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In order to improve the therapeutic efficiency of the chemotherapeutic drug paclitaxel in tumors, a folate-based Paclitaxel nanoemulsion (FNEs) was developed for tumor targeted treatment.

In this study, we designed a folate-targeted nanoemulsion (folate/PEG-DSPE/nanoemulsion, FNEs) based on the traditional nanoemulsion using the principle of long-circulation targeting receptor mediated. The nanoemulsion (folate/PEG-DSPE/nanoemulsion, FNEs) was fabricated using high-pressure homogenization with a microfluidizer.

The nanoemulsion (folate/PEG-DSPE/nanoemulsion, FNEs) can improve the delivery efficiency of nanocarriers at the tumor site by virtue of the high expression of folate receptors on the tumor surface. Malvern Nanoseries device and transmission electron microscopy (TEM) analyses showed that the nanoemulsions were spherical with an average diameter of 140nm. The nanoemulsions can effectively carry paclitaxel (PTX) with an encapsulation rate of about 95%. And in vitro experiments have shown that it camors, and provide an useful reference for solving the problem of low efficacy of chemotherapy drugs in clinical treatment of tumors. Graphical Abstract Schematic representation of Folic acid/PEG-DSPE/nano-emulsion (FNEs) specifically target tumor cells and enhanced anti-tumor effects.This study aimed to investigate the correlation between bone mineral density (BMD) with hemoglobin and ferritin levels in Palestinian patients suffering from various types of hemoglobinopathies. The study revealed the thresholds of hemoglobin and ferritin to protect against low BMD in these patients.

Iron overload is the main cause of low BMD in subjects with hemoglobinopathies. We used iron overload-related parameters like hemoglobin and ferritin to estimate the cutoff values required to maintain bone health and identify subjects with low BMD.

Palestinian patients (135) suffering from various types of hemoglobinopathies were recruited from various medical centers including 87 β thalassemia major (TM), 13 thalassemia intermedia (TI), 16 sickle cell anemia (SCA), 17 sickle cell thalassemia (SCT), and 1 thalassemia trait (TT). AZD5305 Most subjects (84%) were below the age of 30 years. BMD was measured and the z score was used to identify subjects with low BMD (z < – 2.0). Receiver operator characteristic (ROC) cMD with an area under the ROC curve (AUC) 0.699 and sensitivity and specificity were 87.9% and 47.7%, respectively. Similar analysis revealed that Ferritin threshold to protect against low BMD should be maintained below 2300 ng/ml with AUC 0.619 and sensitivity and specificity were 55.0% and 71.4%, respectively.

The results of this study strongly recommend to maintain hemoglobin levels above 9.3 g/dL and ferritin below 2300 ng/ml to protects against low BMD in TM subjects and patients suffering from the other related hemoglobinopathies.

The results of this study strongly recommend to maintain hemoglobin levels above 9.3 g/dL and ferritin below 2300 ng/ml to protects against low BMD in TM subjects and patients suffering from the other related hemoglobinopathies.Six-transmembrane protein of prostate (Stamp2) protects from diabetes and atherosclerosis in mice via anti-inflammatory mechanisms. As chronic inflammation is a hallmark of pulmonary arterial hypertension (PAH), we investigated the role of Stamp2. Stamp2 expression was substantially reduced in the lung of humans with idiopathic PAH, as well as in experimental PAH. In Stamp2-deficient mice, hypoxia modestly aggravated pulmonary vascular remodeling and right ventricular pressure compared to WT. As endothelial cell (EC) and pulmonary arterial smooth muscle cell (PASMC) phenotypes drive remodeling in PAH, we explored the role of Stamp2. Knock-down of Stamp2 in human EC neither affected apoptosis, viability, nor release of IL-6. Moreover, Stamp2 deficiency in primary PASMC did not alter mitogenic or migratory properties. As Stamp2 deficiency augmented expression of inflammatory cytokines and numbers of CD68-positive cells in the lung, actions of Stamp2 in macrophages may drive vascular remodeling. Thus, PASMC responses were assessed following treatment with conditioned media of primary Stamp2-/- or WT macrophages. Stamp2-/- supernatants induced PASMC proliferation and migration stronger compared to WT. A cytokine array revealed CXCL12, MCP-1 and IL-6 as most relevant candidates. Experiments with neutralizing antibodies confirmed the role of these cytokines in driving Stamp2’s responses. In conclusion, Stamp2 deficiency aggravates pulmonary vascular remodeling via cross-talk between macrophages and PASMC. Despite a substantial pro-inflammatory response, the hemodynamic effect of Stamp2 deficiency is modest suggesting that additional mechanisms apart from inflammation are necessary to induce severe PAH.Oral propranolol is the treatment of choice for infantile hemangiomas. The growth relapse rate following oral propranolol therapy is not well established in the literature. The present study aimed at determining predictors of growth relapse of infantile hemangiomas after discontinuation of oral propranolol therapy. A retrospective analysis was performed of all cases of infantile hemangiomas aged ≤ 12 months undergoing oral propranolol therapy in a 6-year period. Of the 198 cases, regrowth after oral propranolol therapy was observed in 35 patients (18%). Facial hemangiomas showed a higher (p = 0.003) relapse rate as compared with other hemangiomas (27 out of 107 facial cases vs. 8 out of 91 with other location, respectively 25% and 8.8%). Of 35 growth relapses cases, 66% of cases (23 in total, 18 facial and 5 otherwise located hemangiomas) underwent a second cycle of oral propranolol therapy (median length of treatment 3 months, interquartile range 2-3). All cases had a successful outcome, either after a single cycle oral propranolol therapy (163 cases, 82%), or in case of regrowth, after a second therapy cycle (23 cases, 12%) or further conservative management (12 cases, 6%).Conclusion Facial infantile hemangiomas relapse earlier and more frequently after oral propranolol therapy. We suggest to closely monitor these patients, as a second cycle of propranolol may be indicated. Prolonged oral propranolol therapy might be considered for facial infantile hemangiomas. What is Known • Oral propranolol is the treatment of choice for infantile hemangiomas. • The growth relapse rate following oral propranolol is not well established. What is New • The present study points out that facial infantile hemangioma relapse earlier and more frequently after oral propranolol therapy. • Patients with facial infantile hemangiomas should be monitored after propranolol therapy discontinuation.