January, 2005
Asthma:
11127.
Beier J, Beeh KM, Kornmann O, Buhl R. Induced sputum methodology:
Validity and reproducibility of total glutathione measurement in supernatant of
healthy and asthmatic individuals. J Lab Clin Med. 2004 Jul;144(1):38-44.
11128.
Mak JC, Leung HC, Ho SP, Law BK, Lam WK, Tsang KW, Ip MS, Chan-Yeung M.
Systemic oxidative and antioxidative status in Chinese patients with asthma. J
Allergy Clin Immunol. 2004 Aug;114(2):260-4.
Depression:
11129.
Aktas MK, Ozduran V, Pothier CE, Lang R, Lauer MS. Global risk scores and
exercise testing for predicting all-cause mortality in a preventive medicine
program. JAMA. 2004 Sep 22;292(12):1462-8.
11130.
Beck CT. Post-traumatic stress disorder due to childbirth: the aftermath.
Nurs Res. 2004 Jul-Aug;53(4):216-24.
11131.
Boscarino JA, Figley CR, Adams RE, Galea S, Resnick H, Fleischman AR,
Bucuvalas M, Gold J. Adverse reactions associated with studying persons recently
exposed to mass urban disaster. J Nerv Ment Dis. 2004 Aug;192(8):515-24.
11132.
Burton E, Stice E, Seeley JR. A prospective test of the stress-buffering
model of depression in adolescent girls: no support once again. J Consult Clin
Psychol. 2004 Aug;72(4):689-97.
11133.
Gilligan PJ, Li YW. Corticotropin-releasing factor antagonists: recent
advances and exciting prospects for the treatment of human diseases. Curr Opin
Drug Discov Devel. 2004 Jul;7(4):487-97. Review.
11134.
Kano M, Fukudo S, Tashiro A, Utsumi A, Tamura D, Itoh M, Iwata R, Tashiro
M, Mochizuki H, Funaki Y, Kato M, Hongo M, Yanai K. Decreased histamine H1
receptor binding in the brain of depressed patients. Eur J Neurosci. 2004
Aug;20(3):803-10.
11135.
Murakami Y, Okamura H, Sugano K, Yoshida T, Kazuma K, Akechi T, Uchitomi
Y. Psychologic distress after disclosure of genetic test results regarding
hereditary nonpolyposis colorectal carcinoma. Cancer. 2004 Jul
15;101(2):395-403.
11136.
Trask PC. Quality of life and emotional distress in advanced prostate
cancer survivors undergoing chemotherapy. Health Qual Life Outcomes. 2004 Jul
23;2(1):37. Review.
11137.
Vythilingam M, Vermetten E, Anderson GM, Luckenbaugh D, Anderson ER, Snow
J, Staib LH, Charney DS, Bremner JD. Hippocampal volume, memory, and cortisol
status in major depressive disorder: effects of treatment. Biol Psychiatry. 2004
Jul 15;56(2):101-12.
Hypertension:
11138.
Bountioukos M, Elhendy A, van Domburg RT, Schinkel AF, Bax JJ, Krenning
BJ, Biagini E, Rizzello V, Simoons ML, Poldermans D. Prognostic value of
dobutamine stress echocardiography in patients with previous coronary
revascularisation. Heart. 2004 Sep;90(9):1031-5.
11139.
Cook S, Hugli O, Egli M, Menard B, Thalmann S, Sartori C, Perrin C, Nicod
P, Thorens B, Vollenweider P, Scherrer U, Burcelin R. Partial gene deletion of
endothelial nitric oxide synthase predisposes to exaggerated high-fat
diet-induced insulin resistance and arterial hypertension. Diabetes. 2004
Aug;53(8):2067-72.
11140.
Mehra MR, Uber PA, Potluri S, Ventura HO, Scott RL, Park MH. Usefulness
of an elevated B-type natriuretic peptide to predict allograft failure, cardiac
allograft vasculopathy, and survival after heart transplantation. Am J Cardiol.
2004 Aug 15;94(4):454-8.
11141.
Uzun H, Karter Y, Aydin S, Curgunlu A, Simsek G, Yucel R, Vehiyd S,
Erturk N, Kutlu A, Benian A, Yaldiran A, Ozturk E, Erdine S. Oxidative stress in
white coat hypertension; role of paraoxonase. J Hum Hypertens. 2004
Jul;18(7):523-8.
