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The anti-tumoral activity of somatostatin has been demonstrated in both animal experiments and human tumors. Clinical trials have reported conflicting results. We therefore hypothesized that somatostatin might have different effects in various hepatocellular carcinoma cells. Their clarification would possibly allow for the better selection of patients suitable for the optimal treatment results. We studied the mRNA and protein expression of TNF receptors and the TNFa-induced apoptosis using the HepG2 and the Hep3B human hepatocellular carcinoma cells after incubation with the somatostatin analog octreotide. RT-PCR, Western blot, and parameters associated with apoptosis (NF-kB nuclear translocation, P65 Ser536 and P65 Ser468 phosphorylation, DNA fragmentation) were assessed. Only TNFR1 was constitutively present in the two cell lines. Octreotide incubation led to an earlier reduction in TNFR1 mRNA and protein in HepG2 compared to Hep3B cells (1 h and 6–12 h, respectively). NF-kB translocation to the nucleus was induced by TNFa and was more prominent in Hep3B. Translocation was unaffected by octreotide. Serine phosphorylation was significantly induced by TNFa and was more evident in the Hep3B cells. TNFa-induced Ser536 phosphorylation was inhibited by octreotide only in the HepG2 cells. DNA fragmentation was not influenced by either octreotide or TNFa in the HepG2 cells, but TNFa induced fragmentation in the Hep3B cells (1.8-fold increase) verified by the TUNEL index (43 compared to 19 for the HepG2 cells). Octreotide and TNFa co-incubation induced apoptosis in the HepG2 cells (1.7-fold increase compared to controls) but inhibited apoptosis in the Hep3B cells. We conclude that: (1) octreotide reduced TNFR1 receptor expression in both cell lines, (2) parameters of apoptosis were differentially affected by octreotide in the two cell lines, and (3) this might be a partial explanation for the conflicting results of somatostatin analog treatment in human hepatocellular carcinoma trials. [ABSTRACT FROM AUTHOR]

Respiratory disorders significantly impact adolescents' health, often resulting in hospital admissions. Meteorological elements such as wind patterns have emerged as potential contributors to respiratory symptoms. However, it remains uncertain whether fluctuations in wind characteristics over extended periods have a tangible impact on respiratory health, particularly in regions characterized by distinct annual wind patterns. Crete is situated in the central-eastern Mediterranean Sea and frequently faces southerly winds carrying Sahara Desert sand from Africa and northerly winds from the Aegean Sea. This retrospective study analyzes long-term wind direction data and their relationship to respiratory symptoms observed in children up to 14 years old admitted at the University Hospital of Heraklion between 2002 and 2010. Symptoms such as headache, dyspnea, dry cough, dizziness, tachypnea, throat ache, and earache were predominantly reported during the presence of southern winds. Fever, productive cough, and chest pain were more frequently reported during northern winds. Cough was the most common symptom regardless of the wind pattern. Southern winds were significantly associated with higher probabilities of productive or non-productive cough, headache, dyspnea, tachypnea, dizziness, earache, and throat ache. Northern winds were related to a higher incidence of productive cough. Rhinitis, asthma, allergies, pharyngitis, and sinusitis were related to southern winds, while bronchiolitis and pneumonia were associated with northern winds. These findings underscore the critical role of local climatic factors, emphasizing their potential impact on exacerbating respiratory conditions in children. Moreover, they point out the need for further research to elucidate the underlying mechanisms and develop targeted interventions for at-risk populations. [ABSTRACT FROM AUTHOR]

Chronic inflammation is an important factor in the development of cancer. Macrophages found in tumors, known as tumor associated macrophages (TAMs), are key players in this process, promoting tumor growth through humoral and cellular mechanisms. 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE), an arachidonic acid metabolite, has been described to possess a potent chemoattractant activity for human white blood cells (WBCs). The biological actions of 5-oxo-ETE are mediated through the GPCR 5-oxo-6E,8Z,11Z,14Z-eicosatetraenoic acid receptor (OXER1). In addition, we have previously reported OXER1 as one of the membrane androgen receptors with testosterone antagonizing 5-oxo-ETE's actions. OXER1 is highly expressed in inflammatory cells and many normal and cancer tissues and cells, including prostate and breast cancer, promoting cancer cell survival. In the present study we investigate the expression and role of OXER1 in WBCs, THP-1 monocytes, and THP-1 derived macrophages, as well as its possible role in the interaction between macrophages and cancer cells (DU-145 and T47D). We report that OXER1 is differentially expressed between WBCs and macrophages and that receptor expression is modified by LPS treatment. Our results show that testosterone and 5-oxo-ETE can act in an antagonistic way affecting Ca2+ movements, migration, and cytokines' expression in immune-related cells, in a differentiation-dependent manner. Finally, we report that 5-oxo-ETE, through OXER1, can attract macrophages to the tumor site while tumor cells' OXER1 activation in DU-145 prostate and T47D breast cancer cells, by macrophages, induces actin cytoskeletal changes and increases their migration. [ABSTRACT FROM AUTHOR]

