Diagnostic study of trypanosomiasis of cats in Mosul, Iraq.

Background: Trypanosomiasis is a zoonotic parasitic disease endemic in Iraq but with limited information about its occurrence in cats. Aim: This study was designed to detect Trypanosoma spp. in cats using microscopic examination by Giemsa stain and conventional polymerase chain reaction (PCR) technique in Mosul, Iraq. Methods: A total of 120 blood samples from cats were microscopically examined using Giemsa stain. Only 35 positive blood samples were examined by the conventional PCR technique. Hematological changes were also reported. Results: The infection rate of Trypanosoma spp. was 34.2% (41 out of 120). Results of conventional PCR technique for the positive 35 blood samples indicated 31.4% as Trypanosoma spp. and 20% Trypanosoma evansi. This study showed that the infection in younger cats was significantly more than in older cats, with significant differences between females and males. Affected cats suffered from fever, dullness, pale mucous membranes, emaciation, muco-purulent ocular discharge, anorexia, incoordination, and anemia. Results of the blood picture indicated increase in total leukocyte count and decrease in hemoglobin concentration, packed cell volume, and total red blood cells. Conclusion: Trypanosoma spp. and T. evansi infection in Mosul of Iraq is reported for the first time in cats, and younger cats were more affected than older cats.

Evaluation of goserelin effectiveness based on assessment of inflammatory cytokines and symptoms in uterine leiomyoma.

Background Uterine leiomyoma is a benign tumour of the uterine smooth muscles associated with an elevated level of inflammatory cytokines. Goserelin, a synthetic gonadotropin-releasing hormone analogue, suppresses the production of sex hormones and release of inflammatory cytokines in uterine leiomyoma cells. Objective The primary objective of this study was to find out the effectiveness of subcutaneous goserelin therapy on lowering serum levels of inflammatory cytokines and improving uterine leiomyoma-related symptoms in female patients diagnosed with uterine leiomyoma. The secondary objective was to assess the tolerability to goserelin therapy used in the management of this tumour. Setting Outpatient gynaecological clinic of the medical consultation department of Baghdad Teaching Hospital, Baghdad province, Iraq. Methods A single centre, prospective, longitudinal, cohort study was carried out on female patients diagnosed with uterine leiomyoma. Goserelin 3.6 mg subcutaneous injection was given in a consecutive monthly dose for the total time duration of three months. Serum levels of inflammatory cytokines, tumour necrosis factor-α and monocyte chemotactic protein-1 were detected before and after goserelin therapy in a consecutive monthly assessment. The study also assessed the improvement in uterine leiomyoma-related symptoms, including pelvic pain alongside the incidence of goserelin-related side effects during therapy schedules. Main Outcome Measures Assessment of serum levels of tumour necrosis factor-α and monocyte chemotactic protein-1 alongside uterine leiomyoma-related symptoms, including pelvic pain and goserelin-related side effects. Results There was a significant decrease in serum levels of tumour necrosis factor-α and monocyte chemotactic protein-1 compared to the baseline level over the 3-month duration of goserelin therapy (0.11 ± 0.02 vs. 0.74 ± 0.19) pg/mL; (0.07 ± 0.00 vs. 0.44 ± 0.18) pg/mL respectively. Patients showed a clinical improvement regarding uterine leiomyoma-related symptoms following each of the consecutive monthly doses of goserelin therapy (n = 11, 55%, P < 0.0001; n = 15, 75%, P < 0.0001; n = 18, 90%, P < 0.0001) respectively. This also includes a significant decrease in the intensity of leiomyoma-related pelvic pain before and after goserelin therapy (7.2 ± 1.43 vs. 3.05 ± 1.14, P < 0.0001). The majority of patients reported vaginal dryness (60%) as the main goserelin-related side effect. Conclusion Goserelin therapy reduces serum levels of inflammatory cytokines, tumour necrosis factor- α and monocyte chemotactic protein-1, improving leiomyoma-related symptoms with good tolerability in patients with uterine leiomyoma.

Potential Confounders and a Modified Framingham Risk Score for the Prediction of Pregnancy-related Medical Conditions Occurrence among Pregnant Women: A Retrospective Study from Baghdad, Iraq.

