The effect of Bongardia Chrysogonum on prostate tissue in a rat model of STZ-induced diabetes.

BACKGROUND: Bongardia chrysogonum is widely used in Turkey for treating urinary tract infections and prostate hypertrophy, and it also has potent hypoglycemic effects and aids glucose homeostasis. Because of the inflammatory conditions in diabetes mellitus (DM), the prostate tissue of men with diabetes is particularly susceptible to developing hypoplasia, and DM produces characteristic pathological changes in prostate tissue. Here, we examined the effects of B. chrysogonum on the prostate tissue of rats with streptozotocin (STZ)-induced diabetes. RESULTS: The glucose levels were statistically significantly higher in the diabetic rats than in healthy controls (P < 0.001). Further, they were significantly lower in the healthy and diabetic rats administered B. chrysogonum than in the untreated diabetic rats (P < 0.001 and 0.05, respectively). The total cholesterol levels were significantly lower in the healthy rats administered B. chrysogonum than the healthy controls (P < 0.05) and diabetic rats (P < 0.01). They were also significantly lower in the diabetic rats administered B. chrysogonum than those that were left untreated (P < 0.05). The testosterone levels were significantly lower in the untreated diabetic rats than in the controls (untreated ones and those administered B. chrysogonum) and diabetic rats administered the herb (P < 0.001, 0.05 and 0.01, respectively). The oxidative stress index was significantly higher in the untreated diabetic rats than the healthy controls (P < 0.05). It was also significantly lower in the healthy and diabetic groups treated with B. chrysogonum than the untreated diabetic rats (P < 0.05). Histological examination showed no changes in the prostate tissue of the non-diabetic rats. In the diabetic group, the glandular lumens were filled with cellular debris and leucocytic infiltrate, and the glandular epithelium was degenerated and thickened. In the diabetic group treated with B. chrysogonum, the epithelium was better preserved and less debris was seen in the glandular lumen. CONCLUSION: To our knowledge, this is the first study to histologically prove the effects of B. chrysogonum on prostate tissue in diabetes. Our findings may be useful in developing B. chrysogonum into a therapeutic agent against diabetes and benign prostate hyperplasia.

The protective effects of caffeic acid phenethyl ester against toluene-induced nephrotoxicity in rats.

Caffeic acid phenethyl ester (CAPE) has antioxidant and anti-inflammatory properties. The aim of this study is to examine the negative effects of toluene on kidney tissues and functions and to investigate the protective effects of CAPE against toluene-induced nephrotoxicity in rats. A total of 21 male Wistar rats were divided into three groups of equal number in each. The rats in group I were the controls. Toluene was intraperitoneally injected into the rats in group II with a dose of 500 mg/kg. Rats in group III received CAPE daily while exposed to toluene. After 14 days of experimental period, all rats were killed by decapitation. Enzymatic activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) and malondialdehyde (MDA) levels were studied in the rat kidneys. Blood urea nitrogen (BUN) and serum creatinine levels were measured for renal function. The CAT and SOD enzyme activities and serum creatinine levels were significantly increased in rats treated with toluene when compared with the controls. But GSH-Px activity, MDA, and BUN levels showed statistically nonsignificant changes. However, increased CAT and SOD enzyme activities and decreased serum creatinine levels were detected in the rats that received CAPE while exposed to toluene. The GSH-Px activity and MDA and BUN levels in the same group did not show statistically significant changes. The results of our study demonstrated that toluene damages kidney tissue and is a nephrotoxic substance. CAPE was able to prevent the renal damage as antioxidant, antitoxic, and nephroprotective agent.

Investigation of the protective effect of erdosteine against cyclosporine-induced injury in rat liver with histological and biochemical methods.

