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Ametropic Amblyopia Wikipedia

This article is an orphan , as no other articles link to it . Please introduce links to this page from related articles ; try the Find link tool for suggestions. ( April 2014 ) Ametropic amblyopia Human eye anatomy(retina) Specialty Neurology Ametropic amblyopia , is a medical condition in which the retina cannot focus on the image of a distant object, a condition often described as reduced visual acuity.

PTPN11
Urogenital Pelvic Malignancy Wikipedia

This article is an orphan , as no other articles link to it . Please introduce links to this page from related articles ; try the Find link tool for suggestions. ( May 2011 ) This article needs additional citations for verification .
Apple Scab Wikipedia

Under optimal conditions, this cycle may repeat every 1–2 weeks during the growing season. [4] At the end of the season, heavily-infected fruit and foliage fall from the canopy, allowing for the development of pseuothecia , which serve as a source of primary inoculum for the next spring. [5] The reproductive conidia of Venturia inaequalis erupting through the cuticle of a crabapple leaf. Predicting infection [ edit ] First developed in 1944 by American plant pathologist, W.D. ... The most notable revision was made in 1989 by plant pathologists William MacHardy and David Gadoury, who determined that ascospores required 3 hours less than originally calculated in order to establish a new infection. [10] While other methods of prediction include ascospore maturation models and leaf orchard leaf canopy models, the Mills Table, combined with electronic weather monitoring, remains the most-widely used tool for predicting apple scab infection periods. [7] Management of apple scab [ edit ] Cultural controls [ edit ] Cultural controls may be used as a first step when seeking to reduce the incidence of new infections . ... As water triggers ascospore release and promotes germination on vulnerable tissue, growers are advised to monitor watering periods and avoid using overhead watering systems. ... As such, fungicides are typically applied early in the season, when ascospores are first released. [5] However, fungicide applications may also be made later in the season to prevent infection of old leaves, which can help reduce the amount of primary inoculum for the following season. [11] Benzimidazole fungicides are among the most commonly-used classes of fungicide for managing apple scab in conventional orchards; however, there is some evidence that the disease is developing resistance to this class of fungicides, along with several others, including demethylation inhibitors and quinone outside inhibitors . [12] To manage the development of fungicide resistance, growers can reduce the number of applications made throughout the season and alternate between different classes of fungicide. [7] In organic production systems, growers commonly use copper- or sulfur-based protectant sprays to reduce the efficacy of primary inoculum. ... This was indicated in a 2015 study, which found that applications of C. cladosporioides could reduce leaf scab incidence by 42-98% and apple scab incidence by 41-94% in both conventionally and organically managed orchards. [17] Resistance breeding programs [ edit ] The first formal resistance breeding programs for apple scab began in the early 20th century with the development of the PRI Apple Breeding Program by Purdue University , Rutgers University , and the University of Illinois .
Oculocutaneous Albinism Type 4 Gene_reviews

Individuals with OCA4 are usually recognized within the first year of life because of hypopigmentation of the hair and skin and the ocular features of nystagmus and strabismus. ... In some individuals pigmentation increases during the first decade of life [Suzuki & Tomita 2008]. ... Variants may include small intragenic deletions/insertions and missense, nonsense, and splice site variants; typically, exon or whole-gene deletions/duplications are not detected. ... Individuals with albinism (including OCA4) are usually recognized within the first year of life because of the ocular features of nystagmus and strabismus. ... Recently, a family with autosomal dominant OCA4 has been reported [Oki et al 2017], with a novel heterozygous pathogenic variant: c.208T>C (p.Tyr70His).

SLC45A2
- Albinism, Oculocutaneous, Type Iv Omim
  
  A number sign (#) is used with this entry because oculocutaneous albinism type IV (OCA4) is caused by homozygous or compound heterozygous mutation in the MATP gene (SLC45A2; 606202) on chromosome 5p13. For a general phenotypic description and a discussion of genetic heterogeneity of oculocutaneous albinism, see OCA1 (203100). Clinical Features Newton et al. (2001) reported a Turkish patient with generalized hypopigmentation and ocular abnormalities consistent with OCA. He had white hair, pale skin, and translucent blue-gray irides. The phenotype was reminiscent of the relatively mild OCA2 (203200). Inagaki et al. (2004) reported Japanese patients with OCA4. Hair color ranged from white to yellow to brown, and iris color ranged from blue to brown.
- Oculocutaneous Albinism Type 4 Orphanet
  
  Clinical description Cutaneous hypopigmentation is often visible at birth and signs of nystagmus and strabismus present in the first year of life. Nystagmus is not always present at birth and can develop at 3 to 4 months of age.
Aging Omim

The 414T-G transversion occurred in the middle of the promoter for mtDNA H-strand replication primer synthesis and L-transcription, at a position immediately adjacent to a segment with high affinity for mitochondrial transcription factor A (TFAM; 600438). ... DNA damage is markedly increased in the promoters of genes with reduced expression in the aged cortex. Moreover, these gene promoters are selectively damaged by oxidative stress in cultured human neurons, and show reduced base-excision DNA repair.
Candida Hypersensitivity Wikipedia

