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Carpenter Syndrome 1 Omim

Gershoni-Baruch (1990) described a brother and sister with rather striking differences in severity. The first born had craniosynostosis of the sagittal suture, normal intelligence, and no abnormalities of the hands and feet.

MEGF8, RAB23, ATRX, GLI3, ZC4H2, AASDHPPT, ARL13B
- Carpenter Syndrome 2 Omim
  
  Altunhan et al. (2011) stated that this was the first report of Carpenter syndrome in association with situs inversus totalis.
- Carpenter Syndrome Orphanet
  
  A rare syndromic craniosynostosis with variable phenotypic expression characterized by craniosynostosis, intellectual disability, distinctive facies, abnormalities of the fingers and toes (brachydactyly, polydactyly and syndactyly), short stature, congenital heart disease, skeletal defects, obesity, genital abnormalities and umbilical hernia. Epidemiology Over 70 cases have been described in the literature. Clinical description Presentation at birth is with macrosomia, umbilical hernia and craniosynostosis which ranges from cloverleaf configuration to predominant involvement of the metopic ridge to craniofacial asymmetry. Cranial anomalies may lead to raised intercranial pressure, difficulty in articulation, frequent otitis media and resultant hearing loss. Typical abnormalities of the digits include brachydactyly, cutaneous syndactyly, preaxial polydactyly in the toes and postaxial polydactlyly in the hands with broad thumbs and absent middle phalanges. Characteristic facial features may include flat nasal bridge with epicanthal folds, down-slanting palpebral fissures, corneal anomalies, low-set, posteriorly rotated malformed ears, and an underdeveloped maxilla and mandible.
- Carpenter Syndrome Wikipedia
  
  Carpenter syndrome Other names Acrocephalopolysyndactyly type II Specialty Medical genetics Carpenter syndrome , also called acrocephalopolysyndactyly type II , [1] is an extremely rare autosomal recessive [2] congenital disorder characterized by craniofacial malformations, obesity , and syndactyly . [2] It was first characterized in 1909, and is named for George Alfred Carpenter . [3] [4] Contents 1 Presentation 1.1 Description 2 Genetics 3 Diagnosis 3.1 Types 4 Treatment 5 Occurrence 6 See also 7 References 8 External links Presentation [ edit ] Carpenter syndrome presents several features: [ citation needed ] Tower-shaped skull ( craniosynostosis ) Additional or fused digits (fingers and toes) Obesity Reduced height Intellectual disability is also common with the disorder, although some patients may have average intellectual capacity. [5] Description [ edit ] Carpenter Syndrome belongs to a group of rare genetic disorders known as acrocephalopolysyndactyly, abbreviated ACPS (RN, 2007). ... Treatment [ edit ] Operations to correct the malformations of the skull should be performed within the first year of infancy in patients affected by Carpenter Syndrome.
- Carpenter Syndrome Gard
  
  Carpenter syndrome is a condition characterized by premature fusion of skull bones (craniosynostosis); finger and toe abnormalities; and other developmental problems. The features in affected people vary. Craniosynostosis can give the head a pointed appearance; cause asymmetry of the head and face; affect the development of the brain; and cause characteristic facial features. Other signs and symptoms may include dental abnormalities; vision problems; hearing loss; heart defects; genital abnormalities; obesity; various skeletal abnormalities; and a range of intellectual disability. Carpenter syndrome can be caused by mutations in the RAB23 or MEGF8 gene and is inherited in an autosomal recessive manner. Treatment focuses on the specific features in each affected person. Life expectancy is shortened but very variable.
Complement Component 2 Deficiency Omim

They designated the defect in the first family as type I; no detectable C2 protein was synthesized.

