Full Classification of Transport on an Equilibrated 5/2 Edge via Shot Noise.

The nature of the bulk topological order of the 5/2 non-Abelian fractional quantum Hall state and the steady state of its edge are long-studied questions. The most promising non-Abelian model bulk states are the Pfaffian (Pf), anti-Pffafian (APf), and particle-hole symmetric Pfaffian (PHPf). Here, we propose to employ a set of dc current-current correlations (electrical shot noise) in order to distinguish among the Pf, APf, and PHPf candidate states, as well as to determine their edge thermal equilibration regimes: full vs partial. Using other tools, measurements of GaAs platforms have already indicated consistency with the PHPf state. Our protocol, realizable with available experimental tools, is based on fully electrical measurements.

Punctured-Chern Topological Invariants for Semimetallic Band Structures.

Topological insulator-based methods underpin the topological classification of gapped bands, including those surrounding semimetallic nodal defects. However, multiple bands with gap-closing points can also possess nontrivial topology. We construct a general wave-function-based "punctured-Chern" invariant to capture such topology. To show its general applicability, we analyze two systems with disparate gapless topology: (1) a recent two-dimensional fragile topological model to capture the various band-topological transitions and (2) a three-dimensional model with a triple-point nodal defect to characterize its semimetallic topology with half integers that govern physical observables such as anomalous transport. This invariant also gives the classification for Nexus triple points (Z×Z) with certain symmetry restrictions, which is reconfirmed by abstract algebra.

Coexistence of Canted Antiferromagnetism and Bond Order in ν=0 Graphene.

Motivated by experimental studies of graphene in the quantum Hall regime, we revisit the phase diagram of a single sheet of graphene at charge neutrality. Because of spin and valley degeneracies, interactions play a crucial role in determining the nature of the ground state. We show that, generically within the Hartree-Fock approximation, in the regime of interest there is a region of coexistence between magnetic and bond orders in the phase diagram. We demonstrate this result both in continuum and lattice models, and argue that the coexistence phase naturally provides a possible explanation for unreconciled experimental observations on the quantum Hall effect in graphene.

Genome-wide detection and classification of terpene synthase genes in Aquilaria agallochum.

Agarwood, one of the precious woods in the globe, is produced by Aquilaria plant species during an upshot of wounding and infection. Produced as a defence response, the dark, fragrant resin gets secreted in the plant's duramen, which is impregnated with fragrant molecules with the due course. Agarwood has gained worldwide popularity due to its high aromatic oil, fragrance, and pharmaceutical value, which makes it highly solicited by numerous industries. Predominant chemical constituents of agarwood, sesquiterpenoids, and 2-(2-phenylethyl) chromones have been scrutinized to comprehend the scientific nature of the fragrant wood and develop novel products. However, the genes involved in the biosynthesis of these aromatic compounds are still not comprehensively studied in Aquilaria. In this study, publicly available genomic and transcriptomics data of Aquilaria agallochum were integrated to identify putative functional terpene synthase genes (TPSs). The in silico study enabled us to identify ninety-six TPSs, of which thirty-nine full-length genes were systematically classified into TPS-a, TPS-b, TPS-c, TPS-e, TPS-f, and TPS-g subfamilies based on their gene structure, conserve motif, and phylogenetic comparison with TPSs from other plant species. Analysis of the cis-regulatory elements present upstream of AaTPSs revealed their association with hormone, stress and light responses. In silico expression studies detected their up-regulation in stress induced tissue. This study provides a basic understanding of terpene synthase gene repertoire in Aquilaria agallochum and unlatches opportunities for the biochemical characterization and biotechnological exploration of these genes. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12298-021-01040-z.

Focused Gaussian beam in the paraxial approximation.

A focused Gaussian beam represents a case of highly practical importance in many areas of optics and photonics. We derive analytical expressions for a focused Gaussian beam in the paraxial approximation, considering an arbitrary lens filling factor. We discuss the role of higher-order Bessel functions of the first kind in defining the electric field in the focal region.

Intra-tumor ROS amplification by melatonin interferes in the apoptosis-autophagy-inflammation-EMT collusion in the breast tumor microenvironment.