Candida hypersensitivity systemic candidiasis, chronic candidiasis Pseudomedical diagnosis Risks Nocebo This article is part of a series on Alternative medicine General information Alternative medicine Alternative veterinary medicine Quackery (Health fraud) History of alternative medicine Rise of modern medicine Pseudoscience Antiscience Skepticism Skeptical movement National Center for Complementary and Integrative Health Terminology of alternative medicine Therapeutic nihilism Fringe medicine and science Acupressure Acupuncture Alkaline diet Anthroposophic medicine Apitherapy Applied kinesiology Aromatherapy Auriculotherapy Bates method Black salve Bodywork Bonesetter Bowen technique Breathwork Fake COVID-19 treatments Cancer treatments Charcoal cleanse Chiropractic Chiropractic treatment techniques Vertebral subluxation Christian Science Chromotherapy Colon cleansing Coffee enema Colorpuncture Colloidal silver Craniosacral therapy Crystal healing Cupping therapy Dental amalgam controversy Detoxification Foot detox Ear candling Energy medicine Esoteric energy Therapeutic touch Fabunan Antiviral Injection Facilitated communication Feldenkrais Method Functional medicine Hair analysis Herbal medicine Holistic dentistry Hologram bracelet Homeopathy Bach flower remedies Biological terrain assessment Hypnotherapy Iridology Ionized jewelry Jilly Juice Lightning Process Lymphotherapy Medical intuitive Mesmerism Magnet therapy Manual therapy Megavitamin therapy Mind–body interventions MMS Myofascial release NAET Naturopathy Oil pulling Orgone Orthomolecular medicine Orthopathy Osteomyology Osteopathy Ozone therapy Parapsychology Phrenology Psychic surgery Psychodermatology Radionics Rapid prompting method RBOP Reiki Reflexology Rolfing Scientific racism ThetaHealing Thought Field Therapy Urophagia Vaginal steaming Vision therapy Vitalism Young blood transfusion Zero balancing Conspiracy theories ( list ) Big Pharma conspiracy theory HIV/AIDS denialism OPV AIDS hypothesis Anti-vaccination Vaccines and autism MMR vaccine and autism Water fluoridation controversy GMO conspiracy theories Misinformation related to the COVID-19 pandemic Classifications Alternative medical systems Mind–body intervention Biologically-based therapy Manipulative methods Energy therapy Traditional medicine African Muti Southern Africa Ayurveda Ayurvedic acupressure Dosha Maharishi Vedic Approach to Health Balneotherapy Brazilian Bush medicine Cambodian Chinese Blood stasis Chinese herbology Dit Da Gua sha Gill plate trade Meridian Moxibustion Pressure point Qi San Jiao Tui na Zang-fu Chumash Curandero Faith healing Iranian Jamu Kambo Japanese Korean Mien Shiang Mongolian Prophetic medicine Shamanism Shiatsu Siddha Sri Lankan Thai massage Tibetan Unani Vietnamese Diagnoses Adrenal fatigue Aerotoxic syndrome Candida hypersensitivity Chronic Lyme disease Electromagnetic hypersensitivity Heavy legs Leaky gut syndrome Multiple chemical sensitivity Wilson's temperature syndrome v t e Candida hypersensitivity is a pseudoscientific disease promoted by William G. Crook, M.D. [1] It is spuriously claimed that chronic yeast infections are responsible for many common disorders and non-specific symptoms including fatigue , weight gain , constipation , dizziness , muscle and joint pain , asthma , and others. [2] Contents 1 Background 2 Symptoms 3 Criticism 4 Legal action 5 See also 6 References Background [ edit ] Candida albicans is a fungus that colonizes a large majority of the population (meaning it is present in the body but not causing an infection or any problems). ... Because allergic symptoms can be influenced by many factors, including emotions, experiments must be designed to separate the effects of the procedure being tested from the effects of other factors. [4] [6] By 2005, scientists were taking note of "a large pseudoscientific cult" [7] that had developed around the topic of yeast infections , with claims that up to one in three people were affected by yeast-related illnesses including Candida hypersensitivity. [4] Legal action [ edit ] Some practitioners of alternative medicine have promoted dietary supplements as supposed cures for this non-existent illness, rendering themselves liable to prosecution. [4] [8] In 1990, alternative health vendor Nature's Way signed a FTC consent agreement not to misrepresent in advertising any self-diagnostic test concerning yeast conditions or to make any unsubstantiated representation concerning any food or supplement's ability to control yeast conditions, with a fine of US$30,000 payable to the National Institutes of Health for research in genuine candidiasis. [8] See also [ edit ] List of topics characterized as pseudoscience References [ edit ] ^ Crook, William G. (1986). ... Retrieved 18 January 2014 . v t e Pseudoscience Terminology Cargo cult science Charlatan Crank Fringe theory Fringe science Pseudoarchaeology Pseudohistory Junk science Paranormal Pathological science Quackery Snake oil Crocodile oil Superseded scientific theory True-believer syndrome Voodoo Science Topics characterized as pseudoscience 2012 phenomenon Acupuncture Adrenal fatigue Alchemy Alternative medicine Ancient astronauts Anthroposophic medicine Applied kinesiology Aquatic ape hypothesis Astrology Bates method Biodynamic agriculture Biorhythms Bloodletting Body memory Catastrophism Chiropractic Chromotherapy Conspiracy theory 5G conspiracy 9/11 conspiracy theories Chemtrail conspiracy theory Climate change denial Misinformation related to the COVID-19 pandemic Moon landing conspiracy theories Conversion therapy Correactology Creation science Cryonics Cryptozoology Crystal healing Cupping Detoxification Colon cleansing Dianetics Doctrine of signatures Doktor Koster's Antigaspills Dowsing Ear candling Electromagnetic hypersensitivity Electronic voice phenomenon Eugenics Facilitated communication Feng shui Flat Earth theory Germ theory denialism Graphology HIV/AIDS denialism Hollow Earth theory Homeopathy Humorism Indigo children Intelligent design Japhetic theory Levitation Lunar effect Lysenkoism Magnet therapy Mediumship Miracle Mineral Supplement Naturopathy Nazi archaeology Nibiru cataclysm Numerology Orgone Palmistry Panchagavya Patent medicine Perpetual motion Phrenology Polygraph Primal therapy Pseudoarchaeology Pseudohistory Genocide denial Historical negationism Holocaust denial Pseudoscientific metrology Psychohistory Quantum mysticism Rapid prompting method Recovered-memory therapy Reiki Scientific racism Aryan race Melanin theory Statement analysis Trepanning Ufology Vertebral subluxation Voice stress analysis Water memory Promoters of pseudoscience Sucharit Bhakdi Deepak Chopra Gaia, Inc.
Simple-Type Schizophrenia Wikipedia

Occurrence of this type of paresis is altogether uncommon (Lishman 1998). [8] Diagnosis [ edit ] Classification [ edit ] ICD [ edit ] The WHO first listed the condition in the 6th revision of the International Classification of Diseases ICD-6 (1949) and it stayed in the manual until the present version ICD-10 . [9] ICD-9 [ edit ] The ICD-9 simple-type schizophrenia description: A psychosis in which there is insidious development of oddities of conduct , inability to meet the demands of society , and decline in total performance. ... In the ICD-11, there is no longer a diagnostic category of simple schizophrenia, and all subtypes of schizophrenia have been eliminated. [2] [9] [13] DSM [ edit ] Simple-type schizophrenia also appeared in the first two editions of the DSM as an official diagnosis: [9] This psychosis is characterized chiefly by a slow and insidious reduction of external attachments and interests and by apathy and indifference leading to impoverishment of interpersonal relations, mental deterioration, and adjustment on a lower level of functioning. ... Appendix B: Criteria Sets and Axes Provided for Further Study. [3] Treatment [ edit ] The use of antipsychotic medication is commonly the first line of treatment; however, the effectiveness after treatment is in question. ... National Institute of Health), Paul Harrison (University Department of Psychiatry Oxford) - Schizophrenia - 736 pages John Wiley & Sons, 13 Jul 2011 Retrieved 2012-01-22 ISBN 1-4443-4774-8 ^ Jean-Etienne-Dominique Esquirol - Des maladies mentales considerées sous les rapports médical, hygiènique et médico-légal Chez J. ... Weinberger - Chief, Clinical Brain Disorders Branch Intramural Research Program [1] Retrieved 2012-01-31 ^ Ben Green 2009 - Problem-Based Psychiatry - 253 pages Radcliffe Publishing, 2009 Retrieved 2012-01-22 ISBN 1-84619-042-8 ^ John Cutting, Michael Shepherd: The clinical roots of the schizophrenia concept.
Panic Attacks And Panic Disorder Mayo_clinic

Psychotherapy Psychotherapy, also called talk therapy, is considered an effective first choice treatment for panic attacks and panic disorder. ... Generally safe with a low risk of serious side effects, SSRI antidepressants are typically recommended as the first choice of medications to treat panic attacks. ... Keep in mind that it can take several weeks after first starting a medication to notice an improvement in symptoms. ... Questions to ask your primary care provider at your first appointment What do you believe is causing my symptoms? ... Are there any brochures or other printed material that I can have? What websites do you recommend? Don't hesitate to ask any other questions.
Sudden Infant Death Syndrome Omim

The 50% male excess was consistent with an X-linked dominant allele that is protective of terminal hypoxia, with a frequency of approximately 33%. ... Furthermore, in 8 of the families with 1 parent who had prolonged QT, 9 of the 23 sibs also had prolonged QT interval, consistent with an autosomal dominant pattern of inheritance. However, the Maron report did not have measurements of QT in the SIDS victims. ... Narita et al. (2001) examined the long/short promoter polymorphism of the SLC6A4 gene (182138.0001) in Japanese SIDS cases and found an excess of the L/L genotype and L allele in the SIDS group relative to controls. Weese-Mayer et al. (2003) investigated this variable tandem repeat sequence polymorphism in the promoter region in a cohort of 87 SIDS cases (43 African American and 44 Caucasian) and gender/ethnicity-matched controls.

