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PubMed2002

Resistance of prostate cancer cells to soluble TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) can be overcome by doxorubicin or adenoviral delivery of full-length TRAIL.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) has been shown to induce apoptosis in malignant cells without harming normal cells. To determine the antitumor potential of TRAIL against prostate cells, we undertook a comprehensive study that included eight prostate cancer cells lines (CWR22Rv1, Du145, DuPro, JCA-1, LNCaP, PC-3, PPC-1, and TsuPr1) and primary cultures of normal prostate epithelial cells (PrEC). Cells were tested for susceptibility to soluble TRAIL in the presence or absence of the chemotherapeutic agent doxorubicin. TRAIL was also delivered by an adenoviral vector. Our results reveal that Du145, DuPro, LNCap, TsuPr1, and PrEC were resistant to 100 ng/mL TRAIL. JCA-1 and PPC-1 were slightly sensitive (20% killing) and PC-3 and CWR22Rv1 exhibited the highest sensitivity to TRAIL (30% and 50% killing, respectively). The combination of 10 ng/mL TRAIL with doxorubicin resulted in 60-80% cytotoxicity in seven of eight prostate cancer cells. TRAIL-mediated apoptosis involved cleavage of Bid, caspase-3, and PARP, and required caspase-8 and -9 activity. Full-length TRAIL delivered by an adenoviral vector (AdTRAIL-IRES-GFP) killed prostate cancer cell lines and PrEC without requisite doxorubicin cotreatment. Therefore, expression of the transgene from a tissue-specific promotor would make gene therapy with AdTRAIL-IRES-GFP a possibility.

Adenoviridae↗
PubMed2006

Immunosensitization of tumor cells to dendritic cell-activated immune responses with the proteasome inhibitor bortezomib (PS-341, Velcade).

Proteasome inhibition results in proapoptotic changes in cancer cells, which may make them more sensitive to immune effector cells. We established a murine model to test whether the proteasome inhibitor bortezomib could sensitize established B16 melanoma tumors to dendritic cell (DC)-activated immune effector cells. Day 3-established s.c. B16 tumors had significantly decreased tumor outgrowth when treated with a combination of bortezomib and DC, regardless of whether the DC were loaded or not with a tumor Ag. In vivo Ab-depletion studies demonstrated that the effector cells were NK and CD8+ cells, but not CD4+ cells. NF-kappaB nuclear transcription factor assay and gene-expression profiling of B16 treated with bortezomib was consistent with inhibition of NF-kappaB target genes leading to a proapoptotic phenotype. In vitro lytic assays demonstrated that TNF-alpha, but not perforin, Fas-ligand, or TRAIL, was responsible for bortezomib-sensitized B16 cytotoxicity. In conclusion, the proteasome inhibitor bortezomib can pharmacologically sensitize tumor cells to the lytic effects of DC-activated immune effector cells.

Animals↗
PubMed2006

Synthesis, characterization and in vitro evaluation of triptolide-lysozyme conjugate for renal targeting delivery of triptolide.

A triptolide-lysozyme (TP-LZM) conjugate was synthesized to achieve renal specific delivery and to reduce the side effects of triptolide. Triptolide was coupled to lysozyme through succinic via an ester bond with an average coupling degree of 1 mol triptolide per 1 mol lysozyme. The lysozyme can specifically accumulate in the proximal tubular cells of the kidney, making it a potential carrier for targeting drugs to the kidney. The structure of triptolide succinate (TPS) was confirmed by IR, 1H-NMR, MS and UV. The concentrations of triptolide in various samples were determined by reversed-phase high-performance liquid chromatography (HPLC). In this study, the physicochemical and stability profiles of TP-LZM under various conditions were investgated the stability and releasing profiles of triptolide-lysozyme (TP-LZM) under various conditions. In vitro release trails showed triptolide-lysozyme was relatively stable in plasma (less than 30% of free triptolide released) and could release triptolide quickly in lysosome (more than 80% of free triptolide released) at 37 degrees C for 24 h. In addition, the biological activities of the conjugate on normal rat kidney proximal tubular cells (NRK52E) were also tested. The conjugate can effectively reduce NO production in the medium of NRK52E induced by lipopolysaccharide (LPS) but with much lower toxicity. These studies suggest the possibility to promote curative effect and reduce its extra-renal toxicity of triptolide by TP-LZM conjugate.