Epidemiological as well as experimental studies have established that the pineal hormone melatonin has inhibitory effects on different types of cancers. Several mechanisms have been proposed for the anticancer activities of melatonin, but the fundamental molecular pathways still require clarity. We developed a mouse model of breast cancer using Ehrlich's ascites carcinoma (injected in the 4th mammary fat pad of female Swiss albino mice) and investigated the possibility of targeting the autophagy-inflammation-EMT colloquy to restrict breast tumor progression using melatonin as intervention. Contrary to its conventional antioxidant role, melatonin was shown to augment intracellular ROS and initiate ROS-dependent apoptosis in our system, by modulating the p53/JNK & NF-κB/pJNK expressions/interactions. Melatonin-induced ROS promoted SIRT1 activity. Interplay between SIRT1 and NF-κB/p65 is known to play a pivotal role in regulating the crosstalk between autophagy and inflammation. Persistent inflammation in the tumor microenvironment and subsequent activation of the IL-6/STAT3/NF-κB feedback loop promoted EMT and suppression of autophagy through activation of PI3K/Akt/mTOR signaling pathway. Melatonin disrupted NF-κB/SIRT1 interactions blocking IL-6/STAT3/NF-κB pathway. This led to reversal of pro-inflammatory bias in the breast tumor microenvironment and augmented autophagic responses. The interactions between p62/Twist1, NF-κB/Beclin1 and NF-κB/Slug were altered by melatonin to strike a balance between autophagy, inflammation and EMT, leading to tumor regression. This study provides critical insights into how melatonin could be utilized in treating breast cancer via inhibition of the PI3K/Akt/mTOR signaling and differential modulation of SIRT1 and NF-κB proteins, leading to the establishment of apoptotic and autophagic fates in breast cancer cells.

Metformin instigates cellular autophagy to ameliorate high-fat diet-induced pancreatic inflammation and fibrosis/EMT in mice.

BACKGROUND: Chronic pancreatic dysfunction is frequently observed as a consequence of prolonged high-fat diet consumption and is a serious public health concern. This pro-diabetic insult aggravates inflammation-influenced fibrotic lesions and is associated with deregulated autophagy. Metformin, a conventional anti-hyperglycemic drug, might be beneficial for pancreatic health, but the complex molecular regulations are not clarified. Considering the worldwide prevalence of chronic pancreatic dysfunction in obese individuals, we aimed to unwind the molecular intricacies explaining the involvement of oxidative stress, inflammation and fibrosis and to approbate metformin as a plausible intervention in this crossroad. MAIN METHODS: Age-matched Swiss Albino mice were exposed to high-fat diet (60 kcal%) against control diet (10 kcal%) to establish diet-induced stress model. Metformin treatment was introduced after 4 weeks to metformin-control and HFD-exposed metformin groups. After 8 weeks, metabolic and molecular outcomes were assessed to establish the impact of metformin on chronic consequences of HFD-mediated injury. KEY FINDINGS: High-fat diet administration to healthy mice primes oxidative stress-mediated chronic inflammation through Nrf2/Keap1/NF-κB interplay. Besides, pro-inflammatory cytokine bias leading to fibrotic (increased TGF-ß, α-SMA, and MMP9) and pro-EMT (Twist1, Slug, Vimentin, E-cadherin) repercussions in pancreatic lobules were evident. Metformin distinctly rescues high-fat diet-induced remodeling of pancreatic pro-diabetic alterations and cellular survival/death switch. Further, metformin abrogates the p62-Twist1 crosstalk in an autophagy-dependent manner (elevated beclin1, LC3-II/I, Lamp2) to restore pancreatic homeostasis. CONCLUSION: Our research validates the therapeutic potential of metformin in the inflammation-fibrosis nexus to ameliorate high-fat diet-induced pancreatic dysfunction and related metabolic alterations.

Evaluation of morphological traits, biochemical parameters and seeding availability pattern among Citrus limon 'Assam lemon' accessions across Assam.

