Stress

1.                  Alim TN, Graves E, Mellman TA, Aigbogun N, Gray E, Lawson W, Charney DS.  Trauma exposure, posttraumatic stress disorder and depression in an African-American primary care population. J Natl Med Assoc. 2006 Oct;98(10):1630-6. 

Department of Psychiatry, Howard University, Washington, DC 20060, USA. talim@howard.edu

OBJECTIVE: Trauma exposure is high in African Americans who live in stressful urban environments. Posttraumatic stress disorder (PTSD) and depression are common outcomes of trauma exposure and are understudied in African Americans. African Americans are more likely to seek treatment for psychiatric disorders in a primary care setting. Our study evaluated trauma exposure, PTSD and major depression in African Americans attending primary care offices. METHOD: Six-hundred-seventeen patients (96% African Americans) were surveyed for trauma exposure in the waiting rooms of four primary care offices. Those patients reporting significant traumatic events were invited to a research interview. Of the 403 patients with trauma exposure, 279 participated. RESULTS: Of the 617 participants, 65% reported > or = 1 clearly traumatic event. The most common exposures were transportation accidents (42%), sudden unexpected death of a loved one (39%), physical assault (30%), assault with a weapon (29%) and sexual assault (25%). Lifetime prevalence of PTSD and a major depressive episode (MDE) among those with trauma exposure (n=279) was 51% and 35%, respectively. The percent of lifetime PTSD cases (n=142) with comorbid MDE was 46%. Lifetime PTSD and MDE in the trauma-exposed population were approximately twice as common in females than males, whereas current PTSD rates were similar. CONCLUSIONS: Our rate of PTSD (approximately 33% of those screened) exceeds estimates for the general population. Rates of MDE comorbid with PTSD were comparable to other studies. These findings suggest the importance of screening African Americans for PTSD, in addition to depression, in the primary care setting.

2.                  Altemus M.  Sex differences in depression and anxiety disorders: potential biological determinants. Horm Behav. 2006 Nov;50(4):534-8.

Department of Psychiatry, Weill Medical College, Cornell University, New York, NY 10021, USA. maltemus@med.cornell.edu

The phenomenon of higher rates of affective disorders in women illustrates many of the difficulties as well as promises of translating preclinical models to human disorders. Abnormalities in the regulation of the hypothalamic-pituitary adrenal axis and the sympathoadrenomedullary system have been identified in depression and anxiety disorders, and these disorders are clearly precipitated and exacerbated by stress. Despite the striking sex difference in the prevalence of depression and anxiety disorders, attempts to identify corresponding sex differences in stress response reactivity in animal models have met with limited success. Processes which may contribute to increased rates of affective disorders in women are greater fluxes in reproductive hormones across the life span, and increased sensitivity to catecholamine augmentation of emotional memory consolidation.

3.                  Bale TL.  Stress sensitivity and the development of affective disorders. Horm Behav. 2006 Nov;50(4):529-33.

Department of Animal Biology, University of Pennsylvania, 3800 Spruce Street, Philadelphia, PA 19104, USA. tbale@vet.upenn.edu

Depressive disorders are the most common form of mental illness in America, affecting females twice as often as males. The great variability of symptoms and responses to therapeutic treatment emphasize the complex underlying neurobiology of disease onset and progression. Evidence from human and animal studies reveals a vital link between individual stress sensitivity and the predisposition toward mood disorders. While the stress response is essential for maintenance of homeostasis and survival, chronic stress and maladaptive responses to stress insults can lead to depression or other affective disorders. A key factor in the mediation of stress responsivity is the neuropeptide corticotropin-releasing factor (CRF). Studies in animal models of heightened stress sensitivity have illustrated the involvement of CRF downstream neurotransmitter targets, including serotonin and norepinephrine, in the profound neurocircuitry failure that may underlie maladaptive coping strategies. Stress sensitivity may also be a risk factor in affective disorder development susceptibility. As females show an increased stress response and recovery time compared to males, they may be at an increased vulnerability for disease. Therefore, examination of sex differences in CRF and downstream targets may aid in the elucidation of the underlying causes of the increased disease presentation in females. While we continue to make progress in our understanding of mood disorder etiology, we still have miles to go before we sleep. As an encouraging number of new animal models of altered stress sensitivity and negative stress coping strategies have been developed, the future looks extremely promising for the possibility of a new generation of drug targets to be developed.

