Analyzing Anger: How to Make People Mad.

Comments on the article by L. Berkowitz and E. Harmon-Jones (see record 2004-15096-001). Does simple displeasure cause anger without appraisals or agency attributions? The authors offer 8 observations: (a) Appraisal theory also predicts that displeasure promotes anger, (b) An emotion of frustration can be usefully distinguished from anger, (c) Aggressive reactions to norm violations among animals suggest that they too distinguish bad behavior from bad outcomes, (d) Attributions to agency are perceptual and automatic in social situations, (e) It is tenuous to argue that agency attributions are enacted in angry aggression, but absent in anger elicitation. (f) The contextualized meanings of expressive movements, rather than movements themselves, elicit emotion, (g) Expressions may be better seen as constituents than as causes of emotions, (h) Cognitive components of emotion generally come before, not after, eliciting events. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Mad King George: the impact of personal and political stress on mental and physical health

Both historians and psychiatrists have tried to explain the recurrent attacks of mental and physical illness experienced by King George III of Great Britain. Although the porphyria hypothesis is widely accepted, this diagnosis assumes that the king's breakdowns were not precipitated by extreme stress. This assumption was tested using single-case historiometric methods. Biographical data were compiled to form two extensive chronologies of the monarch's life, one for stressful events and the other for pathological symptoms. From this information 22 independent judges reliably assessed fluctuations in stress (total, personal, and political) and health (total, physical, and mental) across 624 consecutive months between 1760 and 1811. The cross-correlations were then calculated for the raw, first-differenced, and prewhitened time series. A consistent tendency appeared for the king's health to deteriorate after increases in stress, most frequently with a 9-month delay. The current study demonstrates the utility of applying quantitative techniques to a psychobiographical debate hitherto examined solely by qualitative approaches.     

Localization of Mad2 to kinetochores depends on microtubule attachment, not tension

A single unattached kinetochore can delay anaphase onset in mitotic tissue culture cells (Rieder, C.L., A. Schultz, R. Cole, G. Sluder. 1994. J. Cell Biol. 127:1301-1310). Kinetochores in vertebrate cells contain multiple binding sites, and tension is generated at kinetochores after attachment to the plus ends of spindle microtubules. Checkpoint component Mad2 localizes selectively to unattached kinetochores (Chen, R.-H., J.C. Waters, E.D. Salmon, and A.W. Murray. 1996. Science. 274:242-246; Li, Y., and R. Benezra. Science. 274: 246-248) and disappears from kinetochores by late metaphase, when chromosomes are properly attached to the spindle. Here we show that Mad2 is lost from PtK1 cell kinetochores as they accumulate microtubules and re-binds previously attached kinetochores after microtubules are depolymerized with nocodazole. We also show that when kinetochore microtubules in metaphase cells are stabilized with taxol, tension at kinetochores is lost. The phosphoepitope 3f3/2, which has been shown to become dephosphorylated in response to tension at the kinetochore (Nicklas, R.B., S.C. Ward, and G.J. Gorbsky. 1995. J. Cell Biol. 130:929-939), is phosphorylated on all 22 kinetochores after tension is reduced with taxol. In contrast, Mad2 only localized to an average of 2.6 out of the 22 kinetochores in taxol-treated PtK1 cells. Therefore, loss of tension at kinetochores occupied by microtubules is insufficient to induce Mad2 to accumulate on kinetochores, whereas unattached kinetochores consistently bind Mad2. We also found that microinjecting antibodies against Mad2 caused cells arrested with taxol to exit mitosis after approximately 12 min, while uninjected cells remained in mitosis for at least 6 h, demonstrating that Mad2 is necessary for maintenance of the taxol-induced mitotic arrest. We conclude that kinetochore microtubule attachment stops the Mad2 interactions at kinetochores which are important for inhibiting anaphase onset.     

