Tides are the rise and fall of sea levels caused by the combined effects of the gravitational forces exerted by the Moon and the Sun, the rotation of the Earth. Tide tables can be used for any given locale to find the predicted times and amplitude; the predictions are influenced by many factors including the alignment of the Sun and Moon, the phase and amplitude of the tide, the amphidromic systems of the oceans, the shape of the coastline and near-shore bathymetry. They are however only predictions, the actual time and height of the tide is affected by wind and atmospheric pressure. Many shorelines experience low tides each day. Other locations have a diurnal tide -- one low tide each day. A "mixed tide"—two uneven magnitude tides a day—is a third regular category. Tides vary on timescales ranging from hours to years due to a number of factors, which determine the lunitidal interval. To make accurate records, tide gauges at fixed stations measure water level over time. Gauges ignore; these data are compared to the reference level called mean sea level.

While tides are the largest source of short-term sea-level fluctuations, sea levels are subject to forces such as wind and barometric pressure changes, resulting in storm surges in shallow seas and near coasts. Tidal phenomena are not limited to the oceans, but can occur in other systems whenever a gravitational field that varies in time and space is present. For example, the shape of the solid part of the Earth is affected by Earth tide, though this is not as seen as the water tidal movements. Tide changes proceed via the following stages: Sea level rises over several hours, covering the intertidal zone; the water rises to its highest level. Sea level falls over several hours; the water stops reaching low tide. Oscillating currents produced by tides are known as tidal streams; the moment that the tidal current ceases is called slack tide. The tide reverses direction and is said to be turning. Slack water occurs near high water and low water, but there are locations where the moments of slack tide differ from those of high and low water.

Tides are semi-diurnal, or diurnal. The two high waters on a given day are not the same height; the two low waters each day are the higher low water and the lower low water. The daily inequality is not consistent and is small when the Moon is over the Equator. From the highest level to the lowest: Highest astronomical tide – The highest tide which can be predicted to occur. Note that meteorological conditions may add extra height to the HAT. Mean high water springs – The average of the two high tides on the days of spring tides. Mean high water neaps – The average of the two high tides on the days of neap tides. Mean sea level – This is the average sea level; the MSL is constant for any location over a long period. Mean low water neaps – The average of the two low tides on the days of neap tides. Mean low water springs – The average of the two low tides on the days of spring tides. Lowest astronomical tide and Chart datum – The lowest tide which can be predicted to occur; some charts use this as the chart datum.

Note that under certain meteorological conditions the water may fall lower than this meaning that there is less water than shown on charts. Tidal constituents are the net result of multiple influences impacting tidal changes over certain periods of time. Primary constituents include the Earth's rotation, the position of the Moon and Sun relative to the Earth, the Moon's altitude above the Earth's Equator, bathymetry. Variations with periods of less than half a day are called harmonic constituents. Conversely, cycles of days, months, or years are referred to as long period constituents. Tidal forces affect the entire earth. In contrast, the atmosphere is much more fluid and compressible so its surface moves by kilometers, in the sense of the contour level of a particular low pressure in the outer atmosphere. In most locations, the largest constituent is the "principal lunar semi-diurnal" known as the M2 tidal constituent, its period is about 12 hours and 25.2 minutes half a tidal lunar day, the average time separating one lunar zenith from the next, thus is the time required for the Earth to rotate once relative to the Moon.

Simple tide clocks track this constituent. The lunar day is longer than the Earth day because the Moon orbits in the same direction the Earth spins; this is analogous to the minute hand on a watch crossing the hour hand at 12:00 and again at about 1:05½. The Moon orbits the Earth in the same direction as the Earth rotates on its axis, so it takes more than a day—about 24 hours and 50 minutes—for the Moon to return to the same location in the sky. During this time, it has passed overhead once and underfoot once, so in many places the period of strongest tidal forcing is the above-mentioned, about 12 hours and 25 minutes; the moment of highest tide is not when the Moon is nearest to zenith or nadir, but the period of the forcing still determines the time between high tides. Because the gravitational field created by the Moon weakens with dist

Detachment Kit is an American indie rock band formed in 1999. Detachment Kit was started in Chicago, IL in 1999, by Toddrick Spalding, Josh Hight, Ian Menard. Toddrick met Charlie Davis III through his roommates and the band was completed, they were all art school students and Spalding attended Columbia College and Menard and Charlie H. Davis III attended Art Institute of Chicago; the band recorded a demo soon after the line up congealed, released as the Attacks On Bright America EP in 2001 on limited 10" vinyl on Chris Newmyer's Self-Starter Foundation label. The follow-up full-length album They Raging. Quiet Army was recorded in two days at Steve Albini's Electrical Audio by engineer Greg Norman and released on Self-Starter Foundation; the album was a hit on college radio. The band built a loyal fanbase. Spalding and Hight left the band during the writing of their second album, so Davis and Menard continued on to make the record Of This Blood... recorded by Greg Norman, on which Menard played guitar and drums and Davis played bass and guitar.