4.                  Dyrbye LN, Thomas MR, Huschka MM, Lawson KL, Novotny PJ, Sloan JA, Shanafelt TD.   A multicenter study of burnout, depression, and quality of life in minority and nonminority US medical students. Mayo Clin Proc. 2006 Nov;81(11):1435-42. 

Division of Primary Care Internal Medicine, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905, USA. dyrbye.liseiotte@mayo.edu

OBJECTIVE: To determine the well-being of minority medical students in a multicenter sample of US medical students. PARTICIPANTS AND METHODS: All 1098 medical students at 3 medical schools in Minnesota were surveyed in April 2004. Validated instruments were used to assess burnout, depression, and quality of life (QOL). Students were also asked about the prevalence of significant personal life events in the previous 12 months and strategies used to cope with stress. RESULTS: Although symptoms of depression and overall burnout were similar among minority and nonminority students, minority students were more likely to have a low sense of personal accomplishment (P=.02) and lower QOL In a number of domains (all P< or =.05). These differences persisted on multivariate analysis that controlled for demographic characteristics and recent life events. Minority students were also more likely to have a child (P=.01), originate from outside Minnesota (P<.001), and experience a major personal Illness in the last 12 months (P=.03). CONCLUSION: As a group, the minority medical students in this survey had a lower sense of personal accomplishment and QOL than nonminority students. Additional studies are needed to provide insight regarding the causes of these inequities and the unique challenges faced by minority medical students. Efforts to improve minority students' well-being, QOL, and learning experience may help prevent attrition among minority medical students and promote diversification in the physician workforce.

5.                  Edwards RR, Smith MT, Kudel I, Haythornthwaite J.  Pain-related catastrophizing as a risk factor for suicidal ideation in chronic pain. Pain. 2006 Dec 15;126(1-3):272-9.

Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Meyer 1-108, Baltimore, MD 21287, USA. redwar10@jhmi.edu

Living with chronic pain is associated with many deleterious outcomes, including a substantially increased risk of suicide. While many general risk factors for suicidal ideation and behavior have been identified, few studies have examined pain-related factors that confer increased or decreased risk for suicidality. The present study assessed individual differences in the use of pain-related coping strategies and pain-related catastrophizing as correlates of suicidal ideation in patients with chronic pain. A total of 1512 patients seeking treatment for chronic pain completed a variety of questionnaires assessing pain, coping, and psychosocial functioning. On written questionnaires, approximately 32% of this clinic sample reported some form of recent suicidal ideation. The two most consistent predictors of the presence and degree of suicidal ideation were the magnitude of depressive symptoms and the degree of pain-related catastrophizing, a maladaptive cognitive/emotional pain-coping strategy. Demographic and other pain-related variables such as pain severity and duration were not generally robust predictors of suicidal ideation in this sample of patients with chronic pain. These are the first findings to suggest a unique (e.g., independent of pain severity or depressive symptomatology) association between pain-coping strategies and suicide-related cognitions in the context of chronic pain. Further research in this area, including the addition of suicide prevention materials to pain-coping skills training programs, may benefit large numbers of individuals who are at elevated suicide risk as a consequence of chronic pain.

6.                  Ercan H, Birben E, Dizdar EA, Keskin O, Karaaslan C, Soyer OU, Dut R, Sackesen C, Besler T, Kalayci O. Oxidative stress and genetic and epidemiologic determinants of oxidant injury in childhood asthma. J Allergy Clin Immunol. 2006 Nov;118(5):1097-104. 

Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Meyer 1-108, Baltimore, MD 21287, USA. redwar10@jhmi.edu

Living with chronic pain is associated with many deleterious outcomes, including a substantially increased risk of suicide. While many general risk factors for suicidal ideation and behavior have been identified, few studies have examined pain-related factors that confer increased or decreased risk for suicidality. The present study assessed individual differences in the use of pain-related coping strategies and pain-related catastrophizing as correlates of suicidal ideation in patients with chronic pain. A total of 1512 patients seeking treatment for chronic pain completed a variety of questionnaires assessing pain, coping, and psychosocial functioning. On written questionnaires, approximately 32% of this clinic sample reported some form of recent suicidal ideation. The two most consistent predictors of the presence and degree of suicidal ideation were the magnitude of depressive symptoms and the degree of pain-related catastrophizing, a maladaptive cognitive/emotional pain-coping strategy. Demographic and other pain-related variables such as pain severity and duration were not generally robust predictors of suicidal ideation in this sample of patients with chronic pain. These are the first findings to suggest a unique (e.g., independent of pain severity or depressive symptomatology) association between pain-coping strategies and suicide-related cognitions in the context of chronic pain. Further research in this area, including the addition of suicide prevention materials to pain-coping skills training programs, may benefit large numbers of individuals who are at elevated suicide risk as a consequence of chronic pain.

