Effects of Acupuncture Treatment on Fibromyalgia Symptoms, Serotonin, and Substance P Levels: A Randomized Sham and Placebo-Controlled Clinical Trial.

Objective: The aim of this study was to evaluate the effects of acupuncture treatment on serum levels of serotonin and substance P (SP) as well as on clinical parameters in patients with fibromyalgia (FM). Methods: This is a randomized controlled clinical trial. Seventy-five women with FM were randomized into one of three kinds of acupuncture treatment: real acupuncture group (AcG), sham acupuncture group (ShG), and simulated acupuncture group (SiG). Treatments were applied semiweekly for four weeks. The serum levels of serotonin and SP were evaluated before and after the eight sessions. Patients were clinically assessed by visual analog scale (VAS), the number of tender points (NTP), Fibromyalgia Impact Questionnaire (FIQ), Beck Depression Inventory (BDI), and Nottingham Health Profile (NHP) at baseline, after the last treatment, and one and three months after completion of all treatments. Results: Serum serotonin values increased significantly after treatment in AcG and ShG (P < 0.001 and P < 0.01, respectively). The increase in the AcG was also different from both of the other groups (P < 0.01). While SP levels decreased in the AcG, they increased in the SiG (P = 0.001). In the AcG, significant improvements were found in almost all clinical outcomes after treatment. These usually continued for three months. In the ShG, there were also significant changes on the NTP, VAS, FIQ, and BDI scores after treatment. Improvements on the NTP and FIQ scores lasted for three months. In the SiG, significant improvements were found only in the NTP, VAS, and BDI scores after treatment. Conclusions: Acupuncture, rather than sham or placebo acupuncture, may lead to long-term improvements on clinical outcomes and pain neuromediator values. Changes in serum serotonin and SP levels may be a valuable explanation for acupuncture mechanisms in FM treatment.

The Relationship Between Skinfold Thickness and Leptin, Ghrelin, Adiponectin, and Resistin Levels in Infants of Diabetic Mothers.

This study aimed to investigate the relationship between skinfold thickness and serum leptin, ghrelin, adiponectin, and resistin levels in infants of diabetic mothers. Biochemical parameters were also similar for the two groups (infants of diabetic mothers and controls) (p > 0.05). We confirmed that there was a negative correlation between birth weight and serum ghrelin level (p < 0.05) in the two groups. When it was evaluated for control newborns, a positive correlation between abdominal circumference and serum resistin level was found in the controls (p < 0.05). Our results indicate that gestational diabetes by appropriate diet or insulin treatment may be effective in the protection of fetuses of diabetic mothers from the negative effects of gestational diabetes. Ghrelin alone was negatively correlated with birth weight. This negative correlation could be potentially advantageous to infants, because a reduction in appetite might prevent excessive food intake and postnatal weight gain.

Clinical and biochemical comparison of guided tissue regeneration versus guided tissue regeneration plus low-level laser therapy in the treatment of class II furcation defects: A clinical study.

OBJECTIVE: The present study was aimed to compare the clinical and biochemical effectiveness of guided tissue regeneration (GTR) alone and combined with low-level laser therapy (LLLT) application in the treatment of furcation II periodontal defects, over a period of 6 months. MATERIAL AND METHODS: Thirty-three furcation defects were included in the study. Seventeen of these defects were treated with GTR plus LLLT, and sixteen of them were treated with GTR alone. Probing pocket depth (PPD), clinical attachment level (CAL), horizontal probing depth (HPD), and alkaline phosphatase (ALP) and osteocalcin (OC) levels in the gingival crevicular fluid (GCF) were recorded at baseline and at postoperative 3rd and 6th months. RESULTS: Healing was uneventful in all cases. At the 3rd and 6th months, both treatment modalities-GTR and GTR plus LLLT--showed improved PPD, CAL, and HPD values compared to their baseline values. ALP and OC levels in GCF increased after the treatment in both groups (p < 0.05). When compared the two groups, at the 6th month, PPD, CAL, HPD, and ALP values showed significantly more improvement in laser group than non-laser group (p < 0.05). CONCLUSIONS: The results of this study showed that both treatments led to significantly favorable clinical improvements in furcation periodontal defects. LLLT plus GTR may be a more effective treatment modality compared to GTR alone.

