Thermal Regulation and acclimatization.
THERMOREGULATION AND ACCLIMATIZATION Adapted from: Haymes EM, Wells CL. Environment and Human Performance. Champaign, IL: Human Kinetics; 1986. Reference List available upon request. Thermal Regulation in the Human Organism Ecology is the branch of biology that deals with the relations between living organisms and their environments. Today, it is widely recognized that an organism is at the center of an ecosystem. As such, it is influenced by a multitude of physical and biological environmental factors. It is the essence of living things to be part of an ecosystem and yet to be capable of resisting, to some extent, the impact of the environment (Prosser, 1964). Organisms progress in complexity from a clump of cells that must closely conform to the conditions of their environment to more highly organized accumulations of soft tissues and organs that are capable of independent action. No organism's internal composition is exactly similar to its environment. Regulating organisms are capable of maintaining a relatively constant internal condition (homeostasis) despite widely fluctuating environmental conditions. The internal conditions of conforming organisms, on the other hand, are more closely restricted to the conditions of the surrounding environment. The human is an excellent example of a regulating organism that is able to maintain a relatively constant internal
Cell cycle abnormalities in cancer
Cell Cycle Abnormalities in Cancer. Introduction The cell cycle is a complex topic, parts of which are still being explored today. As cancer grows more prolific in today's society, affecting 1 in 3 of us in the UK in our lifetime, the topic is under scrutiny as the complete understanding of these processes could one day give us a cure for cancer. In this report, I plan to outline the processes that lead to cell proliferation, identify and explain the checkpoints that protect and maintain the integrity of the genome of all human cells, identify key processes that, when mutated, can lead to unchecked cell proliferation, and to highlight the oncogenes involved in most cancers. I will show, that in many of the processes, the loss of key factors could lead to damaged DNA being passed on to daughter cells, leading to mutations that cause tumour genesis. I will also identify, explain the relevance of, and explain the role of key genes that have been discovered to have a major role in cancer. Abstract. The cell cycle consists of five main phases: G0, G1, S, G2 and M phase. G0 phase is described as cells senescence, when, due to signals from checkpoints, such as a cyclin cascade initiated by p53, a prevalent cell cycle blockade, the cell halts all cell cycle progress. This may be due to a signal being shown that DNA has been damaged; this would mean that cell cycle progress would
How does dietary status affect carcinogenesis?
How does dietary status affect carcinogenesis? Cancer is a multi-factoral disease resulting from the perturbation of the normal regulatory processes of a cell. Cancer cells are generated from healthy cells by an accumulation of genetic alterations [1]. These alterations can take the form of mutations, losses, amplifications or re-arrangements in so called "oncogenes" or "tumour suppresser genes" [1]. The many potential mutations giving rise to cancer are initiated by carcinogenic substances and by certain environmental conditions [1]. Carcinogenic substances can be loosely classified as "endogenous", which may be naturally occurring, iatrogenic, environmental contaminants or life style-related or endogenous, for example reactive oxygen species which can be produced in vivo. The human diet consists of an array of microbial, animal and plant derived material and a link between diet and health has been recognised for many centuries [2]. The specific relationship between diet and cancer however is ill defined and uncertain and the evidence is contradictory. Dietary constituents are believed to play both a protective and causative role in the aetiology of the disease and the link between dietary factors and carcinogenesis has been relentlessly investigated by way of animal experiments. Numerous, albeit rather general epidemiological studies have also supported the notion that
Discuss the use of ACE and Angiotensin 2 receptor blockers in diabetic nephropathy. Is there a role for a double blockade?
Discuss the use of ACE and Angiotensin 2 receptor blockers in diabetic nephropathy. Is there a role for a double blockade? What is diabetic nephropathy? Diabetic nephropathy can be defined as a microvascular complication of diabetes marked by albuminuria and a deteriorating course from normal renal function to end-stage renal disease (ESRD). Diabetes is a disease which is caused by the inadequate production of insulin by the body or by the body not being able to properly use the insulin that is produced thereby resulting in hyperglycaemia. The high glucose and other abnormalities of diabetes may lead to kidney damage known as diabetic nephropathy. There are two main types of diabetes, type I, which is insulin dependent, and type II, which is non-insulin dependent. Type 2 diabetes is characterised by insulin resistance, i.e., the failure to respond to normal concentrations of insulin1. Type 1 diabetes is when the body no longer makes insulin. Diabetic nephropathy occurs in 30-40% of all diabetic patients and has become the leading cause of end stage renal disease in the western world2. Persistent albuminuria is the hallmark of diabetic nephropathy, which can be diagnosed in the presence of diabetic retinopathy but in the absence of any clinical or laboratory evidence of other kidney or renal tract diseases 3-6. This definition is valid in-patients with either type 1 or type
For the completion of the Applied Physiology assignment, students are asked to research and discuss the structure and function of three of the bodies systems, these systems are respiratory, cardiovascular and renal.
