Anxiety and caffeine consumption in people with anxiety disorders

Forthy-three anxiety disorder patients (DSM-III) who completed the Hopkins Symptom Checklist (SCL-90-R) and a caffeine questionnaire were compared to 124 medical inpatients. Eighty-four percent of the anxious patients were low caffeine consumers (0-249 mg/day) compared to 41% of medical inpatients; 65% of anxiety patients consumed < 100 mg/day. In anxiety patients, there were no significant correlations between subscale scores of the SCL-90-R and amount of caffeine consumption. Patients who consumed < 100 mg/day did not differ on anxiety subscale scores of the SCL-90-R from those who consumed more. However, patients who reported becoming anxious in response to dringking coffee had higher SCL-90-R anxiety subscale scores than patients who did not, even though their daily consumption was not different. It appears that anxiety disorder patients have increased caffeine sensitivity which leads to decreased consumption.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25630/1/0000180.pd

Circadian fluctuations in anxiety disorders

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26184/1/0000263.pd

Chronic caffeine consumption and the dexamethasone suppression test in depression

Acute caffeine administration increases cortisol and converts the dexamethasone suppression test (DST) to nonsuppression in normal humans; data concerning chronic administration as well as effects in depressed patients are minimal. To determine whether caffeine intake influenced DST results in depression, we retrospectively studied the relationship between regular daily caffeine consumption and pretreatment DST status in major depressives. Daily intake was not correlated with either post-DST cortisol levels or symptom ratings. These data suggest that chronic caffeine use is unlikely to be a major factor in dysregulation of the hypothalamic-pituitary-adrenal axis in depression, perhaps because of the development of tolerance.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27342/1/0000367.pd

Circadian symptom fluctuations in people with anxiety disorders

Circadian rhythm abnormalities have been demonstrated in people with depression, including a tendency toward maximal symptom severity in the morning. Although a few studies have suggested that symptoms in people with anxiety are worse later in the day, no detailed study of this observation has been reported. In 86 patients with anxiety disorders (63 with panic disorder or agoraphobia with panic attacks), anxiety symptoms tended to be more severe in the afternoon or evening than in the morning, with no abnormalities of heart rate or oral temperature. This is the first systematic demonstration of a circadian fluctuation of mood in any disorder other than depression.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25991/1/0000057.pd

Endocrine and physiological changes during "spontaneous" panic attacks

Eight patients with DSM-III-defined panic attacks were compared to four normal subjects on hormonal and physiological variables measured at six predetermined times through 24 hr and also during nine "spontaneous" attacks. Levels at predetermined times were not different, other than a reduction of urinary unconjugated epinephrine in patients. Plasma prolactin was elevated at the peak of most of the attacks and correlated with attack severity. Plasma cortisol and growth hormone, and heart rate, were elevated during some attacks, and plasma norepinephrine showed small increases. Significant plasma epinephrine and MHPG changes were not observed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26943/1/0000509.pd

The antioxidant and chemopreventive potentialities of Mosidae (Adenophora remotiflora) leaves

Our study focused on the antioxidant activities of Mosidae leaf ethanol extract (MLE) and included measurements of reducing power, total phenolic compounds, DPPH radical scavenging activity, and hydroxyl radical scavenging activity. In order to determine whether or not MLE evidences any chemopreventive activities, experimental lung metastasis was induced via the i.v. inoculation of colon26-M3.1 carcinoma cells into BALB/c mice. Additionally, we attempted to characterize any possible cytotoxic effects in murine normal splenocytes and tumor cells (B16-BL6 and colon26-M3.1). The total phenolic content and reducing capacity were measured at 39 mg/100 mL and 1.24, respectively, whereas the DPPH and hydroxyl radical scavenging activities of MLE were measured to be 88.89% and 22.10%, respectively. Prophylactic i.v. treatment with MLE resulted in a dose-dependent and significant inhibition of lung metastasis. Specifically, a MLE dose of 200 ug per mouse resulted in an 88.90% inhibition of lung metastasis. For the cytotoxicity assay, MLE doses up to 100 ug/mL were not shown to affect the growth of normal murine splenocytes. Additionally, the survival of normal cells was not affected at MLE doses below 500 ug/mL. However, MLE doses up to 500 ug/mL reduced the percentage of tumor cell growth for B16BL6 (67% alive) and colon26-M3.1 (62% alive) cells

CTCF cooperates with CtIP to drive homologous recombination repair of double-strand breaks

The pleiotropic CCCTC-binding factor (CTCF) plays a role in homologous recombination (HR) repair of DNA double-strand breaks (DSBs). However, the precise mechanistic role of CTCF in HR remains largely unclear. Here, we show that CTCF engages in DNA end resection, which is the initial, crucial step in HR, through its interactions with MRE11 and CtIP. Depletion of CTCF profoundly impairs HR and attenuates CtIP recruitment at DSBs. CTCF physically interacts with MRE11 and CtIP and promotes CtIP recruitment to sites of DNA damage. Subsequently, CTCF facilitates DNA end resection to allow HR, in conjunction with MRE11-CtIP. Notably, the zinc finger domain of CTCF binds to both MRE11 and CtIP and enables proficient CtIP recruitment, DNA end resection and HR. The N-terminus of CTCF is able to bind to only MRE11 and its C-terminus is incapable of binding to MRE11 and CtIP, thereby resulting in compromised CtIP recruitment, DSB resection and HR. Overall, this suggests an important function of CTCF in DNA end resection through the recruitment of CtIP at DSBs. Collectively, our findings identify a critical role of CTCF at the first control point in selecting the HR repair pathway