Two apparently identically affected stillborn infants, a male and a female, had been born previously at 28 weeks' gestation. Urioste et al. (1991) described 2 female sibs, the offspring of healthy nonconsanguineous parents, who died shortly after birth.
Campomelia, Cumming type, is characterized by the association of limb defects and multivisceral anomalies. Epidemiology The syndrome has been reported in eight infants from four different families. Clinical description Skeletal features include tetramelic campomelia and short long bones. Extraskeletal manifestations may include cervical lymphocele, generalized hydrops, polycystic kidneys, pancreas and liver, fibrotic liver or pancreas, polysplenia, heterotaxia (see this term), lung hypoplastia, short bowel. All newborns reported so far were either stillborn or died shortly after birth.
Similarly, Tassabehji et al. (1993) demonstrated an almost perfect in-frame tandem duplication of 42 bases in exon 28 of the NF1 gene in 3 members of a family with Watson syndrome (613113.0010).
Neurofibromatosis-Noonan syndrome (NFNS) is a RASopathy and a variant of neurofibromatosis type 1 (NF1) characterized by the combination of features of NF1, such as café-au-lait spots, iris Lisch nodules, axillary and inguinal freckling, optic nerve glioma and multiple neurofibromas, and Noonan syndrome (NS), such as short stature, typical facial features (hypertelorism, ptosis, downslanting palpebral fissures, low-set posteriorly rotated ears with a thickened helix, and a broad forehead), congenital heart defects and unusual pectus deformity. As these three entities have significant phenotypic overlap, molecular genetic testing is often necessary for a correct diagnosis (such as when café-au-lait spots are present in patients diagnosed with NS).
A number sign (#) is used with this entry because the lethal form of multiple pterygium syndrome (LMPS) is caused by homozygous or compound heterozygous mutation in the CHRNG gene, which encodes the gamma subunit of the acetylcholine receptor (AChR), (100730) on chromosome 2q. Mutations in this gene can also cause the nonlethal (Escobar) variant of this phenotype (EVMPS; 265000). Mutations in the CHRNA1 (100690) and CHRND (100720) genes can also result in lethal multiple pterygium syndrome; mutations in these genes can also cause fast- or slow-channel congenital myasthenic syndromes (608930 and 601462, respectively). Clinical Features In addition to a lethal multiple pterygium syndrome (Gillin and Pryse-Davies, 1976), Hall (1984) identified 2 other possibly distinct forms: one with spinal fusion and one with congenital bone fusions (van Regemorter et al., 1984). Chen et al. (1984) reported 6 cases. Van Regemorter et al. (1984) documented the lethal multiple pterygium syndrome in 2 spontaneously aborted fetuses from first-cousin parents of Moroccan origin.
Multiple pterygium syndrome lethal type is a very rare genetic condition affecting the skin, muscles and skeleton. It is characterized by minor facial abnormalities, prenatal growth deficiency, spine defects, joint contractures, and webbing (pterygia) of the neck, elbows, back of the knees, armpits, and fingers. Fetuses with this condition are usually not born. Some of the prenatal complications include cystic hygroma , hydrops , diaphragmatic hernia , polyhydramnios , underdevelopment of the heart and lungs, microcephaly, bone fusions, joint dislocations, spinal fusion, and bone fractures. Both X-linked and autosomal recessive inheritance have been proposed. Mutations in the CHRNG , CHRNA1 , and CHRND genes have been found to cause this condition.
Mapping By linkage analysis of a family with X-linked parkinsonism and spasticity, Poorkaj et al. (2010) found linkage to a 28-Mb region on chromosome Xp11.2-q13.3 (multipoint lod score of 2.068 was obtained between markers DXS991 and DXS993).
A rare, genetic, neurological disorder characterized by parkinsonian features (including resting or action tremor, cogwheel rigidity, hypomimia and bradykinesia) associated with variably penetrant spasticity, hyperactive deep tendon reflexes and Babinski sign.
ISBN 978-3-662-04491-9 . ^ Wayne J.G. Hellstrom (28 November 2012). Androgen Deficiency and Testosterone Replacement: Current Controversies and Strategies .