C2, CYP21A2, MBL2, ACADVL, C4A, C4B, CFH, HLA-A, HLA-DRB5, OTOA, C4B_2
- Complement 2 Deficiency Wikipedia
  
  Complement 2 deficiency Specialty Hematology Complement 2 deficiency is a type of complement deficiency caused by any one of several different alterations in the structure of complement component 2 . It has been associated with an increase in infections . [1] [2] It can present similarly to systemic lupus erythematosus (SLE). [3] References [ edit ] ^ Alper CA, Xu J, Cosmopoulos K, et al. (July 2003). "Immunoglobulin deficiencies and susceptibility to infection among homozygotes and heterozygotes for C2 deficiency" (PDF) . J. Clin. Immunol . 23 (4): 297–305. doi : 10.1023/A:1024540917593 . PMID 12959222 . ^ Sherwood L. Gorbach; John G. Bartlett; Neil R. Blacklow (2004). Infectious diseases .
- Complement Component 2 Deficiency Medlineplus
  
  Complement component 2 deficiency is a disorder that causes the immune system to malfunction, resulting in a form of immunodeficiency. Immunodeficiencies are conditions in which the immune system is not able to protect the body effectively from foreign invaders such as bacteria and viruses. People with complement component 2 deficiency have a significantly increased risk of recurrent bacterial infections, specifically of the lungs (pneumonia), the membrane covering the brain and spinal cord (meningitis), and the blood (sepsis ), which may be life-threatening. These infections most commonly occur in infancy and childhood and become less frequent in adolescence and adulthood. Complement component 2 deficiency is also associated with an increased risk of developing autoimmune disorders such as systemic lupus erythematosus (SLE) or vasculitis.
- Complement Component 2 Deficiency Gard
  
  Complement component 2 deficiency (C2D) is a genetic condition that affects the immune system. Signs and symptoms include recurrent bacterial infections and risk for a variety of autoimmune conditions . Infections can be very serious and are common in early life. They become less frequent during the teen and adult years. The most frequent autoimmune conditions associated with C2D are lupus (10-20%) and vasculitis. C2D is caused by mutations in the C2 gene and is inherited in an autosomal recessive fashion.
Complement Component 9 Deficiency Omim

Witzel-Schlomp et al. (1998) studied the genetic basis of inherited C9 deficiency in an adult of Irish origin reported previously by Hobart et al. (1997) and in an unrelated Irish family in which 1 member had died at the age of 22 years of meningitis, probably meningococcal. In the first case, heterozygosity for C6, C7, and C9 DNA markers was found, indicating probable compound heterozygosity of the C9 mutations.

C9, TBX1
Mental Retardation, X-Linked, Syndromic, Nascimento Type Omim

INHERITANCE - X-linked recessive GROWTH Weight - Increased weight HEAD & NECK Head - Large head Face - Midface hypoplasia - Wide face - Prominent supraorbital ridges Eyes - Synophrys - Upslanting palpebral fissures - Deep-set eyes - Almond-shaped eyes Nose - Low nasal bridge Mouth - Large mouth - Downturned corners of the mouth - Thin lips Neck - Short, broad neck CHEST Breasts - Widely spaced nipples GENITOURINARY External Genitalia (Male) - Small penis SKELETAL Feet - Flat feet - Small feet - Broad first toe SKIN, NAILS, & HAIR Skin - Dry skin - Hypopigmented spots (less common) Nails - Onychodystrophy Hair - Hirsutism, generalized - Low posterior hairline - Synophrys - Hair whorls MUSCLE, SOFT TISSUES - Myxedematous appearance NEUROLOGIC Central Nervous System - Mental retardation - Seizures - Lack of speech or poor speech - White matter hypodensities on brain imaging Behavioral Psychiatric Manifestations - Echolalia - Aggression MOLECULAR BASIS - Caused by mutation in the ubiquitin-conjugating enzyme E2A gene (UBE2A, 312180.0001 ) ▲ Close

UBE2A
- X-Linked Intellectual Disability, Nascimento Type Orphanet
  
  X-linked intellectual disability, Nascimento type is a rare X-linked intellectual disability syndrome characterized by intellectual disability (with severe speech impairment), a myxedematous appearance, dysmorphic facial features (including large head, synophrys, prominent supraorbital ridges, almond-shaped and deep-set eyes, large ears, wide mouth with everted lower lip and downturned lip corners), low posterior hairline, short, broad neck, marked general hirsutism and abnormal hair whorls, skin changes (e.g. dry skin or hypopigmented spots), widely spaced nipples, obesity, micropenis, onychodystrophy and seizures.
Ichthyosis, Spastic Quadriplegia, And Mental Retardation Omim

The patients were of Saudi Arabian and Asian Indian descent, respectively. The first patient was noted to have a collodion membrane covering the skin at birth, which resolved and was replaced with dry ichthyotic skin affecting all regions of the body.