Animals↗
PubMed1991

Evaluation of a Computerized Clinical Information System (Micromedex).

This paper summarizes data collected as part of a project designed to identify and assess the technical and organizational problems associated with the implementation and evaluation of a Computerized Clinical Information System (CCIS), Micromedex, in three U.S. Department of Veterans Affairs Medical Centers (VAMCs). The study began in 1987 as a national effort to implement decision support technologies in the Veterans Administration Decentralized Hospital Computer Program (DHCP). The specific objectives of this project were to (1) examine one particular decision support technology, (2) identify the technical and organizational barriers to the implementation of a CCIS in the VA host environment, (3) assess the possible benefits of this system to VA clinicians in terms of therapeutic decision making, and (4) develop new methods for identifying the clinical utility of a computer program designed to provide clinicians with a new information tool. The project was conducted intermittently over a three-year period at three VA medical centers chosen as implementation and evaluation test sites for Micromedex. Findings from the Kansas City Medical Center in Missouri are presented to illustrate some of the technical problems associated with the implementation of a commercial database program in the DHCP host environment, the organizational factors influencing clinical use of the system, and the methods used to evaluate its use. Data from 4581 provider encounters with the CCIS are summarized. Usage statistics are presented to illustrate the methodological possibilities for assessing the "benefits and burdens" of a computerized information system by using an automated collection of user demographics and program audit trails that allow evaluators to monitor user interactions with different segments of the database.

Computer Systems↗
PubMed2005

Enhancing TRAIL-induced apoptosis by Bcl-X(L) siRNA.

We previously found that a change in the balance between mitochondrial pro- and anti-apoptotic proteins caused by ectopic expression of the Bax gene led to increased induction of apoptosis by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). To investigate whether a similar effect can be elicited by down-regulating Bcl-X(L), an anti-apoptotic protein, we tested the effects of a small interfering RNA (siRNA) specific for Bcl-X(L) in TRAIL-resistant cells. The down-regulation of Bcl-X(L) by siRNA inhibited cell proliferation and sensitized TRAIL-induced apoptosis in human cancer cells with both acquired and intrinsic TRAIL resistance. Combining the Bcl-X(L) siRNA with TRAIL protein treatment resulted in an increase in the percentage of apoptotic cells and increased cleavage of caspase-8, caspase-9, caspase-3 and PARP. Furthermore, the release of cytochrome c but not Smac from mitochondria was induced by Bcl-X(L) siRNA alone, and this release was dramatically amplified by combining the Bcl-X(L) siRNA and TRAIL protein treatment. Together, our data suggest that simultaneous triggering of the death receptor and mitochondrial apoptotic pathways leads to enhanced induction of apoptosis, which makes it potentially useful for the treatment of resistant cancers.

Apoptosis↗
PubMed2001

Effect of interferon-gamma on the susceptibility to Fas (CD95/APO-1)-mediated cell death in human hepatoma cells.