SLC6A4, SCN5A, CAV3, KCNJ8, ACADM, MAOA, PHOX2B, AQP4, FEV, SCN1B, CHRNA7, CHRNB2, VHL, KCNQ1, ADCYAP1, IL10, IDS, KCNH2, IL6, LOC110806262, KLF6, IL1B, PSMG1, RYR2, DUSP2, ADCYAP1R1, SLC9A3, IL1A, IL1RN, GSTT1, C4B, TAC1, TNF, TGFB1, HSPD1, TH, SLC6A3, TSPYL1, VEGFA, CASP3, CHAT, VIPR1, CXCL8, GPD1L, MZB1, TPH2, MYD88, KCNK3, CYP2C9, CYP2C19, GSTM1, CYP2C18, HCRT, G6PC, FUT2, SLC5A5, C4A, CYP2D6, UCP1, DMBT1, EPHX2, TLR4, FGFR3, FMO3, SLC22A5, TACR1, FOS, SLC37A4, SULT1A1, SSTR2, SOD2, SNTA1, VIP, HSP90AA1, TRPV1, HSPA14, LOC107987479, MALAT1, PTF1A, OR2AG1, CYP2B6, PRRT2, AP1AR, TNFRSF17, HPGDS, SFTPD, B3GAT1, SETBP1, CYP2C8, CD160, SRA1, NOS1AP, ZBED1, BDNF, SI, SEA, HSPA4, APOE, FAS, CD14, KCND3, KCNA5, KCNA4, IREB2, HADHA, CHRNA4, IL4, HIF1A, HMOX1, IGHMBP2, IFNG, IFNA13, IFNA1, HSPA1B, HTR2A, HTR1A, HTC2, KCNJ10, ATF4, CASP9, PRF1, SCN4A, GFI1, SCN1A, GJA1, RPS27A, PRNP, PRKCB, PRKCA, POMC, CYP4F3, PIK3CA, P2RY1, CYP1A1, TRNL1, ND1, MIF, MBL2, GNB3, CPT1A
- Sudden Infant Death Syndrome Gard
  
  Sudden infant death syndrome (SIDS) is the unexpected, sudden death of a child under age 1 which cannot be explained after a thorough investigation is conducted. Infants who are affected by the condition generally appear healthy with no suspicious signs and symptoms prior to the incident. It is the leading cause of death in infants age 1 to 12 months old. The exact underlying cause of SIDS is unknown; however, scientists suspect that it is likely a multifactorial condition (associated with the effects of multiple genes in combination with lifestyle and environmental factors). Although there is no guaranteed way to prevent SIDS, the American Academy of Pediatrics has a published list of recommendations for risk reduction. Please click on the link to access this resource.
- Sudden Infant Death Syndrome Wikipedia
  
  They are not recommended for children under one year of age as this risk of suffocation greatly outweighs the risk of head bumping or limbs getting stuck in the bars of the crib. [5] Sharing a bed with parents or siblings increases the risk for SIDS. [29] This risk is greatest in the first three months of life, when the mattress is soft, when one or more persons share the infant's bed, especially when the bed partners are using drugs or alcohol or are smoking. [5] The risk remains, however, even in parents who do not smoke or use drugs. [30] The American Academy of Pediatrics thus recommends "room-sharing without bed-sharing", stating that such an arrangement can decrease the risk of SIDS by up to 50%. ... SIDS incidence rises from zero at birth, is highest from two to four months of age, and declines toward zero after the infant's first year. [39] Genetics [ edit ] Genetics plays a role, as SIDS is more prevalent in males. [40] [41] There is a consistent 50% male excess in SIDS per 1000 live births of each sex. ... The X-linkage hypothesis for SIDS and the male excess in infant mortality have shown that the 50% male excess could be related to a dominant X-linked allele , occurring with a frequency of 1 ⁄ 3 that is protective of transient cerebral anoxia . ... The incidence of SIDS has fallen in a number of countries in which this recommendation has been widely adopted. [68] Sleeping on the back does not appear to increase the risk of choking even in those with gastroesophageal reflux disease . [5] While infants in this position may sleep more lightly this is not harmful. [5] Sharing the same room as one's parents but in a different bed may decrease the risk by half. [5] Pacifiers [ edit ] The use of pacifiers appears to decrease the risk of SIDS although the reason is unclear. [5] The American Academy of Pediatrics considers pacifier use to prevent SIDS to be reasonable. [5] Pacifiers do not appear to affect breastfeeding in the first four months, even though this is a common misconception. [69] Bedding [ edit ] Product safety experts advise against using pillows, overly soft mattresses, sleep positioners, bumper pads (crib bumpers), stuffed animals, or fluffy bedding in the crib and recommend instead dressing the child warmly and keeping the crib "naked." [70] Blankets or other clothing should not be placed over a baby's head. [71] The use of a " baby sleep bag " or "sleep sack", a soft bag with holes for the baby's arms and head can be used as a type of bedding that warms the baby without covering its head. [72] Vaccination [ edit ] Higher rates of DTP immunization is associated with lower rates of SIDS supporting recommendations on timely DTP immunization. [73] Many other studies have also reached conclusions that vaccinations reduce the risk of SIDS. ... PMID 16818592 . ^ =1225 "About Statistics and the Law" =1225 Archived 2007-09-02 at the Wayback Machine (Website). Royal Statistical Society. (2001-10-23) Retrieved on 2007-09-22 ^ "Reduce the Risk of SIDS & Suffocation - AAP general recommendations" .
- Sudden Infant Death Syndrome (Sids) Mayo_clinic
  
  Be sure to use the back position every time you or anyone else puts your baby to sleep for the first year of life. Don't trust that others will place your baby to sleep in the correct position: Insist on it. ... And there are ways to help your baby sleep safely. For the first year, always place your baby to sleep on the back.
Autosomal Dominant Intermediate Charcot-Marie-Tooth Disease Type A Orphanet

It presents with usual clinical features of Charcot-Marie-Tooth disease (progressive muscle weakness and atrophy of the distal extremities, distal sensory loss, reduced or absent deep tendon reflexes, and feet deformities) in the first to second decade of life with steady progression until the fourth decade, severe progression and stabilization afterwards.

MAD2L1BP, KIF1B
- Charcot-Marie-Tooth Disease, Dominant Intermediate A Omim
  
  For a phenotypic description and a discussion of genetic heterogeneity of dominant intermediate CMT neuropathy, see CMTDIB (606482). Clinical Features Rossi et al. (1985) and Villanova et al. (1998) reported a large kinship in which 15 individuals, ranging in age from 7 to 72 years, had onset of slowly progressive CMT in the first or second decades of life. Patients presented with lower limb weakness, resulting in muscle cramps and difficulty walking and running. ... Inheritance The transmission pattern of CMTDIA in the family reported by Rossi et al. (1985) was consistent with autosomal dominant inheritance. Mapping In an Italian family with dominant intermediate CMT, described earlier by Rossi et al. (1985) and Villanova et al. (1998), Verhoeven et al. (2001) demonstrated linkage to chromosome 10q24.1-q25.1. Sural nerve biopsy in affected members of this family showed axonal degeneration, loss of large diameter fibers, rare segmental demyelination, and remyelination with onion bulb formation. INHERITANCE - Autosomal dominant SKELETAL Feet - Pes cavus NEUROLOGIC Peripheral Nervous System - Distal limb muscle weakness due to peripheral neuropathy - Distal limb muscle atrophy due to peripheral neuropathy - Muscles cramps - 'Steppage' gait - Foot drop - Hyporeflexia - Areflexia - Distal sensory impairment - Low to normal range of motor nerve conduction velocity (NCV) (25-45 m/s) - Axonal degeneration/regeneration on nerve biopsy - Segmental demyelination/remyelination - Rare 'onion bulb' formations MISCELLANEOUS - Onset in second decade - Begins in feet and legs (peroneal distribution) - Upper limb involvement occurs later - Rapid disease progression from ages 40 to 50 years - Features intermediate between demyelinating CMT and axonal CMT - Genetic heterogeneity (see, e.g., CMTDIB 606482 , CMTDID 607791 ) ▲ Close
Cataract 17, Multiple Types Omim

Willoughby et al. (2005) reported a large 3-generation family from the UK segregating autosomal dominant congenital cataract and microcornea. ... Wang et al. (2011) reported a 5-generation Chinese family segregating autosomal dominant congenital cataract and microcornea. ... All affected individuals showed cataract within the first year of life and had similar poor vision, ranging from 20/100 to 20/400. ... Inheritance The mode of inheritance of CTRCT17 is autosomal dominant in some families (see, e.g., Mackay et al., 2002) and autosomal recessive in others (see Cohen et al., 2007). Mapping In a family with autosomal dominant pulverulent cataract, Mackay et al. (2002) found that the disorder mapped to the beta-crystallin gene cluster on 22q11.2.

