In medicine, a Holter monitor is a type of ambulatory electrocardiography device, a portable device for cardiac monitoring for at least 24 to 48 hours. The Holter's most common use is for monitoring ECG heart activity, its extended recording period is sometimes useful for observing occasional cardiac arrhythmias which would be difficult to identify in a shorter period. For patients having more transient symptoms, a cardiac event monitor which can be worn for a month or more can be used; the Holter monitor was developed at the Holter Research Laboratory in Helena Montana by experimental physicists Norman J. Holter and Bill Glasscock, who started work on radio telemetry in 1949. Inspired by a suggestion from cardiologist Paul Dudley White in the early 1950s, they redirected their efforts toward development of a wearable cardiac monitoring device; the Holter monitor was released for commercial production in 1962. When used to study the heart, much like standard electrocardiography, the Holter monitor records electrical signals from the heart via a series of electrodes attached to the chest.
Electrodes are placed over bones to minimize artifacts from muscular activity. The number and position of electrodes varies by model, but most Holter monitors employ between three and eight; these electrodes are connected to a small piece of equipment, attached to the patient's belt or hung around the neck, keeping a log of the heart's electrical activity throughout the recording period. A 12 lead Holter system is available when precise ECG signal information is required to analyse the exact nature and origin of the rhythm signal. Older devices used reel-to-reel tapes or a standard C90 or C120 audio cassette and ran at a 1.7 mm/s or 2 mm/s speed to record the data. Once a recording was made, it could be played back and analyzed at 60x speed so 24 hours of recording could be analyzed in 24 minutes. More modern units record an EDF-file onto digital flash memory devices; the data is uploaded into a computer which automatically analyzes the input, counting ECG complexes, calculating summary statistics such as average heart rate and maximum heart rate, finding candidate areas in the recording worthy of further study by the technician.
Each Holter system consists of two basic parts – the hardware for recording the signal, software for review and analysis of the record. Advanced Holter recorders are able to display the signal, useful for checking the signal quality. There is a “patient button” located on the front site allowing the patient to press it in specific cases such as sickness, going to bed, taking pills, etc.. The size of the recorder differs depending on the manufacturer of the device; the average dimensions of today’s Holter monitors are about 110x70x30 mm but some are only 61x46x20 mm and weigh 99 g. Most of the devices operate with two AA batteries. In case the batteries are depleted, some Holters allow their replacement during monitoring. Most of the Holters monitor the ECG via three channels. Today’s trend is to minimize the number of leads to ensure the patient’s comfort during recording. Although two/three channel recording has been used for a long time in the Holter monitoring history, as mentioned above, 12 channel Holters have appeared.
These systems use the classic Mason-Likar lead system, i.e. producing a signal in the same format as during the common rest ECG and/or stress test measurement. These Holters can provide information similar to that of a ECG stress test examination, they are suitable when analyzing patients after myocardial infarction. Recordings from these 12-lead monitors are of a lower resolution than those from a standard 12-lead ECG and in some cases have been shown to provide misleading ST segment representation though some devices allow setting the sampling frequency up to 1000 Hz for special-purpose exams such as detection of "late potential". Another innovation is the inclusion of a triaxial movement sensor, which records the patient's physical activity, on examination and software processing, extracts three movement statuses: sleeping, standing up, or walking; some modern devices have the ability to record a vocal patient diary entry that can be listened to by the doctor. These data help the cardiologist to better identify events in relation to the patient's activity and diary.
When the recording of ECG signal is finished, it is up to the physician to perform the signal analysis. Since it would be time demanding to browse through such a long signal, there is an integrated automatic analysis process in the software of each Holter device which automatically determines different sorts of heart beats, etc; however the success of the automatic analysis is closely associated with the signal quality. The quality itself depends on the attachment of the electrodes to the patient body. If these are not properly attached, electromagnetic disturbance can influence the ECG signal resulting in a noisy record. If the patient moves the distortion will be bigger; such record is very difficult to process. Besides the attachment and quality of electrodes, there are other factors affecting the signal quality, such as muscle tremors, sampling rate and resolution of the digitized signal; the auto
Technetium is a chemical element with symbol Tc and atomic number 43. It is the lightest element. Nearly all technetium is produced synthetically, only about 18,000 tons can be found at any given time in the Earth's crust. Occurring technetium is a spontaneous fission product in uranium ore and thorium ore, the most common source, or the product of neutron capture in molybdenum ores; this silvery gray, crystalline transition metal lies between rhenium and manganese in group 7 of the periodic table, its chemical properties are intermediate between those of these two adjacent elements. The most common occurring isotope is 99Tc. Many of technetium's properties were predicted by Dmitri Mendeleev before the element was discovered. Mendeleev noted a gap in his periodic table and gave the undiscovered element the provisional name ekamanganese. In 1937, technetium became the first predominantly artificial element to be produced, hence its name. One short-lived gamma ray-emitting nuclear isomer of technetium—technetium-99m—is used in nuclear medicine for a wide variety of diagnostic tests, such as bone cancer diagnoses.
