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The hormone, responsible for normal growth, is not being released at normal levels by the pituitary gland. Fall Asleep by Ten at Night Ben Franklin truly understood the importance of following the natural rhythm of the body when he suggested that those who go to sleep early and wake up early find themselves more wise, healthy, and wealthy. The practice of consuming inadequate amounts of protein actually had the opposite effect, leading to depletion of glycogen and contributing to negative alterations of the cortisol rhythm. Her parents told us that it was incredibly difficult to rouse Melissa from bed in the morning. Somatostatin slows down the Growth Hormone release from the Pituitary.

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Mechanisms of Aging

Other structures and tissues of the ovaries include the hilum. The ovaries lie within the pelvic cavity, on either side of the uterus, to which they are attached via a fibrous cord called the ovarian ligament.

The ovaries are uncovered in the peritoneal cavity but are tethered to the body wall via the suspensory ligament of the ovary which is a posterior extension of the broad ligament of the uterus. The part of the broad ligament of the uterus that covers the ovary is known as the mesovarium.

The ovarian pedicle is made up part of the fallopian tube , mesovarium , ovarian ligament, and ovarian blood vessels. The surface of the ovaries is covered with membrane consisting of a lining of simple cuboidal -to-columnar shaped mesothelium.

The outermost layer is called the germinal epithelium. The outer layer is the ovarian cortex , consisting of ovarian follicles and stroma in between them. Included in the follicles are the cumulus oophorus , membrana granulosa and the granulosa cells inside it , corona radiata , zona pellucida , and primary oocyte. Theca of follicle , antrum and liquor folliculi are also contained in the follicle.

Also in the cortex is the corpus luteum derived from the follicles. The innermost layer is the ovarian medulla. Follicular cells flat epithelial cells that originate from surface epithelium covering the ovary, are surrounded by Granulosa cells - that have changed from flat to cuboidal and proliferated to produce a stratified epithelium.

The ovary also contains blood vessels and lymphatics. At puberty, the ovary begins to secrete increasing levels of hormones. Secondary sex characteristics begin to develop in response to the hormones. The ability to produce eggs and reproduce develops. The ovary changes structure and function beginning at puberty.

The ovaries are the site of production and periodical release of egg cells , the female gametes. In the ovaries, the developing egg cells or oocytes mature in the fluid-filled follicles. Typically, only one oocyte develops at a time, but others can also mature simultaneously.

Follicles are composed of different types and number of cells according to the stage of their maturation , and their size is indicative of the stage of oocyte development.

When the oocyte finishes its maturation in the ovary, a surge of luteinizing hormone secreted by the pituitary gland stimulates the release of the oocyte through the rupture of the follicle, a process called ovulation. At maturity, ovaries secrete estrogen , testosterone , [12] [13] inhibin, and progesterone. Progesterone prepares the uterus for pregnancy, and the mammary glands for lactation. Progesterone functions with estrogen by promoting menstrual cycle changes in the endometrium.

As women age, they experience a decline in reproductive performance leading to menopause. This decline is tied to a decline in the number of ovarian follicles.

Although about 1 million oocytes are present at birth in the human ovary, only about about 0. The decline in ovarian reserve appears to occur at a constantly increasing rate with age, [17] and leads to nearly complete exhaustion of the reserve by about age As ovarian reserve and fertility decline with age, there is also a parallel increase in pregnancy failure and meiotic errors resulting in chromosomally abnormal conceptions. Women with an inherited mutation in the DNA repair gene BRCA1 undergo menopause prematurely, [18] suggesting that naturally occurring DNA damages in oocytes are repaired less efficiently in these women, and this inefficiency leads to early reproductive failure.

The BRCA1 protein plays a key role in a type of DNA repair termed homologous recombinational repair that is the only known cellular process that can accurately repair DNA double-strand breaks. Primordial follicles contain oocytes that are at an intermediate prophase I stage of meiosis. Meiosis is the general process in eukaryotic organisms by which germ cells are formed, and it is likely an adaptation for removing DNA damages, especially double-strand breaks, from germ line DNA.