April, 2005
Some Selected Abstracts: | |
1. |
Cohen JA, Mannarino AP, Knudsen K. Treating childhood
traumatic grief: a pilot study. J Am Acad Child Adolesc Psychiatry. 2004
Oct;43(10):1225-33. Drexel University College of Medicine, Allegheny General Hospital,
Pittsburgh 15212, USA. jcohen@wpahs.org OBJECTIVE: To examine the potential efficacy and specific timing of
treatment response of individual child and parent trauma-focused
cognitive-behavioral therapy for childhood traumatic grief (CTG), a
condition in which trauma symptoms impinge on the child's ability to
successfully address the normal tasks of grieving. METHOD: Twenty-two
children and their primary caretakers received a manual-based 16-week
treatment with sequential trauma- and grief-focused interventions.
RESULTS: Children experienced significant improvements in CTG,
posttraumatic stress disorder (PTSD), depressive, anxiety, and behavioral
problems, with PTSD symptoms improving only during the trauma-focused
treatment components and CTG improving during both trauma- and
grief-focused components. Participating parents also experienced
significant improvement in PTSD and depressive symptoms. CONCLUSIONS: The
timing of improvements in CTG and PTSD symptoms lends support to providing
sequential trauma- and grief-focused interventions and to the concept that
CTG is related to but distinct from PTSD. The results also suggest the
benefit of individual treatment for CTG and for including parents in the
treatment of CTG. Randomized, controlled trials are needed to further test
the efficacy of this treatment model. |
2. |
Highet NJ, McNair BG, Davenport TA, Hickie IB. How much more
can we lose?": carer and family perspectives on living with a person
with depression. Med J Aust. 2004 Oct 4;181(7 Suppl):S6-9. OBJECTIVE: To explore the experiences of carers and families of people with depression. DESIGN AND SETTING: Structured focus groups conducted in six Australian capital cities between February 2002 and July 2002. Thematic analyses were conducted using the QSR NUD*IST software package for qualitative data. PARTICIPANTS: Thirty-seven carers or family members. RESULTS: Thematic analyses highlighted five key themes. Most notably, the carer's role is made more difficult by the lack of community awareness about depression, and, in some instances, an unwillingness of other family and friends to provide ongoing support. Carers experience a resulting sense of isolation, often exacerbated by adverse experiences with healthcare providers. Carers and family members are frequently excluded when key decisions are made, and report that emergency services are relatively unresponsive to their concerns. By contrast, community support organisations usually provided a sense of inclusion and common purpose. CONCLUSIONS: The experiences of carers and families of people with depression highlight the urgent need for more extensive community education about the illness and more productive collaboration within the healthcare system. |
3. |
Myers MF. Medical marriages and other intimate relationships.
Med J Aust. 2004 Oct 4;181(7):392-4. |
4. |
Verma S, Szmitko PE, Anderson TJ. Endothelial function: ready
for prime time? Can J Cardiol. 2004 Nov;20(13):1335-9. Division of Cardiac Surgery, University of Toronto, Toronto, Canada.
Subodh.Verma@Sympatico.ca The strategic location of the endothelium allows it to detect changes in hemodynamic forces and blood-borne signals, and to respond by releasing a number of autocrine and paracrine substances. The balanced release of these bioactive factors facilitates vascular homeostasis. If disrupted, endothelial cell dysfunction ensues. This predisposes the vessel wall to vasoconstriction, leukocyte adherence, platelet activation, thrombosis, vascular inflammation and atherosclerosis. Given the central role of the endothelium in the development and progression of atherosclerosis, endothelial function testing may serve as a useful biomarker of atherosclerotic disease. The present review highlights the current modalities used in assessing endothelial function, explores how endothelial function may serve as a biomarker for atherosclerosis, comments on the prognostic relevance of endothelial function and describes its use in the clinical setting. |
5. |
Verma S, Szmitko PE, Anderson TJ. Endothelial function: ready
for prime time? Can J Cardiol. 2004 Nov;20(13):1335-9. Division of Cardiac Surgery, University of Toronto, Toronto, Canada.
Subodh.Verma@Sympatico.ca The strategic location of the endothelium allows it to detect changes in hemodynamic forces and blood-borne signals, and to respond by releasing a number of autocrine and paracrine substances. The balanced release of these bioactive factors facilitates vascular homeostasis. If disrupted, endothelial cell dysfunction ensues. This predisposes the vessel wall to vasoconstriction, leukocyte adherence, platelet activation, thrombosis, vascular inflammation and atherosclerosis. Given the central role of the endothelium in the development and progression of atherosclerosis, endothelial function testing may serve as a useful biomarker of atherosclerotic disease. The present review highlights the current modalities used in assessing endothelial function, explores how endothelial function may serve as a biomarker for atherosclerosis, comments on the prognostic relevance of endothelial function and describes its use in the clinical setting. |
Asthma: |
11733.