ELOVL4
Congenital Disorder Of Glycosylation, Type Iik Omim

Clinical Features Foulquier et al. (2012) reported 5 patients from 4 families with CDG2K. The first family contained 2 affected sibs, born of Georgian Jewish parents.

TMEM165
- Tmem165-Cdg Orphanet
  
  TMEM165-CDG is a form of congenital disorders of N-linked glycosylation characterized by a psychomotor delay-dysmorphism (pectus carinatum, dorsolumbar kyphosis and severe sinistroconvex scoliosis, short distal phalanges, genua vara, pedes planovalgi syndrome) with postnatal growth deficiency and major spondylo-, epi-, and metaphyseal skeletal involvement. Additional features include facial dysmorphism (midface hypoplasia, internal strabism of the right eye, low-set ears, moderately high arched palate, small teeth), nephrotic syndrome, cardiac defects, and feeding problems. The disease is caused by mutations in the gene TMEM165 (4q12).
Sessile Serrated Lesion Wikipedia

The surveillance interval is dependent on (1) the number of adenomas, (2) the size of the adenomas, and (3) the presence of high-grade microscopic features. [5] Epidemiology [ edit ] Sessile serrated lesions account for about 25% of all serrated polyps. [6] History [ edit ] Sessile serrated adenomas were first described in 1996. [7] In 2019, the World Health Organization recommended the use of the term "sessile serrated lesion ," rather than sessile serrated polyp or adenoma . [6] See also [ edit ] Polyp table Colonic polyps Colorectal polyps Colorectal carcinoma Microsatellite instability References [ edit ] ^ Rüschoff J, Aust D, Hartmann A (2007).

TTR, BRAF, CALR, TRIM21, SST, ANXA10, MLH1, KRAS, PIK3CA, PTCH1, PTGS2, SLC6A2, SOD1, SOD2, GRK2, TP53, NOS1, GATD3A, AIP, SLIT2, RNF43, REEP1, MIR200A, MIR31, MIR96, NOS2, MUC5AC, NFE2L2, HBA2, BMP4, CTNNB1, ELK3, EPHB1, EPHB2, GABPA, GSTP1, HBA1, HBB, AR, HP, HES1, MAPT, MARK1, MCM2, MGMT, MME, MUC2, GATD3B
- Wild-Type Transthyretin Amyloid Wikipedia
  
  Wild-type transthyretin amyloid ( WTTA ), also known as senile systemic amyloidosis ( SSA ) and abbreviated as ATTR , [1] is a disease that typically affects the heart and tendons of elderly people. It is caused by accumulation of a wild-type (that is to say a normal ) protein called transthyretin . This is in contrast to a related condition called transthyretin-related hereditary amyloidosis where a genetically mutated transthyretin protein tends to deposit at a much earlier age than in WTTA, due to abnormal conformation and bioprocessing. It belongs to a group of diseases called amyloidosis , chronic progressive conditions linked to abnormal deposition of normal or abnormal proteins, because these proteins are misshapen and cannot be properly degraded and eliminated by the cell metabolism. Contents 1 Signs and symptoms 2 Natural course 3 Diagnosis 4 Treatment 4.1 Orphan drug status for transthyretin (TTR) amyloidosis 5 See also 6 References 7 External links Signs and symptoms [ edit ] Wild-type transthyretin amyloid accumulates mainly in the heart , where it causes stiffness and often thickening of its walls, leading consequently to shortness of breath and intolerance to exercise, called diastolic dysfunction .
Coloboma, Ocular, Autosomal Recessive Omim

Ophthalmologic examination of their unaffected first-cousin parents and 3 other brothers showed no abnormalities.

