistochemistry and RNA-Seq, and genomic alterations by NGS. We assessed functional consequences of ALK overexpression and pharmacological ALK inhibition by cell proliferation and cell viability assays. Among 372 primary prostate cancer cases we identified one case with uniformly high ALK protein expression. Genomic analysis revealed a SLC45A3-ALK fusion which promoted oncogenesis in in vitro assays. We observed ALK protein expression in 5/52 (9%) of metastatic prostate cancer cases, of which 4 of 5 had neuroendocrine features. ALK-expressing neuroendocrine prostate cancer had a distinct transcriptional program, and earlier disease progression. An ALK-expressing neuroendocrine prostate cancer model was sensitive to pharmacological ALK inhibition. In summary, we found that ALK overexpression is rare in primary prostate cancer, but more frequent in metastatic prostate cancers with neuroendocrine differentiation. Further, ALK fusions similar to lung cancer are an occasional driver in prostate cancer. Our data suggest that ALK-directed therapies could be an option in selected patients with advanced prostate cancer., Competing Interests: Conflict of interest disclosure statement: No potential conflicts of interest were disclosed by the other authors.

The discovery of small, "cave-like" invaginations at the plasma membrane, called caveola, has opened up a new and exciting research area in health and diseases revolving around this cellular ultrastructure. Caveolae are rich in cholesterol and orchestrate cellular signaling events. Within caveola, the caveola-associated proteins, caveolins and cavins, are critical components for the formation of these lipid rafts, their dynamics, and cellular pathophysiology. Their alterations underlie human diseases such as lipodystrophy, muscular dystrophy, cardiovascular disease, and diabetes. The expression of caveolins and cavins is modulated in tumors and in tumor stroma, and their alterations are connected with cancer progression and treatment resistance. To date, although substantial breakthroughs in cancer drug development have been made, drug resistance remains a problem leading to treatment failures and challenging translation and bench-to-bedside research. Here, we summarize the current progress in understanding cancer drug resistance in the context of caveola-associated molecules and tumor stroma and discuss how we can potentially design therapeutic avenues to target these molecules in order to overcome treatment resistance.

Introduction: The negative impact of the coronavirus disease 2019 (COVID-19) pandemic on mental health and physical activity is well reported. While prior studies showed a positive influence of pet ownership on physical activity and mental health, the interactions between the pandemic and pet ownership are not well studied., Objective: To determine the association between pet ownership, physical activity levels and mental health during the COVID-19 pandemic., Materials and Methods: A cross-sectional study was conducted from May 19 to July 13, 2020 among Singapore residents aged 21 to 64 years through a previously published questionnaire. Inverse probability treatment weighting was used to develop mixed-effects models for outcome comparisons. We recorded participant data on pet ownership, duration and intensity of physical activity, and RAND 36-item Health Survey mental health domains during the COVID-19 pandemic., Results: The questionnaire was completed by 431 pet owners and 103 non-pet owners. A greater proportion of pet owners were female, non-married, employed and owned pets in the past. Pet owners reported 31.8 (95% CI 13.6 to 50; p  = .001) more minutes per week of mild-intensity physical activity compared to non-pet owners. No statistically significant differences were found for moderate- and vigorous-intensity physical activity. Pet owners had better emotional well-being ( ꞵ  = 9.66, 95% CI 4.97 to 14.4; p  < .001), energy ( ꞵ  = 8.29, 95% CI 3.46 to 13.1; p  = .001) and social functioning ( ꞵ  = 11.2, 95% CI 5.03 to 17.4; p  < .001) scores than non-pet owners. However, no statistically significant difference was observed for general health scores. Pet owner physical activity levels, general health, emotional well-being and energy scores correlated positively with pet attachment scores., Conclusion: Pet ownership was associated with greater physical activity levels and better mental health, particularly in main caregivers with higher pet attachment scores. These findings suggest that pet ownership is beneficial to physical and mental well-being during periods of social isolation amidst a global pandemic., Competing Interests: The authors declare no competing interests., (© 2021 The Author(s).)

