Androgen insensitivity syndrome is an intersex condition that results in the partial or complete inability of the cell to respond to androgens. The unresponsiveness of the cell to the presence of androgenic hormones can impair or prevent the masculinization of male genitalia in the developing fetus, as well as impairing or preventing the development of male secondary sexual characteristics at puberty, but does not impair female genital or sexual development; as such, the insensitivity to androgens is clinically significant only when it occurs in genetic males. Clinical phenotypes in these individuals range from a typical male habitus with mild spermatogenic defect or reduced secondary terminal hair, to a full female habitus, despite the presence of a Y-chromosome. AIS is divided into three categories that are differentiated by the degree of genital masculinization: complete androgen insensitivity syndrome is indicated when the external genitalia are those of a typical female. Androgen insensitivity syndrome is the largest single entity that leads to 46,XY undermasculinized genitalia.

Management of AIS is limited to symptomatic management. Areas of management include sex assignment, gonadectomy in relation to tumor risk, hormone replacement therapy, genetic counseling, psychological counseling; the human androgen receptor is a protein encoded by a gene located on the proximal long arm of the X chromosome. The protein coding region consists of 2,757 nucleotides spanning eight exons, designated 1-8 or A-H. Introns vary in size between 26 kb. Like other nuclear receptors, the AR protein consists of several functional domains: the transactivation domain, the DNA-binding domain, the hinge region, the steroid-binding domain; the transactivation domain is encoded by exon 1, makes up more than half of the AR protein. Exons 2 and 3 encode the DNA-binding domain, while the 5' portion of exon 4 encodes the hinge region; the remainder of exons 4 through 8 encodes the ligand binding domain. The AR gene contains two polymorphic trinucleotide microsatellites in exon 1; the first microsatellite contains 8 to 60 repetitions of the glutamine codon "CAG" and is thus known as the polyglutamine tract.

The second microsatellite contains 4 to 31 repetitions of the glycine codon "GGC" and is known as the polyglycine tract. The average number of repetitions varies by ethnicity, with Caucasians exhibiting an average of 21 CAG repeats, Blacks 18. In men, disease states are associated with extremes in polyglutamine tract length; some studies indicate that the length of the polyglutamine tract is inversely correlated with transcriptional activity in the AR protein, that longer polyglutamine tracts may be associated with male infertility and undermasculinized genitalia in men. However, other studies have indicated. A comprehensive meta-analysis of the subject published in 2007 supports the existence of the correlation, concluded these discrepancies could be resolved when sample size and study design are taken into account; some studies suggest longer polyglycine tract lengths are associated with genital masculinization defects in men. Other studies find no such association; as of 2010, over 400 AR mutations have been reported in the AR mutation database, the number continues to grow.

Inheritance is maternal and follows an X-linked recessive pattern. About 30% of the time, the AR mutation is a spontaneous result, is not inherited; such de novo mutations are the result of a germ cell mutation or germ cell mosaicism in the gonads of one of the parents, or a mutation in the fertilized egg itself. In one study, three of eight de novo mutations occurred in the postzygotic stage, leading to the estimate that up to one-third of de novo mutations result in somatic mosaicism. Not every mutation of the AR gene results in androgen insensitivity; some individuals with CAIS or PAIS do not have any AR mutations despite clinical and histological features sufficient to warrant an AIS diagnosis. In one patient, the underlying cause for presumptive PAIS was a mutant steroidogenic factor-1 protein. In another patient, CAIS was the result of a deficit in the transmission of a transactivating signal from the N-terminal region of the androgen receptor to the basal transcription machinery of the cell.

A coactivator protein interacting with the activation function 1 transactivation domain of the androgen receptor may have been deficient in this patient. The signal disru

VPro known as Odyssey, is a computer graphics architecture for Silicon Graphics workstations. First released on the Octane2, it was subsequently used on the Fuel, Tezro workstations and the Onyx visualization systems, where it was branded InfinitePerformance. VPro provides some advanced capabilities such as per-pixel lighting known as "phong shading", 48-bit RGBA color. On the other hand designs suffered from constrained bandwidth and poorer texture mapping performance compared to competing GPU solutions, which caught up to SGI in the market. Four different Odyssey-based VPro graphics board revisions existed, designated V6, V8, V10 and V12; the first series were the V8, with 32 MB and 128 MB of RAM respectively. The V6 and V10 can have up to 8MB RAM allocated to textures, while V8 and V12 can have up to 108MB RAM used for textures; the V10 and V12 boards used in Fuel and Onyx 3000 computers use a different XIO connector than the cards used in Octane2 workstations. The VPro graphics subsystem consists of associated software.

The chip set consists of the buzz ASIC, the pixel blaster and jammer ASIC, associated SDRAM. The buzz ASIC is a single-chip graphics pipeline, it operates at 251 MHz and contains on-chip SRAM. The buzz ASIC has three interfaces: Host SDRAM PB&J ASICAs a result of a patent infringement settlement, SGI acquired rights to some of the Nvidia Quadro GPUs and released VPro-branded products based on these; these cards share nothing with the original Odyssey line and could not be used in SGI MIPS workstations. All VPro boards support the OpenGL ARB imaging extensions, allowing for hardware acceleration of numerous imaging operations at real-time rates. SGI page about Octane2 graphics

Olivewood Cemetery, in Houston, lies near a bend in White Oak Bayou, along the rail line to Chaney Junction, where the First and Sixth wards meet just northwest of downtown. The 6-acre cemetery is an historic resting place for many freed slaves and some of Houston’s earliest black residents. In 1875, the land, used for slave burials, was purchased by Richard Brock, Houston's first black alderman, it opened as a cemetery for black Methodists in 1877. When Olivewood was platted, it was the first African-Americans burial ground within the Houston city limits. Many 19th century influential African-Americans were buried in the cemetery, including Reverend Elias Dibble, first minister of Trinity United Methodist Church; the cemetery includes more than 700 family plots around a graceful, elliptical drive that originated at an ornate entry gate. It contains graves of those who died in poverty. Burials at Olivewood Cemetery continued through the 1960s. In 2003, after decades of neglect and abandonment, the "Descendants of Olivewood," a nonprofit organization, was established to take guardianship of the cemetery, "to provide care and to protect its historical significance."Olivewood was designated an Historic Texas Cemetery.

By 2010 water and vandals threatened to damage graves in a portion of the cemetery. By 2013, a digital database for the cemetery has been created consisting of the years 1910-1940 and can be found at www.findagrave.com. This database can be searched by using first and or last names. Over the years, there have been numerous reports of mysterious after-dark sightings and strange movements within the graveyard. Cathi Bunn, a paranormal investigator, began exploring Olivewood in 1999. One moonlit midnight, Bunn said she videotaped the ghost of Mary White, buried in 1888, hovering above her headstone. Descendants of Olivewood http://www.findagrave.com/cgi-bin/fg.cgi?page=cr&GSsr=41&GSmcid=47179842&CRid=2136702&pt=Olivewood%20Cemetery&