The Assam lemon is a highly valued Citrus cultivar known for its unique aroma, flavor, and appearance. This study aimed to investigate the morphological, seeding pattern and biochemical variations within 132 populations of Assam lemon from across 22 districts of Assam along with the control samples, with the objective to offer comprehensive understanding that could facilitate the improvement of breeding programs and further improvement of this important cultivar. Clustering based on UPGMA algorithm for morphological and seeding pattern data were analysed at population level, revealed two major clusters, where all the populations of Upper Assam districts were in the same cluster with the original stock (control population). The populations from Tinsukia and Dhemaji districts displayed more close similarities with the control population in comparison to populations of Upper Assam districts. Another interesting observation was regarding flowering patterns, while populations from Upper Assam districts excluding Golaghat district displayed both bisexual and unisexual flowers with less concentration of unisexual flowers, other remaining districts had bisexual and unisexual flowers of almost equal concentration. Unisexual flowers contained only the male reproductive organs with 40 anthers, while bisexual flowers had 36 anthers. Seeding patterns were examined across the districts, and it was found that populations from Tinsukia, Dhemaji, Lakhimpur, Dibrugarh, Jorhat, and the control population exhibited seedless characteristic while populations from other selected districts displayed a combination of seedless and seeded traits. Interestingly, Golaghat district appears as the linking district and showed availability of both seeded and seedless Assam lemon fruit, connecting the regions of Barak valley, Central, Lower, North and Upper Assam. Biochemical analysis showed significant variations across districts, however, the populations from Dhemaji, Tinsukia, Lakhimpur, Dibrugarh, and Jorhat districts displayed similarity with the control population. The study also investigated variability in soil nutrient content revealing substantial variation among the populations studied. This comprehensive investigation provides valuable insights into the morphological, seeding pattern, and biochemical diversity within the Assam lemon cultivar. These findings can be instrumental in breeding programs to enhance the cultivar, particularly in producing high-quality seedless fruits to meet consumer demands.

An integrated strategy to explore the potential role of melatonin against copper-induced adrenaline toxicity in rat cardiomyocytes: Insights into oxidative stress, inflammation, and apoptosis.

AIMS: Circumstantial anxiety as well as chronic stress may stimulate the release of stress hormones including catecholamines. Adrenaline toxicity has been implicated in many cardiovascular conditions. Considering previous literature that suggests the oxidative potential of the adrenaline-copper entity, we have investigated its potential nocuous role in isolated adult rat cardiomyocytes, the underlying molecular mechanism, and its possible protection by melatonin. MAIN METHODS: Given the mechanistic congruity of adrenaline-copper (AC) with the well-established H2O2-copper-ascorbate (HCA) system of free radical generation, we have used the latter as a representative model to study the cytotoxic nature of AC. We further investigated the cardioprotective efficacy of melatonin in both the stress models through scanning electron microscopy, immunofluorescence, flow cytometry, and western blot analysis. KEY FINDINGS: Results show that melatonin significantly protects AC-treated cardiomyocytes from ROS-mediated membrane damage, disruption of mitochondrial membrane potential, antioxidant imbalance, and distortion of cellular morphology. Melatonin protects cardiomyocytes from inflammation by downregulating pro-inflammatory mediators viz., COX-2, NF-κB, TNF-α, and upregulating anti-inflammatory IL-10. Melatonin significantly ameliorated cardiomyocyte apoptosis in AC and HCA-treated cells as evidenced by decreased BAX/BCL-2 ratio and subsequent suppression of caspase-9 and caspase-3 levels. The isothermal calorimetric study revealed that melatonin inhibits the binding of adrenaline bitartrate with copper in solution, which fairly explains the rescue potential of melatonin against AC-mediated toxicity in cardiomyocytes. SIGNIFICANCE: Findings suggest that the multipronged strategy of melatonin that includes its antioxidant, anti-inflammatory, anti-apoptotic, and overall cardioprotective ability may substantiate its potential therapeutic efficacy against adrenaline-copper-induced damage and death of adult rat cardiomyocytes.