Many tumors, including hepatocellular carcinomas (HCCs), resist Fas-mediated cell death, which is one of the effector mechanisms in the host's anti-tumor response; however, this resistance can be abolished by interferon-gamma (IFN-gamma). IFN-gamma may sensitize Fas-mediated cell death in several ways, but the exact mechanism in HCCs is uncertain. In this study, we thoroughly investigated the effect of IFN-gamma on the susceptibility of one human normal liver cell line and 12 HCC cell lines to Fas-mediated cell death. We also investigated the effect of IFN-gamma on the expression of various apoptosis-related genes such as the Fas/TNF-related genes, the bcl-2 family, and the caspase family of genes. Although most cell lines showed considerable constitutive expression of Fas, all tested cell lines resisted Fas-mediated cell death without IFN-gamma. When cells were pretreated with IFN-gamma, only three cell lines were made significantly susceptible to Fas-mediated cell death (SNU-354, SNU-387 and SNU-423); the other 10 cell lines were not affected. IFN-gamma increased the mRNA expression of Fas, TRAIL and caspase-1, and surface Fas was also increased. The strongly sensitized cell lines (SNU-354, SNU-387 and SNU-423) showed a particularly potent increment in surface Fas after IFN-gamma treatment (increase in surface Fas > 1.7-fold). This result enabled us to conclude that a potent increment of surface Fas expression is a major sensitizing mechanism of IFN-gamma. We conclude that IFN-gamma cannot play a sensitizing role in most HCC cell lines and that IFN-gamma makes HCC cells susceptible to Fas-mediated cell death through a marked up-regulation of surface Fas in some HCC cells.

Apoptosis↗
PubMed2006

Cognitive deficits and levels of IQ in adolescent onset schizophrenia and other psychotic disorders.

Cognitive deficits have been found to be prevalent in early onset schizophrenia. Whether these deficits also characterise other early onset psychotic disorders to a similar degree is unclear, as very few comparative studies have been done. The primary purpose of this study was to compare the profile and severity of cognitive impairments in first-episode early onset psychotic patients who received the schizophrenia diagnosis to those diagnosed with other non-organic, non-affective psychotic disorders. The secondary purpose was to examine whether the profile of cognitive deficits, in terms of intelligence, executive functions, memory, attention and processing speed was global or specific. First-episode psychotic adolescents (N = 39) between the ages 11 and 17 years were included, 18 of whom were diagnosed with schizophrenia, and 21 with other non-organic, non-affective psychoses, using ICD-10 criteria. A healthy control group (N = 40) was included, matched on gender and age. Cognitive functions were assessed using WISC-III/R, the CANTAB battery, WCST, Trail Making B, fluency tasks, and Buschke's selective reminding task. A similar profile and level of impairment was found on measures of attention, executive functions, reaction time, and memory in the schizophrenic and psychotic adolescent groups. However, analyses of WISC-III factor profiles suggested that early onset schizophrenia patients may have more global IQ deficits than non-organic, non-affective psychoses when examined recently after illness onset. Compared to the deficits of adult schizophrenia described in the literature, the results suggest relatively spared simple reaction times in early onset patients.

Adolescent↗
PubMedDate not supplied

Protracted neurotoxicity from chlordane sprayed to kill termites.

Over 250 adults and children were exposed to chlordane when the wooden building surfaces and soil around an apartment complex were sprayed in 1987. Two hundred-sixteen adults had neurobehavioral functions measured and completed questionnaires for symptom frequency, mood status, confounding factors, and medical, rheumatic, and respiratory disorders in 1994. Measurements included simple and choice reaction time, balance, blink reflex latency, color vision, cognitive, perceptual motor, memory, and recall functions. We analyzed 216 exposed and 174 referent adults. Age, educational level, weight, height, and gender ratio were similar for the exposed and referent groups. Performance of balance, reaction times, Culture Fair, digit symbol, verbal recall, and trail-making were significantly impaired in exposed persons compared to referents. Mood-state scores were elevated, as were the frequencies of respiratory, neurobehavioral, and rheumatic symptoms. In contrast, long-term memory function was similar in both groups, consistent with its status before exposure. There was no identified bias or confounding factors. Chlordane exposure was associated with protracted impairment of neurophysiological and psychological functions. The central nervous system is the most important target of chlorinated cyclodiene insecticides. Human exposure should be prohibited.

