International Standard Serial Number
An International Standard Serial Number is an eight-digit serial number used to uniquely identify a serial publication, such as a magazine. The ISSN is helpful in distinguishing between serials with the same title. ISSN are used in ordering, interlibrary loans, other practices in connection with serial literature; the ISSN system was first drafted as an International Organization for Standardization international standard in 1971 and published as ISO 3297 in 1975. ISO subcommittee TC 46/SC 9 is responsible for maintaining the standard; when a serial with the same content is published in more than one media type, a different ISSN is assigned to each media type. For example, many serials are published both in electronic media; the ISSN system refers to these types as electronic ISSN, respectively. Conversely, as defined in ISO 3297:2007, every serial in the ISSN system is assigned a linking ISSN the same as the ISSN assigned to the serial in its first published medium, which links together all ISSNs assigned to the serial in every medium.
The format of the ISSN is an eight digit code, divided by a hyphen into two four-digit numbers. As an integer number, it can be represented by the first seven digits; the last code digit, which may be 0-9 or an X, is a check digit. Formally, the general form of the ISSN code can be expressed as follows: NNNN-NNNC where N is in the set, a digit character, C is in; the ISSN of the journal Hearing Research, for example, is 0378-5955, where the final 5 is the check digit, C=5. To calculate the check digit, the following algorithm may be used: Calculate the sum of the first seven digits of the ISSN multiplied by its position in the number, counting from the right—that is, 8, 7, 6, 5, 4, 3, 2, respectively: 0 ⋅ 8 + 3 ⋅ 7 + 7 ⋅ 6 + 8 ⋅ 5 + 5 ⋅ 4 + 9 ⋅ 3 + 5 ⋅ 2 = 0 + 21 + 42 + 40 + 20 + 27 + 10 = 160 The modulus 11 of this sum is calculated. For calculations, an upper case X in the check digit position indicates a check digit of 10. To confirm the check digit, calculate the sum of all eight digits of the ISSN multiplied by its position in the number, counting from the right.
The modulus 11 of the sum must be 0. There is an online ISSN checker. ISSN codes are assigned by a network of ISSN National Centres located at national libraries and coordinated by the ISSN International Centre based in Paris; the International Centre is an intergovernmental organization created in 1974 through an agreement between UNESCO and the French government. The International Centre maintains a database of all ISSNs assigned worldwide, the ISDS Register otherwise known as the ISSN Register. At the end of 2016, the ISSN Register contained records for 1,943,572 items. ISSN and ISBN codes are similar in concept. An ISBN might be assigned for particular issues of a serial, in addition to the ISSN code for the serial as a whole. An ISSN, unlike the ISBN code, is an anonymous identifier associated with a serial title, containing no information as to the publisher or its location. For this reason a new ISSN is assigned to a serial each time it undergoes a major title change. Since the ISSN applies to an entire serial a new identifier, the Serial Item and Contribution Identifier, was built on top of it to allow references to specific volumes, articles, or other identifiable components.
Separate ISSNs are needed for serials in different media. Thus, the print and electronic media versions of a serial need separate ISSNs. A CD-ROM version and a web version of a serial require different ISSNs since two different media are involved. However, the same ISSN can be used for different file formats of the same online serial; this "media-oriented identification" of serials made sense in the 1970s. In the 1990s and onward, with personal computers, better screens, the Web, it makes sense to consider only content, independent of media; this "content-oriented identification" of serials was a repressed demand during a decade, but no ISSN update or initiative occurred. A natural extension for ISSN, the unique-identification of the articles in the serials, was the main demand application. An alternative serials' contents model arrived with the indecs Content Model and its application, the digital object identifier, as ISSN-independent initiative, consolidated in the 2000s. Only in 2007, ISSN-L was defined in the
A ventricle is one of two large chambers toward the bottom of the heart that collect and expel blood received from an atrium towards the peripheral beds within the body and lungs. The atrium primes the pump. Interventricular means between the ventricles. In a four-chambered heart, such as that in humans, there are two ventricles that operate in a double circulatory system: the right ventricle pumps blood into the pulmonary circulation to the lungs, the left ventricle pumps blood into the systemic circulation through the aorta. Ventricles generate higher blood pressures; the physiological load on the ventricles requiring pumping of blood throughout the body and lungs is much greater than the pressure generated by the atria to fill the ventricles. Further, the left ventricle has thicker walls than the right because it needs to pump blood to most of the body while the right ventricle fills only the lungs. On the inner walls of the ventricles are irregular muscular columns called trabeculae carneae which cover all of the inner ventricular surfaces except that of the conus arteriosus, in the right ventricle.