Genome-wide analysis of respiratory burst oxidase homolog (Rboh) genes in Aquilaria species and insight into ROS-mediated metabolites biosynthesis and resin deposition.

Respiratory burst oxidase homolog (Rboh) generates reactive oxygen species (ROS) as a defense response during biotic and abiotic stress. In Aquilaria plants, wounding and fungal infection result in biosynthesis and deposition of secondary metabolites as defense responses, which later form constituents of fragrant resinous agarwood. During injury and fungal invasion, Aquilaria tree generates ROS species via the Rboh enzymes. Despite the implication of Rboh genes in agarwood formation, no comprehensive genomic-level study of the Rboh gene family in Aquilaria is present. A systematic illustration of their role during stress and involvement in initiating signal cascades for agarwood metabolite biosynthesis is missing. In this study, 14 Rboh genes were retrieved from genomes of two Aquilaria species, A. agallocha and A. sinensis, and were classified into five groups. The promoter regions of the genes had abundant of stress-responsive elements. Protein-protein network and in silico expression analysis suggested their functional association with MAPK proteins and transcription factors such as WRKY and MYC2. The study further explored the expression profiles of Rboh genes and found them to be differentially regulated in stress-induced callus and stem tissue, suggesting their involvement in ROS generation during stress in Aquilaria. Overall, the study provides in-depth insight into two Rboh genes, AaRbohC and AaRbohA, highlighting their role in defense against fungal and abiotic stress, and likely during initiation of agarwood formation through modulation of genes involved in secondary metabolites biosynthesis. The findings presented here offer valuable information about Rboh family members, which can be leveraged for further investigations into ROS-mediated regulation of agarwood formation in Aquilaria species.

Genome-wide investigation of Cytochrome P450 superfamily of Aquilaria agallocha: Association with terpenoids and phenylpropanoids biosynthesis.

Agarwood is a dark resinous wood, produced when Aquilaria tree responds to wounding and microbial infection resulting in the accumulation of fragrant metabolites. Sesquiterpenoids and 2-(2-phenylethyl) chromones are the major phytochemicals in agarwood and Cytochrome P450s (CYPs) are one of the important enzymes in the biosynthesis of these fragrant chemicals. Thus, understanding the repertoire of CYP superfamily in Aquilaria can not only give insights into the fundamentals of agarwood formation, but can also provide a tool for the overproduction of the aroma chemicals. Therefore, current study was designed to investigate CYPs of an agarwood producing plant, Aquilaria agallocha. We identified 136 CYP genes from A. agallocha genome (AaCYPs) and classified them into 8 clans and 38 families. The promoter regions had stress and hormone-related cis-regulatory elements which indicate their participation in the stress response. Duplication and synteny analysis revealed segmental and tandem duplicated and evolutionary related CYP members in other plants. Potential members involved in the biosynthesis of sesquiterpenoids and phenylpropanoids were identified and found to be upregulated in methyl jasmonate-induced callus and infected Aquilaria trees by real-time quantitative PCR analyses. This study highlights the possible involvement of AaCYPs in agarwood resin development and their complex regulation during stress exposure.

Targeted tumor killing by pomegranate polyphenols: Pro-oxidant role of a classical antioxidant.

One of the key biochemical features that distinguish a cancer cell from normal cells is its persistent pro-oxidative state that leads to intrinsic oxidative stress. Malignant cells have evolved sophisticated adaptation systems that involve high dependency on antioxidant functions and upregulation of pro-survival molecules to counteract the deleterious effects of reactive species and to maintain dynamic redox balance. This situation renders them vulnerable to further oxidative challenges by exogenous agents. In the present study, we advocated that pomegranate polyphenols act as pro-oxidants and trigger ROS-mediated apoptosis in cancer cells. With the help of both in vitro and in vivo models, we have established that pomegranate fruit extract (PFE) can cause a significant reduction in tumor proliferation while leaving normal tissues and cells unharmed. Administration of PFE (0.2% v/v) in Erhlich's ascites carcinoma-bearing mice for 3 weeks, inhibited the nuclear factor (erythroid-derived 2)-like 2-antioxidant response element signaling cascade, increased intracellular reactive oxygen species content, altered glutathione cycle thereby activating reactive oxygen species-induced apoptotic pathway in Erhlich's ascites carcinoma cells. Moreover, PFE mitigated epithelial to mesenchymal transition and migration in triple negative breast cancer cells (MDA-MB 231 cells) by down-regulating nuclear factor kappa light-chain-enhancer of activated B cells. Pre-treatment of tumor cells with N-acetyl cysteine protected these cells from undergoing PFE-induced apoptosis while siRNA-mediated silencing of Nuclear factor (erythroid-derived 2)-like 2 and nuclear factor kappa light-chain-enhancer of activated B cells in tumor cells increased the cytotoxic potential and pro-oxidative activity of PFE, indicating a clear role of these transcription factors in orchestrating the anticancer/pro-oxidative properties of PFE. The seminal findings provided may be exploited to develop potential therapeutic targets for selective killing of malignant cells.