Vitamin D Treatment Effect on Serum Endocan and High-Sensitivity C-Reactive Protein Levels in Renal Transplant Patients.

CONTEXT: Endocan is a marker showing endothelial dysfunction and inflammation. Significantly increased endocan levels have been observed in serum of patients with sepsis and cancer. OBJECTIVE: Our aim was to investigate the relationship between vitamin D treatment and serum endocan and high-sensitivity C-reactive protein (hs-CRP) levels as inflammatory markers in transplant patients. DESIGN: Prospective. SETTING: Nephrology clinic. PATIENTS: Thirty-eight renal transplant patients with serum 25-hydroxy-vitamin D (25-OH-vitamin D) levels below 20 ng/mL and transplanted at least 12 months. INTERVENTION: One-time oral dose of 300 000 IU vitamin D3. MAIN OUTCOME MEASURES: Before and after vitamin D treatment, serum endocan, hs-CRP, calcium, phosphorus, and parathyroid hormone (PTH) levels were measured. RESULTS: Median serum endocan and PTH values before vitamin D were significantly higher than those of after treatment values ( P = .001 and P < .001, respectively). On the other hand, serum total calcium and phosphorus levels before vitamin D treatment were lower than the values obtained after vitamin D treatment ( P = .0013 and P < .001, respectively). Serum hs-CRP was lower after vitamin D therapy than before, but the difference was not statistically significant ( P = .06). A moderate negative correlation was determined between endocan and 25-OH-vitamin D levels after treatment with vitamin D ( r = -.36, P = .02). CONCLUSION: This study has revealed that vitamin D treatment reduced markers of endothelial dysfunction in patients with renal transplantation and vitamin D deficiency.

Serum YKL-40 and MDA levels in Behcet disease.

OBJECTIVE: To measure plasma levels of chitinase-3-like 1 protein and its association with malondialdehyde in Behcet's disease patients. METHODS: The case-control study was conducted at Faculty of Medicine, Ataturk University Erzurum, Turkey, from October 2012 to March 2014, and comprised patients with Behcet's disease and healthy subjects. The patients were divided into two groups, as active and inactive, based on the classification of phases of activity in Behcet's disease. Differences between groups were analysed. SPSS 20 was used for data analysis. RESULTS: Of the 79 participants, 51(64.56%) were patients and 28(35.44%) were controls. The mean age of the first group was 29.45±7.82 years and the second group was 32.21±9.61 years. Among patients, 37(72.55%) were categorised as "active" and 14(27.45%) as "inactive". Median serum Chitinase-3-like 1 protein and malondialdehyde levels were 37.57 ng/mL (interquartilerange: 13.7-293.0 ng/mL) in patients and 26.25 ng/mL (interquartile range: 17.0-44.7 ng/mL) in controls. There was no significant correlation between Chitinase-3-like 1 protein and malondialdehyde (p>0.05). CONCLUSIONS: Chitinase-3-like 1 protein might be associated with Behcet's disease. Elevated malondialdehyde levels were not only the cause of inflammation but also indicator of oxidative stress in Behcet's disease.

Vitamin D supplementation blocks pulmonary structural and functional changes in a rat model of perinatal vitamin D deficiency.

