Public hospital-based level I trauma centers: financial survival in the new millennium

BACKGROUND: The medical benefits of trauma centers have been well documented; studies have reported substantial financial losses attributed to trauma care. This study demonstrates the dependence of Level I trauma centers on Disproportionate Share Hospital (DSH) governmental funds and tax dollars. Furthermore, specific injury groups have greater dependence on these funds. METHODS: Records of 553 trauma patients admitted to a public urban Level I trauma center during a 6-month period were reviewed. Patients were grouped according to blunt, penetrating, and thermal injuries. Data for each group included charges, costs, payments, and the source of reimbursement. Profit and loss margins were compared with and without government funds. RESULTS: With diminished DSH funds and tax dollars, a net loss over $2.1 million was incurred. The greatest disparity originates from Medicaid, self-pay, and prisoner patient groups. Inclusion of government funds provided a positive return of over $600,000. CONCLUSION: The financial stability of urban public Level I trauma centers without additional funding is tenuous because of a high proportion of uninsured and underinsured patients. Government tax dollars and DSH funds are required for their continued solvency.     

New method to generate enzymatically deficient Clostridium difficile toxin B as an antigen for immunization

The family of the large clostridial cytotoxins, encompassing Clostridium difficile toxins A and B as well as the lethal and hemorrhagic toxins from Clostridium sordellii, monoglucosylate the Rho GTPases by transferring a glucose moiety from the cosubstrate UDP-glucose. Here we present a new detoxification procedure to block the enzyme activity by treatment with the reactive UDP-2', 3'-dialdehyde to result in alkylation of toxin A and B. Alkylation is likely to occur in the catalytic domain, because the native cosubstrate UDP-glucose completely protected the toxins from inactivation and the alkylated toxin competes with the native toxin at the cell receptor. Alkylated toxins are good antigens resulting in antibodies recognizing only the C-terminally located receptor binding domain, whereas formaldehyde treatment resulted in antibodies recognizing both the receptor binding domain and the catalytic domain, indicating that the catalytic domain is concealed under native conditions. Antibodies against the native catalytic domain (amino acids 1 through 546) and those holotoxin antibodies recognizing the catalytic domain inhibited enzyme activity. However, only antibodies against the receptor binding domain protected intact cells from the cytotoxic activity of toxin B, whereas antibodies against the catalytic domain were protective only when inside the cell.     

Cardiac abnormalities in end stage renal failure and anaemia

Thirteen anaemic children on dialysis were assessed to determine the incidence of cardiac changes in end stage renal failure. Nine children had an increased cardiothoracic ratio on radiography. The electrocardiogram was abnormal in every case but no child had left ventricular hypertrophy as assessed by voltage criteria. However, left ventricular hypertrophy, often gross, was found on echocardiography in 12 children and affected the interventricular septum disproportionately. Cardiac index was increased in 10 patients as a result of an increased left ventricular stroke volume rather than heart rate. Left ventricular hypertrophy was significantly greater in those on treatment for hypertension and in those with the highest cardiac index. Abnormal diastolic ventricular function was found in 6/11 children. Children with end stage renal failure have significant cardiac abnormalities that are likely to contribute to the high cardiovascular mortality in this group. Anaemia and hypertension, or its treatment, probably contribute to these changes. Voltage criteria on electrocardiogram are of no value in detecting left ventricular hypertrophy. Echocardiography must be performed, with the results corrected for age and surface area, in order to detect and follow these abnormalities.     

Erythropoietin receptor expression in human melanoma cells

Erythropoietin is well known for its role in the control of erythropoiesis, where it acts by binding to its cognate receptor (EpoR) on the surface of erythroid progenitor cells. Here we present the novel finding that the EpoR is also expressed in cells of the melanocytic lineage. It is expressed in transformed cell lines established from normal melanocytes and also in established human melanoma cell lines derived from melanoma metastases, but not in normal primary human melanocytes. The analysis of individual subclones isolated from spontaneously transformed melanocytes revealed that approximately 50% of all the clones examined expressed the EpoR. Further analysis of the individual growth characteristics of EpoR-positive and EpoR-negative clones indicated that, under standard cell culture conditions, expression of the receptor did not affect cell growth. Expression of this receptor is consequently most likely driven by an event that is associated with, but not absolutely required for, the transformed phenotype. While the definite function of this receptor in melanoma cells is still unknown and additional studies are required, our findings support the hypothesis that the EpoR may serve as a progression marker for human melanoma. This observation might be useful in the early diagnosis of melanoma.     

Frequency-dependent effects of phenytoin on frog junctional transmission: Presynaptic mechanisms

The action of the antiepileptic drug, phenytoin, on junctional transmission at various frequencies of synaptic activation was studied in frog nerve-muscle preparation. Intracellular recordings were made from muscle end-plates, and extracellular focal and subsendothelial recordings were obtained from motor nerve terminals and their parent axons, respectively. When the motor nerve was stimulated at 100-200 Hz, exposure to the drug (0.1-0.3 mM) induced intermittent failures of junctional transmission which appeared faster as the rate of stimulation was increased. At these and at lower stimulation frequencies (30-50 Hz), in which failures of transmission occurred only rarely, phenytoin markedly limited the buildup of end-plate potential amplitude during the period of repetitive nerve stimulation (tetanic potentiation). Several lines of evidence suggest that both drug effects are consequent to a frequency-dependent depression of the action potential at motor axons and terminals, which could lead to an intermittent conduction block at the higher rates of stimulation. The selective action of phenytoin on high frequency synaptic transmission may contribute to the specificity shown by this drug in suppressing epileptic seizures while sparing neuronal activity.     

Rotator cuff tear: clinical experience with sonographic detection

Between June 1986 and April 1988, 86 sonographic examinations of the shoulder were performed on patients suspected of having rotator cuff tears. Major sonographic diagnostic criteria included (a) a well-defined discontinuity usually visible as a hypoechoic focus within the cuff, (b) nonvisualization of the cuff and (c) an echogenic focus within the cuff. Seventy-five patients underwent both sonography and arthrography. Compared with arthrography alone, ultrasound examinations enabled detection of 92% of rotator cuff tears (24 of 26 tears), with a specificity of 84% and a negative predictive value of 95%. Correlation was obtained in 30 of these patients who underwent surgery for rotator cuff tear or other soft-tissue abnormality. In this group, the sensitivity of sonography for detection of a tear was 93%, with a specificity of 73%, while for arthrography sensitivity was 87% and specificity was 100%. These data indicate that sonography is a useful, noninvasive screening procedure for patients suspected of having rotator cuff injury.     

On the temperature sensitivity of multiple sclerosis patients (author's transl)]

Aggravation of neurological symptoms in MS patients in heating is well known. This phenomenon is explained by the change of conduction in demyelinated nerve fibers. In raised temperature conduction block occurs. The threshold of conduction block dependent on temperature, is probably proportional to the degree of demyelination. It is possible to inhibit this effect by tyrosin. This model may present a view to a part of neurophysiological mechanisms of MS, on which we possibly can take therapeutical influence. By way of a questionnaire 125 MS patients were asked about changes of their symptoms in heating or cooling. 93% had marked sensitivity to heating. In 90% worsening of neurological symptoms or of general feeling occured in a hot bath. On the other hand about half the patients reported improvement in a cold bath. Therefore we suggest, that a noticeable part of neurological deficit is reversible, if we were able to raise the threshold of conduction block, which depends on temperature, ph, electrolytes and neurotransmitters.