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Salmonella is the leading cause of food-borne zoonotic disease worldwide. Non-typhoidal Salmonella serotypes are the primary etiological agents associated with salmonellosis in poultry. Contaminated poultry eggs and meat products are the major sources of human Salmonella infection. Horizontal and vertical transmission are the primary routes of infection in chickens. The principal virulence genes linked to Salmonella pathogenesis in poultry are located in Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2). Cell-mediated and humoral immune responses are involved in the defense against Salmonella invasion in poultry. Vaccination of chickens and supplementation of feed additives like prebiotics, probiotics, postbiotics, synbiotics, and bacteriophages are currently being used to mitigate the Salmonella load in poultry. Despite the existence of various control measures, there is still a need for a broad, safe, and well-defined strategy that can confer long-term protection from Salmonella in poultry flocks. This review examines the current knowledge on the etiology, transmission, cell wall structure, nomenclature, pathogenesis, immune response, and efficacy of preventative approaches to Salmonella.

The abscission process is initiated by changes in the auxin gradient across the abscission zone (AZ) and is triggered by ethylene. Although changes in gene expression have been correlated with the ethylene-mediated execution of abscission, there is almost no information on the molecular and biochemical basis of the increased AZ sensitivity to ethylene. We examined transcriptome changes in the tomato (Solanum lycopersicum 'Shiran 1335') flower AZ during the rapid acquisition of ethylene sensitivity following flower removal, which depletes the AZ from auxin, with or without preexposure to 1-methylcyclopropene or application of indole-3-acetic acid after flower removal. Microarray analysis using the Affymetrix Tomato GeneChip revealed changes in expression, occurring prior to and during pedicel abscission, of many genes with possible regulatory functions. They included a range of auxin- and ethylene-related transcription factors, other transcription factors and regulatory genes that are transiently induced early, 2 h after flower removal, and a set of novel AZ-specific genes. All gene expressions initiated by flower removal and leading to pedicel abscission were inhibited by indole-3-acetic acid application, while 1-methylcyclopropene pretreatment inhibited only the ethylene-induced expressions, including those induced by wound-associated ethylene signals. These results confirm our hypothesis that acquisition of ethylene sensitivity in the AZ is associated with altered expression of auxin-regulated genes resulting from auxin depletion. Our results shed light on the regulatory control of abscission at the molecular level and further expand our knowledge of auxin-ethylene cross talk during the initial controlling stages of the process.

The gut of warm-blooded animals is colonized by microbes possibly constituting at least 100 times more genetic material of microbial cells than that of the somatic cells of the host. These microbes have a profound effect on several physiological functions ranging from energy metabolism to the immune response of the host, particularly those associated with the gut immune system. The gut of a newly hatched chick is typically sterile but is rapidly colonized by microbes in the environment, undergoing cycles of development. Several factors such as diet, region of the gastrointestinal tract, housing, environment, and genetics can influence the microbial composition of an individual bird and can confer a distinctive microbiome signature to the individual bird. The microbial composition can be modified by the supplementation of probiotics, prebiotics, or synbiotics. Supplementing these additives can prevent dysbiosis caused by stress factors such as infection, heat stress, and toxins that cause dysbiosis. The mechanism of action and beneficial effects of probiotics vary depending on the strains used. However, it is difficult to establish a relationship between the gut microbiome and host health and productivity due to high variability between flocks due to environmental, nutritional, and host factors. This review compiles information on the gut microbiota, dysbiosis, and additives such as probiotics, postbiotics, prebiotics, and synbiotics, which are capable of modifying gut microbiota and elaborates on the interaction of these additives with chicken gut commensals, immune system, and their consequent effects on health and productivity. Factors to be considered and the unexplored potential of genetic engineering of poultry probiotics in addressing public health concerns and zoonosis associated with the poultry industry are discussed.