Whereas epidemiological data strongly link vitamin D (VD) deficiency to childhood asthma, the underlying molecular mechanisms remain unknown. Although VD is known to stimulate alveolar epithelial-mesenchymal interactions, promoting perinatal lung maturation, whether VD supplementation during this period protects against childhood asthma has not been demonstrated experimentally. Using an in vivo rat model, we determined the effects of perinatal VD deficiency on overall pulmonary function and the tracheal contraction as a functional marker of airway contractility. One month before pregnancy, rat dams were put on either a no cholecalciferol-added or a 250, 500, or 1,000 IU/kg cholecalciferol-added diet, which was continued throughout pregnancy and lactation. At postnatal day 21, offspring plasma 25(OH)D levels and pulmonary function (whole body plethysmography and tracheal contraction response to acetylcholine) were determined. 25(OH)D levels were lowest in the no cholecalciferol-supplemented group, increasing incrementally in response to cholecalciferol supplementation. Compared with the 250 and 500 IU/kg VD-supplemented groups, the no cholecalciferol-supplemented group demonstrated a significant increase in airway resistance following methacholine challenge. However, the cholecalciferol deficiency-mediated increase in tracheal contractility in the cholecalciferol-depleted group was only blocked by supplementation with 500 IU/kg cholecalciferol. Therefore, in addition to altering alveolar epithelial-mesenchymal signaling, perinatal VD deficiency also alters airway contractility, providing novel insights to asthma pathogenesis in perinatally VD-deficient offspring. Perinatal VD supplementation at 500 IU/kg appears to effectively block these effects of perinatal VD deficiency in the rat model used, providing a strong clinical rationale for effective perinatal VD supplementation for preventing childhood asthma.

Serum and bronchial aspiration fluid HE-4 levels in lung cancer.

Human epididymis 4 (HE-4) protein has been proposed as a tumor marker for lung and ovarian cancer. This study was designed to measure HE-4 levels in bronchial aspiration fluid (BAF) of patients with lung cancer and to describe the relationship of BAF HE-4 with known systemic increase in serum HE-4 levels. Sixty-four patients with lung cancer, 38 with benign lung disease and 19 healthy subjects, were enrolled in our study. The BAF was obtained during routine bronchoscopic procedure in patient groups. HE-4 levels in serum and BAF were measured with the commercially available kit by an enzyme-linked immunosorbent assay. Serum HE-4 levels were significantly higher in patients with lung cancer group (204.2 ± 22.9 pmol/L) than in benign lung disease group (135 ± 26.9 pmol/L, p = 0.001) and healthy subjects (14.8 ± 7.0 pmol/L, p < 0.0001). No significant difference was observed in terms of BAF HE-4 values in two patient groups. BAF HE-4 levels were significantly higher than those of serum levels in both patient groups (p < 0.0001). Serum HE-4 level was correlated with tumor stage (p = 0.001) and age (p < 0.0001) in the lung cancer group. The areas under the receiver operating characteristic (ROC) curve of serum HE-4 was 0.784 (95 % confidence interval (CI), 0.701-0.867) and that of BAF HE-4 was 0.496 (95 % CI, 0.382-0.610). This study shows that a systemic increase in serum of HE-4 is more prominent than a local increase of HE-4 (BAF), so this may suggest the feasibility of using serum instead of BAF samples for HE-4 measurements in lung cancer cases.

An investigation about the inhibition of acute ischemia/reperfusion damage by dexmedetomidine in rat ovarian tissue.

Reperfusion has always been "the emergency intervention" to ischemic tissue. For a given period of time, tissue injury due to ischemia and reperfusion is more serious than injury due to ischemia only. Groups were as: Group 1: 25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 2: 10 mg/kg yohimbine +25 µg/kg dexmedetomidine + ischemia/reperfusion group. Group 3: Ischemia/reperfusion (control) group. Group 4: Healthy rats. Rat ovaries were exposed to a 3-hour ischemia and then reperfusion ensured for 2 hours. After ischemia/reperfusion, total glutathione, malondialdehyde, 8-hydroxyguanine levels and histopathological investigation were studied. The highest total glutathione and the lowest malondialdehyde and DNA damage levels were determined in dexmedetomidine group when compared to control group. The difference between yohimbine + dexmedetomidine and the control group was insignificant. Dexmedetomidine protects the ovarian tissue of the rat from I/R injury. It is hypothesized that this protective effect of dexmedetomidine is mediated by the α-2 adrenergic receptors. Dexmedetomidine could be useful for attenuation of tissue damage after I/R and prevention of I/R-related complications.

