MATERIALS AND METHODS: This study involved 396 subjects (198 NDHT, age and gender matched 198 normotensives; age, 30 to 50 years). Parameters of LVDF included Doppler-echocardiographic measurements of peak early (E) and late (A) diastolic velocities, E-wave deceleration time (DT) and isovolumetric relaxation time (IVRT). E/A ratio of <1 was taken as an indicative of DD.
RESULTS: Patients with NDHT had reduced E/A ratio (1.27 +/- 0.41 vs 1.37 +/- 0.35, P <0.001) and shortened DT (180.0 +/- 40.0 ms vs 190.0 +/- 30.0 ms, P = 0.025). The peak A velocity and IVRT were increased in the NDHT group [(62.73 +/- 13.82 ms vs 58.26 +/- 12.40 ms, P = 0.002) and (90.0 +/- 20.0 ms vs 80.0 +/- 10.0 ms, P <0.001), respectively]. Peak E velocity was similar in both groups. The prevalence of DD was increased in the NDHT group, 18.6% (32) vs 3.4% (6), P <0.001. Of the 32 NDHT subjects who had DD, 84.4% (27) had no left ventricular hypertrophy (LVH) and 15.7% (5) had LVH. Diastolic function was negatively correlated with age, body mass index, systolic blood pressure, diastolic blood pressure and left ventricular mass index.
CONCLUSION: Impairment in LVDF occurs in NDHT which may precede structural abnormalities. Hypertension, obesity, older age and LVH are associated with worsening of diastolic function.
METHODS: Initially, MTT proliferation assay was used to test the cell viability with various doses of MNQ (5-100 µM). As the half maximal inhibitory concentration (IC50) was obtained, glucose uptake and lactate assays of the cells were tested with IC50 dose of MNQ. The treated cells were also subjected to gene and protein analysis of glycolysis-related molecules (GLUT1 and Akt).
RESULTS: The results showed that MNQ decreased the percentage of MDA-MB-231 cell viability in a dose-dependent manner with the IC50 value of 29 µM. The percentage of glucose uptake into the cells and lactate production decreased significantly after treatment with MNQ as compared to untreated cells. Remarkably, the expressions of GLUT1 and Akt molecules decreased in MNQ-treated cells, suggesting that the inhibition of glycolysis by MNQ is GLUT1-dependent and possibly mediated by the Akt signaling pathway.
CONCLUSION: Our findings indicate the ability of MNQ to inhibit the glycolytic activities as well as glycolysis-related molecules in MDA-MB-231 cells, suggesting the potential of MNQ to be further developed as an effective anticancer agent against TNBC cells.
METHODS: A single-blinded randomised hospital-based trial was undertaken involving 540 nurses assigned to two intervention groups and a waitlist group. Intervention group-1 received a face-to-face training course comprising 20 h spread over six weeks and a hard copy of the module, while intervention group-2 only received the hard copy of the module "without training". In contrast, the waitlist group did not receive anything during the period of collecting data. A self-administered NI control measures-evaluation questionnaire was utilised in collecting the data from the participants; before the intervention, at six weeks and 3 months after the end of the intervention. The period of data collection was between 1st May and 30th October 2016.
RESULTS: The results from collecting and analysing the data showed a statistically significant difference in the mean knowledge scores between the intervention groups that were detectable immediately post-intervention with a mean difference (MD) of 4.31 (P
MATERIALS AND METHODS: We analyzed Ki 67 immuno-histochemistry of 31 consecutive cases staged III giant cell tumor to determine the clinico-pathological correlation. There were 19 male patients compare to 12 females. The mean age was 33.8 years ranged from 18 to 59 years. Five cases presented with local recurrence prior to wide resection and one case had multiple recurrences there after. Six cases had pulmonary metastases. Expression of Ki 67 antigen was evaluated by immuno-histochemical staining techniques using the avidin-biotin perioxidase complex method using an LSAB2 kit (Dako, Glostrup, Denmark). The primary antibody used in this study was Ki-67 (MIB-I clone, dilution 1:25; Dako).
RESULTS: The mean value of Ki-67 index obtained as a percentage of 1000 background cells was 8.15 (ranged 1.00 - 20.0). The median Ki 67 index was 7.5 with standard deviation of 5.12. The Ki 67 index of recurrence tumor was 4.323 compared to 6.05 without recurrence and was not statistically significant (mean difference of 0.865 with p value in independent t test of 0.736). The Ki 67 index was also not statistically significant in the presence of pulmonary metastases with the mean value of metastases group of 6.681 compared to 2.890 without metastases (mean difference of 1.895 with p value in independent t test of 0.424).
CONCLUSION: Ki 67 index is not use-full prognostic marker for aggressive type of giant cell tumor of the bone.