High prevalence of insulin resistance (IR) has been reported in bipolar disorder (BD) patients. Importantly, impaired insulin sensitivity could modulate the course and treatment outcome in BD. Here, we hypothesized that insulin sensitivity could be potentially associated with the neurocognitive trajectory in euthymic BD. We aimed to examine differences in insulin sensitivity and executive function between BD patients and controls.

Sixty-two patients with BD receiving mood stabilizer treatment and 62 controls, matching age, sex, and body mass index, were recruited in this study. Insulin sensitivity was estimated using the homeostasis model assessment of insulin resistance (HOMA-IR). The Wisconsin card-sorting test (WCST) was applied to test participants’ ability to shift cognitive set. Group differences were measured and multivariate regression analysis was performed to examine relationships among factors.

The results indicated that the HOMA-IR (P = .048) value in the patients with BD were significantly higher than those in controls. With regards to executive function, the BD patients performed significantly poorer than the control subjects (P < .05). Moreover, the interaction effect between BD diagnosis and HOMA-IR value on the WCST-preservation errors was significant (P = .01), and post-hoc analyses showed that the cognitive abilities were worse in the BD patients with a higher IR than in the others groups.

Insulin sensitivity is associated with the neurocognitive performance in euthymic BD patients. Although the underlying mechanisms remain unclear, interventions to improve insulin sensitivity could potentially improve the functional outcome of BD.

Previous studies suggested that a disturbance of the dopamine system underlies the pathophysiology of bipolar disorder (BD). In addition, the therapeutic action of medications for treating BD, such as valproate (VPA), might modulate dopamine system activity, but it remains unclear. Here, we aimed to investigate the role of the striatal dopamine transporter (DAT) in BD patients and in social defeat (SD) mice treated with VPA.

We enrolled community-dwelling controls (N = 18) and BD patients (N = 23) who were treated with VPA in a euthymic stage. The striatal DAT availabilities were approached by TRODAT-1 single photon emission computed tomography. We also established a chronic SD mouse model and treated mice with 350 mg/kg VPA for 3 weeks. Behavioral tests were administered, and striatal DAT expression levels were determined.

In humans, the level of striatal DAT availability was significantly higher in euthymic BD patients (1.52 ± 0.17 and 1.37 ± 0.23, p = 0.015). Moreover, the level of striatal DAT availability was also negatively correlated with the VPA concentration in BD patients (r = −0.653, p = 0.003). In SD mice, the expression of striatal DAT significantly increased (p < 0.001), and the SD effect on DAT expression was rescued by VPA treatment.

The striatal DAT might play a role in the pathophysiology of BD and in the therapeutic mechanism of VPA. The homeostasis of DAT might represent a new therapeutic strategy for BD patients.

To describe the epidemiology of vancomycin-resistant enterococci (VRE) in a university hospital in Taipei, Taiwan.

Retrospective review over a 27-month period, from March 1996 to May 1998.

A tertiary-care teaching hospital in Taiwan.

Patients with VRE isolated from any body site.

Patients were identified through hospital microbiology and infection control records. Patient charts were reviewed for clinical and epidemiology data, including age, gender, previous hospital admissions, underlying diseases, types of infection, and recent antibiotic use. VRE isolates were characterized by their typical biochemical reactions, cellular fatty acid profiles, and the presence of van genes. Antibiotypes using the E-test and randomly amplified polymorphic DNA (RAPD) patterns of these isolates were used to determine the clonality.

Twenty-five isolates of VRE recovered from 12 patients were identified. One patient with a perianal abscess had 12 isolates of VRE (4 Enterococcus faecalis, 7 Enterococcus faecium, and 1 Enterococcus casseliflavus) recovered from perianal lesions. Among 3 patients who were hospitalized in the same room, 1 had a community-acquired cellulitis over the left leg caused by E faecalis, and the other 2 patients both had anal colonization with 2 isolates of E faecalis. The other 8 patients had 1 E faecalis isolate each from various clinical specimens. All isolates possessed vanA resistance phenotype and vanA genes. Different antibiotypes and RAPD patterns of the isolates from different patients excluded the possibility of nosocomial spread at the hospital.

Multiple species of VRE (E faecalis, E faecium, and E casseliflavus) and multiple clones of E faecium could colonize or infect hospitalized patients. In addition, clones of VRE can persist long-term in patients' lower gastrointestinal tracts. These results extend our knowledge of the coexistence and the persistence of multiple species and multiple clones of VRE in hospitalized patients.