Adolescent↗
PubMed2003

Early and pre-symptomatic neuropsychological dysfunction in the PPND family with the N279K tau mutation.

The N279K mutation on the tau gene of chromosome 17 leads to an inherited condition that involves pallido-ponto-nigral degeneration (PPND). Patients with PPND develop dementia, but the pattern and onset of cognitive dysfunction has not yet been delineated. Four affected patients underwent neurocognitive evaluation within the first 2 years of PPND motor onset; one of whom underwent five serial neurocognitive evaluations, and another who was not diagnosed with PPND until the third annual evaluation. Impaired letter fluency was found in the early stages of PPND and was also shown to precede the onset of motor symptoms by 2 years. Trail Making A (visual scanning and motor speed) and Trail Making B (divided attention) were impaired within the first 2 years of the disease in all but one patient, but this individual showed clinically significant decline on these tasks by the third year of the disease. Learning, memory, and timed visuospatial sequencing skills were variably affected. Results reveal disproportionate frontal-executive dysfunction early in PPND disease course, a pattern similar to what has been reported in other FTDP-17 kindreds and in sporadic PSP. In addition, results suggest that letter fluency may be a sensitive predictor of incipient PPND.

Chromosomes, Human, Pair 17↗
PubMed1976

[The possibility of a standardization of clinical trials concerning materials for root canal obturation].

Clinical trials constitute epidemiologic experiments, in comparable groups of human populations designed to assess the preventive of curative effects of agents or measures. International organizations (FDI, WHO, CIOMS, ISO) have been instrumental in creating uniform methods, so that the findings from different sources can be validly compared. The need for a standardization of clinical trials in dentistry is particularly felt: - by the dental profession in order to make the choice of materials with the best clinically proven qualities - by the manufacturers in order to develop materials of improved clinical quality - by the public health administrators (or social security agencies), in order to either evaluate the benefit of instituted preventive and curative measure or to ascertain the best possible services A centennial history of efforts is shown to have resulted today in a broad international understanding (Table III). 1. The first chapter of this paper presents a review of the principal requirements for controlled clinical trails [8] such as officially adopted by FDI (Table V). 2. The second chapter offers a first-hand apercu of impending recommendations proposed by COMIET in two protocols [11] for the uniform conduct and evaluation of clinical trials of restorative techniques and materials. 2.1 Three standardized forms (A, B: Table IX, and C) serve to uniformly record data of the operative procedures. 2.2 The proposed standardized criteria (Tables X, XI) for the clinical appraisal of distinct materials give the advantage of having been tested already very extensively. 3. A critical review of the proposed protocols [11] reveals the necessity of: 3.1 referring to and coordinating with the already adopted principal requirements for controlled clinical trials. 3.2 generally adopting the excellent guidelines for the conduct of the study and the evaluation of observations (Tables X, XI) 3.3 taking advantage of the possibilities for reducing the recommended sample of 100 paired restorations (200 cavities)--difficult to implement in many countries--by certain measure such as preliminary in-vitro experiments, consideration of results already reported in the literature and a more systematic use of a standardized photographic serial documentation, a topic which will be the object of an ensuing paper.

International Cooperation↗
PubMed2005

A proposed stoichiometrical calibration procedure to achieve transferability of D-dimer measurements and to characterize the performance of different methods.

BACKGROUND: There is little transferability between D-dimer levels obtained by different reagents today. This makes it difficult to compare results from different clinical studies. OBJECTIVES: We give a comprehensive proposal for calibration of D-dimer assays. All crucial steps and underlying assumptions are made explicit. METHODS: The new approach is based on using a set of fibrinolysates of patient samples clotted and treated with tPA to obtain maximal conversion to D-dimers. Their expected maximal D-dimer concentrations are calculated stoichiometrically from their different fibrinogen values and the published molecular masses of fibrinogen and average D-dimer. The characteristics of five latex enhanced D-dimer immunoassays were also tested against early and late fibrin fragments using this procedure. These were produced by prolonged fibrinolysis of a set of patient samples of varying fibrinogen concentrations. RESULTS: These varied typically between methods and lysis times. One of the methods showing the highest yield irrespective of lysis time was used for calibration. A linear standard curve with zero intercept and R2 = 0.95 was obtained. CONCLUSION: Following this procedure will allow better transferability of D-dimer in future clinical trails.

