Association Between Use of FK506 and Prevalence of Post-transplantation Diabetes Mellitus in Kidney Transplant Patients

Background

Tacrolimus (FK506) use has been suggested as a risk factor for post-transplantation diabetes mellitus (PTDM) because it can impair insulin secretion. This association warrants further investigation. This study aimed to examine the prevalence of PTDM and its association with FK506 use in kidney transplant recipients. The study also aimed to examine the relationship of FK506 use and diabetes-related biologic markers.

Methods

A retrospective chart review was used to collect data at a medical center in northern Taiwan from September 2003 to February 2012. PTDM was defined with the use of the criteria of the American Diabetes Association.

Results

Among 166 patients included in the analysis, PTDM was reported in 49 patients (29.5%). A total of 93 patients used the FK506 regimen, of whom 34 (36.6%) were PTDM cases. Logistic regression showed that FK506 use (odds ratio [OR], 2.71; 95% confidence interval [CI], 1.20–6.11; P = .016) and older age (OR,1.08; 95% CI, 1.03–1.13; P = .001) were significant risk factors for PTDM. In addition, FK506 use in PTDM cases was associated with a significantly higher hemoglobin A1c level (7.55 vs 5.81; P = .01) and a borderline significantly higher insulin resistance index (3.24 vs 1.92; P = .053) than was FK506 use without the presence of PTDM.

Conclusions

Older age and an FK506 regimen were important predictors of the prevalence of PTDM. Greater early detection and prevention efforts for PTDM are needed for older transplant recipients. PTDM patients with an FK506 regimen had higher hemoglobin A1c levels and insulin resistance index than did patients who did not use FK506. The association of serum indicators with FK506 use in the prevalence of PTDM warrants further investigation.     

脑缺血再灌对小鼠学习记忆的影响及药物防护

在建立及管性学习记忆障碍模型的基础上，观察脑缺血再灌对小鼠学习记忆的影响及服用尼莫地平、７６４－３、醒脑灵对其的防护作用。重复脑缺血再灌可明显的降低动物的学习和记忆能力，并可通过药物改善小鼠学习记忆障碍的程度。     

Detection of deception based on fMRI activation patterns underlying the production of a deceptive response and receiving feedback about the success of the deception after a mock murder crime

The ability of a deceiver to track a victim’s ongoing judgments about the truthfulness of the deceit can be critical for successful deception. However, no study has yet investigated the neural circuits underlying receiving a judgment about one’s lie. To explore this issue, we used a modified Guilty Knowledge Test in a mock murder situation to simultaneously record the neural responses involved in producing deception and later when judgments of that deception were made. Producing deception recruited the bilateral inferior parietal lobules (IPLs), right ventral lateral prefrontal (VLPF) areas and right striatum, among which the activation of the right VLPF contributed mostly to diagnosing the identities of the participants, correctly diagnosing 81.25% of ‘murderers’ and 81.25% of ‘innocents’. Moreover, the participant’s response when their deception was successful uniquely recruited the right middle frontal gyrus, bilateral IPLs, bilateral orbitofrontal cortices, bilateral middle temporal gyrus and left cerebellum, among which the right IPL contributed mostly to diagnosing participants’ identities, correctly diagnosing 93.75% of murderers and 87.5% of innocents. This study shows that neural activity associated with being a successful liar (or not) is a feasible indicator for detecting lies and may be more valid than neural activity associated with producing deception.     

Genes in the serotonin pathway are associated with bipolar affective disorder in a Han Chinese population

Serotonin plays an important role in mood regulation, but the involvement of serotonin pathway genes in the development of bipolar I disorder (BP-I), a mood disorder, is not clear. We selected 21 singlenucleotide polymorphisms (SNPs) within the HTR2A gene, 8 within the SLC6A4 gene and 23 within the TPH2 gene for genotyping using the GoldenGate genotyping assay. A total of 375 patients with BP-I and 475 normal controls were recruited. Two out of 21 SNPs (rs1475196 and rs9567747) in the HTR2A gene and 1/23 SNPs (rs17110566) in the TPH2 gene were significantly associated with BP-I, both genotype-wise and allele-wise. Furthermore, a specific haplotype in the HTR2A gene showed a significant association with BP-I. Our results indicate that the HTR2A and TPH2 genes in the serotonin pathway play important roles in susceptibility to BP-I.