What is the full form of HLI1. HLI: Human Life InternationalHLI stands for Human Life International. An anti-abortion Roman Catholic organization in the United States is called Human Life International (HLI). It is among the biggest anti-abortion groups in the country. With affiliations and associates in more than 80 countries and representatives dispatched to around 160, it bills itself as "the largest international pro-life organization in the world. "The leaders of the group are clergy. Since 1996, its headquarters have been in Front Royal, Virginia. Establishment and AgendaPaul Marx started Human Life International in 1981 in Gaithersburg, Maryland, as an extension of the Human Life Center. Its goal is to educate and train leaders of the anti-abortion movement, including family counsellors, radio and television programmers, priests, crisis pregnancy centres, and civic leaders. HLI's anti-abortion activism is based on Catholic teachings that hold that life begins at conception. The group opposes contraceptives as well. It supports Uganda's efforts to make homosexuality a crime. Human Life International provided initial assistance to the Center for Family and Human Rights in 1997. The Population Research Institute is connected to HLI. Between 2000 and 2014, the organization donated $7.9 million to anti-abortion charities. 2. HLI: Highland Light InfantryHLI Stands for Highland Light Infantry. In 1881, the British Army established the Highland Light Infantry (HLI), a light infantry regiment. It fought in both World Wars I and II until 1959, when it was combined with the Royal Scots Fusiliers to become the Princess Margaret's Own Glasgow and Ayrshire Regiment, also known as the Royal Highland Fusiliers. Later, it joined forces with the Black Watch (Royal Highland Regiment), the Highlanders (Seaforth, Gordons, and Camerons), the Argyll and Sutherland Highlanders, and the Royal Scots Borderers to form the Royal Regiment of Scotland, with the 2nd Battalion of the new regiment. Regular ArmyIn December 1914, the 1st Battalion arrived in Marseille to serve on the Western Front as a part of the Sirhind Brigade of the 3rd (Lahore) Division. They went into the trenches close to Festubert. It participated in the March 1915 Battle of Neuve Chapelle, the May 1915 Battle of St. Julien, and the May 1915 Second Battle of Ypres. After that, in December 1915, it relocated to Mesopotamia, where it participated in the Battle of Sharqat in October 1918 and the Siege of Kut in spring 1916. In August 1914, the 2nd Battalion embarked on its mission to the Western Front, landing in Boulogne-sur-Mer as part of the 5th Brigade in the 2nd Division. Territorial ForceAs part of the 157th Brigade in the 52nd (Lowland) Division, the 1/5th (City of Glasgow) Battalion, the 1/6th (City of Glasgow) Battalion, and the 1/7th (Blythswood) Battalion landed at Cape Helles in Gallipoli in July 1915. They were evacuated to Egypt in January 1916 and then moved to Marseille in April 1918 to serve on the Western Front. In November 1914, as part of the 5th Brigade in the 2nd Division, the 1/9th (Glasgow Highland) Battalion landed in France to serve on the Western Front. Between the WarsThe regiment was renamed the City of Glasgow Regiment (Highland Light Infantry) in 1923. In 1930, David Niven received his commission into the regiment and was assigned to the 2nd Battalion. Second World WarAs part of the 42nd Division's 127th Brigade, the 1st Battalion arrived in France in September 1939 to serve with the British Expeditionary Force. In June 1940, the Battalion took part in the evacuation of Dunkirk. Following its participation in the June 1944 Normandy landings, it was a member of the 53rd (Welsh) Division's 71st Infantry Brigade, which saw combat in the Battle of the Bulge in January 1945, the Battle of the Reichswald in March 1945, and the final advance into Germany. Early in the war, the 2nd Battalion relocated to Egypt and participated in the Battle of Keren in March 1941. After that, it moved to the Western Desert, where it fought in the Battle of Fuka in July 1942 and the Battle of Knightsbridge in June 1942 as a member of the 5th Indian Infantry Division's 10th Indian Infantry Brigade. It participated in the July 1943 Allied invasion of Sicily and, following a spell of duty in Greece, Albania, and Yugoslavia, took part in the last push into Northern Italy. As part of the 157th Brigade in the 52nd (Lowland) Division, the 5th and 6th Battalions arrived in France in June 1940. Later that month, they were evacuated from Cherbourg, and in October 1944, they landed in Belgium. In November 1944, they participated in Operation Infatuate, and in April 1945, they captured Bremen. In 1942, the 11th Battalion was transformed into an armoured unit and joined the Royal Armoured Corps as the 156th regiment. However, the troops kept their Highland Light Infantry hat logo on the RAC's black beret. After the WarIn 1959, the Royal Scots Fusiliers and the Highland Light Infantry combined to become the Royal Highland Fusiliers. At Redford Barracks in Edinburgh, the regular 1st battalions of the two Regiments amalgamated to form the 1st Battalion of the newly formed regiment (1 RHF). UniformThe HLI's entire uniform in 1914 was unique; it included a red doublet with buff facings, a dark green shako with a diced border and green cords, and trews of Mackenzie tartan. Officers donned the same tartan plaids, and all ranks wore green Glengarry helmets and white shell coats with trews when in drill order. Before kilts were approved in 1947, the HLI was the only regular Highland regiment that wore trews for full dress. The Glasgow Highlanders, a territorial battalion of the HLI who wore kilts, was an earlier example of an exception. Up until 1900, the regiment had been dressed in khaki-drab tropical service uniforms with plaid trews. 