Bender
BG, Annett RD, Strunk RC. Retrospective and prospective parental reports
of sleep in children with asthma. J Allergy Clin Immunol. 2004
Oct;114(4):985-8. |
Depression: |
11734.
Ben-Ezra
M, Essar N. Depression and anxiety in developing countries. Lancet. 2004
Oct 23;364(9444):1488. 11735.
Cohen
JA, Mannarino AP, Knudsen K. Treating childhood traumatic grief: a pilot
study. J Am Acad Child Adolesc Psychiatry. 2004 Oct;43(10):1225-33. 11736.
Girod
JP, Brotman DJ. Does altered glucocorticoid homeostasis increase
cardiovascular risk? Cardiovasc Res. 2004 Nov 1;64(2):217-26. Review. 11737.
Gross
D, Fogg L, Garvey C, Julion W. Behavior problems in young children: an
analysis of cross-informant agreements and disagreements. Res Nurs
Health. 2004 Dec;27(6):413-25. 11738.
Highet
NJ, McNair BG, Davenport TA, Hickie IB. How much more can we
lose?": carer and family perspectives on living with a person with
depression. Med J Aust. 2004 Oct 4;181(7 Suppl):S6-9. 11739.
Luby
JL, Mrakotsky C, Heffelfinger A, Brown K, Spitznagel E. Characteristics
of depressed preschoolers with and without anhedonia: evidence for a
melancholic depressive subtype in young children. Am J Psychiatry. 2004
Nov;161(11):1998-2004. 11740.
Myers
MF. Medical marriages and other intimate relationships. Med J Aust. 2004
Oct 4;181(7):392-4. 11741.
Sala
M, Perez J, Soloff P, Ucelli di Nemi S, Caverzasi E, Soares JC,
Brambilla P. Stress and hippocampal abnormalities in psychiatric
disorders. Eur Neuropsychopharmacol. 2004 Oct;14(5):393-405. Review. 11742.
Sjostrom
H, Langius-Eklof A, Hjertberg R. Well-being and sense of coherence
during pregnancy. Acta Obstet Gynecol Scand. 2004 Dec;83(12):1112-8. 11743.
Visser
A, Huizinga GA, van der Graaf WT, Hoekstra HJ, Hoekstra-Weebers JE. The
impact of parental cancer on children and the family: a review of the
literature. Cancer Treat Rev. 2004 Dec;30(8):683-94. Review. 11744.
Zimmerman
M, Chelminski I, Young D. On the threshold of disorder: a study of the
impact of the DSM-IV clinical significance criterion on diagnosing
depressive and anxiety disorders in clinical practice. J Clin
Psychiatry. 2004 Oct;65(10):1400-5. |
Heart Disease: |
11745.
Chesebro
JH. Acute coronary syndromes: pathogenesis, acute diagnosis with risk
stratification, and treatment. Am Heart Hosp J. 2004 Fall;2(4 Suppl
1):21-30. Review. 11746.
Ellestad
MH. Stress testing: Problems and appropriate use in acute coronary
syndromes. Am J Cardiol. 2004 Dec 15;94(12):1534-6. 11747.
Kojda
G. Direct vasoprotection by aspirin: a significant bonus to antiplatelet
activity? Cardiovasc Res. 2004 Nov 1;64(2):192-4. 11748.
Macleod
J, Smith GD. Re: "does job strain increase the risk for coronary
heart disease or death in men and women? The Framingham offspring
study". Am J Epidemiol. 2004 Nov 15;160(10):1031-2; author reply
1032. 11749.
Scarabelli
T, Knight R. Urocortins: take them to heart. Curr Med Chem Cardiovasc
Hematol Agents. 2004 Oct;2(4):335-342. Review. 11750.
Verma
S, Szmitko PE, Anderson TJ. Endothelial function: ready for prime time?
Can J Cardiol. 2004 Nov;20(13):1335-9. Review. 11751.
Wang
G, Mao JM, Wang X, Zhang FC. Effect of homocysteine on plaque formation
and oxidative stress in patients with acute coronary syndromes. Chin Med
J (Engl). 2004 Nov;117(11):1650-4. |
Hypertension: |
11752.
