Protective effects of curcumin against gamma radiation-induced ileal mucosal damage

The major objective of this study was to test curcumin as a potential radioprotectant for the ileum goblet cells of the rat. Wistar albino rats were used in the study. Group A was the control group and group B was the single dose radiation group. Group C was the two dose radiation group (4 days interval). The rats in groups D and E were given a daily dose of 100 mg/kg of curcumin for 14 and 18 days, respectively. During the curcumin administration period, the rats in group D were exposed to abdominal area gamma (γ)-ray dose of 5 Gy on the 10th day and group E was exposed to same dose radiation on the 10th and 14th day. Irradiation and treatment groups were decapitated on the 4th day after exposure to single or two-dose irradiation and ileum tissues were removed for light and electron microscopic investigation. Single or two dose 5 Gy γ-irradiation caused a marked intestinal mucosal injury in rats on the 4th day. Radiation produced increases in the number of goblet cells. Curcumin appears to have protective effects against radiation-induced damage, suggesting that clinical transfer is feasible.     

Nicotine withdrawal alleviates acetic acid-induced gastric injury in rats

Epidemiological and experimental studies have demonstrated that cigarette smoking intensifies gastric ulceration. Although nicotine can act as an anxiolytic and antidepressant, its withdrawal may also lead to increased anxiety and depression. In order to associate the toxic actions of nicotine on gastric mucosa with alterations of anxiety level and to evaluate the impact of nicotine withdrawal on the anxiety level and the severity of ulcer, an acetic acid-induced ulcer model was used. Male Sprague-Dawley rats were given either tap water or nicotine bitartarate (50μg/ml in drinking water) for 15 days, while another group of rats had 5 days of withdrawal following 10 days of nicotine treatment. Ulcer was induced by acetic acid on the 15th day of the treatments, and the rats were followed for 3 days until they were decapitated and the gastric tissues were obtained. Using the hole-board test, basal anxiety levels measured on the first day of the treatments were compared with the measurements made at the early and late phases of ulcer induction. Chronic administration of nicotine did not have a potentiating effect on acetic acid-induced gastric ulcer, since the gastric injury, as assessed by both macroscopic and microscopic evaluation and increased gastric myeloperoxidase activity indicating neutrophil recruitment, was not exaggerated or attenuated by nicotine intake. On the other hand, nicotine withdrawal attenuated gastric mucosal injury, despite an increased level of anxiety. Smoking cessation, which triggers the onset of depressive symptoms with nicotine withdrawal, still has a worthwhile positive effect on the gastric mucosa.     

Evaluation of GLUT1, IGF-2, VEGF,FGF 1, and angiopoietin 2 in infantile hemangioma

IntroductionInfantile hemangioma (IH) is a common vascular tumor in children. It is reported that IHs are associated with immunochemical markers such as vascular endothelial growth factor (VEGF)-A, glucose transporter isoform 1 (GLUT1), and insulin-like growth factor-2 (IGF-2).Material and methodsThis cross-sectional study focused on pediatric patients with IH. A total of 46 patients (mean age 14.2 ± 21.9 months) with IH and 45 healthy controls (mean age 21.8 ± 15.08 months) were enrolled. Demographic data, clinical findings, and laboratory parameters were recorded. Blood samples were collected. Serum GLUT1, IGF-2, VEGF-A, fibroblast growth factor 1 (FGF1), and angiopoietin 2 levels were assessed by enzyme-linked immunosorbent assay.ResultsSerum GLUT1, IGF-2, and VEGF-A levels were significantly higher in patients with IH than in healthy controls (8.80 ± 4.07 pg/mL vs. 5.66 ± 4.34 pg/mL, 281.10 ± 84.12 pg/mL vs. 234.19 ± 75.38 pg/mL, 1196.99 ± 389.34 pg/mL vs. 996.99 ± 349.16 pg/mL, respectively, p = 0.026, p = 0.030, and p = 0.036). Serum GLUT1, IGF-2, and VEGF-A levels in patients with complicated hemangioma were significantly higher than in healthy controls (9.69 ± 3.94 pg/mL vs. 5.66 ± 4.34 pg/mL, 289.94 ± 83.18 pg/mL vs. 234.19 ± 75.38 pg/mL, 1276.22 ± 388.24 pg/mL vs. 996.99 ± 349.16 pg/mL, respectively, p = 0.017, p = 0.022, and p = 0.011). Serum GLUT1, IGF-2, and VEGF-A levels in patients with hemangioma receiving propranolol treatment were significantly higher than in healthy controls. Serum FGF1 levels were higher in patients with IH, complicated hemangioma, and hemangioma receiving propranolol treatment than in healthy controls but the difference was not statistically significantly.ConclusionSerum GLUT1, IGF-2, and VEGF-A levels were positively correlated with disease severity in patients with hemangioma, for example, in complicated hemangioma and hemangioma requiring propranolol treatment. However, further research on larger and different age subgroups is warranted to assess these markers.     

