A subclinical infection is an infection that, being subclinical, is nearly or asymptomatic. A subclinically infected person is thus an asymptomatic carrier of a microbe, intestinal parasite, or virus, a pathogen causing illness, at least in some individuals. Many pathogens spread by being silently carried in this way by some of their host population; such infections occur both in humans and nonhuman animals. An example of an asymptomatic infection is a mild common cold, not noticed by the infected individual. Since subclinical infections occur without eventual overt sign, their existence is only identified by microbiological culture or DNA techniques such as polymerase chain reaction. An individual may only develop signs of an infection after a period of subclinical infection, a duration, called the incubation period; this is the case, for example, for subclinical sexually transmitted diseases such as AIDS and genital warts. Individuals with such subclinical infections, those that never develop overt illness, creates a reserve of individuals that can transmit an infectious agent to infect other individuals.
Because such cases of infections do not come to clinical attention, health statistics can fail to measure the true prevalence of an infection in a population, this prevents the accurate modeling of its infectious transmission. The following pathogens are known to be carried asymptomatically in a large percentage of the potential host population: Fever and sickness behavior and other signs of infection are taken to be due to them. However, they are evolved physiological and behavioral responses of the host to clear itself of the infection. Instead of incurring the costs of deploying these evolved responses to infections, the body opts to tolerate an infection as an alternative to seeking to control or remove the infecting pathogen. Subclinical infections are important since they allow infections to spread from a reserve of carriers, they can cause clinical problems unrelated to the direct issue of infection. For example, in the case of urinary tract infections in women, this infection may cause preterm delivery if the person becomes pregnant without proper treatment.
Endara, Pablo. S.. "Symptomatic and Subclinical Infection with Rotavirus PG9, Rural Ecuador". Emerging Infectious Diseases. 13: 574–580. Doi:10.3201/eid1304.061285. ISSN 1080-6040. PMC 2391297. PMID 17553272
A cardiac shunt is a pattern of blood flow in the heart that deviates from the normal circuit of the circulatory system. It may be described as right-left, left-right or bidirectional, or as systemic-to-pulmonary or pulmonary-to-systemic; the direction may be controlled by left and/or right heart pressure, a biological or artificial heart valve or both. The presence of a shunt may affect left and/or right heart pressure either beneficially or detrimentally; the left and right sides of the heart are named from a dorsal view, i.e. looking at the heart from the back or from the perspective of the person whose heart it is. There are four chambers in a heart: a ventricle on both the left and right sides. In mammals and birds, blood from the body goes to the right side of the heart first. Blood enters the upper right atrium, is pumped down to the right ventricle and from there to the lungs via the pulmonary artery. Blood going to the lungs is called the pulmonary circulation; when the blood returns to the heart from the lungs via the pulmonary vein, it goes to the left side of the heart, entering the upper left atrium.
Blood is pumped to the lower left ventricle and from there out of the heart to the body via the aorta. This is called the systemic circulation. A cardiac shunt is when blood follows a pattern that deviates from the systemic circulation, i.e. from the body to the right atrium, down to the right ventricle, to the lungs, from the lungs to the left atrium, down to the left ventricle and out of the heart back to the systemic circulation. A left-to-right shunt is when blood from the left side of the heart goes to the right side of the heart; this can occur either through a hole in the ventricular or atrial septum that divides the left and the right heart or through a hole in the walls of the arteries leaving the heart, called great vessels. Left-to-right shunts occur when the systolic blood pressure in the left heart is higher than the right heart, the normal condition in birds and mammals; the most common congenital heart defects which cause shunting are atrial septal defects, patent foramen ovale, ventricular septal defects, patent ductus arteriosi.
In isolation, these defects may be asymptomatic, or they may produce symptoms which can range from mild to severe, which can either have an acute or a delayed onset. However, these shunts are present in combination with other defects; some acquired shunts are modifications of congenital ones: a balloon septostomy can enlarge a foramen ovale, PFO or ASD. Biological tissues may be used to construct artificial passages. Evaluation can be done during a cardiac catheterization with a "shunt run" by taking blood samples from superior vena cava, inferior vena cava, right atrium, right ventricle, pulmonary artery, system arterial. Abrupt increases in oxygen saturation support a left-to-right shunt and lower than normal systemic arterial oxygen saturation supports a right-to-left shunt. Samples from the SVC & IVC are used to calculate mixed venous oxygen saturation S v O 2 = 3 4 × S V C + 1 4 × I V C and Qp:Qs ratio Q p: Q s = change in oxygen concentration across the pulmonary circulation change in oxygen concentration across the systemic circulation = P V − P A S A − S V where P V is the pulmonary vein, P A is the pulmonary artery, S A is the systemic arterial, S V is the mixed-venous The Qp:Qs ratio is based upon the Fick principle and it is reduced to the above equation and eliminates the need to know cardiac output and hemoglobin concentration.
