scholarly journals Etiology of differentiated carcinoma of the thyroid current apprehension

2003 ◽  
Vol 50 (3) ◽  
pp. 51-55
Author(s):  
Ruben Han

It is apparent that in the last decade carcinoma of the thyroid is becoming increasingly prevalent. The multistage complex theory of thyroid carcinogenesis is based on observations made on cohort patients studies and during animal experiments over a period of last fifty years. The process of thyroid oncogenesis is conceived to be a series of events induced by genetic and environmental factors which alter follicular cells division and growth control. These factors can be considered as initiators (chemical agents and ionising radiation) and promoters (some goitrogenes and drugs). The first class of factors induce incipient tumorigenesis while the second augments TSH secretion and radically increases tumour growth. Normally silent, intracellular proto-oncogenes (of which Ret/PTC series are the most conceived ones) can become activated by chromosomal translocations, deletions or mutations and can transform normal follicular cell into a condition of uncontrolled division and growth. The most significant known cause of thyroid carcinomas in men is exposure to external or internal ionising radiation. Beside that, long-term iodine deficiency, effects of certain chemical carcinogens, drugs and goitrogenes must be considered as significant risk factors. Possible role of sodium/iodide symporter is becoming an objective of the most recent investigations.

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Ghulam Murtaza ◽  
Abida Kalsoom Khan ◽  
Rehana Rashid ◽  
Saiqa Muneer ◽  
Syed Muhammad Farid Hasan ◽  
...  

Several pathologies such as neurodegeneration and cancer are associated with aging, which is affected by many genetic and environmental factors. Healthy aging conceives human longevity, possibly due to carrying the defensive genes. For instance, FOXO (forkhead box O) genes determine human longevity. FOXO transcription factors are involved in the regulation of longevity phenomenon via insulin and insulin-like growth factor signaling. Only one FOXO gene (FOXO DAF-16) exists in invertebrates, while four FOXO genes, that is, FOXO1, FOXO3, FOXO4, and FOXO6 are found in mammals. These four transcription factors are involved in the multiple cellular pathways, which regulate growth, stress resistance, metabolism, cellular differentiation, and apoptosis in mammals. However, the accurate mode of longevity by FOXO factors is unclear until now. This article describes briefly the existing knowledge that is related to the role of FOXO factors in human longevity.


Author(s):  
Nitesh D. Sharma ◽  
Esra’a Keewan ◽  
Ksenia Matlawska-Wasowska

Involvement of the Central Nervous System (CNS) in acute leukemia confers poor prognosis and lower overall survival. Existing CNS-directed therapies are associated with a significant risk of short- or long-term toxicities. Leukemic cells can metabolically adapt and survive in the microenvironment of the CNS. The supporting role of the CNS microenvironment in leukemia progression and dissemination has not received sufficient attention. Understanding the mechanism by which leukemic cells survive in the nutrient-poor and oxygen-deprived CNS microenvironment will lead to the development of more specific and less toxic therapies. Here, we review the current literature regarding the roles of metabolic reprogramming in leukemic cell adhesion and survival in the CNS.


2021 ◽  
Vol 11 (6) ◽  
pp. 320-333
Author(s):  
Danielle L. Stutzman

Abstract It is estimated that 8% to 12% of youth are prescribed psychotropic medications. Those in foster care, juvenile justice systems, residential treatment facilities, and with developmental or intellectual disabilities are more likely to be prescribed high-risk regimens. The use of psychotropic medications in this age group is often off-label and can be associated with significant risk, warranting critical evaluation of their role. Landmark trials, pediatric-specific guidelines, and state-driven initiatives play critical roles in supporting evidence-based use of psychotropic medications in children. Overall, there is a lack of literature describing the long-term use of psychotropic medications in youth—particularly with regard to neurobiological, physical, and social changes that occur throughout development. Deprescribing is an important practice in child and adolescent psychiatry, given concerns for over-prescribing, inappropriate polytherapy, and the importance of reevaluating the role of psychotropic medications as children develop.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S482-S483
Author(s):  
Yun-Ting Huang ◽  
Paola Zaninotto ◽  
Andrew Steptoe ◽  
Li Wei

