Organic waste-to-bioplastics: Conversion with eco-friendly technologies and approaches for sustainable environment.

Petrochemical-based synthetic plastics poses a threat to humans, wildlife, marine life and the environment. Given the magnitude of eventual depletion of petrochemical sources and global environmental pollution caused by the manufacturing of synthetic plastics such as polyethylene (PET) and polypropylene (PP), it is essential to develop and adopt biopolymers as an environment friendly and cost-effective alternative to synthetic plastics. Research into bioplastics has been gaining traction as a way to create a more sustainable and eco-friendlier environment with a reduced environmental impact. Biodegradable bioplastics can have the same characteristics as traditional plastics while also offering additional benefits due to their low carbon footprint. Therefore, using organic waste from biological origin for bioplastic production not only reduces our reliance on edible feedstock but can also effectively assist with solid waste management. This review aims at providing an in-depth overview on recent developments in bioplastic-producing microorganisms, production procedures from various organic wastes using either pure or mixed microbial cultures (MMCs), microalgae, and chemical extraction methods. Low production yield and production costs are still the major bottlenecks to their deployment at industrial and commercial scale. However, their production and commercialization pose a significant challenge despite such potential. The major constraints are their production in small quantity, poor mechanical strength, lack of facilities and costly feed for industrial-scale production. This review further explores several methods for producing bioplastics with the aim of encouraging researchers and investors to explore ways to utilize these renewable resources in order to commercialize degradable bioplastics. Challenges, future prospects and Life cycle assessment of bioplastics are also highlighted. Utilizing a variety of bioplastics obtained from renewable and cost-effective sources (e.g., organic waste, agro-industrial waste, or microalgae) and determining the pertinent end-of-life option (e.g., composting or anaerobic digestion) may lead towards the right direction that assures the sustainable production of bioplastics.

A comprehensive review on glycation and its potential application to reduce food allergenicity.

Food allergens are a major concern for individuals who are susceptible to food allergies and may experience various health issues due to allergens in their food. Most allergenic foods are subjected to heat treatment before being consumed. However, thermal processing and prolonged storage can cause glycation reactions to occur in food. The glycation reaction is a common processing method requiring no special chemicals or equipment. It may affect the allergenicity of proteins by altering the structure of the epitope, revealing hidden epitopes, concealing linear epitopes, or creating new ones. Changes in food allergenicity following glycation processing depend on several factors, including the allergen's characteristics, processing parameters, and matrix, and are therefore hard to predict. This review examines how glycation reactions affect the allergenicity of different allergen groups in allergenic foods.

Development of a sandwich enzyme-linked immunosorbent kit for reliable detection of milk allergens in processed food.

The inclusion of undeclared cow's milk proteins may cause health complications to milk-allergic consumers and is one of the leading cause of food recall in many countries all over the world. Therefore, to keep control on such incidences in processed products, we established a milk sandwich ELISA test kit by incorporating two polyclonal antibodies against milk proteins obtained from different species. Its analytical effectiveness in terms of sensitivity, specificity, accuracy, trueness, and precision were all analyzed. The limit of detection (LOD) of the test kit was 0.011 ppm, with high specificity for milk protein residues. The test kit was highly specific, apart from considerable cross-reactivity with goat milk and minor cross-reactivity with donkey and horse milk. The coefficient of variation of the test kit for intra-assay ranged from 4.02% to 14.62% and inter-assay ranged from 6.05% to 15.08% respectively. The sandwich ELISA was highly specific in detecting commercial food products. In a limited retail survey, 5/6 of the milk proteins declared on the ingredient labels tested positive for milk proteins. The study offers effective technical support for the sensitive detection of milk products both for food manufacturers and regulatory authorities.

Crustacean shellfish allergens: influence of food processing and their detection strategies.