BACKGROUND: The incidence of pregnancy-related medical conditions relied on a set of potential factors that could be available even before the term of pregnancy and may be associated with poor outcomes later in life. This study aimed to investigate the association between some potential predictive factors related to maternal, gestational, and clinical parameters and the incidence of pregnancy-related medical conditions in a sample of Iraqi pregnant women. MATERIALS AND METHODS: A retrospective, observational, single-center study was carried out on 92 pregnant women during their routine visit to the obstetric clinic in a certain distinct of Baghdad province, Iraq. Demographic, gestational, and clinical records of the participants were collected and analyzed to detect the predictive factors for pregnancy-related medical conditions. RESULTS: 56.5% of the participants were at a gestational age of 25-37 weeks. 32.6% complained of pregnancy-related medical conditions, mainly gestational hypertension and diabetes mellitus. Pregnant women with pregnancy-related medical conditions were significantly correlated with a family history (P < 0.0001), previous gestational medical conditions (P < 0.001), diastolic blood pressure (P = 0.0011), different lipid panels (P = 0.0001), and maternal blood phenotype O (P = 0.0001). CONCLUSION: Some predictive factors related to maternal, gestational, and health characteristics are correlated with the incidence of pregnancy-related medical conditions. Interventions to adjust and recognize these confounders are essentials even before pregnancy which could improve maternal health and reduce the overall risk of pregnancy-related medical conditions.

Downregulation of S100a7a antimicrobial peptide in acne vulgaris patients after isotretinoin therapy.

The S100a7a protein is expressed in keratinocytes, its level is increased in acne condition. As isotretinoin therapy is known to alter some of S100 peptides, these could be important specific targets for acne therapy and may have an important role in clinical remission. A randomized controlled trial was held in a dermatology clinic in Baghdad, where 30 patients with moderate to severe acne vulgaris condition aged 16-31 years were enrolled. Five milliliters of venous blood samples were taken before and after 6 weeks of isotretinoin therapeutic trial. A placebo-control group of 26 acne patients was also enrolled. The S100a7a peptide was measured in both groups using the ELISA technique before and after the trial. High levels of serum S100a7a were found in acne patients of both groups before therapeutic trial. Following the trial, a significant statistical difference (p = .0003) was noticed between mean S100a7a protein level of study and control groups. By comparing the mean S100a7a protein level before and after isotretinoin therapy in the study group, a highly significant statistical difference was also found (p = .001). The current study showed a downregulatory effect of isotretinoin therapy on the S100a7a peptide mean level.

Clinical Characteristics of Pregnant Women on the Use of Daily Low-dose Aspirin in Different Hypertensive Pregnancy Disorders: A Retrospective Comparative Study.

BACKGROUND: Hypertensive disorders represent major causes of maternal and fetal complications. It includes a range of conditions, most notably preeclampsia. Aspirin is a well-accepted therapy for the primary and secondary prevention of cardiovascular events. The indications for the use of aspirin during pregnancy are, however, the subject of much concern. This study aimed to assess the clinical characteristics from the benefits of daily low-dose aspirin administration alongside antihypertensive in pregnant women with different hypertensive disorders. MATERIALS AND METHODS: A retrospective observational study was carried out on pregnant women during their routine visit to the obstetric clinic at Baghdad Teaching Hospital. Patients diagnosed during pregnancy with different hypertensive disorders on the prescription of antihypertensive medication with or without daily low-dose aspirin administration were selected. Data were collected to structure a detailed assessment regarding the patients' demographic, gestational, and medical records. RESULTS: Methyldopa was the main antihypertensive agent (98%). Among pregnant women with daily aspirin use, 68% had gestational hypertension, 24% had preeclampsia alongside proteinuria (P = 0.0001), the frequency of daily dose intake of methyldopa (250 mg) tablet (two vs. three times) was significant (P = 0.0001). All pregnant women within the group of daily low-dose aspirin were safe from the incidence of eclampsia (P = 0.0001). CONCLUSION: This study provides intriguing evidence for the benefits of daily low-dose aspirin use during pregnancy as it is considered as a simple protective measure from serious maternal complications of hypertensive disorders, where these complications continue to affect maternal health long after delivery.

Protection by Neostigmine and Atropine Against Brain and Liver Injury Induced by Acute Malathion Exposure.