SALL2
Marjolin's Ulcer Wikipedia

The term was named after French surgeon , Jean-Nicolas Marjolin , who first described the condition in 1828. [7] The term was later coined by J C De Costa .
Somatoparaphrenia Wikipedia

"Mirror-view reverses somatopharaphrenia: Dissociation between first- and third-person perspectives on body ownership".
Indium Lung Wikipedia

Indium lung disease has been fatal in several cases. [2] History [ edit ] It was first described by a group of Japanese researchers in 2003. [1] [4] Epidemiology [ edit ] Cases have been reported in Japan , the United States , and China . [1] [2] [5] The indium industry is mainly based in Japan, where the bulk of cases have occurred; indium industry is also present in the US, China, Taiwan , and South Korea . [4] As of 2010, 10 cases had been described, though more than 100 indium workers had documented respiratory abnormalities. [1] References [ edit ] ^ a b c d e f g h i Sauler, Maor; Gulati, Mridu (December 2012).
Puppy Pregnancy Syndrome Wikipedia

PMID 12793514 . v t e Superstition Main topics Amulet Evil eye Luck Omen Talismans Myth and ritual Lists List of superstitions List of lucky symbols List of bad luck signs Sailors' superstitions Theatrical superstitions Africa Buda Gris-gris Sampy Sleeping child Americas Ascalapha odorata Carranca Cooties Curupira Djucu Fortune cookie Groundhog Day I'noGo tied Oscar love curse Susto White lighter myth Witch window Asia Superstition in India Superstition in Pakistan Japanese superstitions Bhoot (ghost) Chhaupadi Churel Ghosts in Bengali culture Jackal's horn Kuai Kuai culture Muhurta Navaratna Nazar battu Pichal Peri Puppy pregnancy syndrome Akabeko Kanai Anzen Maneki-neko Okiagari-koboshi Omamori Fan death Agimat Arbularyo Barang Kulam Lihi Pagtatawas Pasma Usog Kuman Thong Palad khik Takrut Nang Kwak White elephant Curse of 39 Jin Chan Numbers in Chinese culture Superstitions of Malaysian Chinese Europe August curse Barbary macaques in Gibraltar Bayern-luck Blarney Stone Cimaruta Cornicello The Goodman's Croft Himmelsbrief Icelandic magical staves In bocca al lupo Kitchen witch Klabautermann Mooncalf Nazar Need-fire Painted pebbles Powder of sympathy Rabbit rabbit rabbit Ravens of the Tower of London Russian traditions and superstitions Spilling water for luck The Scottish Play Troll cross Tycho Brahe days Witch post Wolfssegen General 11:11 4 ( Four-leaf clover , Tetraphobia ) 7 ( Seventh son of a seventh son ) 8 9 13 ( Friday the 13th , The Thirteen Club , Thirteenth floor , Triskaidekaphobia ) 108 111 666 ( Number of the Beast ) Ace of spades Auspicious wedding dates Baseball superstition Beginner's luck Black cat Bread and butter Break a leg Chain letter Cramp-ring Curse Davy Jones' Locker Dead man's hand End-of-the-day betting effect Fear of frogs Fear of ghosts First-foot Flying Dutchman Four Eleven Forty Four Gambler's conceit Good luck charm Human sacrifice Jinx Knocking on wood Law of contagion Literomancy Lock of hair Maternal impression Miasma theory Nelson Numismatic charm Penny Rabbit's foot Rainmaking Ship sponsor Shoes on a table Sign of the horns Something old Spilling salt Statue rubbing Three on a match Threshold Toi toi toi 27 Club Wishing well Witch ball Witching hour Related Apotropaic magic Astrology and science Coincidence Debunker Divination Folk religion Fortune-telling Magic and religion Magical thinking Numerology Perceptions of religious imagery in natural phenomena Post hoc ergo propter hoc Traditional medicine Urban legend Jew Muslim
Free-Living Amoebozoa Infection Wikipedia

"A rare but fatal case of granulomatous amebic encephalitis with brain abscess: the first case reported from Turkey". Turkish Neurosurgery . 19 (3): 256–259.
Nasal Glial Heterotopia Wikipedia