CRYBB1
Ovarian Hyperstimulation Syndrome Mayo_clinic

Preparing for your appointment Depending on how severe your ovarian hyperstimulation syndrome is, your first appointment may be with your primary care provider, your gynecologist or infertility specialist, or possibly with a treating doctor in the emergency room. ... List your most important questions first. Some basic questions to ask include: What's the most likely cause of my symptoms? ... Do you have any printed material or brochures I can take home with me? What websites do you recommend? Make sure that you completely understand everything that your provider tells you.

FSHR, NR1H3, DRD2, VEGFA, BRD2, AMH, CGB8, CGB5, LHCGR, KDR, CGA, CGB3, CYP19A1, BMP15, HTC2, IL2, IL18, STAR, SERPINF1, FLT1, F2, MTHFR, CYP11A1, PROC, KISS1R, PGR, PROK1, PLG, IL23A, CHST3, PCOS1, TNF, ARTN, SOCS1, THBS1, ZNF217, CLDN5, VWF, PTGS2, AGRP, MCL1, LPL, AMHR2, ANGPT2, AREG, CD44, CFTR, CISH, CRP, S1PR1, EDN1, EGR1, ERBB2, ESR2, F5, FLT4, HP, IGF2, IL6, CXCL8, IL11, IL17A, LEP, OCLN
- Ovarian Hyperstimulation Syndrome Orphanet
  
  A rare non-malformative gynecological disease affecting pre-menopausal women usually following treatment with ovarian stimulating hormones, characterized by ovarian enlargement and, to varying degrees, shift of serum from the intravascular space to the third space, mainly into the peritoneal, pleural, and to a lesser extent to the pericardial cavities. Presenting symptoms include abdomen distention, pain, nausea, and vomiting. Severity ranges from mild to life-threatening and is complicated by increased risk of thrombosis, acute hepato-renal failure, acute respiratory distress syndrome, and ovarian torsion and rupture.
- Ovarian Hyperstimulation Syndrome Omim
  
  In a 21-year-old Turkish woman who developed OHSS in the first trimester of her first pregnancy, previously described by Cepni et al. (2006), De Leener et al. (2008) identified heterozygosity for a mutation in the FSHR gene (S128Y; 136435.0013). Her beta-HCG level was normal for a 3-month singleton pregnancy, and her TSH (see 118850) level was normal; her symptoms regressed during the second and third trimester with conservative medical treatment, and resolved postpartum. INHERITANCE - Autosomal dominant ABDOMEN - Abdominal pain - Ascites Gastrointestinal - Nausea GENITOURINARY Internal Genitalia (Female) - Enlarged multilocular ovaries - Pathology shows multiple serous and hemorrhagic follicular cysts lined by luteinized cells ('hyperreactio luteinalis') - Ovaries return to normal size after delivery MISCELLANEOUS - Symptoms occur only during pregnancy (usual onset after 6 weeks gestation) - Major fluid shifts may occur in severe cases MOLECULAR BASIS - Caused by mutations in the follicle-stimulating hormone receptor gene (FSHR, 136435.0008 ) ▲ Close
- Ovarian Hyperstimulation Syndrome Wikipedia
  
  Typically, even in severe OHSS with a developing pregnancy, the duration does not exceed the first trimester. [ citation needed ] Cause [ edit ] Sporadic OHSS is very rare, and may have a genetic component. ... PMID 21450755 . ^ a b c d e f Textbook of Assisted Reproductive Techniques, Laboratory and Clinical Perspectives, edited by David K. Gardner, 2001 [ page needed ] ^ Severi, F.M.; Bocchi, C.; Vannuccini, S.; Petraglia, F. (2012).
Triple X Syndrome Mayo_clinic

What you can do Before your appointment, make a list of: Any signs or symptoms you've noticed in your child, including any that may seem unrelated to the reason for the appointment Your child's developmental milestones and when they were met, such as learning to say first words or learning to walk Key personal information about your pregnancy, including any significant illnesses you may have experienced or any medications that you may have used Any problems your child may be having with learning, emotions or behavior Questions to ask your child's health care provider Some basic questions to ask the health care provider include: What's the most likely cause of my child's symptoms? ... Are there any brochures or other printed materials that I can have? What websites do you recommend? Don't hesitate to ask any other questions during your appointment. ... Your health care provider may ask: When did you first notice your child's symptoms? Does anything seem to improve the symptoms?

SHOX, SRY, AMH, STS, ARSC2, ATM, CD38, CYBB, GDF9, GNRHR, MECP2, FIGLA
- Triple X Syndrome Medlineplus
  
  Triple X syndrome, also called trisomy X or 47,XXX, is characterized by the presence of an additional X chromosome in each of a female's cells. Although females with this condition may be taller than average, this chromosomal change typically causes no unusual physical features. Most females with triple X syndrome have normal sexual development and are able to conceive children. Triple X syndrome is associated with an increased risk of learning disabilities and delayed development of speech and language skills. Delayed development of motor skills (such as sitting and walking), weak muscle tone (hypotonia), and behavioral and emotional difficulties are also possible, but these characteristics vary widely among affected girls and women.
- Trisomy X Orphanet
  
  Trisomy X is a sex chromosome anomaly with a variable phenotype caused by the presence of an extra X chromosome in females (47,XXX instead of 46,XX). Epidemiology It is the most common female chromosomal abnormality occurring in approximately 1 in 1,000 female births. However, as most individuals are only mildly affected or asymptomatic, it is estimated that only 10% of individuals with trisomy X are actually diagnosed. Clinical description The most common physical features include tall stature, epicanthal folds, hypotonia and clinodactyly. Seizures, renal and genitourinary abnormalities, and premature ovarian failure (POF; see this term) are also associated findings.
- Triple X Syndrome Wikipedia
  
  Triple X syndrome Other names Triplo-X syndrome, trisomy X, XXX syndrome, 47,XXX syndrome [1] Increased distance between the eyes in a 9-year-old girl with trisomy X [2] Specialty Medical genetics Symptoms Taller than average [1] Complications Learning difficulties , decreased muscle tone , seizures , kidney problems [1] Causes Random event [1] Diagnostic method Chromosomal analysis [3] Treatment Speech therapy, physical therapy, counseling [3] Frequency 1 per 1,000 female births [2] Triple X syndrome , also known as trisomy X and 47,XXX , is characterized by the presence of an extra X chromosome in each cell of a female . [1] Those affected are often taller than average. [1] Usually there are no other physical differences and normal fertility . [1] Occasionally there are learning difficulties , decreased muscle tone , seizures , or kidney problems . [1] Triple X is due to a random event. [1] Triple X can result either during the division of the mother's reproductive cells or during division of cells during early development. [2] It is not typically inherited from one generation to the next. [1] A form where only a percentage of the body cells contain XXX can also occur. [1] Diagnosis is by chromosomal analysis . [3] Treatment may include speech therapy, physical therapy, and counseling . [3] It occurs in about one in every 1,000 female births. [2] It is estimated that 90% of those affected are not diagnosed as they either have no or only few symptoms. [2] It was first identified in 1959. [4] Contents 1 Signs and symptoms 1.1 Physical 1.2 Psychological 2 Cause 3 Diagnosis 4 Treatment 5 Epidemiology 6 History 7 References 8 External links Signs and symptoms Because the vast majority of triple X females are never diagnosed, it may be very difficult to make generalizations about the effects of this syndrome. ... On average, five to ten girls with triple X syndrome are born in the United States each day. [8] History The first published report of a woman with a 47,XXX karyotype was by Patricia A.
- 47 Xxx Syndrome Gard
  
  47 XXX syndrome , also called trisomy X or triple X syndrome, is characterized by the presence of an additional (third) X chromosome in each of a female's cells (which normally have two X chromosomes). An extra copy of the X chromosome is associated with tall stature, learning problems, and other features in some girls and women. Seizures or kidney abnormalities occur in about 10 percent of affected females. 47 XXX syndrome is usually caused by a random event during the formation of reproductive cells (eggs and sperm). An error in cell division called nondisjunction can result in reproductive cells with an abnormal number of chromosomes. Treatment typically focuses on specific symptoms, if present. Some females with 47 XXX syndrome have an extra X chromosome in only some of their cells; this is called 46,XX/47,XXX mosaicism .
Kawasaki Disease Mayo_clinic

With treatment, a child might start to improve soon after the first gamma globulin treatment. Without treatment, Kawasaki disease lasts about 12 days. ... Preparing for your appointment You'll probably first see your family health care provider or pediatrician. ... Can you give me brochures or other printed information? What websites do you recommend? Don't hesitate to ask additional questions.