7.                Hood SD, Hince DA, Robinson H, Cirillo M, Christmas D, Kaye JM.  Serotonin regulation of the human stress response. Psychoneuroendocrinology. 2006 Oct;31(9):1087-97.

School of Psychiatry and Clinical Neurosciences (M521), University of Western Australia, QEII Medical Centre, Perth, Nedlands, Western Australia 6009, Australia. sean.hood@uwa.edu.au

Acute tryptophan depletion (ATD) is a technique that has been used to evaluate the effects on humans of acutely reducing serotonin neurotransmission. We have developed a model using a single breath of 35% CO(2) that activates the hormonal axis and produces autonomic and behavioural arousal, thus modelling a stress response. This study combines ATD and single breath 35% CO(2) inhalation to study stress responses in volunteers. A randomised, double-blinded, placebo-controlled, cross-over trial involving 14 healthy adult volunteers aged between 18 and 65 years was undertaken. Subjects underwent double-blind tryptophan depletion over 2 days and were then crossed over 1 week later. During each study day, at the time of peak depletion, participants were single blinded to receive a single breath of 35% CO(2) or air. This was followed 40 min later by the other gas. Psychological outcomes were assessed with the Spielberger State Anxiety Inventory (SSAI), Visual Analogue Scales (VAS), Panic Inventory (PI), Panic and Agoraphobia Scale (PSI) and Beck Depression Inventory (BDI). Physiological outcome was measured by serial plasma cortisol, prolactin and tryptophan levels, pulse and blood pressure. Tryptophan depletion did not exacerbate 35% CO(2) inhalation effects on anxiety symptoms. Single breath CO(2) robustly increased plasma cortisol levels in comparison to an air inhalation; this was less certain for prolactin levels. ATD influenced the HPA axis (associated with higher cortisol levels), apparently independent of CO(2) or air inhalation stressors. ATD and 35% CO(2) inhalation both induced a pressor response and bradycardia in these normal volunteers. Thirty-five percent CO(2) inhalation and ATD independently activate the human stress response, but do not appear to produce synergistic effects when combined, at least for the conditions produced in this study.

8.                  Mulder DJ, Water TV, Lutgers HL, Graaff R, Gans RO, Zijlstra F, Smit AJ.  Skin autofluorescence, a novel marker for glycemic and oxidative stress-derived advanced glycation endproducts: an overview of current clinical studies, evidence, and limitations. Diabetes Technol Ther. 2006 Oct;8(5):523-35. Review. 

Department of Internal Medicine, University Medical Center Groningen, Groningen, The Netherlands. d.j.mulder@int.umcg.nl

BACKGROUND: Advanced glycation endproducts (AGEs) predict long-term complications in agerelated diseases. However, there are no clinically applicable markers for measuring AGEs in vivo. METHODS: We have recently introduced the AGE-Reader (DiagnOptics B.V., Groningen, The Netherlands) to noninvasively measure AGE accumulation in the human skin of the forearm, making use of the characteristic autofluorescence (AF) pattern that AGEs encompass. Skin AF is calculated as a ratio of mean intensities detected from the skin between 420-600 nm and 300-420 nm. It correlates with collagen-linked fluorescence and specific skin AGE levels from skin biopsies in diabetes, renal failure, and control subjects. Skin AF levels are increased in patients with diabetes and renal failure and are associated with the presence of vascular complications. Additionally, skin AF is strongly related to the progression of coronary heart disease and mortality, independently of traditional risk factors. Since skin pigmentation might influence skin AF, we have investigated the relation of relative skin reflectance (R%) to skin AF in subjects with varying skin phototypes (SPT). RESULTS: The data presented in this article suggest that only in subjects with an SPT of V and VI or R% <12%, no reliable measurement can be performed. Therefore, the current prototype of the AGE-Reader is suitable for subjects with SPT I-IV or R% >12%, and more research is needed for a broader application. CONCLUSION: The AGE-Reader is useful as a noninvasive clinical tool for assessment of risk for long-term vascular complications in diabetes and in other conditions associated with AGE accumulation.