BACKGROUND/AIM: In the present study, the protective effect of erdosteine against cyclosporine-induced injury in rat liver was investigated with histological and biochemical methods. MATERIALS AND METHODS: Thirty-two Wistar albino male rats were randomly divided into 4 groups: control (n = 8), cyclosporine (n = 8, 20 mg kg(-1) day(-1) i.p.), cyclosporine + erdosteine (n = 8, erdosteine 12 mg kg(-1) day(-1) orally), and erdosteine (n = 8). At the end of day 12, liver tissues were removed for histological and biochemical analysis. After liver tissues were fixed in 10% buffered neutral formalin, routine histological processes were applied and tissue sections were stained with hematoxylin and eosin, periodic acid-Schiff, and elastic fiber stain methods. One hundred lobules of liver were examined for each group and evaluated statistically. The levels of malondialdehyde and glutathione peroxidase, as well as the activities of superoxide dismutase, were determined. RESULTS: The cyclosporine group showed significant histopathological changes compared to the control. In the cyclosporine + erdosteine group, histopathological changes of hepatic damage were markedly reduced. Histological findings were supported by biochemical results. CONCLUSION: Erdosteine could attenuate cyclosporine-induced liver injury.

Protective effects of caffeic acid phenethyl ester on the dose-dependent acute nephrotoxicity with paraquat in a rat model.

Paraquat (PQ), which is used extensively as a potent herbicide throughout the world, is highly toxic in humans. We aimed to determine PQ-induced biochemical and histologic changes in the kidneys, and to evaluate the ability of the protective effects of caffeic acid phenethyl ester (CAPE) against PQ-induced injury in rats. Forty-eight rats were divided into eight groups of six: Group 1: Control; Group 2: 10 µmol/kg CAPE; Group 3: 15 mg/kg PQ; Group 4: 30 mg/kg PQ; Group 5: 45 mg/kg PQ; Group 6: 15 mg/kg PQ+CAPE; Group 7: 30 mg/kg PQ+CAPE; Group 8: 45 mg/kg PQ+CAPE. PQ and CAPE were injected intraperitoneally. The levels of the total oxidant status (TOS) and total antioxidant status (TAS) were determined in the supernatants of the excised left kidney. Right kidney tissue of each rat was removed to obtain a histologic score. When PQ-administrated (15, 30, 45) groups compared with other groups, TOS values were found to be significantly higher (p < 0.01). PQ (15, 30, 45) groups had significantly diminished values of TAS than the other groups (p < 0.001). Of histologic score evaluation, only the PQ45 group had a significantly higher value than the sham, and CAPE groups (p < 0.05). Moreover, in CAPE+PQ45 group, the level of histologic score was decreased compared to PQ45 group (p < 0.001). In conclusion, the evaluation of the data suggests that CAPE can be used to prevent the acute effects of PQ nephrotoxicity.

Caffeic acid phenethyl ester (CAPE) protects against acute urogenital injury following pneumoperitoneum in the rat.

PURPOSE: Our aim is to determine the biochemical and histologic changes induced in the kidneys, testis and prostate on possible ischemia and reperfusion (I/R) injury caused by pneumoperitoneum (PNP) in a rat model and to evaluate the ability of protective effects of caffeic acid phenethyl ester (CAPE). METHODS: Twenty-eight adult male Wistar albino rats were randomly divided to one of three treatment groups, with seven animals in each group. Sham, laparoscopy (L), and laparoscopy plus CAPE (L + C) group were subjected to 60 min of PNP with 15 mmHg one hour before the desufflation period. Total oxidant status (TOS) and total antioxidant status (TAS) levels were determined in kidney, testis, and prostate. Kidney and testis tissues were removed to obtain a histologic score. Also, Johnsen scoring system was used for testicular tissue analysis. RESULTS: L group had significantly higher TOS and lower TAS levels on kidney and testis compared to the other groups. In prostate biochemical analysis, there was not any difference between groups. No difference was found between groups according to kidney and testis tissues' histologic evaluation. In evaluation of Johnsen scoring, L group showed significant lower score compared to the other two groups. CONCLUSIONS: Increased intraabdominal pressure (IAP) had an oxidative effect on kidney and testis but not on prostate in rats. Moreover, it could affect the testicular Johnsen score. All these adverse effects of IAP on both kidney and testis could be prevented by CAPE administration.

Antioxidative and anti-inflammatory effect of thymoquinone in an acute Pseudomonas prostatitis rat model.

