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Pillai K. R. Upadhyaya Pallavi Prakash Ashish Viswanath Ramaprasad Badrinarayan Srirangam Mukesh H. V. Pai Yogesh 《Education and Information Technologies》2021,26(4):3677-3698
Education and Information Technologies - The current study examines students’ coping process of a forced technological intervention in academic outcome assessment in a higher education... 相似文献
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Mukesh Nandave Ipseeta Mohanty T. C. Nag Shreesh Kumar Ojha Rajan Mittal Santosh Kumari Dharamvir Singh Arya 《Indian journal of clinical biochemistry : IJCB》2007,22(1):22-28
The present study evaluated the cardioprotective potential of vitamin-E by studying its effect on hemodynamic parameters,
lipid peroxidation, myocyte injury marker and ultrastructural changes in model of isoproterenol-induced myocardial necrosis
in rats. Wistar albino male rats (150–200 g) were randomly divided into saline, ISP control, and vit E groups. Vitamin E group
was administered vitamin E at a dose of 100mg/kg/day while saline and ISP control groups received saline orally for one month.
On 29th and 30th day, ISP (85 mg/kg, sc) was administered at an interval of 24 h to vit E and ISP control rats. On 31st day, rats of all groups were anesthetized and hemodynamic parameters were recorded. At the end of experimentation, animals
were sacrificed; hearts were excised and processed for biochemical and ultrastructural studies. ISP administration produced
marked cardiac necrosis as evidenced by significant decrease in my ocardial creatine kinase-MB as well as increase in malonaldialdehyde
levels. ISP-induced myocardial necrosis resulted in myocardial dysfunction as evidenced by significant depression in heart
rate and mean arterial pressure in the ISP control group as compared to saline control. Salient ultrastructural changes including
extensive loss of myofibrils, muscle necrosis, loss of mitochondria, and formation of several intracytoplasmic vacuoles and
lipid droplets further confirmed the ISP-induced myocardial damage. However, subsequent to ISP challenge, vit E treatment
significantly preserved the myocardium by restoring myocardial CK-MB activity, inhibiting the ISP-induced lipid peroxidation
and ultrastructural changes. Additionally, pre-and co-treatment of vit E prevented the deleterious ultrastructural changes
caused by ISP. These beneficial effects of chronic vit E treatment also translated into significant restoration of the altered
hemodynamic parameters. The present study clearly demonstrated the cardioprotective potential of vit E at dose of 100 mg/kg
in ISP-induced model of myocardial necrosis in rats. The significant restoration of altered hemodynamic parameters, myocardial
CK-MB activity, prevention of ISP-induced rise in lipid peroxidation and ultrastructural changes may confirm its cardioprotective
effect. 相似文献
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Mukesh Nandave S K Ojha Ranjit Kaur 《Indian journal of clinical biochemistry : IJCB》2005,20(2):154-157
The present study deals with estimation of levels of fractions of serum glycoproteins, protein bound hexose (PBH), protein
bound hexosamine (PBHex), protein bound fucose (PBF), protein bound sialic acid (PBS) and protein bound carbohydrate (PBC)
in thirty patients of Major Depressive Disorders (MDD) in comparison with thirty normal subjects. In patients of MDD, the
level of PBH, PBHex, PBF, PBS and PBC were significantly higher as compared to the normal subjects (p<0.05). In patients,
of MDD, after one-month treatment with fluoxetine, the levels of PBH, PBHex, PBF, PBS and PBC were significantly decreased
as compared to the levels of these fractions in same patients of MDD before beginning of the treatment (p<0.05). Based on
findings of the present study, it can be concluded that changes in the level of serum glycoproteins level before and after
treatment with fluoxetine can be correlated with clinical status of MDD. 相似文献
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Present study investigated the effects of isoproterenol-induced oxidative stress on hemodynamic and ventricular functions
in rats. Subcutaneous injections of isoproterenol (85 mg/kg for two consecutive days at 24 h interval) significantly decreased
myocardial antioxidant enzymes; superoxide dismutase, catalase and glutathione peroxidase in heart. Isoproterenol-induced
oxidative stress was also evidenced by significant depletion of reduced glutathione and increased formation of lipid peroxidation
product, thiobarbituric acid reactive substances along with depletion of myocyte injury specific marker enzymes; creatine
phosphokinase isoenzyme and lactate dehydrogenase. The deleterious outcome of oxidative stress on hemodyanmic parameters and
ventricular function were further evidenced by decreased systolic, diastolic and mean arterial blood pressure, heart rate,
ventricular contractility; [(+)LVdP/dt] and relaxation; [(−)LVdP/dt], along with an increased left ventricular end diastolic
pressure (LVEDP). Subsequent to changes in heart rate and arterial pressure, isoproterenol also decreased rate pressure product.
Present study findings clearly demonstrate the detrimental outcome of isoproterenol induced-oxidative stress on cardiac function
and tissue antioxidant defense and substantiate its suitability as an animal model for the evaluation of cardioprotective
agents. 相似文献
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Vikram Thakkar Purvi Patel Neelam Prajapati Ranjit Kaur Mukesh Nandave 《Indian journal of clinical biochemistry : IJCB》2014,29(3):345-350
Identification of reliable biomarkers for detection and staging of cancer and monitoring the outcome of anticancer therapy has been considered to be of high importance. We aimed to estimate the levels of serum glycoproteins, protein bound-hexose, protein bound hexosamine, protein bound fucose, protein bound sialic acid and protein bound carbohydrate in 32 ovarian cancer patients and compared them with the levels that found in 25 normal subjects. As compared to the normal subjects, all the four fractions of glycoproteins level were significantly elevated in ovarian cancer patients (p < 0.05). Chemotherapy in these patients significantly decreased the levels of serum glycoproteins (p < 0.05). Thus, high levels of serum glycoproteins in ovarian cancer patients could be due to abnormal protein glycosylation indicating malignant transformation of the cells. 相似文献
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