Browsing by Author "Kumar, Santosh"

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DeepQSP: Identification of Quorum Sensing Peptides Through Neural Network Model
(Elsevier, 2024-09-13) Rahman, Md. Ashikur; Ali, Md. Mamun; Ahmed, Kawsar; Mahmud, Imran; Bui, Francis M.; Chen, Li; Kumar, Santosh; Moni, Mohammad Ali
Quorum Sensing Peptides (QSP) are small molecules crucial for microbial communication, enabling bacterial populations to coordinate behaviors such as biofilm formation and virulence. The identification of QSP is vital for understanding these biological processes. While existing clinical and lab-based methods are available, they can be costly and time-consuming. This study introduces Deep QSP, a novel technique for QSP identification, which combines Latent Semantic Analysis (LSA), a word embedding feature extraction method, with classical amino acid-based extraction Pseudo Amino Acid Composition (PAAC), and a convolutional neural network (CNN) classifier. The DeepQSP model was evaluated using a dataset of 440 peptide sequences, achieving impressive performance metrics: 0.9697 accuracy, 0.9655 sensitivity, 0.9730 specificity, and a Matthews correlation coefficient (MCC) of 0.9385. The LSA combined with PAAC improves peptide sequence representation, while the CNN effectively captures complex patterns, leading to accurate QSP identification. These quantified results demonstrate the effectiveness of the Deep QSP method, offering a powerful tool for advancing the study of microbial interaction and quorum sensing. The enhanced identification of QSPs is critical for microbiology and bioengineering, aiding in the understanding of cell-to-cell communication in microorganisms.
Mycobacterium tuberculosis : a new hitchhiker in the etiopathogenesis of periodontitis
(2024-06-01) MohanaSundaram, ArunSundar; Gohil, Namra Vinay; Etekochay, Maudlyn O; Patel, Premalkumar; Gurajala, Swathi; Sathanantham, Shanmugarajan Thukani; Nsengiyumva, Mugisha; Kumar, Santosh; Bin Emran, Talha
Periodontitis, a chronic inflammatory disease of the gums affects both the ligament and alveolar bone. A severe form of periodontal disease affects a strikingly high number of one billion adults globally. The disease permutes both the soft and hard tissues of the oral cavity leading to localized and systemic diseases. Periodontitis has a deleterious impact on systemic health causing diabetes, cardiovascular diseases (CVD), and other disease. The cause of the enhanced inflammatory process is due to dysbiosis and an unregulated immune response. Innate immune response and T cells trigger uninhibited cytokine release causing an unwarranted inflammatory response. The RANK- RANKL interaction between osteoblasts, immune cells, and progenitor osteoclasts results in the maturation of osteoclasts, which promote bone resorption. It is well established that dysbiosis of the oral cavity has been implicated in periodontitis. But emerging reports suggest that the pulmonary pathogen, Mycobacterium tuberculosis (Mtb), causes extrapulmonary diseases such as periodontitis. Many clinical case reports advocate the involvement of Mtb in periodontitis, which poses a threat with the surge of tuberculosis in HIV and other immunocompromised individuals. Fostering a better understanding of the mechanism, causative agents and control on inflammatory response is imperative in the prevention and treatment of periodontitis.
Mycobacterium Tuberculosis : A New Hitchhiker in the Etiopathogenesis of Periodontitis
(Wolters Kluwer Health, 2024-01-17) Sundaram, Arun Sundar Mohana; Gohil, Namra Vinay; Etekochay, Maudlyn O.; Patel, Premalkumar; Gurajala, Swathi; Sathanantham, Shanmugarajan Thukani; Nsengiyumva, Mugisha; Kumar, Santosh; Emran, Talha Bin
Periodontitis, a chronic inflammatory disease of the gums affects both the ligament and alveolar bone. A severe form of periodontal disease affects a strikingly high number of one billion adults globally. The disease permutes both the soft and hard tissues of the oral cavity leading to localized and systemic diseases. Periodontitis has a deleterious impact on systemic health causing diabetes, cardiovascular diseases (CVD), and other disease. The cause of the enhanced inflammatory process is due to dysbiosis and an unregulated immune response. Innate immune response and T cells trigger uninhibited cytokine release causing an unwarranted inflammatory response. The RANK- RANKL interaction between osteoblasts, immune cells, and progenitor osteoclasts results in the maturation of osteoclasts, which promote bone resorption. It is well established that dysbiosis of the oral cavity has been implicated in periodontitis. But emerging reports suggest that the pulmonary pathogen, Mycobacterium tuberculosis (Mtb), causes extrapulmonary diseases such as periodontitis. Many clinical case reports advocate the involvement of Mtb in periodontitis, which poses a threat with the surge of tuberculosis in HIV and other immunocompromised individuals. Fostering a better understanding of the mechanism, causative agents and control on inflammatory response is imperative in the prevention and treatment of periodontitis.