Biological Assay↗
PubMed2006

Testing the recommendations of the Washington State Nutrition and Physical Activity Plan: the Moses Lake case study.

BACKGROUND: The Washington State Nutrition and Physical Activity Plan provides a framework in which policy makers can work together to build and support healthy environments for nutrition and physical activity. The city of Moses Lake, Wash, was chosen to serve as a pilot site to test the conceptual approaches and recommendations of the plan and to develop a model for healthy communities elsewhere in the state. CONTEXT: Moses Lake is an ethnically diverse, geographically isolated town with a population of about 15,000. METHODS: An advisory committee used data from an inventory of local policies and environments, along with the recommendations from the state plan, to develop a plan for Healthy Communities Moses Lake. Three initiatives were chosen for the first actions: a connected system of trails and paths, enhanced facilities for breastfeeding in the community, and a community garden. CONSEQUENCES: Records of cumulative actions demonstrated that Healthy Communities Moses Lake continued to be an active and productive project. Initial measures of success were collected by each of the three first action teams. Environmental changes will be monitored by comparison with the initial inventory of local policies. Long-term health outcomes in Moses Lake will be monitored by the Washington State Department of Health. INTERPRETATION: Healthy Communities Moses Lake was successful because the city had leaders and volunteers who were committed to making the city a healthier place. Lessons learned about community-based planning and evaluation are now being applied to Healthy Communities initiatives.

Community Health Services↗
PubMed2006

Neuropsychological predictors of decision-making capacity over 9 months in mild-to-moderate dementia.

BACKGROUND: Older adults with dementia may have diminished capacity to make medical treatment decisions. OBJECTIVE: To examine rates and neuropsychological predictors of treatment decision making, or consent capacity, among older adults with dementia over 9 months. DESIGN: Consent capacity was assessed initially and 9 months later in subjects with and without dementia using a longitudinal repeated measures design. PARTICIPANTS: Fifty-three older adults with dementia and 53 similarly aged adults without dementia. MEASUREMENTS: A standardized measure MacArthur Competence Assessment Tool-Treatment of 4 legal standards for capacity (Understanding, Appreciation, Reasoning, and Expressing a Choice) and a neuropsychological battery. RESULTS: In the dementia group, 9.4% had impaired capacity initially, and 26.4% had impaired capacity at 9 months. Mean scores in the dementia group were impaired relative to controls initially and at 9 months for Understanding (initial t=2.49, P=.01; 9-month t=3.22, P<.01) and Reasoning (initial t=2.18, P=.03; 9-month t=4.77, P<.01). Declining capacity over 9 months was attributable to a further reduction in Reasoning (group x time F=9.44, P=.003). Discriminant function analysis revealed that initial scores on naming, delayed Logical Memory, and Trails B were associated with impaired capacity at 9 months. CONCLUSIONS: Some patients with mild-to-moderate dementia develop a clinically relevant impairment of consent capacity within a year. Consent capacity in adults with mild-to-moderate dementia should be reassessed periodically to ensure that it is adequate for each specific informed consent situation. Interventions that maximize Understanding and Reasoning by supporting naming, memory, and flexibility may help to optimize capacity in this patient group.

Aged↗
PubMedDate not supplied

Building brands without mass media.