It states that a person who causes an abortion after 28 weeks of pregnancy is guilty of "child destruction", a felony, and is punishable with life imprisonment with or without hard labour. [2] Saint Kitts and Nevis also follows precedents set in British abortion law, such as Rex v.
Voen Med Zh 1:47–51 ^ Solozhenkin VG (1978) Scarlet fever-like disease in children. Pediatriia (1):27–28 ^ Fukushima H Matsuda Y, Seki R, Tsubokura M, Takeda N, Shubin FN, Paik IK, Zheng XB (2001) Geographical heterogeneity between Far Eastern and Western countries in prevalence of the virulence plasmid, the superantigen Yersinia pseudotuberculosis -derived mitogen, and the high-pathogenicity island among Yersinia pseudotuberculosis strains.
Patient fibroblasts showed decreased levels of the MRPS2 protein, as well as decreased levels of certain other MRPS proteins and the mt-DNA-encoded 12S rRNA, which are part of the smaller mitochondrial-specific ribosomal subunit 28S (mt-SSU). Complexome profiling of mitochondrial extracts from patient cells showed impaired assembly of the mt-SSU, resulting in a lack of functional mitoribosomes, inhibition of mitochondrial translation, and multiple deficiencies of the oxidative phosphorylation enzymes (OXPHOS).
Clinical Features Shohat et al. (1993) described a preterm (28 weeks) female fetus with a 'new' lethal skeletal dysplasia characterized by distinctive epiphyseal stippling, periosteal cloaking, and unusual microscopic morphology.
Pacman dysplasia Other names Epiphyseal stippling with osteoclastic hyperplasia Pacman dysplasia is inherited in an autosomal recessive manner Pacman dysplasia is a lethal autosomal recessive skeletal dysplasia . The dysplasia is present during fetal development. [1] References [ edit ] ^ http://www.omim.org/entry/167220 Wilcox WR, Wenger DA, Lachman RS, Rimoin DL (2005). "Distinguishing Pacman dysplasia from mucolipidosis II: comment on Saul et al. [2005]". Am J Med Genet A . 135 (3): 333. doi : 10.1002/ajmg.a.30717 . PMID 15887286 . Saul RA, Proud V, Taylor HA, Leroy JG, Spranger J (2005). "Prenatal mucolipidosis type II (I-cell disease) can present as Pacman dysplasia".
A rare disorder characterized by epiphyseal stippling and osteoclastic overactivity. It has been described in less than 10 patients but may be underdiagnosed. It is characterized radiographically by severe stippling of the lower spine and long bones, and periosteal cloaking. Patients also have short metacarpals. The syndrome may be inherited as an autosomal recessive trait. This disorder should be included in the differential diagnosis of mucolipidosis type II.
"Ceruminous adenomas: a clinicopathologic study of 41 cases with a review of the literature". Am J Surg Pathol . 28 (3): 308–18. doi : 10.1097/00000478-200403000-00003 .
No mutations in ADGRG2 were found in 28 men with CBAVD and unilateral renal agenesis, suggestive of a different pathophysiologic mechanism in those cases.
Congenital bilateral absence of the vas deferens occurs in males when the tubes that carry sperm out of the testes (the vas deferens) fail to develop properly. Although the testes usually develop and function normally, sperm cannot be transported through the vas deferens to become part of semen. As a result, men with this condition are unable to father children (infertile) unless they use assisted reproductive technologies. This condition has not been reported to affect sex drive or sexual performance. This condition can occur alone or as a sign of cystic fibrosis, an inherited disease of the mucus glands.
A number sign (#) is used with this entry because at least one form of congenital bilateral aplasia of the vas deferens (CBAVD) is caused by homozygous or compound heterozygous mutation in the cystic fibrosis transmembrane conductance regulator gene (CFTR; 602421) on chromosome 7q31. Mutations in the same gene cause cystic fibrosis (219700). Description Congenital bilateral absence of the vas deferens is found in more than 25% of men with obstructive azoospermia, involving a complete or partial defect of the Wolffian duct derivatives. In 80% of men with CBAVD, mutations are identified in the CFTR gene (summary by Patat et al., 2016). Genetic Heterogeneity of Congenital Bilateral Aplasia of Vas Deferens Also see CBAVDX (300985), caused by mutation in the ADGRG2 gene (300572). Clinical Features Congenital bilateral aplasia of the vas deferens (CBAVD), which leads to male infertility, may occur in isolation or as a manifestation of cystic fibrosis.