INTRODUCTION: The aim of this study is to investigate the potential antioxidant and anti-inflammatory effects of thymoquinone (TQ) to improve acute bacterial prostatitis (ABP) induced by Pseudomonas aeruginosa. MATERIAL AND METHODS: A total of 42 male Wistar albino rats were divided into 7 groups as follows: control, ABP (24, 48, and 72 h), and TQ-ABP (24, 48, and 72 h). The prostate tissue samples were assayed for prostate tissue malondialdehyde (MDA) and nitric oxide (NO) levels, and catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities. Sections were examined for characteristic histological changes, and a histological scoring system was used. RESULTS: When the ABP groups given TQ (24, 48, and 72 h) were compared to the ABP groups not given TQ, the levels of MDA and NO and the GPX activity were found to be significantly lower in the groups given TQ. Concerning SOD values, the TQ-ABP-72 group was lower in comparison with the ABP-72 and control groups, but statistically higher than the TQ-ABP-48 group (p < 0.05). Concerning CAT activity, only the TQ-ABP-72 and ABP-72 groups had a significant difference with the control group. TQ improved prostate histology significantly only in the TQ-ABP-24 group compared to the ABP-24 group (p < 0.001). CONCLUSION: Our study demonstrated for the first time that ABP induced by P. aeruginosa had an oxidative effect on prostate tissue and could regress following TQ administration as shown with the biochemical and histological findings.

Ceftriaxone ameliorates cyclosporine A-induced oxidative nephrotoxicity in rat.

A growing body of evidence now suggested that cyclosporine A (CycA)-induced nephrotoxicity is a crucial clinical problem and oxidative stress is importantly responsible for its toxicity. Ceftriaxone induced antioxidant effect in brain and neuronal tissues against oxidative damage although its antioxidant potential effect on kidney has not been clarified. The aim of this study was to evaluate whether ceftriaxone protects CycA-induced oxidative stress kidney injury in rats. Twenty-four rats were equally divided into four groups. First group was used as control. Ceftriaxone (200 mg/kg) and CycA (15 mg/kg) were administrated to second and third groups for 10 days, respectively. The ceftriaxone and CycA combination was given to rats constituting the fourth group for 10 days. Lipid peroxidation (LP), urea nitrogen and lactate dehydrogenase (LDH) levels were higher in CycA group than in control and ceftriaxone groups although LP, urea nitrogen and LDH levels were lower in ceftriaxone + CycA group than in control and ceftriaxone groups. Glutathione peroxidase and catalase activities were lower in CycA group than in control whereas their activities were increased in control and ceftriaxone groups. Superoxide dismutase activity did not change by the treatments. Ceftriaxone administration recovered also CycA-induced atrophy, vacuolization and exfoliations of tubular epithelium and glomerular collapse in histopathological evaluation of kidney. In conclusion, we observed that ceftriaxone is beneficial on CycA-induced oxidative stress in kidney of rats by modulating oxidative and antioxidant system.

New perspective for the treatment of Alzheimer diseases: liposomal rivastigmine formulations.

The aim of this study was to determine the transportations of rivastigmine containing from various liposome formulations through Madin Darby Canine Kidney (MDCK) cells monolayer and to compare the in vitro test results with in vivo. There is no other liposome formulation of rivastigmine and the transportations of rivastigmine through MDCK cell monolayers or related study available in the literature. Cytotoxicity (MTT) test was used to determine cell viabilities. The effect of sodium-taurocholate or dimethyl-beta-cyclodextrine as penetration enhancer was also investigated. Characterization and stability studies for liposome formulations were performed. Permeation experiments of rivastigmine were performed through MDCK cells and dialysis membrane. The kinetic of release from liposomes was also investigated. The highest apparent permeability coefficient (log. values) was obtained with sodium-taurocholate liposomes for -1.15 ± 0.16 for MDCK cell. Rivastigmine liposomes and solutions were also administered to mice orally and intraperitonally. Acetylcholinesterase (AChE) activity was determined by Ellman method. AChE% inhibition values were calculated for both blood and brain after administration of rivastigmine solution and liposomes. The highest AChE inhibition was observed for rivastigmine-sodium-taurocholate liposomes. Histological observations of the mice' brains were performed under transmission electron microscope (TEM). The histological results were also indicated and supported all these findings.