Cancers of the colon and rectum have been classically viewed as the same disease entity, namely colorectal cancer (CRC), one of the most common cancers in humans and the third [...], Background: Colorectal cancer is one of the most common cancers and the third leading cause of cancer death in both sexes. The disease progresses as a multistep process and is associated with genetic alterations. One of the characteristic features of cancer is telomerase activation. We sought to evaluate the differences in telomerase activity between colon cancer and adjacent normal tissue and to correlate the differences in telomerase activity between different locations with clinicopathological factors and survival. Methods: Matched colon tumour samples and adjacent normal mucosa samples 10 cm away from the tumour were collected during colectomy. We assessed telomerase activity using real time polymerase chain reaction. Several pathological characteristics of tumours, including p53, Ki-67, p21, bcl2 and MLH1 expression were also studied. Results: We collected samples from 49 patients. There was a significantly higher telomerase activity in colon cancer tissue than normal tissue. Adenocarcinomas of the right colon express significantly higher telomerase than left-side cancers. Colon cancers and their adjacent normal tissue had significantly more telomerase and were more positive to MLH1 than rectal cancers. The expression of p53 negatively correlated to telomerase activity and was linked to better patient survival. Conclusion: Colon and rectal cancers seem to have different telomerase and MLH1 profiles, and this could be another factor for their different biologic and clinical behaviour and progression. These results support the idea that the large bowel cannot be considered a uniform organ, at least in the biology of cancer. Contexte: Le cancer colorectal est l'un des cancers les plus repandus; il arrive au troisieme rang des deces attribuables au cancer chez les hommes et les femmes. La maladie progresse en plusieurs etapes et est associee a des anomalies genetiques. L'une des principales caracteristiques du cancer est l'activation de la telomerase. Nous avons voulu evaluer les differences d'activite de la telomerase entre les tissus touches par le cancer du colon et les tissus adjacents normaux afin d'etablir une correlation entre les differences d'activite de la telomerase selon la localisation d'une part et les facteurs clinicopathologiques et la survie d'autre part. Methodes: Lors de colectomies, nous avons recueilli des echantillons tissulaires jumeles de tumeur du colon et de muqueuse adjacente normale a 10 cm du foyer tumoral. Nous avons mesure l'activite de la telomerase a l'aide de la reaction en chaine de la polymerase en temps reel. Plusieurs caracteristiques pathologiques des tumeurs ont aussi ete analysees, y compris l'expression des genes p53, Ki-67, p21, bcl2 et MLH1. Resultats: Nous avons recueilli des echantillons aupres de 49 patients. Nous avons note une activite nettement plus intense de la telomerase dans les tissus touches par le cancer du colon que dans les tissus normaux. Les adenocarcinomes du colon ascendant expriment une activite de la telomerase significativement plus intense que les cancers du colon descendant. Les cancers du colon et les tissus adjacents normaux presentaient une activite significativement plus intense de la telomerase et etaient plus souvent positifs a l'egard du MLH1 comparativement aux cancers rectaux. L'expression du p53 a ete en correlation negative avec l'activite de la telomerase et a ete associee a une meilleure survie chez les patients. Conclusion: Les cancers du colon et du rectum semblent avoir des profils differents au plan de la telomerase et du gene MLH1. Ce facteur pourrait entre autre expliquer leur comportement et leur progression biologiques et cliniques distincts. Ces resultats appuient l'hypothese selon laquelle le colon ne peut etre considere comme un organe uniforme, du moins en ce qui concerne la biologie du cancer.