Positive intervention effect of mobile health application based on mindfulness and social support theory on postpartum depression symptoms of puerperae.

OBJECTIVE: This study investigated the effects of mobile health application designed based on mindfulness and social support theory on parenting self-efficacy and postpartum depression symptoms of puerperae. METHODS: We recruited 130 puerperae from a hospital in China and randomized them to an App use group (n = 65) and a waiting control group (n = 65). The App group underwent an 8-week app use intervention while the control group underwent no intervention. We measured four main variables (mindfulness, perceived social support, maternal parental self-efficacy and postpartum depressive symptoms) before and after the App use intervention. RESULTS: In the App group, perceived social support, maternal parental self-efficacy were significantly higher and postpartum depressive symptoms was significantly lower. In the control group, there were no significant differences in any of the four variables between the pre-test and post-test. CONCLUSIONS: Our findings indicated that the mobile health application may help to improve perceived social support, maternal self-efficacy and reduce postpartum depressive symptoms. The finding of the mobile health application's effect extends our understanding of integrative effects of mindfulness and perceived social support on reduction of postpartum depressive symptoms and suggests clinical potentials in the treatment of postpartum depressive symptoms.

Alpha-Mangostin Reverses Multidrug Resistance by Attenuating the Function of the Multidrug Resistance-Linked ABCG2 Transporter.

The ATP-binding cassette (ABC) drug transporter ABCG2 can actively efflux a wide variety of chemotherapeutic agents out of cancer cells and subsequently reduce the intracellular accumulation of these drugs. Therefore, the overexpression of ABCG2 often contributes to the development of multidrug resistance (MDR) in cancer cells, which is one of the major obstacles to successful cancer chemotherapy. Moreover, ABCG2 is highly expressed in various tissues including the intestine and blood-brain barrier (BBB), limiting the absorption and bioavailability of many therapeutic agents. For decades, the task of developing a highly effective synthetic inhibitor of ABCG2 has been hindered mostly by the intrinsic toxicity, the lack of specificity, and complex pharmacokinetics. Alternatively, considering the wide range of diversity and relatively nontoxic nature of natural products, developing potential modulators of ABCG2 from natural sources is particularly valuable. α-Mangostin is a natural xanthone derived from the pericarps of mangosteen (Garcinia mangostana L.) with various pharmacological purposes, including suppressing angiogenesis and inducing cancer cell growth arrest. In this study, we demonstrated that at nontoxic concentrations, α-mangostin effectively and selectively inhibits ABCG2-mediated drug transport and reverses MDR in ABCG2-overexpressing MDR cancer cells. Direct interactions between α-mangostin and the ABCG2 drug-binding site(s) were confirmed by stimulation of ATPase activity and by inhibition of photolabeling of the substrate-binding site(s) of ABCG2 with [125I]iodoarylazidoprazosin. In summary, our findings show that α-mangostin has great potential to be further developed into a promising modulator of ABCG2 for reversing MDR and for its use in combination therapy for patients with MDR tumors.

Berberine protects against neuronal damage via suppression of glia-mediated inflammation in traumatic brain injury.

Traumatic brain injury (TBI) triggers a series of neuroinflammatory processes that contribute to evolution of neuronal injury. The present study investigated the neuroprotective effects and anti-inflammatory actions of berberine, an isoquinoline alkaloid, in both in vitro and in vivo TBI models. Mice subjected to controlled cortical impact injury were injected with berberine (10 mg·kg(-1)) or vehicle 10 min after injury. In addition to behavioral studies and histology analysis, blood-brain barrier (BBB) permeability and brain water content were determined. Expression of PI3K/Akt and Erk signaling and inflammatory mediators were also analyzed. The protective effect of berberine was also investigated in cultured neurons either subjected to stretch injury or exposed to conditioned media with activated microglia. Berberine significantly attenuated functional deficits and brain damage associated with TBI up to day 28 post-injury. Berberine also reduced neuronal death, apoptosis, BBB permeability, and brain edema at day 1 post-injury. These changes coincided with a marked reduction in leukocyte infiltration, microglial activation, matrix metalloproteinase-9 activity, and expression of inflammatory mediators. Berberine had no effect on Akt or Erk 1/2 phosphorylation. In mixed glial cultures, berberine reduced TLR4/MyD88/NF-κB signaling. Berberine also attenuated neuronal death induced by microglial conditioned media; however, it did not directly protect cultured neurons subjected to stretch injury. Moreover, administration of berberine at 3 h post-injury also reduced TBI-induced neuronal damage, apoptosis and inflammation in vivo. Berberine reduces TBI-induced brain damage by limiting the production of inflammatory mediators by glial cells, rather than by a direct neuroprotective effect.