Congenital bilateral absence of the vas deferens (CBAVD) occurs in males when the tubes that carry sperm out of the testes (vas deferens) fail to develop properly. Although the testes usually develop and function normally, sperm cannot be transported through the vas deferens to become part of semen. As a result, men with this condition are unable to father children (infertile) unless they use assisted reproductive technologies. This condition has not been reported to affect sex drive or sexual performance. This condition can occur alone or as a sign of cystic fibrosis , an inherited disease of the mucus glands.
Congenital bilateral absence of the vas deferens (CBAVD) is a condition leading to male infertility. Epidemiology It accounts for 6% to 8% of cases of obstructive azoospermia and affects about 1/1,000 males. It is also found in 98% of males with cystic fibrosis. Clinical description Infertile patients with CBAVD produce small volumes of acidic sperm (<1 ml with a pH<7.0). Etiology In 1990, mutations in the CFTR gene (the causative gene for cystic fibrosis) were identified in 42% of patients in a population of infertile males with CBAVD, suggesting that CBAVD is a genital form of cystic fibrosis. Since then, an exhaustive analysis of the 27 exons of the CFTR gene has led to the classification of CBAVD patients into four groups: i) patients with two mutations in the CFTR gene (19%), ii) patients with one mutation in the CFTR gene and having the IVS8-5T allele in the trans position (33%), iii) patients with either a mutation in the CFTR gene or having the IVS8-5T allele (27%) and iv) patients with neither the IVS8-5T allele nor a mutation in the CFTR gene (21%).
A child with multiple anomalies, smooth muscle hamartoma, and familial paracentric inversion of chromosome 7q". J Am Acad Dermatol . 28 (2 Pt 2): 364–70. doi : 10.1016/0190-9622(93)70056-Y .
A number sign (#) is used with this entry because of evidence that congenital symmetric circumferential skin creases-2 (CSCSC2) is caused by heterozygous mutation in the MAPRE2 gene (605789) on chromosome 18q12. Description Congenital symmetric circumferential skin creases is characterized by the folding of excess skin, which leads to ringed creases, primarily of the limbs. Affected individuals also exhibit intellectual disability, cleft palate, and dysmorphic features (summary by Isrie et al., 2015). For a discussion of genetic heterogeneity of congenital symmetric circumferential skin creases, see CSCSC1 (156610). Clinical Features Tinsa et al. (2009) described a 9-year-old Tunisian boy, born of consanguineous parents, who had an increased number of deep skin creases of the limbs, mental retardation, seizures, and cleft palate.
A number sign (#) is used with this entry because of evidence that congenital symmetric circumferential skin creases-1 (CSCSC1) is caused by heterozygous mutation in the TUBB gene (191130) on chromosome 6p21. Description Congenital symmetric circumferential skin creases is characterized by the folding of excess skin, which leads to ringed creases, primarily of the limbs. Affected individuals also exhibit intellectual disability, cleft palate, and dysmorphic features (summary by Isrie et al., 2015). Genetic Heterogeneity of Congenital Symmetric Circumferential Skin Creases CSCSC2 (616734) is caused by mutation in the MAPRE2 gene (605789) on chromosome 18q12. Clinical Features Kunze and Riehm (1982) reported 3 families segregating multiple benign ring-shaped skin creases as an autosomal dominant trait.
Circumferential skin creases Kunze type (CSC-KT) is a rare congenital disorder that affects the skin, but can also affect other areas of the body. Babies with CSC-KT are born with excess skin that folds over to form thin rings (creases) that circle the arms and legs. CSC-KT was originally called the “Michelin tire baby syndrome” because of the similarity of the rings on the arms and legs to the cartoon mascot of the French company. The rings on the arms and legs are usually found on both sides of the body. These skin folds do not cause any problems and typically disappear naturally as the child grows.
