The accuracy of non-contrast brain CT scan in predicting the presence of a vascular etiology in patients with primary intracranial hemorrhage.

Spontaneous intraparenchymal cerebral hemorrhages (SIPH) account for 10-15% of acute strokes. Sorting these patients according to the risk of harboring an underlying vascular etiology may help selecting the patients who would mostly benefit from Multidetector CT Angiography (MDCTA). The aim of this study was to evaluate the accuracy of Non-Contrast brain CT (NCCT) in predicting possible vascular etiologies in patients with SIPH. In this retrospective study, we evaluated the NCCT of 334 patients who presented with SIPH from March 2017 to March 2021 and we looked for vascular etiologies in the CTA which was performed for these patients. We used NCCT criteria to predict the presence of any vascular etiologies in SIPH patients and proposed a scoring system based on these criteria which might predict the risk of vascular ICH (VICH score). Out of 334 evaluated patients, 9.3% had an underlying vascular etiology. Independent predictors of the vascular etiology included: age < 46 years, no history of hypertension and coagulation disorders, lobar hemorrhages, and presence of significant perilesional edema. We used these criteria and NCCT classification to create a practical scoring system to predict the risk of vascular ICH (VICH). In our study, VICH score ≥ 4 had 51.6% sensitivity and 96.4% specificity for predicting a positive MDCTA as the maximum optimal cut-off point. The VICH score seemed to be successful in predicting vascular etiologies in this retrospective cohort of 334 patients. This scoring system can be used to select patients if there are limited resources to perform CT angiography.

The utility of early post-liver transplantation model for end-stage liver disease score in prediction of long-term mortality.

BACKGROUND: Little is known about the prognostic ability of post-liver transplantation (LT) model for end-stage liver disease (MELD) score measurement in assessing long-term outcomes. The aim of the present study was to investigate this possible relationship. METHODS: In this retrospective cohort study, the medical records of LT recipients operated under a LT program were reviewed. The accuracy of post-operation MELD score for predicting mortality was evaluated based on receiver operating characteristic (ROC) curves. Univariate and Cox proportional hazard regression models were used to assess the risk factors associated with mortality. RESULTS: Eight hundred twenty-six consecutive LT recipients were included in the study. The areas under the ROC curve on postoperative days (POD) 5 and 9 for predicting 1-year mortality were 0.712 (95% confidence interval [CI] 0.614-0.811) and 0.682 (95%CI 0.571-0.798), respectively. A cutoff point of 14.5 was obtained for MELD score on POD5 that significantly differentiated between survivors and non-survivors with a sensitivity of 69.8% (95%CI 50.7-83.1) and a specificity of 57.2% (95%CI 50.6-63.6). In the Cox multivariate analysis, factors including MELD score on POD5 (hazard ratio [HR] 1.83, 95%CI 1.07-3.12; P=0.026), pre-transplant MELD (HR 1.064, 95%CI 1.025-1.104; P=0.001) and operation duration (min) (HR 1.004, 95%CI 1.003-1.006; P=0.013) were identified as independent risk factors for predicting overall survival. CONCLUSION: The immediate postoperative MELD scores after LT may be of value in predicting mortality and could be used as a tool for postoperative risk assessment of patients.

Effect of berberine chloride on caspase-3 dependent apoptosis and antioxidant capacity in the hippocampus of the chronic cerebral hypoperfusion rat model.

OBJECTIVES: The main goal of the current research was to examine the effects of Berberine (BBR) on apoptotic signaling and hippocampal oxidative stress induced by common carotid artery occlusion. MATERIALS AND METHODS: Chronic cerebral hypoperfusion (CCH) model was created by occluding the two common carotid arteries (two-vessel occlusion [2VO]) permanently. BBR (50 and 100 mg/kg/daily) was intra-gastrically administered to ischemic rats. Neuronal survival was evaluated by Nissl staining. The levels of malondialdehyde (MDA) and antioxidant enzymes, including catalase (CAT) and superoxide dismutase (SOD), along with the activities of caspase 3 were estimated in the hippocampus 2 month after treating the rats with 2VO. RESULTS: According to findings of the present research, the BBR therapy inhibited the neuro-degeneration of hippocampus. BBR also significantly decreased the amount of MDA and activity of caspase 3 in the hippocampus. Furthermore, the administration of BBR alleviated the lowered activities of SOD and CAT after 2VO surgery. CONCLUSION: The antioxidant and antiapoptotic properties of BBR might play important roles in improving functional outcomes and might have significant neuroprotective effects on the CCH damage.

Antidiabetic potential of salvianolic acid B in multiple low-dose streptozotocin-induced diabetes.

