1,720,967 research outputs found
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Grapefruit juice ameliorates nephropathy in streptozotocin induced diabetes.
Full text linkM. Pharm. University of KwaZulu-Natal, Durban 2012.Background
Diabetic Nephropathy (DN) is the leading cause of end stage renal disease and mortality in diabetic patients. Over the years, medicinal plants have been used to manage diabetes and its complications. Metformin, the synthetic analogue of galegine is used as first line therapy for Diabetes Mellitus (DM) but its use is contraindicated in patients with kidney dysfunction. The management of DN currently is limited to the use of anti-hypertensive agents; ACE inhibitors and angiotensin receptor blockers. Grapefruit juice (GFJ) has shown potential as an anti-diabetogenic agent because of its ability to ameliorate hyperglycaemia and dyslipidemia but its effect on fluid and electrolyte disturbance is not known. This study was designed to investigate the effect of GFJ on renal dysfunction in streptozotocin (STZ) induced male wistar rats.
Materials and Methods
Male wistar rats weighing between 250-300g were divided into 7 groups (n=7) and kept in cages for the treatment period of 8 weeks. Laboratory conditions of 12 hour light/dark cycle, temperature 25±20C and humidity 50-55 % were maintained throughout the study period. Non-diabetic animals group 1 (Control) were treated orally with 1.0 ml /Kg BW of distilled water, while group 2 (ND-GFJ) were treated orally with 3.0 ml /kg BW of GFJ. The diabetic groups 3, 4, 5, 6 and 7 were starved overnight in preparation for the STZ injection. Fasting blood glucose concentration was obtained via tail prick before 45 mg or 60 mg of STZ was administered via a single injection in the peritoneal cavity. STZ was prepared by dissolving it in 0.2 ml of 0.1 M Citrate buffer at pH 4.5. Groups 3, 4 and 7 received 60.0 mg/ Kg BW of STZ while group 5 and 6 received 45 mg/kg BW of STZ. Three days following STZ induction, the diabetic state was confirmed by measuring fasting blood glucose and animals with glucose concentration greater than 6 mmol/L were included in the study. Group 4 (INS- D60) and group 5 (INS- D45) were additionally treated with 4.0 U/kg BW of insulin via subcutaneous injection (S.C) twice a day while Group 6 (GFJ-D45) and group 7 (GFJ-D60) were treated orally with 3.0ml/Kg BW of GFJ. Group 3 (D-60) were similarly treated with 1.0 ml /Kg BW of distilled water. Fasting blood glucose (FBG) and glucose tolerance tests (GTT) were done on days 1 and 58 respectively in all the treatment groups. Urine was collected for a period of 24 hours on day 59 and on the last day
animals were sacrificed by halothane overdose. Blood samples were obtained via cardiac puncture; kidney tissues were removed and preserved in formalin while the liver was snap frozen with liquid nitrogen and stored in a freezer (-800C) before analysis.
Results
Reduced plasma insulin was accompanied by decrease in body weight and an increase in FBG accompanied by polyuria, polydipsia and glucose intolerance in the non-treated diabetic animals compared to the control. Fasting blood glucose was significantly (p<0.0001) increased in the diabetic groups and treatment with GFJ or insulin lowered FBG in groups (GFJ-D45, GFJ-D60 & INS-D60) compared to the diabetic control (D60). GFJ significantly (p=0.0034) improved glucose intolerance in diabetic animals (GFJ-D60 & GFJ-D45) when compared to diabetic control groups D-60 & D-45 respectively. Hepatic glycogen content was reduced in diabetic animals (P=0.024) and treatment with GFJ significantly (P=0.00016) increased the glycogen concentration. In the non-diabetic group (GFJ-ND) treatment with GFJ significantly (P=0.0013) increased the glycogen concentration when compared to the control group. In the diabetic animals, decreased GFR was accompanied by Na+ retention accompanied by low urinary K+ and Cl- concentration. Treatment with GFJ significantly (p<0.05) increased urinary Na+ and K+ and Cl- in the diabetic group (GFJ-D60) but did not increase urinary Cl- in non-diabetic group and consequently improved GFR in the diabetic group. Renal pathology showed structural changes in the glomerulus and treatment with GFJ had some reno-protective effect.
Conclusion
GFJ lowered the fasting blood glucose and improved glucose tolerance in the STZ-induced diabetic rats in a comparable manner to insulin treated diabetic rats. GFJ decreased Na+ retention and increased GFR in the diabetic animals. This study suggests that GFJ could ameliorate nephropathy associated with diabetes mellitus. These results are the first to show that GFJ has renoprotective effects in STZ-Induced diabetic rats
Potential hepatoprotective effects of naringenin in nucleoside reverse transcriptase inhibitor-induced oxidative stress and apoptosis in hepatocytes in vitro.