Mechanical shunts such as the Blalock-Taussig shunt are used in some cases of CHD to control blood flow or blood pressure. All reptiles have the capacity for cardiac shunts
Optic pit, optic nerve pit, or optic disc pit is a congenital excavation of the optic disc, resulting from a malformation during development of the eye. Optic pits are important because they are associated with posterior vitreous detachments and serous retinal detachments. Many times, an optic pit is asymptomatic and is just an incidental finding on examination of the eye by a physician. However, some patients may present with the symptoms of a posterior vitreous detachment or serous retinal detachment; this is because optic pits are associated with these disorders and are speculated to be the actual cause of these disorders when they arise in patients with optic pits. The most common visual field defects include a scotoma. Visual acuity is not affected by the pit but may get worse if serous detachment of the macula occurs. Metamorphopsia may result. Optic pits were first described in 1882 as dark gray depressions in the optic disc, they may, appear white or yellowish instead. They can range in size.
Optic pits are associated with other abnormalities of the optic nerve including large optic nerve size, large inferior colobomas of the optic disc, colobomas of the retina. The optic disc originates from the optic cup when the optic vesicle invaginates and forms an embryonic fissure. Optic pits may develop due to failure of the superior end of the embryonic fissure to close completely. No particular risk factors have been conclusively identified. Therefore, a family history of optic pits may be a possible risk factor. Optic pits have been associated with serous retinal detachments in up to as many as 50% of all cases; these detachments may occur at any age but most present in early adulthood. The most popular theory behind this association is a separation of the layers of the retina, known as retinoschisis, due to fluid entering the optic pit and traveling between the inner and outer layers of the retina; the outer layer may subsequently detach. Evidence of retinoschisis has been demonstrated using OCT.
Centrally located optic pits are less to cause changes in the retina. However, if located more peripherally in the optic disc it is more to cause a serous retinal detachment. Furthermore, if the optic pit is located temporally it is more to cause detachment of the macula because of the macula's proximity to the temporal side of the optic disc. If serous macular detachment occurs, a patient’s visual acuity may become as poor as 20/200 or worse. Treatment for optic pit-associated macular detachment involves photocoagulation of the retina by use of an ion laser; this procedure works by burning one or more rows in between the optic disc and areas of serous retinal detachment. In most cases, macular reattachment results and visual acuity can be restored to about 20/80; this procedure may be utilized prior to macular detachment in order to help prevent the future development of macular detachment. Other treatments for optic pit-associated macular detachment include macular buckling, gas tamponade, or vitrectomy.
Some experts feel that the best results can be attained when the use of any of the above-mentioned modalities are used in combination. Optic pits should be diagnosed by an eye care professional who can perform a thorough exam of the back of the eye using an ophthalmoscope. More the development of a special technology called optical coherence tomography has allowed better visualization of the retinal layers, it has been used to demonstrate a marked reduction in the thickness of the retinal nerve fiber layer in the quadrant corresponding to the optic pit. This is not yet in standard use for diagnosis of an optic pit, but may be helpful in supporting a diagnosis. Optic pits. However, patients should follow up with their eye care professional annually or sooner if the patient notices any visual loss whatsoever. Treatment of PVD or serous retinal detachment will be necessary if either develops in a patient with an optic pit. Optic pits occur between men and women, they are seen in 1 in 10,000 eyes, 85% of optic pits are found to be unilateral.