FCGR2A, ITPKC, BLK, CD40, KCNN2, NEBL, MED30, MDGA1, ATP5MF, NAALADL2, FHAD1, TECRL, SLC35F5, ZSCAN25, CRP, CENPU, PTCD1, TNF, SGCD, MESP2, IL10, PREX1, LDLRAD3, ZNF618, IL6, IRF8, DAB1, ATP5MF-PTCD1, IL1A, IL1B, MIA, MIA-RAB4B, IL1RAP, FHAD1-AS1, BUD31, SETBP1, VEGFA, MMP9, IL18, CASP3, ALB, HLA-DRB1, IL4, IL1RN, ACE, PECAM1, IL17A, HSPD1, MIR223, ORAI1, SMAD3, IFNG, CCR5, MBL2, CD40LG, VCAM1, CD14, CD68, S100A9, NLRP3, RBM45, HMGB1, HAMP, HLA-B, HLA-C, CCL2, S100A12, GPT, CCL3L1, FCGR3B, FCGR2B, TNFRSF1A, CCR2, IL6ST, FOXP3, SEMA6A, HSPA14, GOPC, RETN, IL2RA, PTX3, MMP3, S100A8, ISG20, SLC11A1, SLC8A1, LTA, CCL5, MPO, SDC1, MEFV, IL2, MMP2, MIF, FBLIM1, IL1R1, TGFB2, CDR3, AIF1, TRIP10, VWF, CSF3, ABCC4, CYP2C9, NOD1, ESR1, FCN1, FLT1, TIMP2, LINC01194, TGFBR2, MIR145, HMOX1, TGFB1, HLA-A, HLA-DQA1, COPB2, CD209, IL22, CCL4L2, AIM2, STOML1, AMACR, KLRK1, POT1, SPATA2, MAP7, SPAG9, NMNAT2, PLCB1, SUCO, SOCS3, IL23A, ADA2, FCMR, PYCARD, WDR1, ATP6AP2, UTS2, HCP5, TNFSF13B, LILRB4, ADAMTS13, POSTN, GCA, ANP32B, FGF21, PHLPP1, SP140, TLR6, NLRP1, IL17D, TRBV6-5, ABO, ABCC11, TET2, MIR155, MIR222, MIR21, MIR200C, MIR186, MIR183, MIR182, MIR146A, LCE3B, MIR134, MIR125A, MIRLET7I, CCL4L1, IL31, PEAR1, MIR27A, MIR27B, MIR31, MIR320A, MIR371A, WG, TIFAB, MIR483, BRD7P2, MIR671, KIR2DS2, CD24, AD12, RPL17-C18orf32, KLRC4-KLRK1, MIR4515, MTCO2P12, LCE3C, NLRP14, PBK, CLEC7A, GGCT, VKORC1, WNK1, P2RY12, GORASP1, EBF2, CDH22, OR10A4, IL21, NLRC4, PELI1, CD177, BTNL2, MYDGF, NLRX1, GSDMD, ULBP1, ZBP1, SYTL1, CD84, NLRP12, CLEC6A, SFXN1, C1QTNF1, GRIN3A, LRG1, TPH2, HT, SAMD9L, IL27, CERS6, NR1I2, TAC1, TNFSF13, SMAD7, HP, HLA-G, HLA-E, HLA-DQB2, HLA-DPB1, HLA-DOB, HLA-DOA, HIF1A, HGF, GZMB, CXCL2, NR3C1, GLS, GLB1, KAT2A, HSD11B2, HSPA5, TNC, KDR, SMAD5, SMAD1, LDHA, KLRC1, KIR3DL2, KIR2DL2, ITPR3, ICAM1, INSR, IL15, IL12B, CXCL8, IL7, IGF1R, GATA3, GAPDH, FUT1, ANGPT1, CACNB2, VPS51, STS, AQP1, APOB, ANGPT2, AKT1, CAT, AGTR1, AGT, JAG1, AGER, ADM, ADA, CASP4, SEPTIN7, VEGFD, CYP2E1, FCER2, BPTF, ERBB2, EPHB2, ELN, ELAVL2, CTNNB1, CEACAM5, CTLA4, CCN2, MAPK14, COL11A2, CCR3, CHI3L1, SMAD6, MICB, BECN1, MMP11, TIMP4, TIMP1, THBD, TFRC, TRBV20OR9-2, ZEB1, TBXA2R, ACHE, SYT1, ABCC8, SULT1A1, STAT1, SRC, SNCA, SIX1, TLR1, TLR2, TLR4, VEGFC, NCOA1, FGF23, PLA2G7, ABHD16A, PRRC2A, SEMA3B, VDR, TNFAIP3, UCP2, TYK2, TNFRSF4, TNFSF4, TUBA3C, TP53, ST6GAL1, SELP, SELE, NGF, SERPINE1, OTX2, OLR1, NR4A2, NOTCH4, NOS2, NFATC2, PDE2A, NFATC1, NCAM1, MYO5B, COX2, MMP13, MMP12, PDCD1, PGK1, CCL17, PTGS2, CCL4, SCN3A, SAG, RPL17, RELA, NECTIN1, MAP2K7, SERPINA1, MAPK3, MAPK1, PRF1, PPARG, PPARD, PLCB4, LINC02605
- Kawasaki Disease Omim
  
  Several lines of evidence suggested the importance of genetic factors in disease susceptibility and outcome. First, the incidence of Kawasaki disease is 10 to 20 times higher in Japan than in Western countries (Cook et al., 1989). ... Based on a Japanese survey of parents of children with Kawasaki disease, Fujita et al. (1989) reported that within 1 year after the onset of the first case in a family, the overall second-case rate was 2.1% for sibs, compared to an overall incidence of approximately 0.19% in the general population of children 0 to 4 years of age.
- Kawasaki Disease Orphanet
  
  A rare inflammatory disease characterized by an acute febrile, systemic, self-limiting, medium-vessel vasculitis primarily affecting children. It often causes acute coronary arteritis which is associated with coronary arterial aneurysms (CAA) that may be life threatening when untreated. Epidemiology Although it has been reported worldwide, Kawasaki disease (KD) is over-expressed among Asian populations. In Europe, the annual incidence for children under 5 years of age ranges between 1/6,500-20,500. The disease is the most common cause of acquired heart disease in children in developed countries.
- Kawasaki Disease Medlineplus
  
  Kawasaki disease is a sudden and time-limited (acute) illness that affects infants and young children. Affected children develop a prolonged fever lasting several days, a skin rash, and swollen lymph nodes in the neck (cervical lymphadenopathy). They also develop redness in the whites of the eyes (conjunctivitis) and redness (erythema) of the lips, lining of the mouth (oral mucosa), tongue, palms of the hands, and soles of the feet. Without treatment, 15 to 25 percent of individuals with Kawasaki disease develop bulging and thinning of the walls of the arteries that supply blood to the heart muscle (coronary artery aneurysms) or other damage to the coronary arteries, which can be life-threatening. Frequency In the United States and other Western countries, Kawasaki disease occurs in approximately 1 in 10,000 children under 5 each year.
- Kawasaki Disease Gard
  
  Kawasaki disease is a disease that involves inflammation of the blood vessels. It is typically diagnosed in young children, but older children and adults can also develop this condition. Kawasaki disease begins with a fever that lasts at least five days. Other classic symptoms may include red eyes, lips, and mouth; rash; swollen and red hands and feet; and swollen lymph nodes. Sometimes the disease affects the coronary arteries which carry oxygen-rich blood to the heart, which can lead to serious heart problems. Kawasaki disease occurs most often in people of Asian and Pacific Island descent.
Soft Tissue Sarcoma Mayo_clinic

Types Symptoms A soft tissue sarcoma may not cause any symptoms at first. As the cancer grows, it may cause: A noticeable lump or swelling. ... Are there any brochures or other printed material that I can take with me? What websites do you recommend? Are there other specialists that I should meet with for my cancer? ... Questions might include: When did you first notice your symptoms? Are you experiencing pain?