The ground state of this nuclide, technetium-99, is used as a gamma-ray-free source of beta particles. Long-lived technetium isotopes produced commercially are by-products of the fission of uranium-235 in nuclear reactors and are extracted from nuclear fuel rods; because no isotope of technetium has a half-life longer than 4.21 million years, the 1952 detection of technetium in red giants helped to prove that stars can produce heavier elements. From the 1860s through 1871, early forms of the periodic table proposed by Dmitri Mendeleev contained a gap between molybdenum and ruthenium. In 1871, Mendeleev predicted this missing element would occupy the empty place below manganese and have similar chemical properties. Mendeleev gave it the provisional name ekamanganese because the predicted element was one place down from the known element manganese. Many early researchers, both before and after the periodic table was published, were eager to be the first to discover and name the missing element.
Its location in the table suggested that it should be easier to find than other undiscovered elements. German chemists Walter Noddack, Otto Berg, Ida Tacke reported the discovery of element 75 and element 43 in 1925, named element 43 masurium; the group bombarded columbite with a beam of electrons and deduced element 43 was present by examining X-ray emission spectrograms. The wavelength of the X-rays produced is related to the atomic number by a formula derived by Henry Moseley in 1913; the team claimed to detect a faint X-ray signal at a wavelength produced by element 43. Experimenters could not replicate the discovery, it was dismissed as an error for many years. Still, in 1933, a series of articles on the discovery of elements quoted the name masurium for element 43. Whether the 1925 team did discover element 43 is still debated; the discovery of element 43 was confirmed in a 1937 experiment at the University of Palermo in Sicily by Carlo Perrier and Emilio Segrè. In mid-1936, Segrè visited the United States, first Columbia University in New York and the Lawrence Berkeley National Laboratory in California.
He persuaded cyclotron inventor Ernest Lawrence to let him take back some discarded cyclotron parts that had become radioactive. Lawrence mailed him a molybdenum foil, part of the deflector in the cyclotron. Segrè enlisted his colleague Perrier to attempt to prove, through comparative chemistry, that the molybdenum activity was indeed from an element with the atomic number 43. In 1937 they succeeded in isolating the isotopes technetium-95m and technetium-97. University of Palermo officials wanted them to name their discovery "panormium", after the Latin name for Palermo, Panormus. In 1947 element 43 was named after the Greek word τεχνητός, meaning "artificial", since it was the first element to be artificially produced. Segrè met Glenn T. Seaborg, they isolated the metastable isotope technetium-99m, now used in some ten million medical diagnostic procedures annually. In 1952, astronomer Paul W. Merrill in California detected the spectral signature of technetium in light from S-type red giants.