Introduction For the completion of the Applied Physiology assignment, students are asked to research and discuss the structure and function of three of the bodies systems, these systems are respiratory, cardiovascular and renal. Research will then be done on the composition and function of blood, explaining the normal function of red and white blood cells and platelets. This will also include the destruction process and the normal clotting mechanism. Students are also asked to describe the relationship between the three systems and homeostatic mechanisms in maintaining physiological function. This will also mean looking at the structure of the trachea and nose, the bronchi and the lungs and the heart and the lungs to explain homeostasis. All of these systems may experience disorders within their normal mechanisms i.e. coronary heart disease, cardiovascular disease, chronic respiratory diseases and renal diseases. Blood groups will also be identified and the Rhesus factor described, this will also include the causes of iron deficiency and anaemia. Relate structure and function of the respiratory system, the cardiovascular system and the renal system The respiratory system The respiratory system consists of the nasal cavity, pharynx, larynx, trachea, bronchi, the lungs, alveoli, rib cage and the diaphragm. Working together with breathing muscles the respiratory system
Metabolic Homeostasis.
CONTENTS . INTRODUCTION: PAGE 3 2. OVERVIEW OF METABOLIC HOMEOSTASIS: PAGE 4 * GLYCOLYSIS * GLYCONEOGENESIS 3. METABOLIC FUELS AND THE BODY'S ORGANS: PAGE 6 * METABOLIC FUELS * PRINCIPAL ORGANS INVOLVED IN REGULATION * METABOLISM AND THE G.I. TRACT * METABOLISM AND THE HEART * METABOLISM AND THE KIDNEYS * METABOLISM, BLOOD AND OTHER BODY FLUIDS 4. REGULATION HORMONES: PAGE 13 * HORMONAL RATE OF EFFECT * HORMONAL EFFECTS ON MUSCLE * HORMONAL EFFECTS ON LIVER * REGULATION OF INSULIN SECRETION * CELLULAR INSULIN ACTION * REGULATION OF GLUCAGON SECRETION * REGULATION OF FUEL METABOLISM IN EXERCISE 5. APPETITE, HUNGER AND FOOD INTAKE: PAGE 16 * INFLUENCES DICTATING HUNGER * INFLUENCES DICTATING APPETITE * FOOD INTAKE AND ENERGY BALANCE 6. GLUCOSE AND CARBOHYDRATE HOMEOSTASIS: PAGE 19 * DISPOSITION OF HIGH GLUCOSE INTAKE * GLYCOGENOLYSIS IN "FED" STATE * REGULATION OF GLYCOGENOLYSIS 7. CONCLUSIONS: PAGE 22 8. REFERENCES: PAGE 23 THIS ASSIGNMENT IS MY OWN WORK. IT HAS NOT BEEN, AND WILL NOT BE, PRESENTED FOR ASSESSMENT FOR ANY OTHER MODULE OR PIECE OF WORK WHICH ACCRUES CREDIT FOR THE AWARD FOR WHICH I AM CURRENTLY STUDYING OR FOR ANY OTHER AWARD. SIGNED: _____________________________________ . INTRODUCTION: The normal function of cells, tissues, and organisms requires energy. This energy is obtained by the oxidation
The Relationship Between Protein Misfolding and Human Diseases
THE RELATIONSHIP BETWEEN PROTEIN MISFOLDING AND HUMAN DISEASES DEFINITION AND SCOPE OF PROTEIN MISFOLDING: Folding and unfolding of proteins are crucial factors which determine the biological activity and targeting to various cellular locations (Vendruscolo et al., 2003). Synthesis of various proteins is initiated by ribosomes through the cellular information contained in the DNA. Formation of proteins begins by synthesis of amino acids and the process in which the amino acids transform is described as protein folding (Hardesty and Kramer, 2001). Protein folding depends upon multiple contributing and intrinsic properties of amino acids and forms the basis of many cellular functions. One of the most common mechanisms which are prevalent in many diseases is the aggregation of misfolded proteins escaping the quality control measures of the cell (Vendruscolo et al., 2003). The relative thermodynamic and kinetic properties are responsible for the interconversion of folding and misfolding states. These conversions are highly regulated by proteolytic enzymes, molecular chaperones and environment and the failure of the regulation is main cause for protein misfolding and diseases associated with it (Dobson, 2004). Figure 1: Depiction of Amyloid fibril with a representation of its highly misfolded structure (Adapted from Dobson, 2004) In relation to protein misfolding and the
Rosiglitazone maleate: combating insulin resistance.
