Hooked In Annus 1984
Towanda Tuning
In 1984, the Anal Position Index (API) was proposed by Reisner and colleagues to determine the position of the anal opening in the pelvic floor [38]. API is the ratio of the perineal length divided by the length of the complete posterior pelvic floor, that is, the distance of the fourchette/the scrotal-perineal junction to the center of the anus divided by the distance from the fourchette/scrotal-perineal junction to the tip of the coccyx in girls/boys, respectively (Figure 3).
L. Larry. Larry White taught psychology at Beloit from 1984 to 2020. His special field of inquiry, in which he published widely, was the interrogation of children and teens by law enforcement officials and attorneys, and he was featured on that subject in the famed Netflix documentary, MAKING A MURDERER.
The Stones' momentum sucked everyone, including themselves, into its vortex. "I decided that if Keith and I kept dipping into the same bag, there would be no book and we'd both be dead," writes Stanley Booth, one of the walking wounded of the rock 'n' roll wars, in the coda to his firsthand account of the Stones' infamous 1969 tour, Dance with the Devil. Booth puts a metaphysical shellac on the Stones' greed, while Philip Norman's Symphony for the Devil blandly passes off the Stones' saga of self-destruction as a saga of success. In both books the "devil" is a kind of glib folly, Neither author is prepared to see the moral and intellectual bankruptcy behind so much of their hard-driving rock 'n' rolling. The Stones' songs played at evil; but their lives embodied it. Evil is the inability to acknowledge the suffering of others. The destruction of life that seems to have followed the Stones is a barometer of their indifference. Illegitimate children are bom and forgotten. Their friends get hooked on drugs; some of them die. The Stones' lives were self-fulfilling prophecies of their songs. Their great early hit "I Can't Get No Satisfaction" (1965) announced the dilemma of their new wealth and fame: they were numb. The song was a blues by people who had everything:
The distinctive look of these clouds is created by the wind. The clouds develop when ice crystals within the clouds grow. The clouds become heavier and begin to descend. They are then whipped by strong winds below, sometimes jet stream winds, and spread horizontally across the sky. The clouds' hooked tails indicate the direction of winds aloft.
Androgen Insensitivity Syndrome, or AIS, is a genetic condition, inherited (except for occasional spontaneous mutations), occurring in approximately 1 in 20,000 individuals. In an individual with complete AIS, the body's cells are unable to respond to androgen, or "male" hormones. ("Male" hormones is an unfortunate term, since these hormones are ordinarily present and active in both males and females.) Some individuals have partial androgen insensitivity. In an individual with complete AIS and karyotype 46 XY, testes develop during gestation. The fetal testes produce mullerian inhibiting hormone (MIH) and testosterone. As in typical male fetuses, the MIH causes the fetal mullerian ducts to regress, so the fetus lacks uterus, fallopian tubes, and cervix plus upper part of vagina. However, because cells fail to respond to testosterone, the genitals differentiate in the female, rather than the male pattern, and Wolffian structures (epididymis, vas deferens, and seminal vesicles) are absent. The newborn AIS infant has genitals of normal female appearance, undescended or partially descended testes, and usually a short vagina with no cervix. Occasionally the vagina is nearly absent. AIS individuals are clearly women. At puberty, the testes are stimulated by the pituitary gland, and produce testosterone. Because testosterone is chemically very similar to estrogen, some of the testosterone converts back to estrogen ("aromatizes") in the bloodstream. This estrogen produces breast growth, though it may be late. Women with AIS do not menstruate, and are not fertile. Because the development of pubic and underarm hair, in women as well as in men, depends upon testosterone, most AIS women have no pubic or underarm hair, but some have sparse hair. When an AIS girl is diagnosed during infancy, physicians often perform surgery to remove her undescended testes. Although removal of testes is advisable, because of the risk of cancer, ISNA advocates that surgery be offered later, when the girl can choose for herself. Testicular cancer is rare before puberty. Vaginoplasty surgery is frequently performed on AIS infants or girls to increase the size of the vagina, so that she can engage in penetrative intercourse with a partner with an average size penis. Vaginoplasty surgery is problematic, with many failures. ISNA advocates against vaginal surgery on infants. Such surgery should be offered to, not imposed on, the pubertal girl, and she should have an opportunity to speak with adult AIS women about their sexual experience and about surgery in order to make a fully informed decision. Not all AIS women will choose surgery. Some women have successfully increased the depth of their vagina with a program of regular pressure dilation, using aids designed for that purpose. Contact the "AIS Support Group": Physicians and parents have been most reluctant to be honest with AIS girls and women about their condition, and this secrecy and stigma has unnecessarily increased the emotional burden of being different. Because AIS is a genetic defect located on the X chromosome, it runs in families. Except for spontaneous mutations, the mother of an AIS individual is a carrier, and her XY children have a 1/2 chance of having AIS. Her XX children have a 1/2 chance of carrying the AIS gene. Most AIS women should be able to locate other AIS women among siblings or maternal relatives. *Is there a test to find out if you have AIS?