Homologous recombinational repair is especially promoted during meiosis. They hypothesized that DNA double-strand break repair is vital for the maintenance of oocyte reserve and that a decline in efficiency of repair with age plays a key role in ovarian aging.

Ovarian diseases can be classified as endocrine disorders or as a disorders of the reproductive system. If the egg fails to release from the follicle in the ovary an ovarian cyst may form. Small ovarian cysts are common in healthy women. Some women have more follicles than usual polycystic ovary syndrome , which inhibits the follicles to grow normally and this will cause cycle irregularities. Cryopreservation of ovarian tissue, often called ovarian tissue cryopreservation , is of interest to women who want to preserve their reproductive function beyond the natural limit, or whose reproductive potential is threatened by cancer therapy, [27] for example in hematologic malignancies or breast cancer.

Tissue can then be thawed and implanted near the fallopian, either orthotopic on the natural location or heterotopic on the abdominal wall , [28] where it starts to produce new eggs, allowing normal conception to take place. Birds have only one functional ovary the left , while the other remains vestigial. Ovaries in females are analogous to testes in males, in that they are both gonads and endocrine glands.

Ovaries of some kind are found in the female reproductive system of many animals that employ sexual reproduction , including invertebrates.

However, they develop in a very different way in most invertebrates than they do in vertebrates, and are not truly homologous. Many of the features found in human ovaries are common to all vertebrates, including the presence of follicular cells, tunica albuginea, and so on.

However, many species produce a far greater number of eggs during their lifetime than do humans, so that, in fish and amphibians, there may be hundreds, or even millions of fertile eggs present in the ovary at any given time. In these species, fresh eggs may be developing from the germinal epithelium throughout life. Corpora lutea are found only in mammals, and in some elasmobranch fish; in other species, the remnants of the follicle are quickly resorbed by the ovary.

In birds, reptiles, and monotremes , the egg is relatively large, filling the follicle, and distorting the shape of the ovary at maturity.

Amphibians and reptiles have no ovarian medulla; the central part of the ovary is a hollow, lymph -filled space. The ovary of teleosts is also often hollow, but in this case, the eggs are shed into the cavity, which opens into the oviduct. In most birds and in platypuses , the right ovary never matures, so that only the left is functional.

Exceptions include the kiwi and some, but not all raptors , in which both ovaries persist. In the primitive jawless fish , and some teleosts, there is only one ovary, formed by the fusion of the paired organs in the embryo.

From Wikipedia, the free encyclopedia. This article is about the reproductive organ. For other uses, see Ovary disambiguation. For the plant part, see Ovary botany. In botany, this is a proposed section and a synonym of Solanum. The ovaries form part of the female reproductive system , and attach to the fallopian tubes.

Blood supply of the human female reproductive organs. Worldwide in the early 21st century, preventable cancers linked to lifestyle factors were responsible for several million new cancer cases annually. Such cancers are especially common in developed countries. For example, in the United States some 25 to 30 percent of major cancers, such as colorectal cancer , endometrial cancer , breast cancer , and esophageal cancer , have been linked to obesity and physical inactivity.

In fact, in in that country, researchers estimated that about 3. The impact of obesity on cancer risk varies widely by cancer type. Likewise, about one-third of cancers commonly diagnosed in the United Kingdom are considered preventable through improvements in diet, physical activity, and weight control. Less-developed countries, however, are not immune to rising rates of preventable cancers.

Less-active lifestyles and increased availability of processed foods have placed many people in developing countries at increased risk of cancer as well as conditions such as diabetes mellitus and heart disease.

Less-developed countries are often home to high rates of disease caused by infectious agents, including human papillomavirus HPV , which can give rise to cervical cancer , and hepatitis B and C viruses, which can cause liver cancer. Vaccines that have been developed against papillomaviruses and hepatitis B virus are helping to control the rates of associated cancers in heavily affected countries.