Costs, market fragmentation, and new media channels that let customers bypass advertisements seem to be in league against the old ways of marketing. Relying on mass media campaigns to build strong brands may be a thing of the past. Several companies in Europe, making a virtue of necessity, have come up with alternative brand-building approaches and are blazing a trail in the post-mass-media age. In England, Nestlé's Buitoni brand grew through programs that taught the English how to cook Italian food. The Body Shop garnered loyalty with its support of environmental and social causes. Cadbury funded a theme park tied to its history in the chocolate business. Häagen-Dazs opened posh ice-cream parlors and got itself featured by name on the menus of fine restaurants. Hugo Boss and Swatch backed athletic or cultural events that became associated with their brands. The various campaigns shared characteristics that could serve as guidelines for any company hoping to build a successful brand: senior managers were closely involved with brand-building efforts; the companies recognized the importance of clarifying their core brand identity; and they made sure that all their efforts to gain visibility were tied to that core identity. Studying the methods of companies outside one's own industry and country can be instructive for managers. Pilot testing and the use of a single and continuous measure of brand equity also help managers get the most out of novel approaches in their ever more competitive world.

Advertising↗
PubMed2001

Green fluorescent protein as a novel tool to measure apoptosis and necrosis.

BACKGROUND: Several apoptosis-detecting methods are currently available. Many of them are work intensive and require the additional use of antibodies, dyes, specific substrates, or enzymatic reactions. A simple, fast, and reliable method was developed to test for apoptosis or necrosis using mouse and human cell lines (e.g., Jurkat, A20.2J, and PB3c cells) stably transfected with a vector coding for green fluorescent protein (GFP) as indicator cells. METHODS: Apoptosis in GFP-transfected cell lines was induced either by soluble Fas-Ligand (sFasL), recombinant human TRAIL (rhTRAIL), or interleukin-3 (IL-3) deprivation. Necrosis was induced by polyclonal anti-A20 and complement treatment of GFP-transfected A20. Cells were analyzed by flow cytometry for GFP fluorescence. Propidium iodide and Annexin V staining were used to confirm the results obtained with the GFP-method. RESULTS: Live GFP-transfected cells show a strong fluorescence intensity, which is significantly diminished upon induction of apoptosis, whereas necrotic GFP-transfected cells almost completely lose their GFP-associated fluorescence. Apoptosis but not necrosis of GFP-transfected cells was blocked by the use of a caspase inhibitor. The results are highly comparable to conventional apoptosis-detecting methods. CONCLUSIONS: The advantage of our GFP-based assay compared with other methods is the analysis of apoptosis or necrosis without the necessity for additional staining or washing steps, making it an ideal tool for screening apoptotic or necrotic stimuli.

Animals↗
PubMed2005

Inhibition of TRAIL-induced apoptosis by IL-8 is mediated by the p38-MAPK pathway in OVCAR3 cells.

INTRODUCTION: TRAIL (TNF-Related Apoptosis Inducing Ligand) is a member of the TNF superfamily of cell death inducing ligands. Interestingly, while malignant cells are responsive to TRAIL-induced cell death when used alone or in combination with other agents, normal cells do not appear to be sensitive to this ligand, making it a desirable therapeutic compound against many cancers, including many ovarian carcinomas. Interleukin-8 (IL-8), a member of the C-X-C chemokine family, has been found to be at significantly higher level in the ascites from patients with ovarian cancer. We have previously demonstrated a role for IL-8 in blocking TRAIL's ability to induce apoptosis in the ovarian cancer cell line, OVCAR3, possibly by repressing the DR4 TRAIL receptor expression and blocking caspase-8 cleavage. In addition, we showed a member of the mitogen-activated protein kinase (MAPK) superfamily, p38gamma, is among the genes regulated in OVCAR3 cells by TRAIL and IL-8. The present study further investigates involvement of the p38 MAPK pathway in IL-8's ability to block TRAIL-induced apoptosis in the ovarian surface epithelial cancer cell line, OVCAR3. RESULTS: In this study we demonstrate that p38gamma as well as p38alpha play a significant role in IL-8's ability to block TRAIL-induced apoptosis. Through array analysis, as well as confirmation with other methods, we detected regulation of p38gamma and p38alpha following treatment of the cancer cell line with IL-8 or TRAIL. We also tested two other isoforms of p38 MAPK, p38beta and p38delta, but did not find significant regulation by IL-8 or TRAIL. We also examined activation of the p38 MAPK pathway, up-stream as well as down-stream, and noticed activation of the pathway following treatment with TRAIL and decreased activity when IL-8 was introduced. With the use of specific inhibitors, we were able to further confirm the role of this pathway in TRAIL-induced apoptosis, and IL-8's ability to block this apoptosis, in ovarian cancer cell lines. CONCLUSION: Taken together, these results further solidify the role of IL-8 in blocking the TRAIL-induced apoptosis in these ovarian carcinoma cells and provide new molecular insight into this potentially important therapeutic target.

