Evaluation of NaOH treatment of human dura mater implants to obviate Creutzfeldt-Jakob disease transmission.

One of the few disinfectants known to inactivate the causative agent of Creutzfeldt-Jakob Disease is NaOH. In this study, NaOH was evaluated as a possible routine treatment for human dura mater alloimplants. Use of high concentration NaOH (1 M) resulted in protein loss and macroscopic changes to the tissue. Lower concentrations (0.1 M), although exhibiting little direct detrimental effect, greatly increased the susceptibility of the tissue to collagenase digestion. The use of NaOH treated commercial or institutionally prepared human dura mater should be approached with caution.     

Medical problem solving and uncertainty in the emergency department

STUDY OBJECTIVE: To compare the diagnostic processes of experienced emergency physicians with those of novices. DESIGN: Prospective, convenience sample of patients. SETTING: Emergency department of a county university medical center in a large southwestern urban community. PARTICIPANTS: Experienced emergency physicians (attending and senior residents) and novice clinicians (junior residents and senior medical students). INTERVENTIONS: Participants developed initial diagnostic impressions after reviewing the chief complaint, nurse triage notes, and vital signs. Tests were then selected, and a final diagnostic impression was identified after results were known. Clinicians also marked a visual analog scale corresponding to their estimate that each diagnostic possibility was correct. RESULTS: Experienced physicians increased their certainty more than novices (P = .014). They deviated from a standard history-physical-laboratory sequence more often than novices (P = .008). CONCLUSION: Expertise in medical decision making is characterized by a moderate initial level of certainty concerning a diagnosis that significantly increases as the experienced clinician follows a flexible strategy of testing to arrive at a final diagnosis.     

Retroviruses and schizophrenia in Jamaica

Reports of an 18-fold higher incidence of schizophrenia among second-generation Afro-Caribbeans, and especially Jamaican migrants in the United Kingdom were soon called “an epidemic of schizophrenia,” with the inference that a novel virus, likely to be perinatally transmitted, was a possible etiological agent. This intriguing observation led us to explore a possible link with human T-cell lymphotropic virus type one (HTLV-I), because it is a virus that is endemic in the Caribbean Islands, is perinatally transmitted, known to be neuropathogenic, and the cause of a chronic myelopathy (tropical spastic paraparesis/ HTLV-I associated myelopathy). We therefore examined inpatients at the Bellevue Mental Hospital, Kingston, Jamaica and did standard serological tests for retroviruses HTLV-I and HTLV-II and HIV-I and HIV-II on 201 inpatients who fulfilled ICD-9 and DSM III-R criteria for schizophrenia. Our results produced important negative data, since the seropositivity rates for HTLV-I, the most likely pathogen, were no greater than the seropositivity range for HTLV-I carriers in this island population, indicating that HTLV-I and the other retroviruses tested do not play a primary etiological role in Jamaican schizophrenics.     

Poliomyelitis outbreak in Natal/KwaZulu, South Africa, 1987-1988. 1. Epidemiology.

An epidemic of type 1 poliomyelitis occurred in Natal/KwaZulu in the eastern part of South Africa between December 1987 and November 1988. 412 poliomyelitis cases were reported, of whom 74% were younger than 5 years. The case-fatality rate was 8%. It is suggested that massive floods, experienced in the area 2 months earlier, triggered the outbreak.     

Examination of the roles of glycoprotein Ib and glycoprotein IIb/IIIa in platelet deposition on an artificial surface using clinical antiplatelet agents and monoclonal antibody blockade

The mechanism of platelet thrombus growth on an artificial surface is incompletely understood. While glycoprotein (GP)Ib and GPIIb/IIIa are required for normal attachment and thrombus formation on subendothelium, their roles in platelet deposition to artificial surfaces remain unclear. Using selected platelet inhibitors (aspirin [ASA], low molecular weight dextran, monoclonal antibodies 10E5 [v GPIIb/IIIa], and 6D1 [GPIb]) we examined the mechanism of platelet deposition to polyethylene (PE) surfaces under steady laminar and oscillatory flow conditions. Polyethylene-100 (PE-100) tubes (0.86 mm internal diameter) were perfused under steady laminar flow with citrated human whole blood reconstituted with 111indium-labeled platelets at 312 seconds-1 shear rate in the presence and absence of platelet inhibitors. The effect of oscillatory flow on platelet deposition was examined in a microwell system using 3/16-inch diameter discs of National Heart, Lung, and Blood Institute primary reference PE as the test surface. ASA and dextran did not significantly (P greater than .05) inhibit platelet deposition in laminar flow (not tested in oscillatory). Antibody 10E5 was a potent inhibitor (laminar less than 1%, P less than .0001, oscillatory less than 1.6%, P less than .01) of platelet deposition in both systems, and in this case, true adhesion (first attached layer) was blocked. Antibody 6D1 unexpectedly inhibited 70% of platelet deposition (P less than .01) in steady laminar flow and 56.5% in oscillatory flow (P less than .01). Scanning electron microscopy demonstrated platelets atop platelets in the controls, rare platelets in the 10E5 group, and a patchy monolayer of platelets in the 6D1 group. Transmission electron microscopy of cross-sections confirmed these observations. We conclude that the adhesion of the first platelet layer to an artificial surface requires GPIIb/IIIa. The data also suggest that GPIb is required for the development of the second layer in vertical platelet thrombus growth.