Transcription factor NF-κB plays a central role in immunity from fruit flies to humans, and NF-κB activity is altered in many human diseases. To investigate a role for NF-κB in immunity and disease on a broader evolutionary scale we have characterized NF-κB in a sea anemone (Exaiptasia pallida; called Aiptasia herein) model for cnidarian symbiosis and dysbiosis (i.e., “bleaching”). We show that the DNA-binding site specificity of Aiptasia NF-κB is similar to NF-κB proteins from a broad expanse of organisms. Analyses of NF-κB and IκB kinase proteins from Aiptasia suggest that non-canonical NF-κB processing is an evolutionarily ancient pathway, which can be reconstituted in human cells. In Aiptasia, NF-κB protein levels, DNA-binding activity, and tissue expression increase when loss of the algal symbiont Symbiodinium is induced by heat or chemical treatment. Kinetic analysis of NF-κB levels following loss of symbiosis show that NF-κB levels increase only after Symbiodinium is cleared. Moreover, introduction of Symbiodinium into naïve Aiptasia larvae results in a decrease in NF-κB expression. Our results suggest that Symbiodinium suppresses NF-κB in order to enable establishment of symbiosis in Aiptasia. These results are the first to demonstrate a link between changes in the conserved immune regulatory protein NF-κB and cnidarian symbiotic status.

This study surveys Vietnamese refugees attending two psychiatric clinics to determine both the prevalence of panic disorder (PD) as well as panic attack subtypes in those suffering PD. A culturally valid adaptation of the SCID-panic module (the Vietnamese Panic Disorder Survey or VPDS) was administered to 100 Vietnamese refugees attending two psychiatric clinics. Utilizing culturally sensitive panic probes, the VPDS provides information regarding both the presence of PD and panic attack subtypes during the month prior to interview. Of 100 patients surveyed, 50 (50%) currently suffered PD. Among the 50 patients suffering PD, the most common panic attack subtypes during the previous month were the following: "orthostatic dizziness" (74% of the 50 panic disorder patients [PDPs]), headache (50% of PDPs), wind-induced/temperature-shift-induced (24% of PDPs), effortinduced (18% of PDPs), gastro-intestinal (16% of PDPs), micturition-induced (8% of PDPs), outof-the-blue palpitations (24% of PDPs), and out-of-the-blue shortness of breath (16% of PDPs). Five mechanisms are adduced to account for this high PD prevalence as well as the specific profile of subtypes: 1) a trauma-caused panic attack diathesis; 2) trauma-event cues; 3) ethnic differences in physiology; 4) catastrophic cognitions generated by cultural syndromes; and 5) a modification of Clark's spiral of panic.

Viewed historically and cross-culturally, orthostatic-induced dizziness, i.e., dizziness caused by standing up from a sitting or a lying position, forms a key aspect of many syndromes: irritable heart (American Civil War), effort syndrome (World War I and World War II), chronic fatigue syndrome (contemporary USA), Gulf War syndrome (contemporary USA), and orthostatic dysregulation (contemporary Japan). Among Vietnamese refugees attending a psychiatric clinic, this study documents a high rate of orthostatic panic (OP), as well as certain processes seemingly generating these panic attacks, viz., flashbacks and culturally specific catastrophic cognitions. Case examples are used to demonstrate OP's phenomenology and relevance to clinical care. To illustrate the mechanisms producing OP, we adduce the multiplex model of panic generation. Culturally appropriate care of Vietnamese refugees should include assessment and treatment of OP.

The purpose of this study was to compare toxicity rates and types between obese and non-obese women during adjuvant chemotherapy for breast cancer, adjusting for regimen type and received dose. We conducted a retrospective cohort study of 537 women receiving chemotherapy, initially treated between 2007 and 2010 at two tertiary hospitals in Brisbane, Australia. Demographic, chemotherapy and toxicity data were extracted from patient charts and analyzed using multivariate logistic regression. Three hundred and seventy-four women were eligible for inclusion. Obese women (body mass index (BMI) > 30 kg/m(2); mean age 52.58 ± 9.49) were older than non-obese women (BMI ≤ 29.9 kg/m(2); mean age 50.19 ± 11.15, P = 0.05) and had more comorbidities (P < 0.01). After adjustment for potential confounders, obesity was not statistically related to chemotherapy-related admission risk (OR 1.27; 95 % CI 0.78-2.09) or febrile neutropenia risk (OR 0.56; 95% CI 0.28-1.21). However, obese women received chemotherapy with proportionally lower mean relative dose intensity than non-obese women (94 vs. 97% of reference dose, P = 0.03). Eighteen (15.8%) obese and zero non-obese women (P < 0.01) had their chemotherapy dose capped at an arbitrary body surface area. Compared with non-obese women, obese women receive different chemotherapy regimens and relatively lower chemotherapy doses. There was no significant evidence of increased toxicity among obese women with either full or adjusted chemotherapy doses. Full body surface areas-based dosing appears to be tolerated as well in obese as in lean women.

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