Evidence for hepatocarcinogenic activity of pentachlorobenzene with intralobular variation in foci incidence

Pentachlorobenzene (PeCB) is an important environmental contaminant derived primarily from the by-product contamination of the popular fungicides hexachlorobenzene and pentachloronitrobenzene. Its tumor-promoting activity was studied in a medium-term initiation/promotion assay in male F344 rats. Animals were given a single i.p. injection of diethylnitrosamine (200 mg/kg body weight) and 2 weeks later were administered 0.1 or 0.4 mmol/kg per day PeCB by gavage in a corn oil vehicle, 7 days/week. At the end of week 3, rats were subjected to a partial hepatectomy. Results showed that PeCB, at both doses, significantly increased both the number and area of glutathione S-transferase pi (GST-P) foci (>0.2 mm diameter) (P < 0.05). This trend was dose-dependent. In addition to increases in preneoplastic foci, liver glutathione concentrations and glutathione-associated enzymes showed significant changes in animals treated with PeCB. Glutathione reductase (GR) and gamma-glutamylcysteine synthetase (gamma-GCS) were both significantly induced in the centrilobular region. Changes in oxidized glutathione concentrations corresponded with the increase in GR activity with decreases of 40 and 30% in the low and high dose groups, respectively. No significant changes were detected in reduced glutathione concentrations. Together with changes in GR and gamma-GCS expression, a decrease in GST-P foci around the central veins was significant (P = 0.004) at the high dose. In these animals, 26% of the foci were classified as centrilobular whereas 37 and 39% of the foci were centrilobular in the low dose and control groups, respectively. Because of the co-localized nature of the changes in glutathione-associated enzymes and the decreased incidence of centrilobular foci, our results suggest that the reduced cellular environment may ultimately play a role in negatively selecting for foci growth.     

Beyond regulatory focus.

Comments on the article by E. T. Higgins (see record 1997-43865-002) regarding a regulatory focus theory of pleasure and pain. It is argued that although Higgins's concepts of promotion and prevention foci advance out understanding of approach and avoidance motivation, they leave some important questions unanswered. To address these questions, S. Reiss's sensitivity theory is offered as potentially useful in integration with Higgins's concepts to move beyond the Hedonic Principle. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Pathologic anatomy of experimental listeriosis

The authors present a survey of the Soviet and foreign literature and findings of their own experimental studies. On the basis of these data the pathologo-anatomic picture of listerosis in laboratory animals (white mice, guinea-pigs and rabbits) is given in dynamics and histogenesis of focal changes in this disease in elucidated. The most typical feature of listerosis in animals is lesions of the kidney where focal changes in the form of granulems could be detected macroscopically at an early period and with great consistency. Several stages in its histogenesis may be discerned: I. focal necroses of hepatic cells associated with their invasion with lister Listeria; 2. appearance of cellular elements around the foci of necroses with subsequent formation of granulemas consisting mainly of leucocytes and lymphoid cells; 3. development of necrobiotic changes in the central areas of granulemas with concomitance of exudative processes; 4. organization of necrotic foci with subsequent scarring.     

Neuron loss localizes human temporal lobe epilepsy by in vivo proton magnetic resonance spectroscopic imaging

Temporal lobe epileptogenic foci were blindly localized in 8 patients with medically refractory unilateral complex partial seizures using noninvasive in vivo proton magnetic resonance spectroscopic imaging (1H-MRSI) with 4-ml effective voxel size. The brain proton metabolite signals in 8 matched normal controls were bilaterally symmetrical within +/- 10%. The hippocampal seizure foci had 21 +/- 5% less N-acetyl aspartate signal than the contralateral hippocampal formations (p < 0.01). The focal N-acetyl aspartate reductions were consistent with pathology findings of mesial temporal sclerosis with selective neuron loss and gliosis in the surgically resected epileptogenic foci. Proton MRSI correctly localized the seizure focus in all 8 cases. By comparison, MR imaging correctly localized 7 of 8 cases and single photon emission computed tomography correctly localized 2 of 5 cases. No lactate was detected in these interictal studies. No significant changes in choline or creatine were observed. In conclusion, 1H-MRSI is a useful tool for the noninvasive clinical assessment of intractable focal epilepsy. These preliminary results suggest that 1H-MRSI can accurately localize temporal lobe epileptogenic foci.     

