Aims
To establish whether RNA degrades in long-term storage at −80°C and whether RNA integrity numbers (RINs) determine ‘fitness for purpose’ in severely degraded RNA.
Methods
RNA was extracted from 549 thyroid biospecimens stored at −80°C for 0.1–10.9 years then their RINs correlated with storage time. RT-PCR for 65, 265, 534 and 942 base pair amplicons of hydroxymethylbilane synthase was used to measure amplicon length in RNA from cryopreserved and FFPE biospecimens that were equally degraded according to RIN.
Results
Storage time did not correlate with RIN. Longer amplicons were obtained from cryopreserved samples than FFPE samples with equal RINs.
Conclusions
RNA does not degrade in thyroid biospecimens stored for long periods of time at −80°C. Although RINs are known to predict amenability to analytical platforms in good quality samples, this prediction is unreliable in severely degraded samples.
Neuroendocrine dysfunctions (NED) are often observed in patients with schizophrenia spectrum disorders and could be a component of the etiopathogenesis of the disease as well as effect associated with use of atypical neuroleptics. The most common NED symptoms and syndromes are described in the literature review: neuroleptic-induced hyperprolactinemia syndrome, the frequency of occurrence 2–100 %, metabolic syndrome — a 49.3 %, increasing in body weight (neuroleptics obesity) — 40–92 %, diabetes mellitus type 2 — 6.2–25.0 %, violation of thyroid metabolism — 20–49 %, a polymorphic syndrome — 9.9–32.9 %. Metabolic syndrome is more often observed in patients with schizoaffective disorder than in patients with schizophrenia; however, explanatory factors of this association deserve further research. Patients, receiving atypical neuroleptics, must undergo regular endocrinological examination and psychiatrists must draw attention to the endocrinological component of the patient’s health. Diabetologists and psychiatrists must work together to monitor patients treated with atypical antipsychotics, with the aim of identifying their impaired glucose tolerance and diabetes management.
Резюме. В обзоре литературы обобщен и проанализирован материал, посвященный воспалительным процессам, сопровождающим сердечно-сосудистые осложнения при сахарном диабете (СД). Показана роль эндотелиальной дисфункции, приводящей к повышению проницаемости эндотелия, накоплению в стенке сосуда липопротеинов, их модификации, образованию и секреции молекул клеточной адгезии, что, в свою очередь, приводит к привлечению моноцитов и их дифференциации в воспалительные макрофаги. Отмечена роль рецепторов-скавенджеров в депонировании холестерина и формировании пенистых клеток. Детально рассмотрены механизмы инициации воспалительного процесса и образования инфламмасом. Описана схема трансдукции провоспалительных сигналов в клетке и участие ключевого фактора NF-κB, интегрирующего всю поступающую информацию и контролирующего трансактивацию генов, участвующих в воспалении. Показано, что воспалительные процессы являются ключевыми в развитии заболеваний сосудов при СД, а подавление этих процессов тормозит прогрессирование болезни, уменьшая повреждения артерий и способствуя их заживлению.
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