9.                  Nierop A, Bratsikas A, Zimmermann R, Ehlert U. Are stress-induced cortisol changes during pregnancy associated with postpartum depressive symptoms? Psychosom Med. 2006 Nov-Dec;68(6):931-7.   

Department of Clinical Psychology and Psychotherapy, University of Zurich, Zurichbergstrasse 43, CH-8044 Zurich, Switzerland.

OBJECTIVE: The purpose of this study was to examine the association between psychobiological stress reactivity during healthy pregnancy and depressive symptoms in the early puerperium. METHODS: A sample of healthy nulliparous pregnant women (N = 57) between the ages of 21 and 35 years underwent a standardized psychosocial stress test during pregnancy. Within an average of 13 days after delivery, postpartum depressive symptoms were assessed using the German version of the Edinburgh postnatal depression scale (EPDS). The sample was divided into a group with probable cases (EPDS score >9, N = 16) and a group with probable noncases (EPDS score < or =9, N = 41). RESULTS: The probable case group showed significantly higher cortisol responses to the stress test compared with the probable noncase group, whereas baseline levels did not differ. Additionally, women in the probable case group showed significantly higher state anxiety and lower mood state throughout the experiment. Furthermore, the probable case group showed higher stress susceptibility, higher trait anxiety, and higher levels in the Symptom Checklist. No differences were found for prior episodes of psychiatric disorders, obstetrical complications, birth weight, or mode of delivery. CONCLUSIONS: Our data provide evidence that healthy pregnant women developing postpartum depressive symptoms might already be identified during pregnancy by means of their higher cortisol reactivity and their higher psychological reactivity in response to psychosocial stress. Further investigations are required to explore whether higher psychobiological stress responses not only precede depressive symptoms within 2 weeks after birth, but might also predict postpartum major depression.

 Asthma:

15530.  Bacsi A, Choudhury BK, Dharajiya N, Sur S, Boldogh I.  Subpollen particles: carriers of allergenic proteins and oxidases. J Allergy Clin Immunol. 2006 Oct;118(4):844-50.

15531.  Campbell TS, Lavoie KL, Bacon SL, Scharf D, Aboussafy D, Ditto B.  Asthma self-efficacy, high frequency heart rate variability, and airflow obstruction during negative affect in daily life. Int J Psychophysiol. 2006 Oct;62(1):109-14.

15532.  Chu EK, Cheng J, Foley JS, Mecham BH, Owen CA, Haley KJ, Mariani TJ, Kohane IS, Tschumperlin DJ, Drazen JM.  Induction of the plasminogen activator system by mechanical stimulation of human bronchial epithelial cells. Am J Respir Cell Mol Biol. 2006 Dec;35(6):628-38.

15533.  Heck JE, Jacobson JS.  Asthma diagnosis among individuals in same-sex relationships. J Asthma. 2006 Oct;43(8):579-84. 

15534.  Tessier DM, Pascal LE.  Activation of MAP kinases by hexavalent chromium, manganese and nickel in human lung epithelial cells. Toxicol Lett. 2006 Dec 1;167(2):114-21.

15535.  Umetsu DT, Dekruyff RH.  Immune dysregulation in asthma. Curr Opin Immunol. 2006 Dec;18(6):727-32.

Depression:

15536.  Ahola K, Honkonen T, Kivimaki M, Virtanen M, Isometsa E, Aromaa A, Lonnqvist J.   Contribution of burnout to the association between job strain and depression: the health 2000 study. J Occup Environ Med. 2006 Oct;48(10):1023-30. 

15537.  Avdibegovic E, Sinanovic O.  Consequences of domestic violence on women's mental health in Bosnia and Herzegovina. Croat Med J. 2006 Oct;47(5):730-41. 

15538.  Bogdan R, Pizzagalli DA. Acute stress reduces reward responsiveness: implications for depression. Biol Psychiatry. 2006 Nov 15;60(10):1147-54.

15539.  Bornstein SR, Schuppenies A, Wong ML, Licinio J.  Approaching the shared biology of obesity and depression: the stress axis as the locus of gene-environment interactions. Mol Psychiatry. 2006 Oct;11(10):892-902.