In vitro and in vivo experiments were conducted to study the effects of synbiotic supplementation on Salmonella enterica ser. Enteritidis (SE) proliferation, cecal content load, and broiler carcass contamination. Lactobacillus reuteri, Enterococcus faecium, Bifidobacterium animalis, and Pediococcus acidilactici culture supernatants decreased (P < 0.05) the in vitro proliferation of SE at 1:1 supernatant: pathogen dilution. A total of 240 Cobb-500 broiler chicks were randomly allotted to three treatment groups (8 replicates/group with 10 birds/replicate): control (basal diet), antibiotic (Virginiamycin at 20 mg/kg feed), synbiotic (PoultryStar® ME at 0.5 g/kg feed containing L. reuteri, E. faecium, B. animalis, P. acidilactici and a Fructooligosaccharide) from day of hatch. At 21 d of age, all birds in experimental groups were orally inoculated with 250 μl of 1 X 109 CFU SE. Antibiotic supplementation increased (P < 0.05) body weight and feed consumption, compared to the control group. Birds in the synbiotic supplementation had intermediate body weight and feed consumption that were not significantly different from both the control and antibiotic group at 42 d of age in SE infected birds. No significant effects were observed in feed efficiency at 42 d of age among the groups. Antibiotic and synbiotic supplementation decreased (P < 0.05) SE load in cecal contents by 0.90 and 0.85 log units/ g and carcass SE load by 1.4 and 1.5 log units/mL of rinsate compared to the control group at 42 d of age (21 dpi). The relative abundance of IL-10, IL-1, TLR-4, and IFNγ mRNA was decreased (P < 0.05) in the antibiotic and synbiotic supplementation groups compared to the control birds at 42 d of age (21 dpi). It can be concluded that synbiotic supplementation decreased SE proliferation in vitro and decreased SE load in the cecal contents and broiler carcass.

The rapid development of online products paves the way to share customers’ opinions on amazon products. Unstructured text reviews and customer feedback are popular resources for customers when making decisions. However, reading through all the evaluations is tiresome, but the volume of customer feedback is enormous. The ability to forecast the precise sentiment polarities of user textual feedback evaluations for a particular entity is still difficult because of phrase length restrictions, textual order variations, and logical complexities. Therefore, an aspect level of analysis is needed, which support the retailers in understanding customer expectation and then modifying the product accordingly. However, many existing machine learning algorithms are available for sentiment detection but fail in accuracy rate. This paper proposes a novel sigTan-Beta Activation Function for Convolution Neural Networks (CNN) to attain remarkable and effective results. First, the sample dataset is pre-processed, and text strings are converted into the vector using Word2Vec, which computes the distance between words and groups them based on similarity. Afterwards, CNN extracts the sensitive features from the data and classifies the product reviews. The proposed model uses the sigTan-Beta Activation Function, which tunes the weight of the neurons to gain accurate performance. The proposed classified as positive or negative classes using the amazon review dataset. The proposed sigTan-Beta Activation Function for Convolution Neural Network (CNN) experiment performs better than existing methods in terms of accuracy, precision and F1-score. Our proposed sigTan-Beta Activation Function for Convolution Neural Network (CNN) achieves 94.5% accuracy to the existing ABO-RF algorithm (89.9%).

This research addresses the challenge of accurate load forecasting in cluster microgrids, where distributed energy systems interlink to operate seamlessly. As renewable energy sources become more widespread, ensuring a consistent and reliable power supply in the face of variable weather conditions is a significant challenge for power providers. The variability in energy consumption patterns, influenced by human behavior and environmental conditions, further complicates load prediction. The inherent instability of solar and wind energies adds complexity to forecasting load demand accurately. This paper suggests a solution in addressing some challenges by proposing a Modified Temporal Convolutional Feed Forward Network (MTCFN) for load forecasting in cluster microgrids. The Fire Hawk Optimization algorithm is employed to determine optimal configurations, addressing the intricacies of this complex optimization problem. Data collected from the Microgrid Market Share and Forecast 2024–2032 report, the efficiency of the proposed approach is evaluated through metrics such as Mean Absolute Error (MAE), Root Mean Square Error (RMSE), Mean Absolute Percentage Error (MAPE), Mean Square Error (MSE), and R-squared. The RMSE, MSE, MAE, MAPE, and R-squared values of the MTCFN are 0.4%, 1.5%, 0.6%, 6.8%, and 0.8%, respectively. The optimization algorithm's effectiveness is cross-validated through rigorous testing, training, and validation processes, revealing that the FFNN model based on the Fire Hawk Optimization algorithm yields superior load forecasting results. This research contributes to the advancement of signal, image, and video processing in the context of resilient and accurate energy management in cluster microgrids.