There are three types of these muscles. The third type, the papillary muscles give origin at their apices to the chordae tendinae which attach to the cusps of the tricuspid valve and to the mitral valve; the mass of the left ventricle, as estimated by magnetic resonance imaging, averages 143 g ± 38.4 g, with a range of 87–224 g. The right ventricle is equal in size to that of the left ventricle and contains 85 millilitres in the adult, its upper front surface is circled and convex, forms much of the sternocostal surface of the heart. Its under surface is flattened, forming part of the diaphragmatic surface of the heart that rests upon the diaphragm, its posterior wall is formed by the ventricular septum, which bulges into the right ventricle, so that a transverse section of the cavity presents a semilunar outline. Its upper and left angle forms a conical pouch, the conus arteriosus, from which the pulmonary artery arises. A tendinous band, called the tendon of the conus arteriosus, extends upward from the right atrioventricular fibrous ring and connects the posterior surface of the conus arteriosus to the aorta.
The left ventricle is longer and more conical in shape than the right, on transverse section its concavity presents an oval or nearly circular outline. It forms a small part of the sternocostal surface and a considerable part of the diaphragmatic surface of the heart; the left ventricle is thicker and more muscular than the right ventricle because it pumps blood at a higher pressure. The right ventricle is triangular in shape and extends from the tricuspid valve in the right atrium to near the apex of the heart, its wall is thickest at the apex and thins towards its base at the atrium. By early maturity, the walls of the left ventricle have thickened from three to six times greater than that of the right ventricle; this reflects the typical five times greater pressure workload this chamber performs while accepting blood returning from the pulmonary veins at ~80mmHg pressure and pushing it forward to the typical ~120mmHg pressure in the aorta during each heartbeat. During systole, the ventricles contract.
During diastole, the ventricles fill with blood again. The left ventricle receives oxygenated blood from the left atrium via the mitral valve and pumps it through the aorta via the aortic valve, into the systemic circulation; the left ventricular muscle must relax and contract and be able to increase or lower its pumping capacity under the control of the nervous system. In the diastolic phase, it has to relax quickly after each contraction so as to fill with the oxygenated blood flowing from the pulmonary veins. In the systolic phase, the left ventricle must contract and forcibly to pump this blood into the aorta, overcoming the much higher aortic pressure; the extra pressure exerted is needed to stretch the aorta and other arteries to accommodate the increase in blood volume. The right ventricle receives deoxygenated blood from the right atrium via the tricuspid valve and pumps it into the pulmonary artery via the pulmonary valve, into the pulmonary circulation; the typical healthy adult heart pumping volume is ~5 liters/min, resting.