Detection and effects of helicobacters in healthy dogs and dogs with signs of gastritis

OBJECTIVES: To determine prevalence, colonization density, and distribution of helicobacters and gastric histologic findings in healthy dogs and dogs with signs of gastritis; to evaluate association of colonization density and gastric inflammation; and to compare the number of Helicobacter spp with degree of inflammation. DESIGN: Cross-sectional prevalence survey. ANIMALS: 25 healthy dogs and 21 dogs with signs of gastritis. PROCEDURE: During endoscopy, gastric mucosal biopsy specimens were obtained from healthy and affected client-owned dogs. Histologic and cytologic evaluation and results of a urease test were used for detecting helicobacters, which were identified definitively by use of transmission electron microscopy and bacterial culture. RESULTS: Helicobacters were detected in all 25 healthy and 20 of 21 affected dogs. Cytologic examination was a more sensitive method than histologic examination or the urease test. Helicobacters were found least frequently and in fewest number in the antrum in both groups of dogs. Gastric inflammation was evident in both groups of dogs and did not differ significantly between groups. A significant association was not detected between colonization density or the number of Helicobacter spp and degree of gastric inflammation. In both groups, H bizzozeronii, H felis, and H salomonis were cultured. CLINICAL IMPLICATIONS: Histologically verified chronic gastritis is common in dogs with signs of gastritis as well as in healthy dogs. Colonization density of helicobacters was not associated with degree of gastric inflammation in the dogs of our study. It remains to be determined whether certain strains of Helicobacter spp can induce gastritis in dogs.     

Histomorphometry of the optic nerves of normal dogs and dogs with hereditary glaucoma

The beagle dog with hereditary primary open-angle glaucoma, unlike other animal models of human glaucoma, possesses a slowly progressive, sustained elevation of intraocular pressure. The effects of this insidious elevation in intraocular pressure on the axons of the optic nerves of three beagles at early stages of glaucoma and two beagles with advanced signs of glaucoma were compared to the optic nerves of four age-matched normal dogs. Plastic embedded optic nerve cross-sections (1 micron) 1 mm posterior to the lamina cribrosa were osmicated and stained with Toluidine Blue. Axons from 0.2 to > 2.0 microns in diameter were counted and measured in 16 cross-sectional regions of equal size within the whole optic nerve using a computerized image analysis system. The mean optic nerve axon diameters in the normal, early glaucomatous, and advanced glaucomatous dogs were 1.53, 1.25 and 1.13 microns respectively. The average total optic nerve axon count in the normal dogs was 148,303. Approximately 16% of the total axonal fibers were counted in each nerve. The counts of optic nerve axons 2.0 microns or greater in diameter were reduced by up to 60% in the central regions of the optic nerves of affected beagles. The large diameter axons of the peripheral optic nerve of the beagle dogs with glaucoma were more resistant to the elevated intraocular pressure. The counts of axons > 0.6 to 0.8 micron in diameter were significantly increased in glaucomatous beagles.     

Mad2 transiently associates with an APC/p55Cdc complex during mitosis

Activation of the mitotic checkpoint pathway in response to mitotic spindle damage in eukaryotic cells delays the exit from mitosis in an attempt to prevent chromosome missegregation. One component of this pathway, hsMad2, has been shown in mammalian cells to physically associate with components of a ubiquitin ligase activity (termed the anaphase promoting complex or APC) when the checkpoint is activated, thereby preventing the degradation of inhibitors of the mitotic exit machinery. In the present report, we demonstrate that the inhibitory association between Mad2 and the APC component Cdc27 also takes place transiently during the early stages of a normal mitosis and is lost before mitotic exit. We also show that Mad2 associates with the APC regulatory protein p55Cdc in mammalian cells as has been reported in yeast. In contrast, however, this complex is present only in nocodazole-arrested or early mitotic cells and is associated with the APC as a Mad2/p55Cdc/Cdc27 ternary complex. Evidence for a Mad2/Cdc27 complex that forms independent of p55Cdc also is presented. These results suggest a model for the regulation of the APC by Mad2 and may explain how the spindle assembly checkpoint apparatus controls the timing of mitosis under normal growth conditions.     