Full text linkMaster’s Degree. University of KwaZulu-Natal, Durban.Abstract available in PDF
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Metformin does not prevent glucose intolerance but improves renal function and reduces oxidative stress in type 1 diabetes.
Full text linkMaster of Science in Pharmaceutical Sciences. University of KwaZulu-Natal, Durban 2016.Type 1 diabetes (T1D) is a chronic condition caused by the complete destruction of insulin
producing pancreatic β-cells. Increased oxidative stress and impaired antioxidant capacity are
associated with the development of diabetic complications such as diabetic nephropathy.
Metformin, a drug commonly used in the treatment of type 2 diabetes, has been suggested to
have antioxidant capacity. We hypothesise that metformin, when used as an adjunct to insulin
in T1D may help prevent the development of diabetic nephropathy by decreasing oxidative
stress.
Sprague-Dawley rats (230-250g) were divided into 5 groups, (Group A: untreated controls,
B: diabetic control, C: T1D + insulin (4U/kg twice daily), D: T1D + metformin (250mg/kg
via oral gavage), E: T1D + metformin + insulin). Diabetes was induced in groups B-E by
intraperitoneal streptozotocin injection at a dose of 65mg/kg body weight and diabetes was
confirmed 48 hours later. Glucose tolerance test, serum and urinary electrolytes (K+,Cl-
,Na+), creatinine, urea, superoxide dismutase activity, glutathione concentration and
malondialdehyde concentration were analysed.
Metformin alone did not improve glucose intolerance. Both the diabetic control group as well
as the group treated with metformin alone experienced hyperglycemia, polydipsia, polyuria,
weight loss and impaired glucose tolerance. However, when metformin was added to insulin
there was a significant increase in electrolyte excretion and also greatly improved creatinine
clearance when compared to the diabetic control group. Metformin with insulin further
reduced superoxide dismutase activity compared to the diabetic control, increased glutathione
concentration as well as reduced malondialdehyde concentrations in both plasma and renal
tissue. In conclusion, metformin has positive additive effects on oxidative stress and renal
function when used as an adjunct therapy to insulin for T1D
Naringin reversal of some aspects of diabetic nephropathy in rats type 1 streptozotocin induced diabetes.
Full text linkM. Sc. University of KwaZulu-Natal, Durban 2014.The role of naringin on streptozotocin-induced diabetic nephropathy was investigated. Male Wister rats (200-300 g) were divided into six groups (n=7). Group A was treated with a vehicle (0.2 ml of 0.1M citrate buffer pH4.5) by a single intraperitoneal injection (IP) and 3.0 ml/kg/BW of distilled water and group B was treated naringin (50 mg/kg/BW) daily. Groups C, D, E and F were rendered diabetic by a single IP of STZ (60 mg/kg/BW) in 0.1M citrate buffer (pH4.5). Diabetes was confirmed after 2 days (48 hours). Group C was treated with subcutaneous insulin (4 U/kg/BW) twice a day while groups D and F were treated with naringin (50 mg/kg/BW) and ramipril (20 mg/kg/BW) which is the drug that is currently used to treat diabetic nephropathy orally, daily, respectively. On day 55, 24-hours urine samples were collected and on day 56 rats were sacrificed; blood samples were collected by cardiac puncture and kidney and liver samples were excised and snap-frozen in liquid nitrogen for further analysis.
Diabetic groups (C, D, E and F) showed significant (p<0.001) hyperglycemia, weight loss, polydipsia, polyuria, impaired glucose tolerance and low fasting plasma insulin compared to the controls. Treatment with naringin improved weight loss, polydipsia, fasting plasma glucose and fasting plasma insulin. Naringin decreased fasting blood glucose but did not improve glucose intolerance and it significantly (p<0.001) improved fasting plasma insulin compared to diabetic control. Furthermore, non-treated diabetic groups significantly (p<0.001) showed elevated plasma malondialdehyde (MDA) and reduced superoxide dismutase (SOD) activities compared to the controls. Naringin further reduced renal lipid peroxidation and increased SOD activities in diabetic rats. Moreover, naringin reversed electrolytes retention and also increased glomerular filtration rate in diabetic rats.
Naringin therefore ameliorates some aspects of diabetic nephropathy (GFR, serum and urine electrolytes) by reversing oxidative stress associated with DN
Naringing reverses HIV-1 protease inhibitors-associated pancreatic beta-cell dysfunction in vitro.
Full text linkM. Pharm. University of KwaZulu-Natal, Durban 2014.Introduction: Chronic exposure to HIV-1 Protease Inhibitors (PIs) has been associated with
pancreatic β-cell dysfunction and impairment of insulin secretion. PIs have been suggested to
induce β-cell dysfunction through increasing oxidative stress leading to impaired insulin
secretion. The study investigated whether naringin, a naturally occurring antioxidant, could
reverse PIs-induced β-cell dysfunction by reducing oxidative stress.
