Increased Great Saphenous Vein Diameter at the Level of Knee among Patients with Varicose Veins in a Tertiary Care Centre: A Descriptive Cross-sectional Study.

Introduction: Colour Doppler ultrasonography plays an important role in determining the morphological and hemodynamic information of the venous system. This study aimed to find out the prevalence of increased great saphenous vein diameter at the level of the knee among patients with varicose veins in a tertiary care centre. Methods: A descriptive cross-sectional study was carried out in the Department of Radiology at a tertiary care centre from 30 October 2021 to 31 March 2022 after taking ethical approval from the Institutional Review Committee (Reference number: 028-077/078). A convenience sampling technique was used for the study. The study group consisted of patients over 18 years, coming for ultrasonography examination of the lower limb with the clinical symptoms and signs of varicose veins. The great saphenous vein diameter was measured at the level of the medial femoral condyle of the knee using the software in the ultrasonography unit. B mode, colour Doppler and spectral analysis were done. A cut-off value of 5 mm for the diameter of the great saphenous vein was taken to indicate the presence or absence of varicosity and saphenofemoral reflux. Point estimate and 90% Confidence Interval were calculated. Results: Among 72 patients with varicose veins, the diameter of the great saphenous vein was increased in 59 (81.94%) (74.50-89.38, 90% Confidence Interval) patients. Conclusions: The mean diameter of the great saphenous vein in our study was similar when compared to other studies conducted in similar settings. Keywords: saphenous vein; ultrasonography; varicose veins.

An indirect role for oncomir-519b in the expression of truncated neurokinin-1 in breast cancer cells.

Neurokinin 1 (NK1) encodes full-length (NK1-FL) and truncated (NK1-Tr) receptors, with distinct 3' UTR. NK1-Tr exerts oncogenic functions and is increased in breast cancer (BC). Enhanced transcription of NK1 resulted in higher level of NK1-Tr. The 3' UTR of these two transcripts are distinct with NK1-Tr terminating at a premature stop codon. NK1-Tr mRNA gained an advantage over NK1-FL with regards to translation. This is due to the ability of miR519B to interact with sequences within the 3' UTR of NK1-FL, but not NK1-Tr since the corresponding region is omitted. MiR519b suppressed the translation of NK1-FL in T47D and MDA-MB-231 resulting in increased NK1-Tr protein. Cytokines can induce the transcription of NK1. However, our studies indicated that translation appeared to be independent of cytokine production by the BC cells (BCCs). This suggested that transcription and translation of NK1 might be independent. The findings were validated in vivo. MiR-519b suppressed the growth of MDA-MB-231 in 7/10 nude BALB/c. In total, increased NK1-Tr in BCCs is due to enhanced transcription and suppressed translation of NK1-FL by miR-519b to reduced tumor growth. In summary, we report on miRNA as a method to further regulate the expression of a spiced variant to promote oncogenesis. In addition, the findings have implications for therapy with NK1 antagonists. The oncogenic effect of NK1-Tr must be considered to improve the efficacy of current drugs to NK1.

CD34 cells from patients with trisomy 8 myelodysplastic syndrome (MDS) express early apoptotic markers but avoid programmed cell death by up-regulation of antiapoptotic proteins.

CD34 cells from patients with trisomy 8 myelodysplastic syndrome (MDS) are distinguished from other MDS cells and from normal hematopoietic cells by their pronounced expression of apoptotic markers. Paradoxically, trisomy 8 clones can persist in patients with bone marrow failure and expand following immunosuppression. We previously demonstrated up-regulation of c-myc and CD1 by microarray analysis. Here, we confirmed these findings by real-time polymerase chain reaction (PCR), demonstrated up-regulation of survivin, c-myc, and CD1 protein expression, and documented comparable colony formation by annexin(+) trisomy 8(-) CD34(+) and annexin(-) CD34 cells. There were low levels of DNA degradation in annexin(+) trisomy 8 CD34 cells, which were comparable with annexin(-) CD34 cells. Trisomy 8 cells were resistant to apoptosis induced by gamma irradiation. Knock-down of survivin by siRNA resulted in preferential loss of trisomy 8 cells. These results suggest that trisomy 8 cells undergo incomplete apoptosis and are nonetheless capable of colony formation and growth.