Maximum capacity pumping volume extends from ~25 liters/min for non-athletes to as high as ~45 liters/min for Olympic level athletes. In cardiology, the performance of the ventricles are measured with several volumetric parameters, including end-diastolic volume, end-systolic volume, stroke volume and ejection fraction. Ventricular pressure is a measure of blood pressure within the ventricles of the heart. During most of the cardiac cycle, ventricular pressure is less than the pressure in the aorta, but during systole, the ventricular pressure increases, the two pressures become equal to each other, the aortic valve opens, blood is pumped to the body. Elevated left ventricular end-diastolic pressure has been described as a risk factor in cardiac surgery. Noninvasive approximations have been described. An elevated pressure difference between the aortic pressure and the left ventricular pressure may be indicative of aortic stenosis. Right
The atrioventricular node, or AV node is a part of the electrical conduction system of the heart that coordinates the top of the heart. It electrically ventricles; the AV node lies at the lower back section of the interatrial septum near the opening of the coronary sinus, which conducts the normal electrical impulse from the atria to the ventricles. The AV node is quite compact; the AV node lies at the lower back section of the interatrial septum near the opening of the coronary sinus, which conducts the normal electrical impulse from the atria to the ventricles. The AV node is quite compact, it is located at the center of Koch's triangle—a triangle enclosed by the septal leaflet of the tricuspid valve, the coronary sinus, the membranous part of the interatrial septum. The blood supply of the AV node is from the atrioventricular nodal branch; the origin of this artery is most a branch of the right coronary artery, with the remainder originating from the left circumflex artery. This is associated with the dominance of the coronary artery circulation.
In right-dominant individuals the blood supply is from the right coronary artery while in left dominant individuals it originates from the left circumflex artery. BMP cell signaling plays a key role in diverse aspects of cardiac differentiation and morphogenesis. are multifunctional signaling molecules critical for the development of AV node. BMP influences AV node development through Alk3 receptor. Abnormalities seen in BMP and Alk3 are associated with some cardiovascular diseases like Ebstein’s anomaly and AV conduction disease; the AV node receives two inputs from the right atrium: posteriorly, via the crista terminalis, anteriorly, via the interatrial septum. Contraction of heart muscle cells requires depolarization and repolarization of their cell membranes. Movement of ions across cell membranes causes these events; the cardiac conduction system coordinates myocyte mechanical activity. A wave of excitation spreads out from the sinoatrial node through the atria along specialized conduction channels.
This activates the AV node. The atrioventricular node delays impulses by 0.09s. This delay in the cardiac pulse is important: It ensures that the atria have ejected their blood into the ventricles first before the ventricles contract; this protects the ventricles from excessively fast rate response to atrial arrhythmias. AV conduction during normal cardiac rhythm occurs through two different pathways: the first “pathway” has a slow conduction velocity but shorter refractory period the second “pathway” has a faster conduction velocity but longer refractory period. An important property, unique to the AV node is decremental conduction, in which the more the node is stimulated the slower it conducts; this is the property of the AV node that prevents rapid conduction to the ventricle in cases of rapid atrial rhythms, such as atrial fibrillation or atrial flutter. The AV node's normal intrinsic firing rate without stimulation is 40-60 times/minute; this property is important because loss of the conduction system before the AV node should still result in pacing of the ventricles by the — slower — pacemaking ability of the AV node.
Atrioventricular conduction disease describes impairment of the electrical continuity between the atria and ventricles. It occurs when the atrial depolarization fail to reach the ventricles or is conducted with an abnormally long delay, it can be a genetically inherited disorder. Atrioventricular nodal re-entry tachycardia. Cystic tumour of atrioventricular nodal region CTAVN is of endodermal origin and occurs in the area of the AV node, tricuspid valve, interatrial septum. Junctional rhythm Anatomy figure: 20:06-02 at Human Anatomy Online, SUNY Downstate Medical Center - "The conduction system of the heart." Thoraxlesson4 at The Anatomy Lesson by Wesley Norman https://web.archive.org/web/20070929080346/http://www.healthyheart.nhs.uk/heart_works/heart03.shtml
In medicine, a disease is considered asymptomatic if a patient is a carrier for a disease or infection but experiences no symptoms. A condition might be asymptomatic if it fails to show the noticeable symptoms with which it is associated. Asymptomatic infections are called subclinical infections. Other diseases might be considered subclinical if they present some but not all of the symptoms required for a clinical diagnosis; the term clinically silent is used. Knowing that a condition is asymptomatic is important because: It may develop symptoms and so require watch and wait or early treatment, it may become benign. It is required that a person undergoes treatment so it does not cause medical problems such as high blood pressure and hyperlipidaemia. Be alert to possible problems: asymptomatic hypothyroidism makes a person vulnerable to Wernicke-Korsakoff syndrome or beri-beri following intravenous glucose; the affected person may be infectious and unknowingly spread the infection to others. An example of an asymptomatic disease is Cytomegalovirus, a member of the herpes virus.