Background: The re-introduction of medical students into healthcare systems struggling with the COVID-19 pandemic raises concerns as to whether they will be supported when confronted with death and dying patients in resource-limited settings and with reduced support from senior clinicians. Better understanding of how medical students respond to death and dying will inform educationalists and clinicians on how to best support them., Methods: We adopt Krishna's Systematic Evidence Based Approach to carry out a Systematic Scoping Review (SSR in SEBA) on the impact of death and dying on medical students. This structured search process and concurrent use of thematic and directed content analysis of data from six databases (Split Approach) enhances the transparency and reproducibility of this review., Results: Seven thousand six hundred nineteen were identified, 149 articles reviewed and 52 articles included. The Split Approach revealed similar themes and categories that correspond to the Innate, Individual, Relational and Societal domains in the Ring Theory of Personhood., Conclusion: Facing death and dying amongst their patients affect how medical students envisage their personhood. This underlines the need for timely, holistic and longitudinal support systems to ensure that problems faced are addressed early. To do so, there must be effective training and a structured support mechanism.

Although existing literature increasingly suggests a positive influence of pet ownership on human physical activity levels, results from many European, American, and Japanese studies have been inconsistent. How pet ownership impacts mental health and atopy is likewise controversial and whether distinct demographic subgroups experience differential effects is unclear. This cross-sectional study surveyed participants (n = 823) via a self-administered online questionnaire. Comparisons of outcomes between pet owners and non-pet owners with subgroup analyses were performed within a propensity score-matched subset (n = 566) of respondents. There were no differences in physical activity levels or mental health scores between pet owners and non-pet owners. In subgroup analyses, compared to non-pet owners, main pet caregivers reported 14.1 (95% CI 2.79-25.3) and 19.0 (95% CI 4.70-33.3) more minutes per week of moderate- and vigorous-intensity physical activity respectively and higher SF-36 emotional well-being (β = 2.7, 95% CI 0.100-5.32) and energy scores (β = 3.8, 95% CI 0.410-7.27). Age was a significant effect modifier of the association between pet ownership and emotional well-being, energy and social functioning scores, with greater scores above the ages of 39, 35 and 39 years old respectively (interaction p = 0.043, 0.044, 0.042). Finally, pet acquisition was associated with worsening of allergic rhinitis, while pet ownership cessation was associated with improvement of allergic rhinitis and eczema symptoms. To our knowledge, this is the first study addressing the public health impact of pet ownership in Southeast Asia and its findings add contextual nuance to suggest potential benefits derived from pet ownership.

Lipid uptake occurs through caveolae, plasma membrane invaginations formed by caveolins (CAV) and caveolae-associated protein 1 (CAVIN1). Genetic alterations of CAV1N1 and CAV1 modify lipid metabolism and underpin lipodystrophy syndromes. Lipids contribute to tumorigenesis by providing fuel to cancer metabolism and supporting growth and signaling. Tumor stroma promotes tumor proliferation, invasion, and metastasis, but how stromal lipids influence these processes remain to be defined. Here, we show that stromal CAVIN1 regulates lipid abundance in the prostate cancer microenvironment and suppresses metastasis. We show that depletion of CAVIN1 in prostate stromal cells markedly reduces their lipid droplet accumulation and increases inflammation. Stromal cells lacking CAVIN1 enhance prostate cancer cell migration and invasion. Remarkably, they increase lipid uptake and M2 inflammatory macrophage infiltration in the primary tumors and metastasis to distant sites. Our data support the concept that stromal cells contribute to prostate cancer aggressiveness by modulating lipid content and inflammation in the tumor microenvironment. IMPLICATIONS: This study showed that stromal CAVIN1 suppresses prostate cancer metastasis by modulating tumor microenvironment, lipid content, and inflammatory response., (©2020 American Association for Cancer Research.)

We report an incidental discovery of the superior pulmonary vein coming from a strange anatomical location when performing a robotic left lower lobectomy. When trying to identify the superior pulmonary vein, an aberrant pulmonary vein was found leading into the innominate vein., (© The Author 2017. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery. All rights reserved.)