Chronic subdural hematoma after endoscopic third ventriculostomy: a case report and literature review

Chronic subdural hematoma is a very rarely observed complication after endoscopic third ventriculostomy (ETV). A 21-year-old male patient was admitted to our clinic with complaining of headache, weakness and tremor. The fundoscopic examination revealed slightly indistinct border of the papilla and neurological examination findings were normal. The cranial computed tomographic (CT) and magnetic resonance imaging (MRI) findings demonstrated three-ventricular hydrocephalus due to aqueductal stenosis and ETV was performed. The symptoms got better after the operation. At 1? month postoperatively the patient reapplied to our clinic with a symptom of severe headache. Cranial BT imaging demonstrated enlargement of subdural hematoma. The hematoma was treated by burr-hole evacuation and drainage and totally disappeared in the postoperative period. The follow-up CT scan was evaluated as normal. Nowadays, ETV is accepted as a safe and an alternative method for the treatment of obstructive hydrocephalus instead of shunt operation. Chronic subdural hematoma is a rarely observed complication after ETV.     

Increased plasma levels of cystatin C and transforming growth factor-beta1 in patients with coronary artery ectasia: can there be a potential interaction between cystatin C and transforming growth factor-beta1

Cystatin C, known as an inhibitor of the cathepsin family of cysteine proteases, has been evaluated in several cardiovascular disorders such as atherosclerosis and acute myocardial infarction. The potential interaction between transforming growth factor-beta1 and cystatin C has also been demonstrated in some cell types. Accordingly, we aimed to compare the plasma levels of cystatin C and transforming growth factor-beta1 in patients with coronary artery ectasia coexisting with coronary artery disease and those with coronary artery disease alone. Thirty-nine patients with coronary artery ectasia and coronary artery disease and 35 age and sex-matched patients with coronary artery disease alone were prospectively enrolled in the study. Blood samples of all patients and control participants for measuring plasma cystatin C and transforming growth factor-beta1 levels were drawn>or=24 h after the coronary angiography. Cystatin C concentrations in plasma were measured by latex-enhanced reagent on a Behring Nephelometer II. Plasma levels of transforming growth factor-beta1 were measured by using transforming growth factor-beta1 enzyme-linked immunosorbent assay kit (BioSource International, Inc., Camarillo, California, USA). Plasma level of cystatin C was significantly higher in patients with coronary artery ectasia+coronary artery disease than in patients with coronary artery disease alone (1.05+/-0.30 mg/dl vs. 0.92+/-0.18 mg/mdl, P=0.025, respectively). Transforming growth factor-beta1 was also found to be significantly higher in patients with coronary artery ectasia+coronary artery disease compared with those with coronary artery disease (2.47+/-0.43 vs. 2.22+/-0.43 pg/ml, P=0.02, respectively). The plasma level of cystatin C was significantly but weakly correlated with that of transforming growth factor-beta1 (r=0.217 P=0.02). We conclude that plasma levels of cystatin C and transforming growth factor-beta1 are significantly higher in patients with combined coronary artery ectasia and coronary artery disease than in those with coronary artery disease. Correlation between transforming growth factor-beta1 and cystatin C may also suggest that pathogenesis of coronary artery ectasia might have some different pathways from atherosclerosis with respect to the regulation of extracellular matrix remodeling. Therefore, the role of cystatin in the pathogenesis of coronary artery ectasia and its potential interaction with transforming growth factor-beta1 should be evaluated in further studies.     

Neuropsychiatric symptoms in patients with Parkinson's disease and dementia: frequency, profile and associated care giver stress

Objective

To explore the profile of neuropsychiatric symptoms in patients with dementia associated with Parkinson''s disease (PDD).

Methods

537 patients with PDD drawn from an international multicentre clinical trial of rivastigmine were assessed using the 10‐item Neuropsychiatric Inventory (NPI). A cluster analysis was used to investigate the inter‐relationship of NPI items. Associations between the clusters and demographic and clinical variables were analysed.

