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Background/Objectives: Lower extremity amputations (LEAs) are a burdensome complication of peripheral artery disease (PAD) and/or arterial embolism and thrombosis (AET). We assessed the trends in PAD- and/or AET-related LEAs in Romania. Methods: This retrospective study (2015–2019) analyzed data on minor and major LEAs in hospitalized patients recorded in the National School for Public Health, Management, and Health Education database. The absolute numbers and incidences of LEAs were analyzed by diagnosis type, year, age, sex, and amputation level. Results: Of 38,590 vascular disease-related amputations recorded nationwide, 36,162 were in PAD and 2428 in AET patients. The average LEA incidence in the general population was 34.73 (minimum: 31.96 in 2015; maximum: 36.57 in 2019). The average incidence of major amputations, amputations above the knee, hip amputations, amputations below the knee, and minor amputations was 16.21 (15.62 in 2015; 16.84 in 2018), 13.76 (13.33 in 2015; 14.28 in 2018), 0.29 (0.22 in 2017; 0.35 in 2019), 2.15 (2.00 in 2015; 2.28 in 2019), and 18.52 (16.34 in 2015; 20.12 in 2019), respectively. Yearly PAD- and/or AET-related amputations were significantly higher in men versus women. The overall number of LEAs increased with age, particularly in patients ≥ 70 years. The increase in the total number of amputations was mainly due to a constant rise in minor amputations for both groups, regardless of gender. Conclusions: PAD- and/or AET-related LEAs in Romania increased from 2015 to 2019, with men having a greater incidence than women. Raising awareness and effective management strategies are needed to prevent LEAs. [ABSTRACT FROM AUTHOR]

Aim: The present study aimed at identifying the pattern of patients with critical limb ischemia (CLI) compared with those with peripheral arterial occlusive disease (PAOD).

Abstract Epithelioid hemangioendothelioma (EHE) is a rare, well-differentiated endothelial tumor with intermediate malignancy which develops more frequently from the peripheral veins, generally in the lower limb. Bone EHE comprises less than 1% of the bone neoplasms. We present the case of a young man, 24-year-old, with EHE of the forearm with secondary involvement of the distal radius. The location and the extension of the tumor allowed a wide excision, without the reconstruction of radius, followed by adjuvant radiotherapy, with a subsequent favorable evolution. Based on the clinical, radiographic, and pathological features of the EHE review, we concluded that it is difficult to adopt a standardized therapeutic approach due to the extremely low incidence of the bone involvement in EHE and the variable tendencies towards malignancy of this tumor. To our knowledge this is the third case of EHE with the involvement of the radius.

Tumor necrosis factor alpha (TNF-a) is a pro-inflammatory cytokine involved in the promotion and progression of cancer, including triple negative breast cancer cells. Thus, there is significant interest in understanding the molecular signaling pathways that connect TNF-a with the survival of tumor cells. In our experiments, we used as an in vitro model for triple negative breast cancer the cell line Hs578T. The purpose of this study is to determine the gene expression profiling of apoptotic signaling networks after blocking TNF-a formation by using specially designed siRNA molecules to target TNF-a messenger RNA. Knockdown of TNF-a gene was associated with cell proliferation inhibition and apoptosis, as observed by monitoring the cell index using the xCELLigence RTCA System and flow cytometry. PCR array technology was used to examine the transcript levels of 84 genes involved in apoptosis. 15 genes were found to be relevant after comparing the treated group with the untreated one of which 3 were down-regulated and 12 up-regulated. The down-regulated genes are all involved in cell survival, whereas the up-regulated ones are involved in and interact with pro-apoptotic pathways. The results described here indicate that the direct target of TNF-a in the Hs578T breast cancer cell line increases the level of certain pro-apoptotic factors that modulate different cellular networks that direct the cells towards death. [ABSTRACT FROM AUTHOR]

Previous studies indicate that green tea extract may inhibit breast cancer progression by blocking angiogenesis, although the molecular mechanisms are not well defined. Epigallocatechin-3-gallate (EGCG) is the major biologically active component of green tea. In this study we evaluated the cell proliferation and relative gene expression of vascular endothelial growth factor (VEGF) expression on Hs578T human breast cancer cell line at 24, 48 and 72 hours after 10 microM of EGCG treatment. Also, we evaluated the effect of this natural compound on the cell migratory behaviour based on real-time XCELLigence data. Cell proliferation becomes significantly low at 72 hours. EGCG had a dual effect on the VEGF gene expression timeline: after a first increase at 24 hours, it started to decrease at 48 and 72 hours. The inhibition of cell proliferation at 72 hours suggests a possible reactivation of apoptosis. The dual effect on VEGF expression in the presence of EGCG suggests the complexity of the angiogenic switch leading to the modulation of the cell migration processes. It also emphasizes the importance of the metabolite products in the modulation of these effects. Our findings have shown that EGCG suppresses the growth, migration and invasion of human breast cancer cells by inhibiting VEGF expression. A better understanding of this mechanism may lead to an improved strategy for tumor therapy based on the inhibition of angiogenesis.

Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine involved in the promotion and progression of cancer, including triple negative breast cancer cells. Thus, there is significant interest in understanding the molecular signaling pathways that connect TNF-α with the survival of tumor cells. In our experiments, we used as an in vitro model for triple negative breast cancer the cell line Hs578T. The purpose of this study is to determine the gene expression profiling of apoptotic signaling networks after blocking TNF-α formation by using specially designed siRNA molecules to target TNF-α messenger RNA. Knockdown of TNF-α gene was associated with cell proliferation inhibition and apoptosis, as observed by monitoring the cell index using the xCELLigence RTCA System and flow cytometry. PCR array technology was used to examine the transcript levels of 84 genes involved in apoptosis. 15 genes were found to be relevant after comparing the treated group with the untreated one of which 3 were down-regulated and 12 up-regulated. The down-regulated genes are all involved in cell survival, whereas the up-regulated ones are involved in and interact with pro-apoptotic pathways. The results described here indicate that the direct target of TNF-α in the Hs578T breast cancer cell line increases the level of certain pro-apoptotic factors that modulate different cellular networks that direct the cells towards death.