Tension pneumocephalus as a complication of hyperbaric oxygen therapy in a patient with chronic traumatic brain injury.

Although hyperbaric oxygen therapy has not been accepted as a standard therapy for traumatic brain injuries, it has been used, along with rehabilitative exercises, for traumatic brain injuries, and the standard protocol has a low risk of complications. We report a case of chronic traumatic brain injury that progressed to tension pneumocephalus after hyperbaric oxygen therapy. The patient was a 25-yr-old man who presented with left occipital bone fracture and subarachnoid and subdural hemorrhage after being hit by a car. He underwent craniectomy to remove the hematoma and cerebrospinal fluid diversion with a ventriculoperitoneal shunt for the treatment of hydrocephalus. Fifteen months after the trauma, the patient received hyperbaric oxygen therapy to promote functional recovery. Tension pneumocephalus developed after the first session of hyperbaric oxygen therapy, and immediate burr hole drainage followed by ligation of the ventriculoperitoneal shunt was performed. The patient's consciousness recovered gradually, and he was discharged home. We suggest that patients with unrepaired skull base fracture and cerebrospinal fluid diversion should be carefully evaluated before receiving hyperbaric oxygen therapy.

Wogonin improves histological and functional outcomes, and reduces activation of TLR4/NF-κB signaling after experimental traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) initiates a neuroinflammatory cascade that contributes to neuronal damage and behavioral impairment. This study was undertaken to investigate the effects of wogonin, a flavonoid with potent anti-inflammatory properties, on functional and histological outcomes, brain edema, and toll-like receptor 4 (TLR4)- and nuclear factor kappa B (NF-κB)-related signaling pathways in mice following TBI. METHODOLOGY/PRINCIPAL FINDINGS: Mice subjected to controlled cortical impact injury were injected with wogonin (20, 40, or 50 mg·kg(-1)) or vehicle 10 min after injury. Behavioral studies, histology analysis, and measurement of blood-brain barrier (BBB) permeability and brain water content were carried out to assess the effects of wogonin. Levels of TLR4/NF-κB-related inflammatory mediators were also examined. Treatment with 40 mg·kg(-1) wogonin significantly improved functional recovery and reduced contusion volumes up to post-injury day 28. Wogonin also significantly reduced neuronal death, BBB permeability, and brain edema beginning at day 1. These changes were associated with a marked reduction in leukocyte infiltration, microglial activation, TLR4 expression, NF-κB translocation to nucleus and its DNA binding activity, matrix metalloproteinase-9 activity, and expression of inflammatory mediators, including interleukin-1ß, interleukin-6, macrophage inflammatory protein-2, and cyclooxygenase-2. CONCLUSIONS/SIGNIFICANCE: Our results show that post-injury wogonin treatment improved long-term functional and histological outcomes, reduced brain edema, and attenuated the TLR4/NF-κB-mediated inflammatory response in mouse TBI. The neuroprotective effects of wogonin may be related to modulation of the TLR4/NF-κB signaling pathway.

Differential effects of concomitant use of vitamins C and E on trophoblast apoptosis and autophagy between normoxia and hypoxia-reoxygenation.

BACKGROUND: Concomitant supplementation of vitamins C and E during pregnancy has been reportedly associated with low birth weight, the premature rupture of membranes and fetal loss or perinatal death in women at risk for preeclampsia; however, the cause is unknown. We surmise that hypoxia-reoxygenation (HR) within the intervillous space due to abnormal placentation is the mechanism and hypothesize that concomitant administration of aforementioned vitamin antioxidants detrimentally affects trophoblast cells during HR. METHODOLOGY/PRINCIPAL FINDINGS: Using villous explants, concomitant administration of 50 microM of vitamins C and E was observed to reduce apoptotic and autophagic changes in the trophoblast layer at normoxia (8% oxygen) but to cause more prominent apoptosis and autophagy during HR. Furthermore, increased levels of Bcl-2 and Bcl-xL in association with a decrease in the autophagy-related protein LC3-II were noted in cytotrophoblastic cells treated with vitamins C and E under standard culture conditions. In contrast, vitamin treatment decreased Bcl-2 and Bcl-xL as well as increased mitochondrial Bak and cytosolic LC3-II in cytotrophoblasts subjected to HR. CONCLUSIONS/SIGNIFICANCE: Our results indicate that concomitant administration of vitamins C and E has differential effects on the changes of apoptosis, autophagy and the expression of Bcl-2 family of proteins in the trophoblasts between normoxia and HR. These changes may probably lead to the impairment of placental function and suboptimal growth of the fetus.