Rosiglitazone maleate: combating insulin resistance Introduction Diabetes mellitus is a growing problem across the world. By the year 2010 it is estimated that over 221 million people will be afflicted with the disease1. Type 1 diabetes is the result of absolute insulin deficiency and is treated through the addition of exogenous insulin. Type 2 diabetes, non-insulin dependent diabetes (NIDDM), is characterized by a relative insulin deficiency and increased insulin resistance; it accounts for 90% of all cases of diabetes. Insulin resistance is the inability of cells to use insulin effectively which results in hyperglycemia even in the presence of adequate amounts of insulin. Insulin resistance contributes not only to diabetes, but to a plethora of other metabolic abnormalities including dyslipidemia, hypertension, and vasculopathy which are collectively termed the insulin resistance or cardiovascular dysmetabolic syndrome.2 Rosiglitazone, also known as Avandia, is effective only in the presence of insulin; its antihyperglycemic effect is the result of lowered insulin resistance in cells. Its development as a drug is described in this paper. Bioassay used to discover lead compound When GlaxoSmithKline started targeting insulin resistance in 1984 virtually nothing was known of the molecular mechanisms of insulin action, let alone what defects contribute to insulin
Cardiovascular system and health promotion
This assignment is going to be based on the structure and function of the cardiovascular system and how homeostatic mechanisms work with the system to regulate it. The many functions of the heart will be recognised, but the main focus will be on the regulation of heart beat. Various Health Promotion initiatives will then be looked at in context to how they help people maintain a healthy heart and how successful these initiatives are in doing this. At some point, a definition of homeostasis and a definition of health promotion will also be given. Throughout the assignment, my own personal thoughts and accounts will be given to demonstrate the workings of the cardiovascular system and how effective health promotion is in reality. The cardiovascular system consists of two components. Firstly there is the heart and secondly the blood vessels. The heart is a muscular organ which is about the size of a fist and is cone shaped, according to Mader (2006). It is situated in-between the lungs directly behind the sternum. There are three layers of tissue that make up the heart according to Waugh and Grant (2006); the myocardium, which makes up the largest proportion of the heart and consists largely of cardiac muscle; the endocardium which consists of connective tissue and the pericardium, which consists of two sacs and secretes a small amount of lubricating liquid to ensure
Serum Leptin Levels and Adiposity in Chinese.
Serum Leptin Levels and Adiposity in Chinese* *This work was financially supported by the Rockefeller Foundation of the United States and Natural Science Fund of Shanghai Secondary Medical University 98-11-25 SUMMARY Objective: To establish normal serum leptin levels in Chinese and to investigate the relationships between serum leptin levels and body fat, gender, age and androgen. Methods: Serum leptin levels were measured in 77 lean (BMI<25) and 28 overweight or obese(BMI?25) subjects by a RIA method. Results: The serum leptin levels in lean Chinese were 2.15?1.46ng/ml in male and 7.85?3.60ng/ml in female, which are similar to those of Caucasians, while in overweight or obese ones, the levels were 4.87?3.47ng/ml and 16.59?6.92ng/ml respectively, lower than those in Caucasians. A 2-3 times higher leptin concentrations were found in women than in men in both conditions. Even when the number of lean males were expanded to 79 subjects aged from 17-80, no significant leptin-age relationship was found. Despite 25% of obese subjects manifested a relative deficiency of leptin, as a whole, leptin levels in both men and women were significantly correlated with BMI (r=0.69, P<0.001 in male and r=0.63, P<0.001 in female). Conclusion: Serum leptin levels in Chinese lean people are similar to those in Caucasians and in both lean and obese groups, the leptin levels are correlated with