A rare genetic disease characterized by benign circumferential skin creases, mainly on the limbs, due to folding of excess skin. The creases often improve spontaneously in childhood. Patients also exhibit variable degrees of intellectual disability, short stature, cleft palate, and facial dysmorphism (including epicanthal folds, microphthalmia, broad nasal bridge, low-set, posteriorly rotated ears, and microstomia, among others). Variable additional features have been reported, such as seizures, infantile hypotonia, hearing impairment, strabismus, and urogenital anomalies. Brain imaging may show hypoplastic corpus callosum or mildly dilated ventricles.
Other associated malformations seen in MRKH type 2 include upper urinary tract malformations (40% of cases), unilateral renal agenesis (23-28%; see this term), ectopia of one or both kidneys (17%; see this term), renal hypoplasia (4%), horseshoe kidney and hydronephrosis.
MURCS association stands for (MU)llerian, (R)enal, (C)ervicothoracic (S)omite abnormalities and is a developmental disorder that primarily affects the reproductive and urinary systems. Most individuals with MURCS association are female, although males can also have this condition. Females with MURCS association can have an absent or abnormally shaped uterus. In rare cases, the vagina is also affected. Both males and females with MURCS association can have absent or abnormally formed reproductive tubes (usually the fallopian tubes in females and the vas deferens in males), kidney abnormalities, and short stature (adult height of less than 5 feet). Additional symptoms might include fused spinal bones in the neck and upper back and hearing loss.
This article needs more links to other articles to help integrate it into the encyclopedia . Please help improve this article by adding links that are relevant to the context within the existing text. ( April 2014 ) ( Learn how and when to remove this template message ) MURCS association Other names Müllerian duct aplasia-renal dysplasia-cervical somite anomalies syndrome This condition can be inherited in an autosomal dominant manner(though not always) [1] Specialty Medical genetics MURCS association (a variant of Mayer-Rokitansky-Küster-Hauser syndrome ) is a very rare developmental disorder [2] that primarily affects the reproductive and urinary systems involving MU llerian agenesis , R enal agenesis , C ervicothoracic S omite abnormalities. [3] It affects only females. Contents 1 Genetics 2 Diagnosis 3 Treatment 4 Notes 5 References 6 External links Genetics [ edit ] Genetic heterogeneity is observed in MURCS association. [4] Diagnosis [ edit ] This section is empty. You can help by adding to it . ( August 2017 ) Treatment [ edit ] This section is empty. You can help by adding to it . ( August 2017 ) Notes [ edit ] ^ RESERVED, INSERM US14 -- ALL RIGHTS. of diseases=Mayer-Rokitansky-Kuster-Hauser-syndrome-type-2&title=Mayer-Rokitansky-Kuster-Hauser-syndrome-type-2&search=Disease_Search_Simple "Orphanet: Mayer Rokitansky Kuster Hauser syndrome type 2" Check |url= value ( help ) . www.orpha.net .
"Case analysis of purple urine-bag syndrome at a long-term care service in a community hospital" . Chang Gung Medical Journal . 28 (9): 636–642. PMID 16323555 . ^ Barlow, GB; Dickson JAS (March 1978).
Haplotype analysis suggested the presence of 2 founder mutations. In 28 affected and 22 healthy sibs from 22 unrelated Norwegian and Swedish families with ichthyosis prematurity syndrome, 13 of which had been previously studied by Klar et al. (2004), Melin et al. (2006) confirmed linkage to chromosome 9q33.3-q34.13 and refined the IPS haplotype to a 76-kb core region.
