Frequently asked questions (and answers) about Hawaii's new Uniform Health Care Decisions Act (Modified)

The Hawaii Uniform Health Care Decisions Act (Modified) became law, effective July 1, 1999. The Act makes major changes the law pertaining to Advance Directives and surrogate decision-making. While some of the changes seem to be confusing, most practitioners should find the new law helpful in attempting to assure that the rights of their patients to self-determination and autonomy are preserved and their wishes are followed. Using a question and answer format, this article will provide a basic guide to the new law. The "frequently asked questions" and the answers follow a brief overview of the Uniform Health Care Decisions Act. For busy practitioners, a conclusion summarizes key points.     

Innervation of supporting cells in the apical turns of the guinea pig cochlea is from type II afferent fibers

The outer supporting cells in the apical turns of the guinea pig cochlea receive a dense innervation. Our previous study (Fechner et al. [1998] J. Comp. Neurol. 400:299-300) suggested that this innervation of the Deiters' and Hensen's supporting cells was not derived from efferent fibers of the olivocochlear bundle, but its origin has not been further specified. To test the hypothesis that the innervation was afferent in origin, we traced apical afferent fibers that were retrogradely labeled by extracellular injections of horseradish peroxidase. Labeled afferent fibers were of two types: type I fibers contacted inner hair cells, whereas type II fibers crossed the tunnel and contacted outer hair cells. Significantly, most of the type II fibers also formed branches to the outer supporting cells. Although a few olivocochlear efferent fibers formed such branches, counts indicated that the overwhelming majority of the branches were produced by type II afferent fibers. These branches were not produced by basal type II fibers. Apical type II fibers also differed from basal fibers by having shorter lengths, spiraling both apically and basally, and contacting all three rows of outer hair cells. These innervation differences suggest differences in the ways that information from outer hair cells is processed in the apex versus the base of the cochlea.     

Are outbreaks and sporadic respiratory infections byMycoplasma pneumoniae due to two distinct subtypes?

Thirty-seven clinical isolates ofMycoplasma pneumoniae, cultured from patients' respiratory material between 1986 and 1994, were typed by immunological methods and by polymerase chain reaction (PCR). For immunological typing two monoclonal antibodies (mAb) were used that recognized the P1 adhesion ofMycoplasma pneumoniae strain FH but differed in their ability to inhibit the adherence ofMycoplasma pneumoniae to erythrocytes. The mAb P1.58, which was not able to inhibit adherence, showed reactions with all patients' isolates in immunoblots, whereas the adherence-inhibiting mAb P1.62 reacted with only seven patients' isolates. Due to variations within the P1adhesin genome ofMycoplasma pneumoniae group 1 (Mycoplasma pneumoniae type strain M129) and group 2 (Mycoplasma pneumoniae type strain FH), two primer sets were designed. According to the size of the PCR-amplification products, all clinical isolates that showed no mAb P1.62 reactivity belonged toMycoplasma pneumoniae group 1, whereas mAb P1.62-positive-reacting mycoplasma isolates were characterized as group 2 strains. During an outbreak ofMycoplasma pneumoniae diseases in 1992, all 19 clinical isolates showed no cross-reactivity in immunoblots with the mAb P1.62 and were typed by PCR asMycoplasma pneumoniae group 1 strains. Furthermore, 206Mycoplasma pneumoniae complement fixation test — positive patient sera (titer>140) from the study period were tested for adherence-inhibiting antibodies towards both type strains. Thirty-two sera showed adherence-inhibiting antibodies towards group 1 and 22 towards group 2 mycoplasmas. In only seven sera were adherence-inhibiting antibodies directed to bothMycoplasma pneumoniae groups. The serological data of the outbreak in 1992 revealed that patients withMycoplasma pneumoniae group 1 infections developed adherence-inhibiting antibodies more frequently than did patients infected with group 2, which might have implications for the pathogenesis ofMycoplasma pneumoniae diseases and subsequent infections.     