"It is estimated that 1% of all newborns are infected with CMV, but the majority of infections are asymptomatic." In some diseases, the proportion of asymptomatic cases can be important. For example, in multiple sclerosis it is estimated that around 25% of the cases are asymptomatic, being these cases detected postmortem or just by coincidence while treating other diseases. Asymptomatic conditions may not be discovered; some people may remain asymptomatic for a remarkably long period of time. If a patient is asymptomatic, precautionary steps must be taken. A patient's individual genetic makeup may prevent the onset of symptoms; some diseases are defined only clinically, like AIDS being opposed to HIV infection. Therefore, it makes no sense to speak about "asymptomatic AIDS"; this concept of clinically defined diseases is related in some way to the concept of syndrome. These are conditions for which there is a sufficient number of documented individuals that are asymptomatic that it is clinically noted.
For a complete list of asymptomatic infections see subclinical infection. Symptomatic Subclinical infection
Atrial natriuretic peptide
Atrial natriuretic peptide or atrial natriuretic factor is a natriuretic peptide hormone secreted from the cardiac atria. Natriuretic peptides are a family of hormone/paracrine factors; the main function of ANP is causing a reduction in expanded extracellular fluid volume by increasing renal sodium excretion. ANP is synthesized, secreted by cardiac muscle cells in the walls of the atria in the heart; these cells contain volume receptors which respond to increased stretching of the atrial wall due to increased atrial blood volume. Reduction of blood volume by ANP can result in secondary effects such as reduction of extracellular fluid volume, improved cardiac ejection fraction with resultant improved organ perfusion, decreased blood pressure, increased serum potassium; these effects may be blunted or negated by various counter-regulatory mechanisms operating concurrently on each of these secondary effects. Brain natriuretic peptide – a misnomer, it acts via the same receptors as ANP does, but with 10-fold lower affinity than ANP.
The biological half-life of BNP, however, is twice as long as that of ANP, that of NT-proBNP is longer, making these peptides better choices than ANP for diagnostic blood testing. The discovery of ANP was reported in 1981, when rat atrial extracts were found to contain a substance that increased salt and urine output in the kidney; the substance was purified from heart tissue by several groups and named atrial natriuretic factor or ANP. ANP is a 28-amino acid peptide with a 17-amino acid ring in the middle of the molecule; the ring is formed by a disulfide bond between two cysteine residues at positions 7 and 23. ANP is related to BNP and CNP, which all share a similar amino acid ring structure. ANP is one of a family of nine structurally similar natriuretic hormones: seven are atrial in origin. ANP is synthesized as an inactive preprohormone, encoded by the human NPPA gene located on the short arm of chromosome 1; the NPPA gene is expressed in atrial myocytes and consists of two introns and three exons, with translation of this gene yielding a high molecular mass 151 amino acid polypeptide known as preproANP.
The preprohormone is activated via post-translational modification that involves cleavage of the 25 amino acid signal sequence to produce proANP, a 126 amino acid peptide, the major form of ANP stored in intracellular granules of the atria. Following stimulation of atrial cells, proANP is released and converted to the 28-amino-acid C-terminal mature ANP on the cell surface by the cardiac transmembrane serine protease corin. ANP is secreted in response to: Stretching of the atrial wall, via Atrial volume receptors Increased Sympathetic stimulation of β-adrenoceptors Increased sodium concentration, though sodium concentration is not the direct stimulus for increased ANP secretion Endothelin, a potent vasoconstrictor Three types of atrial natriuretic peptide receptors have been identified on which natriuretic peptides act, they are all cell surface receptors and designated: guanylyl cyclase-A known as natriuretic peptide receptor-A or NPR1 guanylyl cyclase-B known as natriuretic peptide receptor-B or NPR2 natriuretic peptide clearance receptor or NPR3NPR-A and NPR-B have a single membrane-spanning segment with an extracellular domain that binds the ligand.
