Hypervascular liver metastasis from hypovascular ductal cell carcinoma of the pancreas

In a case of hypervascular metastatic liver tumor, the vascularity of primary focus, pancreatic carcinoma was hypovascular. Based on the imaging findings, we thought before the operation that the two lesions were double cancers. Histological examination showed that the stromal volume of metastatic tumorous tissue was richer than that of the primary focus. It was suggested that the difference in the stromal volume was related to the difference of the vascularity. Some foctors originating in stromal cells might be involved in angiogenesis.     

Ablation of the microglial protein DOCK2 reduces amyloid burden in a mouse model of Alzheimer's disease

Alzheimer's disease (AD) neuropathology is characterized by innate immune activation primarily through prostaglandin E2 (PGE₂) signaling. Dedicator of cytokinesis 2 (DOCK2) is a guanyl nucleotide exchange factor expressed exclusively in microglia in the brain and is regulated by PGE₂ receptor EP2. DOCK2 modulates microglia cytokine secretion, phagocytosis, and paracrine neurotoxicity. EP2 ablation in experimental AD results in reduced oxidative damage and amyloid beta (Aβ) burden. This discovery led us to hypothesize that genetic ablation of DOCK2 would replicate the anti-Aβ effects of loss of EP2 in experimental AD. To test this hypothesis, we crossed mice that lacked DOCK2 (DOCK2 −/−), were hemizygous for DOCK2 (DOCK2 +/−), or that expressed two DOCK2 genes (DOCK2 +/+) with APPswe-PS1Δe9 mice (a model of AD). While we found no DOCK2-dependent differences in cortex or in hippocampal microglia density or morphology in APPswe-PS1Δe9 mice, cerebral cortical and hippocampal Aβ plaque area and size were significantly reduced in 10-month-old APPswe-PS1Δe9/DOCK2 −/− mice compared with APPswe-PS1Δe9/DOCK2 +/+ controls. DOCK2 hemizygous APPswe-PS1Δe9 mice had intermediate Aβ plaque levels. Interestingly, soluble Aβ₄₂ was not significantly different among the three genotypes, suggesting the effects were mediated specifically in fibrillar Aβ. In combination with earlier cell culture results, our in vivo results presented here suggest DOCK2 contributes to Aβ plaque burden via regulation of microglial innate immune function and may represent a novel therapeutic target for AD.     

Quantitative evaluation of the diagnostic thinking process in medical students

OBJECTIVE: To explore the diagnostic thinking process of medical students. SUBJECTS AND METHODS: Two hundred twenty-four medical students were presented with 3 clinical scenarios corresponding to high, low, and intermediate pre-test probability of coronary artery disease. Estimates of test characteristics of the exercise stress test, and pre-test and post-test probability for each scenario were elicited from the students (intuitive estimates) and from the literature (reference estimates). Post-test probabilities were calculated using Bayes' theorem based upon the intuitive estimates (Bayesian estimates of post-test probability) and upon the reference estimates (reference estimates of post-test probability). The differences between the reference estimates and the intuitive estimates, and between Bayesian estimates and the intuitive estimates were used for assessing knowledge of test characteristics, and ability of estimating pre-test and post-test probability of disease. RESULTS: Medical students could not rule out disease in low or intermediate pre-test probability settings, mainly because of poor pre-test estimates of disease probability. They were also easily confused by test results that differed from their anticipated results, probably because of their inaptitude in applying Bayes' theorem to real clinical situations. These diagnostic thinking patterns account for medical students or novice physicians repeating unnecessary examinations. CONCLUSIONS: Medical students' diagnostic ability may be enhanced by the following educational strategies: 1) emphasizing the importance of ruling out disease in clinical practice, 2) training in the estimation of pre-test disease probability based upon history and physical examination, and 3) incorporation of the Bayesian probabilistic thinking and its application to real clinical situations.     

Impact of respiratory function on the progression from metabolically healthy non-overweight to metabolically abnormal phenotype

Background and aims

Recent studies identified that metabolically abnormal non-overweight phenotype is a risk factor for cardiovascular diseases. However, only little is known about risk factors for the progression from metabolically healthy non-overweight (MHNO) to metabolically abnormal phenotype. In this study, we investigated the impact of respiratory function on the progression from MHNO to metabolically abnormal phenotype.