Axonal cytoskeletal changes after non-disruptive axonal injury

In animal models of human diffuse axonal injury, axonal swellings leading to secondary axotomy occur between 2 and 6 h after injury. But, analysis of cytoskeletal changes associated with secondary axotomy has not been undertaken. We have carried out a quantitative analysis of cytoskeletal changes in a model of diffuse axonal injury 4 h after stretch-injury to adult guinea-pig optic nerves. The major site of axonal damage was the middle portion of the nerve. There was a statistically significant increase in the proportion of small axons with a diameter of 0.5 micron and smaller in which there was compaction of neurofilaments. Axons with a diameter greater than 2.0 microns demonstrated an increased spacing between cytoskeletal elements throughout the length of the nerve. However, in the middle segment of the nerve these larger axons demonstrated two different types of response. Either, where periaxonal spaces occurred, there was a reduction in axonal calibre, compaction of neurofilaments but no change in their number, and a loss of microtubules. Or, where intramyelinic spaces occurred there was an increased spacing between neurofilaments and microtubules with a significant loss in the number of both. Longitudinal sections showed foci of compaction of neurofilaments interspersed between regions where axonal structure was apparently normal. Neurofilament compaction was correlated with disruption of the axolemma at these foci present some hours after injury. We suggest that the time course of these axonal cytoskeletal changes after stretch-injury to central axons is shorter than those changes documented to occur during Wallerian degeneration.     

The effects of promotion and prevention cues on creativity.

This study tested whether cues associated with promotion and prevention regulatory foci influence creativity. The authors predicted that the "risky," explorative processing style elicited by promotion cues, relative to the risk-averse, perseverant processing style elicited by prevention cues, would facilitate creative thought. These predictions were supported by two experiments in which promotion cues bolstered both creative insight (Experiment 1) and creative generation (Experiment 2) relative to prevention cues. Experiments 3 and 4 provided evidence for the process account of these findings, suggesting that promotion cues, relative to prevention cues, produce a riskier response bias (Experiment 3) and bolster memory search for novel responses (Experiment 4). A final experiment provided evidence that individual differences in regulatory focus influence creative problem solving in a manner analogous to that of incidental promotion and prevention cues. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

A case of neuro-Behcet's syndrome in a woman (author's transl)

An autopsy case of Neuro-Beh?et's syndrome is reported with review of the previous 13 cases. A 48-year-old woman who had recurrent oral aphthae and genital ulcers beginning at the age of 27 years suddenly developed several neurological symptoms including headache, paraplegia and disturbance of speech. She died of septicemia due to the urinary infection 22 years after the appearance of the first symptoms and one year after the neurological manifestation. Autopsy revealed a marked atrophy of the frontal lobes of the cerebral hemispheres. Microscopic changes in the central nervous system were consisted of edema and lymphocytic cuffing around the vessels, small foci of softening of the white matter and accumulation of fat-laden cells around these foci, and demyelination. These histologic lesions showed a diffuse distribution in the entire brain without a characteristic localisation, but involvement of the basilar nuclei and the pons was most intense in the present case as observed in most of the previous reports. Microscopic examination of other organs revealed severe pyelonephritis and fatty changes of the liver.     

Historical overview of key issues in food safety

Foodborne transmission of pathogenic and toxigenic microorganisms has been a recognized hazard for decades. Even half a century ago we knew about the dangers of botulism from underprocessed canned foods; staphylococcal poisoning from unrefrigerated cream-filled pastries, sliced ham, meat, and poultry salads; and salmonellosis from infected animal products. Despite new protective measures, changes in preservation techniques and failure to follow recognized procedures have created new dangers. Moreover, we now recognize new organisms that can cause foodborne illness--Listeria monocytogenes, Escherichia coli O157:H7, Campylobacter jejuni, Vibrio parahaemolyticus, Yersinia enterocolitica, and others. Controlling these organisms will require widespread education and possibly new regulatory initiatives.     

Gallbladder cancer with intratumoral anechoic foci: a mimic of adenomyomatosis

We report a case of advanced gallbladder cancer in a 58-year-old man. On ultrasonography, there were anechoic foci within the tumor. Although anechoic foci within a thickened gallbladder wall usually represent intramural diverticula (dilated Rokitansky-Aschoff sinuses) of adenomyomatosis, cystically dilated cancerous glands were the etiology of these foci in this case. Thus, gallbladder cancer may also have anechoic foci within the tumor.     

Employee Commitment and Motivation: A Conceptual Analysis and Integrative Model.

