Predictive factors for development of the no-reflow phenomenon in patients with reperfused anterior wall acute myocardial infarction.

OBJECTIVES: We sought to elucidate the clinical factors related to the development of no-reflow phenomenon after successful coronary reperfusion in patients with an acute myocardial infarction (AMI). BACKGROUND: Myocardial contrast echocardiography revealed that the no-reflow phenomenon is observed in some patients with a reperfused AMI, and those patients usually have poor functional and clinical outcomes. It is still unknown what clinical factors are related to the development of the no-reflow phenomenon. METHODS: Myocardial contrast echocardiography was performed 15 min after successful coronary reperfusion therapy in 199 patients with an anterior wall AMI who underwent successful coronary reperfusion with primary coronary angioplasty within 24 h after the onset of AMI. Multiple logistic regression analysis was used to identify independent predictors of the no-reflow phenomenon. RESULTS: Seventy-nine patients showed the no-reflow phenomenon. Univariate analysis indicated that pre-infarction angina within 48 h before symptom onset, Killip class, Thrombolysis in Myocardial Infarction flow grade 0 on the initial coronary angiogram, the number of abnormal Q-waves and the wall motion score (WMS) on the echocardiogram obtained at hospital admission are related to the no-reflow phenomenon. Multivariate logistic regression analysis revealed that all of these factors, except for Killip class, are independent predictive factors of the no-reflow phenomenon. CONCLUSIONS: Development of the no-reflow phenomenon is related to the severity of myocardial damage (number of Q-waves), the size of the risk area (WMS) and the occlusion status of infarct-related artery. In addition, ischemic preconditioning (pre-infarction angina) seems to be the factor that attenuates the no-reflow phenomenon.

Specific immune response to a synthetic peptide derived from outer surface protein C of Borrelia burgdorferi predicts protective borreliacidal antibodies.

In a previous study, we described the development of a new specific serodiagnostic test for Lyme disease involving enzyme-linked immunosorbent assay and a synthetic peptide, OspC-I. The OspC-I peptide is derived from part of the outer surface protein C (OspC) amino acid sequence of Borrelia burgdorferi and is located in the region conserved among B. burgdorferi sensu stricto or sensu lato isolates. In this study, we demonstrate that sera containing antibodies against OspC-I from patients with early Lyme disease had borreliacidal activity against isolates of three genospecies of Lyme disease spirochete, B. burgdoreferi B31, B. garinii HPI and B. afzelii HT61. However, the borreliacidal activity against B. burgdorferi, which has not been isolated in Japan, was weaker than that against the other species. Vaccination of mice with OspC-I induced the production of anti-OspC-I antibodies in serum with borreliacidal activity. The immune mouse serum had significantly higher levels of borreliacidal activity against HP1 and HT61, than against B31. Neutralization of borreliacidal activity with anti-IgM antibodies showed that the borreliacidal activity of anti-OspC-I antibodies in serum was due to IgM. Furthermore. mice vaccinated with OspC-I were protected against challenge with HPI and HT61. but not fully protected against infection with B31. These results suggest that OspC-I is not only a specific antigen for use in serodiagnostic tests for Lyme disease, but is also a potential candidate for a Lyme disease vaccine in Japan.

Antibody response to OspC-I synthetic peptide derived from outer surface protein C of Borrelia burgdorferi in sera from Japanese forestry workers.

The prevalence of antibodies against Lyme disease spirochaetes in serum samples from 80 forestry workers at high occupational risk of Lyme disease was surveyed by enzyme-linked immunosorbent assay (ELISA) with the OspC-I synthetic peptide. The peptide is part of the outer surface protein C (OspC) amino acid sequence located in the region conserved among Borrelia burgdorferi sensu stricto or sensu lato. Positivity for antibodies against OspC-I was observed in 25 (313%) of the forestry workers. Of these positive cases, 12 (15.0%) and 19 (23.8%) were positive for immunoglobulin M (IgM) and IgG antibody, respectively. Among 62 workers who were negative for IgG antibody against B. garinii or B. japonica in our previous study, 9 (14.5%) and 4 (6.5%) were positive for IgM and IgG antibody, respectively, in OspC-I ELISA. These results demonstrate for the first time that Lyme disease in forestry workers can be revealed using OspC-I ELISA. We conclude that forestry workers who show positive results for antibodies against OspC-I have very likely been exposed to Lyme disease spirochaetes, and that those who show positivity for IgM antibody against OspC-I may be in the early stage of Lyme disease.