Methods: The RIN-5F cells were cultured in RPM1-1640 medium, allowed to grow to 80%
confluence, exposed to different concentrations of PIs [nelfinavir (1-10 μM), saqanavir (1-10
μM) and atazanavir (5-20 μM)] in the presence of 11 mM glucose for 24 hr then subjected to
insulin ELISA assay to assess dose-dependent suppression of insulin of secretion by PIs. To
determine glucose-induced insulin secretion, the cells were exposed to nelfinavir (10 μM),
saquinavir (10 μM), atazanavir (20 μM) 24 hr with or without glibenclamide (10 μM) in the
presence of varying glucose concentrations (11-25 mM) then harvested and subjected to
biochemical assays for the measurement of insulin levels, lipid peroxidation, ATP generation,
Glutathione levels (GSH), Superoxide dismutase (SOD) and caspase-3 and -9 activities.
Cells were further exposed to naringin (0-50 μM) in the presence of 11 mM glucose for 24 hr
then subjected to insulin ELISA for insulin secretion determination. To investigate the role of
PIs relative to naringin on RIN-5F cells, the cells were exposed to nelfinavir (10 μM),
saquinavir (10 μM) and atazanavir (20 μM) with or without naringin (10 μM) also in the
presence of 11 mM for 24 hr and similarly subjected to biochemical assays.
Results: Linear regression analysis showed significant decrease in insulin levels in response
to nelfinavir, saqunavir and atazanavir (r2= 0.86, 0.76, 0.95, respectively) in a dose-dependent
manner. PIs significantly (p < 0.05) reduced insulin secretion and ATP production, increased
lipid peroxidation, SOD and caspase-3 and -9 activities and also reduced GSH in a glucosexv
dependent manner. These effects were reversed by glibenclamide. Naringin (0-50 μM) caused
dose-dependent increased in insulin secretion and also reduced lipid peroxidation, SOD,
caspase-3 and -9 activities, increased GSH and ATP levels in cells that were exposed to PIs.
Conclusion: PIs induced β-cell dysfunction and impairment of insulin secretion by increasing
oxidative stress and ATP depletion. Naringin ameliorated PIs-induced impairment of β-cell
dysfunction by reducing oxidative stress
The effects of naringin on glucose tolerance and ketoacidosis in type 1 diabetes.
Full text linkM. Pharm. University of KwaZulu-Natal, Durban 2014.The effects of naringin (4’,5,7-trihydroxy flavonone-7-rhamnoglucoside), a flavonoid isolated from the grapefruit and other citrus fruit species were investigated on diabetic ketoacidosis (DKA) in a type 1 diabetic rat model. DKA is an acute life threatening complication of diabetes mellitus. Male Sprague-Dawley rats (225-250g) were divided into 5 groups (n=7). Group 1 (control) was treated daily with 1.0 ml/kg distilled water while group 2 was treated with 50 mg/kg of naringin, via gastric gavage respectively. Diabetes was induced in groups 3, 4 and 5 by a single intraperitoneal injection of 60 mg/kg streptozotocin in 0.1 M citrate buffer and was confirmed after 48 hours. Group 3 was further treated with subcutaneous insulin (4 IU/kg) twice daily respectively. Blood samples for analysis were collected by cardiac puncture. The animals were handled humanely according to the guidelines of the Animal Ethics Committee, University of KwaZulu Natal, number 106/13/Animal.
The untreated diabetic rats (group 5) showed significant (p<0.0001) hyperglycemia, polydipsia, polyuria, weight loss, impaired glucose tolerance, low fasting plasma insulin (FPI) and low glycogen levels compared to the normal control. They also showed significantly (p<0.0001) elevated acetoacetate (AcAc), β-hydroxybutyrate (3HB), total ketone body (TKB), anion gap (AG) and potassium (p<0.05) levels compared to normal control. Furthermore, significant (p<0.01) reductions blood pH, sodium, chloride and bicarbonate (p<0.0001) levels were recorded compared to the normal control. Treatment of the diabetic groups with naringin did not improve fasting blood glucose and serum electrolyte levels but significantly improved weight loss (p<0.0001), water consumption (p<0.0001), hepatic glycogen level (p<0.05), 3HB (p<0.05), AcAc (p<0.05), TKB (p<0.01), bicarbonate (p<0.01), blood pH (p<0.01) and AG (p<0.05) compared to the diabetic control group.
The results in this study therefore suggest that naringin reverses ketoacidosis but does not improve glucose tolerance in a diabetes type 1 rat model
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