Ichthyosis prematurity syndrome Specialty Dermatology Ichthyosis prematurity syndrome ( IPS ) is a dermatological disease with known genetic causes. This syndrome is a rare subcategory of autosomal recessive congenital ichthyosis (ARCI). [1] It is associated with complications in the mid-trimester of a pregnancy leading to premature births. [2] Although most prevalent in individuals of Scandinavian origin, there have also been scattered cases in people of Japanese, Italian and Indian ethnicity. [1] [3] [4] This disorder is also referred to as ichthyosis congenital type IV. [1] Contents 1 Signs and symptoms 1.1 Premature birth 1.2 Thick caseous layer of skin 1.3 Desquamating skin 1.4 Respiratory problems 1.5 Eosinophilia 2 Genetics 2.1 Mode of inheritance 2.2 Genetic cause 3 Diagnosis 4 Treatment 5 Prognosis 6 Epidemiology 7 References 8 External links Signs and symptoms [ edit ] Eosinophils in peripheral blood The symptoms associated with the disorder are often confused for other dermatological disorders. The symptoms below are ones specifically associated with IPS. Premature birth [ edit ] Pregnancies that have a foetus affected with this syndrome are complicated because of polyhydramnion . Complications arise because of opaque amnionic fluid resulting from the shedding of skin. As a result, ultrasounds are difficult to conduct. [1] Triggered by the harsh environment in the uterus, delivery results around 30– 34 weeks of gestation (pregnancy) and the baby is born in prematurely. [1] Thick caseous layer of skin [ edit ] A white layer of thick scaly substance covers the surface of the skin of the infant.
Ichthyosis prematurity syndrome is a rare, syndromic congenital ichthyosis characterized by premature birth (at gestational weeks 30-32, in general) in addition to thick, caseous and desquamating epidermis, neonatal respiratory asphyxia, and persistent eosinophilia. After the perinatal period, a spontaneous improvement in the health of affected patients is observed and skin features (vernix caseosa-like scale) evolve into a mild presentation of flat follicular hyperkeratosis with atopy.
Disease onset occurred between the ages of 28 and 69 years and was characterized by lower proximal muscle weakness, usually followed by upper proximal muscle weakness.
Myasthenia gravis is a disorder that causes weakness of the skeletal muscles, which are muscles that the body uses for movement. The weakness most often starts in the muscles around the eyes, causing drooping of the eyelids (ptosis) and difficulty coordinating eye movements, which results in blurred or double vision. In a form of the disorder called ocular myasthenia, the weakness remains confined to the eye muscles. In most people with myasthenia gravis, however, additional muscles in the face and neck are affected. Affected individuals may have unusual facial expressions, difficulty holding up the head, speech impairment (dysarthria), and chewing and swallowing problems (dysphagia) that may lead to choking, gagging, or drooling.
Myasthenia gravis (MG; see 254200) is an autoimmune disease of the neuromuscular junction that is often found in association with other autoimmune disorders. Association studies using case-control designs, i.e., comparisons of unrelated patients and control subjects, had demonstrated an increased frequency of the extended HLA haplotype A1-B8-DR3 (8.1) in Caucasian MG patients with thymus hyperplasia, in women, and in patients with an early onset of disease (Fritze et al., 1974; Vieira et al., 1993; Machens et al., 1999). To reevaluate the association of HLA with MG in 656 patients with generalized disease, and to test linkage of HLA to MG with thymus hyperplasia, Giraud et al. (2001) studied transmission of parental alleles to MG offspring with thymus hyperplasia in simplex (single-case) families using the transmission/disequilibrium test (TDT) as a test of linkage. Their results indicated linkage of HLA to MG with thymus hyperplasia, defining a locus on chromosome 6p21.3 that they designated MYAS1. They found that DR3 and DR7, or closely linked genes, had opposing effects on MG phenotypes.
Tola et al. (1994) examined HLA antigens in 47 Italian patients with sporadic myasthenia gravis. The frequency of B8 and DR3 in patients was 19.1 and 27.3%, respectively, compared to 9.7 and 14.1% in controls. There was also an association between the B8 allele and early onset of generalized myasthenia gravis sustained by thymic hyperplasia. The DR1 antigen was found in 55% of patients with ocular myasthenia and in only 2.8% of patients with generalized myasthenia. DR3 was present in 50% of patients with concurrent autoimmune conditions and in only 4.54% of patients without a more generalized disorder of autoimmunity.
Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disease characterized by weakness of the skeletal muscles. Common symptoms include weakness of the muscles that control the eye and eyelid, facial expressions, chewing, talking, and swallowing. Weakness tends to increase during periods of activity and improve after periods of rest. The condition results from a defect in the transmission of nerve impulses to muscles, which is due to the presence of antibodies against acetylcholine . The exact reason this occurs is not known. Some cases have been linked to tumors in the thymus gland .
In some cases, the mother remains asymptomatic . [27] Diagnosis [ edit ] MG can be difficult to diagnose, as the symptoms can be subtle and hard to distinguish from both normal variants and other neurological disorders. [15] Three types of myasthenic symptoms in children can be distinguished: [28] Transient neonatal myasthenia occurs in 10 to 15% of babies born to mothers afflicted with the disorder, and disappears after a few weeks.
Overview Myasthenia gravis (my-us-THEE-nee-uh GRAY-vis) causes muscles under your voluntary control to feel weak and get tired quickly. This happens when the communication between nerves and muscles breaks down. There's no cure for myasthenia gravis. Treatment can help with symptoms. These symptoms can include weakness of arm or leg muscles, double vision, drooping eyelids, and problems with speaking, chewing, swallowing and breathing. This disease can affect people of any age, but it's more common in women younger than 40 and in men older than 60.
Myasthenia gravis (MG) is a rare, clinically heterogeneous, autoimmune disorder of the neuromuscular junction characterized by fatigable weakness of voluntary muscles. Epidemiology The prevalence is estimated to be 1/5,000 and the incidence to be 1/250,000 to 1/33,000 in Europe. MG affects both males and females: mainly females before the age of 40 years and males and females equally after the age of 50 years. Clinical description Myasthenia gravis can develop at any age but there is a bimodal peak in the age of onset in the adult-onset form, with primarily female patients before 40 years of age, and primarily males after 50 years of age (adult-onset myasthenia gravis; see this term). Patients have fluctuating weakness, worsening with repetitive activities, heat and stress while improving with rest and with involvement of skeletal muscle groups of ocular, bulbar, extremities and neck.
Acatalasemia is a condition characterized by very low levels of an enzyme called catalase. Many people with acatalasemia never have any health problems related to the condition and are diagnosed because they have affected family members. Some of the first reported individuals with acatalasemia developed open sores (ulcers) inside the mouth that led to the death of soft tissue (gangrene). When mouth ulcers and gangrene occur with acatalasemia, the condition is known as Takahara disease. These complications are rarely seen in more recent cases of acatalasemia, probably because of improvements in oral hygiene.
A rare congenital disorder resulting from a deficiency in erythrocyte catalase, an enzyme responsible for the breakdown of hydrogen peroxide. Epidemiology The disorder is very rare in the general population with an estimated prevalence of 1 in 31250. Clinical description The disorder is usually asymptomatic but may be associated with oral ulcerations and gangrene, or diabetes mellitus and atherosclerosis in certain populations. Genetic counseling Transmission is autosomal recessive.
A number sign (#) is used with this entry because acatalasemia is caused by homozygous mutation in the CAT gene (115500) on chromosome 11p13. Description Acatalasemia, also known as acatalasia, is a metabolic disorder characterized by a total or near total loss of catalase activity in erythrocytes. About half of cases originate from ulcerating oral gangrenes, and these cases are referred to as having Takahara disease. Half-normal levels of catalase in heterozygotes is referred to as hypocatalasemia or hypocatalasia (Ogata, 1991). Clinical Features Acatalasemia was first discovered in Japan by Takahara, an otolaryngologist who found that in cases of progressive oral gangrene, hydrogen peroxide applied to the ulcerated areas did not froth in the usual manner (Takahara and Miyamoto, 1948).
.: "I read it somewhere," "Somebody must have told me," etc.). [27] Diagnostic tests [ edit ] Wisconsin Card Sorting Test (WCST) [ edit ] The Wisconsin Card Sorting Test is widely used in clinical settings to test for cognitive impairments, such as frontal lobe disorder which has been associated with source amnesia. [28] Procedure The visuo-spatial component of this test is devised of two sets of 12 identical cards. ... The goal is to say as many different words possible that begin with the given letter. [28] Results The Verbal fluency test can assess for damage in the prefrontal lobes, which has been associated with patients suffering from source amnesia. ... These memory impairments may be due to degeneration of the frontal lobe and other age related changes. [28] It is very common for older adults to experience increased source amnesia for memories compared to younger adults. ... Psychological Bulletin . 95 (1): 3–28. doi : 10.1037/0033-2909.95.1.3 . ... Psychological Bulletin . 114 (1): 3–28. doi : 10.1037/0033-2909.114.1.3 .
