Suicidal risk and demoralization in Parkinson disease

Journal of Neurology - We aimed to determine suicide risk and lifetime suicidal ideation in Parkinson disease (PD) patients versus controls and how depression, demoralization, and insomnia are...     

Circulating adhesion molecules in sera of asthmatic children before and after steroid therapy.

The aim of this study was to evaluate respiratory function tests, total eosinophil counts, serum immune globulin E (IgE), and serum concentrations of soluble intercellular adhesion molecule (sICAM)1, soluble vascular cell adhesion molecule (sVCAM) 1, and soluble P-selectin (sP-selectin) levels in the children with mild and/or moderate asthma before and 3 months after inhaled steroids and to determine whether adhesion molecule levels showed any difference between asthmatic and healthy children and whether these levels changed with disease activity. A total of 28 children with bronchial asthma and 24 children as a control group were included in the study. All of the patients in the study group were administered inhaled budesonide treatment. The patients were reevaluated 3 months later. Respiratory functions tests were performed and total eosinophil count and serum total IgE level were determined. Serum levels of sICAM-1, sVCAM-1, and sP-selectin were determined and skin-prick tests were performed. Significant difference paralleled to clinical improvement was found in the study group for respiratory function tests, total eosinophil count, serum IgE level, and sICAM-1 levels determined before and after the treatment. However, no significant difference was found for sP-selectin and sVCAM-1 levels before and after the treatment. The higher level of sICAM-1 before the treatment suggests that leukocyte-endothelial adhesion have a role in bronchial asthma, which is an inflammatory airway disease. Reduction in the level of sICAM-1 after the treatment may be related to the decreased inflammation in response to therapy. However, no strong relationships were found between the determinants representing the inflammation and respiratory function tests.     

Evaluation of staining susceptibility of resin artificial teeth and stain removal efficacy of denture cleansers

Objective. To assess the staining susceptibility of four acrylic resin (Ivostar, SR Vivodent PE, Major Dent, Integral) and a nanocomposite resin (Veracia) artificial teeth and to evaluate the stain removal efficacy of denture cleansers. Materials and methods. Sixty maxillary incisors of each brand (total = 300) were divided into three groups according to staining solution as coffee, red wine and tea. Baseline color measurements were performed with a spectrophotometer. Specimens were immersed in staining solutions for 14 h (2 h × 7 days) and then second color measurements were performed. Each group was further divided into four sub-groups according to denture cleanser as Corega tabs, Fittydent, NaOCl (0.5%) and distilled water (control) (n = 5). Specimens were immersed in denture cleansers for 8 h and third color measurements were made. Thus, the weekly simulation period was completed. This cycle was repeated 12 times to simulate a 3-month time period and measurements were performed at the end of the 4th, 8th and 12th cycles. ΔE values were calculated and data were analyzed with 3-way repeated measures ANOVA and Bonferroni tests. Results. Significant color differences were found among the teeth and staining solutions, but all of the color differences were in the clinically acceptable range (ΔE < 5.5). Integral showed the highest ΔE values for all solutions, while Ivostar and Vivodent demonstrated the lowest ΔE values for red wine and tea solutions. There was no significant difference among the denture cleansers in terms of stain removal efficacy. Conclusions. Cross-linked acrylic (Integral) and nanocomposite (Veracia) resin teeth were more susceptible to staining. Denture cleansers were efficient on stain removal from artificial teeth.     

The effect of bolus methylprednisolone in prevention of brain edema in hypoxic ischemic brain injury: an experimental study in 7-day-old rat pups

One of the major mechanisms responsible for tissue injury in hypoxic ischemic brain damage is the formation of free radicals. We studied the efficacy of methylprednisolone, which is claimed to cause rapid congealing of membranes, and to protect the cells against the free radicals present in the environment, in preventing the brain edema that occurs in hypoxic ischemic brain injury. Hypoxic ischemic brain injury to the right hemisphere in 7-day-old rat pups is produced by cauterization of the right common carotid artery followed by hypoxia in 8% oxygen and 92% nitrogen for 3 h. The animals were divided into the groups. One group received methylprednisolone at 30 mg/kg body weight and the other an equal volume of saline 40 min before hypoxia. At 42 h of recovery, some of the rats were killed for measurement of water content in the right and left hemispheres whereas others were killed at 40 days for neuropathological examination. The water content in the right hemisphere was significantly lower in the 19 methylprednisolone-treated pups than it was in 20 saline-treated pups, mean +/- S.E.M. was 83.913 +/- 0.313% and 86.681 +/- 0.377%, respectively. The differences between the means were significant (P less than 0.001) according to the Mann-Whitney U-test. The difference of the mean water contents between the two hemispheres was significantly higher in the saline-treated group (2.695 +/- 0.372%) than it was in the methylprednisolone-treated group (0.432 +/- 0.088%), P less than 0.0001 by independent samples t-test. Neuropathological study was performed on 4 rat pups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum endostatin levels and regenerative capacities of normal and cirrhotic livers following partial hepatectomy in mice: the response to different resection sizes

