Background and Purpose : Many cases of amnesia caused by thalamic hemorrhage involve anterior nucleus hemorrhage, dorsomedial nucleus hemorrhage, and intraventricular rupture. In the present study, intraventricular rupture was studied with a focus on cases with hematoma compression at the fornix. Methods : Of 116 patients with thalamic hemorrhage admitted to our hospital, 50 patients aged <70 years who had hemorrhage during their first stroke confined to the thalamus, internal capsule, and corona radiata, and who neither developed hydrocephalus nor showed dementia prior to onset were investigated. Thalamic hemorrhages were classified by CT findings and the extent of intraventricular rupture. Memory was studied by the FIM memory scores on admission and discharge. Results and Conclusion : Patients with dorsomedial nucleus hemorrhage showed no tendency toward amnesia and were equivalent to patients with posterolateral nucleus hemorrhage, which does not usually result in amnesia on its own. Of the 30 patients with posterolateral nucleus hemorrhage, a high degree of amnesia was observed in the 18 with intraventricular rupture. A high proportion of patients with dorsomedial nucleus hemorrhage experienced intraventricular rupture (5 of 6 patients). Equivalent degrees of amnesia were observed in patients with intraventricular rupture with dorsomedial nucleus hemorrhage and those with posterolateral nucleus hemorrhage. The present findings in conjunction with the fact that amnesia in thalamic hemorrhage involves episodic memory impairment suggest that amnesia in patients with dorsomedial or posterolateral nucleus hemorrhage or with intraventricular rupture does not stem from damage to the dorsomedial nucleus, which is part of the Yakovlev circuit involved in emotional memory. Instead, the primary cause appears to be the effects of intraventricular rupture on the Papez circuit surrounding the lateral ventricle and foramen of Monro.

BACKGROUND AND OBJECTIVES: Reactive oxygen species (ROS) mediate various signaling pathways that underlie vascular inflammation in atherogenesis and cardiovascular diseases. Cardiac rehabilitation (CR) has a variety of multiple beneficial effects, including anti-inflammatory effects. The purpose of the present study was to investigate the effects of CR on ROS in patients with cardiovascular diseases. SUBJECTS AND METHODS: The serum level of derivatives of reactive oxidative metabolites, an index of oxidative stress, was measured in 100 patients with cardiovascular diseases before, and, subsequently, 3 and 6 months after, CR. A biological antioxidant potential (BAP) test was applied to assess the antioxidant power of the serum. RESULTS: The resting reactive oxidative metabolite levels decreased 3-6 months after CR {pre: 351+/-97 Carratelli unit (CARR U), 3 months: 329+/-77 CARR U, 6 months: 325+/-63 CARR U, all p<0.01} with the increase of the percentage of the predicted values of VO2 peak and the percentage of the predicted values of VO2 at the anaerobic threshold (VO2 AT) and the decrease of the B-type natriuretic peptide (BNP). The BAP test and antioxidative/oxidative stress ratio increased 6 months after CR. The % changes of the antioxidative/oxidative stress ratio was positively correlated with the % changes of VO2 AT, and negatively correlated with the % changes of the BNP. CONCLUSION: These results suggest that intensive supervised CR significantly improved exercise capacity, which may be attributable to an adaptive response involving more efficient oxidative metabolites or the increased capacity of endogenous anti-oxidative systems in patients with cardiovascular diseases.
Anaerobic Threshold ; Antioxidants ; Atherosclerosis ; Cardiovascular Diseases ; Exercise Therapy ; Humans ; Inflammation ; Natriuretic Peptide, Brain ; Oxidative Stress ; Oxygen Consumption ; Reactive Oxygen Species

Background/Aims: 5-Aminosalicylic acid (ASA) causes intolerance reactions in some patients. This study was performed to examine the prognosis of patients with ulcerative colitis (UC) and 5-ASA intolerance, and to evaluate the potential interaction between 5-ASA intolerance and the intestinal microbiota. Methods: We performed a retrospective cohort study of patients with UC who visited participating hospitals. The primary endpoint was to compare the incidence of hospitalization within 12 months between the 5-ASA intolerance group and the 5-ASA tolerance group. The secondary endpoint was to compare the risk of adverse clinical outcomes after the start of biologics between the 2 groups. We also assessed the correlation between 5-ASA intolerance and microbial change in an independently recruited cohort of patients with UC. Results: Of 793 patients, 59 (7.4%) were assigned to the 5-ASA intolerance group and 734 (92.5%) were assigned to the 5-ASA tolerance group. The admission rate and incidence of corticosteroid use were significantly higher in the intolerance than tolerance group (P< 0.001). In 108 patients undergoing treatment with anti-tumor necrosis factor biologics, 5-ASA intolerance increased the incidence of additional induction therapy after starting biologics (P< 0.001). The 5-ASA intolerance group had a greater abundance of bacteria in the genera Faecalibacterium, Streptococcus, and Clostridium than the 5-ASA tolerance group (P< 0.05). Conclusions In patients with UC, 5-ASA intolerance is associated with a risk of adverse clinical outcomes and dysbiosis. Bacterial therapeutic optimization of 5-ASA administration may be important for improving the prognosis of patients with UC.