About 70% are found on the temporal side of the optic disc. Another 20% are found centrally, while the remaining pits are located either superiorly, inferiorly, or nasally. "Optic Nerve Pit". American Association for Pediatric Ophthalmology and Strabismus. March 2014. "Optic Pits". EyeWiki. American Academy of Ophthalmology
X-rays make up X-radiation, a form of electromagnetic radiation. Most X-rays have a wavelength ranging from 0.01 to 10 nanometers, corresponding to frequencies in the range 30 petahertz to 30 exahertz and energies in the range 100 eV to 100 keV. X-ray wavelengths are shorter than those of UV rays and longer than those of gamma rays. In many languages, X-radiation is referred to with terms meaning Röntgen radiation, after the German scientist Wilhelm Röntgen who discovered these on November 8, 1895, credited as its discoverer, who named it X-radiation to signify an unknown type of radiation. Spelling of X-ray in the English language includes the variants x-ray, X ray. Before their discovery in 1895 X-rays were just a type of unidentified radiation emanating from experimental discharge tubes, they were noticed by scientists investigating cathode rays produced by such tubes, which are energetic electron beams that were first observed in 1869. Many of the early Crookes tubes undoubtedly radiated X-rays, because early researchers noticed effects that were attributable to them, as detailed below.
Crookes tubes created free electrons by ionization of the residual air in the tube by a high DC voltage of anywhere between a few kilovolts and 100 kV. This voltage accelerated the electrons coming from the cathode to a high enough velocity that they created X-rays when they struck the anode or the glass wall of the tube; the earliest experimenter thought to have produced. In 1785 he presented a paper to the Royal Society of London describing the effects of passing electrical currents through a evacuated glass tube, producing a glow created by X-rays; this work was further explored by his assistant Michael Faraday. When Stanford University physics professor Fernando Sanford created his "electric photography" he unknowingly generated and detected X-rays. From 1886 to 1888 he had studied in the Hermann Helmholtz laboratory in Berlin, where he became familiar with the cathode rays generated in vacuum tubes when a voltage was applied across separate electrodes, as studied by Heinrich Hertz and Philipp Lenard.
His letter of January 6, 1893 to The Physical Review was duly published and an article entitled Without Lens or Light, Photographs Taken With Plate and Object in Darkness appeared in the San Francisco Examiner. Starting in 1888, Philipp Lenard, a student of Heinrich Hertz, conducted experiments to see whether cathode rays could pass out of the Crookes tube into the air, he built a Crookes tube with a "window" in the end made of thin aluminum, facing the cathode so the cathode rays would strike it. He found that something came through, that would cause fluorescence, he measured the penetrating power of these rays through various materials. It has been suggested that at least some of these "Lenard rays" were X-rays. In 1889 Ukrainian-born Ivan Pulyui, a lecturer in experimental physics at the Prague Polytechnic who since 1877 had been constructing various designs of gas-filled tubes to investigate their properties, published a paper on how sealed photographic plates became dark when exposed to the emanations from the tubes.
Hermann von Helmholtz formulated mathematical equations for X-rays. He postulated a dispersion theory before Röntgen made his announcement, it was formed on the basis of the electromagnetic theory of light. However, he did not work with actual X-rays. In 1894 Nikola Tesla noticed damaged film in his lab that seemed to be associated with Crookes tube experiments and began investigating this radiant energy of "invisible" kinds. After Röntgen identified the X-ray, Tesla began making X-ray images of his own using high voltages and tubes of his own design, as well as Crookes tubes. On November 8, 1895, German physics professor Wilhelm Röntgen stumbled on X-rays while experimenting with Lenard tubes and Crookes tubes and began studying them, he wrote an initial report "On a new kind of ray: A preliminary communication" and on December 28, 1895 submitted it to Würzburg's Physical-Medical Society journal. This was the first paper written on X-rays. Röntgen referred to the radiation as "X"; the name stuck.
They are still referred to as such in many languages, including German, Danish, Swedish, Estonian, Japanese, Georgian and Norwegian. Röntgen received the first Nobel Prize in Physics for his discovery. There are conflicting accounts of his discovery because Röntgen had his lab notes burned after his death, but this is a reconstruction by his biographers: Röntgen was investigating cathode rays from a Crookes tube which he had wrapped in black cardboard so that the visible light from the tube would not interfere, using a fluorescent screen painted with barium platinocyanide, he noticed a faint green glow from the screen, about 1 meter away. Röntgen realized some invisible rays coming from the tube were passing through the cardboard to make the screen glow, he found they could pass through books and papers on his desk. Röntgen threw himself into investigating these unknown rays systematically. Two months after his initial discovery, he published his paper. Röntgen discovered their medical use when he made a picture of his wife's hand on a photographic plate formed due to X-rays.
The photograph of his wife's hand was the first photograph of a human body part using X-rays. When she saw the picture, she said "I have seen my death."The discovery of X-rays stimul