However, lack of health care infrastructure in some of those countries means that many persons affected by cancer may receive late diagnosis or inadequate care and that the general public may remain unaware of the risk factors for preventable cancers because information may not be disseminated effectively. Cancer is to a great degree a disease of the elderly , and age is thus a very important factor in cancer development.

However, individuals of any age, including very young children, can be stricken with the disease. In many developed countries cancer deaths in children are second only to accidental deaths. In the United States the most-striking increase in cancer mortality is seen in persons between the ages of 55 and A decline in cancer mortality in persons older than 75 simply reflects the lower number of persons in that population.

Age-adjusted death rates deaths per , population for specific types of tumours have changed significantly over the years. In , for the first time since data began being compiled, cancer deaths in the United States decreased almost 3 percent , and the declines continued through the first decade of the 21st century.

Worldwide, however, death rates from cancer were on the rise. In the United States and certain other developed countries, decreases in death rates from cancer can be attributed to successes of therapy or prevention. For example, a reduction in the number of deaths due to lung cancer has been attributed to warnings that have altered cigarette-smoking habits.

Therapy has greatly lessened mortality from Hodgkin disease and testicular cancer , and it also has improved the chances of surviving breast cancer. Preventive measures have played a major role in the decrease of cancer mortality as well. For example, colonoscopy, which is used to detect early asymptomatic cancers or premalignant growths polyps in the colon, has contributed to declines in death rates from colon cancer.

Routine Pap smear , an examination used to screen for carcinoma of the uterine cervix , has resulted in a downward trend in mortality observed for that disease. The identification of certain types of HPV as the causal agents of cervical cancer has improved cervical-cancer-screening programs by enabling samples obtained from asymptomatic women to be tested for the presence of harmful viral types that could later give rise to cancer.

The effectiveness of preventative measures for cervical cancer is thought to have been greatly increased by the availability of HPV vaccines such as Gardasil , which was approved for the immunization of young girls and boys prior to their becoming sexually active. Striking differences in incidence and age-adjusted death rates of specific forms of cancer are seen in various parts of the world. For example, deaths caused by malignant melanoma , a cancer of the pigmented cells in the skin, are six times more frequent in New Zealand than in Iceland, a variation attributed to differences in sun exposure.

Most observed geographic differences probably result from environmental or cultural influences rather than from differences in the genetic makeup of separate populations. That view is illustrated by examining the differing incidences of stomach cancer that occur in Japanese immigrants to the United States, in Japanese-Americans born to immigrant parents, and in long-term resident populations of both countries. Gastric cancer mortality rates are much higher in Japan than they are in California probably because of dietary and lifestyle differences.

Rates for first-generation Japanese immigrants, on the other hand, are intermediate between those of native Japanese and native Californians, and mortality rates among descendants of Japanese immigrants approach those of the general Californian population with each passing generation. Such observable trends clearly suggest that environmental and cultural factors play an important role in the causation of cancer. Exposure to high levels of carcinogens substances or forms of energy that are known to cause cancer—for instance, asbestos or ionizing radiation can occur in the workplace.

Occupational exposure can result in small epidemics of unusual cancers, such as an increase in angiosarcoma of the liver documented in among American workers who cleaned vinyl chloride polymerization vessels.

Likewise, dramatic increases of certain types of cancer, such as leukemia and thyroid cancer, have been detected in populations exposed to high doses of radiation associated with the malfunction of nuclear reactors. The transition of cells through the different stages from normal to cancerous can be thought of as an evolutionary process, in which there occurs a succession of genetic changes that undergo selection and determine the ultimate genotype genetic constitution of a tumour and its metastases.

Many benign tumours are encased in a well-formed capsule. Malignant tumours, on the other hand, lack a true capsule and, even when limited to a specific location, invariably can be seen to have infiltrated surrounding tissues.

The ability to invade adjacent tissues is a major characteristic that distinguishes malignant tumours from benign tumours. A tumour mass is composed not only of abnormal tumour cells but also of normal host cells, which nourish the tumour, and immune cells, which attempt to react to the tumour. In some instances, tumour cells and cells in the tumour stroma cooperate or compete with one another, resulting in complex tumour behaviour. The rate of tumour growth is determined by comparing the excess of cell production with cell loss.