Effect of aging on HbA1c in a working male Japanese population.

OBJECTIVE: To evaluate whether there is any change in HbA1c with age and to determine the effects of body mass index (BMI), exercise, and family history of diabetes on this change. RESEARCH DESIGN AND METHODS: A cross-sectional survey of 7,664 male Japanese workers aged 20-59 years was performed. All subjects received a physical examination that included measurement of HbA1c as an indicator of plasma glucose level. The subjects were classified according to their ages and BMIs, and any relationship with HbA1c levels was evaluated. Information on physical activity and family history of diabetes was obtained by a questionnaire. RESULTS: In all BMI groups, HbA1c increased with age. The greatest increase in HbA1c was observed in the 40- to 49-year-old age-group in subjects with a BMI < or = 26 kg/m2 and in the 30- to 39-year-old age-group in subjects with a BMI > 26. HbA1c in the subjects aged 20-29 years did not change with BMI. In contrast, HbA1c in subjects aged 30-59 years was significantly higher in those with a BMI > 26 when compared with those with BMI < or = 20. The age-dependent increase in HbA1c was greater in subjects with a positive rather than negative family history of diabetes. This age-dependent increase was not affected by active participation in sporting activities of mild to moderate intensity for 3 or more days per week. CONCLUSIONS: The age-dependent increase in HbA1c may be a consequence of the aging process itself. Furthermore, both BMI and a hereditary predisposition to diabetes, but not active participation in sports, affect this age-dependent increase in HbA1c.

[The survey of prevalence of Lyme borreliosis in forestry workers in Saitama prefecture].

Forestry workers in Saitama Prefecture are in high occupational risk to Lyme borreliosis transmitted by ticks. We surveyed the incidence of tick bites and the prevalence of antibodies against Borrelia burgdorferi in 80 forestry workers. ELISA with the antigen from B. burgdorferi sensu stricto B31 as well as Borrelia garinii HP3 and Borrelia japonica HO14 isolated in Japan was used for the detection of antibodies. Antibody-positive cases against B31, HP3 and HO14 was 3.8, 23.8 and 13.8%, respectively. Antibody-positive cases by ELISA were subjected to Western blotting with the antigens from three borrelias. Finally, 20.0% of the workers were antibody-positive by specific antibodies, anti-OspA antibody. The correlation between ELISA and Western blotting was better when HP3 was used as an antigen. One out of 30 normal control individuals was positive in ELISA with HP3 antigen, but negative in Western blotting. Thirty percent of the workers had a history of tick bites, and these cases had no characteristic symptoms of Lyme borreliosis. However, the rate of tick bites in antibody-positive cases was significantly higher than that in antibody-negative cases. These results suggested that the forestry workers in Saitama are very likely to be infected with Lyme borreliosis transmitted by ticks.

Hyper-infusion pressure for diabetic membrane dissection.

Vitrectomy was performed on 17 eyes (16 cases) with diabetic macular traction detachment with highly active fibrovascular proliferative tissue. Membrane dissection was performed with the central retinal artery temporarily occluded by hyper-infusion pressure from 82 to 105 mmHg, introduced over a duration of 0.9 to 16.5 minutes (average 4.1 minutes). With this technique, nearly complete hemostasis was achieved during membrane dissection. The retina was anatomically reattached in 16 eyes (94%); visual improvement of two lines or better was obtained in 15 eyes (88%). Membrane dissection under temporary hyper-infusion pressure prevented complications by allowing good visualization, remarkably reducing the surgical time requirement.

Distribution and morphology of retinal ganglion cells in the Japanese quail.

A ganglion cell density map was produced from the Nissl-stained retinal whole mount of the Japanese quail. Ganglion cell density diminished nearly concentrically from the central area toward the retinal periphery. The mean soma area of ganglion cells in isodensity zones increased as the cell density decreased. The histograms of soma areas in each zone indicated that a population of small-sized ganglion cells persists into the peripheral retina. The total number of ganglion cells was estimated at about 2.0 million. Electron microscopic examination of the optic nerve revealed thin unmyelinated axons to comprise 69% of the total fiber count (about 2.0 million). Since there was no discrepancy between both the total numbers of neurons in the ganglion cell layer and optic nerve fibers, it is inferred that displaced amacrine cells are few, if any. The spectrum in optic nerve fiber diameter showed a unimodal skewed distribution quite similar to the histogram of soma areas of ganglion cells in the whole retina. This suggests a close correlation between soma areas and axon diameters. Retinal ganglion cells filled from the optic nerve with horseradish peroxidase were classified into 7 types according to such morphological characteristics as size, shape and location of the soma, as well as dendritic arborization pattern. Taking into account areal ranges of somata of each cell type, it can be assumed that most of the ganglion cells in the whole retinal ganglion cell layer are composed of type I, II and III cells, and that the population of uniformly small-sized ganglion cells corresponds to type I cells and is an origin of unmyelinated axons in the optic nerve.