Results

89% of the patients presented at least one symptom on the NPI, 77% had two or more symptoms and 64% had at least one symptom with a score ⩾4. The most common symptoms were depression (58%), apathy (54%), anxiety (49%) and hallucinations (44%). Patients with more severe dementia and advanced Parkinson''s disease had more neuropsychiatric symptoms. Nearly 60% of the care givers reported at least one NPI symptom to be of at least moderate severe distress. Five NPI clusters were identified: one group with few and mild symptoms (52%); a mood cluster (11%, high scores on depression, anxiety and apathy); apathy (24%; high apathy and low scores on other items); agitation (5%, high score on agitation and high total NPI score); and a psychosis cluster (8%; high scores on delusions and hallucinations). The psychosis and agitation clusters had the lowest Mini‐Mental State Examination score and the highest Unified Parkinson''s Disease Rating Scale and care giver distress scores.

Conclusion

Neuropsychiatric symptoms are common in patients with PDD. The profile of these symptoms differs from that in other types of dementia. Subgroups with different neuropsychiatric profiles were identified. These subgroups may be associated with distinct neurobiological changes, which should be explored in future studies.A wide range of neuropsychiatric disturbances commonly occurs in patients with Parkinson''s disease.^1,2 Neuropsychiatric disturbances contribute considerably to reduced quality of life,³ distress for the care giver⁴ and increased risk for admission to nursing home^5,6 in patients with Parkinson''s disease. Most patients with Parkinson''s disease will eventually develop dementia,⁷ and neuropsychiatric symptoms are more common in those with Parkinson''s disease with dementia (PDD).^1,8 Knowledge of the wide variety of psychiatric symptoms and diagnostic skills to identify and implement optimal treatment of these symptoms are thus of major importance in the management of patients with Parkinson''s disease and those with PDD.The multiple psychiatric symptoms in patients with dementia tend to cluster into discrete psychiatric syndromes,^9,10 indicating that the underlying pathophysiological constructs may explain the relationship between observed variables. Identifying these underlying constructs is important, as it may prove to be more valuable to correlate neurochemical measures with syndromes rather than with individual symptoms. Also, from the clinical point of view, treatment might be best directed towards syndromes rather than towards each specific, individual behavioural symptom. Finally, there is emerging evidence of subtypes within the major neurodegenerative disorders, including Parkinson''s disease,¹¹ and exploring psychiatric syndromes may help in distinguishing such subtypes.Statistical methods such as factor analysis, cluster analysis and latent class analysis have been used to identify empirically based classifications of neuropsychiatric clusters in patients with neurodegenerative disorders, with high face validity.^9,10,12 These empirically based classifications could enhance our understanding of the heterogeneity of patients with dementia, and lead to clearer treatment strategies for different subgroups. Although factor analysis can provide information on how symptoms correlate in a sample, it is of limited value in understanding how the symptoms occur in groups of patients, and is thus of limited value in identifying groups of patients on the basis of symptoms. Rather, classification of individual patients is possible using cluster analysis, a data‐driven, exploratory classification method.¹³Five different clusters of neuropsychiatric symptoms were recently identified in patients with Parkinson''s disease.¹² However, to the best of our knowledge, no studies have explored how neuropsychiatric symptoms cluster in patients with PDD. Therefore, to explore whether natural subgroups of patients with Parkinson''s disease can be identified on the basis of their neuropsychiatric profile, we administered the Neuropsychiatric Inventory (NPI) to a large sample of patients with PDD, and used cluster analysis to identify the inter‐relationship of neuropsychiatric symptoms. The analysis is based on the baseline data obtained in a large phase III clinical trial evaluating the safety and efficacy of rivastigmine in PDD.¹⁴     

Liver Fibrosis Is Associated with Decreased Peripheral Platelet Count in Patients with Chronic Hepatitis B and C

Thrombocytopenia is a common complication of chronic liver diseases, but its pathogenesis is not clear. Although generally attributed to hypersplenism, other factors should also be considered. We investigated the relationship between the peripheral platelet count and the degree of fibrosis in patients with chronic viral hepatitis. In an effort to avoid the effects of hypersplenism, we excluded patients with splenomegaly and/or bi- or pan-cytopenia. Seven hundred eighty-four patients (265 chronic viral hepatitis C and 519 chronic viral hepatitis B) were included in the study. Univariate analysis showed that the peripheral platelet count had a negative correlation with fibrosis score, necroinflammatory activity, and age in both groups. In multivariate analysis, the peripheral platelet count had a similar correlation with the fibrosis score and age, but not with necroinflammatory activity, in both groups. The peripheral platelet count decreased more significantly in females with chronic hepatitis C but not in the chronic hepatitis B group. In conclusion, a decrease in peripheral platelet count may be a sign of an increase in the degree of fibrosis during the course of chronic viral hepatitis B and C and factors other than hypersplenism may play a role in this decrease in the peripheral platelet count.