Возвращаясь к старой дискуссии . Попалась работа 1996 г.,не нашедшая продолжения . Группа исследователей из Лейпцигского университета занимается разработкой лекарственных препаратов на основе 5-фенокситиофенов ,рассматривая эти вещества как потенциальные ингибиторы клеточного захвата Т3.
Хотя группе и удалось доказать снижение захвата т3 клетками печени под влиянием рядавеществ,очевидно ,что клиничесоке применение в данном случае ,даже если и станет возможным ,ограничится периодом предоперационной подготовки ,поскольку препарат не влияет на механизмы собственно активации щитовидной железы .
Любопытно ,что с 1996 г. новых публикаций на эту тему практически нет .

Некоторые заключения по генетическим маркерам( 2002 г )S27-2
AUTOIMMUNE DISEASES: WHAT NEXT AFTER GENOMICS?@
DL Faustman1
1 Immunobiology Laboratory, Massachusetts General Hospital, Boston, Massachusetts
Autoimmune diseases, the improper attack of white blood cells against self tissues, come in many guises based on a clinical definition of what target organs are destroyed. For instance, Type 1 diabetes represents the self destruction of the insulin secr eting islets, rheumatoid arthritis represents the self destruction of select peripheral joints, Sjogren s disease represents the self destruction of one s own salivary and lacrimal glands, etc. The genetics of these d iseases are comp lex but some unique h uman features of these diseases define a challenge that will not be uncovered by conventional genetic sequencing approaches.

It is well known that human cohorts can have identical autoimmune causing genes but are u n likely to co-e xpre ss the disease. Thi s means that large sequencing efforts to identify every combination of autoimmune causing genes in every population is unlikely to be consistently diagnostic of disease expression. DNA sequencing does not define t he rol e of pr eferen tial autoimmune disease expression in females or the reason for the frequent protection of individuals that carry the "bad" genes, as is the case with unaffected identical twins.

Recent human and murine autoimmunity studies have def in e d cell ular phe notypes of disease that track with disease expression in such diverse autoimmune diseases as Type 1 diabetes, rheumatoid arthritis and subsets of premature ovarian failure patients. These complex phenotypes in many cases localize the de fe ct to the prote asome, a large and ubiqui tious multi-enzyme complex found in all mammalian cells. The proteasome defect in some models results in the defective production and activation of transcription factor NF-B. These autoimmune phenotyp e s, i ndicative o f disease expression, could be impor tant in disease treatment even in genetically diverse cohorts with identical clinical disease.
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