Objective: To evaluate clinical pharmacist-led pain-medication education in patients with cancer. Methods: A controlled study was conducted prospectively at six tertiary hospitals in China. In-patients with cancer were randomized to receive conventional treatment plus medication education or no education (controls). Education consisted of access to information booklets and eight 30-min face-to-face counselling sessions given by clinical pharmacists over 4 weeks. Patients completed pain-and analgesic-knowledge assessments and a Brief Pain Inventory, pre-and poststudy. Results: A total of 123 and 114 patients in the education and control groups, respectively, completed follow-up. At the end of the study, patient knowledge regarding cancer pain and pain control was significantly increased in both groups; pain and analgesic knowledge scores were significantly higher in the education group compared with controls. In the control group, the increase in total pain-related knowledge was significantly greater in analgesic-naïve patients compared with those who were using/had used analgesics. Pain intensity scores and pain interference of daily activities were significantly reduced in the education group compared with controls. Conclusions: Clinical pharmacist-led medication education resulted in improved pain control in patients with cancer.

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Many diabetic patients complicated with wild to severe depression. It is unclear in diabetic medication whether depression perturbs the drug metabolic process of the hypoglycemic agents or not. The present study was designed to investigate the impact of chronic unpredicted mild stress (CUMS) –induced depression on mitiglinide (MGN) pharmacokinetics in rats. Adult female Sprague-Dawley rats in CUMS group were subjected to different types of stressors and the stress procedures lasted for 8 weeks. Control group without receiving stress had free access to food and water. Open-field test and 5-HT levels were assayed to evaluate the depression. After CUMS all rats were given 2.5 mg/kg of mitiglinide per os. The blood samples were collected at different time and mitiglinide plasma concentration was measured by high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Non-compartmental statistical moment analysis was processed with DAS software. In CMUS-induced depression group, peak concentration (Cmax), peak time (Tmax), area under curve (AUC0 → ∞), mean residence time (MRT0 → ∞), and half-life (T1/2z) were reduced while total plasma clearance (CLz/F) was increased compared to control group. These preliminary results indicated that CUMS-induced depression alter the drug metabolic process of mitiglinide in rats. This finding will be significant in clinic.

Neuroplasticity refers to the capacity of the nervous system to modify its organization such that the brain can be shaped by environmental input. Individuals exhibit different degrees of neuroplasticity because of their different courses of growth. Neuroplasticity may thus play a role in individual differences in the treatment of neuropsychiatric diseases. The nervous system monitors and coordinates internal organ function. Thus neuroplasticity may also be associated with the pathogenesis and the treatment of some other diseases besides neuropsychiatric diseases. The cardiovascular system is controlled by the nervous system, mainly by the autonomic nervous system. Stress may lead to depression and cardiovascular disease (CVD). CVD is associated with depression, which is a disorder of decreased neuroplasticity. And the mechanisms of depression and CVD are related. So we conclude that decreased neuroplasticity causes the coexistence of depression with CVD, and increased neuroplasticity may be beneficial against the development of CVD. This theory provides another angle that can explain some of the reported phenomena related to CVD and neuropsychiatry and provide a potential treatment to protect against CVD.

Cancer is one of the most eminent diseases of modern times and numerous natural products derived from medicinal plants have been identified as potential sources of antitumor drugs. A successful anticancer drug must target or inhibit tumor cells whilst causing minimal damage to healthy cells. The present study aimed to investigate the antitumor efficacy of ethyl acetate extract, and other isolated compounds from Artemisia indica, on MCF‑7, BHY, Miapaca‑2, Colo‑205 and A‑549 cell lines. The apoptotic activity of the compounds was studied using flow cytometry. The different cancer cell lines were treated with the ethyl acetate extract and varying concentrations of compounds (denoted a‑g) isolated from the A. indica. The cytotoxicity was evaluated by MTT assay and the apoptotic properties of the compounds and the extract were assessed using flow cytometry. In MCF‑7 cells, the effect on mitochondrial membrane potential loss (ΛΨm) induced by compounds b and d was also studied. Bioassay‑guided fractionation of the ethyl acetate extract from the shoot and root parts of A. indica led to the identification of the compounds a‑g as: 5‑hydroxy‑3,7,4'‑trimethoxyflavone; ludartin; maackiain; lupeol; cis‑matricaria ester; trans‑matricaria ester; and 6‑methoxy‑7,8‑methylenedioxy coumarin, respectively. All the compounds exhibited mild to potent inhibition of cell proliferation in all the cell lines, with the half maximal inhibitory concentration values ranging from 25.18‑88.12 µM. Ludartin and lupeol were observed to have the most potent inhibitory effects. Based on the initially identified antiproliferative effects, these two compounds were evaluated for their effects on cell cycle phase distribution, DNA damage and their effects on mitochondrial membrane potential loss (ΛΨm). The two compounds induced DNA damage and mitochondrial membrane potential loss in MCF‑7 cells. The results of the current study suggest that lupeol and ludartin, isolated from A. indica, produce anticancer effects by inducing DNA damage and a reduction of mitochondrial membrane potential, and may be used as potent anticancer agents, subsequent to further study.

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PGE2 may promote cardiac fibrosis via EP1 receptor and calcium signal pathway.

The aim of this study was to explore the impact of depression mood disorder on the incidence of adverse drug reactions of anticancer drugs in cancer patients. The Hamilton Depression Scale 17 was used to evaluate the depression mood disorder level in 73 cancer patients before chemotherapy. Pharmacists monitored adverse drug reactions during the chemotherapy period. The relationship between depression mood disorder level and the incidence of adverse drug reactions was analysed. The frequency and extent of total adverse drug reactions were not related to depression mood disorder level. The frequency and extent of subjectively experienced adverse drug reactions such as anorexia, nausea and fatigue were related to depression mood disorder level. In conclusion, psychological support and intervention should be provided to cancer patients in order to improve patient adherence and cancer chemotherapy effectiveness, and to decrease the incidence of adverse drug reactions.