Activating Transcription Factor 2↗
PubMed2002

Effects of acute hypoglycaemia on auditory information processing in adults with Type I diabetes.

AIMS/HYPOTHESIS: Acute hypoglycaemia in humans causes general impairment of cognitive function, but information about its effects on more specific cognitive processes is limited. METHODS: Basic aspects of auditory function were studied in 15 adults with uncomplicated Type I (insulin-dependent) diabetes mellitus. Two separate hyperinsulinaemic glucose clamp procedures were done on different study days, in a counterbalanced fashion, either maintaining euglycaemia (blood glucose 5.0 mmol x l(-1)) or inducing hypoglycaemia (blood glucose 2.6 mmol x l(-1)). During each study, the subjects performed a battery of auditory and cognitive function tasks. RESULTS: Hypoglycaemia caused deterioration in mental efficiency as assessed by Digit Symbol (p<0.001) and Trail Making B (p=0.004) tasks. Acute hypoglycaemia also caused deterioration in one of three measures of simple auditory processing (single-tone loudness, p=0.001) and in auditory temporal processing (p=0.007). The amplitude and latency of auditory N100, P200 and P300 event-related potentials were not affected, but the amplitude of the N240 potential was reduced during acute hypoglycaemia. CONCLUSION/INTERPRETATION: Our findings are consistent with other recognised disruptive effects of acute hypoglycaemia on sensory information processing in non-diabetic and diabetic adults, including adverse effects on auditory information processing in non-diabetic subjects. These derangements have implications for the everyday activities of people with Type I diabetes who are frequently exposed to acute hypoglycaemia.

Acute Disease↗
PubMed1996

Relationship between alcohol withdrawal seizures and temporal lobe white matter volume deficits.

A previous magnetic resonance imaging study from our laboratory reported significant temporal lobe volume deficits in cortical gray matter, white matter, and anterior hippocampus in chronic alcoholic men relative to controls. In the present study, we reexamined these data and asked whether withdrawal seizure history was predictive of either the hippocampal or the extrahippocampal volume deficits. A review of the medical charts indicated that 11 alcoholics had experienced one or more alcohol-related seizures and 35 were seizure-free; no patient had a seizure disorder unrelated to alcohol. The two alcoholic groups did not differ significantly in age, education, alcohol consumption variables, premorbid intelligence, Memory Quotient, Trail Making, or detection of hidden figures. Although each alcoholic group showed significant bilateral volume deficits of the anterior hippocampus and frontal-parietal and temporal gray matter, relative to controls, the seizure group had significantly smaller temporal lobe white matter volumes than either the control or the seizure-free groups; the latter two groups did not differ from each other. Both alcoholic groups, however, had white matter volume deficits in the frontal-parietal region. Thus, the seizure group accounted for the white matter volume deficits in the temporal lobe previously reported in the full sample of alcoholics. It seems, then, that reduced white matter volume in the temporal lobes may be either a risk factor for or sequela of alcohol withdrawal seizures.

Adult↗