We examined the effect of treatment with neostigmine alone or with atropine on brain oxidative stress and on brain and liver tissue damage following acute malathion toxicity. Rats were intraperitoneally treated with malathion 150 mg/kg along with neostigmine (200 or 400 µg/kg) or neostigmine (200 µg/kg) + atropine (1 mg/kg) and euthanized 4 h later. Results indicated that compared with the saline group, malathion resulted in (i) higher brain malondialdehyde (MDA) and nitric oxide (46.4% and 86.2%); (ii) decreased brain reduced glutathione (GSH) (67.6%); (iii) decreased brain paraoxonase-1 (PON1), acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) activities (31.2%, 21.6% and 60%); (iv) decreased brain glucose (-38.1%); (v) neuronal degeneration in cortex and hippocampus and markedly increased glial fibrillary acidic protein (GFAP) immunostaining in the hippocampus; (v) hydropic and fatty degeneration in liver. Rats treated with malathion along with neostigmine or neostigmine + atropine showed no change in brain MDA but decreased nitric oxide (-34.2%-48%). GSH increased after neostigmine 200 µg/kg or neostigmine + atropine (35.8% and 41%). PON1 activity increased (42%-35.2%) and glucose concentrations increased (91.5%-81.5%) by 400 µg/kg neostigmine or neostigmine + atropine. Brain AChE activity remained unchanged but BChE activity showed 18.3% increment after 400 µg/kg neostigmine. Rats treated with 400 µg/kg neostigmine or neostigmine + atropine had normal neuronal appearance in cortex and hippocampus and weak GFAP expression in hippocampus. Liver damage was prevented by neostigmine + atropine. These results suggest that treatment with neostigmine + atropine afforded protection against the deleterious effects of acute malathion on the brain and liver.

Nitric oxide synthase inhibitors protect against brain and liver damage caused by acute malathion intoxication.

OBJECTIVE: To investigate the effect of NG-nitro-l-arginine methyl ester (l-NAME), a non-selective nitric oxide synthase (NOS) inhibitor, and 7-nitroindazole (7-NI), a selective neuronal NOS inhibitor, on oxidative stress and tissue damage in brain and liver and on DNA damage of peripheral blood lymphocytes in malathion intoxicated rats. METHODS: Malathion (150 mg/kg) was given intraperitoneally (i.p.) along with l-NAME or 7-NI (10 or 20 mg/kg, i.p.) and rats were euthanized 4 h later. The lipid peroxidation product malondialdehyde (MDA), nitric oxide (nitrite), reduced glutathione (GSH) concentrations and paraoxonase-1 (PON-1) activity were measured in both brain and liver. Moreover, the activities of glutathione peroxidase (GPx) acetylcholinesterase (AChE), and butyrylcholinesterase (BChE), total antioxidant capacity (TAC), glucose concentrations were determined in brain. Liver enzyme determination, Comet assay, histopathological examination of brain and liver sections and inducible nitric oxide synthase (iNOS) immunohistochemistry were also performed. RESULTS: (i) Rats treated with only malathion exhibited increased nitric oxide and lipid peroxidation (malondialdehyde) accompanied with a decrease in GSH content, and PON-1 activity in brain and liver. Glutathione peroxidase activity, TAC, glucose concentrations, AChE and BChE activities were decreased in brain. There were also raised liver aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities and increased DNA damage of peripheral blood lymphocytes (Comet assay). Malathion caused marked histopathological changes and increased the expression of iNOS in brain and liver tissues. (ii) In brain of malathion-intoxicated rats, l-NAME or 7-NI resulted in decreased nitrite and MDA contents while increasing TAC and PON1 activity. Reduced GSH and GPx activity showed an increase by l-NAME. AChE activity increased by 20 mg/kg l-NAME and 10 mg/kg 7-NI. AChE activity decreased by the higher dose of 7-NI while either dose of 7-NI resulted in decreased BChE activity. (iii) In liver of malathion-intoxicated rats, decreased MDA content was observed after l-NAME or 7-NI. Nitrite level was unchanged by l-NAME but increased after 7-NI which also resulted in decreased GSH concentration and PON1 activity. Either inhibitor resulted in decreased liver ALT activity. (iv) DNA damage of peripheral blood lymphocytes was markedly inhibited by l-NAME or 7-NI treatment. (v) iNOS expression in brain and liver decreased by l-NAME or 7-NI. (vi) More marked improvement of the histopathological alterations induced by malathion in brain and liver was observed after 7-NI compared with l-NAME. CONCLUSIONS: In malathion intoxicated rats, the neuronal NOS inhibitor 7-NI and to much less extent l-NAME were able to protect the brain and liver tissue integrity along with improvement in oxidative stress parameters. The decrease in DNA damage of peripheral blood lymphocytes by NOS inhibitors also suggests the involvement of nitric oxide in this process.