The stars were near the end of their lives, yet were rich in this short-lived element, indicating that it was being produced in the stars by nuclear reactions. This evidence bolstered the hypothesis that heavier elements are the product of nucleosynthesis in stars. More such observations provided evidence that elements are formed by neutron capture in the s-process. Since that discovery, there have been many searches in terrestrial materials for natural sources of technetium. In 1962, technetium-99 was isolated and identified in pitchblende from the Belgian Congo in small quantities; the Oklo natural nuclear fission reactor contains evidence that significant amounts of technetium-99 were produced and have since decayed into ruthenium-99. Technetium is a silvery-gray radioactive metal with an appearance similar to platinum obtained as a gray powder; the crystal structure of the pure metal is hexagonal close-packed. Atomic technetium has characteristic emission lines at these wavelengths of light: 363.3 nm, 403.1 nm
Low-density lipoprotein is one of the five major groups of lipoprotein which transport all fat molecules around the body in the extracellular water. These groups, from least dense, compared to surrounding water to most dense, are chylomicrons low-density lipoprotein, intermediate-density lipoprotein, low-density lipoprotein and high-density lipoprotein. LDL delivers fat molecules to the cells and can drive the progression of atherosclerosis if they become oxidized within the walls of arteries, it is important to note that LDL is not "bad cholesterol". LDL is not cholesterol at all, not bad, it is an essential transport system for lipids the human body needs to survive, including cholesterol. There is both "large" and "small" particle LDL, while only small is associated with cholesterol-related issues, neither is "bad". "small" LDL is necessary to conduct nutrients to vessels that "large" LDL can't reach. Lipoproteins transfer lipids around the body in the extracellular fluid, making fats available to body cells for receptor-mediated endocytosis.
Lipoproteins are complex particles composed of multiple proteins 80–100 proteins/particle. A single LDL particle is about 220–275 angstroms in diameter transporting 3,000 to 6,000 fat molecules/particle, varying in size according to the number and mix of fat molecules contained within; the lipids carried include all fat molecules with cholesterol and triglycerides dominant. For years, it was believed that LDL particles posed a risk for cardiovascular disease when they invaded the endothelium and became oxidized, since the oxidized forms would be more retained by the proteoglycans, but there is growing evidence that this belief was supported by bad methodology, that there is no actual correlation between LDL and heart disease. A complex set of biochemical reactions regulates the oxidation of LDL particles, chiefly stimulated by presence of necrotic cell debris and free radicals in the endothelium. Increased concentrations of LDL particles is associated with the development of atherosclerosis over time.
Each native LDL particle enables emulsification, i.e. surrounding/packaging all fatty acids being carried, enabling these fats to move around the body within the water outside cells. Each particle contains a single apolipoprotein B-100 molecule, along with 80 to 100 additional ancillary proteins; each LDL has a hydrophobic core consisting of polyunsaturated fatty acid known as linoleate and hundreds to thousands esterified and unesterified cholesterol molecules. This core carries varying numbers of triglycerides and other fats and is surrounded by a shell of phospholipids and unesterified cholesterol, as well as the single copy of Apo B-100. LDL particles are 22 nm to 27.5 nm in diameter and have a mass of about 3 million daltons. Since LDL particles contain a variable and changing number of fatty acid molecules, there is a distribution of LDL particle mass and size. Determining the structure of LDL has been a tough task because of its heterogeneous structure; the structure of LDL at human body temperature in native condition, with a resolution of about 16 Angstroms using cryogenic electron microscopy, has been described.
LDL particles are formed as VLDL lose triglyceride through the action of lipoprotein lipase and they become smaller and denser, containing a higher proportion of cholesterol esters. When a cell requires additional cholesterol, it synthesizes the necessary LDL receptors as well as PCSK9, a proprotein convertase that marks the LDL receptor for degradation. LDL receptors are inserted into the plasma membrane and diffuse until they associate with clathrin-coated pits; when LDL receptors bind LDL particles in the bloodstream, the clathrin-coated pits are endocytosed into the cell. Vesicles containing LDL receptors bound to LDL are delivered to the endosome. In the presence of low pH, such as that found in the endosome, LDL receptors undergo a conformation change, releasing LDL. LDL is shipped to the lysosome, where cholesterol esters in the LDL are hydrolysed. LDL receptors are returned to the plasma membrane, where they repeat this cycle. If LDL receptors bind to PCSK9, transport of LDL receptors is redirected to the lysosome, where they are degraded.
