Search

Cognitive impairment is a common complication observed after a stroke. Currently there are no definitively proven pharmacologic therapies for recovery from post-stroke cognitive impairment and vascular dementia. In this meta-analysis, we evaluated the efficacy and safety of cholinesterase inhibitors in their improvement of cognition in patients with post-stroke cognitive impairment and vascular dementia. We conducted a meta-analysis using seven eligible studies from 305 published articles. We investigated the differences in Mini-Mental State Examination (MMSE) and Alzheimer's Disease Assessment Scale-Cognitive subscale (ADAS-Cog) scores, before and after cholinergic augmentation in patients with post-stroke cognitive impairment and vascular dementia. MMSE and ADAS-cog scores were also compared during the subsequent follow-up periods. MMSE score of patients with post-stroke cognitive impairment was increased after cholinergic augmentation throughout the 24 weeks with mean differences [MD] of 3.000, 1.732, 1.578 1.516, and 1.222, at 4, 4-8, 8-12, 12-18, and 18-24 weeks, respectively. In addition, ADAS-cog scores decreased at 6, 12, 18, and 24 weeks by pharmaceutical augmentation, but not with placebo with mean differences [MD] of -2.333, -2.913, -2.767, -2.416, and -1.859, respectively. This meta-analysis shows that acetylcholinesterase inhibitors maintain a stable pattern of improved cognitive function in patients with post stroke cognitive impairment and vascular dementia without the increased risk of side effects.

Tumor lysis syndrome is rare in hepatocellular carcinoma (HCC), but it has been reported more frequently recently in response to treatments such as transcatheter arterial chemoembolization (TACE), radiofrequency thermal ablation (RFTA), and sorafenib. Tumor lysis syndrome induced by low-dose steroid appears to be very unusual in HCC. We report a patient with hepatitis-C-related liver cirrhosis and HCC in whom tumor lysis syndrome occurred due to low-dose steroid (10 mg of prednisolone). The patient was a 90-year-old male who presented at the emergency room of our hospital with general weakness and poor oral intake. He had started to take prednisolone to treat adrenal insufficiency 2 days previously. Laboratory results revealed hyperuricemia, hyperphosphatemia, and increased creatinine. These abnormalities fulfilled the criteria in the Cairo-Bishop definition of tumor lysis syndrome. Although the patient received adequate hydration, severe metabolic acidosis and acute kidney injury progressed unabated. He finally developed multiple organ failure, and died 3 days after admission. This was a case of tumor lysis syndrome caused by administration of low-dose steroid in a patient with HCC.

Many patients with diabetes are at increased risk of cognitive dysfunction and dementia. Diabetes mellitus is a vascular risk factor that may increase the risk of dementia through its associations with vascular dementia. We tested whether cognitive impairment could be exacerbated in combined injury using a rat model of chronic cerebral hypoperfusion with diabetes. We also determined whether a potent inhibitor of type III phosphodiesterase could prevent the cognitive decline caused by this combined injury.We used Otsuka Long–Evans Tokushima Fatty (OLETF) rats as a model of type II diabetes (T2DM) and Long–Evans Tokushima Otsuka (LETO) rats as a control. Chronic cerebral hypoperfusion was modeled by permanent bilateral common carotid artery occlusion (BCCAO). At 24 weeks, the non-diabetic and T2DM rats were randomly assigned into groups for the following experiments: analysis I (1) sham non-diabetic rats (n = 8); (2) hypoperfused non-diabetic rats (n = 9); (3) sham T2DM rats (n = 8); (4) hypoperfused T2DM rats (n = 9); analysis II- (1) sham T2DM rats without treatment (n = 8); (2) cilostazol-treated T2DM rats (n = 8); (3) hypoperfused T2DM rats (n = 9); and (4) hypoperfused T2DM rats and cilostazol treatment (n = 9). The rats were orally administered cilostazol (50 mg/kg) or vehicle once a day for 2 weeks after 24 weeks. Rats performed Morris water maze tasks, and neuronal cell death and neuroinflammation were investigated via Western blots and histological investigation.Spatial memory impairment was exacerbated synergistically in the hypoperfused T2DM group compared with the hypoperfused non-diabetic group and sham T2DBM group (P

Background/AimsBecause of the similarities in the clinical presentations of Crohn's disease (CD) and intestinal tuberculosis (ITB), differential diagnosis is critical. Mesenteric adipose tissue hypertrophy and creeping fat are characteristic features of CD. The purpose of this study was to assess the usefulness of visceral fat for the differential diagnosis of CD and ITB.MethodsWe conducted a retrospective review of 50 patients with findings of CD or ITB between January 2005 and July 2008. Abdominal computed tomography (CT) was performed on all subjects during their first evaluation. The abdominal fat area was assessed using quantitative abdominal CT.ResultsThe ratio of visceral fat to total fat (VF/TF) was significantly higher in male CD patients than in male ITB patients. The ratio of visceral fat to subcutaneous fat (VF/SF) was also higher in CD patients than in patients with ITB. For a VF/TF cut-off value of 0.46, the sensitivity and specificity for the diagnosis of CD were 42.1% and 93.3% respectively, with positive and negative predictive values of 88.9% and 56.0%, respectively.ConclusionMeasurement of the abdominal fat area using CT can be clinically useful for the differential diagnosis of CD and ITB.

Sedum middendorffianum Maxim (SMM) is a Korean endemic plant belonging to the Crassulaceae family. This study aimed to investigate the antitumor effects of the SMM extract on human ovarian cancer cells. Among five endemic plants grown in Korea, the SMM extract showed the most potent cytotoxicity in ovarian cancer cells and had little effect on normal ovarian surface epithelial cells. Furthermore, we revealed that the SMM extract dose-dependently induced apoptosis in human ovarian cancer A2780 and SKOV3 cells. The SMM extract markedly stimulated the activation of caspase-3/8, while the broad-spectrum caspase inhibitor and caspase-8 selective inhibitor significantly reversed SMM extract-induced apoptosis. In addition, the SMM extract significantly inhibited cell invasion and the expression levels of matrix metalloproteinase (MMP)-2 and MMP-9 in ovarian cancer cells. Notably, the SMM extract increased the generation of intracellular ROS, and pretreatment with antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed SMM-induced cytotoxicity and anti-invasive activity. Moreover, NAC treatment reversed the SMM-induced inhibition of MMP-2/9 expression. Taken together, these data suggest that the SMM extract induces caspase-dependent apoptotic cell death and inhibits MMP-dependent invasion via ROS regulation.

Skin photoaging, characterized by collagen degradation and upregulation of matrix metalloproteinases (MMPs), is a major concern caused by UVB irradiation. In this study, we investigated the potential of Acanthopanax sessiliforum extract (ASE) and Chaenomeles sinensis (CSE) extracts to mitigate the efects of UVB-induced photodamage in human fbroblast and hairless mice. Water extracts of AS (ASE) and CS (CSE) were found to inhibit the expression of MMP-1/-3 in vitro. Furthermore, the extract of mixture of AS and CS (ACE) showed more potent inhibitor efect, as compared to ASE and CSE. In UVB-irradiated hairless mice, oral administration of ACE efectively reduced wrinkle formation, skin roughness, and epidermal thickness while promoting the deposition of collagenous fbers. These results indicate that ACE has the potential to protect against skin photoaging by restoring the impaired skin via downregulation of MMP-1/-3 expression and secretion. Our fndings highlight the therapeutic potential of ACE in mitigating skin photoaging. [ABSTRACT FROM AUTHOR]