Prolonged stress has long been shown to have major effects on the development of both type of diabetes mellitus, Type 1 and Type 2. Type 1 diabetes is an autoimmune disease that is characterized by the immune system attacking self-antigens. There is a failure or breakdown in immunological tolerance to allow this to happen. Prolonged physical or emotional stress can activate the hypothalamus-pituitary-adrenal (HPA) axis to induce production of the stress hormone glucocorticoid, causing abrupt thymus involution and result in escape of autoreactive T- cells. Though regulatory T-cells (Treg) are present in the circulation, they are unable to suppress the autoreative T-cells from initiating the destruction of -cells and the subsequent development of Type 1 diabetes. Stress also causes metabolic disturbances, including altered hepatic glucose metabolism, increased peripheral insulin resistance and hyperglycemia. Glucocorticoid is the potential contributor to the chronic hyperglycemia that results in insulin resistance and -cell dysfunction via the generation of oxidative stress which ultimately leads to the development of Type 2 diabetes."

G Protein Coupled Receptors (GPCRs) are a large family of seven transmembrane (TM) helical structural motif containing proteins that regulate cellular communication. Based on sequence similarity within the seven TM segment in human, the major five GPCR families are rhodopsin, secretin, glutamate, adhesion and frizzled/taste. GPCRs are principle signal transducer that activate senses of sight, smell and test, and responsible for many signaling disorders and diseases. Molecular mechanisms of GPCR activation are always implicated as a therapeutic purpose to discover new drug targets. Several molecular mechanisms and models of GPCR activation have been proposed. Dimerization, protonation, conformations due to intramolecular interaction and specific conformational changes are thought to be responsible for receptor activation. In this review, these mechanisms and proposed model systems are discussed in detail.

Psychological stress has extreme adverse consequences on health. However, the molecular mechanisms that mediate and accelerate the process of aging due to stress hormone are not well defined. This review has focused on diverse molecular paths that come out in response to chronic psychological stress via releasing of excessive glucocorticoids (GCs), involved in the aging process. GCs suppress transcription of nuclear cell adhesion molecules which impair synaptic plasticity, memory formation, and cognitive ability. Again, GCs promote muscle atrophy by means of motivating ubiquitin proteasome system and can repress muscle protein synthesis by inhibition of PI3-kinase/Akt pathway. GCs also inhibit interleukin-2 synthesis through suppressing T cell receptor signal that leads to loss of T cell activation, proliferation, and B-cell activation. Moreover, GCs increase the expression of collagenase-3, RANK ligand, and colony stimulating factor-1 that induce bone resorption. In general, stress-induced GCs can play causal role for aging and age-related disorders.

Chronic Psychological stress has several adverse effects both on HIV- people and on HIV+ patient. When the HIV- people are concerned, stress makes them more susceptible to HIV infection. T-cells have CXCR4 receptor and Macrophage have CCR5 receptor which can bind with both glucocorticoid and catecholamine hormone. HIV has GP120 protein which has to bind with both CD4 and CXCR4/CCR5 receptor for its entry into the host cells. Mental stress increases glucocorticoid and catecholamine concentration in blood. When these stress hormones, glucocorticoid and catecholamine, bind with the CXCR4/CCR5 receptors, cAMP signaling pathway gets activated. This signal transduction pathway leads to the synthesis of more CXCR4 and CCR5 receptors by those cells, which in turn become more susceptible to HIV infection. Stress inhibits Th2 when the cell produces INF- as a response to viral attacks. So that other cells remain vulnerable to viral infection. When T-cell count is decreased in the blood, the body cannot protect itself from other opportunistic infectious pathogens. As a result progression of AIDS is increased."

Cancer is a class of diseases in which a group of cells display the traits of uncontrolled growth, invasion, and sometimes metastasis. These three malignant properties of cancers differentiate them from benign tumors, which are self-limited, do not invade or metastasize. Most cancers form a tumor but not all cancer e.g. leukemia.Cancer may affect people at all ages, even fetuses, but risk for the more common varieties tends to increase with age. Nearly all cancers are caused by abnormalities in the genetic material of the transformed cells. These abnormalities may be due to the effects of carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents. Other cancer-promoting genetic abnormalities may be randomly acquired through errors in DNA replication or are inherited and thus present in all cells from birth. Complex interactions between carcinogens and the host genome can explain mechanism of cancers develop after exposure to a known carcinogen.This book addresses the biomolecular mechanisms of new aspects of genetics in the initiation of Cancer and progression of Tumor.

Atherosclerosis is a disease that causes medium-size and larger blood vessels in the body to harden and narrow which is not a clinical symptoms but it is the ultimate stage of any types of coronary heart disease like stroke, heart attack, myocardial infarction, paralysis and so on. In recent decades, there has been increasing interest in exploring the relationship between psychological stress and various health conditions. Extensive studies support that behavioral and psychological factors contribute significantly to the development and progression of atherosclerosis. Psychological factors, specifically depression, anxiety, personality factors, social isolation, and chronic and sub-acute life stress, are known to be related to the risk of heart disease. This spurred on the relentless effort to explore how behaviour and biological systems could interact in the endeavour to uncover more mysteries of the human body. This review addresses the biomolecular mechanism of understanding the role of chronic psychological stressors on the immune system and development of atherosclerosis as well as established the relationship between the chronic psychological stress and the atherosclerosis.

Programmed cell death, which is termed as apoptosis, is essential for normal development and maintenance of tissue homeostasis in multicellular organisms. Aberrant regulation of this pathway is linked to multiple human diseases, including cancer, autoimmunity, neurodegenerative disorders and diabetes. Apoptosis is pursued by two pathways; extrinsic and intrinsic pathway. The intrinsic pathway of apoptosis mainly relies on mitochondria where Bcl-2 family proteins serve as the master regulators. Mitochondria mainly execute their function through mitochondrial outer membrane permeabilization (MOMP). MOMP leads to the release of several apoptogenic factors from mitochondrial intermembrane space, such as cytochrome c and Smac/Diablo, into the cytosol that activate downstream caspase and promote cell death. Bcl-2 family proteins play key role by regulating MOMP. The complex interaction among pro-and anti-apoptotic Bcl-2 family members determine the possibility of MOMP and thereby determine the cellular commitment to apoptosis. This review focuses on the mitochondrial pathway of apoptosis, mechanism of MOMP and its regulation by Bcl-2 family proteins.