LDL interfere with the quorum sensing system that upregulates genes required for invasive Staphylococcus aureus infection. The mechanism of antagonism entails binding Apolipoprotein B to a S. aureus autoinducer pheromone, preventing signaling through its receptor. Mice deficient in apolipoprotein B are more susceptible to invasive bacterial infection. LDL can be grouped based on its size: large low density LDL particles are described as pattern A, small high density LDL particles are pattern B. Pattern B has been associated by some with a higher risk for coronary heart disease; this is thought to be because the smaller particles are more able to penetrate the endothelium of arterial walls. Pattern I, for intermediate, indicates that most LDL particles are close in size to the normal gaps in the endothelium. According to one study, sizes 19.0–20.5 nm were designated as pattern B and LDL sizes 20.6–22 nm were designated as pattern A. Other studies have shown no such correlation at all; some evidence suggests the correlation between Pat
Cholesterol is an organic molecule. It is a type of lipid. Cholesterol is biosynthesized by all animal cells and is an essential structural component of animal cell membranes. Cholesterol serves as a precursor for the biosynthesis of steroid hormones, bile acid and vitamin D. Cholesterol is the principal sterol synthesized by all animals. In vertebrates, hepatic cells produce the greatest amounts, it is absent among prokaryotes, although there are some exceptions, such as Mycoplasma, which require cholesterol for growth. François Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769. However, it was not until 1815 that chemist Michel Eugène Chevreul named the compound "cholesterine". There is only one kind of cholesterol. There is no "good cholesterol" or "bad cholesterol"; the system that transports cholesterol where it is needed in the human body uses LDL and HDL to do so. Those are proteins, not lipids like cholesterol, neither of them are "bad", both are necessary to human health.
Cholesterol is essential for all animal life, with each cell capable of synthesizing it by way of a complex 37-step process. This begins with the mevalonate or HMG-CoA reductase pathway, the target of statin drugs, which encompasses the first 18 steps; this is followed by 19 additional steps to convert the resulting lanosterol into cholesterol. A human male weighing 68 kg synthesizes about 1 gram of cholesterol per day, his body contains about 35 g contained within the cell membranes. Typical daily cholesterol dietary intake for a man in the United States is 307 mg. Most ingested cholesterol is esterified; the body compensates for absorption of ingested cholesterol by reducing its own cholesterol synthesis. For these reasons, cholesterol in food, seven to ten hours after ingestion, has little, if any effect on concentrations of cholesterol in the blood. However, during the first seven hours after ingestion of cholesterol, as absorbed fats are being distributed around the body within extracellular water by the various lipoproteins, the concentrations increase.
Cholesterol is recycled in the body. The liver excretes it in a non-esterified form into the digestive tract. About 50% of the excreted cholesterol is reabsorbed by the small intestine back into the bloodstream. Plants make cholesterol in small amounts. Plants manufacture phytosterols, which can compete with cholesterol for reabsorption in the intestinal tract, thus reducing cholesterol reabsorption; when intestinal lining cells absorb phytosterols, in place of cholesterol, they excrete the phytosterol molecules back into the GI tract, an important protective mechanism. The intake of occurring phytosterols, which encompass plant sterols and stanols, ranges between ~200–300 mg/day depending on eating habits. Specially designed vegetarian experimental diets have been produced yielding upwards of 700 mg/day. Cholesterol, given that it composes about 30% of all animal cell membranes, is required to build and maintain membranes and modulates membrane fluidity over the range of physiological temperatures.
The hydroxyl group of each cholesterol molecule interacts with the water molecules surrounding the membrane as do the polar heads of the membrane phospholipids and sphingolipids, while the bulky steroid and the hydrocarbon chain are embedded in the membrane, alongside the nonpolar fatty-acid chain of the other lipids. Through the interaction with the phospholipid fatty-acid chains, cholesterol increases membrane packing, which both alters membrane fluidity and maintains membrane integrity so that animal cells do not need to build cell walls; the membrane remains stable and durable without being rigid, allowing animal cells to change shape and animals to move. The structure of the tetracyclic ring of cholesterol contributes to the fluidity of the cell membrane, as the molecule is in a trans conformation making all but the side chain of cholesterol rigid and planar. In this structural role, cholesterol reduces the permeability of the plasma membrane to neutral solutes, hydrogen ions, sodium ions.
Within the cell membrane, cholesterol functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of invaginated caveolae and clathrin-coated pits, including caveola-dependent and clathrin-dependent endocytosis; the role of cholesterol in endocytosis of these types can be investigated by using methyl beta cyclodextrin to remove cholesterol from the plasma membrane. Recent studies show that cholesterol is implicated in cell signaling processes, assisting in the formation of lipid rafts in the plasma membrane, which brings receptor proteins in close proximity with high concentrations of second messenger molecules. In multiple layers and phospholipids, both electrical insulators, can facilitate speed of transmission of electrical impulses along nerve tissue. For many neuron fibers, a myelin sheath, rich in cholesterol since it is derived from compacted layers of Schwann cell membrane, provides insulation for more efficient conduction of impulses.
