Cyclooxygenase-2 expression and its association with thyroid lesions

Cyclooxygenase (COX), also known as prostaglandin H synthase, catalyses the formation of prostaglandins from arachidonic acid. It can be expressed in response to various stimuli, such as hormones, mitogens, cytokines, other inflammatory mediators and growth factors. The product of COX-2 activity has been implicated in carcinogenesis by promoting angiogenesis, inhibiting apoptosis, increasing cell invasion and stimulating cell proliferation. It has also been proved that the regular intake of non-steroidal anti-inflammatory drugs (NSAIDs) decreases the risk of developing colon and breast cancers. Thus, it speaks for an important role of COX-2 in growth processes of various types of neoplasms. The connection between COX-2 activity and carcinogenesis has also been examined in human thyroid neoplasms. COX-2 overexpression has been reported in thyroid cancers and also in inflammatory conditions. In consequence there is significant interest whether COX-2 could be of importance as a molecular marker of malignancy in the case of thyroid carcinoma

A brand new medical condition - 6 years old patient with neurological symptoms diagnosed with PIMS-TS (Paediatric Inflammatory Multisystem Syndrome – Temporally Associated with SARS-CoV-2) - case report

Children's multi-system inflammatory syndrome PIMS-TS is a completely new challenge for pediatricians, which has established a separate branch of the fight against the still active COVID-19 pandemic. It turns out that even a pediatric patient who has not suffered symptomatic infection with the SARS-CoV-2 virus, as a result of contact with this pathogen, can develop a severe systemic inflammatory reaction rich in symptoms originating in almost every system of the human body. The first reports of the inflammatory syndrome that is the subject of this work come from May 2020. It is known that the symptoms of PIMS are caused by a multi-system inflammatory response in the body, potentially related to the immune system. The course of this disease may bring to mind other inflammatory diseases in children, such as Kawasaki disease, toxic shock syndrome and MAS macrophage activation syndrome

Impact of biological treatment on intestinal microbiom in children with Crohn's disease

Crohn’s disease (CD) is a chronic, inflammatory illness of the digestive tract, characterized by alternating periods of remission and recurrence. The pathogenesis of CD is still unclear but probably is a result of a complex interaction between immunological, genetic and microbiological disorders. In recent years, there has been an increasing extent of evidence that gut microbiota plays a very important role in the pathogenesis of CD. Currently, the most effective treatment is biological therapy using anti-TNF monoclonal antibodies. It is interesting whether biological drugs resulting in fast remission, contributes to the normalization of the gut microbiota. Due to the fact that the children’s population is a significant percentage of all patients with CD, it is important to pay close attention to the problem of microbiological disorders in this age group. The aim of this study was to investigate whether there are quantitative changes of chosen bacteria species and fungi of the genus Candida in children with Crohn's disease relative to healthy children and assesment of quantitative changes in patients after biological treatment. In the group of children with Crohn’s disease, the numbers in Candida were significantly higher (9.74×1017 CFU/g) than in the control group (9.35×1010 CFU/g, p = 0.011). Biological therapy led to a significant reduction in the amount Candida (5.91×1011) and was comparable with the number in the control group. In the case of bacteria, we observed an increase in S. marcescens (3,4×108) in the patients group compared to the controls (1,85×108) and an increase in L. fermentum (2,34×1010) in relation to healthy children (3,31×108, p = 0,048) Biological treatment had an impact on the decrease in L. fermentum (4,76×109, p = 0.05)

Relative quantification of PIK3CA gene expression level in fine-needle aspiration biopsy thyroid specimens collected from patients with papillary thyroid carcinoma and non-toxic goitre by real-time RT-PCR

<p>Abstract</p> <p>Background</p> <p>Recent studies have shown that the phosphatidylinositol 3-kinase (PI3K) signaling pathway is important regulator of many cellular events, including apoptosis, proliferation and motility. PI3K pathway alterations (<it>PIK3CA </it>gene mutations and/or amplification) have been observed in various human tumours. In the majority of diagnosed cases, mutations are localized in one of the three "hot spots" in the gene, responsible for coding catalytic subunit α of class I PI3K (<it>PIK3CA</it>). Mutations and amplification of <it>PIK3CA </it>gene are characteristic for thyroid cancer, as well.</p> <p>Methods</p> <p>The aim of our study was to examine a gene expression level of <it>PIK3CA </it>in fine-needle aspiration biopsy (FNAB) thyroid specimens in two types of thyroid lesions, papillary thyroid carcinoma (PTC) and non-toxic goitre (NTG). Following conventional cytological examination, 42 thyroid FNAB specimens, received from patients with PTC (n = 20) and NTG (n = 22), were quantitatively evaluated regarding <it>PIK3CA </it>expression level by real-time PCR in the ABI PRISM^®7500 Sequence Detection System.</p> <p>Results</p> <p>Significantly higher expression level (RQ) of <it>PIK3CA </it>in PTC group has been noted in comparison with NTG group (p < 0.05).</p> <p>Conclusion</p> <p>These observations may suggest role of <it>PIK3CA </it>alterations in PTC carcinogenesis.</p

COX-2 expression in papillary thyroid carcinoma (PTC) in cytological material obtained by fine needle aspiration biopsy (FNAB)

<p>Abstract</p> <p>Background</p> <p>COX-2 is an enzyme isoform that catalyses the formation of prostanoids from arachidonic acid. An increased <it>COX-2 </it>gene expression is believed to participate in carcinogenesis. Recent studies have shown that <it>COX-2 </it>up-regulation is associated with the development of numerous neoplasms, including skin, colorectal, breast, lung, stomach, pancreas and liver cancers. <it>COX-2 </it>products stimulate endothelial cell proliferation and their overexpression has been demonstrated to be involved in the mechanism of decreased resistance to apoptosis. Suppressed angiogenesis was found in experimental animal studies as a consequence of null mutation of <it>COX-2 </it>gene in mice. Despite the role of <it>COX-2 </it>expression remains a subject of numerous studies, its participation in carcinogenesis or the thyroid cancer progression remains unclear.</p> <p>Methods</p> <p>Twenty three (23) patients with cytological diagnosis of PTC were evaluated. After FNAB examination, the needle was washed out with a lysis buffer and the obtained material was used for <it>COX-2 </it>expression estimation. Total RNA was isolated (RNeasy Micro Kit), and RT reactions were performed. β-actin was used as endogenous control. Relative <it>COX-2 </it>expression was assessed in real-time PCR reactions by an ABI PRISM 7500 Sequence Detection System, using the ΔΔC_Tmethod.</p> <p>Results</p> <p><it>COX-2 </it>gene expression was higher in patients with PTC, when compared to specimens from patients with non-toxic nodular goitre (NTG).</p> <p>Conclusions</p> <p>The preliminary results may indicate <it>COX-2 </it>role in thyroid cancer pathogenesis, however the observed variability in results among particular subjects requires additional clinical data and tumor progression analysis.</p