Despite the increasing popularity of crustacean shellfish among consumers due to their rich nutrients, they can induce a serious allergic response, sometimes even life-threatening. In the past decades, a variety of crustacean allergens have been identified to facilitate the diagnosis and management of crustacean allergies. Although food processing techniques can ease the risk of crustacean shellfish allergy, no available processing methods to tackle crustacean allergies thoroughly. Strict dietary avoidance of crustacean shellfish and its component is the best option for the protection of sensitized individuals, which should rely on the compliance of food labeling and, as such, on their verification by sensitive, reliable, and accurate detection techniques. In this present review, the physiochemical properties, structure aspects, and immunological characteristics of the major crustacean allergens have been described and discussed. Subsequently, the current research progresses on how various processing techniques cause the alterations and modifications in crustacean allergens to produce hypoallergenic crustacean food products were summarized and discussed. Particularly, various analytical methodologies employed in crustacean shellfish allergen detection, and the effect of food processing and matrix on these techniques, are also herein emphasized for the appropriate selection of analytical detection tools to safeguard consumers safety.

Infection-induced signals generated at the plasma membrane epigenetically regulate Wnt signaling in vitro and in vivo.

Wnt signaling regulates immunomodulatory functions during infection and inflammation. Employing NCCIT and HCT116 cells, having high endogenous Wnt signaling, we observed elevated levels of low-density lipoprotein receptor-related protein 5/6 (LRP5/6) and Frizzled class receptor 10 (FZD10) and increases in ß-catenin, doublecortin-like kinase 1 (DCLK1), CD44 molecule (CD44), and aldehyde dehydrogenase 1 family member A1 (ALDH1A1). siRNA-induced knockdown of these receptors antagonized TOPflash reporter activity and spheroid growth in vitro and elevated Wnt-inhibitory factor 1 (WIF1) activity. Elevated mRNA and protein levels of LRP5/6 and FZD10 paralleled expression of WNT2b and WNT4 in colonic crypts at days 6 and 12 post-infection with Citrobacter rodentium (CR) and tended to decline at days 20-34. The CR mutant escV or the tankyrase inhibitor XAV939 attenuated these responses. A three-dimensional organoid assay in colonic crypts isolated from CR-infected mice revealed elevated levels of LRP5/6 and FZD10 and ß-catenin co-localization with enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2). Co-immunoprecipitation in the membrane fraction revealed that axin associates with LRP5/6 in CR-infected crypts, and this association was correlated with increased ß-catenin. Colon tumors from either CR-infected ApcPMin/+ or azoxymethane/dextran sodium sulfate (AOM/DSS)-treated mice had high LRP5/6 or FZD10 levels, and chronic Notch blockade through the γ-secretase inhibitor dibenzazepine down-regulated LRP5/6 and FZD10 expression. In CR-responsive CT-26 cells, siRNA-induced LRP5/6 or FZD10 knockdown antagonized TOPflash reporter activity. Elevated miR-153-3p levels correlated with LRP5/6 and FZD10, and miR-153-3p sequestration via a plasmid-based miR inhibitor system attenuated Wnt signaling. We conclude that infection-induced signals from the plasma membrane epigenetically regulate Wnt signaling.

Dynamics of the preterm gut microbiome in health and disease.

Advances in metagenomics have allowed a detailed study of the gut microbiome, and its role in human health and disease. Infants born prematurely possess a fragile gut microbial ecosystem that is vulnerable to perturbation. Alterations in the developing gut microbiome in preterm infants are linked to life-threatening diseases such as necrotizing enterocolitis (NEC) and late-onset sepsis; and may impact future risk of asthma, atopy, obesity, and psychosocial disease. In this mini-review, we summarize recent literature on the origins and patterns of development of the preterm gut microbiome in the perinatal period. The host-microbiome-environmental factors that portend development of dysbiotic intestinal microbial patterns associated with NEC and sepsis are reviewed. Strategies to manipulate the microbiome and mitigate dysbiosis, including the use of probiotics and prebiotics will also be discussed. Finally, we explore the challenges and future directions of gut microbiome research in preterm infants.

Dietary Interventions Ameliorate Infectious Colitis by Restoring the Microbiome and Promoting Stem Cell Proliferation in Mice.