Mirtazapine protects against cisplatin-induced oxidative stress and DNA damage in the rat brain.

AIM: Cisplatin chemotherapy is associated with neurotoxicity, and oxidative stress might play an important role in the pathogenesis. Mirtazapine may be a preventative agent via its less-known antioxidant properties. The aim of this study was to examine the potential chemoprotective effects of mirtazapine against cisplatin-induced oxidative stress and DNA damage. METHODS: Twenty-four rats were divided equally into four groups: control; cisplatin (10 mg/kg i.p.); cisplatin plus mirtazapine (10-30 mg/kg, respectively i.p and p.o.); and mirtazapine (30 mg/kg p.o.). The rats were killed at the end of the 14th day of treatment. Brain tissue was examined with regard to antioxidant/oxidant biochemical parameters. RESULTS: Although glutathione (tGSH) and nitric oxide (NO) end product mean scores were found to be statistically higher in the control group when compared with the cisplatin group (72.44% and 61.99% percentage change [PC], respectively), malondialdehyde (MDA), myeloperoxidase (MPO), and 8-hydroxyguanine (8-OH-GUA) mean scores were statistically lower in the control group in comparison with the cisplatin group (-55.48%, -67.99%, and -48.81% PC, respectively; P < 0.01). Finally, tGSH and NO end product levels were restored to normal (85.90% and 55.30% PC, respectively), and MDA, MPO, and 8-OH-GUA were significantly reduced by treatment with mirtazapine (-60.50%, -78.59%, and -38.10% PC, respectively; P < 0.01). CONCLUSION: Mirtazapine has chemoprotective effects against cisplatin-induced oxidative stress and DNA damage in the rat brain, which may be attributed to its antioxidant capabilities. It would be useful to investigate whether cisplatin at the desired doses can be given concurrently with mirtazapine.

The role of thiamine pyrophosphate in prevention of cisplatin ototoxicity in an animal model.

OBJECTIVE: The aim of this study was to evaluate the effectiveness of thiamine pyrophosphate against cisplatin-induced ototoxicity in guinea pigs. MATERIALS AND METHODS: Healthy guinea pigs (n = 18) were randomly divided into three groups. Group 1 (n = 6) received an intraperitoneal injection of saline solution and cisplatin for 7 days, group 2 (n = 6) received an intraperitoneal injection of thiamine pyrophosphate and cisplatin for 7 days, and group 3 (n = 6) received only intraperitoneal injection of saline for 7 days. The animals in all groups were sacrificed under anesthesia, and their cochleas were harvested for morphological and biochemical observations. RESULTS: In group 1, receiving only cisplatin, cochlear glutathione concentrations, superoxide dismutase, and glutathione peroxidase activities significantly decreased (P < 0.05) and malondialdehyde concentrations significantly increased (P < 0.05) compared to the control group. In group 2, receiving thiamine pyrophosphate and cisplatin, the concentrations of enzymes were near those of the control group. Microscopic examination showed that outer hair cells, spiral ganglion cells, and stria vascularis were preserved in group 2. CONCLUSION: Systemic administration of thiamine pyrophosphate yielded statistically significant protection to the cochlea of guinea pigs from cisplatin toxicity. Further experimental animal studies are essential to determine the appropriate indications of thiamine pyrophosphate before clinical use.

Do the effects of aggregate and disaggregate energy consumption on different environmental quality indicators change in the transition to sustainable development? Evidence from wavelet coherence analysis.