* The answer depends upon exactly what you are looking for--diagnostic information, or carrier status. If were born with female genitals and testes, and have very sparse or absent pubic hair, you most likely have complete AIS. If you were born with ambiguous genitals and testes, there are a number of possible etiologies, including partial AIS. Testing for partial AIS is more problematic than the complete form. Hormonal tests in a newborn with 46 XY karyotype and ambiguous genitals will show normal to elevated testosterone and LH, and a normal ratio of testosterone to DHT. A family history of ambiguous genitals in maternal relatives suggests partial androgen insensitivity. If you are wondering if you are a carrier, or if you know that you are a carrier and are wondering about the status of your fetus, genetic testing is possible. AIS has been diagnosed as early as 9-12 weeks gestation by chorionic villus sampling (sampling tissue from the fetal side of the placenta). By the 16th week it can be detected by ultrasound and amniocentesis. However, prenatal diagnosis is not indicated unless there is a family history of AIS. See the following for details of testing. Hodgins M. B., Duke E. M., Ring D.: Carrier detection in the testicular feminization syndrome: deficient 5 alpha-dihydrotestosterone binding in cultured skin fibroblasts from the mothers of patients with complete androgen insensitivity. J. Med. Genet. Jun 1984, 21, (3), p178-81. Batch J. A., Davies H. R., Evans B. A. J., Hughes I. A., Patterson M. N.: Phenotypic variation and detection of carrier status in the partial androgen insensitivity syndrome. Arch. Dis. Childh. 1993; 68: 453-457.
The extent of androgen insensitivity in 46 XY individuals is quite variable, even in a single family. Partial androgen insensitivity typically results in "ambiguous genitalia." The clitoris is large or, alternatively, the penis is small and hypospadic (these are two ways of labeling the same anatomical structure). Partial androgen insensitivity may be quite common, and has been suggested as the cause of infertility in many men whose genitals are of typically male appearance. Individuals with ambiguous genitals have typically been subjected to "corrective" surgery during infancy. Based on our own painful experiences, ISNA believes that such cosmetic surgery of the genitals is harmful and unethical. Surgery is justified only when it is necessary for the health and well-being of the child. Surgery which is intended to make the genitals appear more male or more female should be offered, but not imposed, only when the child is old enough to make an informed decision for her/himself. *Is there a test to find out if you have androgen insensitivity?* The answer depends upon exactly what you are looking for--diagnostic information, or carrier status. If were born with female genitals and testes, and have very sparse or absent pubic hair, you most likely have complete AIS. If you were born with ambiguous genitals and testes, there are a number of possible etiologies, including partial AIS. Testing for partial AIS is more problematic than the complete form. Hormonal tests in a newborn with 46 XY karyotype and ambiguous genitals will show normal to elevated testosterone and LH, and a normal ratio of testosterone to DHT. A family history of ambiguous genitals in maternal relatives suggests partial androgen insensitivity. If you are wondering if you are a carrier, or if you know that you are a carrier and are wondering about the status of your fetus, genetic testing is possible. AIS has been diagnosed as early as 9-12 weeks gestation by chorionic villus sampling (sampling tissue from the fetal side of the placenta). By the 16th week it can be detected by ultrasound and amniocentesis. However, prenatal diagnosis is not indicated unless there is a family history of AIS. See the following for details of testing. Hodgins M. B., Duke E. M., Ring D.: Carrier detection in the testicular feminization syndrome: deficient 5 alpha-dihydrotestosterone binding in cultured skin fibroblasts from the mothers of patients with complete androgen insensitivity. J. Med. Genet. Jun 1984, 21, (3), p178-81. Batch J. A., Davies H. R., Evans B. A. J., Hughes I. A., Patterson M. N.: Phenotypic variation and detection of carrier status in the partial androgen insensitivity syndrome. Arch. Dis. Childh. 1993; 68: 453-457.
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