TP53, SMARCA4, PIK3CA, CIC, MDM2, HRAS, PAX3, MDM4, TNF, RB1, CSF2, SOX2, NF1, MCL1, FLT4, JUN, MAML3, IFNG, ZNF667-AS1, PRAME, GSTP1, EWSR1, KIT, PDGFRA, CDKN2A, MLH1, PMS2, WT1, WRN, IL6, ATM, CHEK2, GNAS, SS18, DICER1, TBC1D9, CTNNB1, SYT1, FOXO1, CDK4, SMARCB1, PTEN, RAF1, SSX2, GDF5, ERBB2, SDHA, SDHB, SDHC, EGFR, ABCB1, CD274, BMPR1B, KRAS, DUX4, AKT1, MET, ALK, IGF1R, IGF1, C11orf65, CCNB3, CCND1, VEGFA, FUS, BCOR, BRAF, FLI1, HIF1A, YAP1, SSX2B, MYC, IGF2, ZHX2, ATF1, ERG, BCL2, KDR, SMUG1, PIK3CG, GLI1, PIK3CD, CD248, PIK3CB, BRCA2, CRP, DDIT3, CDKN1A, BRCA1, CD44, FN1, MSH2, MUC4, CD99, H3-3A, EGF, TFE3, NTRK1, RET, NFATC2, H3-3B, H3P10, PARP1, YWHAE, PATZ1, CD34, ETV4, PDCD1, PDGFB, MTOR, TSPAN31, MIR182, NRAS, DES, STAT3, CTAG1A, JAZF1, CAV1, NKX2-2, PTGS2, CD6, ASPSCR1, FOLH1, PROM1, EZR, VEGFC, PAX7, NANS, LAG3, SERPINE1, CTAG1B, COL1A1, TLE1, TERT, RASSF1, MYOG, PLIN1, NUTM1, FGFR4, NME1, HGF, UVRAG, VIM, CSF1R, STS, EZH2, LOC110806263, MAPK14, HTC2, COL18A1, CKAP4, 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ERCC1, CD82, ERCC5, C3CER1, POT1, SH2B1, KDM1A, RNF19A, CAMP, ZNF281, CBL, SUZ12, CASR, MGA, CRTC1, CASP3, LPAR3, MAPK8IP2, CASP9, SIRT1, POLDIP2, TARDBP, HEY1, CAPN6, KCNJ4, CALM3, ATRAID, PIWIL2, BTC, LAMTOR1, PTTG1IP, FEV, UGT1A1, KRT20, MOV10L1, CALB2, FGFRL1, TPPP3, GDE1, ISYNA1, CALD1, KLF3, CYFIP2, GP6, PHF11, TMED7, FOXP3, F11R, OBP2A, CALM1, NXT1, DROSHA, SIRT2, POLM, TNFRSF21, B3GAT1, CALM2, EML4, TUSC2, ATF6, GDF15, CLOCK, TCL1B, RGS6, ESPL1, SART3, CD28, HDAC4, PCLAF, KEAP1, MS4A1, MELK, RUSC2, NR1I3, CCS, CD14, EEF1E1, NAPSA, ADGRG2, ABCG2, ENDOU, CD63, CD47, GPRC5A, USP6, CD40, P2RX6, AURKB, PIWIL1, COPB2, KLF4, CD163, SLIT2, GRAP2, KCNK6, G3BP1, ZNF197, MMRN1, LYVE1, OS9, CCNE1, SLC27A5, TDRKH, CNMD, TOPBP1, ZWINT, CCND3, CCND2, DUSP12, FBXW7, CBX3, CHSY1, KRIT1, CCK, SUB1, HPSE, TRIM13, PLK2, TUBB3, MYL9, NDC80, CD247, CD3E, CD3D, CIB2, CIB1, ZNRD2, MRPL28, AHSA1, MYL12A, DCTN6, CD1D, NES, ZNF654, CMAS, LARP6, MIR127, ABCB5, C16orf96, TICAM2, GSTK1, XIAP, ANXA5, 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MPIG6B, PER2, BAP1, CDH11, PHF1, FRZB, ENPP2, FPR1, PGF, PGR, FOSB, SERPINB9, GAB1, MLANA, PLAGL1, PLAUR, PLD2, PLG, FHIT, FSHR, PDGFA, ESD, OPRM1, NPY1R, GPC3, GHRHR, NTRK3, GH1, ROR2, P4HB, GABRG2, PEBP1, GFAP, GCG, PAX5, GATA3, GAS6, GPC5, POU4F1, PPARG, EXTL3, PTX3, PVR, FABP3, RAC1, RAD51B, F2R, RARA, PPP1R1A, RASA1, ETV5, RBL2, RBP1, ESRRB, REST, PTPRG, PTPRC, PTPN11, ACSL3, ACSL4, PSMD9, PSMD4, FAU, FCGR3A, MAPK8, FCGR3B, FER, PRKDC, PRKAR1A, PRF1, FES, FGF1, GCLC, NPAS2, GLUL, CXCR2, MCM3, MDK, ING1, ILK, IL15, IL10, IL3RA, MMP8, MKI67, IL2RG, FOXO4, RBPJ, IGFBP7, MMP2, MCM2, ING2, MCAM, MAPT, MAGEA3, SMAD4, MAD2L1, LSS, LOX, LMNA, LGALS1, LEP, LCP1, LCK, CXCL10, ITGB3, JAK2, MMP3, IGFBP3, GSK3B, HIC1, MYL2, HSPB1, HNRNPM, HPRT1, HK2, NFATC1, HDGF, MMP11, NFKBIA, NGFR, H2AX, NMB, MSH6, NOS1, IRF8, MYCL, ID2, MXI1, MUC6, MUC1, MTTP, MTHFR, COX2, IDH2, IFI27, MST1, IFNA1, IFNA13, IGFALS, IGFBP2, MMP14, ESR2, ROM1, CDK2, UQCRH, TWIST1, TYK2, CPE, TYRO3, UBE2I, NR1H2, MAP3K8, TTF1, COMP, COL9A3, COL9A2, VIP, VIPR1, WEE1, HIRA, TSG101, ROS1, TLN1, CSF2RA, THBD, THBS1, THBS2, CSF1, TIA1, TM7SF2, TSC2, CRHR1, TOP2A, CREB1, TPM3, TPM4, HSP90B1, WNT1, COL9A1, ABCC2, CUL4A, ARID1A, AXIN1, KIF22, FZD4, ULK1, CDKN2C, CDKN1C, XPA, PLPP2, DYNLL1, IRS2, ABCC3, CDK9, FBP2, CEL, CFL1, HMGA2, SLC25A16, CHEK1, KAT6A, TFPI2, FZD3, MAFK, AIMP2, SCG2, CLU, PAX8, LEPQTL1, ZAP70, CLIC1, YES1, CSF2RB, TGFA, TFPI, SRSF1, ELAVL1, SELE, SELP, SFRP1, SFRP2, SFRP4, FBXW4, FSCN1, ATN1, SLAMF1, SLC9A3, SLC12A3, DPP4, DHFR, CTTN, ENG, CX3CL1, EPAS1, SCN8A, SCN1A, CLEC11A, ATXN2, STOM, SALL2, EPHB4, S100A11, S100A10, RREB1, RRBP1, RPS6, ERN1, SNAI1, SOD1, CSF3, TAF12, STK3, STK4, CXADR, SYN1, CUX1, ADAM17, CTLA4, SOD2, CCN2, TCF21, VPS72, PPP1R11, CSK, TFAP2A, STAT6, STAT5B, STAT5A, CYP3A4, STAT1, DAXX, BRINP1, DCN, SSTR2, SST, DCTN1, SPG7, SP3, SP1, SOX10, SOX9, TIMM8A, AADAC
- Sarcoma Mayo_clinic
  
