Comorbid depressive symptoms can aggravate the functional changes of the pain matrix in patients with chronic back pain: A resting-state fMRI study.

Objective: The purposes of this study are to explore (1) whether comorbid depressive symptoms in patients with chronic back pain (CBP) affect the pain matrix. And (2) whether the interaction of depression and CBP exacerbates impaired brain function. Methods: Thirty-two patients with CBP without comorbid depressive symptoms and thirty patients with CBP with comorbid depressive symptoms were recruited. All subjects underwent functional magnetic resonance imaging (fMRI) scans. The graph theory analysis, mediation analysis, and functional connectivity (FC) analysis were included in this study. All subjects received the detection of clinical depressive symptoms and pain-related manifestations. Result: Compared with the CBP group, subjects in the CBP with comorbid depressive symptoms (CBP-D) group had significantly increased FC in the left medial prefrontal cortex and several parietal cortical regions. The results of the graph theory analyses showed that the area under the curve of small-world property (t = -2.175, p = 0.034), gamma (t = -2.332, p = 0.023), and local efficiency (t = -2.461, p = 0.017) in the CBP-D group were significantly lower. The nodal efficiency in the ventral posterior insula (VPI) (t = -3.581, p = 0.0007), and the network efficiency values (t = -2.758, p = 0.008) in the pain matrix were significantly lower in the CBP-D group. Both the topological properties and the FC values of these brain regions were significantly correlated with self-rating depression scale (SDS) scores (all FDR corrected) but not with pain intensity. Further mediation analyses demonstrated that pain intensity had a mediating effect on the relationship between SDS scores and Pain Disability Index scores. Likewise, the SDS scores mediated the relationship between pain intensity and PDI scores. Conclusion: Our study found that comorbid depressive symptoms can aggravate the impairment of pain matrix function of CBP, but this impairment cannot directly lead to the increase of pain intensity, which may be because some brain regions of the pain matrix are the common neural basis of depression and CBP.

Temporal changes and prognostic value of plasma ghrelin level in patients with acute heart failure: a prospective study.

BACKGROUND: Plasma ghrelin levels can be elevated in patients with acute heart failure (AHF). This study aimed to analyze the temporal changes and prognostic value of ghrelin levels in patients with AHF. METHODS: This prospective study included patients with AHF at the Cardiology Department, Weifang People's Hospital (May 2018-October 2019), and age- and sex-matched healthy controls. Plasma ghrelin levels were measured. Multivariable logistic regression and receiver operating characteristic (ROC) curve analyses were used to evaluate whether ghrelin levels could predict major cardiac adverse events (MACEs) during a 1-year follow-up. RESULTS: Finally, 92 patients with AHF and 50 healthy controls were enrolled. Ghrelin levels were higher in patients with AHF at 1, 3, 12, and 24 h compared with controls (all P < 0.01). Ghrelin levels in the AHF group were higher at 3 and 12 h than at 1 and 24 h (P < 0.001). Ghrelin level at 3 h in patients with AHF was negatively correlated with the left ventricular end-diastolic diameter and left ventricular ejection fraction (both P < 0.05). MACEs occurred in 48 patients with AHF. Ghrelin levels were higher in the MACE group than in the non-MACE group at 1 (P = 0.011) and 3 h (P = 0.034). Multivariable regression showed that ghrelin level at 3 h was independently associated with MACEs [OR = 0.629, 95% confidence interval (CI): 0.515-0.742, P = 0.010], but the area under the ROC curve was only 0.629 (95% CI 0.515-0.742). CONCLUSIONS: Plasma ghrelin levels are elevated in AHF and patients with MACEs during follow-up.

The ORF4 protein of porcine circovirus type 2 antagonizes apoptosis by stabilizing the concentration of ferritin heavy chain through physical interaction.

Porcine circovirus type 2 (PCV2) is the primary aetiological agent of porcine circovirus-associated disease in swine. The mechanism of PCV2 pathogenesis remains largely unknown. A newly identified viral protein of PCV2, ORF4, has been suggested to be involved in virus-induced apoptosis. However, there is still no information regarding the molecular mechanism by which ORF4 regulates apoptosis. In this study, we reveal that a physical interaction between the PCV2 ORF4 protein and ferritin heavy chain (FHC) in the cytoplasm of host cells reduced the cellular concentration of FHC. The ORF4-mediated reduction of FHC inhibited reactive oxygen species accumulation in PCV2-infected cells. Consequently, the ORF4 protein inhibited apoptosis in host cells. This may be the first report to describe the mechanism of ORF4 cytoprotection against apoptosis during the early stages of PCV2 infection.

Effect of routine heparins treatment in acute coronary syndrome on serum pregnancy-associated plasma protein a concentration.

BACKGROUND: Pregnancy-associated plasma protein A (PAPP-A) has been suggested as a useful marker of acute coronary syndrome (ACS). Serum PAPP-A concentrations are affected by unfractionated heparin (UFH) in ACS population, and we tried to investigate the time profile of effects of routine heparins treatment on serum PAPP-A concentrations in ACS population thoroughly and give advice to sample collection of related study. METHODS: Twenty cases were involved in this study: ten patients with acute myocardial infarction received subcutaneous low molecular weight heparin (LMWH) twice a day (group A), and the other ten percutaneous coronary intervention patients with stenting received intravenous UFH (group B). Samples were collected before and after heparin administration and serum PAPP-A concentrations were analyzed in these samples. RESULTS: Serum PAPP-A concentration increased in both group A and B. In group A, PAPP-A concentration elevated gradually (14.5 to 29.4 mIU/L, P<0.05) throughout the observation period and normalized at 48h after drug discontinuation. In group B, there was a rapid and intense increase after intravenous heparin injection (13.1 to 49.3 mIU/L, P<0.05), and a new PAPP-A peak was induced by additional heparin administration. CONCLUSIONS: Heparins-induced increase in serum PAPP-A concentration lasted until 48h after drug use was discontinued. We recommend that samples from these patients for PAPP-A measurement should be collected at least 48h after the last administration if its not available before the administration of heparins.