Letrozole induces hepatotoxicity without causing oxidative stress: the protective effect of melatonin.

AIM: The aim of this study was to determine the effects of letrozole (LTZ), an aromatase inhibitor (AI), and melatonin (MLT) on hepatic function and oxidative stress in female rats. MATERIAL AND METHODS: A total of 32 female rats were divided equally into four groups (n = 8). Control group received saline (0.5 ml/day, oral gavage). LTZ was administered to rats by daily oral gavage at 1 mg/kg dose. LTZ + MLT group was given LTZ (1 mg/kg, oral gavage) plus MLT (0.5 mg/kg/day, s.c.). MLT group was given MLT (0.5 mg/kg/day) by s.c. injection. The activities of superoxide dismutase (SOD) and catalase (CAT) and malondialdehyde (MDA) levels were measured in liver tissue. Total antioxidant capacity (TAC), total oxidant status (TOS), ALT, AST, GGT, ALP, LDH, bilirubin, BUN, creatinine, total cholesterol (TC), high-density lipoprotein (HDL) and triglyceride (TG) were assayed in serum samples. RESULTS: The oxidative stress parameters did not differ between groups. LTZ administration increased hepatic function parameters such as AST, LDH, ALP, bilirubin and MLT improved the disturbances of hepatic function. LTZ caused minimal histological changes in liver tissue and MLT treatment reversed those dejenerations. DISCUSSION: LTZ may cause hepatotoxicity without inducing oxidative stress and MLT restores hepatic activity.

Effects of caffeic acid phenethyl ester on isoproterenol-induced myocardial infarction in rats.

OBJECTIVE: Caffeic acid phenethyl ester (CAPE) is a natural product with potent anti-inflammatory, antitumor and antioxidant activities and attenuates inflammation and lipid peroxidation induced by ischemia-reperfusion injury. The purpose of the present study was to investigate the effects of CAPE on isoproterenol (ISO) -induced myocardial infarction. METHODS: A randomized controlled experimental design was used in this study. Rats were divided into four groups and treated with saline, CAPE, ISO and ISO+CAPE. Rats were treated with CAPE (10 micromol kg/day i.p.) or saline starting 3 days before injecting ISO (150 mg /kg s.c., 24 hours). Seven days later, rats were sacrificed and the hearts were excised for biochemical analyses and microscopic examination. One-way ANOVA test with post hoc multiple comparisons using LSD method were used for statistical analysis of the data. RESULTS: The administration of ISO alone resulted in higher myeloperoxidase (MPO) activity, lipid peroxidation, superoxide dismutase (SOD) and catalase (CAT) than in the control. The enzyme activities did not change in rat given CAPE alone. CAPE treatment prevented the increase in MPO activity and malondialdehyde, but did not affect the activities SOD and CAT enzymes. CONCLUSION: In light of these results, we conclude that CAPE prevents MPO-and lipid peroxidation-mediated myocardial injury via inhibition of neutrophil's MPO activity.

Effects of ß-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats.