3. HLI: Human Longevity IncorporationHLI stands for Human Longevity Incorporation. In order to develop life-enhancing therapies, HLI is sequencing up to 40,000 human genomes annually and combining the results with clinical data, the metabolome, and the microbiome to create the largest genotype/phenotype database in the world. With the help of funding from HLI, the world's largest human sequencing operation is being built to create the most extensive and complete database of human genotypes, microbiomes, and phenotypes, which will help combat diseases linked to aging-related biological decline in humans. To address the age-related loss in endogenous stem cell function, HLI is also spearheading the development of cell-based therapies. Database licensing to pharmaceutical, biotechnology, and academic institutions, sequencing, and the creation of cutting-edge diagnostics and treatments will be the sources of income. Intending to quickly scale to 100,000 human genomes annually, HLI has originally purchased two Illumina HiSeq X Ten sequencing systems (with the potential to acquire three additional systems) to sequence up to 40,000 human genomes annually. HLI will sequence a wide range of people, including kids, adults, supercentenarians, people with illnesses, and healthy people. Focusing on some of the most common and practical areas, HLI is well-positioned to identify therapeutic solutions to retain a healthy, high-performing body. With its team of highly skilled scientists and physicians, HLI focuses on cancer, diabetes and obesity, heart and liver illnesses, and dementia. The J. Craig Venter Institute (JCVI), University of California, San Diego, and Metabolon Inc. have all formed strategic partnerships with the company. HLI is concentrating its initial efforts on the clinical sequencing of cancer. Although many are addressing this field with gene sequencing and other cutting-edge technologies, no thorough clinical endeavour has combined germ line, human genome, and tumour genome sequencing with detailed biochemical data from every patient. In order to enable whole genome, microbiome, and tumour sequencing and analysis of consenting UC San Diego research patients, HLI and UC San Diego have inked a collaborative research agreement. In order to improve patient outcomes and diagnostic capabilities, the collected data must be analyzed, used, and shared. The UC San Diego Moores Cancer Center, under the direction of Director Scott Lippman, M.D., has welcomed the collaboration. The business plans to expand this kind of partnership and initiative with UC San Diego to additional clinical facilities across the globe. Pioneers in the fields of stem cell therapy and genomics formed HLI, a privately held corporation with its headquarters located in San Diego, California, in 2013. HLI is creating the most comprehensive database of human genotypes and phenotypes in the world using advancements in genomic sequencing, the human microbiome, proteomics, informatics, computing, and cell therapy technologies. This database will serve as a foundation for numerous commercialization opportunities aimed at addressing ageing-related diseases and human biological decline. As part of its product offerings, HLI will be creating new treatments and diagnostics as well as licensing access to its database. Other Strategic CollaborationsProteomics, infectious disease diagnostics, and the human microbiome are the topics of a collaboration and research services agreement that HLI is building with the JCVI. The creator and CEO of JCVI, a pioneer in the fields of synthetic, microbial, and human genomics, is Dr. Venter. HLI intends to get intellectual property licenses from JCVI. Stem Cell TherapyThe company plans to use the latest advancements in stem cell therapy in an ambitious multi-pronged endeavour to extend and improve a healthy life span. The foundation of HLI's work is the assumption that numerous biological changes, including significant alterations and degradation to the genome of the differentiated, specialized cells present in all bodily tissues, take place as the human body ages. Over time, the body experiences a loss and deterioration of healthy populations of regenerating stem cells. HLI will keep an eye on the genetic alterations brought on by stem cell differentiation, normal ageing, and disease onset. 4. HLI: Heart Lung InteractionHLI stands for Human Lung Interaction. Changes in transpulmonary pressure and pleural pressure are the two main causes of lung inflation that lead to heart-lung interactions. Among these, pleural pressure variations during spontaneous breathing are the most prominent. The environment of the heart decreases in relation to the rest of the body during inspiration because the heart is surrounded by pleural pressure. This modifies the left heart's outflow and the right heart's inflow. The inflow into the left heart and the outflow from the right heart can both change in response to changes in transpulmonary pressure. Ventricular function, respiratory effort, and cardiac and respiratory frequency all affect these relationships. IntroductionOne of the fundamental rhythms of life is the connection between the heart and lungs, which varies according to the frequency of breathing and heartbeat. Amphibians were the first animals to develop the arrangement of the circulatory system that is seen in mammals and birds, where blood flow in the pulmonary circulation is divided from the systemic circulation and flows between the right and left hearts. The benefit of this arrangement was that it allowed the pulmonary vascular pressure to be significantly lower than the systemic vascular pressure, allowing the alveoli to be delicate structures with superior gas exchange. However, because of its location in the middle of the chest and the necessity for blood flow to travel through the lungs as they expand and contract, the heart is susceptible to the mechanical forces that cause the lungs to expand. These are