For a transformed tumour cell to produce a tumour of about one billion cells a mass that weighs about 1 gram [0. A tumour nodule can grow to only a certain diameter 1 to 2 millimetres [0. For tumour expansion to occur, new capillaries tiny blood vessels must form within the tumour—a process called vascularization, or angiogenesis.

At some point, after months or even years as a harmless cluster of cells, tumours may suddenly begin to generate blood vessels. This occurs because they develop the ability to synthesize growth factors that specifically stimulate the formation of vessels. Once they have begun to grow, tumours are able to sustain their own growth in a semi-independent fashion. This results from growth factors produced by the tumour cells themselves a self-stimulatory process called autocriny and by the stromal cells a process called paracriny.

Cancer cells can be distinguished from normal cells, and even from benign tumour cells, by microscopic examination. Differences in appearance include inconsistencies in size and shape and misshapen internal structures such as the nucleus , where genetic material is found. Genetic instability of the cell often gives rise to abnormal cells with giant nuclei that contain enormous amounts of DNA deoxyribonucleic acid. When those highly abnormal cells divide by mitosis , the number of chromosomes formed is abnormally elevated, and the mitotic figures the structures that help to coordinate the division of the chromosomes are often distorted.

Cancer cells also tend to be less-well-differentiated than normal cells, a characteristic that is called anaplasia. When a malignant tumour no longer resembles the tissue of origin, it is said to be undifferentiated, or anaplastic. Most tumours take many years to grow and form to the point where they produce clinical manifestations.

Laryngeal cancer , for instance, appears only after several years of constant exposure to alcohol and tobacco smoke—a behaviour shared by many common tumours caused by environmental conditions. Careful studies of individuals with polyps of the colon benign tumours of the inner lining of the large intestine show that it takes three to five years for a new polyp to form and the same amount of time for the polyp to transform or progress into a carcinoma.

Thus, when malignant tumours finally present with clinical manifestations, they are well into the last phase of their life. In some instances it is known that certain abnormal cellular changes precede cancer. Those alterations are collectively referred to as precancerous lesions. A number of terms, such as hyperplasia , dysplasia , and neoplasia , are used to describe precancerous lesions. For example, endometrial hyperplasia increased cell growth in the endometrium, or inner lining of the uterus often precedes, and may even set the stage for, cancer of the endometrium.

Some clinical conditions are also known to be associated with an increased risk of carcinoma. Indeed, long-standing ulcerative colitis and leukoplakia of the oral cavity carry such an increase in risk that they are known as preneoplastic conditions for adenocarcinoma of the colon and squamous cell carcinoma of the mouth.

Throughout the extended period of time that it takes for cells to acquire the abnormal changes that lead to cancer, they transmit encoded information to their daughter cells. Ultimately, it is the accumulation of that information that is responsible for giving rise to the gene products that in turn cause the abnormal behaviour displayed by cancer cells. In other words, the natural history of a tumour is similar to the natural history of an organism—both obey the tenets of evolutionary theory.

Before tumours metastasize, or spread to other tissues of the body, they pass through a long period as noninvasive lesions. During that stage the earliest stage in which cancer is recognized as such the tumour remains in the anatomic site where it arose and does not invade beyond those confines. An example of such a lesion might be a carcinoma that has arisen from an epithelial cell lining the uterine cervix; as long as this carcinoma is confined to the mucosal lining and has not penetrated the basement membrane, which separates the lining from other tissue layers, it is known as a noninvasive tumour or an in situ tumour.

A tumour at that stage lacks its own network of blood vessel s to supply nutrients and oxygen, and it has not sent cells into the circulatory system to give rise to new tumours.

It also is usually asymptomatic—an unfortunate circumstance, because in situ tumours are curable. In the next stage of tumour progression, a solid tumour invades nearby tissues by breaching the basement membrane. The basement membrane, or basal lamina, is a sheet of proteins and other substances to which epithelial cells adhere and that forms a barrier between tissues. Once tumours are able to break through this membrane, cancerous cells not only invade surrounding tissue substances but also enter the bloodstream—often via a lymphatic vessel, which discharges its contents into the blood.