BACKGROUND: NSAIDs have been found to induce gastrointestinal tract damage. Recently, it has been suggested that this might be mediated by lipid peroxidation. OBJECTIVE: The aim of this study was to assess the potential protective effects of ß-glucan against acetylsalicylic acid (ASA-induced gastric damage by means of its antioxidant capacity in an experimental rat model. METHODS: Thirty-two male Wistar albino rats (200-250 g) were randomized into 4 groups consisting of 8 rats each. The ß-glucan group received 50 mg/kg ß-glucan once a day for 10 days and 30 minutes before anesthesia. The ASA group received saline once a day for 10 days and 300 mg/kg (20 mg/mL) ASA as a single dose, 4 hours before anesthesia. The ASA+ß-glucan group was administered 50 mg/kg ß-glucan once a day for 10 days and 30 minutes before anesthesia. Additionally, 300 mg/kg (20 mg/mL) ASA was administered as a single dose, 4 hours before anesthesia. The control group received saline once a day for 10 days and 30 minutes before anesthesia. All medications were administered by intragastric gavage. The stomach from each rat was dissected and divided into 2 parts for histologic and biochemical analysis. Gastric tissue malondialdehyde (MDA), nitric oxide (NO) levels, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were determined for oxidative parameter analysis. RESULTS: The gastroprotective and antioxidant effects of ß-glucan appeared to attenuate the ASA-induced gastric tissue damage. Compared with the control group, MDA and NO levels and CAT and GSH-Px activities were significantly increased in the stomachs of ASA-treated rats (MDA, 4.12 [0.44] to 13.41 [1.05] µmol/L; NO, 8.04 [7.25-9.10] vs 30.35 [22.34-37.95] µmol/g protein; CAT, 0.050 [0.004] to 0.083 [0.003] k/g protein; GSH-Px, 0.57 [0.42-0.66] to 1.55 [1.19-1.76] U/L; all, P < 0.001), whereas SOD activity was significantly decreased in the same group (291 [29] to 124 [6] U/mL; P < 0.001). In the ASA+ß-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P < 0.001). CONCLUSION: ß-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.

Alport syndrome: significance of gingival biopsy in the initial diagnosis and periodontal evaluation after renal transplantation.

Alport Syndrome (AS) is an important hereditary disorder affecting the glomerular basement membrane. Diagnosis of AS is based on the presence of hematuric nephropathy, renal failure, hearing loss, ocular abnormalities and changes in the glomerular basement membrane of the lamina densa. The aims of this case report were to show the changes in the gingival tissues in a patient with AS under therapy with cyclosporin-A after renal transplantation and to discuss the possible role of type IV collagen in gingival basal lamina as an alternative approach for the diagnosis of AS. A 20-year-old male patient with AS underwent periodontal therapy including a series of gingivectomy surgeries. Gingival samples obtained during the second surgery were examined histopathologically and by transmission electron microscopy for further pathological examination. Gingivectomy procedures have been performed every 6 months over the last 4 years. The excessive and fibrous gingival enlargements resulted in migration of the anterior teeth, but no alveolar bone loss occurred. This is the first report to demonstrate the possible changes in the gingival tissues caused by AS. It is suggested that gingival biopsy can be an initial diagnostic tool instead of renal or skin biopsies. Proper dental and periodontal care and regular visits to the dentist could provide limited gingival hyperplasia to patients with AS.

Alport syndrome: significance of gingival biopsy in the initial diagnosis and periodontal evaluation after renal transplantation

Alport Syndrome (AS) is an important hereditary disorder affecting the glomerular basement membrane. Diagnosis of AS is based on the presence of hematuric nephropathy, renal failure, hearing loss, ocular abnormalities and changes in the glomerular basement membrane of the lamina densa. The aims of this case report were to show the changes in the gingival tissues in a patient with AS under therapy with cyclosporin-A after renal transplantation and to discuss the possible role of type IV collagen in gingival basal lamina as an alternative approach for the diagnosis of AS. A 20-year-old male patient with AS underwent periodontal therapy including a series of gingivectomy surgeries. Gingival samples obtained during the second surgery were examined histopathologically and by transmission electron microscopy for further pathological examination. Gingivectomy procedures have been performed every 6 months over the last 4 years. The excessive and fibrous gingival enlargements resulted in migration of the anterior teeth, but no alveolar bone loss occurred. This is the first report to demonstrate the possible changes in the gingival tissues caused by AS. It is suggested that gingival biopsy can be an initial diagnostic tool instead of renal or skin biopsies. Proper dental and periodontal care and regular visits to the dentist could provide limited gingival hyperplasia to patients with AS.

Nogo-A inhibitory peptide (NEP1-40) increases pan-cadherin expression following mild cortical contusion injury in rats.