Seckl
JR. Prenatal glucocorticoids and long-term programming. Eur J Endocrinol.
2004 Nov;151 Suppl 3:U49-62. Review. 11753.
Vanderheyden
M, Goethals M, Verstreken S, De Bruyne B, Muller K, Van Schuerbeeck E,
Bartunek J. Wall stress modulates brain natriuretic peptide production
in pressure overload cardiomyopathy. J Am Coll Cardiol. 2004 Dec
21;44(12):2349-54. |
July, 2005
Some Selected Abstracts: | |
1. |
Jammes Y, Steinberg JG,
Mambrini O, Bregeon F, Delliaux S. Chronic fatigue syndrome:
assessment of increased oxidative stress and altered muscle excitability
in response to incremental exercise. J Intern Med. 2005 Mar;257(3):299-310. Laboratoire de Physiopathologie Respiratoire (UPRES EA 2201),
Faculte de Medecine, Institut Federatif de Recherche Jean Roche,
Marseille, France. jammes.y@jean-roche.univ-mrs.fr OBJECTIVES:
Because the muscle response to incremental exercise is not well documented
in patients suffering from chronic fatigue syndrome (CFS), we combined
electrophysiological (compound-evoked muscle action potential, M wave),
and biochemical (lactic acid production, oxidative stress) measurements to
assess any muscle dysfunction in response to a routine cycling exercise.
DESIGN: This case-control study compared 15 CFS patients to a gender-,
age- and weight-matched control group (n=11) of healthy subjects.
INTERVENTIONS: All subjects performed an incremental cycling exercise
continued until exhaustion. MAIN OUTCOME MEASURES: We measured the oxygen
uptake (VO2), heart rate (HR), systemic blood pressure, percutaneous O2
saturation (SpO2), M-wave recording from vastus lateralis, and venous
blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid
(LA), and three markers of the oxidative stress (thiobarbituric
acid-reactive substances, TBARS, reduced glutathione, GSH, and ascorbic
acid, RAA). RESULTS: Compared with control, in CFS patients (i) the slope
of VO2 versus work load relationship did not differ from control subjects
and there was a tendency for an accentuated PvO2 fall at the same exercise
intensity, indicating an increased oxygen uptake by the exercising
muscles; (ii) the HR and blood pressure responses to exercise did not
vary; (iii) the anaerobic pathways were not accentuated; (iv) the
exercise-induced oxidative stress was enhanced with early changes in TBARS
and RAA and enhanced maximal RAA consumption; and (v) the M-wave duration
markedly increased during the recovery period. CONCLUSIONS: The response
of CFS patients to incremental exercise associates a lengthened and
accentuated oxidative stress together with marked alterations of the
muscle membrane excitability. These two objective signs of muscle
dysfunction are sufficient to explain muscle pain and postexertional
malaise reported by our patients. |
2. |
Jammes Y, Steinberg JG,
Mambrini O, Bregeon F, Delliaux S. Chronic fatigue syndrome:
assessment of increased oxidative stress and altered muscle excitability
in response to incremental exercise. J Intern Med. 2005 Mar;257(3):299-310. Laboratoire de Physiopathologie Respiratoire (UPRES EA 2201),
Faculte de Medecine, Institut Federatif de Recherche Jean Roche,
Marseille, France. jammes.y@jean-roche.univ-mrs.fr OBJECTIVES:
Because the muscle response to incremental exercise is not well documented
in patients suffering from chronic fatigue syndrome (CFS), we combined
electrophysiological (compound-evoked muscle action potential, M wave),
and biochemical (lactic acid production, oxidative stress) measurements to
assess any muscle dysfunction in response to a routine cycling exercise.
DESIGN: This case-control study compared 15 CFS patients to a gender-,
age- and weight-matched control group (n=11) of healthy subjects.