Decreases in short-chain-fatty-acids (SCFAs) are linked to inflammatory bowel disease (IBD). Yet, the mechanisms through which SCFAs promote wound healing, orchestrated by intestinal stem cells, are poorly understood. We discovered that, in mice with Citrobacter rodentium (CR)-induced infectious colitis, treatment with Pectin and Tributyrin diets reduced the severity of colitis by restoring Firmicutes and Bacteroidetes and by increasing mucus production. RNA-seq in young adult mouse colon (YAMC) cells identified higher expression of Lgr4, Lgr6, DCLK1, Muc2, and SIGGIR after Butyrate treatment. Lineage tracing in CR-infected Lgr5-EGFP-IRES-CreERT2/ROSA26-LacZ (Lgr5-R) mice also revealed an expansion of LacZ-labeled Lgr5(+) stem cells in the colons of both Pectin and Tributyrin-treated mice compared to control. Interestingly, gut microbiota was required for Pectin but not Tributyrin-induced Lgr5(+) stem cell expansion. YAMC cells treated with sodium butyrate exhibited increased Lgr5 promoter reporter activity due to direct Butyrate binding with Lgr5 at -4.0 Kcal/mol, leading to thermal stabilization. Upon ChIP-seq, H3K4me3 increased near Lgr5 transcription start site that contained the consensus binding motif for a transcriptional activator of Lgr5 (SPIB). Thus, a multitude of effects on gut microbiome, differential gene expression, and/or expansion of Lgr5(+) stem cells seem to underlie amelioration of colitis following dietary intervention.

Quantification of crustacean tropomyosin in foods using high-performance liquid chromatography-tandem mass spectrometry method.

BACKGROUND: Allergic reactions to crustacean products have been increasing owing to the rising consumption. Tropomyosin (TM) is the main crustacean allergen; it has a coiled-coil structure, which shows stability to various food processing methods. Crustacean processed products have been used in several food products, thereby causing greater difficulties in detecting TM in these products. We aimed to develop an assay based on high-performance liquid chromatography-tandem mass spectrometry for the accurate and reproducible quantification of crustacean TM in foods. RESULTS: The three peptides IQLLEEDLER, LAEASQAADESER, and IVELEEELR were selected as peptide markers, and the peptide IVELEEELR was selected as the quantitative marker. Extraction conditions and enzymatic digestion conditions were completely optimized. The extraction solution of Tris-hydrochloric acid buffer (50 mmol L-1 , pH 7.4) containing 1 mol L-1 potassium chloride and the enzymatic treatment at 1:15 ratio (enzyme/protein, m/m) for 13 h showed excellent efficiency. The method exhibited a good linear relationship, with the qualified coefficient of determination (R2  = 0.9994) in the wide range of 1 to 1000 µg L-1 . The accuracy was validated based on spiked recovery at three spiking levels (12.5, 25.0, and 50.0 µg kg-1 , TM/matrix) in blank matrices that included chicken sausages, beef balls, and egg-milk biscuits. The recoveries ranged from 91% to 109% with qualified relative standard deviations <15% with the limit of quantification (of 1.6 mg kg-1 , TM/matrix). CONCLUSION: This new approach can be used for the qualitative and quantitative detection of crustacean TM in various food matrices. © 2021 Society of Chemical Industry.

Enzymatic crosslinking and food allergenicity: A comprehensive review.

Food allergy has become a major global public health concern. In the past decades, enzymatic crosslinking technique has been employed to mitigate the immunoreactivity of food allergens. It is an emerging non-thermal technique that can serve as a great alternative to conventional food processing approaches in developing hypoallergenic food products, owing to their benefits of high specificity and selectivity. Enzymatic crosslinking via tyrosinase (TYR), laccase (LAC), peroxidase (PO), and transglutaminase (TG) modifies the structural and biochemical properties of food allergens that subsequently cause denaturation and masking of the antigenic epitopes. LAC, TYR, and PO catalyze the oxidation of tyrosine side chains to initiate protein crosslinking, while TG initiates isopeptide bonding between lysine and glutamine residues. Enzymatic treatment produces a high molecular weight crosslinked polymer with reduced immunoreactivity and IgE-binding potential. Crosslinked allergens further inhibit mast cell degranulation due to the lower immunostimulatory potential that assists in the equilibration of T-helper (Th)1/Th2 immunobalance. This review provides an updated overview of the studies carried out in the last decade on the potential application of enzymatic crosslinking for mitigating food allergenicity that can be of importance in the context of developing hypoallergenic/non-allergenic food products.

