Abin da ya haddasa kwayoyin cututtuka

Kwayoyin cututtuka sun hada da wani babban rukuni na cututtuka wanda taso daga canje-canje a gene tsari. Bari mu gano abin da suke haddasawa daga wadannan pathologies.

Gene na mutum cututtuka suna kagaggun sa ta maye gurbi a cikin tsarin kwayoyin halittu, wanda gudanar da wani aiki ta hanyar kira na polypeptides, a cikin wasu kalmomi - da sunadarai. Duk wani gene maye gurbi entails canje-canje a cikin tsarin ko adadin furotin.

Irin cututtuka fara da farko sakamako na mutant allele. Idan daya yayi kokarin schematically labarun gene maye gurbi mutum, akwai farko za zama mutant allele, wanda gudana a cikin modified farko samfurin, sakamakon wani cell wuce sarkar na biochemical matakai, sakamakon manyan zuwa canje-canje a cikin gabobin da kyallen takarda, sa'an nan dukan kwayoyin.

Idan akai la'akari da kwayoyin cuta a matakin kwayoyin, wadannan bambance-bambancen karatu za a iya gano:

- samar da wani wuce haddi adadin da gene samfurin,

- kira na wani mahaukaci gina jiki

- da rashin samar,

- kazalika da samar da wata rage adadin farko samfurin.

Kwayoyin cuta ba ya kawo karshen a matakin kwayoyin. Su pathogenesis ci gaba wajen samar da a salon salula matakin. A wannan connection ya kamata a lura da cewa batu na aikace-aikace na modified gene a cututtuka daban-daban na iya zama duka jikuna a general, da kuma raba salula Tsarin kamar membranes, peroxisomes, lysosomes, mitochondria.

An muhimmanci alama kayyade munanan ne cewa su na asibiti manifestations, kazalika da kudi da kuma mai tsanani na ci gaba aka ƙaddara a matakin da genotype da kwayoyin, da muhalli da yanayi, shekaru na haƙuri, kuma kamar.

A halayyar siffa daga cikin kwayoyin heterogeneity ne pathologies. Wannan ya nuna cewa phenotypic magana da cutar na iya zama saboda daban-daban maye gurbi cewa faruwa a cikin guda gene ko a daban-daban da kwayoyin halittu. Wannan aka farko kafa a 1934 ta mashahuri bincike a cikin filin jinsi S.N.Davidenkovym.

Amma monogenic siffofin kayyade munanan, bisa ga dokokin na Mendel, suna gaji. Bi da bi, monogenic siffofin za a iya raba ta da irin gādo, wato autosomal recessive, autosomal rinjaye, da kuma guda biyu tare da Y- ko X-chromosomes.

All kwayoyin cutar za a iya classified da wani yawan halaye, kuma mafi girma a kungiyar a wannan yanayin za a gaji rayuwa cututtuka. Kusan dukkan su kasance a wani autosomal recessive hanya. A sabili da waɗannan pathological yanayi ne rashin wani musamman enzyme wanda yake da alhakin kira na amino acid. Wadannan sun hada da cututtuka kamar phenylketonuria, ido-cutaneous zabiya da homogentisuria.

A gaba most rukuni na kwayoyin cututtuka hade da rayuwa cuta. Glycogen cuta, galactosemia - ne misalai na wannan kungiya.

Biye da cututtuka da cewa an kai tsaye alaka sia metabolism - wato Gaucher cuta, Niemann-sama cuta da kuma kama.

Kwayoyin cuta a cikin mutane, kuma da waɗanda suka riga aka ambata, suna classified

- hereditary cututtuka na pyrimidine da purine metabolism,

- pathologies dangantawa da connective nama cuta,

- gaji cuta da ake zagawa da sunadarai,

- cututtuka na kai tsaye munasaba zuwa metabolism cuta a erythrocytes,

- hereditary Pathology karafa musayar,

- kuma syndromes cewa sa malabsorption matakai a cikin narkewa kamar tsarin.

Bugu da kari ya na sama da muka ƙara da cewa kafa na hereditary yanayi da cutar dogara ne a kan na asibiti da kuma bisa ga asalinsu Hanyar.