15540.  Carlsson JM, Olsen DR, Mortensen EL, Kastrup M. Mental health and health-related quality of life: a 10-year follow-up of tortured refugees. J Nerv Ment Dis. 2006 Oct;194(10):725-31. 

15541.  Clark M, Isaacks-Downton G, Wells N, Redlin-Frazier S, Eck C, Hepworth JT, Chakravarthy B.  Use of preferred music to reduce emotional distress and symptom activity during radiation therapy. J Music Ther. 2006 Fall;43(3):247-65. 

15542.  Davidson J, Baldwin D, Stein DJ, Kuper E, Benattia I, Ahmed S, Pedersen R, Musgnung J.   Treatment of posttraumatic stress disorder with venlafaxine extended release: a 6-month randomized controlled trial. Arch Gen Psychiatry. 2006 Oct;63(10):1158-65. 

15543.  Deblinger E, Mannarino AP, Cohen JA, Steer RA.  A follow-up study of a multisite, randomized, controlled trial for children with sexual abuse-related PTSD symptoms. J Am Acad Child Adolesc Psychiatry. 2006 Dec;45(12):1474-84.

15544.  Dozier M, Peloso E.  The role of early stressors in child health and mental health outcomes. Arch Pediatr Adolesc Med. 2006 Dec;160(12):1300-1.

15545.  Essex MJ, Kraemer HC, Armstrong JM, Boyce WT, Goldsmith HH, Klein MH, Woodward H, Kupfer DJ.  Exploring risk factors for the emergence of children's mental health problems. Arch Gen Psychiatry. 2006 Nov;63(11):1246-56. 

15546.  Geisler S, Berod A, Zahm DS, Rostene W.  Brain neurotensin, psychostimulants, and stress--emphasis on neuroanatomical substrates. Peptides. 2006 Oct;27(10):2364-84.

15547.  Grieger TA, Cozza SJ, Ursano RJ, Hoge C, Martinez PE, Engel CC, Wain HJ.   Posttraumatic stress disorder and depression in battle-injured soldiers. Am J Psychiatry. 2006 Oct;163(10):1777-83; quiz 1860.

15548.  Hosie AM, Wilkins ME, da Silva HM, Smart TG.  Endogenous neurosteroids regulate GABAA receptors through two discrete transmembrane sites. Nature. 2006 Nov 23;444(7118):486-9.

15549.  Karbownik M, Lewinski A. Thyroid gland and oxidative stress; the role of melatonin. J Endocr Reprod 2004, 8(1-2), 69-82.

15550.  Kennedy SE, Koeppe RA, Young EA, Zubieta JK.  Dysregulation of endogenous opioid emotion regulation circuitry in major depression in women. Arch Gen Psychiatry. 2006 Nov;63(11):1199-208. 

15551.  Leck P, Difede J, Patt I, Giosan C, Szkodny L.  Incidence of male childhood sexual abuse and psychological sequelae in disaster workers exposed to a terrorist attack. Int J Emerg Ment Health. 2006 Fall;8(4):267-74. 

15552.  Lucassen PJ, Heine VM, Muller MB, van der Beek EM, Wiegant VM, De Kloet ER, Joels M, Fuchs E, Swaab DF, Czeh B.  Stress, depression and hippocampal apoptosis. CNS Neurol Disord Drug Targets. 2006 Oct;5(5):531-46. Review. 

15553.  McEwen BS.  Sleep deprivation as a neurobiologic and physiologic stressor: Allostasis and allostatic load. Metabolism. 2006 Oct;55(10 Suppl 2):S20-3. Review. 

15554.  Minor TR, Huang Q, Witt AE.  Cytokine-purine interactions in traumatic stress, behavioral depression, and sickness. CNS Neurol Disord Drug Targets. 2006 Oct;5(5):547-60. Review. 

15555.  Rasmusson AM, Pinna G, Paliwal P, Weisman D, Gottschalk C, Charney D, Krystal J, Guidotti A.  Decreased cerebrospinal fluid allopregnanolone levels in women with posttraumatic stress disorder. Biol Psychiatry. 2006 Oct 1;60(7):704-13.

15556.  Schreiber JE, Shirtcliff E, Van Hulle C, Lemery-Chalfant K, Klein MH, Kalin NH, Essex MJ, Goldsmith HH.  Environmental influences on family similarity in afternoon cortisol levels: twin and parent-offspring designs. Psychoneuroendocrinology. 2006 Oct;31(9):1131-7.