Demyelination is believed to be part of the basis for multiple sclerosis. Within cells, cholesterol is a precursor molecule for several biochemical pathways. For example, it is the precursor molecule for the synthesis of vitamin D and all steroid hormones, including the adrenal gland ho
Insulin is a peptide hormone produced by beta cells of the pancreatic islets. It regulates the metabolism of carbohydrates and protein by promoting the absorption of carbohydrates glucose from the blood into liver and skeletal muscle cells. In these tissues the absorbed glucose is converted into either glycogen via glycogenesis or fats via lipogenesis, or, in the case of the liver, into both. Glucose production and secretion by the liver is inhibited by high concentrations of insulin in the blood. Circulating insulin affects the synthesis of proteins in a wide variety of tissues, it is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low insulin levels in the blood have the opposite effect by promoting widespread catabolism of reserve body fat. Beta cells are sensitive to glucose concentrations known as blood sugar levels; when the glucose level is high, the beta cells secrete insulin into the blood. Their neighboring alpha cells, by taking their cues from the beta cells, secrete glucagon into the blood in the opposite manner: increased secretion when blood glucose is low, decreased secretion when glucose concentrations are high.
Glucagon, through stimulating the liver to release glucose by glycogenolysis and gluconeogenesis, has the opposite effect of insulin. The secretion of insulin and glucagon into the blood in response to the blood glucose concentration is the primary mechanism of glucose homeostasis. If beta cells are destroyed by an autoimmune reaction, insulin can no longer be synthesized or be secreted into the blood; this results in type 1 diabetes mellitus, characterized by abnormally high blood glucose concentrations, generalized body wasting. In type 2 diabetes mellitus the destruction of beta cells is less pronounced than in type 1 diabetes, is not due to an autoimmune process. Instead there is an accumulation of amyloid in the pancreatic islets, which disrupts their anatomy and physiology; the pathogenesis of type 2 diabetes is not well understood but patients exhibit a reduced population of islet beta-cells, reduced secretory function of islet beta-cells that survive, peripheral tissue insulin resistance.
Type 2 diabetes is characterized by high rates of glucagon secretion into the blood which are unaffected by, unresponsive to the concentration of glucose in the blood. Insulin is still secreted into the blood in response to the blood glucose; as a result, the insulin levels when the blood sugar level is normal, are much higher than they are in healthy persons. The human insulin protein is composed of 51 amino acids, has a molecular mass of 5808 Da, it is a dimer of a B-chain, which are linked together by disulfide bonds. Insulin's structure varies between species of animals. Insulin from animal sources differs somewhat in effectiveness from human insulin because of these variations. Porcine insulin is close to the human version, was used to treat type 1 diabetics before human insulin could be produced in large quantities by recombinant DNA technologies; the crystal structure of insulin in the solid state was determined by Dorothy Hodgkin. It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system.
Insulin may have originated more than a billion years ago. The molecular origins of insulin go at least as far back. Apart from animals, insulin-like proteins are known to exist in the Fungi and Protista kingdoms. Insulin is produced by beta cells of the pancreatic islets in most vertebrates and by the Brockmann body in some teleost fish. Cone snails Conus geographus and Conus tulipa, venomous sea snails that hunt small fish, use modified forms of insulin in their venom cocktails; the insulin toxin, closer in structure to fishes' than to snails' native insulin, slows down the prey fishes by lowering their blood glucose levels. The preproinsulin precursor of insulin is encoded by the INS gene. A variety of mutant alleles with changes in the coding region have been identified. A read-through gene, INS-IGF2, overlaps with this gene at the 5' region and with the IGF2 gene at the 3' region. In the pancreatic β cells, glucose is the primary physiological stimulus for the regulation of insulin synthesis.