C. jejuni is the leading cause of human foodborne illness associated with poultry, beef, and pork consumption. C. jejuni is highly prevalent in commercial poultry farms, where horizontal transmission from the environment is considered to be the primary source of C. jejuni. As an enteric pathogen, C. jejuni expresses virulence factors regulated by a two-component system that mediates C. jejuni’s ability to survive in the host. C. jejuni survives and reproduces in the avian intestinal mucus. The avian intestinal mucus is highly sulfated and sialylated compared with the human mucus modulating C. jejuni pathogenicity into a near commensal bacteria in poultry. Birds are usually infected from two to four weeks of age and remain colonized until they reach market age. A small dose of C. jejuni (around 35 CFU/mL) is sufficient for successful bird colonization. In the U.S., where chickens are raised under antibiotic-free environments, additional strategies are required to reduce C. jejuni prevalence on broilers farms. Strict biosecurity measures can decrease C. jejuni prevalence by more than 50% in broilers at market age. Vaccination and probiotics, prebiotics, synbiotics, organic acids, bacteriophages, bacteriocins, and quorum sensing inhibitors supplementation can improve gut health and competitively exclude C. jejuni load in broilers. Most of the mentioned strategies showed promising results; however, they are not fully implemented in poultry production. Current knowledge on C. jejuni’s morphology, source of transmission, pathogenesis in poultry, and available preharvest strategies to decrease C. jejuni colonization in broilers are addressed in this review.

Clostridium perfringens type A and C are the primary etiological agents associated with necrotic enteritis (NE) in poultry. The predisposing factors implicated in the incidence of NE changes the physical properties of the gut, immunological status of birds, and disrupt the gut microbial homeostasis, causing an over-proliferation of C. perfringens. The principal virulence factors contributing to the pathogenesis of NE are the α-toxin, β-toxin, and NetB toxin. The immune response to NE in poultry is mediated by the Th1 pathway or cytotoxic T-lymphocytes. C. perfringens type A and C are also pathogenic in humans, and hence are of public health significance. C. perfringens intoxications are the third most common bacterial foodborne disease after Salmonella and Campylobacter. The restrictions on the use of antibiotics led to an increased incidence of NE in poultry. Hence, it is essential to develop alternative strategies to keep the prevalence of NE under check. The control strategies rely principally on the positive modulation of host immune response, nutritional manipulation, and pathogen reduction. Current knowledge on the etiology, pathogenesis, predisposing factors, immune response, effect on the gut microbial homeostasis, and preventative strategies of NE in this post-antibiotic era is addressed in this review.