15557.  Shih M, Hootman JM, Strine TW, Chapman DP, Brady TJ.  Serious psychological distress in U.S. adults with arthritis. J Gen Intern Med. 2006 Nov;21(11):1160-6.

15558.  Taylor SE, Lehman BJ, Kiefe CI, Seeman TE.  Relationship of early life stress and psychological functioning to adult C-reactive protein in the coronary artery risk development in young adults study. Biol Psychiatry. 2006 Oct 15;60(8):819-24.

Hypertension:

15559.  Achari V, Thakur AK, Sinha AK.  Metabolic syndrome: its prevalence and association with coronary artery disease in type 2 diabetes. Journal, Indian Academy of Clinical Medicine. 2006 Jan-Mar; 7(1): 32-8.

15560.  Fujita K, Nishizawa H, Funahashi T, Shimomura I, Shimabukuro M.  Systemic oxidative stress is associated with visceral fat accumulation and the metabolic syndrome. Circ J. 2006 Nov;70(11):1437-42. 

15561.  Sarkar PD, T M S, Madhusudhan B.  Association between paraoxonase activity and lipid levels in patients with premature coronary artery disease. Clin Chim Acta. 2006 Nov;373(1-2):77-81.

15562.  Takami T, Ohata K, Nishi OA, Hara M. Histological Characteristics of arterialized  medullary vein in spinal dural arteriovenous fistulas related with clinical findings: Report of five cases. Neurology India. 2006 Jun; 54(2): 202-4 

15563.  Vaziri ND, Rodriguez-Iturbe B.  Mechanisms of disease: oxidative stress and inflammation in the pathogenesis of hypertension. Nat Clin Pract Nephrol. 2006 Oct;2(10):582-93. Review.

15564.  Wirtz PH, von Kanel R, Mohiyeddini C, Emini L, Ruedisueli K, Groessbauer S, Ehlert U.   Low social support and poor emotional regulation are associated with increased stress hormone reactivity to mental stress in systemic hypertension. J Clin Endocrinol Metab. 2006 Oct;91(10):3857-65.

15565.  Yang H, Schnall PL, Jauregui M, Su TC, Baker D. Work hours and self-reported hypertension among working people in California. Hypertension. 2006 Oct;48(4):744-50.

Heart Disease:

15566.  Fletcher GF, Mills WC, Taylor WC.  Update on exercise stress testing. Am Fam Physician. 2006 Nov 15;74(10):1749-54. Review. 

15567.  Heponiemi T, Ravaja N, Elovainio M, Naatanen P, Keltikangas-Jarvinen L.  Experiencing positive affect and negative affect during stress: relationships to cardiac reactivity and to facial expressions. Scand J Psychol. 2006 Oct;47(5):327-37. 

15568.  Kagan VE, Tyurina YY, Bayir H, Chu CT, Kapralov AA, Vlasova II, Belikova NA, Tyurin VA, Amoscato A, Epperly M, Greenberger J, Dekosky S, Shvedova AA, Jiang J.  The "pro-apoptotic genies" get out of mitochondria: oxidative lipidomics and redox activity of cytochrome c/cardiolipin complexes. Chem Biol Interact. 2006 Oct 27;163(1-2):15-28.

15569.  Kalantar-Zadeh K, Balakrishnan VS.  The kidney disease wasting: inflammation, oxidative stress, and diet-gene interaction. Hemodial Int. 2006 Oct;10(4):315-25. Review. 

15570.  Lash LH.  Mitochondrial glutathione transport: physiological, pathological and toxicological implications. Chem Biol Interact. 2006 Oct 27;163(1-2):54-67. 

15571.  Mirzaei H, Regnier F.  Identification and quantification of protein carbonylation using light and heavy isotope labeled Girard's P reagent. J Chromatogr A. 2006 Nov 17;1134(1-2):122-33.

15572.  Moens AL, Kass DA.  Tetrahydrobiopterin and cardiovascular disease. Arterioscler Thromb Vasc Biol. 2006 Nov;26(11):2439-44. 

15573.  Ramakrishna G, Breen JF, Mulvagh SL, McCully RB, Pellikka PA.  Relationship between coronary artery calcification detected by electron-beam computed tomography and abnormal stress echocardiography: association and prognostic implications. J Am Coll Cardiol. 2006 Nov 21;48(10):2125-31.

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