BACKGROUND: Nogo-A is a myelin-associated neurite outgrowth inhibitory protein that limits elongation of central nerve fibers, neuronal regeneration and plasticity. We investigated the effect of delivering an inhibitory peptide that neutralizes Nogo-A on neuronal recovery following mild cortical contusion injury. METHODS: 41 rats were allocated into the control and NEP1-40 treatment groups. PBS was applied following trauma over the parietal cortex after opening the dura in the control group. NEP1-40 solution was immediately applied following trauma after opening the dura in the treatment group. Each group was further divided into 3 subgroups and sacrificed on the third, eighth, and 21st days after injury. The brains were removed for analysis. RESULTS: Immunohistochemical staining of the injured cortex for pan-cadherin revealed a significant increase in staining in the NEP 1-40 treatment group at the 8th and 21st days after injury. Electron microscopic evaluation revealed better cytoarchitectural preservation in the axons of the animals treated with NEP 1-40. CONCLUSION: We observed improved preservation of injured neurons after topical application of NEP 1-40 following mild cortical injury. Pan-cadherin expression may correlate with the recovery of neurons and axonal bodies. Electron microscopical findings confirmed better preservation of neuronal structures after NEP1-40 treatment. Pan-cadherin is a good marker for neuronal recovery after cortical injury.

Effects of erdosteine on acetaminophen-induced hepatotoxicity in rats.

We investigated the effects of erdosteine on acetaminophen (APAP)-induced hepatotoxicity in rats. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), AST (aspartate aminotransferase), and ALT (alanine transaminase) activities, and malonyldialdehyde (MDA) and nitric oxide levels as oxidant/antioxidant biochemical parameters were investigated with light microscopic evaluation in adult female Wistar Albino rats. APAP administration produced a decrease in hepatic SOD, CAT, and GSH-Px activities, and coadministration of erdosteine (150 and 300 mg/kg) resulted in increases in the activities. MDA and NO levels increased in the APAP group, and erdosteine treatments prevented these increases. Significant elevations in serum AST and ALT levels were observed in the APAP group, and when erdosteine and APAP were coadministered, their serum levels were close to those in the control group. Light microscopic evaluation of livers showed that there were remarkable centrilobular (zone III) hepatic necrosis and mild to moderate sinusoidal congestion in the APAP group, whereas in the erdosteine group, cellular necrosis was minimal and the hepatocytes maintained a better morphology when compared to the APAP group. Erdosteine prevented APAP-induced liver injury and toxic side effects probably through the antioxidant and radical scavenging effects of erdosteine.

Protective effects of N-acetylcysteine on cyclosporine-A-induced nephrotoxicity.

OBJECTIVES: Cyclosporine A (CsA) is used for the treatment of autoimmune and inflammatory disorders. However, CsA-induced nephrotoxicity remains an important clinical problem, and oxidative stress has been implicated as a possible responsible mechanism. We assessed the protective ability of N-acetylcysteine (NAC), an antioxidant, against CsA-induced nephrotoxicity. MATERIALS AND METHODS: Wistar albino rats were randomly assigned into four groups. Group 1 rats were treated with sodium chloride as control, group 2 with CsA, group 3 with CsA and NAC, and group 4 with NAC alone. Animals were sacrificed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), malondialdehyde (MDA) and nitric oxide (NO) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. Kidney sections were analyzed for MDA and NO levels and SOD and GSH-Px activities, as well as histopathological changes. RESULTS: Overall, the treatment of rats with CsA alone produced significant increases in NO and MDA levels and significant decreases in SOD and GSH-Px activities in serum and renal samples. Morphological changes, including tubular epithelial atrophy, vacuolizations, and cellular desquamations, were clearly observed in the rats treated with CsA alone. Concurrent NAC administration with CsA improved renal function, as indicated by lower BUN and Cr values. Moreover, NAC significantly reduced MAD and NO levels and increased SOD and GSH-Px activities in serum and renal tissue, as well as provided a histologically proven protection against CsA-induced nephrotoxicity. CONCLUSION: These results indicate that NAC produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role for oxidative stress in pathogenesis.

Correlation between proteinuria level and renal morphology with special reference to electron microscopy in kidney donors.

