Clinical psychology program #ubc #psychology, #ubc #psych, #psychology #ubc, #university #of #british

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Clinical

UBC s Graduate Program in Clinical Psychology s broad mission is to advance clinical science. We view clinical science as composed of research efforts and practice directed toward:

  1. The promotion of adaptive functioning
  2. Assessment, understanding, amelioration, and prevention of human problems in behaviour, affect, cognition or health
  3. The application of knowledge in ways consistent with scientific evidence

The program s emphasis on the term science underscores its commitment to empirical approaches to evaluating the validity and utility of testable hypotheses and to advancing knowledge and practice by this method.

The Doctoral Program in Clinical Psychology is accredited by the Canadian Psychological Association. If you are interested in more information about our accreditation status, contact the Director of Clinical Training (Lynn Alden ) or:

Initial accreditation 1986-87
Next site visit due 2015-16

As of 2012, CPA and APA signed the First Street Accord which is a mutual recognition agreement on accreditation. It demonstrates that the APA views the accreditation standards and principles of the CPA as equivalent to the Commission on Accreditation guidelines and principles. View the statement .

This webpage presents an overview of important information about the clinical program. To fully understand the Doctoral Program in Clinical Psychology at UBC, please read the material in all the links on this page and in the Graduate Student Handbook.





Dysmenorrhagia #psychology #wiki,psychology,dysmenorrhea,biological #psychology: #genetics,biological #psychology: #evolutionary #psychology,biological #psychology: #neuroanatomy,biological #psychology: #neurochemistry,biological

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Dysmenorrhea

Dysmenorrhea (or dysmenorrhoea ) is a medical condition characterized by severe uterine pain during menstruation. While many individuals experience minor pain during menstruation, dysmenorrhea is diagnosed when the pain is so severe as to limit normal activities, or require medication.

Dysmenorrhea can feature different kinds of pain, including sharp, throbbing, dull, nauseating, burning, or shooting pain. Dysmenorrhea may precede menstruation by several days or may accompany it, and it usually subsides as menstruation tapers off. Dysmenorrhea may coexist with excessively heavy blood loss, known as menorrhagia .

Secondary dysmenorrhea is diagnosed when symptoms are attributable to an underlying disease. disorder. or structural abnormality either within or outside the uterus. Primary dysmenorrhea is diagnosed when none of these are detected.

Contents

Primary dysmenorrhea Edit

Explanation Edit

During a woman’s menstrual cycle, the endometrium thickens in preparation for potential pregnancy. After ovulation. if the ovum is not fertilized and there is no pregnancy, the built-up uterine tissue is thus not needed.

Molecular compounds called prostaglandins are released. These compounds cause the muscles of the uterus to contract. When the uterine muscles contract, they constrict the blood supply to the tissue of the endometrium, which, in turn, breaks down and dies. These uterine contractions continue as they squeeze the old, dead endometrial tissue through the cervix and out of the body through the vagina. These contractions are responsible for the varying degrees of pain and discomfort commonly experienced during menstruation.

Signs and symptoms Edit

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The main symptom of dysmenorrhea is pain concentrated in the lower abdomen. in the umbilical region or the suprapubic region of the abdomen. It is also commonly felt in the right or left abdomen. It may radiate to the thighs and lower back. Other symptoms may include nausea and vomiting. diarrhea. headache. fainting. and fatigue. Symptoms of dysmenorrhea usually begin a few hours before the start of menstruation, and may continue for a few days.

Etiology Edit

Pathophysiology Edit

Prostaglandins are released during menstruation, due to the destruction of the endometrial cells, and the resultant release of their contents. [2] Release of prostaglandins and other inflammatory mediators in the uterus is thought to be a major factor in primary dysmenorrhea. [3] Females with primary dysmenorrhea have increased activity of the uterine muscle with increased contractility and increased frequency of contractions. [4]

Diagnosis Edit

In one research study using MRI. visible features of the uterus were compared in dysmenorrheic and eumenorrheic (normal) participants. The study concluded that in dysmenorrheic patients, visible features on cycle days 1-3 correlated with the degree of pain, and differed significantly from the control group. [5]

Treatments Edit

Nutritional Edit

Research indicates that one mechanism underlying dysmenorrhea is a disturbed balance between antiinflammatory. vasodilator eicosanoids derived from omega-3 fatty acids. and proinflammatory. vasoconstrictor eicosanoids derived from omega-6 fatty acids. [6] Several studies have indicated that intake of omega-3 fatty acids can reverse the symptoms of dysmenorrhea, by decreasing the amount of omega-6 FA in cell membranes. [7] [8] [9] The richest dietary source of omega-3 fatty acids is found in flax oil. [10]