Whey allergens: Influence of nonthermal processing treatments and their detection methods.

Whey and its components are recognized as value-added ingredients in infant formulas, beverages, sports nutritious foods, and other food products. Whey offers opportunities for the food industrial sector to develop functional foods with potential health benefits due to its unique physiological and functional attributes. Despite all the above importance, the consumption of whey protein (WP) can trigger hypersensitive reactions and is a constant threat for sensitive individuals. Although avoiding such food products is the most successful approach, there is still a chance of incorrect labeling and cross-contamination during food processing. As whey allergens in food products are cross-reactive, the phenomenon of homologous milk proteins of various species may escalate to a more serious problem. In this review, nonthermal processing technologies used to prevent and eliminate WP allergies are presented and discussed in detail. These processing technologies can either enhance or mitigate the impact of potential allergenicity. Therefore, the development of highly precise analytical technologies to detect and quantify the existence of whey allergens is of considerable importance. The present review is an attempt to cover all the updated approaches used for the detection of whey allergens in processed food products. Immunological and DNA-based assays are generally used for detecting allergenic proteins in processed food products. In addition, mass spectrometry is also employed as a preliminary technique for detection. We also highlighted the latest improvements in allergen detection toward biosensing strategies particularly immunosensors and aptasensors.

Dietary phosphate restriction attenuates polycystic kidney disease in mice.

Studies in rodents with reduced nephron mass have suggested a strong positive correlation between dietary phosphate consumption and CKD progression. Prior work by our group demonstrated that dietary phosphate restriction can prevent tubular injury and microcyst formation in rodents with glomerulonephritis. Tubular injury and cystic dilation of tubules are key contributors to kidney function decline in polycystic kidney disease (PKD). Here, we determined whether dietary phosphate restriction slows renal cyst growth and fibrosis in a mouse model of PKD. Pcy/pcy mice received a normal phosphate (0.54%) or a phosphate-restricted (0.02%) diet (n = 10/group) from 7 to 20 wk of age. All of the other major dietary constituents, including protein source and content, were comparable between the two diets. At 20 wk, body weight, kidney weight-to-body weight ratio (KW/BW), cystic area, cyst number, and kidney fibrosis were quantified. Pcy/pcy mice fed a phosphate-restricted diet had lower serum phosphate, fibroblast growth factor 23, and parathyroid hormone levels, along with elevated serum calcium levels and increased kidney Klotho gene expression compared with mice that consumed the control diet. Dietary phosphate restriction resulted in a 25% lower KW/BW ratio and reduced the cyst number, cystic index, and gene expression for the tubular injury markers neutrophil gelatinase-associated lipocalin and interleukin-18. Mice fed the phosphate-restricted diet exhibited lower kidney expression for pathways involved in collagen deposition and myofibroblast activation (collagen type I-α1, phosphorylated SMAD3, and α-smooth muscle actin); however, histological differences in kidney fibrosis were not appreciated. Dietary phosphate restriction slows cystogenesis and inhibits the activation of key pathways in the generation of kidney fibrosis in PKD mice.

NEC-like intestinal injury is ameliorated by Lactobacillus rhamnosus GG in parallel with SIGIRR and A20 induction in neonatal mice.