In the 2030 Agenda for Sustainable Development, adopted by the United Nations (UN) member states in 2015, half of the target period has been exceeded. However, China, whose energy consumption relies heavily on fossil resources, remains at the top of the list of global polluters. Therefore, investigating the environmental impacts of energy types is essential to China's path towards Sustainable Development Goals (SDG)-7 and SDG-13. Based on this motivation, the paper offers new insights into the energy-environment literature for China with wavelet coherence analysis (WCA). This approach can investigate the relationship between variables in a periodic manner based on the frequency behavior of the models. The paper separately analyzes the effects of primary energy consumption (PEC), fossil energy consumption (FEC), renewable energy consumption (REC), nuclear energy consumption (NEC), GDP, and population (POP) on three different environmental indicators in China. Using two environmental pollution indicators (carbon emission (CO2) and ecological footprint (EF)) and one environmental quality indicator (load capacity factor (LCF)), the paper allows for comparison and robustness checks on the environmental impacts of energy indicators. Empirical findings reveal the following: (i) Except for REC and POP in the CO2 model, the variables in all three models largely move together during the period under observation; (ii) variables other than POP have consistent coefficient signs; (iii) PEC, FEC, NEC, and GDP increase CO2 and EF while decreasing LCF; (iv) the effect of NEC on LCF is more obvious until 2000; (v) unlike the others, REC affects CO2 and EF negatively and LCF positively; (vi) there is bidirectional causality between PEC and environmental indicators but not for REC; (vii) the causality relations of other variables with environmental indicators differ in terms of model, time, and direction of causality. In light of the findings, the paper highlights that only the REC improves environmental quality in China. Other energy indicators contribute to environmental degradation. China, whose ecological deficit has increased dramatically in recent years, urgently needs to reduce its dependence on fossil energy sources by accelerating investments in REC. Governments should also review nuclear energy policies, which are expected to help achieve carbon neutrality.

Biochemically and histopathologically comparative review of thiamine's and thiamine pyrophosphate's oxidative stress effects generated with methotrexate in rat liver.

BACKGROUND: Oxidative liver injury occurring with methotrexate restricts its use in the desired dose. Therefore, whether or not thiamine and thiamine pyrophosphate, whose antioxidant activity is known, have protective effects on oxidative liver injury generated with methotrexate was comparatively researched in rats using biochemical and histopathological approaches. MATERIAL/METHODS: Thiamine pyrophosphate+methotrexate, thiamine+methotrexate, and methotrexate were injected intraperitoneally in rats for 7 days. After this period, all animals' livers were excised, killing them with high-dose anesthesia, and histopathologic and biochemical investigations were made. RESULT: Biochemical results demonstrated a significant elevation in level of oxidant parameters such as MDA and MPO, and a reduction in antioxidant parameters such as GSH and SOD in the liver tissue of the methotrexate group. Also, the quantity of 8-OHdG/dG, a DNA injury product, was higher in the methotrexate group with high oxidant levels and low antioxidant levels, and the quantity of 8-OHdG/dG was in the thiamine pyrophosphate group with low oxidant levels and high antioxidant levels. In the thiamine and control groups, the 8-OHdG/dG rate was 1.48 ± 0.35 pmol/L (P>0.05) and 0.55 ± 0.1 pmol/L (P<0.0001). Thiamine pyrophosphate significantly decreased blood AST, ALT and LDH, but methotrexate and thiamine did not decrease the blood levels of AST, ALT and LDH. Histopathologically, although centrilobular necrosis, apoptotic bodies and inflammation were monitored in the methotrexate group, the findings in the thiamine pyrophosphate group were almost the same as in the control group. CONCLUSIONS: Thiamine pyrophosphate was found to be effective in methotrexate hepatotoxicity, but thiamine was ineffective.

Effect of mirtazapine on oxidative stress created in rat kidneys by ischemia-reperfusion.

In this study, the effect of mirtazapine on rat kidneys versus ischemia-reperfusion (IR) damage was biochemically and histopathologically investigated. The results have shown that malondialdehyde (MDA) level of healthy rat group is 15.2 mol/g protein. The level of this substance was measured as 26.7 mol/g in only ischemia group. The MDA levels of IR and mirtazapine + renal ischemia-reperfusion (MRIR) groups were 39 ± 17.6 mol/g protein. While myeloperoxidase activity of healthy rat group was 20.2 u/g, the activities of only ischemia, IR, and MRIR groups were 28, 36.3, and 21 u/g, respectively. The glutathione levels were measured as 17.7, 12.8, 7.5, and 16.2 nmol/g in healthy, only ischemia, IR, and MRIR groups, respectively. Finally, glutathione S-transferase activities of healthy, only ischemia, IR, and MRIR groups were determined as 20, 13.8, 7.1, and 18.3 u/g, respectively. Histopathologically, while hemorrhage in interstitial area was observed in only ischemia group, significant tubular epithelial swelling, necrosis, and cast accumulation were seen in IR group. In MRIR group, only mild tubular epithelial swelling and mild hyaline cast accumulation were observed in kidney tissue. Consequently, it can be said that mirtazapine has a protective effect on IR-induced kidney damage.