Oral intake of magnesium has also been indicated in providing relief: two double-blind. placebo -controlled studies demonstrated a positive therapeutic effect of magnesium on dysmenorrhea. [11] [12] A randomized, double-blind, controlled trial demonstrated that oral intake of vitamin E relieves the pain of primary dysmenorrhea and reduces blood loss. [13] A review of case histories indicated that zinc. in 1 to 3 30-milligram doses given daily for one to four days prior to onset of menses, prevents essentially all to all warning of menses and all menstrual cramping. [14] Intake of thiamine (vitamin B1 ) was demonstrated to provide “curative” relief in 87% of females experiencing dysmenorrhea, in a controlled study. [15]

NSAIDs Edit

Non-steroidal anti-inflammatory drugs (NSAIDs) are effective in relieving the pain of primary dysmenorrhea. [16] NSAIDs can have side effects of nausea. dyspepsia. peptic ulcer. and diarrhea. [17] Patients who cannot take the more common NSAIDs, or for whom they are not effective, may be prescribed a COX-2 inhibitor. [18] One study indicated that conventional therapy with NSAIDs “provides symptomatic relief but has increasing adverse effects with long-term use”, [19] another indicated that long-term use of NSAIDs has “severe adverse effects”. [20]

Hormonal contraceptives Edit

Although use of hormonal contraception can improve or relieve symptoms of primary dysmenorrhea, [21] [22] a 2001 systematic review found that no conclusions can be made about the efficacy of commonly used modern lower dose combined oral contraceptive pills for primary dysmenorrhea. [23] Norplant [24] and Depo-provera [25] [26] are also effective, since these methods often induce amenorrhea. The IntraUterine System (Mirena IUD) has been cited as useful in reducing symptoms of dysmenorrhea. [27]

Non-drug therapies Edit

Several non-drug therapies for dysmenorrhea have been studied, including behavioral, acupuncture. acupressure. chiropractic care. and the use of a TENS unit.

Behavioral therapies assume that the physiological process underlying dysmenorrhea is influenced by environmental and psychological factors, and that dysmenorrhea can be effectively treated by physical and cognitive procedures that focus on coping strategies for the symptoms rather than on changes to the underlying processes. A 2007 systematic review found some scientific evidence that behavioral interventions may be effective, but that the results should be viewed with caution due to poor quality of the data. [28]

Acupuncture and acupressure are used to treat dysmenorrhea. A review cited four studies, two of which were patient-blind. indicating that acupuncture and acupressure were effective. [29] This review stated that the treatments appear “promising” for dysmenorrhea, and that the researchers considered further studies to be justified. Another study indicated that acupuncture “reduced the subjective perception of dysmenorrhea”, [30] still another indicated that adding acupuncture in patients with dysmenorrhea was associated with improvements in pain and quality of life. [31]

Although claims have been made for chiropractic care, under the theory that treating subluxations in the spine may decrease symptoms, [32] a 2006 systematic review found that overall no evidence suggests that spinal manipulation is effective for treatment of primary and secondary dysmenorrhea. [33]

Treatment with a transcutaneous electrical nerve stimulation (TENS) unit, often used for chronic pain. was indicated as effective in several studies. [34] [35] [36] [37] One study encouraged providers to try the TENS unit with patients, on the grounds that they found it to be “non-invasive. efficient, and easy to use”. [38] A study led by the same researchers reported proof of TENS’ effectiveness. [39]

Other medications and herbal therapies Edit

Other medications and herbal therapies have been studied in the treatment of dysmenorrhea. A 2008 systematic review found promising evidence for Chinese herbal medicine for primary dysmenorrhea, but that the evidence was limited by its poor methodological quality. [40] One study indicated that two Japanese herbal medicines provided all of the study participants with complete relief. [41] A review indicated the effectiveness of use of transdermal nitroglycerin. [42] A double-blind, controlled study indicated that treatment with an extract of guava leaf resulted in significant reduction of symptoms. [43] In a small double-blind. placebo -controlled study, guaifenesin reduced primary dysmenorrhea, but the effect was not significant. [44]

Hormonal treatments Edit

One study suggested that vasopressin antagonists with V1(a) selectivity might be useful in treating a variety of disorders, including dysmenorrhea. [45]

