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Biomedical subjects

John W Thompson

Publications and source records attributed to John W Thompson.

13 recordsLinked to original sources
PubMed2006

The review panel process: an algorithm for the conditional release of insanity acquittees.

The release of insanity acquittees requires making informed decisions regarding both the presence and severity of an individuals' mental illness and the dangerousness of these individuals. This study evaluated the usefulness of employing structured assessments of mental health and violence risk factors in the conditional release decision-making process. All persons found Not Guilty by Reason of Insanity at East Louisiana Mental Health System, Forensic Division who underwent a review panel between July 1, 1997 and July 1, 1999 were included in this study. The Classification and Regression Tree analysis was utilized to arrive at cutpoints that would optimize the predictive ability of the decision tree analysis. The results indicated that the Community Outpatient Treatment Readiness Profile score was the strongest predictor -- all patients receiving a score of 62 or greater on this scale were recommended to remain at the facility. When women were recommended for release, it was to civil facilities and with moderate levels of symptoms. For males with moderate symptoms, low PCL-R scores were associated with recommendations for release, whereas high scores were associated with recommendations for continued commitment. Our data suggests that algorithms may be useful to governing bodies when making release decisions.

Adult↗
PubMed2004

The New Orleans Forensic Aftercare Clinic: a seven year review of hospital discharged and jail diverted clients.

This paper provides a review of the Forensic Aftercare Clinic Conditional Release Program (FAC), which has been operating since December, 1995, in New Orleans, LA. The FAC is a community based program that provides clinical, rehabilitative, and supervisory services to individuals who have been found not guilty by reason of insanity or unrestorably incompetent to proceed and who have been discharged from inpatient settings or diverted from jail settings and placed on conditional release by district court orders. 119 clients participated in FAC over a 7 year period. Forty-one (34.4%) had their conditional release revoked. Of the total population, 12 (10.1%) were re-arrested on at least one charge, 3 (2.4%) were arrested on felony charges, and 9 (7.6%) on misdemeanors. Only two of these charges were violent, resulting in no significant harm to victims. Twenty (16.8%) were hospitalized at least once due to relapse. Clients diverted from jail to community settings did not differ significantly on most variables from clients who were discharged from long-term hospitalization. Data related to public safety and client diversion demonstrate that clients, when appropriate, can be safely diverted to the community in lieu of hospitalization. The number of statewide clients who have been discharged from the forensic hospital into the community has increased steadily from 13 in 1995 to 29 in 2002, and statewide diversion clients have steadily increased from 0 in 1992 to 20 in 2002. The increase in statewide diversion clients and forensic discharges over this 7 year period indicates that stakeholders see the viability of the program as an alternative to as well as a step-down from long-term forensic hospitalization.

Adult↗
PubMed2004

A unique pathway of cardiac myocyte death caused by hypoxia-acidosis.

Chronic hypoxia in the presence of high glucose leads to progressive acidosis of cardiac myocytes in culture. The condition parallels myocardial ischemia in vivo, where ischemic tissue becomes rapidly hypoxic and acidotic. Cardiac myocytes are resistant to chronic hypoxia at neutral pH but undergo extensive death when the extracellular pH (pH[o]) drops below 6.5. A microarray analysis of 20 000 genes (cDNAs and expressed sequence tags) screened with cDNAs from aerobic and hypoxic cardiac myocytes identified >100 genes that were induced by >2-fold and approximately 20 genes that were induced by >5-fold. One of the most strongly induced transcripts was identified as the gene encoding the pro-apoptotic Bcl-2 family member BNIP3. Northern and western blot analyses confirmed that BNIP3 was induced by 12-fold (mRNA) and 6-fold (protein) during 24 h of hypoxia. BNIP3 protein, but not the mRNA, accumulated 3.5-fold more rapidly under hypoxia-acidosis. Cell fractionation experiments indicated that BNIP3 was loosely bound to mitochondria under conditions of neutral hypoxia but was translocated into the membrane when the myocytes were acidotic. Translocation of BNIP3 coincided with opening of the mitochondrial permeability pore (MPTP). Paradoxically, mitochondrial pore opening did not promote caspase activation, and broad-range caspase inhibitors do not block this cell death pathway. The pathway was blocked by antisense BNIP3 oligonucleotides and MPTP inhibitors. Therefore, cardiac myocyte death during hypoxia-acidosis involves two distinct steps: (1) hypoxia activates transcription of the death-promoting BNIP3 gene through a hypoxia-inducible factor-1 (HIF-1) site in the promoter and (2) acidosis activates BNIP3 by promoting membrane translocation. This is an atypical programmed death pathway involving a combination of the features of apoptosis and necrosis. In this article, we will review the evidence for this unique pathway of cell death and discuss its relevance to ischemic heart disease. The article also contains new evidence that chronic hypoxia at neutral pH does not promote apoptosis or activate caspases in neonatal cardiac myocytes.