Novel neuroprotective and hepatoprotective effects of citric acid in acute malathion intoxication.

OBJECTIVE: To study the effect of citric acid given alone or combined with atropine on brain oxidative stress, neuronal injury, liver damage, and DNA damage of peripheral blood lymphocytes induced in the rat by acute malathion exposure. METHODS: Rats were received intraperitoneal (i.p.) injection of malathion 150 mg/kg along with citric acid (200 or 400 mg/kg, orally), atropine (1 mg/kg, i.p.) or citric acid 200 mg/kg + atropine 1 mg/kg and euthanized 4 h later. RESULTS: Malathion resulted in increased lipid peroxidation (malondialdehyde) and nitric oxide concentrations accompanied with a decrease in brain reduced glutathione, glutathione peroxidase (GPx) activity, total antioxidant capacity (TAC) and glucose concentrations. Paraoxonase-1, acetylcholinesterase (AChE) and butyrylcholinesterase activities decreased in brain as well. Liver aspartate aminotransferase and alanine aminotransferase activities were raised. The comet assay showed increased DNA damage of peripheral blood lymphocytes. Histological damage and increased expression of inducible nitric oxide synthase (iNOS) were observed in brain and liver. Citric acid resulted in decreased brain lipid peroxidation and nitric oxide. Meanwhile, glutathione, GPx activity, TAC capacity and brain glucose level increased. Brain AChE increased but PON1 and butyrylcholinesterase activities decreased by citric acid. Liver enzymes, the percentage of damaged blood lymphocytes, histopathological alterations and iNOS expression in brain and liver was decreased by citric acid. Meanwhile, rats treated with atropine showed decreased brain MDA, nitrite but increased GPx activity, TAC, AChE and glucose. The drug also decreased DNA damage of peripheral blood lymphocytes, histopathological alterations and iNOS expression in brain and liver. CONCLUSIONS: The study demonstrates a beneficial effect for citric acid upon brain oxidative stress, neuronal injury, liver and DNA damage due to acute malathion exposure.

A new mathematical evaluation of smoking problem based of algebraic statistical method.

Smoking problem is considered as one of the hot topics for many years. In spite of overpowering facts about the dangers, smoking is still a bad habit widely spread and socially accepted. Many people start smoking during their gymnasium period. The discovery of the dangers of smoking gave a warning sign of danger for individuals. There are different statistical methods used to analyze the dangers of smoking. In this study, we apply an algebraic statistical method to analyze and classify real data using Markov basis for the independent model on the contingency table. Results show that the Markov basis based classification is able to distinguish different date elements. Moreover, we check our proposed method via information theory by utilizing the Shannon formula to illustrate which one of these alternative tables is the best in term of independent.

Citric acid effects on brain and liver oxidative stress in lipopolysaccharide-treated mice.

Citric acid is a weak organic acid found in the greatest amounts in citrus fruits. This study examined the effect of citric acid on endotoxin-induced oxidative stress of the brain and liver. Mice were challenged with a single intraperitoneal dose of lipopolysaccharide (LPS; 200 µg/kg). Citric acid was given orally at 1, 2, or 4 g/kg at time of endotoxin injection and mice were euthanized 4 h later. LPS induced oxidative stress in the brain and liver tissue, resulting in marked increase in lipid peroxidation (malondialdehyde [MDA]) and nitrite, while significantly decreasing reduced glutathione, glutathione peroxidase (GPx), and paraoxonase 1 (PON1) activity. Tumor necrosis factor-alpha (TNF-α) showed a pronounced increase in brain tissue after endotoxin injection. The administration of citric acid (1-2 g/kg) attenuated LPS-induced elevations in brain MDA, nitrite, TNF-α, GPx, and PON1 activity. In the liver, nitrite was decreased by 1 g/kg citric acid. GPx activity was increased, while PON1 activity was decreased by citric acid. The LPS-induced liver injury, DNA fragmentation, serum transaminase elevations, caspase-3, and inducible nitric oxide synthase expression were attenuated by 1-2 g/kg citric acid. DNA fragmentation, however, increased after 4 g/kg citric acid. Thus in this model of systemic inflammation, citric acid (1-2 g/kg) decreased brain lipid peroxidation and inflammation, liver damage, and DNA fragmentation.