The band relocated to Brooklyn, New York, recruited the rhythm section of Michael Hamilton and Bryan Mayer for live performances. In 2005, Nick Davis replaced Michael Hamilton on drums. Original Detachment Kit bass player Josh Hight went on to form IRONS. In January 2010, Menard and Charlie Davis started a new band with Jess Birch called BRONZE, releasing their self-titled debut EP in May 2010. Detachment Kit toured extensively, playing on the same bill as bands such as Les Savy Fav, Thursday, My Morning Jacket, Burning Brides, The Walkmen, Hot Hot Heat and Cambria, Guided by Voices, The Dismemberment Plan, Jimmy Eat World; the band's sound is influenced by post-punk bands, with Gang of Four and Wire identified as influences, their sound described as "peppered with smart references to post-punk and indie's hallowed past". Some tracks on Of This Blood were described as "a sort of post-punk blues"; the band has drawn comparisons with Les Savy Fav, Built To Spill and Modest Mouse. They Raging Quiet Army, Self-Starter Of This Blood, Frenchkiss Live at Cat's Cradle 16 September 2004 - download only Plus - Self-released Attacks on Bright America, Self-Starter The Detachment Kit on Myspace Bronze website

Activin and inhibin are two related protein complexes that have directly opposite biological effects. Identified in 1986, activin enhances FSH biosynthesis and secretion, participates in the regulation of the menstrual cycle. Many other functions have been found to be exerted by activin, including roles in cell proliferation, apoptosis, homeostasis, immune response, wound repair, endocrine function. Conversely, inhibin downregulates inhibits FSH secretion; the existence of inhibin was hypothesized as early as 1916. Activin is a dimer composed of two identical or similar beta subunits. Inhibin is a dimer wherein the first component is a beta subunit similar or identical to the beta subunit in activin. However, in contrast to activin, the second component of the inhibin dimer is a more distantly-related alpha subunit. Activin, inhibin and a number of other structurally related proteins such as anti-Müllerian hormone, bone morphogenetic protein, growth differentiation factor belong to the TGF-β protein superfamily.

The activin and inhibin protein complexes are both dimeric in structure, and, in each complex, the two monomers are linked to one another by a single disulfide bond. In addition, both complexes are derived from the same family of related genes and proteins but differ in their subunit composition. Below is a list of the most common inhibin and activin complexes and their subunit composition: The alpha and beta subunits share 25% sequence similarity, whereas the similarity between beta subunits is 65%. In mammals, four beta subunits have been described, called activin βA, activin βB, activin βC and activin βE. Activin βA and βB are identical to the two beta subunits of inhibin. A fifth subunit, activin βD, has been described in Xenopus laevis. Two activin βA subunits give rise to activin A, one βA, one βB subunit gives rise to activin AB, so on. Various, but not all theoretically possible, heterodimers have been described; the subunits are linked by a single covalent disulfide bond. The βC subunit is able to form activin heterodimers with βA or βB subunits but is unable to dimerize with inhibin α.

Activin is produced in the gonads, pituitary gland and other organs: In the ovarian follicle, activin increases FSH binding and FSH-induced aromatization. It participates in androgen synthesis enhancing LH action in testis. In the male, activin enhances spermatogenesis. Activin is expressed in wounded skin, overexpression of activin in epidermis of transgenic mice improves wound healing and enhances scar formation, its action in wound repair and skin morphogenesis is through stimulation of keratinocytes and stromal cells in a dose-dependent manner. Activin regulates the morphogenesis of branching organs such as the prostate and kidney. Activin A increased the expression level of type-I collagen suggesting that activin A acts as a potent activator of fibroblasts. Lack of activin during development results in neural developmental defects. Upregulation of Activin A drives pluripotent stem cells into a mesoendodermal fate, thus provides a useful tool for stem cell differentiation and organoid formation.

In both females and males, inhibin inhibits FSH production. Inhibin does not inhibit the secretion of GnRH from the hypothalamus. However, the overall mechanism differs between the sexes: Inhibin is produced in the gonads, pituitary gland, corpus luteum and other organs. FSH stimulates the secretion of inhibin from the granulosa cells of the ovarian follicles in the ovaries. In turn, inhibin suppresses FSH. Inhibin B reaches a peak in the early- to mid-follicular phase, a second peak at ovulation. Inhibin A reaches its peak in the mid-luteal phase. Inhibin secretion is diminished by GnRH, enhanced by insulin-like growth factor-1, it is secreted from the Sertoli cells, located in the seminiferous tubules inside the testes. Androgens stimulate inhibin production; as with other members of the superfamily, activins interact with two types of cell surface transmembrane receptors which have intrinsic serine/threonine kinase activities in their cytoplasmic domains: Activin type 1 receptors: ACVR1, ACVR1B, ACVR1C Activin type 2 receptors: ACVR2A, ACVR2BActivin binds to the Type II receptor and initiates a cascade reaction that leads to the recruitment and activation of Type I activin receptor.

This interacts with and phosphorylates SMAD2 and SMAD3, two of the cytoplasmic SMAD proteins. Smad3 translocates to the nucleus and interacts with SMAD4 through multimerization, resulting in their modulation as transcription factor complexes responsible for the expression of a large variety of genes. In contrast to activin, much less is known about the mechanism of action of inhibin, but may involve competing with activin for binding to activin receptors and/or binding to inhibin-specific receptors. Activin A is more plentiful in the adipose tissue of obese, compared to lean persons. Activin A promotes the proliferation of adipocyte progenitor cells, while inhibiting their differentiation into adipocytes. Activin A increases inflammatory cytokines in macrophages. A mutation in the gene for the activin receptor ACVR1 results in fibrodysplasia ossificans progressiva, a fatal disease that causes muscle and soft tissue to be replaced by bone tissue; this condition is characterized by the formation of an extra skeleton that produces immobilization and death by suffocation.

The mutation in