Tumour cells that have invaded a lymphatic vessel often become trapped in lymph nodes , whereas cells that gain access to blood vessels are disseminated to various parts of the body such as the bones , the lungs , and the brain.

At such distant sites cancer cells form secondary tumours, or metastases. That ability to metastasize is what makes cancer such a lethal disease. The primary tumour the original tumour growing at the site of origin usually can be controlled by available therapies, but it is the disseminated disease that eventually proves fatal to the host.

In order to disseminate throughout the body, the cells of a solid tumour must be able to accomplish the following tasks. They must detach from neighbouring cells, break through supporting membranes, burrow through other tissues until they reach a lymphatic or blood vessel, and then migrate through the lining of that vessel. Next, individual cells or clumps of cells must enter the circulatory system for transport throughout the body. If they survive the journey through lymphatic vessels, veins , and arteries , they will eventually lodge in a capillary of another organ, where they may begin to multiply and form a secondary tumour.

Laboratory researchers have intensively studied this process in the hope that insight into the mechanisms of metastasis will provide ways to devise effective therapies.

Each step has been individualized and studied, and mechanisms have been elucidated at the cellular and even the molecular level. Several of those mechanisms are described in this section. The formation of capillaries, or angiogenesis, is an important step that a tumour undergoes in its transition from a small harmless mass of cells to a life-threatening malignant tumour.

When they first arise in healthy tissue, tumour cells are not able to stimulate capillary development. At some point in their development, however, they call on proteins that stimulate angiogenesis, and they also develop the ability themselves to synthesize proteins with that capacity. One of those proteins is known as vascular endothelial growth factor VEGF.

VEGF induces endothelial cells the building blocks of capillaries to penetrate a tumour nodule and begin the process of capillary development. As the endothelial cells divide, they in turn secrete growth factors that stimulate the growth or motility of tumour cells. Thus, endothelial cells and tumour cells mutually stimulate each other. Cancer cells also produce another type of protein that inhibits the growth of blood vessels. It seems, therefore, that a balance between angiogenesis inhibitors and angiogenesis stimulators determines whether the tumour begins capillary development.

Evidence suggests that angiogenesis begins when cells decrease their production of the inhibiting proteins. Angiogenesis inhibitors are seen as promising therapeutic agents. The process of invasion begins when one cancer cell detaches itself from the mass of tumour cells. Normally, cells are cohesive and stick to one another by a series of specialized molecules.

An important early step in cancer invasion appears to be the loss of this property, known as cellular adhesion. In many epithelial tumours it has been shown that cell-adhesion molecules such as E-cadherin , which helps to keep cells in place, are in short supply. Another type of adhesion that keeps cells in place is their attachment to the extracellular matrix , the network of substances secreted by cells and found between them that helps to provide structure in tissues.

Normally, if a cell is unable to attach to the extracellular matrix, it dies through induction of the cell suicide program known as apoptosis. Cancer cells, however, develop a means to avoid death in that situation. In order to gain access to a blood or lymphatic channel, cancer cells must move through the extracellular matrix and penetrate the basement membrane of the vessel.

To do that, they must be able to forge a path through tissues, a task they perform with the aid of enzymes that digest the extracellular matrix. The cell either synthesizes those proteins or stimulates cells in the matrix to do so. The breakdown of the extracellular matrix not only creates a path of least resistance through which cancer cells can migrate but also gives rise to many biologically active molecules—some that promote angiogenesis and others that attract additional cells to the site.

Once in the bloodstream, tumour cells are disseminated to regions throughout the body. Eventually those cells lodge in capillaries of other organs and exit into those organs, where they grow and establish new metastases. Not all the cancer cells within a malignant tumour are able to spread. Although all the cells in a tumour derive from a single cell, successive divisions give rise to a heterogeneous group of cancer cells, only some of which develop the genetic alterations that allow the cell to seed other tissues.