INTERVENTIONS: All subjects performed an incremental cycling exercise
continued until exhaustion. MAIN OUTCOME MEASURES: We measured the oxygen
uptake (VO2), heart rate (HR), systemic blood pressure, percutaneous O2
saturation (SpO2), M-wave recording from vastus lateralis, and venous
blood sampling allowing measurements of pH (pHv), PO2 (PvO2), lactic acid
(LA), and three markers of the oxidative stress (thiobarbituric
acid-reactive substances, TBARS, reduced glutathione, GSH, and ascorbic
acid, RAA). RESULTS: Compared with control, in CFS patients (i) the slope
of VO2 versus work load relationship did not differ from control subjects
and there was a tendency for an accentuated PvO2 fall at the same exercise
intensity, indicating an increased oxygen uptake by the exercising
muscles; (ii) the HR and blood pressure responses to exercise did not
vary; (iii) the anaerobic pathways were not accentuated; (iv) the
exercise-induced oxidative stress was enhanced with early changes in TBARS
and RAA and enhanced maximal RAA consumption; and (v) the M-wave duration
markedly increased during the recovery period. CONCLUSIONS: The response
of CFS patients to incremental exercise associates a lengthened and
accentuated oxidative stress together with marked alterations of the
muscle membrane excitability. These two objective signs of muscle
dysfunction are sufficient to explain muscle pain and postexertional
malaise reported by our patients. |
3. |
Nutt DJ.
Overview of diagnosis and drug treatments of anxiety disorders.
CNS Spectr. 2005 Jan;10(1):49-56. Psychopharmacology
Unit, University of Bristol, Bristol, UK. david.j.nutt@bristol.ac.uk Anxiety
disorders are common and often disabling. They fall into five main categories:
panic disorder, social anxiety disorder, generalized anxiety disorder,
obsessive-compulsive disorder and posttraumatic stress disorder,
each of which have characteristic symptoms and cognitions. All anxiety
disorders respond to drugs and psychological treatments. This review will
focus on drug treatments. Recent research has emphasized the value of
antidepressants especially the selective serotonin reuptake inhibitors,
benzodiazepines, and related sedative-like compounds. The common
co-existence of depression with all of the anxiety disorders means that
the selective serotonin reuptake inhibitors are now generally considered
to be the first-line treatments but the benzodiazepines have some utility
especially in promoting sleep and working acutely to reduce extreme
distress. |
Asthma: |
12241. Bloomberg GR, Chen E. The relationship of psychologic stress with childhood asthma. Immunol Allergy Clin North Am. 2005 Feb;25(1):83-105. Review. |
Biochemical Indicators: |
|
Depression: |
|
Heart Disease: |
|
Hypertension: |
|
October, 2005
Some Selected Abstracts: | |
1. |
Karasz A Cultural differences in conceptual models of depression. Soc Sci Med. 2005 Apr;60(7):1625-35. Department of Family Medicine and Community Health, Albert Einstein College of Medicine, 3544 Jerome Avenue, Bronx, NY 10467, USA. akkarasz@montefiore.org Members of ethnic minority groups are less likely than white middle class people to seek professional treatment for depression and other mental health problems. One explanation is that the former conceptualize depressive symptoms as social problems or emotional reactions to situations, while the latter are more apt to view depression as a disease requiring professional treatment. Though considerable evidence supports this hypothesis, it is rarely explored directly through cross-cultural comparisons. The present study compares conceptual models of depressive symptoms in two diverse cultural groups in New York City (USA): 36 South Asian (SA) immigrants and 37 European Americans (EA) were presented with a vignette describing depressive symptoms and participated in a semi-structured interview designed to elicit representational models of the symptoms. Results indicate pervasive differences in representational models across the two groups. SA participants identified the "problem" in the vignette in largely social and moral terms. Suggestions for management and health seeking in this group emphasized self-management and lay referral strategies. EAs, by contrast, often proposed alternate, sometimes contradictory, explanatory models for the depressive symptoms. One model emphasized biological explanations ranging from "hormonal imbalance" to "neurological problem." The second model resembled the "situational stress" or "life problem" model described by SAs. The implications of these findings, and directions for future research, are discussed. |
2. |
Kash KM, Mago R, Kunkel EJ. Psychosocial oncology: supportive care for the cancer patient. Semin Oncol. 