Indirect role of beta2-adrenergic receptors in the mechanism of analgesic action of nonsteroidal antiinflammatory drugs.

OBJECTIVE: Adrenal gland hormones have been shown to have a role in the antiinflammatory effect mechanism of nonsteroidal antiinflammatory drugs. This study investigates whether the analgesic effects of indomethacin, diclofenac sodium, aspirin, and nimesulide (IDAN; upper case letters of the four drugs we used) are also related to adrenal gland hormones. DESIGN: The analgesic effects of IDAN were studied in the carrageenan-induced inflammatory pain model using both intact and adrenalectomized rats. Paw withdrawal tests were performed in adrenalectomized rats that had been pretreated with phenoxybenzamine, propranolol, and metoprolol. SETTING: This study was performed in Pharmacology and Biochemistry Laboratories of Faculty of Medicine. PATIENTS/SUBJECTS: A total of 306 (114 intact and 192 adrenalectomized) male Albino Wistar rats were used. INTERVENTIONS: Adrernalectomy, drug administrations, pain model induction and pain threshold measurements were performed during the study. MEASUREMENTS AND MAIN RESULTS: Although the analgesic effects of nonsteroidal antiinflammatory drugs were lost in adrenalectomized rats, they exerted significant analgesia in adrenalectomized rats that had been pretreated with prednisolone and adrenalin. All these drugs were found to decrease serum adrenalin concentration but did not change serum cortisole (corticosterone in rats) concentration. Prednisolone and adrenalin inhibited carrageenan-induced hyperalgesia in adrenalectomized rat groups pretreated with metoprolol or phenoxybenzamine, but not in rats given propranolol. Propranolol also negated the analgesic effects of IDAN in intact rats. The analgesic effects provided by either prednisolone or adrenalin could not be inhibited by the alpha1, alpha2, or beta1 blockers but disappeared when beta2 receptors were blocked. CONCLUSIONS: The analgesic effects of nonsteroidal antiinflammatory drugs appear to be related to endogenous adrenalin and cortisole. We have demonstrated that adrenalin and prednisolone play important roles in the analgesic effect mechanism of IDAN. Prednisolone and adrenalin produce analgesic effects through beta2-adrenergic receptors, suggesting an indirect role for beta2-adrenergic receptors in the analgesic effect mechanism of the nonsteroidal antiinflammatory drugs mentioned.

Dehydroepiandrosterone ameliorates hepatocellular damage in obstructive jaundice.

We aimed to investigate the ameliorating effect of dehydroepiandrosterone (DHEA) on the potential hepatocellular damage in experimental obstructive jaundice. Twenty-four male rabbits in the study were randomly allocated into three groups. In the sham group, the choledochal canal was identified and explored. In the obstructive jaundice and treatment groups, the choledochal canal was ligated. Placebo and DHEA were administered to the obstructive jaundice and treatment groups, respectively. Blood samples were obtained at baseline, and both blood samples and liver tissue samples were obtained by re-laparotomy performed on day 8. Biochemical parameters were measured in blood samples, and liver samples were histopathologically evaluated. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP) and bilirubin levels were lower in the treatment group than in obstructive jaundice. Mononuclear inflammation in the portal region and hepatocyte degeneration were milder in the treatment group compared to obstructive jaundice group. Fibrosis and necrosis were also recovered by the DHEA treatment.In conclusion, these findings suggested that DHEA may reduce the obstructive jaundice-induced hepatocellular damage.