Arsenic-induced differential inflammatory responses in mouse thymus involves NF-κB/STAT-3 disruption, Treg bias and autophagy activation.

AIM: Arsenic contamination in drinking water is a world-wide public health concern. Sustained arsenic ingestion leads to immune alterations and subsequent development of inflammatory and autoimmune diseases; however, the underlying cellular and molecular intricacies of immunotoxicity remains uncharacterized. We aim to understand how exposure to arsenic at different concentrations affects the immune system differentially and whether arsenic-induced differential inflammation dictates altered T-regulatory cell bias and emphasize the role of autophagy in the pathway. MAIN METHODS: Swiss albino mice were exposed to environmentally relevant concentrations of arsenic in drinking water for 28 days. Examination of thymic cyto-architecture was done to evaluate thymic damage. ELISA was performed for key cytokines. Flow cytometry, western blotting, and immunostaining were performed for cell surface and intracellular proteins. Co-immunoprecipitation and transfection with siRNA were performed to examine the direct physical interactions between proteins. KEY FINDINGS: Our study distinctly demonstrates that arsenic-induced oxidative stress instigates NF-κB activation, which not only provokes pro-inflammatory responses, but also exhibits immune-suppressive activity depending on the dose of arsenic. Co-immunoprecipitation of NF-κBp65 and pSTAT-3 reveals that arsenic alters their physical interaction, thereby suppressing IL-6/STAT-3/IL-17A feedback loop. Flow cytometry and silencing studies demonstrate that NF-κB-driven Treg cell differentiation induces immune-suppression through FoxP3 up-regulation at the highest dose of arsenic and such immune-suppression is actively supported by NF-κB-driven autophagy activation. SIGNIFICANCE: Collectively, our findings reveal that exposure to arsenic differentially impacts the immune system and understanding the molecular cascade might provide direction for prevention/treatment of arsenic-induced inflammatory and autoimmune diseases.

Sustained systemic inflammation increases autophagy and induces EMT/fibrotic changes in mouse liver cells: Protection by melatonin.

The unending lifestyle stressors along with genetic predisposition, environmental factors and infections have pushed the immune system into a state of constant activity, leading to unresolved inflammation and increased vulnerability to chronic diseases. Liver fibrosis, an early-stage liver condition that increases the risk of developing liver diseases like cirrhosis and hepatocellular carcinoma, is among the various diseases linked to inflammation that dominate worldwide morbidity and mortality. We developed a mouse model with low-grade lipopolysaccharide (LPS) exposure that shows hepatic damage and a pro-inflammatory condition in the liver. We show that inflammation and oxidative changes increase autophagy in liver cells, a degradation process critical in maintaining cellular homeostasis. Our findings from in vivo and in vitro studies also show that induction of both inflammation and autophagy trigger epithelial-mesenchymal transition (EMT) and pro-fibrotic changes in hepatocytes. Inhibiting the inflammatory pathways with a naturally occurring NF-κB inhibitor and antioxidant, melatonin, could assuage the changes in autophagy and activation of EMT/fibrotic pathways in hepatocytes. Taken together, this study shows a pathway linking inflammation and autophagy which could be targeted for future drug development to delay the progression of liver fibrosis.

