Krill oil (KO) exhibits various biological activities, such as anti-inflammatory and antitumor effects. However, the inhibitory effects of benign prostatic hyperplasia (BPH) <em>in vitro</em> and <em>in vivo </em>have not yet been studied. This study investigated the anti-BPH effects of KO extracted by an enzymatic hydrolysis method. KO treatment inhibited the proliferation of WMPY-1 and BPH-1 cells by induction of G₀/G₁ phase arrest through the modulation of positive and negative regulators in both prostate cell types. KO treatment stimulated phosphorylation of JNK and p38 signaling. In addition, KO changed the expression of BPH-related markers (5α-reductase, androgen receptor, FGF, Bcl-2, and Bax) and the activity of the proliferation-mediated NF-κB binding motif. KO-induced levels of proliferation-mediated molecules of prostate cells were attenuated in the presence of siRNA-specific p-38 (si-p38) and JNK (si-JNK). Furthermore, the administration of KO alleviated prostate size and weight and the cell layer thickness of prostate glands in a testosterone enanthate-induced BPH rat model. KO treatment altered the level of dihydrotestosterone in serum and the expression levels of BPH-related markers in prostate tissues. Finally, KO-mediated inhibition of prostatic growth was validated by histological analysis. These results suggest that KO has an inhibitory effect on BPH in prostate cells <em>in vitro</em> and <em>in vivo</em>. Thus, KO might be a potential prophylactic or therapeutic agent for patients with BPH.

Copyright © by 2015 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

Krill oil (KO) exhibits various biological activities, such as anti-inflammatory and antitumor effects. However, the inhibitory effects of benign prostatic hyperplasia (BPH) <em>in vitro</em> and <em>in vivo </em>have not yet been studied. This study investigated the anti-BPH effects of KO extracted by an enzymatic hydrolysis method. KO treatment inhibited the proliferation of WMPY-1 and BPH-1 cells by induction of G₀/G₁ phase arrest through the modulation of positive and negative regulators in both prostate cell types. KO treatment stimulated phosphorylation of JNK and p38 signaling. In addition, KO changed the expression of BPH-related markers (5α-reductase, androgen receptor, FGF, Bcl-2, and Bax) and the activity of the proliferation-mediated NF-κB binding motif. KO-induced levels of proliferation-mediated molecules of prostate cells were attenuated in the presence of siRNA-specific p-38 (si-p38) and JNK (si-JNK). Furthermore, the administration of KO alleviated prostate size and weight and the cell layer thickness of prostate glands in a testosterone enanthate-induced BPH rat model. KO treatment altered the level of dihydrotestosterone in serum and the expression levels of BPH-related markers in prostate tissues. Finally, KO-mediated inhibition of prostatic growth was validated by histological analysis. These results suggest that KO has an inhibitory effect on BPH in prostate cells <em>in vitro</em> and <em>in vivo</em>. Thus, KO might be a potential prophylactic or therapeutic agent for patients with BPH.

Copyright © by 2015 by the Society of Critical Care Medicine and Wolters Kluwer Health, Inc. All Rights Reserved.

Paraquat (1,1'-dimethyl-4,4'-bipyridinium dichloride; PQ), an effective and widely used herbicide, was commercially introduced in 1962. It is reduced by the electron donor NADPH, and then reduced PQ transfers the electrons to molecular oxygen, resulting in the production of reactive oxygen species (ROS), which are related to cellular toxicity. However, the influence of continuous hypoxia on PQ-induced ROS production has not fully been investigated. We evaluated in vitro the protective effect of continuous hypoxia on PQ-induced cytotoxicity in the human carcinogenic alveolar basal epithelial cell line (A549 cells) by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and live and dead assay, and by measuring lactate dehydrogenase (LDH) release. To elucidate the mechanism underlying this effect, we monitored the immunofluorescence of intracellular ROS and measured malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Continuous hypoxia protected the A549 cells from PQ-induced cytotoxicity. Continuous hypoxia for a period of 24 h significantly reduced intracellular ROS, decreased MDA concentration in the supernatant, and normalized SOD and GPx activities. Continuous hypoxia attenuated PQ-induced cell toxicity in A549 cells. This protective effect might be attributable to the suppression of PQ-induced ROS generation.

In patients with OHCA admitted to the emergency department, MV ventilation during CPR showed clinical outcomes similar to those of BV ventilation in most measures. However, survival at hospital discharge was significantly higher in the MV group, suggesting potential benefits of MV use in selected patients.

This study aimed to evaluate the effectiveness of an empathy-expanding in-depth group counseling program for the recovery of negative symptoms (such as avolition, social withdrawal, and isolation) in individuals with bipolar disorder and schizophrenia who were in a relatively stable phase (with an average illness duration of more than three years) while concurrently receiving outpatient medication. A total of 24 anonymous volunteers (including 3 duplicate participants) were recruited with the cooperation of the Korean Schizophrenia Recovery Association (Simjihoe). Approximately half of the participants were referred to the program involuntarily by their family members. Participants were divided into four groups of six individuals each and engaged in the program for three sessions, meeting once per week for two hours via mobile chat-based counseling. The program was conducted sequentially across the groups and was implemented over a four-month period.To validate the program’s effects, both self-reported feedback and observations from family members were collected through surveys and text messages, and additional phone and face-to-face interviews were conducted to enhance data reliability. At the end of the third session, 78% (n=18/23) of participants reported positive changes in their daily lives, with approximately 40% specifically experiencing improvements in their interpersonal relationships. Furthermore, follow-up assessments conducted three to six months later confirmed that 70% (n=14/20) of participants maintained these positive changes. These findings suggest that this novel approach—digital, empathy-expanding in-depth group counseling—effectively mitigates depression and anxiety in individuals with severe mental disorders while facilitating lasting improvements in interpersonal relationships and external activities. Notably, the participant-friendly design and the significant behavioral changes observed despite the program’s short duration underscore its substantial social and psychological implications.

Pediatric and adult mice exhibited significant time-dependent differences in neuroinflammation and apoptosis following TBI, with pediatric mice showing more intense early responses indicative of age-specific vulnerabilities in post-injury outcomes. Both age groups showed a significant but transient increase in HSP70 expression, suggesting an acute response to stress post-injury.