Vitamin E and Hippophea rhamnoides L. extract reduce nicotine-induced oxidative stress in rat heart.

The effects of vitamin E and Hippophea rhamnoides L. extract (HRe-1) on nicotine-induced oxidative stress in rat heart were investigated. There were eight rats per group and supplementation period was 3 weeks. The groups were: nicotine [0.5 mg kg(-1)day(-1), intraperitoneal (i.p.)]; nicotine plus vitamin E [75 mg kg(-1)day(-1), intragastric (i.g.)]; nicotine plus HRe-1 (250 mg kg(-1)day(-1), i.g.); and the control group (receiving only vehicles). Nicotine increased the malondialdehyde level, which was prevented by both vitamin E and HRe-1. Glutathione peroxidase (GPx) activity in nicotine plus vitamin E supplemented group was higher than the others. Glutathione S-transferase (GST) activity in nicotine plus HRe-1 supplemented group was increased compared with the control group. Catalase activity was higher in nicotine group compared with others. GPx activity in nicotine plus vitamin E supplemented group was elevated compared with the others. Total and non-enzymatic superoxide scavenger activities in nicotine plus vitamin E supplemented group were lower than nicotine plus HRe-1 supplemented group. Superoxide dismutase (SOD) activity was higher in nicotine plus HRe-1 supplemented group compared with others. Glutathione reductase activity and nitric oxide level were not affected. Increased SOD and GST activities might have taken part in the prevention of nicotine-induced oxidative stress in HRe-1 supplemented group in rat heart. Flavonols such as quercetin, and isorahmnetin, tocopherols such as alpha-tocopherol and beta-tocopherol and carotenoids such as alpha-carotene and beta-carotene, reported to be present in H. rhamnoides L. extracts may be responsible for the antioxidant effects of this plant extract.

Hippophae rhamnoides attenuates nicotine-induced oxidative stress in rat liver.

The effects of vitamin E and Hippophae rhamnoides L. (Elaeagnaceae) extract (HRe-1) on nicotine-induced oxidative stress in rat liver were investigated. Four groups, eight rats each, were used in this study, and the supplementation period was 3 weeks. The groups were: nicotine (0.5 mg/kg/day, intraperitoneal (i.p.)); nicotine plus vitamin E (75 mg/kg/day, intragastric (i.g.)); nicotine plus HRe-1 (250 mg/kg/day, i.g.); and the control group. The malondialdehyde and nitric oxide levels, glutathione peroxidase, glutathione S-transferase, glutathione reductase, superoxide dismutase, and total and non-enzymatic superoxide scavenger activities were measured spectrophotometrically in supernatants of the tissue homogenates. Nicotine increased the malondialdehyde level in liver tissue compared with control. This nicotine-induced increase in lipid peroxidation was prevented by both vitamin E and HRe-1. Superoxide dismutase activity was higher in the nicotine plus vitamin E-supplemented group compared with nicotine and control groups. Glutathione reductase activity was higher in the nicotine group compared with the control group. However, glutathione peroxidase activity in the control group was higher than the levels in the nicotine, and the nicotine plus HRe-1 supplemented groups. The nitric oxide level was higher in the nicotine group compared with all other groups. Total and non-enzymatic superoxide scavenger activities and glutathione S-transferase activity were not affected by any of the treatments. Our results suggest that Hippophae rhamnoides extract as well as vitamin E can protect the liver against nicotine-induced oxidative stress.

The Effect of Corrected Inflammation, Oxidative Stress and Endothelial Dysfunction on Fmd Levels in Patients with Selected Chronic Diseases: A Quasi-Experimental Study.

