Spontaneous Resolution of an Aggressive Direct Carotid Cavernous Fistula Following Partial Transvenous Embolization Treatment: A Case Report and Review of Literatures.

Traumatic direct type carotid cavernous fistula (CCF) is an acquired arteriovenous shunt between the carotid artery and the cavernous sinus post severe craniofacial trauma or iatrogenic injury. We reported a 46-year-old woman who had developed a traumatic direct type CCF after severe head trauma with a skull base fracture and brain contusion hemorrhage. The clinical manifestations of the patient included pulsatile exophthalmos, proptosis, bruits, chemosis, and a decline in consciousness.

NF-κB knockdown can modulate amphetamine-mediated feeding response.

This study determined if transcription factor NF-κB is involved in the effect of amphetamine (AMPH)-mediated feeding response. Moreover, possible roles of hypothalamic neuropeptide Y (NPY) and proopiomelanocortin (POMC) were also investigated. AMPH was administered daily to rats for four days.

Role of reactive oxygen species-related enzymes in neuropeptide y and proopiomelanocortin-mediated appetite control: a study using atypical protein kinase C knockdown.

Aims: Studies have reported that redox signaling in the hypothalamus participates in nutrient sensing. The current study aimed to determine if the activation of reactive oxygen species-related enzymes (ROS-RE) in the hypothalamus participates in regulating neuropeptide Y (NPY)-mediated eating. Moreover, possible roles of proopiomelanocortin (POMC) and atypical protein kinase C (aPKC) were also investigated.

Knocking down the transcript of protein kinase C-lambda modulates hypothalamic glutathione peroxidase, melanocortin receptor and neuropeptide Y gene expression in amphetamine-treated rats.

It has been reported that neuropeptide Y (NPY) contributes to the behavioral response of amphetamine (AMPH), a psychostimulant. The present study examined whether protein kinase C (PKC)-λ signaling was involved in this action. Moreover, possible roles of glutathione peroxidase (GP) and melanocortin receptor 4 (MC4R) were also examined.

The effect of protein kinase C-delta knockdown on anti-free radical enzyme and neuropeptide Y gene expression in phenylpropanolamine-treated rats.

Hypothalamic neuropeptide Y (NPY) has been reported to involve in regulating behavioral response of phenylpropanolamine (PPA), a sympathomimetic agent. This study explored if protein kinase C (PKC)-delta signaling participated in this regulation. Moreover, possible roles of anti-free radical enzyme catalase (CAT) and nitrogen oxide synthase (NOS) were also examined.

Amphetamine-evoked changes of oxidative stress and neuropeptide Y gene expression in hypothalamus: regulation by the protein kinase C-delta signaling.

Amphetamine (AMPH), a psychostimulant, is an appetite suppressant and may be regarded as a neurotoxin. It was reported that superoxide dismutase (SOD) and neuropeptide Y (NPY) participated in AMPH-mediated behavior response. However, molecular mechanisms underlying this action are not well known.

Roles of protein kinase Calpha isozyme in the regulation of oxidative stress and neuropeptide Y gene expression in phenylpropanolamine-mediated appetite suppression.

Hypothalamic neuropeptide Y (NPY) is an appetite stimulant in the brain. Although regulation of NPY expression has been reported to contribute to the appetite-suppressing effect of phenylpropanolamine (PPA), it is still unknown if protein kinase C (PKC) is involved in this effect. Rats were daily treated with PPA for 4 days.