Of those cells that are able to break away from the parent tumour and enter the circulation, probably less than 1 in 10, actually ends up creating a new tumour at a distant site. Although the location and nature of the primary tumour determine the patterns of dissemination, many tumours spread preferentially to certain sites. This situation can be explained in part by the architecture of the circulatory system and the natural routes of blood flow. For example, because the lungs are usually the first organ through which the blood flows after leaving most organs, they are the most-common site of metastasis.

But circulation alone does not explain all cases of preferential spread. Clinical evidence suggests that a homing mechanism is responsible for some unlikely metastatic deposits. For example, prostate and breast cancers often disseminate first to the bone, and lung cancer often seeds new tumours in the adrenal glands.

That may occur because of an affinity that exists between receptor proteins on the surface of cancer cells and molecules that are abundant in the extracellular matrix of specific tissues. In some instances, the circulating cells may even home back to the primary source, thus contributing to the growth of the primary tumour by reseeding. Because metastasis is such a biologically complex phenomenon, it is unlikely that a single genetic defect brings it about.

It seems more reasonable to predict that a number of aberrant genes contribute to the process. Attempts to discover what genes are involved are ongoing and, it is hoped, will lead to new therapeutic approaches that halt tumour spread.

The signs and symptoms of benign or malignant tumours result for the most part from the local effects of either the primary tumour or its metastases. In some cases the primary tumour and the secondary metastases do not progress at the same pace, and in such an instance the primary tumour may manifest itself while the metastases do not cause symptoms and, as a result, go undetected for years.

In addition to local effects, malignant neoplasms produce systemic effects such as body wasting cachexia and a variety of clinical manifestations known as paraneoplastic syndromes. Both local and systemic effects are described in this section. Metastatic tumours those that result from the spread of the primary tumour can produce the same consequences.

A tumour affects normal bodily functions by compressing, invading, and destroying normal tissues and also by producing substances that circulate in the bloodstream.

The location of the tumour will determine how fast it manifests itself. Tumours arising in the deep soft tissues of the retroperitoneal space the area next to the kidney can grow very large before they produce discomfort. On the other hand, a relatively small tumour in the lungs can produce partial obstruction of secondary airways and cause pneumonia , which can draw attention to the tumour at an early stage.

The expansive growth of benign neoplasms or the more destructive growth of malignant tumours may erode natural surfaces and lead to the development of ulcers and bleeding and create conditions that favour infection. Tumours of the colon are indicated when small quantities of blood are found in the stools through an occult blood test.

Metastases growing in the adrenal gland , for instance, eventually can destroy the gland and produce adrenal insufficiency a condition called Addison disease. Sometimes the clinical manifestations of a tumour result from a malfunction in the tumour cell itself. This is commonly seen in tumours of endocrine glands, whose cells produce excessive amounts of hormones. For example, benign tumours of the parathyroid gland called parathyroid adenomas oversecrete parathormone, which causes calcium levels in the blood to rise.

Symptoms such as muscle weakness, fatigue , anorexia , nausea , and constipation are caused by the excess calcium levels. In the life of a tumour, acute accidents can produce dramatic symptoms. For example, ovarian cysts can rupture and produce immediate and severe abdominal discomfort. Tumours growing freely in a cavity can become twisted and cut off the blood supply to the tumour. That interruption of blood flow can cause tissue death infarction , which may result in internal bleeding and cause intense pain for the individual.

About 10 percent of persons with cancer have signs and symptoms that are not directly related to the location of a tumour or its metastases. Effects that appear at a distance from the tumour are called paraneoplastic syndromes. Such symptoms may be the first manifestation of a small tumour and thus may allow early detection and treatment of the disease. It is important that those symptoms not be confused with symptoms caused by advanced metastatic disease, as misdiagnosis can lead to inappropriate therapy.

Among the most-dramatic paraneoplastic syndromes are those mediated by abnormal hormone production. For example, small-cell carcinomas of the lung can produce excessive amounts of adrenocortical-stimulating hormone.

The gallbladder serves an important digestive function