Acidosis↗
PubMed2003

Effect of an individualized treatment protocol on restoration of competency in pretrial forensic inpatients.

In this study, we evaluated the effectiveness of individualized treatment on restoration of competency in patients adjudicated incompetent to stand trial. Treatment groups included deficit-focused remediation (six individual sessions and four group sessions; n = 8), legal rights education (control group; six individual sessions and four group sessions; n = 10), and standard hospital treatment (control group; four group sessions; n = 8). There were no significant baseline differences among groups. All groups differed significantly on competency measures obtained before and after testing. The deficit-focused remediation and the legal rights education groups both demonstrated significantly higher post-treatment scores on competency measures than the standard hospital treatment group. Both groups demonstrated approximately 50 percent more improvement on the competency measures than the standard hospital treatment group. There were no significant differences between the deficit-focused remediation and legal rights education groups on post-test competency scores, suggesting that focus on individual deficits may not be a useful treatment strategy. Results demonstrate, however, that more frequent legal rights education is a worthwhile endeavor in treatment of incompetency.

Adolescent↗
PubMed2003

The influence of French, Spanish, and English legal traditions on early mental health proceedings in Louisiana.

Unlike other jurisdictions in the United States where the basis of the law can be traced more exclusively to the common law of England, the legal system in Louisiana also has origins in the laws of France and Spain. In this article, the authors describe the laws and procedures that developed early in Louisiana's history for the involuntary care and civil commitment of the mentally ill, focusing on the laws that were passed after the American takeover in 1803.

Civil Rights↗
PubMed2002

Mechanisms for maintaining extracellular glutamate levels in the anoxic turtle striatum.

The turtle Trachemys scripta is one of a limited group of vertebrates that can withstand hours to days without oxygen. One facet of anoxic survival is the turtle's ability to maintain basal extracellular glutamate levels, whereas in most vertebrates, anoxia triggers massive excitotoxic glutamate release. We investigated glutamate release and reuptake in the anoxic turtle and the effects of adenosine and ATP-sensitive potassium (K(ATP)) channels on glutamate homeostasis. Striatal extracellular glutamate was measured in anesthetized T. scripta by microdialysis in normoxia and over 2-h anoxia. Glutamate release is decreased by 44% in the early anoxic turtle; this anoxia-induced decrease in glutamate release was prevented when K(ATP) channels and adenosine receptors were blocked simultaneously but not when either mechanism was blocked individually. We hypothesize that the continued release and reuptake of glutamate during anoxia help maintain neuronal tone and aid in the recovery of a functional neuronal network after long periods of anoxia, whereas activation of adenosine and/or K(ATP) conserves energy by reducing glutamate release and lowering transport costs.

Adenosine↗
PubMed2002

Novel cases: malingering by animal proxy.

Malingering to obtain medications of abuse is well documented in the general medical setting. However, we have found no cases previously reported of such malingering in a veterinary setting. We report five cases submitted by veterinarians in which clients (pet owners) are strongly suspected or confirmed to have been engaging in malingering to obtain controlled medications for their personal use. Cases bear a striking resemblance to malingering in the general medical setting for drugs to abuse. We propose that veterinarians, like their medical counterparts, are potential targets of malingering by their clients for drugs of abuse. Because of their familiarity with this condition, psychiatrists may have a role in training veterinarians to recognize malingering on the part of their human clients. In addition, psychiatrists may benefit from familiarizing themselves with novel forms of malingering, such as are presented in this case series.