Theorists and researchers interested in employee commitment and motivation have not made optimal use of each other's work. Commitment researchers seldom address the motivational processes through which commitment affects behavior, and motivation researchers have not recognized important distinctions in the forms, foci, and bases of commitment. To encourage greater cross-fertilization, the authors present an integrative framework in which commitment is presented as one of several energizing forces for motivated behavior. E. A. Locke's (1997) model of the work motivation process and J. P. Meyer and L. Herscovitch's (2001) model of workplace commitments serve as the foundation for the development of this new framework. To facilitate the merger, a new concept, goal regulation, is derived from self-determination theory (E. L. Deci & R. M. Ryan, 1985) and regulatory focus theory (E. I. Higgins, 1997). By including goal regulation, it is acknowledged that motivated behavior can be accompanied by different mindsets that have particularly important implications for the explanation and prediction of discretionary work behavior. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Electroencephalographic signs of compensatory reactions following stroke with location of the focus in the right and left cerebral hemispheres

The authors studied 41 patients with acute disorders of cerebral circulation, a focus in the right hemisphere and 14 with foci in the left hemisphere. The traits of compensatory reactions were studied according to the background and functional EEG, depending upon the severity, stage, localization and lateralization of focal vascular brain lesions. The authors indicate to a rigidity of clinical and EEG changes in patients with right hemispheric localization of the focus which is explained by the authors by disturbances of the higher cortical functions in these patients.     

Morphological and biochemical changes in the myocardium after sudden death from ischemic heart disease

The myocardium was examined in 44 persons who had suddenly died of ischemic heart disease, in 37 who had died of injury, and in 28 who had died of alcohol poisoning. Those with ischemic heart disease had foci of necrosis of the muscle fibers, severe disturbances in microcirculation, changes in the activity of certain myocardial enzymes and in the content of lipids in the myocardium. Biochemical changes similar to these in many respects were revealed in individuals who had died of alcohol poisoning, in view of which alcohol poisoning may be a factor conducive to sudden death in ischemic heart disease.     

Personal constructs and psychodynamic psychotherapy: A case study.

[Correction Notice: An erratum for this article was reported in Vol 24(1) of Psychoanalytic Psychology (see record 2007-00135-015). An error was made in the reproduction of figures 5 and 6. The corrected versions are provided with the erratum.] During a short term, psychoanalytically informed psychotherapy, a college student's salient constructs regarding her self and her object representations were elicited via the Role Construct Repertory Test. The course of this psychotherapy is traced and is examined with regard to the information provided by component analyses of these repertory grids. The aims of this article are to demonstrate the utility of an independent measure such as repertory grids for 1) additional understanding of the patient's modes of construing self and others; 2) establishing meaningful foci for a short-term treatment; 3) providing information for a more considered set of interpretive interventions regarding key conflicts; and 4) considering changes and outcome in light of the foci of the treatment. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Metabolic polymorphisms in carcinogen metabolising enzymes and cancer susceptibility

Molecular genetic analysis is providing us with enormous advances in understanding the pathogenesis of human diseases such as cancer. The study of familial disease and the subsequent mapping and identification of the mutations which contribute to disease susceptibility, is not only providing insights into the factors involved in the pathogenesis of the disease but also identifying new targets for therapy. It is now clear that human tumours result from a complex sequence of mutation events. Each individual step makes the mutated cell more independent of its normal growth regulatory processes, eventually resulting in the formation of a metastatic tumour. There are a multitude of biochemical changes that these mutations confer, which provide preneoplastic cells with a selection advantage. In addition to an increased rate of cell division, such changes may make the cells resistant to cytotoxic insult or to programmed cell death. They can also confer an increased ability to survive independent of a normal hormonal environment. It is now clear that all these types of change may contribute to tumour cell progression.     

Work in people's lives: A location for counseling psychologists.

The career development–vocational psychology literature has been marked by 2 persistent problems: a slow response to new developments in basic areas of psychology, such as developmental psychology, and a lack of representation of populations other than White and middle-class groups as research participants or as foci of theoretical explanation. After a brief discussion of 2 factors that may have contributed to these problems, a rationale for a new location for this field is developed. The new location focuses on the study of work in people's lives from the perspective of social constructionism and from the perspective of counseling psychologists as applied psychologists. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The physician in the pharmaceutical industry

The physician's role in the pharmaceutical industry has changed over the past years. This change is a consequence of several factors, namely the evolution of the industry itself, the legislative and regulatory changes in this particular area, the development of medicine, new techniques and research, and finally the physician's needs. The changes that this activity has undergone not only create new stimuli for the physicians in the industry, but also new challenges and needs for the complete achievement of their career. This is a review article of the main functions and responsibilities of the physician in the pharmaceutical industry as well as the new challenges that this group of physicians faces. Finally, special attention is given to post-graduate courses and their relation with the academic structure.     