2005 Apr;32(2):211-8. Department of Psychiatry and Human Behavior, Thomas Jefferson University, Philadelphia, PA 19107, USA. kathryn.kash@jefferson.edu Increasing attention is being paid to the emotional and psychosocial needs of cancer patients. As a result of huge advances in early detection and in treatment modalities, there now are millions of cancer survivors in the United States. There has been a realization that cancer survivors have distinct psychosocial needs. As cancer survivors live longer, reduction of psychological distress has been recognized as being an important part of having an improved quality of life. There have been numerous changes in the field of psychosocial oncology since it first began 25 years ago. Guidelines now exist for the definition of distress and decision trees are available for making the appropriate referrals. Advances in pharmacologic treatment for depression and anxiety have made it possible to decrease distress and increase coping in cancer patients undergoing treatment as well as in cancer survivors. Numerous individual and group therapies have demonstrated effectiveness in improving mood and quality of life in cancer patients and those at high risk for developing cancer. Due to the forthright efforts of cancer patients, there are now many organizations and list serves (e-mailing lists) that cancer survivors can turn to for help before, during, and after cancer treatment. Finally, with the rapid expansion of the internet not only are there websites available as resources, but also the creation of interactive online support is becoming a reality. One of the most important issues in providing supportive care to cancer patients in the future is to meet the individual needs of patients and provide the type of psychological therapy that will work best for them. |
3. |
Laifenfeld D, Karry R, Klein E, Ben-Shachar D Alterations in cell adhesion molecule L1 and functionally related genes in major depression: a postmortem study. Biol Psychiatry. 2005 Apr 1;57(7):716-25. Laboratory of Psychobiology, The Department of Psychiatry, Rambam Medical Center, and B. Rappaport Faculty of Medicine, Technion IIT, Haifa, Israel. BACKGROUND: Current research in depression aims to delineate genes involved in neuronal plasticity that are altered in the disease or its treatment. We have shown antidepressant induced increases in three interrelated genes, cell adhesion molecule L1 (CAM-L1), laminin, and cAMP response element binding protein (CREB), and a reciprocal decrease in these genes consequent to stress. Presently we hypothesized that CAM-L1, CREB, and laminin may be altered in post mortem brains of depressed subjects. METHODS: Studies were performed in the prefrontal and in the ventral parieto-occipital cortices, of 59 brains from depressed, bipolar, and schizophrenic subjects, and normal controls, obtained from the Stanley Foundation Brain Collection. mRNA and protein levels were determined by RT-PCR and Western blot analysis, respectively. RESULTS: Levels of CAM-L1 and of phosphorylated CREB (pCREB) were increased in the prefrontal cortex of the depressed group, while CAM-L1, laminin and pCREB were decreased in the parieto-occipital cortex. Depressed subjects receiving antidepressants differed from subjects not receiving antidepressants in the expression of CAM-L1 and laminin in the parieto-occipital cortex, and in the expression of pCREB in the prefrontal cortex. CONCLUSIONS: The present findings of specific alterations in depression and antidepressant treatment particularly in CAM-L1 suggest that this gene may play an important role in the pathophysiology and treatment of depression. |
4. |
Plante
GE Depression and cardiovascular disease: a reciprocal relationship.
Metabolism. 2005 May;54(5 Suppl 1):45-8. Department
of Medicine (Nephrology), Institute of Geriatrics, University of
Sherbrooke, Quebec, Canada. gerard.e.plante@usherbrooke.ca. Until relatively recently, depression has been considered a purely "mental" disorder and therefore in the natural domain of psychologists and psychiatrists. However, recent epidemiological studies have revealed that aging, physical and psychological stress, chronic pain, several metabolic disorders such as insulin resistance and established diabetes, alcoholism, inflammatory conditions, and vascular disorders such as arterial hypertension all may be associated with depression. The present review examines some of these depression-associated factors and the mechanisms by which they might give rise to vascular disorders such as atherosclerosis, microcirculation endothelial dysfunction, and interstitial disturbances leading to organ damage. A number of disorders involving the circulation can lead progressively and insidiously to large artery rigidity, remodeling of peripheral arteries, and alterations of the microcirculation of large blood vessels. Perturbations in vasa vasorum blood flow may contribute to atherogenesis, in addition to the influence of numerous cellular events involved in inflammation (tumor necrosis factor alpha, interleukin 1 beta, etc). Since Hans Selye first described the neuroendocrine cascade generated by experimentally induced stress half a century ago, phenomena such as the axonal release of neurotransmitters (including serotonin), accumulation of metabolites such as homocysteine, platelet-activating factor, and nitric oxide also have been implicated in the pathogenesis of depression. Moreover, vascular consequences of depression such as heart rate and pulse pressure variations may lead to endothelial dysfunction in critical microcirculation networks (cerebral, myocardial, and renal) and initiate physicochemical alterations in interstitial compartments adjacent to vital organs. The appropriate use of ambulatory monitoring of vascular parameters, such as heart rate and pulse pressure, and eventually, early identification of genetic and metabolic markers may prove helpful in the early detection of events preceding and predicting the clinical manifestations of depression. |
5. |
Schneider
RH, Alexander CN, Staggers F, Rainforth M, Salerno JW, Hartz A, Arndt S,
Barnes VA, Nidich SI. Long-term effects of stress reduction on mortality in persons
> or = 55 years of age with systemic hypertension.