Adult↗
PubMed1989

The detection of psychiatric illness and psychological handicaps in a British pain clinic population.

Ninety-seven successive patients attending the Newcastle Pain Relief Clinic completed a battery of psychiatric, psychological and pain questionnaires, and an extensive personal information form. All patients were seen by a physician who evaluated the extent of the pain arising from physical, psychiatric and psychological causes, and by a psychiatrist, who administered a structured interview schedule. Thirty-two percent of the patients had sufficient symptoms to be classified as psychiatric cases on the Present State Examination (PSE), a further 22% had minor neurotic symptoms and features of illness behaviour, 35% were categorized as organic, and 11% were unclassified. The Leeds General Depression Scale for Depression and Anxiety and the Beck Depression Inventory were the most effective of the psychiatric questionnaires used in separating the psychiatric patients from the remainder, and can be recommended as screening instruments for psychiatric illness in this population. Factors associated with a psychiatric diagnosis included female sex, larger number of present medications, greater reduction in activities compared to the period before the pain developed and increasing subjective pain from the onset of this.

Chronic Disease↗
PubMedDate not supplied

Acidosis regulates the stability, hydrophobicity, and activity of the BH3-only protein Bnip3.

Bnip3 is a prodeath member of the so-called BH3-only subfamily of Bcl-2 proteins. A major function of this class of proteins is to regulate the permeability state of the outer mitochondrial membrane by forming homoand hetero-oligomers inside the membrane. We reported previously that Bnip3 accumulates in cardiac myocytes during exposure to hypoxia, but coincident acidosis is required to activate the death program. Acidosis increased the rate of intracellular accumulation of Bnip3 and promoted a tighter association with mitochondria. Here we report that acidic pH mediates increased half-lives of Bnip3 dimers and monomers (>3-) as well as that of a faster-migrating fragment (>10-) and confers protection against degradation by protease. Hydrophobic partitioning experiments revealed that Bnip3 monomers and oligomers from hypoxia-acidic cell fractions associated significantly with the detergent layer, whereas protein from hypoxia-neutral myocytes did not. Acidosis promoted homodimerization of Bcl-xL but did not increase its association with detergent. Neutralization of the extracellular medium of cardiac myocyte cultures under hypoxia-acidosis resulted in rapid degradation of accumulated Bnip3 (half life, <2 h), coincident with cessation of the death program. Bnip3 monomers appear to be the active species because substitution of alanine for histidine at position 173 within the transmembrane (TM) domain prevented homodimerization but did not inhibit the death function. These results demonstrate a pH-sensitive shift in the stability and apparent hydrophobicity of Bnip3 monomers that correlates closely with membrane binding and function.

Acidosis↗
PubMedDate not supplied

Redox stress and the contributions of BH3-only proteins to infarction.

Ischemia followed by reperfusion is the primary cause of tissue injury and infarction during heart attack and stroke. The initiating stimulus is believed to involve reactive oxygen species that are produced during reperfusion when electron transport resumes in the mitochondria after suppression by ischemia. Programmed death has been shown to be a significant component of infarction, and evidence indicates that multiple pathways are initiated during both ischemia and reperfusion phases. Major infarction is preceded by severe ischemia that includes hypoxia, intracellular acidosis, glucose depletion, loss of ATP, and elevation of cytoplasmic calcium. The superimposition of a reactive oxygen surge on the latter condition provides the impetus for maximal damage. Compelling evidence implicates mitochondria not only as the source of initiating ROS but also as the focal sensors that translate the redox stress signal into a cellular-death response. Pivotal to this response are the BH3-only proteins that are activated by death signals and regulate mitochondrial communication with executioner proteins in the cytoplasm. The BH3-only proteins do this by controlling the activity of pores and channels in the outer mitochondrial membrane. To date at least six BH3-only proteins have been shown to contribute to ischemia-reperfusion death pathways in heart and/or brain; these include Bnip3, PUMA, Bid, Bad, HGTD-P, and Noxa. Here we review the evidence for these cell-death pathways and discuss their relevance to ischemic disease and infarction.

Animals↗