The effect of curcumin on low-passage glioblastoma cells in vitro.

BACKGROUND: Plant extract therapy has been the cornerstone of cancer treatment for many years. The natural component curcumin demonstrated antineoplastic effects on different type of tumor cells. In this study, we explored the effectiveness of curcumin against low-passage human primary glioblastoma (GB) cell cultures. MATERIALS AND METHODS: Early passage GB cell cultures (GB3B, GB4B, and GB5B) were established from fresh samples tissue obtained from GB patients. Growth rate (GR) and doubling time (DT) was determined for each cell line. The cytotoxic effect of curcumin was quantified by hemocytometer cell counting, using trypan blue. To study the changes in cell shape, GB cells exposed to a concentration corresponding to inhibitory concentration 50 (IC50) of curcumin were studied by phase-contrast microscopy by capturing images during the treatment. RESULTS: Our results showed that GB cells proliferate with a GR of 0.2872 and a DT of 2.41 days for GB3B, a GR of 0.2787 and a DT of 2.49 days for GB4B, and a GR of 0.2787 and a DT of 2.49 days for GB5B. Curcumin induced cell death in GB cells in a time- and dose-dependent manner. The IC50 for GB3B was 46.4 µM, for GB4B was 78,3 µM, and for GB5B was 47.7 µM. Phase contrast microscopy showed that cultures treated with curcumin in a concentration corresponding to IC50 contained rounded cells and cell fragments, 72 h after the treatment. CONCLUSIONS: The results of the present investigation proved that curcumin is a natural compound potentially useful in the fight against GB.

[A rare cause of pulmonary arterial hypertension diagnosed in an elderly patient]. / Cauza rara de hipertensiune pulmonara diagnosticata la un pacient vârstnic.

Pulmonary arterial hypertension (PAH) is a rare and incurable disease, related to right ventricle overload and failure, which are late consequences of asymptomatic progressive pulmonary vascular occlusion. The clinical approach requires: a high clinical suspicion; the detection and confirmation of PAH by echo-Doppler and right heart catheterisation; identification of an etiology; assessment of functionality and life expectancy; and reversibility testing. We present the case of a 68-year-old male patient presenting with progressive fatigability and shortness of breath, abnormal heart beats in the last 4 years, aggravated in the last year. Clinical findings showed signs of cardiac failure. Multiple echocardiographies demonstrated right atrial and right ventricular dilatation, with severe PAH, subsequent severe pulmonary and tricuspid regurgitation, mild mitral and aortic regurgitation and efficient left ventricular function. Subsequent cardiac catheterization confirms severe PAH, excludes VSD, and sees a left-to-right shunt but an ASD could not be anatomically localized. Left ventricular function and the coronary arteries were normal. Transesophageal echocardiography demonstrated an ASD sinus venosus with bidirectional shunt associated with partial abnormal in pulmonary venous drainage, with right supranumery pulmonary vein with drainage in the sinus venosus, the upper and inferior right pulmonary veins flowing into the right atrium, the upper and inferior left pulmonary veins Bowing into the left atrium, associated to important superior and inferior vena cava dilatation. The patient receives treatment for right heart failure, oral anticoagulation, antiarrhythmic drugs, cardio-pulmonary rehabilitation is initiated and he is referred to a center specialised in PAH, for bosentan treatment. In this patient, it is surprising that even born with a potentially cyanogenic congenital heart disease, his condition is discovered at an advanced age on the edge for evolution towards an Eisenmenger Syndrome, being fairly asymptomatic until the last year when he receives treatment for left heart failure.