Am J Cardiol. 2005 May 1;95(9):1060-4 Institute
for Natural Medicine and Prevention, Maharishi University of Management,
Fairfield, Iowa, USA. rschneider@mum.edu Psychosocial
stress contributes to high blood pressure and subsequent cardiovascular
morbidity and mortality. Previous controlled studies have associated
decreasing stress with the Transcendental Meditation (TM) program with
lower blood pressure. The objective of the present study was to evaluate,
over the long term, all-cause and cause-specific mortality in older
subjects who had high blood pressure and who participated in randomized
controlled trials that included the TM program and other behavioral
stress-decreasing interventions. Patient data were pooled from 2 published
randomized controlled trials that compared TM, other behavioral
interventions, and usual therapy for high blood pressure. There were 202
subjects, including 77 whites (mean age 81 years) and 125 African-American
(mean age 66 years) men and women. In these studies, average baseline
blood pressure was in the prehypertensive or stage I hypertension range.
Follow-up of vital status and cause of death over a maximum of 18.8 years
was determined from the National Death Index. Survival analysis was used
to compare intervention groups on mortality rates after adjusting for
study location. Mean follow-up was 7.6 +/- 3.5 years. Compared with
combined controls, the TM group showed a 23% decrease in the primary
outcome of all-cause mortality after maximum follow-up (relative risk
0.77, p = 0.039). Secondary analyses showed a 30% decrease in the rate of
cardiovascular mortality (relative risk 0.70, p = 0.045) and a 49%
decrease in the rate of mortality due to cancer (relative risk 0.49, p =
0.16) in the TM group compared with combined controls. These results
suggest that a specific stress-decreasing approach used in the prevention
and control of high blood pressure, such as the TM program, may contribute
to decreased mortality from all causes and cardiovascular disease in older
subjects who have systemic hypertension. |
Asthma: |
12925. Fedorov IA, Wilson SJ, Davies DE, Holgate ST. Epithelial stress and structural remodelling in childhood asthma. Thorax. 2005 May;60(5):389-94. 12926. Nel A. Atmosphere. Air pollution-related illness: effects of particles. Science. 2005. May 6;308(5723):804-6. |
Depression: |
12927. Adewuya AO, Ola BA. Prevalence of and risk factors for anxiety and depressive disorders in Nigerian adolescents with epilepsy. Epilepsy Behav. 2005 May;6(3):342-7. 12928. Azoulay E, Pochard F, Kentish-Barnes N, Chevret S, Aboab J, Adrie C, Annane D, Bleichner G, Bollaert PE, Darmon M, Fassier T, Galliot R, Garrouste-Orgeas M, Goulenok C, Goldgran-Toledano D, Hayon J, Jourdain M, Kaidomar M, Laplace C, Larche J, Liotier J, Papazian L, Poisson C, Reignier J, Saidi F, Schlemmer B; FAMIREA Study Group. Risk of post-traumatic stress symptoms in family members of intensive care unit patients. Am J Respir Crit Care Med. 2005 May 1;171(9):987-94. 12929. Birkeland R, Thompson JK, Phares V. Adolescent motherhood and postpartum depression. J Clin Child Adolesc Psychol. 2005 Jun;34(2):292-300. 12930. Blumenthal JA, Sherwood A, Babyak MA, Watkins LL, Waugh R, Georgiades A, Bacon SL, Hayano J, Coleman RE, Hinderliter A. Effects of exercise and stress management training on markers of cardiovascular risk in patients with ischemic heart disease: a randomized controlled trial. JAMA. 2005 Apr 6;293(13):1626-34. 12931. Chandra PS, Desai G, Ranjan S. HIV & psychiatric disorders. Indian J Med Res. 2005 Apr;121(4):451-67. Review. 12932. Dahlin M, Joneborg N, Runeson B. Stress and depression among medical students: a cross-sectional study. Med Educ. 2005 Jun;39(6):594-604. 12933. Davies V, Gledhill J, McFadyen A, Whitlow B, Economides D. Psychological outcome in women undergoing termination of pregnancy for ultrasound-detected fetal anomaly in the first and second trimesters: a pilot study. Ultrasound Obstet Gynecol. 2005 Apr;25(4):389-92. 