Prognosis Edit

A survey in Norway showed that 14 percent of females between the ages of 20 to 35 experience symptoms so severe that they stay home from school or work. [46] Among adolescent girls, dysmenorrhea is the leading cause of recurrent short-term school absence in this group. [47]

Epidemiology Edit

Reports of dysmenorrhea are greatest among individuals in their late teens and 20s, with reports usually declining with age. One study indicated that 67.2% of adolescent females experienced dysmenorrhea. [48] A study of Hispanic adolescent females indicated a high prevalence and impact in this group. [49] Another study indicated that dysmenorrhea was present in 36.4% of participants, and was significantly associated with lower age and lower parity. [50] Childbearing is said to relieve dysmenorrhea. One study indicated that in nulliparous women with primary dysmenorrhea, the severity of menstrual pain decreased significantly after age 40. [51] A questionnaire concluded that menstrual problems, including dysmenorrhea, were more common in females who had been sexually abused. [52]

Secondary dysmenorrhea Edit





Access: Strigolactone inhibition of shoot branching: Nature #nature, #science, #science #news, #biology,

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Strigolactone inhibition of shoot branching

Victoria Gomez-Roldan 1. Soraya Fermas 2. Philip B. Brewer 3. Virginie Puech-Pag s 1. Elizabeth A. Dun 3. Jean-Paul Pillot 2. Fabien Letisse 4. Radoslava Matusova 5. Saida Danoun 1. Jean-Charles Portais 4. Harro Bouwmeester 5. 6. Guillaume B card 1. Christine A. Beveridge 3. 7. 8. Catherine Rameau 2. 8 Soizic F. Rochange 1. 8

  1. Universit de Toulouse; UPS; CNRS; Surface Cellulaire et Signalisation chez les V g taux, 24 chemin de Borde Rouge, F-31326 Castanet-Tolosan, France
  2. Station de G n tique et d Am lioration des Plantes, Institut J. P. Bourgin, UR254 INRA, F-78000 Versailles, France
  3. ARC Centre of Excellence for Integrative Legume Research, The University of Queensland, Brisbane 4072, Australia
  4. CNRS, UMR5504, INRA, UMR792 Ing nierie des Syst mes Biologiques et des Proc d s, INSA de Toulouse, F-31400 Toulouse, France
  5. Plant Research International, PO Box 16, 6700 AA Wageningen, the Netherlands
  6. Laboratory of Plant Physiology, Wageningen University, Arboretumlaan 4, 6703 BD Wageningen, the Netherlands
  7. School of Integrative Biology, The University of Queensland, Brisbane 4072, Australia
  8. These authors contributed equally to this work.

Abstract

A carotenoid-derived hormonal signal that inhibits shoot branching in plants has long escaped identification. Strigolactones are compounds thought to be derived from carotenoids and are known to trigger the germination of parasitic plant seeds and stimulate symbiotic fungi. Here we present evidence that carotenoid cleavage dioxygenase 8 shoot branching mutants of pea are strigolactone deficient and that strigolactone application restores the wild-type branching phenotype to ccd8 mutants. Moreover, we show that other branching mutants previously characterized as lacking a response to the branching inhibition signal also lack strigolactone response, and are not deficient in strigolactones. These responses are conserved in Arabidopsis. In agreement with the expected properties of the hormonal signal, exogenous strigolactone can be transported in shoots and act at low concentrations. We suggest that endogenous strigolactones or related compounds inhibit shoot branching in plants. Furthermore, ccd8 mutants demonstrate the diverse effects of strigolactones in shoot branching, mycorrhizal symbiosis and parasitic weed interaction.

  1. Universit de Toulouse; UPS; CNRS; Surface Cellulaire et Signalisation chez les V g taux, 24 chemin de Borde Rouge, F-31326 Castanet-Tolosan, France
  2. Station de G n tique et d Am lioration des Plantes, Institut J. P. Bourgin, UR254 INRA, F-78000 Versailles, France
  3. ARC Centre of Excellence for Integrative Legume Research, The University of Queensland, Brisbane 4072, Australia
  4. CNRS, UMR5504, INRA, UMR792 Ing nierie des Syst mes Biologiques et des Proc d s, INSA de Toulouse, F-31400 Toulouse, France
  5. Plant Research International, PO Box 16, 6700 AA Wageningen, the Netherlands
  6. Laboratory of Plant Physiology, Wageningen University, Arboretumlaan 4, 6703 BD Wageningen, the Netherlands
  7. School of Integrative Biology, The University of Queensland, Brisbane 4072, Australia
  8. These authors contributed equally to this work.

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