BACKGROUND: Angiogenesis has an important role in liver regeneration. Antiangiogenic response in remnant liver following resection and its relationship to regeneration is not well known. The aim of this study was to investigate the effect of hepatectomy size on serum endostatin levels, and the effect of endostatin levels to liver regeneration after partial hepatectomy in normal and cirrhotic mice. MATERIALS AND METHODS: Sixty noncirrhotic and 36 carbon tetrachloride-induced cirrhotic mice were included in the study. Noncirrhotic mice were randomly divided into four main groups: sham, 20%, 40%, and 70% hepatectomy groups. Similarly, cirrhotic mice were randomly divided into three main groups: sham, 20%, and 40% hepatectomy groups. The mice in each group were further divided into two subgroups to compare serum endostatin levels and liver regeneration indexes on days 1 and 14. Liver regeneration was evaluated by the proliferating cell nuclear antigen-labeling index. Serum endostatin level was measured to evaluate antiangiogenic response. RESULTS: Serum endostatin levels on the first day and 14th day increased significantly in correlation with the hepatectomy size, both in normal mice and cirrhotic mice (P < 0.05). In normal mice with high regeneration indexes that underwent 40% and 70% hepatectomies, there was a significant increase in serum endostatin levels on the 14th day compared with the first day (P < 0.05). However, the increase in mice that underwent 20% hepatectomies was not significant. After 20% and 40% hepatectomies, first day serum endostatin levels were significantly higher in cirrhotic mice compared with normal mice (P < 0.05), which was independent of regeneration. Nevertheless, after 40% hepatectomies, 14th day serum endostatin levels were significantly lower in cirrhotic mice compared with normal mice, attributable to the limited regeneration capacity of cirrhotic liver (P < 0.05). Regeneration capacity of cirrhotic liver was low at all times. CONCLUSIONS: The current study suggests that there is a significant relationship between serum endostatin levels and regeneration capacity after hepatectomy in normal mice. On the other hand, following resection of cirrhotic liver, regeneration capacity is depressed and high endostatin levels are independent of hepatic regeneration.     

The effect of the nitric oxide synthesis inhibitor L-NAME on amitriptyline-induced hypotension in rats

OBJECTIVE: Hypotension induced by tricyclic antidepressants is multifactorial. Previous animal experiments suggest a contribution from nitric oxide production. Our study aimed to evaluate the role of nitric oxide in amitriptyline-induced hypotension using N-nitro-L-arginine methyl ester, a nitric oxide synthesis inhibitor, and 3-morpholino sydnonimine, a nitric oxide donor, in anesthetized rats. METHODS: Amitriptyline intoxication was induced by the continuous infusion of amitriptyline 0.625 mg/kg/min throughout the experiment in anesthetized rats. Fifteen and 25 minutes after amitriptyline infusion began, two bolus doses of 10 mg/kg of N-nitro-L-arginine methyl ester (n = 8) or an equivalent volume of 5% dextrose solution (n = 8) was administered to each rat (Protocol 1). To investigate whether the effect of N-nitro-L-arginine methyl ester on blood pressure is counteracted by 3-morpholino sydnonimine, after the same protocol of amitriptyline infusion and 5 minutes after an N-nitro-L-arginine methyl ester bolus, a bolus of 3000 nmol/kg of 3-morpholino sydnonimine was administered (n = 8) to each rat (Protocol 2). To investigate the effect of N-nitro-L-arginine methyl ester on 3-morpholino sydnonimine induced hypotension, a group of rats received a continuous infusion of 0.54 mg/kg/h of 3-morpholino sydnonimine until 50% reduction was observed in mean arterial blood pressure followed by a bolus dose of 10 mg/kg of N-nitro-L-arginine methyl ester (n = 6) or 5% dextrose solution (n = 6) (Protocol 3). Outcome measures included mean arterial blood pressure, heart rate, and QRS duration in electrocardiogram. Student's t test and survival analysis were used for selected comparisons. RESULTS: For all parameters, the treatment groups were similar at baseline and at postamitriptyline periods before therapy was rendered. Amitriptyline infusion significantly reduced mean arterial blood pressure by 50.8 +/- 2.2% and prolonged QRS by 23.9 +/- 7.2% after 15 minutes. In Protocol 1, N-nitro-L-arginine methyl ester significantly increased mean arterial blood pressure compared to dextrose-treated control animals within 30 minutes (77.9 +/- 8.5% vs. 49.7 +/- 5.0% mmHg, p < 0.01, 95% CI 57.1-98.7%). QRS duration progressively increased during the amitriptyline infusion; however, there was no significant difference in QRS width between N-nitro-L-arginine methyl ester and control groups at any time point. N-nitro-L-arginine methyl ester increased survival time compared to controls (33.4 +/- 4.1 vs. 19.9 +/- 2.7 minutes, p < 0.01, 95% CI 25.4-41.3) but did not affect mortality. In Protocol 2 of continuous infusion of amitriptyline, 3-morpholino sydnonimine counteracted the N-nitro-L-arginine methyl ester-induced increase in mean arterial blood pressure. In both protocols, heart rate decreased significantly during amitriptyline infusion but there was no difference between treatment and control groups. In Protocol 3, N-nitro-L-arginine methyl ester bolus reversed 3-morpholino sydnonimine-induced hypotension compared to dextrose bolus. (83.8 +/- 5.7% vs. 54.6 +/- 4.8%, p < 0.01, 95% CI 69.2-98.4). CONCLUSION: N-nitro-L-arginine methyl ester is found to be effective in temporarily improving hypotension and prolonging survival time but does not affect overall mortality. Because this effect was antagonized by 3-morpholino sydnonimine, nitric oxide production appears to contribute to the pathophysiology of amitriptyline-induced hypotension.