Population-based survey of complementary and alternative medicine usage, patient satisfaction, and physician involvement. South Carolina Complementary Medicine Program Baseline Research Team.

BACKGROUND: With an increasing proportion of Americans using complementary or alternative medicine (CAM), physicians need to know which patients are using CAM to effectively manage care. METHODS: In this cross-sectional study, telephone interviews were conducted with 1,584 South Carolina adults (ages 18 and older); 66% responded to the survey of demographics, general health, frequency of CAM use, perceived CAM effectiveness, and physician knowledge of CAM use. RESULTS: A total of 44% had used a CAM during the past year. Increasing age and higher education were significantly associated with CAM use. More than 60% perceived CAM therapy as very effective, and 89% said they would recommend CAM to others. Physicians were unaware of CAM use in 57% of their patients using CAM. CONCLUSION: Complementary or alternative medicine use in this rural Southern state is similar to national usage. Users view CAM as effective. Physicians are frequently unaware of patients' CAM use. More research is needed to establish CAM effectiveness and how CAM affects medical care, training, and public health.

Corticotropin-releasing hormone receptor (type I) antisense targeting reduces anxiety.

Two brain-derived corticotropin-releasing hormone receptors have been cloned, termed corticotropin-releasing hormone receptors type I and type 2. Antisense oligodeoxynucleotides targeted to the cloned rat and mouse corticotropin-releasing hormone receptors type I messenger RNA reduced the binding of the natural ligand of the corticotropin-releasing hormone receptors type I and also the release of adenocorticotrophic hormone in primary rat anterior pituitary cells and in clonal mouse pituitary cells (AtT-20) by up to 60% in an application time-dependent manner. Studies on intracellular uptake of fluorescence-labelled oligodeoxynucleotides indicated a cytoplasmic accumulation starting within two to four hours after application of oligodeoxynucleotides in vitro. In vivo, antisense oligodeoxynucleotides infused intra-cerebroventricularly reduced binding of radiolabelled corticotropin-releasing hormone receptors in central sites of the rat brain. Anxiety induced by i.c.v. administration of corticotropin-releasing hormone was attenuated by corticotropin-releasing hormone receptors type I antisense treatment as determined in the elevated plus maze and in the novel open field test. The corticotropin-releasing hormone-induced behavioural changes were absent in corticotropin-releasing hormone receptors type I antisense-pretreated animals. These results show that the selected antisense probes used were able to suppress corticotropin-releasing hormone receptors type I function in vitro as well as in vivo and suggest that the development of drugs blocking this specific receptor might lead to a novel class of anxiolytics.

Rat hypothalamus neuron-like cells in primary culture accumulate and translate mRNA coding for the amphibian P-domain peptide xP1.

1. Neurons seem to possess the intrinsic capability to incorporate and translate exogenous RNA. For further evaluation of this phenomenon, we wanted to study the uptake and processing capacity of rat hypothalamic neurons for species-unspecific heterologous cRNA under in vitro conditions. 2. cRNA coding for the amphibian p-domain peptide xP1 was prepared by in vitro transcription and added to the culture medium of rat hypothalamic cells, derived from E18 fetuses. 3. After 2 hr, a fraction of the hypothalamic neuron-like cells had accumulated the radiolabeled transcripts, as could be demonstrated by autoradiographic assessment. Specific immunostaining for xP1 could be demonstrated 18 hr after incubation with the cRNA. 4. Our findings indicate that hypothalamic neuron-like cells are capable of accumulating and translating nonmammalian transcripts. Since it was only a portion of hypothalamic cells that showed this effect, specific recognition sites for RNA may be presented by certain neurons, further supporting the assumption that binding, uptake, and translation of cRNA transcripts represent a general neural property which is malleable to functional status.

Human intestinal trefoil factor is expressed in human hypothalamus and pituitary: evidence for a novel neuropeptide.