An overview of basic molecular biology of SARS-CoV-2 and current COVID-19 prevention strategies.

Coronavirus Disease 2019 (COVID-19) manifests as extreme acute respiratory conditions caused by a novel beta coronavirus named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) which is reported to be the seventh coronavirus to infect humans. Like other SARS-CoVs it has a large positive-stranded RNA genome. But, specific furin site in the spike protein, mutation prone and phylogenetically mess open reading frame1ab (Orf1ab) separates SARS-CoV-2 from other RNA viruses. Since the outbreak (February-March 2020), researchers, scientists, and medical professionals are inspecting all possible facts and aspects including its replication, detection, and prevention strategies. This led to the prompt identification of its basic biology, genome characterization, structural and expression based functional information of proteins, and utilization of this information in optimizing strategies to prevent its spread. This review summarizes the recent updates on the basic molecular biology of SARS-CoV-2 and prevention strategies undertaken worldwide to tackle COVID-19. This recent information can be implemented for the development and designing of therapeutics against SARS-CoV-2.

Oleic acid as a restorative agent in alleviating adrenaline induced altered morphofunctional milieu of gastric tissue and mitochondria.

The role of oleic acid as a protective antioxidant has recently been recognized. The present study is aimed to explore whether oleic acid can afford protection to rat gastric tissue when challenged with adrenaline. Sixty adult healthy male albino rats were divided into 10 groups comprising of 6 animals each. First group constituted the control. Rats of the second group were injected sub-cutaneously with adrenaline bitartrate at the dose of 0.3mg/kg body weight, every day for a period of 17 days. Rats of the third, to the sixth groups were orally fed with different doses of oleic acid (2.5, 5, 10, 20 mg/kg body weight/day) respectively. The rats of seventh to tenth groups were orally fed with doses of oleic acid as mentioned above and subsequently injected with adrenaline bitartrate at 0.3mg/kg body weight sub-cutaneously. After the treatment period, the animals were euthanized through cervical dislocation following light ether anaesthesia and gastric tissues were collected for morphological and biochemical studies. Subcutaneously administered pharmacological dose of adrenaline bitartrate caused oxidative stress inducing gastric lesion in male albino rats as evident from the altered levels of biomarkers of oxidative stress, activities of antioxidant and mitochondrial enzymes related to energy metabolism with changes in tissue morphology. Pre-treatment of rats with oleic acid dose-dependently protected against these gastric injuries induced by adrenaline indicating the potentiality of oleic acid in protecting against adrenaline induced gastric injury in male albino rats where antioxidant mechanisms appear to play a pivotal role in mediating such protection.

Inflammation-induced behavioral changes is driven by alterations in Nrf2-dependent apoptosis and autophagy in mouse hippocampus: Role of fluoxetine.

Inflammation has been associated with the progression of many neurological diseases. Peripheral inflammation has also been vaguely linked to depression-like symptoms in animal models, but the underlying pathways that orchestrate inflammation-induced behavioral or molecular changes in the brain are still elusive. We have recently shown that intraperitoneal injections of lipopolysaccharide (LPS) to Swiss albino mice triggers systemic inflammation, leading to an activated immune response along with changes in monoamine levels in the brain. Herein we pinpoint the fundamental pathways linking peripheral inflammation and depression-like behavior in a mouse model, thereby identifying suitable targets of intervention to combat the situation. We show that LPS-induced peripheral inflammation provoked a depression-like behavior in mice and a distinct pro-inflammatory bias in the hippocampus, as evident from increased microglial activation and elevated levels of pro-inflammatory cytokines IL-6 and TNF-α, and activation of NFκB-p65 pathway. Significant alterations in Nrf2-dependent cellular redox status, coupled with altered autophagy and increased apoptosis were noticed in the hippocampus of LPS-exposed mice. We and others have previously shown that, fluoxetine (an anti-depressant) has effective anti-inflammatory and antioxidant properties by virtue of its abilities to regulate NFκB and Nrf2 signaling. We observed that treatment with fluoxetine or the Nrf2 activator tBHQ (tert-butyl hydroquinone), could reverse depression-like-symptoms and mitigate alterations in autophagy and cell death pathways in the hippocampus by activating Nrf2-dependent gene expressions. Taken together, the data suggests that systemic inflammation potentiates Nrf2-dependent changes in cell death and autophagy pathway in the hippocampus, eventually leading to major pathologic sequelae associated with depression. Therefore, targeting Nrf2 could be a novel approach in combatting depression and ameliorating its associated pathogenesis.

