Deepak Baby

Bio: Deepak Baby is an academic researcher. The author has contributed to research in topics: Kidney disease & Cancer. The author has an hindex of 2, co-authored 2 publications receiving 143 citations.

Inflammation and cancer.

Abstract: Inflammation is often associated with the development and progression of cancer. The cells responsible for cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance; therefore, the targeting of inflammation represents an attractive strategy both for cancer prevention and for cancer therapy. Tumor-extrinsic inflammation is caused by many factors, including bacterial and viral infections, autoimmune diseases, obesity, tobacco smoking, asbestos exposure, and excessive alcohol consumption, all of which increase cancer risk and stimulate malignant progression. In contrast, cancer-intrinsic or cancer-elicited inflammation can be triggered by cancer-initiating mutations and can contribute to malignant progression through the recruitment and activation of inflammatory cells. Both extrinsic and intrinsic inflammations can result in immunosuppression, thereby providing a preferred background for tumor development. The current review provides a link between inflammation and cancer development.

Calciphylaxis and its diagnosis: A review.

Abstract: Calciphylaxis also known as Calcific uremic arteriolopathy (CUA), is a rare fatal complication usually associated with end-stage renal disease (ESRD). It is characterized by skin ulceration and necrosis leading to significant pain. The disease calciphylaxis is pathological state resulting in accumulation of calcium content in medial wall of small blood vessels along with the fibrotic changes in intima. The aetiopathogenesis of this disease, small vessel vasculopathy, remains complicated, and unclear. It is believed that development of calciphylaxis depends on medial calcification, intimal fibrosis of arterioles and thrombotic occlusion. The disease is rare, life-threatening medical condition that occurs mostly in population with kidney disease or in patients on dialysis. Skin biopsy and radiographic features are helpful in the diagnosis of calciphylaxis, but negative results do not necessarily exclude the diagnosis. This article highlights steps undertaking in the diagnosis of calciphylaxis.

A Cross-Sectional Study of Serum Glutathione Peroxidase: An Antioxidative Marker in Chronic Periodontitis and Chronic Kidney Disease

Abstract: Background and aim: Oxidative stress as an individual risk for periodontitis and chronic kidney disease (CKD) has been elaborated through various mechanical pathways, yet its role in association with both diseases remains unexplored. Thus, the current study aims in evaluating serum glutathione peroxidase, an oxidative stress marker in CKD patients with periodontitis, and compare it with the healthy controls. Methodology: One hundred and twenty subjects were divided into four groups as control (C=30 subjects), periodontitis and non-CKD patients (CP=30 patients), non-periodontitis and CKD patients (CKD=30 patients), and periodontitis and CKD patients (CKD+CP=30 patients). Demographic variables, periodontal parameters, such as plaque index (PI), gingival index (GI), probing pocket depth (PPD), percentage proportion of sites with probing pocket depth more than 5 mm, clinical attachment loss (CAL), percentage proportion of sites with clinical attachment loss more than 3 mm and serum stress marker, and glutathione peroxidase were compared between the groups and the results were statistically analyzed. Results: The demographic variables did not differ significantly between the groups, except for age. The means PI, GI, PPD, percentage proportion of sites with probing pocket depth more than 5 mm, CAL, percentage proportion of sites with clinical attachment loss were higher in CKD+CP. The glutathione peroxidase was significantly higher in CP group (p=0.001) and significantly correlated with periodontal parameters. Conclusion: The oxidative stress marker glutathione peroxidase was higher in CP, followed by the CKD groups. This could pave a strong link of oxidative stress as a risk factor for chronic periodontitis, as well as chronic kidney disease.

Epidemiology of Bladder Cancer

Abstract: Based on the latest GLOBOCAN data, bladder cancer accounts for 3% of global cancer diagnoses and is especially prevalent in the developed world. In the United States, bladder cancer is the sixth most incident neoplasm. A total of 90% of bladder cancer diagnoses are made in those 55 years of age and older, and the disease is four times more common in men than women. While the average 5-year survival in the US is 77%, the 5-year survival for those with metastatic disease is a measly 5%. The strongest risk factor for bladder cancer is tobacco smoking, which accounts for 50-65% of all cases. Occupational or environmental toxins likewise greatly contribute to disease burden (accounting for an estimated 20% of all cases), though the precise proportion can be obscured by the fact bladder cancer develops decades after exposure, even if the exposure only lasted several years. Schistosomiasis infection is the common cause of bladder cancer in regions of Africa and the Middle East and is considered the second most onerous tropical pathogen after malaria. With 81% of cases attributable to known risk factors (and only 7% to heritable mutations), bladder cancer is a prime candidate for prevention strategies. Smoking cessation, workplace safety practices, weight loss, exercise and schistosomiasis prevention (via water disinfection and mass drug administration) have all been shown to significantly decrease the risk of bladder cancer, which poses a growing burden around the world.