Cytoarchitecture and ultrastructure of the avian ectostriatum: afferent terminals from the dorsal telencephalon and some nuclei in the thalamus.

The cytoarchitecture, ultrastructure, and afferent terminals in the ectostriatal complex of the Japanese quail were examined. The complex consists of the central core (Ec) and peripheral belt (Ep). Terminals in the complex were categorized into three main groups according to the shape of synaptic vesicles: S (spherical), P (pleomorphic), and F (flat). S terminals are further classified into three types: Ss, small terminals which have densely packed vesicles and a long active zone and are presynaptic to large spines; Sm, medium-sized to large terminals which have a relatively short active zone and contact dendritic spines, trunks, and somata; Sl, large terminals which have many mitochondria and cored vesicles and form synapses only with somata. Some of the Sm terminals are derived from myelinated axons. The Sl terminals are frequently combined with gap junctions as so-called mixed synapses. The P terminal occasionally surrounds an axon hillock, making symmetric synaptic contacts. The F terminals often cover a wide area of the soma. A few gap junctions are also recognized between adjacent somata. Afferent sources of the ectostriatal complex were examined by means of horseradish peroxidase (HRP) retrograde transport. Many large HRP-labeled cells were recognized in the nucleus rotundus (Rt). HRP-labeled cells were seen in the nucleus triangularis (Tr), nucleus dorsolateralis posterior thalami (DLP), and a few labeled cells were scattered in the hyperstriatum ventrale (HV). Substantial numbers of Sm terminals in Ec degenerated after destruction of Rt; they made synaptic contacts with dendritic trunks (71.8%) and small spines (28.2%). Degenerating and intact Sm terminals were found to form synapses with the same dendritic trunk by the reconstruction of serial thin sections. Among the 167 Sm terminals, 20 terminals (12.0%) degenerated after lesions in Rt. The Sm terminals in Ec degenerated after destruction of Tr and the terminals formed synapses with somata as well as dendritic trunks and spines. After lesions of the dorsal telencephalon including HV, degenerating fibers sparsely entered the ectostriatal complex associated with the Ss terminal degeneration. DLP seemed to project mainly on the medial area of posterior Ep. The terminals from DLP made asymmetric synaptic contacts with dendritic spines, trunks, and somata. Some of the terminals from DLP were identified as the Sl type, but other S types could not be identified.

Histopathological changes of the retina and optic nerve in the albino mutant quail (Coturnix coturnix japonica).

Histopathological changes in the retina and optic nerve in imperfect albino mutant quails with a sex-linked recessive gene were studied ontogenetically. The mutant quail showed eye enlargement 3 months after hatching. The eyes exhibited hazy corneas, lens opacities and deep anterior chambers at 18 months of age. Some ganglion cells in the retina and axons in the optic disc began to degenerate 6 months after hatching. There were many deformed or fragmented ganglion cells at 12 months of age, and axonal degeneration was observed in the optic disc. The optic disc and the retina around it became excavated. At this time, hydropic degeneration was found in the ganglion nerve fibre layer and optic nerve and a small accumulation of acid mucopolysaccharide, which was sensitive to hyaluronidase, was present in the optic disc and optic nerve. The excavation was found to be fully developed around the optic disc at 18 months and most ganglion cells showed degenerative changes. During this period, the inner plexiform and inner nuclear layers showed hydropic degeneration. At 24 months the ganglion cell and ganglion nerve fibre layers had disappeared, the thickness of the inner nuclear layer was reduced and many photoreceptor cells were totally degenerated. The optic nerve was occupied by glial cells, blood vessels and cavernous spaces in which acid mucopolysaccharide accumulated. These histopathological retinal changes in the mutant quail are very similar to those reported in experimentally induced glaucoma of other animal species and to those in human glaucoma. The usefulness of this mutant quail as an animal model for the human disease is discussed.