BACKGROUND: Exaggerated Toll-like receptor (TLR) signaling and intestinal dysbiosis are key contributors to necrotizing enterocolitis (NEC). Lactobacillus rhamnosus GG (LGG) decreases NEC in preterm infants, but underlying mechanisms of protection remain poorly understood. We hypothesized that LGG alleviates dysbiosis and upregulates TLR inhibitors to protect against TLR-mediated gut injury. METHODS: Effects of LGG (low- and high-dose) on intestinal pro-inflammatory TLR signaling and injury in neonatal mice subjected to formula feeding (FF) and NEC were determined. 16S sequencing of stool and expression of anti-TLR mediators SIGIRR (single immunoglobulin interleukin-1-related receptor) and A20 were analyzed. RESULTS: FF induced mild intestinal injury with increased expression of interleukin-1ß (IL-1ß) and Kupffer cell (KC) (mouse homolog of IL-8) compared to controls. LGG decreased IL-1ß and KC in association with attenuated TLR signaling and increased SIGIRR and A20 expression in a dose-dependent manner. Low- and high-dose LGG had varying effects on gut microbiome despite both doses providing gut protection. Subsequent experiments of LGG on NEC revealed that pro-inflammatory TLR signaling and intestinal injury were also decreased, and SIGIRR and A20 expression increased, in a dose-dependent manner with LGG pre-treatment. CONCLUSIONS: LGG protects against intestinal TLR-mediated injury by upregulating TLR inhibitors without major changes in gut microbiome composition.

An overview on marine anti-allergic active substances for alleviating food-induced allergy.

Food provides energy and various nutrients and is the most important substance for the survival of living beings. However, for allergic people, certain foods cause strong reactions, and sometimes even cause shock or death. Food allergy has been recognized by the World Health Organization (WHO) as a major global food safety issue which affect the quality of life of nearly 5% of adults and 8% of children, and the incidence continues to rise but there is no effective cure. Drug alleviation methods for food allergies often have shortcomings such as side effects, poor safety, and high cost. At present, domestic and foreign scientists have turned to research and develop various new, safe and efficient natural sources of hypoallergenic or anti-allergic drugs or foods. There are many kinds of anti-allergic substances obtained from the plants and animals have been reported. Besides, probiotics and bifidobacteria also have certain anti-allergic effects. Of all the sources of anti-allergic substances, the ocean is rich in effective active substances due to its remarkable biodiversity and extremely complex living environment, and plays a huge role in the field of anti-food allergy. In this paper, the anti-food allergic bioactive substances isolated from marine organisms encompassing marine microbial, plant, animal sources and their mechanism were reviewed and the possible targets of anti-allergic substances exerting effects are illustrated by drawing. In addition, the development prospects of marine anti-allergic market are discussed and forecasted, which can provide reference for future research on anti-allergic substances.

Potential efficacy of processing technologies for mitigating crustacean allergenicity.

Crustacean allergy has become a growing food safety concern at a global scale. In the past decades, various food processing approaches have been employed to develop food products with reduced allergenic potential. Thermal treatment can dramatically influence the allergenicity of crustaceans by either reducing or enhancing their allergenic potential. Maillard reaction, enzymatic and acid treatments have shown to be promising in mitigating crustacean allergenicity. Recently, novel processing technologies, namely high-pressure processing, high-intensity ultrasound, irradiation, pulsed ultraviolet light and hurdle technology have attracted special attention from the researchers and the food industry professionals owing to their benefits over the conventional methods. In this context, this review paper provides an updated overview of the current knowledge on how different food processing methods induce structural changes of crustacean allergens and, subsequently, influence their allergenic potential. Data on prevalence and clinical relevance of crustacean allergy are presented, as well as, the molecular characterization of crustacean allergens and the main analytical methods for their detection in processed foods.

Effect of tyrosinase-catalyzed crosslinking on the structure and allergenicity of turbot parvalbumin mediated by caffeic acid.