Campylobacter is one of the major foodborne pathogens causing bacterial gastroenteritis worldwide. The immune response of broiler chickens to C . jejuni is under-researched. This study aimed to characterize the immune response of chickens to Campylobacter jejuni colonization. Birds were challenged orally with 0.5 mL of 2.4 x 10 8 CFU/mL of Campylobacter jejuni or with 0.5 mL of 0.85% saline. Campylobacter jejuni persisted in the ceca of challenged birds with cecal colonization reaching 4.9 log10 CFU/g on 21 dpi. Campylobacter was disseminated to the spleen and liver on 7 dpi and was cleared on 21 dpi from both internal organs. Challenged birds had a significant increase in anti- Campylobacter serum IgY (14&21 dpi) and bile IgA (14 dpi). At 3 dpi, there was a significant suppression in T-lymphocytes derived from the cecal tonsils of birds in the challenge treatment when compared to the control treatment after 72 h of ex vivo stimulation with Con A or C . jejuni . The T-cell suppression on 3 dpi was accompanied by a significant decrease in LITAF, K60, CLAU-2, IL-1β, iNOS, and IL-6 mRNA levels in the ceca and an increase in nitric oxide production from adherent splenocytes of challenged birds. In addition, on 3 dpi, there was a significant increase in CD4+ and CD8+ T lymphocytes in the challenge treatment. On 14 dpi, both pro and anti-inflammatory cytokines were upregulated in the spleen, and a significant increase in CD8+ T lymphocytes in Campylobacter -challenged birds’ ceca was observed. The persistence of C . jejuni in the ceca of challenged birds on 21 dpi was accompanied by an increase in IL-10 and LITAF mRNA levels, an increase in MNC proliferation when stimulated ex-vivo with the diluted C . jejuni , an increase in serum specific IgY antibodies, an increase in both CD4+ and CD8+ cells, and a decrease in CD4+:CD8+ cell ratio. The balanced Th1 and Th2 immune responses against C . jejuni might explain the ceca’s bacterial colonization and the absence of pathology in Campylobacter -challenged birds. Future studies on T lymphocyte subpopulations should elucidate a pivotal role in the persistence of Campylobacter in the ceca.

Poultry infected with Salmonella mount an immune response initially, however the immune responses eventually disappear leading the bird to be a carrier of Salmonella . The hypothesis of this study is that Salmonella infection induces T regulatory cell numbers and cytokine production and suppress host T cells locally in the gut to escape the host immune responses. An experiment was conducted to comparatively analyze the effect of S . enterica ser. Enteritidis ( S . Enteritidis) and S . enterica ser. Heidelberg ( S . Heidelberg) infection on CD4 + CD25 + T regulatory cell properties in chickens. A total of 144 broiler chicks were randomly distributed into three experimental groups of non-infected control, S . Enteritidis infected and S . Heidelberg infected groups. Chickens were orally inoculated with PBS (control) or 5x10 6 CFU/mL of either S . Enteritidis or S. Heidelberg at 3 d of age. Each group was replicated in six pens with eight chickens per pen. Chickens infected with S . Enteritidis had 6.2, 5.4, and 3.8 log 10 CFU/g, and chickens infected with S . Heidelberg had 7.1, 4.8, and 4.1 log 10 CFU/g Salmonella in the cecal contents at 4, 11, and 32 dpi, respectively. Both S . Enteritidis and S . Heidelberg were recovered from the liver and spleen 4 dpi. At 4, 11, and 32 dpi, chickens infected with S . Enteritidis and S . Heidelberg had increased CD4 + CD25 + cell numbers as well as IL-10 mRNA transcription of CD4 + CD25 + cells compared to that in the control group. CD4 + CD25 + cells from S . Enteritidis- and S . Heidelberg-infected chickens and restimulated with 1 μg antigen in vitro , had higher (P < 0.05) IL-10 mRNA transcription than the CD4 + CD25 + cells from the non-infected controls Though at 4dpi, chickens infected with S . Enteritidis and S . Heidelberg had a significant (P < 0.05) increase in CD4 + CD25 - IL-2, IL-1β, and IFNγ mRNA transcription, the CD4 + CD25 - IL-2, IL-1β, and IFNγ mRNA transcription, were comparable to that in the control group at 11 and 32dpi identifying that the host inflammatory response against Salmonella disappears at 11 dpi. It can be concluded that S . Enteritidis and S . Heidelberg infection at 3 d of age induces a persistent infection through inducing CD4 + CD25 + cells and altering the IL-10 mRNA transcription of CD4 + CD25 + cell numbers and cytokine production in chickens between 3 to 32 dpi allowing chickens to become asymptomatic carriers of Salmonella after 18 dpi.