Abstract Diabetes among older people is becoming more common worldwide, and usually accompanied by polypharmacy. However, the role of polypharmacy in older people with diabetes remains uncertain. A nationally representative cross-sectional study, ELSA 2012/2013, was used and 7729 participants aged 50-109 were investigated. Polypharmacy was defined as taking five to nine long-term used medications daily for chronic diseases or chronic symptoms, while using ten or more medications was excessive polypharmacy. The presence of illness was defined as either self-reported diagnosis or being prescribed specific medications for the condition. Data showed the prevalence of polypharmacy was 21.4%, and only 3% was excessive polypharmacy. 51.6% of diabetic people reported polypharmacy and 10.2% excessive polypharmacy. These rates were significantly higher than the 16.4% polypharmacy and 1.8% excessive polypharmacy among people without diabetes (p < 0.001). Among people with three or more comorbidities, polypharmacy was present in 61.5% of people with diabetes, compared with 36.0% in people without diabetes. Significant risk factors for polypharmacy were diabetes (Relative-risk ratios/RRR=4.06, 95% CI 3.38, 4.86), older age (RRR=1.02, 95% CI 1.01, 1.03), male (RRR=0.64, 95% CI 0.55, 0.75), more comorbidity (RRR=2.46, 95% CI 2.30, 2.62), living with a partner (RRR=1.20, 95% CI 1.01, 1.42), and less wealth (RRR=0.93, 95% CI 0.87, 0.98). However, age, cohabitation, and wealth were not significantly related to excessive polypharmacy. Diabetes and the number of comorbidities were predominant risk factors for excessive polypharmacy. Current evidences confirmed both health condition and socioeconomic status were associated with medication use in older adults.


Blood ◽  
2011 ◽  
Vol 118 (14) ◽  
pp. 3853-3861 ◽  
Author(s):  
Yi Zhang ◽  
Sandra Stehling-Sun ◽  
Kimberly Lezon-Geyda ◽  
Subhash C. Juneja ◽  
Lucie Coillard ◽  
...  

Abstract The Mds1 and Evi1 complex locus (Mecom) gives rise to several alternative transcripts implicated in leukemogenesis. However, the contribution that Mecom-derived gene products make to normal hematopoiesis remains largely unexplored. To investigate the role of the upstream transcription start site of Mecom in adult hematopoiesis, we created a mouse model with a lacZ knock-in at this site, termed MEm1, which eliminates Mds1-Evi1 (ME), the longer, PR-domain–containing isoform produced by the gene (also known as PRDM3). β-galactosidase–marking studies revealed that, within hematopoietic cells, ME is exclusively expressed in the stem cell compartment. ME deficiency leads to a reduction in the number of HSCs and a complete loss of long-term repopulation capacity, whereas the stem cell compartment is shifted from quiescence to active cycling. Genetic exploration of the relative roles of endogenous ME and EVI1 isoforms revealed that ME preferentially rescues long-term HSC defects. RNA-seq analysis in Lin−Sca-1+c-Kit+ cells (LSKs) of MEm1 documents near complete silencing of Cdkn1c, encoding negative cell-cycle regulator p57-Kip2. Reintroduction of ME into MEm1 LSKs leads to normalization of both p57-Kip2 expression and growth control. Our results clearly demonstrate a critical role of PR-domain–containing ME in linking p57-kip2 regulation to long-term HSC function.


1986 ◽  
Vol 111 (2) ◽  
pp. 154-161 ◽  
Author(s):  
Ildo Nicoletti ◽  
Paolo Filipponi ◽  
Leone Fedeli ◽  
Franca Ambrosi ◽  
Camillo Giammartino ◽  
...  

Abstract. In order to gain further insight into the role of dopamine (DA) in the control of TSH release and to investigate whether an increased or defective DA inhibition on pituitary thyrotrophs may be considered responsible for the abnormal TSH dynamics in pathological hyperprolactinaemia, we examined the effect of low-dose DA infusion on TRH stimulated TSH secretion in normally cycling women and in patients with pathological hyperprolactinaemia. The effect of long-term bromocriptine therapy on TSH dynamics was also evaluated in a selected group of hyperprolactinaemic women. Fifty-two hyperprolactinaemic patients with no other signs of pituitary or thyroid dysfunction had significantly higher mean TSH serum concentrations and mean TSH peak values after TRH administration than 75 healthy controls. Furthermore, the TSH rises induced by the DA-synthesis inhibitor α-methyl-p-tyrosine (AMPT, 500 mg orally) were enhanced in both prolactinoma and 'idiopathic hyperprolactinaemia' patients as compared with controls. There was a positive correlation between the TRH- and AMPT-induced TSH rises in the hyperprolactinaemic group. Low-dose DA infusion (0.1 μg/kg min) reduced TSH response to TRH in both regularly cycling women and patients with hyperprolactinaemic amenorrhoea. Long-term bromocriptine therapy (2.5 mg tid over 60– 150 days) not only normalized serum Prl levels, but also reduced the TSH response to TRH in 7 hyperprolactinaemic women who had presented exaggerated TSH responses to the basal TRH test. These findings confirm that DA plays a physiological role in the inhibition of TSH release, probably at the level of the anterior pituitary. The fact that both low-dose DA infusion and long-term bromocriptine treatment effectively reduced TSH release in hyperprolactinaemic patients seems to indicate that endogenous DA inhibition of pituitary thyrotrophs is reduced rather than enhanced in pathological hyperprolactinaemia.


