BackgroundInpatient palliative care is important for patients with terminal pancreatic cancer. However, the differences between inpatient palliative care and acute hospital care for inpatients with pancreatic cancer have not been explored in a population-based study.MethodsThis population-based nationwide study was conducted using data from the Taiwan National Health Insurance database to analyze the differences between inpatient palliative care and acute hospital care for inpatients with pancreatic cancer. We identified 854 patients with terminal pancreatic cancer, who had received in-hospital end-of-life care between January 2003 and December 2006. These patients were then sub-divided and matched 1:1 (using propensity score matching) according to whether they received inpatient palliative care (n = 276) or acute hospital care (n = 276). These groups were subsequently compared to evaluate any differences in the use of aggressive procedures, prescribed medications, and medical costs.ResultsInpatient palliative care was typically provided by family physicians (39 %) and oncologists (25 %), while acute hospital care was typically provided by oncologists (29 %) and gastroenterologists (24 %). The inpatient palliative care group used natural opium alkaloids significantly more frequently than the acute hospital care group (84.4 % vs. 56.5 %, respectively; P < 0.001). The inpatient palliative care group also had shorter hospital stays (10.6 ± 11.1 days vs. 20.6 ± 16.3 days, respectively; P < 0.001), fewer aggressive procedures, and lower medical costs (both, P < 0.005).ConclusionsCompared to patients in acute hospital wards, patients with pancreatic cancer in inpatient palliative care units received more frequent pain control treatments, underwent fewer aggressive procedures, and incurred lower medical costs. Therefore, inpatient palliative care should be considered a viable option for patients with terminal pancreatic cancer.

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The hippocampus has long been associated with learning, memory, and modulation of emotional responses. Previous studies demonstrated that stress-induced loss of hippocampal neurons may contribute to the pathogenesis of depression. The recent observations supported that antidepressant drugs increase the production of serotoninergic neurotransmitter and they play a critical role in the initiation of neurogenesis in the hippocampus. In order to explore the possible new mechanism of the treatment of depression, we cultured neural stem cells (NSCs) derived from the hippocampus of adult rats as an in vitro model to evaluate the capabilities of neuroprotection and neural differentiation in NSCs by fluoxetine (FL) treatment. Our results showed that 20 microM FL treatment can significantly increase the proliferation rate of NSCs (p<0.05), and up-regulate the mRNA and protein expressions of Bcl-2 in Day-7 FL-treated NSCs (p<0.01). Using Bcl-2 gene silencing with small interfering RNA, our data verified that FL can prevent Fas ligand-induced caspase-dependent apoptosis in NSCs through the activation of Bcl-2. The in vitro observation and immunofluorescent study further demonstrated that FL treatment can stimulate the neurite development and serotoninergic differentiation of NSCs through the activation of Bcl-2. Using microdialysis with high performance liquid chromatography- electrochemical detection, the functional release of serotonin in the differentiating NSCs with FL treatment was increased and simultaneously regulated by the Bcl-2 expressions. In sum, the study results indicate that antidepressant administration can increase NSCs survival, promote the neurite development, and facilitate NSCs differentiating into the functional serotoninergic neurons via the modulation of Bcl-2 expression.

TACE is associated with the modulation of serum angiogenic, inflammatory, and cell growth cytokines in HCC patients. Serum IL-6 correlates with post-TACE fever, and baseline serum VEGF independently predicts patient survival.

Both diabetic peripheral neuropathy and peripheral arterial disease (PAD) cause foot ulcers and often result in non-traumatic amputations in patients with type 2 diabetes. This study aimed to evaluate the association between clinical variables, PAD, and subclinical diabetic small fiber peripheral neuropathy detected by abnormal thermal thresholds of the lower extremities in patients with type 2 diabetes.We investigated 725 consecutive patients with type 2 diabetes (male/female: 372/353; mean age, 67 ± 11 years) who did not have apparent cardiovascular disease (including coronary artery disease, arrhythmia, and stroke) and who underwent the quantitative sensory test for thermal (warm and cold) thresholds of the lower limbs and ankle-brachial index (ABI)/toe-brachial index (TBI) examinations in 2015. The analyses included glycated hemoglobin, estimated glomerular filtration rate, and other characteristics.In total, 539 (74.3%) patients showed an abnormality of at least 1 thermal threshold in their feet. All patients with an abnormal ABI (<0.9) had concurrent impaired thermal thresholds, and 93% (87/94) of patients with an abnormal TBI experienced abnormal thermal thresholds in the lower limbs. Age- and sex-adjusted TBI and estimated glomerular filtration rate were significantly correlated to abnormal thermal thresholds. In the multivariate analysis, fasting plasma glucose, and glycated hemoglobin were independently associated with abnormal thermal thresholds in the lower extremities.Subclinical thermal threshold abnormalities of the feet are significantly associated with PAD and nephropathy in patients who have type 2 diabetes without cardiovascular disease.