Human intestinal trefoil factor, hITF, a secretory polypeptide found mainly in the human gastrointestinal tract, is a member of the newly characterized trefoil factor or P-domain peptide family representing putative growth factors. Here we describe the identification of this gut peptide in the human brain and pituitary. With reverse transcriptase polymerase chain reaction, we were able to isolate and clone the transcript from human hypothalamus. An antibody generated against a synthetic peptide derived from the carboxyl terminus of hITF was used for immunohistochemical studies of appropriate tissue sections. Neurons expressing hITF were identified in two magnocellular hypothalamic nuclei, the paraventricular and periventricular nuclei. hITF polypeptide was also observed in Herring bodies of the neurohypophysis and in secretory cells of the adenohypophysis. Double immunostaining with antigrowth hormone antibody showed partial coexistence in a selected subpopulation of adenohypophysial cells. Localization of hITF in the hypothalamo-neurohypophysial system may suggest a modulatory action on the classical magnocellular nonapeptides vasopressin and oxytocin, and further indicates an adenohypophysial importance of this peptide. It is likely that hITF represents a novel neuropeptide of yet unknown function.

Molecular and cellular analysis of rP1.B in the rat hypothalamus: in situ hybridization and immunohistochemistry of a new P-domain neuropeptide.

P-domain peptides, a new family of secretory polypeptides, have been identified mainly in the gastroenteropancreatic tract of humans, rodents, and amphibians as well as in amphibian skin. In the present study, with PCR and RNA analysis a transcript has been discovered in rat brain termed rP1.B. The deduced polypeptide consists of a single P-domain and its amino acid sequence matches that of rat intestinal trefoil factor (rITF). Thus far, rP1.B is the only P-domain peptide expressed in neuronal cells of the CNS. Immunostained magnocellular perikarya were visible in the paraventricular, supraoptic and periventricular nuclei. Parvocellular rP1.B neurons were found in the arcuate nucleus. Additionally, specific hybridization signals with radiolabeled transcripts were observed in the same regions. rP1.B in the rat hypothalamus may be involved in the control of hypothalamo-hypophysial functions.

c-fos mRNA is present in axons of the hypothalamo-neurohypophysial system of the rat.

In situ hybridization revealed that c-fos encoding transcripts occur in the median eminence of rats. Osmotic stress resulted within 15 min. in additional labeling of the magnocellular nuclei, while osmotically stimulated rats that had been pretreated with colchicine failed to show c-fos hybridization in the magnocellular perikarya. Rats, pretreated with a polymerase II inhibitor, showed 15 min. after osmotic stimulation c-fos hybridization in the hypothalamic nuclei, whereas the median eminence was depleted of hybridization signal. c-fos is probably among the transcripts, stored in axons of the hypothalamo-neurohypophysial system, to be transported retrogradly upon osmotic stimulation.

Corticotropin-releasing hormone (CRH) antisense oligodeoxynucleotide treatment attenuates social defeat-induced anxiety in rats.

1. The neuropeptide corticotropin-releasing hormone (CRH) is the main mediator of the neuroendocrine and behavioral response to stress. End-capped phosphorothioate antisense and sense oligodeoxynucleotides (ODN) corresponding to the start coding region of rat CRH mRNA were infused intracerebroventricularly (30 micrograms/3 microliters per injection) three times at 12 hr intervals. Six hours after the last injection rats were subjected to social defeat stress and subsequently tested on the elevated plus maze. 2. Socially defeated CRH antisense-treated rats displayed markedly reduced anxiety-related behavior, as they spent significantly more time in the open arms of the plus maze compared to sense ODN- and vehicle-treated animals. 3. In controls, social defeat evoked a stress-induced elevation of CRH mRNA and CRH in the hypothalamus and a significant increase in plasma corticotropin (ACTH) levels. These parameters were attenuated in antisense-injected rats. 4. Our results suggest that CRH antisense treatment is effectively suppressing the neuroendocrine and behavioral effects of social defeat.