Effect of different smoking methods on the quality of pork sausages.

AIM: An experiment was conducted to evaluate the nutritional, physicochemical, microbiological, and sensory attributes of pork sausages treated with conventional smoking (CS) and liquid smoke (LS). MATERIALS AND METHODS: Pork sausages were prepared by employing CS (T1) and by addition of LS at 3% (T2A), 5% (T2B), and 7% (T2C) while smoking was not done in control (C) sausages. The ready-to-eat pork sausages were evaluated in terms of proximate composition, emulsion stability (ES), cooking loss (CL), pH, water activity (aw), texture profile analysis (TPA), and shear force on the day of preparation and the shelf life of the sausages was evaluated on the basis of thiobarbituric acid reactive substance (TBARS) value, organoleptic qualities, total viable plate count, total psychrophilic count, and yeast and mold counts at 5-day interval up to 15 days under refrigerated storage (6±1°C). RESULTS: The mean percentage moisture and percentage ether extract contents of the conventionally smoked sausages (T1) exhibited significant difference (p≤0.01) with the rest of the formulations. However, in terms of mean percentage crude protein and percentage total solids, no significant difference (p≥0.05) was recorded between the treatment groups. The mean ES (ml of oil/100 g emulsion) of the different sausage emulsions ranged from 1.88 to 3.20, while the mean aw values among the sausage formulations were found to be non-significant. In terms of mean percentage, CL and pH values, significantly lowest (p≤0.01) values were recorded by the T1 sausages. The mean TBARS values recorded at different periods of time in respect of all the treatment groups ranged from 0.10 to 0.33 mg malanoldehyde [MDA]/kg of sausages which are well within the permissible limit. The highest shear force values (KgF) were recorded by the sausages of T1 formulation (p≤0.01), while TPA of the sausages did not record any significant difference (p≥0.05) among the treatments. Organoleptic studies revealed acceptability of the sausages up to 10 days of refrigerated storage irrespective of treatments employed; however, the sausages of T1 formulation scored significantly (p≤0.01) higher panel ratings. Microbiologically, sausages with different formulations were found to be within the acceptable limit up to the 15th day of refrigerated storage. CONCLUSION: The study revealed that traditional hot smoking has slightly higher edges over the LS-treated sausages in terms of lipid oxidation, microbiological safety, and sensory panel ratings. However, if not superior, the same was found to be well within the acceptable limit in case of LS-treated sausages proving the potentiality of the use of LS as a suitable replacement for the traditional hazardous hot smoking process.

A 3D-Printed Patient-Specific Phantom for External Beam Radiation Therapy of Prostate Cancer.

This paper presents the design evolution, fabrication, and testing of a novel patient and organ-specific, 3D printed phantom for external beam radiation therapy of prostate cancer. In contrast to those found in current practice, this phantom can be used to plan and validate treatment tailored to an individual patient. It contains a model of the prostate gland with a dominant intraprostatic lesion, seminal vesicles, urethra, ejaculatory duct, neurovascular bundles, rectal wall, and penile bulb generated from a series of combined T2-weighted/dynamic contrast-enhanced magnetic resonance images. The iterative process for designing the phantom based on user interaction and evaluation is described. Using the CyberKnife System at Boston Medical Center a treatment plan was successfully created and delivered. Dosage delivery results were validated through gamma index calculations based on radiochromic film measurements which yielded a 99.8% passing rate. This phantom is a demonstration of a methodology for incorporating high-contrast magnetic resonance imaging into computed-tomography-based radiotherapy treatment planning; moreover, it can be used to perform quality assurance.