Background: Recent studies have proposed that humans may perceive complex carbohydrates and that sensitivity to simple carbohydrates is independent of sensitivity to complex carbohydrates. Variation in oral complex carbohydrate sensitivity may influence food consumption. Objective: This study aimed to investigate the associations between oral complex carbohydrate sensitivity, anthropometry, and dietary intake in adults. Methods: We assessed oral sensitivity to complex carbohydrates (maltodextrin and oligofructose) by measuring detection thresholds (DTs) and suprathreshold intensity perceptions (STs) for 34 participants, including 16 men (mean ± SEM age : 26.2 ± 0.4 y; range: 24-30 y) and 18 women (age: 29.4 ± 2.1 y; range: 24-55 y). We also measured height, weight, and waist circumference (WC) and participants completed a 4-d food diary and a food-frequency questionnaire. Results: Measurements of oral sensitivity to complex carbohydrates were significantly correlated with WC and dietary energy and starch intakes (DT: r = -0.38, P < 0.05; ST: r = 0.36-0.48, P < 0.05). When participants were grouped into tertiles, there were significant differences in WC and total energy or starch intakes for those who were more sensitive or experienced high intensity compared with those who were less sensitive or experienced low intensity. Being more sensitive or experiencing high intensity was associated with greater energy (7968-8954 kJ/d) and starch (29.1-29.8% of energy) intakes and a greater WC (88.2-91.4 cm) than was being less sensitive or experiencing low intensity (6693-7747 kJ/d, 20.9-22.2% of energy, and 75.5-80.5 cm, respectively). Conclusion: Complex carbohydrate sensing is associated with WC and consumption of complex carbohydrates and energy in adults. This trial was registered at anzctr.org.au as ACTRN12616001356459., Competing Interests: Author disclosures: JYQL, KEL, RLM, and RSJK, no conflicts of interest., (© 2017 American Society for Nutrition.)

Sweetness is one of the 5 prototypical tastes and is activated by sugars and non-nutritive sweeteners (NNS). The aim of this study was to investigate measures of sweet taste function [detection threshold (DT), recognition threshold (RT), and suprathreshold intensity ratings] across multiple sweeteners. Sixty participants, 18-52 years of age (mean age in years = 26, SD = ±7.8), were recruited to participate in the study. DT and RT were collected for caloric sweeteners (glucose, fructose, sucrose, erythritol) and NNS (sucralose, rebaudioside A). Sweetness intensity for all sweeteners was measured using a general Labeled Magnitude Scale. There were strong correlations between DT and RT of all 4 caloric sweeteners across people (r = 0.62-0.90, P < 0.001), and moderate correlations between DT and RT for both of the NNS (r = 0.39-0.48, P < 0.05); however, weaker correlations were observed between the DT or RT of the caloric sweeteners and NNS (r = 0.26-0.48, P < 0.05). The DT and RT of glucose and fructose were not correlated with DT or RT of sucralose (P > 0.05). In contrast, there were strong correlations between the sweetness intensity ratings of all sweeteners (r = 0.70-0.96, P < 0.001). This suggests those caloric sweeteners and NNS access at least partially independent mechanisms with respect to DT and RT measures. At suprathreshold level, however, the strong correlation between caloric sweeteners and NNS through weak, moderate, and strong intensity indicates a commonality in sweet taste mechanism for the perceived intensity range., (© The Author 2016. Published by Oxford University Press.)

Variation in ability to detect, recognize, and perceive sweetness may influence food consumption, and eventually chronic nutrition-related conditions such as overweight and obesity. The aim of this study was to investigate the associations between sweet taste function, anthropometry, and dietary intake in adults. Participants' (n = 60; mean age in years = 26, SD = ±7.8) sweet taste function for a range of sweeteners (glucose, fructose, sucrose, sucralose, erythritol, and Rebaudioside A) was assessed by measuring detection and recognition thresholds and sweetness intensity. Height, weight, and waist circumference were also measured, and participants also completed a Food Frequency Questionnaire. There was large inter-individual variation in detection, recognition and sweetness intensity measures. Pearson's correlation coefficient revealed no robust correlations between measures of sweet taste function, anthropometry, and dietary intake, with the exception of suprathreshold intensity, which was moderately correlated with total energy intake (r = 0.23-0.40). One-way analysis of variance revealed no significant differences between the most and least sensitive participants in terms of BMI, waist circumference, and dietary intake for all measures of sweet taste function and sweeteners (all p > 0.01). When stratified into BMI categories, there were no significant differences in any measure of sweet taste function between the normal weight and overweight/obese participants (all p > 0.01). Results show that that sweet taste function is not associated with anthropometry and sweetness intensity measures are the most appropriate measure when assessing links between sweet taste and food consumption.