Intravenous gammaglobulin treatment of chronic idiopathic thrombocytopenic purpura

High-dose intravenous gammaglobulin (IVIgG) was given to 12 children and adults with chronic idiopathic thrombocytopenic purpura (ITP) to avoid splenectomy or because they either failed to respond to or required maintenance with high doses of steroids and/or immunosuppressives. The average platelet count increase to initial therapy was 239,500/microliters (range 23,000-790,000). A concomitant IgG Fc receptor blockade, measured by IgG-sensitized 51Cr-labeled autologous erythrocytes, was seen in 11 of 11 patients tested, both splenectomized and not splenectomized, lasting 3-4 wk. Six or more months after treatment, 2 children are in remission, 2 children and 2 adults are stable requiring no therapy with platelet counts of approximately 50,000 and 30,000, respectively, 3 children require maintenance IVIgG therapy at 2-10-wk intervals, and 1 child and 2 adults have become refractory to further IVIgG. Splenectomy was not performed in 4 children. Two adults were able to discontinue daily prednisone. The 3 patients who became unresponsive to Swiss Red Cross gamma-globulin (IgSRK) therapy did so in conjunction with a markedly elevated platelet-associated IgG and IgM. Serum IgM increased an average of 103 mg/dl after the IVIgG infusions. No significant side effects were seen.     

Contrast timing in computed tomography: effect of different contrast media concentrations on bolus geometry

Objective

To assess the effect of low-osmolar, monomeric contrast media with different iodine concentrations on bolus shape in aortic CT angiography.

Materials and methods

Repeated sequential computed tomography scanning of the descending aorta of eight beagle dogs (5 male, 12.7 ± 3.1 kg) was performed without table movement with a standardized CT scan protocol. Iopromide 300 (300 mg I/mL), iopromide 370 (370 mg I/mL) and iomeprol 400 (400 mg I/mL) were administered via a foreleg vein with an identical iodine delivery rate of 1.2 g I/s and a total iodine dose of 300 mg I/kg body weight. Time-enhancement curves were computed and analyzed.

Results

Iopromide 300 showed the highest peak enhancement (445.2 ± 89.1 HU), steepest up-slope (104.2 ± 17.5 HU/s) and smallest full width at half maximum (FWHM; 5.8 ± 1.0 s). Peak enhancement, duration of FWHM, enhancement at FWHM and up-slope differed significantly between iopromide 300 and iomeprol 400 (p < 0.05). Except for enhancement at FWHM there were no significant differences between iopromide 300 and iopromide 370 and iopromide 370 and iomeprol 400 (p > 0.05).

Conclusions

Low viscous iopromide 300 results in a better defined bolus with a significantly higher peak enhancement, steeper up-slope and smaller FWHM when compared to iomeprol 400. These characteristics potentially affect contrast timing.     

Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group

Multiple sclerosis (MS) is a demyelinating autoimmune disease of the central nervous system. While its etiology is not well understood, genetic factors are clearly involved. Until recently, most genetic studies in MS have been association studies using the case-control design testing specific candidate genes and studying only sporadic cases. The only consistently replicated finding has been an association with the HLA-DR2 allele within the major histocompatibility complex (MHC) on chromosome 6. Using the genetic linkage design, however, evidence for and against linkage of the MHC to MS has been found, fostering suggestions that sporadic and familial MS have different etiologies. Most recently, two of four genomic screens demonstrated linkage to the MHC, although specific allelic associations were not tested. Here, a dataset of 98 multiplex families was studied to test for an association to the HLA-DR2 allele in familial MS and to determine if genetic linkage to the MHC was due solely to such an association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta) in the MHC demonstrated strong genetic linkage (parametric lod scores of 4.60, 2.20 and 1.24, respectively) and a specific association with the HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results by HLA-DR2 status showed that the linkage results were limited to families segregating HLA-DR2 alleles. These results demonstrate that genetic linkage to the MHC can be explained by the HLA-DR2 allelic association. They also indicate that sporadic and familial MS share a common genetic susceptibility. In addition, preliminary calculations suggest that the MHC explains between 17 and 62% of the genetic etiology of MS. This heterogeneity is also supported by the minority of families showing no linkage or association with loci within the MHC.      

The inferior alveolar artery in its bony course

Based on the dissection of 30 hemi-mandibles, the authors report a study of the inferior alveolar artery in its intraosseous course. On morphologic considerations they propose a classification of the collaterals into two groups: the principal collaterals destined for the teeth and the bony alveolar tissue and the secondary collaterals destined for the sheath and the nerve as well as the bony tissue around the canal. Loss of the teeth and absorption of the alveolar bone modify the caliber of the inferior alveolar arterial axis, the distribution of its collaterals and possibly its mode of termination. These facts suggest a consideration of the vascularization of the mandible in terms of four sectors. They arrive at practical conclusions that may be drawn from this study in stomatology.