The involvement of dopamine within the nucleus accumbens in the formation and maintenance of pair bonds was assessed in a series of experiments using the monogamous prairie vole. We show that dopamine transmission that promotes pair bond formation occurs within the rostral shell of the nucleus accumbens, but not in its core or caudal shell. Within this specific brain region, D1- and D2-like receptor activation produced opposite effects: D1-like activation prevented pair bond formation, whereas D2-like activation facilitated it. After extended cohabitation with a female, male voles showed behavior indicative of pair bond maintenance-namely, selective aggression towards unfamiliar females. These voles also showed a significant upregulation in nucleus accumbens D1-like receptors, and blockade of these receptors abolished selective aggression. Thus, neuroplastic reorganization of the nucleus accumbens dopamine system is responsible for the enduring nature of monogamous pair bonding. Finally, we show that this system may also contribute to species-specific social organization.

Delivering CFTR to ciliated cells of cystic fibrosis (CF) patients fully restores ion and fluid transport to the lumenal surface of airway epithelium and returns mucus transport rates to those of non-CF airways.

Intrauterine adhesions (IUAs) can lead to partial or complete closure of the uterine cavity, which may result in symptoms including abnormal menstruation, infertility, and pelvic pain. A network meta-analysis was performed to assess the effect of adjuvant therapy on the prevention and treatment of IUAs. We searched electronic databases, including PubMed, Embase, and the Cochrane Library, up to May 5, 2017, without language restrictions. The primary outcomes in the present analysis were the rate of IUAs for prevention and the rate of IUA recurrence for treatment. The secondary outcomes included the IUA score and the rate of severity of IUAs. The treatments were then ranked by the surface under the cumulative ranking curve (SUCRA). We included 20 articles that involved a total of 1891 patients in our analysis. In the outcomes of prevention-related studies, an alginate hyaluronate-carboxymethylcellulose membrane (ACH) (n = 10, SUCRA score = 93.3%) was the adjuvant treatment that most effectively reduced IUA incidence. It was followed by intercoat (n = 10, SUCRA score = 74.7%) and misoprostol (n = 10, SUCRA score = 68.6%). In addition, auto-cross-linked hyaluronic acid (ACP) (n = 3, SUCRA score = 83.2%) and intercoat (n = 3, SUCRA score = 66.4%) each corresponded to a relatively high preventive effect against severe IUAs. In the treatment-related studies, ACP plus a balloon (n = 4, SUCRA score = 96.3%) and a freeze-dried amnion graft plus a balloon (n = 4, SUCRA score = 62.7%) most effectively reduced IUA recurrence and had a high probability of most effectively reducing IUA scores. Therefore, according to the prophylactic analysis, ACH and intercoat were most likely to prevent IUA development. In our analysis of agents used to prevent severe IUAs, we found that ACP and intercoat provided significant advantages and had high reliability. In our analysis of treatments, ACP plus a balloon and freeze-dried amniotic agents plus a balloon were most likely to reduce IUA recurrence and IUA scores after adhesiolysis.

Background. We performed this meta-analysis to investigate the efficacy of probiotics on prevention of infection-related complications following colorectal resection. Method. PubMed, EMBASE, Cochrane Library, and the Web of Science were searched up to January 2016. According to the results, only randomized controlled trials that compared the efficacy of probiotics on patients with colorectal resection were included for meta-analysis. Results. Nine studies including a total of 1146 patients met the criteria (556 received multistrain probiotic bacteria, 590 with non-multistrain probiotic bacteria). The combination of multistrain probiotics was beneficial in the reduction of total infections (OR = 0.30, 95%CI: 0.15–0.61, p = 0.0009), including surgical site infections (SSI) (OR = 0.48, 95%CI: 0.25–0.89, p = 0.02) and nonsurgical site infections (NSSI) (OR = 0.36, 95%CI: 0.23–0.56, p < 0.00001). However, there was no significant reduction in total infections (OR = 0.74, 95%CI: 0.50–1.09, p = 0.13) or SSI (OR = 0.77, 95%CI: 0.52–1.12, p = 0.17) with the application of non-multistrains of probiotics. Conclusion. Combinations of multistrain probiotic bacteria showed promise in preventing the incidence of infections following colorectal surgery. However, the efficacy of one or two strains of probiotics remains undetermined.

Mossy fiber sprouting (MFS) and neuronal loss are important pathological features of chronic epilepsy closely related to the development of spontaneous recurrent seizures. However, the pathological mechanism of MFS remains unclear. Collapsin response mediator protein 2 (CRMP2) is a cytoplasmic protein highly expressed in the nervous system and is involved in axon/dendrite specification and axonal growth. It is possibly associated with the development of MFS. Lacosamide (LCM), a novel antiepileptic drug, was recently found to inhibit the CRMP2-mediated neurite outgrowth. Therefore, we studied the relationships between LCM, CRMP2, and MFS, seeking potential therapeutic targets for epileptogenesis and a better understanding of the mechanism of action of LCM. We used kainic acid to induce status epilepticus in an animal model and examined the resultant changes in protein expression by Western blot and changes in histology by specific staining for cell death and MFS. Our results showed that the expression level of CRMP2 was elevated and the expression level of phosphorylated CRMP2 (p-CRMP2) was reduced following status epilepticus. Administration of LCM not only reversed this effect but also suppressed spontaneous recurrent seizures and reduced MFS and loss of hippocampal neurons. This study reveals that, in addition to its antiseizure efficacy, LCM has a neuroprotective effect and inhibits the development of epilepsy. CRMP2 is possibly involved in the mechanism by which LCM suppresses MFS and is expected to be a new therapeutic target for treating epileptogenesis.