The aims of this study were to evaluate whether there is a correlation between protein level in urine and renal morphology in kidney transplant donors, as well as to detect the role of electron microscopy. For this purpose, kidney biopsies of 10 donors with urine protein levels were evaluated. Seven patients were female and three were male. Two had physiologic proteinuria (< 150 mg/24h), four had non-significant proteinuria (150-300 mg/24h), and three had significant (> 300 mg/24h) proteinuria. Serum creatinine levels were in normal ranges in all patients except for one who had a slight increase (1.76 mg/dL). Seven cases were reported to have normal or nonspecific light microscopic findings. Two of those seven cases had physiologic proteinuria, three had non-significant proteinuria, and two had significant proteinuria. One case had IgA nephropathy with significant proteinuria. One donor had early stage focal segmental glomerulosclerosis with non-significant proteinuria, and one donor had focal interstitial fibrosis with normal urine protein level. There was no statistically significant difference between score means of ultrastructural morphology of the six patients with same patients' light microscopic results and score means of light microscopic results with urine protein levels of all patients. However, there was a significant difference between score means of ultrastructural morphology with urine protein levels of those six patients. In conclusion, urine protein levels and light microscopic findings did not always reflect the detailed morphology alone and together. Therefore, combining with electron microscopic examination could be more beneficial in relieving problems occurring in long-term prognoses.

Ultrastructure of the thymus in diabetes mellitus and starvation.

INTRODUCTION: The purpose of this study was to investigate the ultrastructural change of the thymus under stress conditions created by diabetes accompanied by fasting, and also the effects of insulin therapy. METHODS: Forty-eight Sprague-Dawley type rats were used in this experiment. Type 1 diabetes symptoms were induced in 24 of the rats by the application of a single dose of intravenous streptozotocin in sodium citrate buffer through the tail vein. A single dose of sodium citrate buffer was given to rats to create a control group. Following the infusions, rats were divided into control, control and fasting, diabetes, diabetes and fasting, and insulin treatment groups. At the end of the experiment tissues from the thymus of the rats were extracted and examined using electron microscopy. RESULTS: Severe degeneration was observed in the prolonged fasting (stress) and diabetes groups without insulin treatment. Insulin treatment was found to mostly reverse this degeneration. CONCLUSION: This study demonstrates that the thymus was affected ultrastructurally by diabetes and concomitant fasting, and insulin treatment can reverse these changes.

Investigation of epidermal growth factor containing liposome formulation effects on burn wound healing.

It was aimed to develop liposome formulations containing epidermal growth factor (EGF) and to investigate the healing effects of these formulations on second-degree burn wounds in rats. Multilamellar type liposomes containing EGF were prepared by film formation method. In vitro releases of EGF from liposome formulations were determined using spectrofluorometer. Second-degree standard burn wounds were formed on rats and liposome formulations containing 10 microg/mL EGF (ELP group), EGF solution (ES group), liposome without containing EGF (LP group), and Silverdine ointment (SIL group) were applied daily. Untreated control groups [unburned (S) and untreated (Y) rats] were also evaluated. Biopsies were taken at the 3rd, 7th, and 14th day of the treatment from the wounds and histological observations were performed under transmission electron microscope. Bromodeoxyuridine (BrdU) staining technique was used for immunohistochemical analysis. After trichrome stainings, the thicknesses of the epidermis and the areas of the fibroblast nucleus were measured using a light microscope and Vision Screening Analysis Program. It was observed that the healing in the ELP group was the fastest among all groups (p < 0.05) at the 14th day of therapy. The healing effect in order from highest to lowest efficacy was found to be ELP>SIL>ES groups, respectively, at the 14th day. All results indicated that the EGF-liposome formulation is effective and can be used for the treatment of burn wounds.

Phagotrophic protozoa: A new weapon against pathogens?

Immune suppression is one of the most important factors contributing mortality in systemic diseases like HIV, cancer or diabetes. Moreover, in autoimmune diseases immune suppression itself becomes the only choice of therapy. Finally, fatal bacterial infections occur. As antibiotics get stronger, severity of their side effects increase and more resistant organisms develop. The war between antibiotics and pathogens becomes a never ending story while human body gets weaker day by day. Therefore we should develop new methods against bacterial infections. We have suggested that the protists controlling the bacterial growth effectively in aquatic environments could be used in the human body to cope with human pathogens. Million years of a balanced aquatic ecosystem could be a clue for us to search for better and more natural fighting methods against human infectious agents.