  Are there brochures or other printed material I can have? What websites do you recommend? Don't hesitate to ask other questions.
- Soft Tissue Sarcoma Gard
  
  Soft tissue sarcoma is a form of cancer that occurs due to abnormal and uncontrolled cell growth of the "soft tissues" of the body. These tissues connect, support and surround other body parts and may include muscle, fat, blood vessels, lymph vessels , nerves, tendons and the lining of joints. Many people with early soft tissue sarcoma have no signs or symptoms of the condition. When present, symptoms depend on the location and size of the tumor but may include a palpable lump under the skin, pain, or difficulty breathing. Most cases occur sporadically in people with little to no family history of the condition.
- Soft-Tissue Sarcoma Wikipedia
  
  Because soft tissue is relatively elastic, tumors can grow rather large, pushing aside normal tissue, before they are felt or cause any problems. The first noticeable symptom is usually a painless lump or swelling.
Breast Cysts Mayo_clinic

You may be referred to a breast-health specialist based on a clinical breast exam or findings on an imaging test. What you can do The first evaluation focuses on your medical history. ... Are there any printed materials that I can take home? What websites do you recommend? Don't hesitate to ask questions anytime you don't understand something. What to expect from your doctor Be prepared to answer questions that your doctor may ask, such as: When did you first notice the breast cyst or lump?

ACP3, TRIM23, CYP17A1, IGF1, IGFBP3, PIP, PPP1R8, NAA10, BCCIP
- Breast Cyst Wikipedia
  
  Otherwise, if the lump is not a cyst, the fluid aspirated may contain blood or there may not be fluid at all. Whereas in the first case, the fluid is sent to the laboratory for further examination, the latter circumstance is a sign that the breast lump is solid. ... Hormone therapy , by the means of oral contraceptives , is sometimes prescribed to reduce their recurrence and to regulate the menstrual cycle of the patient (which is likely to cause them in the first place). Danazol may also be prescribed to treat this condition and it is usually considered in patients on whom the non-medical treatment fails and the symptoms are intense. ... PMID 11348400 . S2CID 46191435 . ^ Mason BR, Page KA, Fallon K (June 1999). "An analysis of movement and discomfort of the female breast during exercise and the effects of breast support in three cases". ... External links [ edit ] Classification D ICD - 10 : N60.0 ICD - 9-CM : 610.0 MeSH : D047688 v t e Breast disease Inflammation Mastitis Nonpuerperal mastitis Subareolar abscess Granulomatous mastitis Physiological changes and conditions Benign mammary dysplasia Duct ectasia of breast Chronic cystic mastitis Mammoplasia Gynecomastia Adipomastia (lipomastia, pseudogynecomastia) Breast hypertrophy Breast atrophy Micromastia Amastia Anisomastia Breast engorgement Nipple Nipple discharge Galactorrhea Inverted nipple Cracked nipples Nipple pigmentation Masses Galactocele Breast cyst Breast hematoma Breast lump Pseudoangiomatous stromal hyperplasia Other Pain Tension Ptosis Fat necrosis Amazia v t e Cystic diseases Respiratory system Langerhans cell histiocytosis Lymphangioleiomyomatosis Cystic bronchiectasis Skin stratified squamous: follicular infundibulum Epidermoid cyst and Proliferating epidermoid cyst Milia Eruptive vellus hair cyst outer root sheath Trichilemmal cyst and Pilar cyst and Proliferating trichilemmal cyst and Malignant trichilemmal cyst sebaceous duct Steatocystoma multiplex and Steatocystoma simplex Keratocyst nonstratified squamous: Cutaneous ciliated cyst Hidrocystoma no epithelium: Pseudocyst of the auricle Mucocele other and ungrouped: Cutaneous columnar cyst Keratin implantation cyst Verrucous cyst Adenoid cystic carcinoma Breast cyst Human musculoskeletal system Cystic hygroma Human digestive system oral cavity: Cysts of the jaws Odontogenic cyst Periapical cyst Dentigerous cyst Odontogenic keratocyst Nasopalatine duct cyst liver: Polycystic liver disease Congenital hepatic fibrosis Peliosis hepatis bile duct: Biliary hamartomas Caroli disease Choledochal cysts Bile duct hamartoma Nervous system Cystic leukoencephalopathy Genitourinary system Polycystic kidney disease Autosomal dominant polycystic kidney Autosomal recessive polycystic kidney Medullary cystic kidney disease Nephronophthisis Congenital cystic dysplasia Other conditions Hydatid cyst Von Hippel–Lindau disease Tuberous sclerosis
Bladder Stones Mayo_clinic

Breaking stones apart In one method, you're first given numbing medication or general anesthesia to make you unconscious. ... Preparing for your appointment If you have signs and symptoms of bladder stones, you're likely to see your primary care doctor first. You may then be referred to a doctor who specializes in treating urinary tract disorders (urologist). ... Do you have any printed materials that I can have? What websites do you recommend? Don't hesitate to ask additional questions that may come up during your appointment.

AHR, AMBP, ANXA1, BSG, CEACAM5, CEACAM3, CEACAM7, DPEP1, IRF1, PSG2
- Bladder Stone Wikipedia
  
  An open cystolithotomy is performed under general anesthesia as an inpatient procedure. The first step is a cystoscopy to examine the bladder, then an incision is made in the lower abdomen. ... Aulus Cornelius Celsus wrote that Lithotomos developed instruments to break up and extract bladder stones. [18] Celsus gave the first description of lithotomy as performed before and during his time, and the operation has ever since borne his name—the Celsian method. [19] Etymology [ edit ] Lithiasis (stone formation) in the bladder is called cystolithiasis ( / ˌ s ɪ s t oʊ l ɪ ˈ θ aɪ ə s ɪ s / ), from cysto- (bladder/cyst) + -lith (stone) + -iasis (disorder).
Mononucleosis Mayo_clinic

But it may not detect the infection during the first week of the illness. A different antibody test requires a longer result time, but can detect the disease even within the first week of symptoms. ... Are there brochures or other printed material that I can take with me? What websites do you recommend? Don't hesitate to ask any other questions.

PDLIM7, SH2D1A, HLA-DRB1, RBM45, IL10, HLA-A, APCS, BCL2, TRBV20OR9-2, IL1A, RTEL1, PLAU, PSMB9, RAG1, RAG2, CCL22, TNF, SERPINE2, AHSG, BSND, APOBEC3B, KLRG1, ARL2BP, ERVW-1, FOXP3, CD244, KRT20, ERVK-6, HAVCR2, IFNL3, MIR449A, NCAM1, KIR3DL1, KLRD1, GEM, KLK3, CD19, MS4A1, CD28, TNFRSF8, CD79A, CDK2, CR2, CRP, GDNF, GLUD1, KIR3DS1, GLUD2, GPT, HLA-B, IFNG, IL1B, IL2RA, IL6, IL16, ISG20, ITGA2B, ERVK-20
- Infectious Mononucleosis Wikipedia
  
  Transmission [ edit ] Epstein–Barr virus infection is spread via saliva , and has an incubation period of four to seven weeks. [32] The length of time that an individual remains contagious is unclear, but the chances of passing the illness to someone else may be the highest during the first six weeks following infection. Some studies indicate that a person can spread the infection for many months, possibly up to a year and a half. [33] Pathophysiology [ edit ] The virus replicates first within epithelial cells in the pharynx (which causes pharyngitis , or sore throat), and later primarily within B cells (which are invaded via their CD21 ). ... Physical examination , including palpation of any enlarged lymph nodes in the neck, or enlarged spleen . [38] The heterophile antibody test is a screening test that gives results within a day, [39] but has significantly less than full sensitivity (70–92%) in the first two weeks after clinical symptoms begin. [21] [40] Serological tests take longer time than the heterophile antibody test, but are more accurate. ... This test is specific but not particularly sensitive (with a false-negative rate of as high as 25% in the first week, 5–10% in the second, and 5% in the third). [21] About 90% of diagnosed people have heterophile antibodies by week 3, disappearing in under a year. ... The atypical lymphocytes resembled monocytes when they were first discovered, thus the term "mononucleosis" was coined. ... Retrieved 10 August 2016 . ^ a b Ebell, MH (12 April 2016). "JAMA PATIENT PAGE. Infectious Mononucleosis" . JAMA . 315 (14): 1532. doi : 10.1001/jama.2016.2474 .
Lip Cancer Mayo_clinic

Each person finds his or her own way of coping with the emotional and physical changes cancer brings. But when you're first diagnosed with cancer, sometimes it's difficult to know what to do next. ... Are there brochures or other printed material that I can take with me? What websites do you recommend? In addition to the questions that you've prepared to ask your doctor, don't hesitate to ask other questions that occur to you. ... Your doctor may ask: When did you first begin experiencing symptoms? Have your symptoms been continuous or occasional?