Insulin is regulated through the transcription factors PDX1, NeuroD1, MafA. PDX1 is in the nuclear periphery upon low blood glucose levels interacting with corepressors HDAC1 and 2, downregulating the insulin secretion. An increase in blood glucose levels causes phosphorylation of PDX1 and it translocates centrally and binds the A3 element within the insulin promoter. Upon translocation it interacts with coactivators HAT p300 and acetyltransferase set 7/9. PDX1 affects the histone modifications through deacetylation as well as methylation, it is said to suppress glucagon. NeuroD1 known as β2, regulates insulin exocytosis in pancreatic β cells by directly inducing the expression of genes involved in exocytosis, it is localized in the cytosol, but in response to high glucose it becomes glycosylated by OGT and/or phosphorylated by ERK, which causes translocation to the nucleus. In the nucleus β2 heterodimerizes with E47, binds to the E1 element of the insulin promoter and recruits co-activator p300 which acetylates β2.
It is able to interact with other transcription factors as well in activation of the insulin gene. MafA is degraded by proteasomes upon low blood glucose levels
Pathology is the study of the causes and effects of disease or injury. The word pathology refers to the study of disease in general, incorporating a wide range of bioscience research fields and medical practices. However, when used in the context of modern medical treatment, the term is used in a more narrow fashion to refer to processes and tests which fall within the contemporary medical field of "general pathology," an area which includes a number of distinct but inter-related medical specialties that diagnose disease through analysis of tissue and body fluid samples. Idiomatically, "a pathology" may refer to the predicted or actual progression of particular diseases, the affix path is sometimes used to indicate a state of disease in cases of both physical ailment and psychological conditions. A physician practicing pathology is called a pathologist; as a field of general inquiry and research, pathology addresses four components of disease: cause, mechanisms of development, structural alterations of cells, the consequences of changes.
In common medical practice, general pathology is concerned with analyzing known clinical abnormalities that are markers or precursors for both infectious and non-infectious disease and is conducted by experts in one of two major specialties, anatomical pathology and clinical pathology. Further divisions in specialty exist on the basis of the involved sample types and physiological systems, as well as on the basis of the focus of the examination. Pathology is a significant field in medical research; the study of pathology, including the detailed examination of the body, including dissection and inquiry into specific maladies, dates back to antiquity. Rudimentary understanding of many conditions was present in most early societies and is attested to in the records of the earliest historical societies, including those of the Middle East and China. By the Hellenic period of ancient Greece, a concerted causal study of disease was underway, with many notable early physicians having developed methods of diagnosis and prognosis for a number of diseases.
The medical practices of the Romans and those of the Byzantines continued from these Greek roots, but, as with many areas of scientific inquiry, growth in understanding of medicine stagnated some after the Classical Era, but continued to develop throughout numerous cultures. Notably, many advances were made in the medieval era of Islam, during which numerous texts of complex pathologies were developed based on the Greek tradition. So, growth in complex understanding of disease languished until knowledge and experimentation again began to proliferate in the Renaissance and Baroque eras, following the resurgence of the empirical method at new centers of scholarship. By the 17th century, the study of microscopy was underway and examination of tissues had led British Royal Society member Robert Hooke to coin the word "cell", setting the stage for germ theory. Modern pathology began to develop as a distinct field of inquiry during the 19th Century through natural philosophers and physicians that studied disease and the informal study of what they termed “pathological anatomy” or “morbid anatomy”.
However, pathology as a formal area of specialty was not developed until the late 19th and early 20th centuries, with the advent of detailed study of microbiology. In the 19th century, physicians had begun to understand that disease-causing pathogens, or "germs" existed and were capable of reproduction and multiplication, replacing earlier beliefs in humors or spiritual agents, that had dominated for much of the previous 1,500 years in European medicine. With the new understanding of causative agents, physicians began to compare the characteristics of one germ’s symptoms as they developed within an affected individual to another germ’s characteristics and symptoms; this realization led to the foundational understanding that diseases are able to replicate themselves, that they can have many profound and varied effects on the human host. To determine causes of diseases, medical experts used the most common and accepted assumptions or symptoms of their times, a general principal of approach that persists into modern medicine.