The Gut Microbiota and Inflammation: An Overview.

Abstract: The gut microbiota encompasses a diverse community of bacteria that carry out various functions influencing the overall health of the host. These comprise nutrient metabolism, immune system regulation and natural defence against infection. The presence of certain bacteria is associated with inflammatory molecules that may bring about inflammation in various body tissues. Inflammation underlies many chronic multisystem conditions including obesity, atherosclerosis, type 2 diabetes mellitus and inflammatory bowel disease. Inflammation may be triggered by structural components of the bacteria which can result in a cascade of inflammatory pathways involving interleukins and other cytokines. Similarly, by-products of metabolic processes in bacteria, including some short-chain fatty acids, can play a role in inhibiting inflammatory processes. In this review, we aimed to provide an overview of the relationship between the gut microbiota and inflammatory molecules and to highlight relevant knowledge gaps in this field. Based on the current literature, it appears that as the gut microbiota composition differs between individuals and is contingent on a variety of factors like diet and genetics, some individuals may possess bacteria associated with pro-inflammatory effects whilst others may harbour those with anti-inflammatory effects. Recent technological advancements have allowed for better methods of characterising the gut microbiota. Further research to continually improve our understanding of the inflammatory pathways that interact with bacteria may elucidate reasons behind varying presentations of the same disease and varied responses to the same treatment in different individuals. Furthermore, it can inform clinical practice as anti-inflammatory microbes can be employed in probiotic therapies or used to identify suitable prebiotic therapies.

Vascular Calcification-New Insights Into Its Mechanism.

Abstract: Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

Epidemiology of lung cancer

Abstract: Lung cancer is the leading cause of global cancer incidence and mortality, accounting for an estimated 2 million diagnoses and 1.8 million deaths. Neoplasms of the lungs are the second most common cancer diagnosis in men and women (after prostate and breast cancer, respectively). With increasing access to tobacco and industrialization in developing nations, lung cancer incidence is rising globally. The average age of diagnosis is 70 years old. Men are twice as likely to be diagnosed with lung cancer, which largely reflects differences in tobacco consumption, although women may be more susceptible due to higher proportions of epidermal growth factor receptor mutations and the effects of oestrogen. African American men in the US are at the highest risk of lung cancer. Family history increases risk by 1.7-fold, with a greater risk among first-degree relatives. Tobacco smoking is the greatest preventable cause of death worldwide, accounting for up to 90% of lung cancer cases, and continued consumption is projected to increase global cancer incidence, particularly in developing nations such as China, Russia, and India. Second-hand smoke among children and spouses has likewise been implicated. Radon from natural underground uranium decay is the second leading cause of lung cancer in the developed world. Occupational hazards such as asbestos and environmental exposures such as air pollution, arsenic, and HIV and Tb infection have all been implicated in lung carcinogenesis, while cannabis smoking, electronic cigarettes, heated tobacco products, and COVID-19 have been hypothesized to increase risk.

Targeting of CD163+ macrophages in inflammatory and malignant diseases

Abstract: The macrophage is a key cell in the pro- and anti-inflammatory response including that of the inflammatory microenvironment of malignant tumors. Much current drug development in chronic inflammatory diseases and cancer therefore focuses on the macrophage as a target for immunotherapy. However, this strategy is complicated by the pleiotropic phenotype of the macrophage that is highly responsive to its microenvironment. The plasticity leads to numerous types of macrophages with rather different and, to some extent, opposing functionalities, as evident by the existence of macrophages with either stimulating or down-regulating effect on inflammation and tumor growth. The phenotypes are characterized by different surface markers and the present review describes recent progress in drug-targeting of the surface marker CD163 expressed in a subpopulation of macrophages. CD163 is an abundant endocytic receptor for multiple ligands, quantitatively important being the haptoglobin-hemoglobin complex. The microenvironment of inflammation and tumorigenesis is particular rich in CD163+ macrophages. The use of antibodies for directing anti-inflammatory (e.g., glucocorticoids) or tumoricidal (e.g., doxorubicin) drugs to CD163+ macrophages in animal models of inflammation and cancer has demonstrated a high efficacy of the conjugate drugs. This macrophage-targeting approach has a low toxicity profile that may highly improve the therapeutic window of many current drugs and drug candidates.