CONTEXT: Salvianolic acids are the most abundant water-soluble compounds extracted from the herb Salvia miltiorrhiza L. (Lamiaceae) with antioxidant and protective effects. OBJECTIVE: This study evaluates the antidiabetic effect of salvianolic acid B (Sal B) in multiple low-dose streptozotocin (MLDS)-induced diabetes in rat. MATERIALS AND METHODS: Rats were divided into control, Sal B40-treated control, diabetic, Sal B20-, and Sal B40-treated diabetic groups. Sal B was daily administered at doses of 20 or 40 mg/kg (i.p.), started on third day post-STZ injection for 3 weeks. Serum glucose and insulin level and some oxidative stress markers in pancreas were measured in addition to the oral glucose tolerance test (OGTT), histological assessment, and apoptosis determination. RESULTS: After 3 weeks, treatment of diabetic rats with Sal B20 and Sal B40 caused a significant decrease of the serum glucose (p < 0.05-0.01) and improvement of OGTT. Meanwhile, serum insulin was significantly higher in Sal B20- and Sal B40-treated diabetics (p < 0.01) and treatment of diabetics with Sal B40 significantly lowered malondialdehyde (MDA) (p < 0.05), raised glutathione (GSH) (p < 0.05), and activity of catalase (p < 0.01) with no significant change of nitrite. Furthermore, the number of pancreatic islets (p < 0.05) and their area (p < 0.01) was significantly higher and apoptosis reactivity was significantly lower (p < 0.05) in the Sal B40-treated diabetic group versus diabetics. DISCUSSION AND CONCLUSION: Three-week treatment of diabetic rats with Sal B exhibited antidiabetic activity which is partly exerted via attenuation of oxidative stress and apoptosis and augmentation of antioxidant system.

Cognitive impairment induced by permanent bilateral common carotid occlusion exacerbates depression-related behavioral, biochemical, immunological and neuronal markers.

There is a strong link between cognitive impairment and depression, but up to date it is not clear whether cognitive impairment is 'cause' or 'consequence' of depression. Therefore, we here examined the effect of cognitive impairment induced by permanent occlusion of common carotid arteries, a model known as two-vessel occlusion (2VO), on chronic unpredictable stress (CUS)-induced depression-related markers in rats. Male Sprague-Dawley rats underwent 2VO or sham surgery. Sixty days after the surgery, the cognitive function of the rats was tested using the radial arm maze task measuring working and reference memory. Subsequently, the animals were randomly assigned to undergo 21 days of CUS or to stay non-stressed. One week after the last stressor, psychomotor retardation, a feature of depression-like behavior, was assessed using the forced swim test (FST) by measuring time spent on immobility. Plasma amino acid (glutamine, glutamate and glycine) and serum pro-inflammatory cytokine (interleukin 6) levels, and hippocampus CA1 neuronal damage were measured 24h after FST exposure. Results show that 2VO increased immobility in the FST only when rats had been exposed to CUS. In addition, 2VO surgery intensified the effect of CUS on IL-6, glutamate and glycine levels and increased CA1 hippocampal damage. In conclusion, our findings show that cognitive impairment may predispose to depression by intensifying the effect of stress on depression-related behavioral, biochemical, immunological and neuronal markers.

Iron administration prevents BDNF decrease and depressive-like behavior following chronic stress.

Pro-inflammatory cytokines play important roles in responses to stresses and affect iron metabolism. Iron is essential for survival of hippocampus neurons and plays a role in depression. Noting the close causal effect relation between stress and depression, in this experimental study we investigated the influence of iron on stress-induced depression. Rats were exposed to chronic mild stress and were treated with three different iron doses (9, 12, and 20mg/kg) three times a week for four weeks with an iron chelator in the first and third week. Serum interleukin-6 (enzyme-linked immune sorbent assay), hippocampus iron content (atomic absorption spectrometry), brain-derived neurotrophic factor (BDNF) gene expression (real-time polymerase chain reaction), CA1 pyramidal cell count (Nissl method) and a behavioral test (forced swimming test) were evaluated. In both the stressed and stressed plus iron groups, hippocampus cell counts were lower than in the control group (non-stressed). The use of deferiprone in the stressed groups markedly prevented neuronal loss. In stressed rats, the iron content of the hippocampus was higher than in the control group (P<0.001). Moreover, in the stressed group with moderate iron administration (12 mg/kg), there was a significant elevation of BDNF expression (P<0.05) and decreased immobility behavior time (P<0.05). These results indicate that high doses of iron in stressful situations augment neuronal degeneration and loss, possibly by iron accumulation. Deferiprone as an iron chelator could reverse this effect. During chronic mild stress, cerebrospinal fluid possibly reduces the iron content and may result in reduction of monoamines being involved in mood regulation. Iron administration in a moderate dose can increase these neurotransmitters and BDNF expression.