The intracellular domain maintains two consensus catalytic domains for guanylyl cyclase activity. Binding of a natriuretic peptide induces a conformational change in the receptor that causes receptor dimerization and activation; the binding of ANP to its receptor causes the conversion of GTP to cGMP and raises intracellular cGMP. As a consequence, cGMP activates a cGMP-dependent kinase that phosphorylates proteins at specific serine and threonine residues. In the medullary collecting duct, the cGMP generated in response to ANP may act not only through PKG but via direct modulation of ion channels. NPR-C functions as a clearance receptor by binding and sequestering ANP from the circulation. All natriuretic peptides are bound by the NPR-C. Maintenance of the ECF volume, its subcompartment the vascular space, is crucial for survival; these compartments are maintained within a narrow range, despite wide variations in dietary sodium intake. There are three volume regulating systems: two salt saving systems, the renin angiotensin aldosterone system and the renal sympathetic system.
When the vascular space contracts, the RAAS and RSS are "turned on". Each system suppresses its counteracting system. NP's are made in cardiac, intestinal and adrenal tissue: ANP in one of a family of cardiac NP's: others at BNP, CNP, DNP. ANP binds to a specific set of receptors – ANP receptors. Receptor-agonist binding causes the increase in renal sodium excretion, which results in a decreased ECF and blood volume. Secondary effects may be an improvement in cardiac ejection fraction and reduction of systemic blood pressure. ANP acts on the kidney to increase sodium and water excretion in the following ways: ANP increases glomerular filtration rate and glomerular permeability. ANP directly dilates the afferent arteriole and counteracts the norepinephrine induced vasoconstriction of the afferent arteriole; some studies suggest that ANP constricts the efferent arteriole, but this is not a unanimous finding. ANP inhibits the effect of Angiotensin II on the mesangia
A myocardial bridge occurs when one of the coronary arteries tunnels through the myocardium rather than resting on top of it. The arteries rest on top of the heart muscle and feed blood down into smaller vessels that populate throughout the myocardium. However, if the muscle grows around one of the larger arteries a myocardial bridge is formed; as the heart squeezes to pump blood, the muscle exerts pressure across the bridge and constricts the artery. This defect is present from birth. Though affected individuals may never exhibit symptoms, clinical manifestations include asymptomatic anomaly, myocardial infarction, to sudden cardiac death; the incidence of the condition in the general population is estimated at 5% based on autopsy findings, but significance when found in association with other cardiac conditions is unknown. The condition is diagnosed on a scale based on. If there is less than 50% blockage the condition is benign. Blockage over 70% causes some pain. Small amounts of myocardial bridging are undetectable, as the blood flows through the coronary while the heart is relaxing in diastole.
This condition can cause complications such as vasospasm, angina pectoris, ventricular tachycardia. Additionally many patients express discomfort in specific positions. Surgery for symptomatic myocardial bridge of the left anterior descending artery may include myotomy, coronary artery bypass surgery, or both. Procedure selection is based on the size of the underlying artery during diastole, the presence of concomitant proximal coronary artery disease, the presence of anatomic factors that would increase the risk of myotomy. Surgical strategy for the management should be customized, the treatment of choice is myotomy but bypass surgery can be added when there is proximal coronary obstruction or anatomic anomalies that increase the risk of recurrence of the obstruction. Cardiac CT Angiography Harlan Krumholz, M. D. discusses myocardial bridging Medical definition of myocardial bridge Myocardial bridge summary by the Texas Heart Institute
OCLC Online Computer Library Center, Incorporated d/b/a OCLC is an American nonprofit cooperative organization "dedicated to the public purposes of furthering access to the world's information and reducing information costs". It was founded in 1967 as the Ohio College Library Center. OCLC and its member libraries cooperatively produce and maintain WorldCat, the largest online public access catalog in the world. OCLC is funded by the fees that libraries have to pay for its services. OCLC maintains the Dewey Decimal Classification system. OCLC began in 1967, as the Ohio College Library Center, through a collaboration of university presidents, vice presidents, library directors who wanted to create a cooperative computerized network for libraries in the state of Ohio; the group first met on July 5, 1967 on the campus of the Ohio State University to sign the articles of incorporation for the nonprofit organization, hired Frederick G. Kilgour, a former Yale University medical school librarian, to design the shared cataloging system.