This is distinctly different from an encephalocele , which is a herniation of brain tissue and/or leptomeninges , that develops through a defect in the skull, where there is a continuity with the cranial cavity . [2] Contents 1 Signs and symptoms 2 Pathology 2.1 Histochemistry 2.2 Immunohistochemistry 3 Diagnosis 3.1 Differential diagnoses 3.2 Imaging findings 3.3 Classification 4 Management 5 Epidemiology 6 References 7 Further reading Signs and symptoms [ edit ] Patients come to clinical attention early in life (usually at birth or within the first few months), with a firm subcutaneous nodule at bridge of nose, or as a polypoid mass within the nasal cavity, or somewhere along the upper border of the nasal bow.
- Nasal Glial Heterotopia Orphanet
  
  Nasal glial heterotopia is a rare developmental abnormality presenting usually at birth or in early childhood (rarely in adulthood) as a benign, non-pulsatile mass that can lead to nasal obstruction, deformation of the septum and nasal bone, and respiratory distress if untreated. Nasal glial heterotopias have no communication with the central nervous system; however an associated defect in the cribriform plate is sometimes reported.
Childhood Rhabdomyosarcoma Wikipedia

Alveolar and anaplastic rhabdomyosarcoma occur in the teenage years. [ citation needed ] Embryonal rhabdomyosarcoma develops within the first seven weeks of the embryo's development.

