Two cases of retroperitoneal hematoma caused by combination of anticoagulant therapy and 5-fluorouracil

We reported two cases of retroperitoneal hematoma in patients who received a combination of anticoagulant therapy and5-fluorouracil (5-FU). We should be aware of the possible interaction of this combination therapy and monitor prothrombin time (PT) prolongation. CT is useful for evaluation of the disease

Influences of Technological Parameters on Cross-Flow Nanofiltration of Cranberry Juice

The paper focused on the influence of operative conditions on the separation of benzoic acid from 10 °Brix cranberry juice by cross-flow nanofiltration with a plate and frame pilot scale (DDS Lab Module Type 20 system). Six kinds of commercial nanofiltration membrane were investigated. The results showed that the rejection of benzoic acid was significantly lower than that of other components in cranberry juice, including sugars and other organic acids. In a range of 2–7.5 L/min, feed flow rate slightly affected the performance of nanofiltration. Higher temperatures resulted in higher permeate flux and lower rejection of benzoic acid, whereas rejection of sugar and organic acid was stable at a high value. In a range of 2.5–5.5, pH also significantly affected the separation of benzoic acid and negative rejection against benzoic acid was observed at pH 4.5 with some of the membranes. This implies that pH 4.5 is considered as an optimum pH for benzoic acid separation from cranberry juice. The lower permeate flux caused a lower rejection of benzoic acid and negative rejection of benzoic acid was observed at the low permeate flux. Pretreatment by ultrafiltration with CR61PP membranes could improve the permeate flux but insignificantly influenced the efficiency of separation. The results also indicated that NF99 and DK membranes can be effectively used to separate benzoic acid from cranberry juice

Corticosteroids Mediate Heart Failure-Induced Depression through Reduced σ1-Receptor Expression

<div><p>Cardiovascular diseases are risk factors for depression in humans. We recently proposed that σ₁ receptor (σ₁R) stimulation rescued cardiac hypertrophy and heart failure induced by transverse aortic constriction (TAC) in mice. Importantly, σ₁R stimulation reportedly ameliorates depression-like behaviors in rodents. Thus, we hypothesized that impaired σ₁R activity in brain triggers depression-like behaviors in animals with cardiovascular disease. Indeed, here we found that cardiac hypertrophy and heart failure induced by TAC were associated with depression-like behaviors concomitant with downregulation of σ₁R expression in brain 6 weeks after surgery. σ₁R levels significantly decreased in astrocytes in both the hippocampal CA1 region and dentate gyrus. Oral administration of the specific σ₁R agonist SA4503 (0.3–1.0mg/kg) significantly improved TAC-induced depression-like behaviors concomitant with rescued astrocytic σ₁R expression in CA1 and the dentate gyrus. Plasma corticosterone levels significantly increased 6 weeks after TAC, and chronic treatment of mice with corticosterone for 3 weeks elicited depression-like behaviors concomitant with reduced astrocytic σ₁R expression in hippocampus. Furthermore, the glucocorticoid receptor antagonist mifepristone antagonized depressive-like behaviors and ameliorated decreased hippocampal σ₁R expression in TAC mice. We conclude that elevated corticosterone levels trigger hippocampal σ₁R downregulation and that σ₁R stimulation with SA4503 is an attractive therapy to improve not only cardiac dysfunction but depression-like behaviors associated with heart failure.</p></div

Schematic representation of the hypothesis tested and results obtained.

<p>Shown is a model depicting mechanisms underlying TAC-induced depressive-like behavior, as suggested by findings presented here. TAC-induced cardiac σ₁R downregulation induces cardiac dysfunction. At the same time, levels of peripheral pro-inflammatory cytokines and corticosterone increase, aggravating cardiac dysfunction and downregulating brain hippocampal σ₁R levels. σ₁R stimulation with SA4503 blocks TAC-induced σ₁R downregulation in heart and in hippocampus.</p