Progress in understanding the molecular pathogenesis of human lung cancer

We review the molecular pathogenesis of lung cancer including alterations in dominant oncogenes, recessive oncogenes/tumor suppressor genes, alterations in growth regulatory signaling pathways, abnormalities in other pathways, such as apoptosis, autocrine and paracrine growth stimulatory loops, angiogenesis, and host immune responses, other mechanisms of genetic changes, such as microsatellite and methylation alterations, and the potential for inherited predisposition to lung cancer. These changes are related to multistage carcinogenesis involving preneoplastic lesions, and lung development and differentiation. The translational applications of these findings for developing new ways of early detection, prevention, treatment, and prognosis of lung cancer are discussed.     

The multiyear changes in the epidemic activity of the foci of zoonotic cutaneous leishmaniasis at the Murgab oasis. I. An analysis of the relations of morbidity to heliogeophysical factors

Attempts were made to analyse the relationships of changes in the pattern of zoonotic cutaneous leishmaniasis (ZCL) morbidity by the 1951-1993 statistics of the Turkmenistan Ministry of Health by the areas of Mary?ski? velaiat with heliogeophysical factors. For quantitative characterization of solar activity changes, various indices were used; among them there was the Wolf number, radio radiation flux at a wavelength of 10.7 cm. and the geomagnetic Aa-index. In some many-year observations, vague cyclic variations were detected on a personal computer by spectral and periodogram analyses proved to be effective in other diseases. Correlation and cross-correlation analyses were used to evaluate the possible relationships between the morbidity rates and the changes in heliogeophysical factors. The study has revealed that the epidemic activity of ZCL foci is characterized by cyclicity with variations of about 2.4, 3.6, 6.9, and 11.2 years. The changes in ZCL morbidity in the areas, including the natural ZCL foci of Murgab delta landscapes, slightly differ from those in the areas with valley foci in the south part of the velayat in the duration and expression of cycles. At the same time sun-caused 11-year cycles are observed in all groups of the areas, though they are slightly more pronounced in the north than in the south. The greatest epidemic outbreaks (1956-1957, 1965, 1977, and 1986-1988) occurred in various areas of the Murgab oasis on an average of 1-3 years after the minimum of 11-year solar cycles. Noteworthy, they are greatly marked in odd solar activity cycles (the 1957 and 1977 outbreaks) in many areas. Among the parameters chosen, the radio flux of solar radiation at a wavelenght of 10.7 cm and the Wolf number (the correlation coefficients are as high as 0.30-0.50 at P = 0.95) are closely related with ZCL morbidity changes when the plot is shifted. At the same time the values of the geomagnetic Aa-index are unlikely to greatly affect changes in the epidemiological situation. The regularities revealed are of particular significance for long-term prediction of the greatest rises of ZCL morbidity rates. Taking into account the estimated solar activity changes within the next years, one may expect activation of natural ZCL foci and, in case of untimely use of prophylactic measures, the following rise in the population's morbidity in 1998-1999.     

Spinal neurilemmomas and neurofibromas: central dot sign in postgadolinium MRI

The MR studies of three histologically proven spinal neurilemmomas and neurofibromas were reviewed retrospectively. There were two benign neurilemmomas (schwannomas) and one neurofibroma. The common characteristic of these cases was a central low intensity focus ("dot") seen on postcontrast T1-weighted imaging. The low intensity foci corresponded histologically to a congeries of changes including edema, microcysts, foam cells, hyalinization of blood vessels, old hemorrhage, and dystrophic calcification.     

Xrcc3 is required for assembly of Rad51 complexes in vivo

Rad51 is a member of a family of eukaryotic proteins related to the bacterial recombinational repair protein RecA. Rad51 protein localizes to multiple subnuclear foci in Chinese hamster ovary cells. Subnuclear Rad51 foci are induced by ionizing radiation or the DNA cross-linking agent cisplatin. Formation of these foci is likely to reflect assembly of a multimeric form of Rad51 that promotes DNA repair. Formation of damage-induced Rad51 foci does not occur in the Chinese hamster ovary cell line irs1SF, which is sensitive to DNA damaging agents. The Rad51 focus formation defect of irs1SF cells is corrected by a construct that encodes the repair protein Xrcc3. Xrcc3 is a human homolog of Rad51 previously isolated by virtue of its ability to correct the radiation sensitivity of irs1SF cells. Changes in the steady state level of Rad51 protein do not account for the irs1SF defect nor do they account for the appearance of foci following DNA damage. These results suggest that Xrcc3 is required for the assembly or stabilization of a multimeric form of Rad51 during DNA repair. Cell lines defective in two different components of DNA protein kinase formed Rad51 foci in response to damage, indicating DNA protein kinase is not required for damaged-induced mobilization of Rad51.