Nifedipine-associated acute psychosis

A 84-year-old man was given nifedipine for control of angina pectoris. Acute psychosis with paranoid ideation developed soon after he began receiving the medication. All symptoms resolved with discontinuation of nifedipine. This is the second reported case of nifedipine-associated acute psychosis. Alternations in calcium-mediated neurotransmitter release, particularly dopamine, may be responsible. Clinicians should consider nifedipine when presented with a patient with acute psychosis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26032/1/0000105.pd

Individual Differences in Emotion Expression: Hierarchical Structure and Relations with Psychological Distress

Several constructs reflecting individual differences in emotion expression have been described in the literature, yet their structural organization is unknown. The present study provided a taxonomy of these individual differences and determined their relations to depression and anxiety symptoms. Exploratory factor analyses suggested seven emotion-expression factors-Affect Intensity, Ambivalence About Expression Disclosure of Negative Emotion, Disclosure of Emotion, Disclosure of Lack of Affect, Expression of Positive Emotion, and Secret Keeping-are explained by two second-order factors: Emotional Constraint and Emotional Expression. Multiple regression and canonical correlation analyses suggested that a reluctance to express emotions is related to heightened psychological symptoms. These findings bridge constructs from disparate literatures, and they provide support for emotion dysregulation models of affective disorders

Evidence that arginine vasotocin inhibits human chorionic gonadotropin and cyclic adenosine 3',5' monophosphate stimulated ovarian steroidogenesis

SummaryA study of the ovary as a site of action of arginine vasotocin, a nonapeptide synthesized in the pineal gland of vertebrates, was conducted in the rat. Progesterone production stimulated by either human Chorionic Gonadotropin or 8Br-cyclic Adenosine 3',5' Monophosphate was significantly reduced in rats prepreated with arginine vasotocin. The affinity and receptor number for human chorionic gonadotropin were uneffected by pretreatment with arginine vasotocin. These results suggest that the antigonadotropic action attributed to arginine vasotocin may be due to an inhibition of ovarian steroidogenesis at a point distal to cyclic Adenosine 3',5' Monophosphate formation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/24374/1/0000643.pd

Long-term follow-up of coronary artery occlusion secondary to blunt chest trauma

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/26913/1/0000479.pd

Plasma levels of immunoreactive atrial natriuretic hormone in patients with diabetes mellitus

In order to determine whether atrial natriuretic hormone (ANH) secretion is altered in diabetic patients with autonomic neuropathy, plasma immunoreactive ANH (IR-ANH) levels were measured in 23 patients with insulin-dependent diabetes mellitus, 12 of whom had definite cardiac autonomic neuropathy determined by noninvasive maneuvers. Levels were also measured in 31 healthy control subjects. Whereas only one of the 11 diabetics without cardiac autonomic neuropathy had elevated IR-ANH levels, four of the 12 diabetics with cardiac autonomic neuropathy had elevated IR-ANH levels (P = 0.03 compared to control subjects). 24-h urinary sodium excetion was not different among the groups. There was no significant correlation between IR-ANH levels and diabetes control and any of the parameters of autonomic nervous system activity nor between IR-ANH levels and plasma norepinephrine or epinephrine levels. Furthermore, no relationship was observed in the diabetic subjects between IR-ANH levels and left ventricular ejection fraction determined by radionuclide ventriculography. Thus, elevated IR-ANH levels occur with greater frequency in diabetic patients with autonomic neuropathy. These elevations do not appear to be due to alterations in dietary sodium intake or left ventricular dysfunction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/25997/1/0000063.pd

Effect of Long-Term Exposure to Lower Low-Density Lipoprotein Cholesterol Beginning Early in Life on the Risk of Coronary Heart Disease A Mendelian Randomization Analysis

ObjectivesThe purpose of this study was to estimate the effect of long-term exposure to lower plasma low-density lipoprotein cholesterol (LDL-C) on the risk of coronary heart disease (CHD).BackgroundLDL-C is causally related to the risk of CHD. However, the association between long-term exposure to lower LDL-C beginning early in life and the risk of CHD has not been reliably quantified.MethodsWe conducted a series of meta-analyses to estimate the effect of long-term exposure to lower LDL-C on the risk of CHD mediated by 9 polymorphisms in 6 different genes. We then combined these Mendelian randomization studies in a meta-analysis to obtain a more precise estimate of the effect of long-term exposure to lower LDL-C and compared it with the clinical benefit associated with the same magnitude of LDL-C reduction during treatment with a statin.ResultsAll 9 polymorphisms were associated with a highly consistent reduction in the risk of CHD per unit lower LDL-C, with no evidence of heterogeneity of effect (I2 = 0.0%). In a meta-analysis combining nonoverlapping data from 312,321 participants, naturally random allocation to long-term exposure to lower LDL-C was associated with a 54.5% (95% confidence interval: 48.8% to 59.5%) reduction in the risk of CHD for each mmol/l (38.7 mg/dl) lower LDL-C. This represents a 3-fold greater reduction in the risk of CHD per unit lower LDL-C than that observed during treatment with a statin started later in life (p = 8.43 × 10−19).ConclusionsProlonged exposure to lower LDL-C beginning early in life is associated with a substantially greater reduction in the risk of CHD than the current practice of lowering LDL-C beginning later in life

PTP1B Regulates Leptin Signal Transduction In Vivo

AbstractMice lacking the protein-tyrosine phosphatase PTP1B are hypersensitive to insulin and resistant to obesity. However, the molecular basis for resistance to obesity has been unclear. Here we show that PTP1B regulates leptin signaling. In transfection studies, PTP1B dephosphorylates the leptin receptor-associated kinase, Jak2. PTP1B is expressed in hypothalamic regions harboring leptin-responsive neurons. Compared to wild-type littermates, PTP1B−/− mice have decreased leptin/body fat ratios, leptin hypersensitivity, and enhanced leptin-induced hypothalamic Stat3 tyrosyl phosphorylation. Gold thioglucose treatment, which ablates leptin-responsive hypothalamic neurons, partially overcomes resistance to obesity in PTP1B−/− mice. Our data indicate that PTP1B regulates leptin signaling in vivo, likely by targeting Jak2. PTP1B may be a novel target to treat leptin resistance in obesity

Location Preferences of Family Firms: Strategic Decision Making or “Home Sweet Home”?

Selecting a business location is among the most important strategic decisions for family firms. Yet the separate demands of the family and the business often prove difficult to balance. A comparison of location preferences in family and nonfamily firms provides insight into the family influence on strategic decision making.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/67069/2/10_1111_j_1741-6248_1992_00271_x.pd