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Campaign for Homosexual Equality Homosexual Law Reform Society Gay Liberation Front Gay Rights Working Party Order of Chaeronea History Topics Timeline List of politicians First LGBT officeholders Violence against LGBT people HIV/AIDS crisis Death penalty Timeline 342 MSM activity made illegal 1533 Death penalty introduced for MSM activity 1543 Buggery Act extended to Wales 1828 Offences Against the Person Act 1828 1835 James Pratt and John Smith executed 1861 Death penalty for buggery abolished 1885 Labouchere Amendment introduced 1889 Cleveland Street scandal 1895 Oscar Wilde found guilty of gross indecency 1912 The Cave of the Golden Calf opens 1921 Plans to make lesbian activity illegal defeated 1936 Mark Weston transitions 1952 John Nott-Bower begins crackdown 1954 Pitt-Rivers , Montagu , Wildeblood imprisoned 1954 Alan Turing commits suicide 1957 Wolfenden report released 1967 MSM activity made legal (England & Wales) 1972 First British Gay Pride Rally 1976 Jeremy Thorpe resigns as Liberal leader 1981 MSM activity made legal (Scotland) 1981 First case of AIDS reported in the UK 1982 MSM activity made legal ( NI ) 1983 Gay men barred from donating blood 1984 Chris Smith elected as first openly gay MP 1987 Operation Spanner begins 1988 Section 28 comes into force 1989 Stonewall UK forms 1994 Age of consent for MSM becomes 18 1997 Angela Eagle becomes first openly lesbian MP 1998 Bolton 7 found guilty 1998 Lord Alli becomes first openly gay Lord 1999 Admiral Duncan bombing 2000 Gay men allowed in HM Armed Forces 2001 Age of consent equalised to 16 2001 MSM activity involving multiple men legal 2002 Same sex couples granted equal rights to adopt 2003 Section 28 repealed 2004 Civil partnerships introduced 2004 Gender Recognition Act 2004 2006 Discrimination made illegal 2008 Equalised access to IVF for lesbian couples 2008 Incitement to homophobic hatred made a crime 2009 Public apology to Alan Turing 2010 Equality Act 2010 2011 Gay men allowed to donate blood (1 yr deferral) 2013 Nikki Sinclaire becomes first openly trans MEP 2013 Marriage (Same Sex Couples) Act 2013 2014 First same-sex marriages take place 2016 MSM activity not grounds for military discharge 2017 Turing law implemented 2017 Blood donation deferral 3 months (excl. ... In October 2018, the Terrence Higgins Trust established the Mags Portman PrEP Access Fund to provide PrEP to those in England and Northern Ireland who cannot afford it. [25] The fund has a maximum size of 1,000 users and will be available until the end of 2020. [26] Timeline [ edit ] 1979, June: a sample shows a UK transmission to a haemophiliac in the UK. [27] 1981, 12 December: A 49-year-old man dies in Brompton hospital due to an AIDS related illness - the first death in the UK. [28] [29] He was homosexual and frequent visitor to the United States. [30] 1982, 4 July: Terry Higgins dies of an AIDS related illness - leading to the establishment of the Terrence Higgins Trust . [31] [32] 1987, 9 April: Diana, Princess of Wales , opens a new ward at Middlesex Hospital for the treatment of HIV patients, shaking the hands of AIDS patients without wearing gloves. [33] [34] [35] 1987: The UK Government launched " AIDS: Don't Die of Ignorance ", a major public information campaign. ... Retrieved 2017-08-29 . ^ "Free HIV treatment on NHS for foreign nationals" . BBC News . 2012-02-28 . Retrieved 2017-08-29 . ^ "Ready to Be Tested?