Oxidative status and the response to pegylated-interferon alpha2a plus ribavirin in chronic genotype 4 HCV hepatitis.

Oxidative stress may play a pathogenic role in chronic hepatitis C (CHC). The present study examined the oxidative status in plasma of patients with CHC who received pegylated interferon and ribavirin therapy. The following groups were included: (1) sustained virological response (28 patients), (2) null response (26 patients), (3) breakthrough (24 patients), (4) relapse (24 patients), (5) spontaneous cure (23 patients) and (6) twenty five normal subjects as a control group. Markers of oxidative stress including plasma malondialdehyde, nitric oxide, reduced glutathione, total antioxidant capacity and uric acid as well as serum ALT, AST, alkaline phosphatase, total bilirubin, albumin, prothrombin time were studied. The study indicated significant decline in reduced glutathione and total antioxidant capacity and markedly elevated levels of malondialdehyde and nitric oxide in all groups compared with the controls. Null response group had the highest levels of malondialdehyde and nitric oxide. Nitric oxide was significantly higher in those with null response compared with all other groups and with control subjects. Uric acid was significantly higher in spontaneous cure group compared with all other groups and with the controls. We concluded that CHC patients had increased oxidative stress. The oxidative status in plasma of these patients was not changed by antiviral therapy. The study also showed an important contribution of nitric oxide in null response patients. High serum uric acid did not interfere with the response and/or did not predict the response to antiviral therapy.

The effect of gabapentin on oxidative stress in a model of toxic demyelination in rat brain.

BACKGROUND: Gabapentin, a structural analog of γ-aminobutyric acid (GABA), is used in the treatment of neuropathic pain in multiple sclerosis. METHODS: This study investigated the effect of gabapentin on oxidative stress in a model of brain demyelination evoked by intracerebral injection (i.c.i) of ethidium bromide (10 µL of 0.1%). Rats received saline (control) or gabapentin at 100 or 300 mg/kg orally daily for 10 days prior to injection of ethidium bromide. Rats were euthanized 1 day later, and then the levels of reduced glutathione (GSH), glutathione peroxidase (GPx) activity, lipid peroxidation (malondialdehyde; MDA), nitrite, acetyl cholinesterase (AChE) and paraoxonase activities were assessed in the brain cortex in different treatment groups. RESULTS: Ethidium bromide resulted in increased oxidative stress in the cortex 1 day after its injection. Malondialdehyde increased by 30.2%, whereas GSH decreased by 17.6%. GPx activity was inhibited by 78.6%. Brain nitrite increased by 55.4%, AChE activity decreased by 33.4% and paraoxonase activity decreased by 27.5%. In ethidium bromide treated rats, gabapentin administered at 300 mg/kg increased cortical MDA by 66%. GSH was unaltered by gabapentin, but GPx activity decreased by 54.3% by the higher dose of gabapentin. Nitrite decreased by 21.4% and 29.2% after 100 and 300 mg/kg of gabapentin, respectively. AChE activity increased by 28.6% and 69.3% by 100 and 300 mg/kg of gabapentin, respectively. Paraoxonase activity showed 83.3% and 73% decreases by 100 and 300 mg/kg of gabapentin, respectively. CONCLUSIONS: These results suggest that gabapentin increases brain lipid peroxidation and decreases brain antioxidant enzymes in this model of chemical demyelination.

Cadmium impact and osteoporosis: mechanism of action.

CONTEXT: Cadmium (Cd) is a widespread environmental pollutant that is associated with increased risk of osteoporosis. It has been proposed that Cd's toxic effect on bone is exerted via impaired activation of vitamin D, secondary to the kidney effects. OBJECTIVE: The present study was designed to investigate the damaging impact of Cd in drinking water on bone from biochemical and histopathological point of view. MATERIALS AND METHODS: This study was conducted on 30, 3-months-old female Sprague Dawley rats exposed to cadmium chloride in a dose of 50 mg Cd/L in drinking water for 3 months. Serum was taken for determination of calcium, phosphorous levels, parathyroid hormone, 1,25 dihydroxy vitamin D(3), osteocalcin (OC) and bone specific alkaline phosphatase (BALP) activity. RESULTS: The result revealed that Cd administration induces significant increase in serum calcium (Ca), phosphorous (P) and parathyroid hormone (PTH) levels in concomitant with significant reduction in serum vitamin D(3), osteocalcin (OC) levels and bone specific alkaline phosphatase (BALP) activity. CONCLUSION: The present study provided clear evidence that long-term exposure to cadmium chloride produced marked abnormalities in bone biomarkers and increasing risk of fracture.