Kilgour wished to merge the latest information storage and retrieval system of the time, the computer, with the oldest, the library. The plan was to merge the catalogs of Ohio libraries electronically through a computer network and database to streamline operations, control costs, increase efficiency in library management, bringing libraries together to cooperatively keep track of the world's information in order to best serve researchers and scholars; the first library to do online cataloging through OCLC was the Alden Library at Ohio University on August 26, 1971. This was the first online cataloging by any library worldwide. Membership in OCLC is based on use of services and contribution of data. Between 1967 and 1977, OCLC membership was limited to institutions in Ohio, but in 1978, a new governance structure was established that allowed institutions from other states to join. In 2002, the governance structure was again modified to accommodate participation from outside the United States.
As OCLC expanded services in the United States outside Ohio, it relied on establishing strategic partnerships with "networks", organizations that provided training and marketing services. By 2008, there were 15 independent United States regional service providers. OCLC networks played a key role in OCLC governance, with networks electing delegates to serve on the OCLC Members Council. During 2008, OCLC commissioned two studies to look at distribution channels. In early 2009, OCLC negotiated new contracts with the former networks and opened a centralized support center. OCLC provides bibliographic and full-text information to anyone. OCLC and its member libraries cooperatively produce and maintain WorldCat—the OCLC Online Union Catalog, the largest online public access catalog in the world. WorldCat has holding records from private libraries worldwide; the Open WorldCat program, launched in late 2003, exposed a subset of WorldCat records to Web users via popular Internet search and bookselling sites.
In October 2005, the OCLC technical staff began a wiki project, WikiD, allowing readers to add commentary and structured-field information associated with any WorldCat record. WikiD was phased out; the Online Computer Library Center acquired the trademark and copyrights associated with the Dewey Decimal Classification System when it bought Forest Press in 1988. A browser for books with their Dewey Decimal Classifications was available until July 2013; until August 2009, when it was sold to Backstage Library Works, OCLC owned a preservation microfilm and digitization operation called the OCLC Preservation Service Center, with its principal office in Bethlehem, Pennsylvania. The reference management service QuestionPoint provides libraries with tools to communicate with users; this around-the-clock reference service is provided by a cooperative of participating global libraries. Starting in 1971, OCLC produced catalog cards for members alongside its shared online catalog. OCLC commercially sells software, such as CONTENTdm for managing digital collections.
It offers the bibliographic discovery system WorldCat Discovery, which allows for library patrons to use a single search interface to access an institution's catalog, database subscriptions and more. OCLC has been conducting research for the library community for more than 30 years. In accordance with its mission, OCLC makes its research outcomes known through various publications; these publications, including journal articles, reports and presentations, are available through the organization's website. OCLC Publications – Research articles from various journals including Code4Lib Journal, OCLC Research, Reference & User Services Quarterly, College & Research Libraries News, Art Libraries Journal, National Education Association Newsletter; the most recent publications are displayed first, all archived resources, starting in 1970, are available. Membership Reports – A number of significant reports on topics ranging from virtual reference in libraries to perceptions about library funding. Newsletters – Current and archived newsletters for the library and archive community.
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