While the pathophysiology of chronic disorders varies there are three basic mechanisms - inflammation, oxidative stress and endothelial dysfunction - that are common in many chronic diseases. However, the failure of these mechanisms to work synchronously can lead to morbidity complicating the course of many chronic diseases. We analyzed data of 178 patients from cohorts with selected chronic diseases in this quasi-experimental study. Endothelial dysfunction was determined by flow-mediated dilatation (FMD) and asymmetric dimethylarginine (ADMA) levels. Serum ADMA, high sensitive C-reactive protein (hs-CRP), serum PTX3, malondialdehyde (MDA), Cu/Zn-superoxide dismutase (Cu/Zn-SOD), glutathione peroxidase (GSH-Px) levels and FMD were studied in baseline and after 12 weeks of Morinda citrifolia (anti-atherosclerotic liquid- AAL), omega-3 (anti-inflammatory capsules- AIC) and extract with Alaskan blueberry (anti-oxidant liquid- AOL). Stepwise multivariate regression analysis was used to evaluate the association of FMD with clinical and serologic parameters. Serum ADMA, MDA, PTX3, hsCRP and albumin levels, and proteinuria were significantly decreased while CuZn-SOD, GSH-Px and FMD levels were significantly increased following AAL, AIC and AOL therapies. The FMD was negatively correlated with serum ADMA, MDA, PTX3, and hsCRP levels and positively correlated with CuZn-SOD and eGFR levels. ADMA and PTX3 levels were independently related to FMD both before and after AAL, AIC and AOL therapies. Our study shows that serum ADMA, MDA, PTX3 levels are associated with endothelial dysfunction in patients with selected chronic diseases. In addition, short-term AAL, AIC and AOL therapies significantly improves a number of parameters in our cohort and can normalize ADMA, PTX3, hsCRP and MDA levels.

Serum lipid profile paraoxonase and arylesterase activities in psoriasis.

Psoriasis is a common chronic and recurrent inflammatory skin disease with unknown etiology that has been associated with abnormal plasma lipid metabolism and oxidative stress. There are controversial results in the previous studies investigating oxidant/antioxidant systems in psoriasis.The aim of this work was to evaluate dyslipidemia, oxidative stress, total antioxidant capacity and serum paraoxonase (PON1) and arylesterase (ARE) activities in psoriasis, and to look for a correlation between these parameters and lesion percentage in psoriasis.Thirty psoriatic patients and twenty three sex- and agematched healthy volunteers were included in the study. From blood samples, lipid profile, malondialdehyde (MDA) levels, total antioxidant capacity (TAO), serum PON1 and ARE activities were determined.No significant differences between the patients and controls were found in terms of total cholesterol, triacylglycerol (TAG), HDL-cholesterol, LDL-cholesterol, VLDL-cholesterol, MDA and TAO levels. Serum PON1 and sodium-stimulated PON1 activities (p < 0.05) and ARE activity (p < 0.01) were found significantly higher in the patients than in the controls. There was not any significant correlation between lesion percentage and the parameters studied.

Prognostic values of lesion volume and biochemical markers in ischemic and hemorrhagic stroke: a stereological and clinical study.

PURPOSE: Our aim was to evaluate the relationship between lesion volume, serum level of biochemical markers, and clinical situation in ischemic and hemorrhagic stroke. METHODS: MRI was obtained on 33 ischemic and 28 hemorrhagic strokes. The Cavalieri method was used to measure the volume. To evaluate neurological situation of the patients, we used the National Institutes of Health Stroke Scale (NIHSS) and Rankin Disability Scores at the first, third, seventh, and thirtieth days. We measured the level of leptin, high sensitivity C-reactive protein (hs-CRP), insulin, cortisol, fibrinogen, protein C, protein S, von Willebrand factor, D-dimer, Antitrombin III, and Factor VIII (F VIII) at the same time intervals. RESULTS: In ischemic events, cortisol level at third and seventh days, and fibrinogen level at the first day were correlated with lesion volumes (r = 0.5, p = .02; r = 0.4, p = .02; r = 0.5, p = .005, respectively). In hemorrhagic events, only fibrinogen level was correlated with lesion volumes at third day (r = 0.6, p = .04). No significant differences were found among all these biochemical parameters, neurological situation (p > .05), and lesion volumes at all times. CONCLUSION: In the prediction of stroke prognosis, lesion volume and all of the evaluated biochemical parameters are not deterministic factors.