BACKGROUND: Enzymatic treatment of allergenic protein can alter their functional properties under a mild reaction condition due to specificity of enzymes. Phenolic compounds act as mediators and enhance the crosslinking reactions. The study aimed to assess the changes in the structure and immunoglobulin G (IgG) binding capacity of turbot parvalbumin (PV) upon crosslinking with tyrosinase (Tyr) in the absence and presence of caffeic acid. RESULTS: Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis revealed the appearance of higher molecular weight bands (24, 36 kDa) in the crosslinked PV. The secondary structure of crosslinked PV became loosened and disordered. The results of intrinsic fluorescence and ultraviolet absorption spectral analyses, as well as surface hydrophobicity and free amino group analyses also revealed structural changes. As observed by western blot analysis, the intensity of the PV bands reduced upon Tyr treatment, indicating reduced binding of specific IgG to PV. Moreover, the indirect ELISA (enzyme-linked immunosorbent assay) analysis confirmed that the IgG binding ability of crosslinked PV was reduced 34.94%. CONCLUSION: Enzymatic treatment mitigated the allergenicity of fish PV, which was closely related to the alterations in the conformational structure. This treatment showed potential for developing hypoallergenic fish products under mild reaction conditions. © 2019 Society of Chemical Industry.

Allergenicity of acrolein-treated shrimp tropomyosin evaluated using RBL-2H3 cell and mouse model.

BACKGROUND: Food processing effects can modify protein functional properties. However, protein was oxidized inevitably by lipid peroxidation during food processing. Acrolein, a primary by-product of lipid peroxidation, can modify the structural and functional properties of protein. The aim of the research was to analyze the effect of acrolein on allergenicity of TM, a major allergen in shrimp. RESULTS: The overall allergenic effects of acrolein-treated TM were evaluated using female BALB/c mice and a mediator-releasing RBL-2H3 cell line. Acrolein-treated TM significantly decreased TM-specific immunoglobulin E/G1 levels, and histamine and mMCP-1 release in mouse serum. Release of inflammatory mediators such as ß-hexosaminidase, histamine, cysteinyl leukotriene and prostaglandin D2 was clearly suppressed after acrolein treatment. CONCLUSION: These results indicate that acrolein-induced tropomyosin modification can decrease the allergenicity of TM. This reduction contributes to allergenic potential changes in shrimp during processing and preservation. © 2018 Society of Chemical Industry.

Determining the effect of malondialdehyde on the IgE-binding capacity of shrimp tropomyosin upon in vitro digestion.

BACKGROUND: Stability in simulated gastric fluids is considered an important parameter for the estimation of food allergenicity. Moreover, proteins in food are highly susceptible to lipid oxidation during processing and preservation. In this study, the change in the IgE-binding capacity of malondialdehyde (MDA)-treated shrimp tropomyosin (TM) following in vitro digestion was investigated by SDS-PAGE and western blot. RESULTS: Shrimp TM treated with different concentrations of MDA was slightly degraded and became increasingly resistant to pepsin digestion over time. While untreated TM was rapidly degraded, MDA-treated TM showed some resistance and was degraded by trypsin only after increasing the digestion time. Results of immunoblotting studies on IgE using sera from patients allergic to shrimp indicated that the IgE-binding capacity of TM and MDA (50 mmol L-1 )-treated TM decreased slightly after pepsin digestion and significantly decreased after trypsin digestion. CONCLUSION: The study indicated that the resistance of TM to degradation increased after oxidation. The treatment with proteases, especially trypsin, is quite effective in decreasing the IgG/IgE-binding capacity of shrimp TM. © 2017 Society of Chemical Industry.

An ornamental plant targets epigenetic signaling to block cancer stem cell-driven colon carcinogenesis.