1991 ◽  
Vol 11 (4) ◽  
pp. 330-332 ◽  
Author(s):  
Michael L. Nicholson ◽  
Paul R. Burton ◽  
Peter K. Donnelly ◽  
Peter S. Veitch ◽  
John Walls

Long-term survival of the peritoneal catheter is essential for successful CAPD. In our unit, all CAPD catheters are now placed by an open surgical technique, which in some cases has included performing a partial omentectomy. The aim of this study was to assess the influence of omentectomy on CAPD catheter survival. Three hundred consecutive CAPD catheters inserted over a 5-year period were analyzed. Omentectomy was performed in 113 cases (38%). Data relating to a number of potentially significant risk/benefit factors were analyzed using multiple regression analysis (proportional hazards method of Cox). Performing a partial omentectomy at the time of catheter insertion was found to significantly improve CAPD catheter survival (p=0.0002).


2018 ◽  
Vol 47 (3-4) ◽  
pp. 327-341 ◽  
Author(s):  
C. Adam-Guillermin ◽  
T. Hertal-Aas ◽  
D. Oughton ◽  
L. Blanchard ◽  
F. Alonzo ◽  
...  

The ALLIANCE working group on effects of ionising radiation on wildlife brings together European researchers to work on the topics of radiosensitivity and transgenerational effects in non-human biota. Differences in radiation sensitivity across species and phyla are poorly understood, but have important implications for understanding the overall effects of radiation and for radiation protection; for example, sensitive species may require special attention in monitoring and radiation protection, and differences in sensitivity between species also lead to overall effects at higher levels (community, ecosystem), since interactions between species can be altered. Hence, understanding the mechanisms of interspecies radiation sensitivity differences may help to clarify mechanisms underpinning intraspecies variation. Differences in sensitivity may only be revealed when organisms are exposed to ionising radiation over several generations. This issue of potential long-term or hereditary effects for both humans and wildlife exposed to low doses of ionising radiation is a major concern. Animal and plant studies suggest that gamma irradiation can lead to observable effects in the F1 generation that are not attributable to inheritance of a rare stable DNA mutation. Several studies have provided evidence of an increase in genomic instability detected in germ or somatic cells of F1 organisms from exposed F0 organisms. This can lead to induced radiosensitivity, and can result in phenotypic effects or lead to reproductive effects and teratogenesis. In particular, studies have been conducted to understand the possible role of epigenetic modifications, such as DNA methylation, histone modifications, or expression of non-coding RNAs in radiosensitivity, as well as in adaptation effects. As such, research using biological models in which the relative contribution of genetic and epigenetic processes can be elucidated is highly valuable.


2015 ◽  
Vol 156 (47) ◽  
pp. 1904-1907 ◽  
Author(s):  
Attila Szijártó

The critical importance of the ischemic-reperfusive injury is well documented with regards to numerous organs and clinical conditions. Oxygen free radicals play a central role in the mediation of the injury, which dominantly influences the prevalence of postoperative complications, (long term) organ damage, and the potential manifestation of systemic reactions. The both anatomically and pathophysiologically unique ischemic-reperfusive injury of the liver, which is expressively vulnerable to free radicals, is of utmost importance in liver surgery. Several techniques (adaptive maneuvers, chemical agents) are known to ameliorate the reperfusive injury. Based on the prior research of the workgroup of the author, the aim of the current article is to overview the set of measures capable of attenuating ischemic-reperfusive injury (ischemic preconditioning, -perconditioning, administration of adenosine, -inosine, -levosimendan, and -poly-ADP-ribose-polymerase inhibitor), with special attention to the ischemic-reperfusive injury of the liver, as well as the special pathophysiological role of free radicals in mediating hepatic damage. Orv. Hetil., 2015, 156(47), 1904–1907.


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