GLI1, PAX3, PIK3CB, PIK3CD, PTCH1, MYOG, IGF2, IGF1R, PIK3CG, TP53, RHD, PIK3CA, MDM2, EPHB2, ALK, PAX7, MYCN, MAPK1, FOXO1, MYOD1, IGF1, AKT1, VEGFA, EGFR, FGFR4, CDKN2A, MIR206, MET, TGFB1, FSD1L, DES, FSD1, TNF, DMD, EWSR1, ABCB1, CAV1, HDAC9, DICER1, EZH2, PLAT, HRAS, MAP2K7, MAPK8, PLK1, EZR, EGR1, TBC1D9, MMP2, CDKN1A, ARHGEF25, CDK4, DUX4, NR4A1, NF1, NRAS, PTPN11, PARP1, RPE65, HGF, SMUG1, PTGS2, MIB1, CASP3, SLC2A1, SIX1, GLI2, TDP1, MYC, PROM1, NCOA2, H19, CCND1, NES, IL15, STIM1, MIR27A, RB1, IFNG, CD274, ABCG2, EIF3K, MGMT, RAG2, AHSA1, GPT, MMP9, HES1, ABCC1, IGFBP2, KIDINS220, GRAP2, YAP1, ILK, ACTB, ACKR3, SLC12A9, KIT, KIF22, ITGA2, OBP2A, MKI67, PTEN, KRAS, POLDIP2, RNF19A, PDGFRA, MSTN, CTNNB1, GABPA, CRKL, CRK, COL11A2, SYT1, TBX2, NOTCH3, TRA, CDKN2B, CCN3, MIR203A, CCND2, CCK, CASP8, BUB1B, BRAF, BMP4, IL24, BCL2, PHB2, BIRC2, AIMP2, MIR450B, VIM, WEE1, MAPK14, MBD2, NOS1, NFE2L2, MTOR, FN1, PLG, FOXM1, SMARCB1, FOXF1, FHL2, SMO, FGFR1, UTS2, SOS1, STAT3, ORAI1, NHS, ERBB2, DNER, EPHB4, EPHA3, DLEU2, EGF, HDAC3, TNFRSF10B, IGF2BP1, PDLIM5, CKAP4, CHEK2, ZHX2, MTMR11, HPSE, AADAC, CIB2, CARM1, NR1I2, KAT2B, DLK1, FADD, TNFSF10, TNFSF14, ABCC3, NCOA1, PTCH2, TP63, LMO4, BFSP2, CLTCL1, TAM, COIL, ST8SIA2, HMGA2, ST8SIA4, CXCR4, SYNJ1, PHOX2B, WASF1, ARPC5, ENOX2, OLFM1, MYCNOS, EFS, SPRY2, SPRY1, OLIG2, LRPPRC, HDAC6, RGN, MAML1, HDAC4, BAG3, NOG, CEP164, DYRK1B, SLC16A3, SLC16A4, LARGE1, MRM2, MMRN1, WDR48, FNDC5, VGLL2, SMYD1, PDIK1L, PWAR1, SLCO6A1, TWIST2, TNFRSF13C, SLFN11, BMF, TANC1, RITA1, MAGT1, SPRY4, WLS, DHDDS, SLC52A2, GGCT, WNK1, MARCKSL1, GORASP1, GOLPH3, IL21, NUTM1, CAVIN1, NANOS1, MIR431, LOC110806263, HBB-LCR, MTCO2P12, DUX4L9, MIR874, MIR605, MIR411, MIR545, MIR486-1, MIR410, MIR378A, CAVIN4, XRCC6P5, PLIN5, MIR223, MIR22, MIR214, MIR197, MIR145, MIRLET7C, PRSS57, GSTK1, CXCL16, VANGL2, SIRT2, PNPLA2, SETD2, TRAC, TRAJ60, TRAV29DV5, DLL1, IGHV1-12, EML4, HPGDS, DUX1, PTPN22, PANX1, BRD1, ZNF281, SUZ12, HEY1, SIRT1, SATB2, VPS13A, CIC, PPRC1, ZNF609, KDM1A, HMGXB3, YES1, IL22, DERL2, MEG3, CHPT1, XAB2, PARD3, PCDHA4, PDGFC, DEPDC1B, NLRP2, FEM1A, HES6, ZNF331, PACC1, SDF4, GOLPH3L, MSTO1, FEV, P4HTM, FAM193B, NANS, LUC7L3, SUFU, ETV7, LEF1, ZBTB16, RRM2, WT1, HOXB6, HMOX1, HMGB1, HLA-DMA, HLA-A, HIF1A, CFHR1, CFH, H2AX, GSK3B, GLI3, GLB1, G6PD, FUS, FLT1, FOXO3, FOXS1, FOXF2, GPC5, FGFR3, FGF2, FCGRT, HNRNPH1, HRG, F2RL2, HSPA4, SMAD4, LTK, LIF, LGALS3, JARID2, ITGAM, IRS1, INSRR, INSR, CXCR2, CXCL8, IL6ST, IL6, IL4, IL1R1, RBPJ, IGFBP6, ICAM1, IAPP, TNC, HSP90AA1, F3, F2R, WNT2, CDC42, CAV3, CAV2, CA5A, SERPING1, BMP2, BCL2L1, ATP2B1, ATM, ARRB1, RHOA, APP, XIAP, ANPEP, ALPP, ALPI, ALB, JAG1, AGER, AP2A1, ACVRL1, ACTL6A, CD47, CDH15, ETV4, CDKN1C, ESR2, ESR1, ERG, ERBB3, EPOR, EPO, ENO2, ENG, EDN3, DNMT3B, DMPK, DCC, DAG1, CYP2B6, CNR1, CLTC, CEACAM7, CEACAM3, CETN1, CEACAM5, CDKN2C, MB, MCL1, MDM4, SP3, SOX11, SOX2, SNRPF, SNAI1, SMARCA4, SMARCA1, SLPI, SHH, FBXW4, SGK1, SGCA, MAP2K4, CXCL12, CCL5, CCL2, TSPAN31, RPS6KA2, ROCK1, RELA, RBBP7, RASGRF1, SP1, SPP1, MEF2C, SRMS, UVRAG, UTRN, UCHL3, TXN, TTN, TNNT1, TH, TGFBR1, TFRC, TFE3, TFCP2, TERT, TRBV20OR9-2, TBX3, TAZ, TAT, SYP, STAT6, SS18, SSX2, SSX1, RAF1, MOK, PVALB, PTPRC, YBX1, NPM1, NOTCH1, NOS2, NM, NGF, NEU2, NELL1, NBN, NACA, PPP1R12A, MYF6, MYF5, COX2, MPST, MMP14, MAP3K10, CD99, CIITA, KITLG, MEF2D, NTRK1, ODC1, SLC22A18, PMS2, PTHLH, PTH, PTBP1, PSG2, MAPK3, PKN1, PRKCI, PPARA, POU4F1, PLAU, SERPINE1, PLAG1, ABCB4, SERPINF1, PECAM1, PDGFRB, PCNA, PAX9, PAM, PAK1, H3P10
Atrioventricular Reentrant Tachycardia Wikipedia