Phytochemicals modulate key cellular signaling pathways and have proven anticancer effects. Alcea rosea(AR; Hollyhock) is an ornamental plant with known anti-inflammatory properties. This study explored its role as an anticancer agent. The AR seed extract (AR extract) inhibited proliferation and colony formation in a dose- and time-dependent manner and promoted apoptosis as was evidenced by cleavage of PARP and increased expression of Bax accompanying reduced levels of BCL-xl protein in HCT116 and SW480 cells, respectively. In addition, AR extract-arrested cells at Go/G1 phase of cell cycle and exhibited decreases in Cyclin D1. AR extract-treated cells exhibited reduced number and size of colonospheres in a dose-dependent manner concomitant with decreases in cancer stem cell (CSC) markers ALDH1A1 and Dclk1. Relative levels of ß-catenin, Notch-ICD, Hes1 and EZH2 were also attenuated by AR extract. TOP-flash reporter activity, a measure of Wnt signaling, decreased significantly in response to treatment while overexpression of wild type but not mutant EZH2, reversed the inhibitory effects. Moreover, WIF1 (a Wnt antagonist) promoter activity increased dramatically following treatment with AR extract which phenocopied increases in WIF1 reporter activity following EZH2 knockdown.In vivo, AR extract attenuated tumor growth due probably to reduced levels of EZH2, ß-catenin, CyclinD1 and Ki-67 along with reduced levels of CSC markers. Since partial purification via HPLC yielded a prominent peak, efforts are underway to identify the active ingredient(s). Taken together, the results clearly suggest that AR extract/active component(s) can be an effective preventative/therapeutic agent to target colon cancer.

High-sensitivity C-reactive protein (hs-CRP) levels and its relationship with components of polycystic ovary syndrome in Indian adolescent women with polycystic ovary syndrome (PCOS).

C-reactive protein (CRP) is a risk marker for type 2 diabetes mellitus and cardiovascular diseases. In polycystic ovary syndrome (PCOS), limited data are available on high-sensitivity C-reactive protein (hs-CRP) levels and its relationship with components of PCOS especially in Indian women. The objective was to determine serum hs-CRP concentration in adolescent women with and without PCOS and to assess possible correlations of serum hs-CRP levels with components of PCOS in Indian women. One hundred and sixty women with PCOS and sixty non-PCOS women having normal menstrual cycles were included. Clinical assessment included anthropometry, Ferriman-Gallwey (FG) score and blood pressure (BP) measurement. Laboratory evaluation included estimation of T4, TSH, LH, FSH, total testosterone, prolactin, cortisol, 17OHP, hs-CRP, lipid profile, and insulin, and glucose after 2-h oral glucose tolerance test. Homeostasis Model Assessment Insulin resistance index (HOMA-IR) and Quantitative Insulin Sensitivity Check Index (QUICKI) and glucose intolerance was calculated. FG score, LH, FSH, total Testosterone, HOMA-IR and QUICKI were significantly different among women with or without PCOS (p < 0.01). Although hs-CRP levels showed a higher trend in women having PCOS, there was no significant difference between the groups (p > 0.05). A significant and positive correlation was found between hs-CRP and body mass index (BMI) (r = 0.308, p < 0.01) among PCOS group. The results in Indian adolescent women suggest that hs-CRP levels may not per se be associated with PCOS, rather can be related to fat mass in this subset of subjects.

Aging induces changes in cancer formation and microbial content in a murine model of bladder cancer.

Bladder cancer (BCa) incidence is tightly linked to aging. Older patients with BCa present with higher grade tumors and have worse outcomes on Bacillus-Calmette-Guerin (BCG) immunotherapy. Aging is also known to result in changes in the gut microbiome over mammalian lifespan, with recent studies linking alterations in the gut microbiome to changes in tumor immunity. There is limited information on the microbiome in BCa models though, despite known links to aging and immunotherapy. The purpose of this study was to evaluate how aging impacts tumor formation, inflammation, and the microbiome of mice given the model BCa carcinogen N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN). We hypothesized old animals would have larger, more inflamed tumors and a shift in their fecal microbiome compared to their younger counterparts. Young (~8-week-old) or old (~78-week-old) C57Bl/6J animals were administered 0.05% BBN in drinking water for 16 weeks and then euthanized or allowed to progress for an additional 4 weeks. After 16 weeks of BBN, old mice had higher bladder to body weight ratio than young mice, and also muscle invasive tumors, which were not seen in their young counterparts. Old animals also had increased innate immune recruitment, but CD4+/CD8+ T cell recruitment did not appear different. BBN dramatically altered the microbiome in both sets of animals as measured by ß-diversity, including changes in multiple genera of bacteria. These data suggest old mice have a differential response to BBN-induced BCa. Given the median age of patients with BCa, understanding how the aged phenotype interacts with BCa is imperative.