TP53, BCL2, MSN, NGFR, PDPN
Dermatomyositis Mayo_clinic

The rash, which can be itchy and painful, is often the first sign of dermatomyositis. Muscle weakness. ... Preparing for your appointment You're likely to first see your family doctor, who might refer you to a doctor who specializes in the treatment of arthritis and other diseases of the joints, muscles and bones (rheumatologist) and to a doctor who specializes skin diseases (dermatologist). ... Do you have brochures or other printed material I can have? What websites do you recommend? Don't hesitate to ask other questions.

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- Dermatomyositis Wikipedia
  
  Specialty Rheumatology Symptoms Rash, muscle weakness, weight loss, fever [1] Complications Calcinosis , lung inflammation, heart disease [1] [2] Usual onset 40s to 50s [3] Duration Long term [1] Causes Unknown [1] Diagnostic method Based on symptoms, blood tests, electromyography , muscle biopsies [3] Differential diagnosis Polymyositis , inclusion body myositis , scleroderma [3] Treatment Medication, physical therapy , exercise, heat therapy, orthotics , assistive devices, rest [1] Medication Corticosteroids , methotrexate , azathioprine [1] Frequency ~ 1 per 100,000 people per year [3] Dermatomyositis ( DM ) is a long-term inflammatory disorder which affects skin and the muscles . [1] Its symptoms are generally a skin rash and worsening muscle weakness over time. [1] These may occur suddenly or develop over months. [1] Other symptoms may include weight loss, fever, lung inflammation, or light sensitivity. [1] Complications may include calcium deposits in muscles or skin . [1] The cause is unknown. [1] Theories include that it is an autoimmune disease or a result of a viral infection . [1] It is a type of inflammatory myopathy . [1] Diagnosis is typically based on some combination of symptoms, blood tests, electromyography , and muscle biopsies . [3] While no cure for the condition is known, treatments generally improve symptoms. [1] Treatments may include medication, physical therapy , exercise, heat therapy, orthotics and assistive devices, and rest. [1] Medications in the corticosteroids family are typically used with other agents such as methotrexate or azathioprine recommended if steroids are not working well. [1] Intravenous immunoglobulin may also improve outcomes. [1] Most people improve with treatment and in some the condition resolves completely. [1] About one per 100,000 people per year are newly affected. [3] The condition usually occurs in those in their 40s and 50s with women being affected more often than men. [3] People of any age, however, may be affected. [3] The condition was first described in the 1800s. [4] Contents 1 Signs and symptoms 1.1 Skin 1.2 Muscles 1.3 Other 2 Causes 3 Diagnosis 3.1 Classification 4 Treatment 5 Prognosis 6 Epidemiology 7 History 8 Society and culture 9 Research 10 References 11 External links Signs and symptoms [ edit ] The main symptoms include several kinds of skin rash along with muscle weakness in both upper arms or thighs. [2] Skin [ edit ] One form the rashes take is called " heliotrope " (a purplish color) or lilac, but may also be red . ... PMID 26563285 . S2CID 7104535 . ^ Page 285 in: Thomson and Cotton Lecture Notes in Pathology , Blackwell Scientific. ... "Polymyositis and dermatomyositis (first of two parts)" . The New England Journal of Medicine . 292 (7): 344–7. doi : 10.1056/nejm197502132920706 . ... This article incorporates public domain material from the United States Department of Health and Human Services document: "NINDS Dermatomyositis Information Page" . Retrieved 12 December 2016 . External links [ edit ] Medicine portal Classification D ICD - 10 : M33.0 - M33.1 ( ILDS M33.910) ICD - 9-CM : 710.3 MeSH : D003882 DiseasesDB : 10343 External resources MedlinePlus : 000839 eMedicine : med/2608 derm/98 Scholia : Q681160 v t e Systemic connective tissue disorders General Systemic lupus erythematosus Drug-induced SLE Libman–Sacks endocarditis Inflammatory myopathy Myositis Dermatopolymyositis Dermatomyositis / Juvenile dermatomyositis Polymyositis * Inclusion body myositis Scleroderma Systemic scleroderma Progressive systemic sclerosis CREST syndrome Overlap syndrome / Mixed connective tissue disease Other hypersensitivity / autoimmune Sjögren syndrome Other Behçet's disease Polymyalgia rheumatica Eosinophilic fasciitis Eosinophilia–myalgia syndrome fibrillin Marfan syndrome Congenital contractural arachnodactyly v t e Paraneoplastic syndromes Endocrine Hypercalcaemia SIADH Zollinger–Ellison syndrome Cushing's syndrome Hematological Multicentric reticulohistiocytosis Nonbacterial thrombotic endocarditis Neurological Paraneoplastic cerebellar degeneration Encephalomyelitis Limbic encephalitis Opsoclonus Polymyositis Transverse myelitis Lambert–Eaton myasthenic syndrome Anti-NMDA receptor encephalitis Musculoskeletal Dermatomyositis Hypertrophic osteopathy Mucocutaneous reactive erythema Erythema gyratum repens Necrolytic migratory erythema papulosquamous Acanthosis nigricans Ichthyosis acquisita Acrokeratosis paraneoplastica of Bazex Extramammary Paget's disease Florid cutaneous papillomatosis Leser-Trélat sign Pityriasis rotunda Tripe palms Other Febrile neutrophilic dermatosis Pyoderma gangrenosum Paraneoplastic pemphigus Authority control NDL : 00563159
- Dermatopolymyositis Wikipedia
  
  References [ edit ] ^ Chraibi S, Ibnabdeljalil H, Habbal R, Bennis A, Tahiri A, Chraibi N (November 1998). "Pericardial tamponade as the first manifestation of dermatopolymyositis".
- Dermatomyositis Orphanet
  
  A type of idiopathic inflammatory myopathy characterized by evocative skin lesions and symmetrical proximal muscle weakness. Epidemiology Annual incidence is estimated between 1 to 10 new cases/million population/year, and prevalence between 1/50,000 and 1/10,000. Dermatomyositis (DM) is more common in women than in men (2:1). In the United States, a Black-to-Caucasian ratio of 3:1 has been reported. Clinical description Onset is generally in adulthood, in some cases earlier (Juvenile DM, see this term). Patients typically present a heliotrope rash (erythema of eyelids with or without edema) and Gottron's papules (lichenoid papules over knuckles and sometimes knees, elbows), violaceous erythema (on extensor surfaces and face), poikiloderma (photoexposed areas), and periungual telangiectasias.
- Dermatomyositis Gard
  
  Dermatomyositis is an autoimmune condition that causes skin changes and muscle weakness. Symptoms can include a red skin rash around the eyelids, red bumps around the joints, and muscle weakness in the arms and legs. Dermatomyositis is most common in adults between ages 40 and 60, or in children between ages 5 and 15. Muscle weakness gets worse over time and can lead to stiff joints and muscle wasting. The cause for dermatomyositis is unknown. Diagnosis is made through a clinical exam and microscopic examination of a piece of skin and muscle.