Modern medicine was advanced by further developments of the microscope to analyze tissues, to which Rudolf Virchow gave a significant contribution, leading to a slew of research developments. By the late 1920s to early 1930s pathology was deemed a medical specialty. Combined with developments in the understanding of general physiology, by the beginning of the 20th century, the study of pathology had begun to split into a number of rarefied fields and resulting in the development of large number of modern specialties within pathology and related disciplines of diagnostic medicine; the term pathology comes from the Ancient Greek roots of pathos, meaning "experience" or "suffering" and -logia, "study of". The modern practice of pathology is divided into a number of subdisciplines within the discrete but interconnected aims of biological research and medical practice. Biomedical research into disease incorporates the
Physiology is the scientific study of the functions and mechanisms which work within a living system. As a sub-discipline of biology, the focus of physiology is on how organisms, organ systems, organs and biomolecules carry out the chemical and physical functions that exist in a living system. Central to an understanding of physiological functioning is the investigation of the fundamental biophysical and biochemical phenomena, the coordinated homeostatic control mechanisms, the continuous communication between cells; the physiologic state is the condition occurring from normal body function, while the pathological state is centered on the abnormalities that occur in animal diseases, including humans. According to the type of investigated organisms, the field can be divided into, animal physiology, plant physiology, cellular physiology and microbial physiology; the Nobel Prize in Physiology or Medicine is awarded to those who make significant achievements in this discipline by the Royal Swedish Academy of Sciences.
Human physiology seeks to understand the mechanisms that work to keep the human body alive and functioning, through scientific enquiry into the nature of mechanical and biochemical functions of humans, their organs, the cells of which they are composed. The principal level of focus of physiology is at the level of systems within systems; the endocrine and nervous systems play major roles in the reception and transmission of signals that integrate function in animals. Homeostasis is a major aspect with regard to such interactions within plants as well as animals; the biological basis of the study of physiology, integration refers to the overlap of many functions of the systems of the human body, as well as its accompanied form. It is achieved through communication that occurs in a variety of both electrical and chemical. Changes in physiology can impact the mental functions of individuals. Examples of this would be toxic levels of substances. Change in behavior as a result of these substances is used to assess the health of individuals.
Much of the foundation of knowledge in human physiology was provided by animal experimentation. Due to the frequent connection between form and function and anatomy are intrinsically linked and are studied in tandem as part of a medical curriculum. Plant physiology is a subdiscipline of botany concerned with the functioning of plants. Related fields include plant morphology, plant ecology, cell biology, genetics and molecular biology. Fundamental processes of plant physiology include photosynthesis, plant nutrition, nastic movements, photomorphogenesis, circadian rhythms, seed germination and stomata function and transpiration. Absorption of water by roots, production of food in the leaves, growth of shoots towards light are examples of plant physiology. Although there are differences between animal and microbial cells, the basic physiological functions of cells can be divided into the processes of cell division, cell signaling, cell growth, cell metabolism. Microorganisms can be found everywhere on Earth.
Types of microorganisms include archaea, eukaryotes, protists and micro-plants. Microbes are important in human culture and health in many ways, serving to ferment foods, treat sewage, produce fuel and other bioactive compounds, they are essential tools in biology as model organisms and have been put to use in biological warfare and bioterrorism. They are a vital component of fertile soils. In the human body microorganisms make up the human microbiota including the essential gut flora, they are the pathogens responsible for many infectious diseases and as such are the target of hygiene measures. Most microorganisms can reproduce and bacteria are able to exchange genes through conjugation and transduction between divergent species; the study of human physiology as a medical field originates in classical Greece, at the time of Hippocrates. Outside of Western tradition, early forms of physiology or anatomy can be reconstructed as having been present at around the same time in China and elsewhere.
Hippocrates incorporated his belief system called the theory of humours, which consisted of four basic substance: earth, water and fire. Each substance is known for having a corresponding humour: black bile, phlegm and yellow bile, respectively. Hippocrates noted some emotional connections to the four humours, which Claudius Galenus would expand on; the critical thinking of Aristotle and his emphasis on the relationship between structure and function marked the beginning of physiology in Ancient Greece. Like Hippocrates, Aristotle took to the humoral theory of disease, which consisted of four primary qualities in life: hot, cold and dry. Claudius Galenus, known as Galen of Pergamum, was the first to use experiments to probe the functions of the body. Unlike Hippocrates, Galen argued that humoral imbalances can be located in specific organs, including the entire body, his modification of this theory better equipped doctors to make more precise diagnoses. Galen played off of Hippocrates idea that emotions were tied to the humours, added the notion of temperaments: sanguine corresponds with blood.
Galen saw the human body consisting of three connected systems: the brain and nerves, which are responsible for thoughts and sensations.