Neuroprotective effect of nitric oxide donor isosorbide-dinitrate against oxidative stress induced by ethidium bromide in rat brain.

This study investigated the effect of systemic administration of isosorbide-dinitrate (ISDN) on oxidative stress and brain monoamines in a toxic model of brain demyelination evoked by intracerebral injection (i.c.i) of ethidium bromide (10 µl of 0.1 %). Rats received saline (control) or ISDN at 5 or 10 mg/kg for 10 days prior to injection of ethidium bromide. Rats were euthanized one day later, and then the levels of reduced glutathione (GSH), lipid peroxidation (malondialdehyde; MDA), nitric oxide (nitrite/nitrate), acetylcholinesterase (AChE) activity, paraoxonase activity as well as monoamine levels (serotonin, dopamine and noradrenaline) were assessed in the brain cortex in different treatment groups. The i.c.i of ethidium bromide resulted in increased oxidative stress in the cortex one day after its injection; (i) MDA increased by 36.9 %; (ii) GSH decreased by 20.8 %, while (iii) nitric oxide increased by 60.3 %; (iv) AChE and paraoxonase activities in cortex decreased by 35.9 % and 29.4 %, respectively; (v) serotonin was significantly increased. In ethidium bromide-treated rats, pretreatment with ISDN at 10 mg/kg decreased cortical MDA by 23.9 %. Reduced glutathione was increased by 25.1 % ISDN at 10 mg/kg, while nitric oxide showed a 32.8 and 41.7 % decrease after 5 and 10 mg/kg of ISDN, respectively. Acetylcholinesterase activity increased by 24.3 % by 10 mg/kg of ISDN. Paraoxonase activity showed further decrease by 72.2 and 83.8 % after treatment with 5 and 10 mg/kg of ISDN, respectively. The administration of ISDN decreased the level of serotonin and noradrenaline compared with the ethidium bromide only treated group. Overall, the present findings suggest neuroprotective effect of ISDN against oxidative stress in this model of chemical demyelination.

Neuroprotective and hepatoprotective effects of micronized purified flavonoid fraction (Daflon®) in lipopolysaccharide-treated rats.

Micronized purified flavonoid fraction (MPFF, Daflon®) is a phlebotonic drug widely used in chronic venous or lymphatic insufficiency. We aimed to investigate the effects of MPFF on hepatic and brain oxidative stress and on liver injury caused by lipopolysaccharide (LPS) in rats. MPFF (4.5, 9, or 18 mg/kg) or saline was administered orally for two days prior to intraperitoneal (i.p.) LPS (300 µg/kg) and at time of LPS administration. Rats were euthanized 4 h after LPS injection. The administration of LPS increased oxidative stress in brain and liver tissue. Malondialdehyde (MDA) increased by 193.5 and 191.8%, reduced glutathione (GSH) decreased by 73.8 and 70.8% and nitric oxide increased by 118.2 and 151.7% in the brain and liver, respectively. Serum paraoxonase 1 (PON1) activity decreased by 42.6%. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were raised by 101.8, 93.6, and 223.2%, respectively. Rats treated with MPFF at 9 and 18 mg/kg showed decreased brain MDA (27.5-34%), nitrite (25.5-41%) and increased GSH (27.2-74.1%). In the liver, MDA decreased by 16.4-59.8%, nitrite decreased by 54.7-56.7%, and GSH increased by 15.2-70.5% with MPFF at 4.5, 9, or 18 mg/kg, respectively. Serum PON1 activity showed 41-65.9% increments with MPFF. Significant reductions in serum AST, ALT, and ALP were seen after treatment with MPFF. Moreover, the degree of histological damage, expression of the inducible form of nitric oxide synthase and the apoptotic enzyme caspase-3 in the liver were substantially reduced. MPFF thus prevented the increased oxidative stress and inflammation in brain and liver as well as the liver dysfunction caused by endotoxemia in the rat.