Function of the c-Myc antagonist Mad1 during a molecular switch from proliferation to differentiation

Mad-Max heterodimers have been shown to antagonize Myc transforming activity by a mechanism requiring multiple protein-protein and protein-DNA interactions. However, the mechanism by which Mad functions in differentiation is unknown. Here, we present evidence that Mad functions by an active repression mechanism to antagonize the growth-promoting function(s) of Myc and bring about a transition from cellular proliferation to differentiation. We demonstrate that exogenously expressed c-Myc blocks inducer-mediated differentiation of murine erythroleukemia cells without disrupting the induction of endogenous Mad; rather, high levels of c-Myc prevent a heterocomplex switch from growth-promoting Myc-Max to growth-inhibitory Mad-Max. Cotransfection of a constitutive c-myc with a zinc-inducible mad1 results in clones expressing both genes, whereby a switch from proliferation to differentiation can be modulated. Whereas cells grown in N'N'-hexamethylene bisacetamide in the absence of zinc fail to differentiate, addition of zinc up-regulates Mad expression by severalfold and differentiation proceeds normally. Coimmunoprecipitation analysis reveals that Mad-Max complexes are in excess of Myc-Max in these cotransfectants. Moreover, we show that the Sin-binding, basic region, and leucine zipper motifs are required for Mad to function during a molecular switch from proliferation to differentiation.     

Microinjection of antibody to Mad2 protein into mammalian cells in mitosis induces premature anaphase

In yeast, the Mad2 protein is required for the M phase arrest induced by microtubule inhibitors, but the protein is not essential under normal culture conditions. We tested whether the Mad2 protein participates in regulating the timing of anaphase onset in mammalian cells in the absence of microtubule drugs. When microinjected into living prophase or prometaphase PtK1 cells, anti-Mad2 antibody induced the onset of anaphase prematurely during prometaphase, before the chromosomes had assembled at the metaphase plate. Anti-Mad2 antibody-injected cells completed all aspects of anaphase including chromatid movement to the spindle poles and pole-pole separation. Identical results were obtained when primary human keratinocytes were injected with anti-Mad2 antibody. These studies suggest that Mad2 protein function is essential for the timing of anaphase onset in somatic cells at each mitosis. Thus, in mammalian somatic cells, the spindle checkpoint appears to be a component of the timing mechanism for normal mitosis, blocking anaphase onset until all chromosomes are aligned at the metaphase plate.     

Lucky dogs.

Psychologists possess unique qualifications to serve as elected public officials. However, psychologists often are unprepared or unable to provide a thoughtful, honest, public statement of their individual core values, what implications these values have for their practice and polities, and why they believe they are representative of, and sensitive to, their respective constituencies. Integrating one's personal experiences, professional training, and commitment to societal change and progress is illustrated with the author's personal development into his positions as both a clinical psychologist and a state legislator. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Cutaneous zoonoses transmitted by dogs and cats

Pets like dogs and cats are responsible for a series of zoonotic disorders. Some of these diseases are inflicted by bites, scratches or licking. Others result from a close contact with fur, or are transmitted by ectoparasites or by the contaminated environment. Some systemic infectious and parasitic diseases are transmitted from animals to humans and vice versa. Such situation may lead to endemic problems in some communities.     

Deafness and its diagnosis in dogs and cats

The problem of inherited deafness in various breeds of dogs and cats catches more and more attention in concerned breeders and owners. This article presents an update in the current knowledge of prevalence, aetiology and genetics of sensorineural deafness and its differentiation against acquired forms of hearing disorders. An electrophysiological method (Auditory Evoked Potentials) to obtain an objective diagnosis of hearing disorders is presented. The usefulness of Auditory Evoked Potentials as an instrument for genetic investigations in inherited deafness is discussed.