12934. de Kloet ER, Sibug RM, Helmerhorst FM, Schmidt M. Stress, genes and the mechanism of programming the brain for later life. Neurosci Biobehav Rev. 2005 Apr;29(2):271-81. 12935. Furlan PM, Ten Have T, Cary M, Zemel B, Wehrli F, Katz IR, Gettes DR, Evans DL. The role of stress-induced cortisol in the relationship between depression and decreased bone mineral density. Biol Psychiatry. 2005 Apr 15;57(8):911-7. 12936. Hamet P, Tremblay J. Genetics and genomics of depression. Metabolism. 2005 May;54(5 Suppl 1):10-5. Review. 12937. Holtzheimer PE 3rd, Russo J, Zatzick D, Bundy C, Roy-Byrne PP. The impact of comorbid posttraumatic stress disorder on short-term clinical outcome in hospitalized patients with depression. Am J Psychiatry. 2005 May;162(5):970-6. 12938. Horowitz JA, Damato EG, Duffy ME, Solon L. The relationship of maternal attributes, resources, and perceptions of postpartum experiences to depression. Res Nurs Health. 2005 Apr;28(2):159-71. 12939. Jacobsen PB, Donovan KA, Trask PC, Fleishman SB, Zabora J, Baker F, Holland JC. Screening for psychologic distress in ambulatory cancer patients. Cancer. 2005 Apr 1;103(7):1494-502. 12940. Karasz A. Cultural differences in conceptual models of depression. Soc Sci Med. 2005 Apr;60(7):1625-35. 12941. Kash KM, Mago R, Kunkel EJ. Psychosocial oncology: supportive care for the cancer patient. Semin Oncol. 2005 Apr;32(2):211-8. Review. 12942. Katerndahl D, Burge S, Kellogg N. Predictors of development of adult psychopathology in female victims of childhood sexual abuse. J Nerv Ment Dis. 2005 Apr;193(4):258-64. 12943. Laifenfeld D, Karry R, Klein E, Ben-Shachar D. Alterations in cell adhesion molecule L1 and functionally related genes in major depression: a postmortem study. Biol Psychiatry. 2005 Apr 1;57(7):716-25. 12944. McEwen BS. Glucocorticoids, depression, and mood disorders: structural remodeling in the brain. Metabolism. 2005 May;54(5 Suppl 1):20-3. Review. 12945. Miyaoka T, Yasukawa R, Yasuda H, Shimizu M, Mizuno S, Sukegawa T, Inagaki T, Horiguchi J. Urinary excretion of biopyrrins, oxidative metabolites of bilirubin, increases in patients with psychiatric disorders. Eur Neuropsychopharmacol. 2005 May;15(3):249-52. 12946. Monroe SM, Harkness KL. Life stress, the "kindling" hypothesis, and the recurrence of depression: considerations from a life stress perspective. Psychol Rev. 2005 Apr;112(2):417-45. Review. 12947. Noble RE. Depression in women. Metabolism. 2005 May;54(5 Suppl 1):49-52. Review. 12948. Plante GE. Depression and cardiovascular disease: a reciprocal relationship. Metabolism. 2005 May;54(5 Suppl 1):45-8. Review. 12949. Steptoe A, Whitehead DL. Depression, stress, and coronary heart disease: the need for more complex models. Heart. 2005 Apr;91(4):419-20. 12950. Wurtman RJ. Genes, stress, and depression. Metabolism. 2005 May;54(5 Suppl 1):16-9. Review. |
Heart Disease: |
12952.
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French D, Maissi E, Marteau TM.
The purpose of attributing cause: beliefs about the causes of
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Friedman E. Neurobiology of managing perceived stress. J Natl Med
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Petix NR, Sestini S, Coppola A, Marcucci G, Nassi F, Taiti A,
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SPECT myocardial perfusion imaging in patients with suspected or known
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Sanfilippo AJ, Abdollah H, Knott TC, Link C, Hopman W. Stress
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stress testing. Can J Cardiol. 2005 Apr;21(5):405-12. |
Hypertension: |
12958. Hogue CJ, Bremner JD. Stress model for research into preterm delivery among black women. Am J Obstet Gynecol. 2005 May;192(5 Suppl):S47-55. Review. 12959. Schneider RH, Alexander CN, Staggers F, Rainforth M, Salerno JW, Hartz A, Arndt S, Barnes VA, Nidich SI. Long-term effects of stress reduction on mortality in persons > or = 55 years of age with systemic hypertension. Am J Cardiol. 2005 May 1;95(9):1060-4. |