The effects of trimetazidine on lipopolysaccharide-induced oxidative stress in mice.

The effects of trimetazidine, a novel anti-ischemic agent, on the development of oxidative stress induced in mice with lipopolysaccharide endotoxin were investigated. The drug was administered orally once daily at doses of 1.8, 3.6 or 7.2 mg/kg for two days prior to intraperitoneal (i.p.) injection of lipopolysaccharide E (200 µg/kg) and at time of endotoxin administration. Mice were euthanized 4 h after administration of the lipopolysaccharide. Lipid peroxidation (malondialdehyde; MDA), reduced glutathione (GSH) and nitric oxide (nitrite/nitrate) concentrations were measured in brain and liver. The administration of lipopolysaccharide increased oxidative stress in both the brain and liver tissue. MDA increased by 33.9 and 107.1 %, GSH decreased by 23.9 and 84.3 % and nitric oxide increased 70.3 and 48.4 % in the brain and liver, respectively. Compared with the lipopolysaccharide control group, brain MDA decreased by 26.2 and 36.7 %, while GSH increased by 18.2 and 25.8 % after the administration of trimetazidine at 3.6 and 7.2 mg/kg, respectively. Brain nitric oxide decreased by 45.3, 50.8 and 57.0 % by trimetazidine at 1.8, 3.6 and 7.2 mg/kg, respectively. In the liver, MDA decreased by 18.7, 30.7 and 49.4 % and GSH increased by 150.3, 204.8 and 335.4 % following trimetazidine administration at 1.8, 3.6 and 7.2 mg/kg. Meanwhile, nitric oxide decreased by 17.3 % by 7.2 mg/kg of trimetazidine. These results indicate that administration of trimetazidine in the presence of mild systemic inflammatory response alleviates oxidative stress in the brain and liver.

Evaluation of the whole genome DNA-DNA hybridization technique to identify bacteria in histological sections of periradicular lesions.

Whole genome DNA-DNA hybridization has been used to identify bacteria in periradicular lesions partly because there is no amplification of the bacteria, therefore, minor contaminants are not detected. There are, however, potential pitfalls with this technique, including inability to distinguish dead bacteria, cross-reactions of species within a genus, and inability to detect species present in low numbers because of loss of DNA during extraction and purification. Alternatively, inadequate extraction and purification of DNA could result in false positives. Therefore, controls are required to monitor DNA loss, DNA cross-reactions, and DNA of pure cultures mixed with bacteria-free tissue to monitor for false positives. We determined that the quality of DNA extracted from histological sections of periradicular lesions is excellent for DNA-DNA hybridization. Although lesions contain large numbers of bacteria, histological sections through lesions barely contain sufficient quantity of bacteria for such analysis. This was confirmed by histological observation of sparsely distributed bacteria within lesions. Furthermore, we found that the bacteria are not distributed evenly throughout periradicular lesions, in numbers or species.

Effect of carbohydrate source on post-prandial blood glucose in subjects with type 1 diabetes treated with insulin lispro.

Our purpose was to determine if the glycemic index (GI) and proportion of carbohydrate absorbed as glucose (Pg) affected glycemic responses and occurrence of post-prandial hypoglycemia in subjects with type 1 diabetes treated with insulin lispro. Subjects (n=8) were studied on five separate occasions after 10-12 h overnight fasts following a standard dinner. After their morning insulin dose, subjects ate 50 g carbohydrate from a starchy food (Pg=1; mashed potato GI=83, white bread GI=71, spaghetti GI=41, barley GI=25) or pineapple juice (Pg=0.5; GI=46). Blood glucose was measured fasting and at 30 min intervals for 4 h. Glucose responses after different foods differed significantly from 30 to 180 min, with mean incremental area under the curve being closely related to GI (r=0.98, P<0.01). By multiple regression analysis, occurrence of post-prandial hypoglycemia was influenced (P<0.05) by subject and Pg. Time to hypoglycemia was affected by subject, fasting glucose, and GI. Thus, in subjects with type 1 diabetes treated with insulin lispro, GI predicts glycemic responses of carbohydrate foods. Pg may affect the occurrence of post-prandial hypoglycemia, while GI may affect its timing. Further studies using mixed meals are required to confirm how carbohydrate source affects glycemic responses and occurrence of hypoglycemia in normal meal setting.