In the absence of shock, inhibition at the AV node is attempted. This is achieved first by a trial of specific physical maneuvers such as holding a breath in or bearing down.

TTN, TTN-AS1
Doege–potter Syndrome Wikipedia

The hypoglycemia is the result of the tumors producing insulin-like growth factor 2 . [2] The syndrome was first described in 1930, by Karl Walter Doege (1867–1932), a German-American physician [3] and by Roy Pilling Potter (1879–1968), an American radiologist, working independently; [4] the full term Doege–Potter syndrome was infrequently used until the publication of a 2000 article [5] using the eponym . [6] DPS is rare (as of 1976, less than one hundred cases were described [7] ), with a malignancy rate of 12–15%.
Abortion In Luxembourg Wikipedia

Abortions may be performed in hospitals, clinics, and a doctor's surgery . [3] Before reforms passed in 2012, only a doctor could determine if a woman was "in distress". Abortions in the first twelve weeks were only permitted in the event of a physical or mental health threat to the mother, a serious risk that the child would be born with a serious disease or serious defects, or a pregnancy resulting from rape.
Post-Kala-Azar Dermal Leishmaniasis Wikipedia

PKDL probably has an important role in interepidemic periods of VL, acting as a reservoir for parasites. PKDL was first identified by Sir Upendranath Brahmachari , who initially called it dermal leishmanoid .

IL10, IFNGR1, IFNG, IL4, ADA, DDX56, GAL, FOXP3, CD207, VDR, TNF, STAT1, SELL, RPS12, LGALS3, IL6, IL9, AQP1, IGHG3, IFNA13, IFNA1, DPP4, CD68, CD40, CD28, CD1A, CAMP, VAMAS6
Mallet Finger Wikipedia

Specialty Emergency medicine , plastic surgery Symptoms Inability to extend the finger tip, pain and bruising of the finger [3] Causes Trauma resulting in over bending of the finger tip [3] Diagnostic method Based on symptoms, X-rays [3] Treatment Splinting for 8 weeks, surgery [3] Prognosis 6 to 10 weeks for healing [3] Frequency Relatively common [2] A mallet finger , also known as hammer finger or PLF finger , is an extensor tendon injury at the farthest away finger joint . [2] This results in the inability to extend the finger tip without pushing it. [3] There is generally pain and bruising at the back side of the farthest away finger joint. [3] A mallet finger usually results from overbending of the finger tip. [3] Typically this occurs when a ball hits an outstretched finger and jams it. [3] This results in either a tear of the tendon or the tendon pulling off a bit of bone . [3] The diagnosis is generally based on symptoms and supported by X-rays . [3] Treatment is generally with a splint that holds the fingertip straight continuously for 8 weeks. [3] The middle joint is allowed to move. [3] This should be begun within a week of the injury. [3] If the finger is bent during these weeks, healing may take longer. [3] If a large piece of bone has been torn off surgery may be recommended. [3] Without proper treatment a permanent deformity of the finger may occur. [2] Contents 1 Diagnosis 2 Treatment 3 See also 4 References 5 External links Diagnosis [ edit ] The diagnosis is generally based on symptoms and supported by X-rays . [3] The injury can be accompanied by swelling and ecchymosis . [4] X-ray showing fracture at the insertion of the extensor tendon A mallet finger without an associated fracture Treatment [ edit ] The management goal is to restore extension of the joint. [5] Treatment is generally with a splint that holds the first joint of the finger straight continuously for 8 weeks. [3] This should begin within a week of the injury. [3] The splint may be worn just at night for a few additional weeks after this. [3] The split acts to immobilize flexing of the joint.