Caveolae are small, "omega-shaped" invaginations at the plasma membrane of the cell which are involved in a variety of processes including cholesterol transport, potocytosis and cell signalling. Within caveolae there are caveolae-associated proteins, and changes in expression of these molecules have been described to play a role in the pathophysiology of various diseases including cancer and cardiovascular disease. Evidence is beginning to accumulate that epigenetic processes may regulate the expression of these caveolae related genes, and hence contribute to disease progression. Here, we summarize the current knowledge of the role of epigenetic modification in regulating the expression of these caveolae related genes and how this relates to changes in cellular physiology and in health and disease.

To better understand lipid biosynthesis in oil palm mesocarp, in particular the differences in gene regulation leading to and including de novo fatty acid biosynthesis, a multi-platform metabolomics technology was used to profile mesocarp metabolites during six critical stages of fruit development in comparatively high- and low-yielding oil palm populations. Significantly higher amino acid levels preceding lipid biosynthesis and nucleosides during lipid biosynthesis were observed in a higher yielding commercial palm population. Levels of metabolites involved in glycolysis revealed interesting divergence of flux towards glycerol-3-phosphate, while carbon utilization differences in the TCA cycle were proven by an increase in malic acid/citric acid ratio. Apart from insights into the regulation of enhanced lipid production in oil palm, these results provide potentially useful metabolite yield markers and genes of interest for use in breeding programmes.

Central composite design of response surface methodology (RSM) was employed to optimize the extraction time (X 1 : 99.5-290.5 min) and temperature (X 2 : 30.1-54.9 °C) of Schizophyllum commune aqueous extract with high antioxidant activities and total phenolic content (TPC). Results indicated that the data were adequately fitted into four second-order polynomial models. The extraction time and temperature were found to have significant linear, quadratic and interaction effects on antioxidant activities and TPC. The optimal extraction time and temperature were: 290.5 min and 35.7 °C (DPPH(•) scavenging ability); 180.7 min and 41.7 °C (ABTS(•+) inhibition ability); 185.2 min and 42.4 °C (ferric reducing antioxidant power, FRAP); 290.5 min and 40.3 °C (TPC). These optimum conditions yielded 85.10%; 94.31%; 0.74 mM Fe(2+) equivalent/100 g; 635.76 mg gallic acid equivalent/100 g, respectively. The yields of antioxidant activities and TPC obtained experimentally were close to its predicted values. The establishment of such model provides a good experimental basis employing RSM for optimizing the extraction time and temperature on antioxidants from S. commune aqueous extract.

Micro RNAs are small non-coding RNAs, which regulate fundamental cellular and developmental processes at the transcriptional and translational level. In breast cancer, miR-145 expression is downregulated compared with healthy control tissue. As several predicted targets of miR-145 potentially regulate cell motility, we aimed at investigating a potential role for miR-145 in breast cancer cell motility and invasiveness. Assisted by Affymetrix array technology, we demonstrate that overexpression of miR-145 in MDA-MB-231, MCF-7, MDA-MB-468 and SK-BR-3 breast cancer cells and in Ishikawa endometrial carcinoma cells leads to a downregulation of the cell-cell adhesion protein JAM-A and of the actin bundling protein fascin. Moreover, podocalyxin and Serpin E1 mRNA levels were downregulated, and gamma-actin, transgelin and MYL9 were upregulated upon miR-145 overexpression. These miR-145-dependent expression changes drastically decreased cancer cell motility, as revealed by time-lapse video microscopy, scratch wound closure assays and matrigel invasion assays. Immunofluorescence microscopy demonstrated restructuring of the actin cytoskeleton and a change in cell morphology by miR-145 overexpression, resulting in a more cortical actin distribution, and reduced actin stress fiber and filopodia formation. Nuclear rotation was observed in 10% of the pre-miR-145 transfected MDA-MB-231 cells, accompanied by a reduction of perinuclear actin. Luciferase activation assays confirmed direct miR-145-dependent regulation of the 3'UTR of JAM-A, whereas siRNA-mediated knockdown of JAM-A expression resulted in decreased motility and invasiveness of MDA-MB-231 and MCF-7 breast cancer cells. Our data identify JAM-A and fascin as novel targets of miR-145, firmly establishing a role for miR-145 in modulating breast cancer cell motility. Our data provide a rationale for future miR-145-targeted approaches of antimetastatic cancer therapy.