mainly composed of two forces: variations in the pressure across the lung, or transpulmonary pressure, and variations in pleural pressure. The decline in pleural pressure that occurs during spontaneous breathing effectively lowers the heart relative to the rest of the body, dominating the interaction. What enters the heart through the great veins and what exits the heart through the aorta are changed by this variation in the heart's environment in relation to atmospheric pressure. The second factor, which applies to both spontaneous negative pressure breathing and positive pressure artificial breaths, is the rise in transpulmonary pressure with lung inflation. An increase in transpulmonary pressure can impact both the left heart's filling and the right heart's emptying. Regulation of Steady State Cardiac OutputIt is vital first to comprehend the typical variables that control steady-state cardiac output in order to comprehend how breathing influences cardiac output. Cardiac output is determined by two functions: the first one describes blood return to the heart, and the second one describes the heart's processing of the returned blood. Return functionThe characteristics of the elastic chambers that make up the vasculature control how blood flows around the closed circuit that is the circulation. The elastic walls of every component in the circulatory system are stretched by the volume filling it. This produces a pressure known as the mean circulatory filling pressure (MCFP), which is the same in all vascular compartments, even in the absence of flow. When there are pressure differences between the compartments, flow between them happens. Even in the absence of heart contractions, blood will flow from the circulation to atmospheric pressure if a major vein is severed until the vascular walls are no longer stretched. In this simple situation, flow is determined by three factors: the volume that stretches the walls of each vascular compartment, the resistance that lowers the system to atmospheric pressure, and the compliance (1/elastance), or stretchiness, of the vascular walls. The bulk of the vascular volume is made up of venules and tiny veins, which control the elastic force that pumps blood back to the heart. Its importance for heart filling is the reason systemic filling pressure (MSFP) is a distinct name for it. The pressure in the veins and venules is typically higher than MCFP under flow conditions, while it can occasionally be lower. Throughout the vascular compartments, volume is redistributed. The pressure inside the ventricles is increased by this brief rise in elastance during systole. Due to the presence of cardiac valves, blood flows out of the ventricles in a single direction. It raises the ventricular pressure in relation to the ventricular outflows (the aorta from the left ventricle and the pulmonary artery from the right). Because of the pressure differential that occurs in one compartment compared to the next, each cycle generates a stroke volume that travels through the vasculature. The stroke volume expelled by the left heart must match the stroke return to the right heart in a steady state. In every heart cycle, just one stroke volume's worth of energy travels through the circuit. Cardiac FunctionAs was mentioned in the preceding section, the elastance of the heart chambers varies cyclically throughout the cardiac cycle. A key factor in determining the volume expelled each beat is the ventricle's starting pressure right prior to the start of systole, as explained by the Frank-Starling connection. This pressure, known as the heart's preload, is established by the ventricle's diastolic elastance and volume at the conclusion of diastole. The preload determines the last stretch of the cardiac sarcomeres before the start of systole. The cardiac function curve is the relationship between cardiac output and preload, as described by Starling. The load the heart experiences upon ejection, known as the afterload, and the rate and magnitude of the brief rise in ventricular elastance throughout the cardiac cycle, known as contractility, are additional factors that affect the volume ejected each beat. The number of times per minute that the heart ejects a stroke volume or heart rate is the final factor that determines how much the heart ejects every minute. The cardiac function curve is shifted higher and leftward by a decrease in afterload, an increase in contractility, or an increase in heart rate. Therefore, an increase in cardiac output for the same preload is characterized as an increase in cardiac function. It's important to distinguish between an increase in cardiac output and an increase in cardiac function. Cardiovascular output represents the amount of blood that leaves the heart per minute, while function describes what the heart can accomplish depending on its filling pressure. Cardiac OutputThe venous return function, which controls how well blood returns to the heart, and the cardiac function curve, which controls how well the heart ejects the blood that returns to it, interact to define the real or "working" cardiac output. Arthur Guyton's pictorial approach to the return function and cardiac function describes this relationship clearly, and it can be utilized to solve the complex mathematical relationships between these two functions. Because he maintained that Pra is a significant controlled variable for the return of blood to the heart, he plotted Pra on the x-axis. The cardiac preload, which is the primary variable in the cardiac function curve at a fixed afterload, heart rate, and contractility, is also the right atrial pressure at the end of diastole. Because it makes clear how the reference system for the heart differs from that of the systemic circulation, Guyton's approach is particularly helpful in understanding how the heart interacts with the venous return during the breathing cycle. Next TopicIAC |