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Biomedical subjects

G L Li

Publications and source records attributed to G L Li.

At least 37 records · Page 2Linked to original sources
PubMed1998

Expression of endothelial barrier antigen immunoreactivity in blood vessels following compression trauma to rat spinal cord. Temporal evolution and relation to the degree of the impact.

The endothelial barrier antigen (EBA) recognised by a monoclonal antibody is expressed in rat cerebral microvessels possessing blood-brain barrier properties but only weakly by fenestrated vessels. We have studied the expression of this marker in the spinal cord of control rats and compared the findings with those seen in rats subjected to compression injury at the T8-9 level with a survival period of 4 h, 24 h, 4 days and 9 days. To that end, formalin-fixed paraffin-embedded material was immunostained by the avidin-biotin-peroxidase complex method. Sections from control rats presented a distinct immunostaining at the site of the endothelial cells of almost all microvessels in the grey and white matter of the cord. The anterior and posterior spinal arteries did not show such staining. Neurons and glial cells were unstained. Rats which had survived 4 h after a moderate or severe compression trauma still showed immunoreactivity in intramedullary microvessels at the site of injury. There was a moderate reduction of vascular immunoreactivity at 24 h and a pronounced loss of such reactivity at 4 days after trauma. At 9 days after compression the expression of the endothelial barrier antigen had almost been normalised in the microvessels of the cord. In conclusion, using immunohistochemistry, EBA can be demonstrated in noninjured rat spinal cord microvessels, while the staining disappears at the site of compression trauma to the cord. The EBA marker can be used to indicate sites of vascular injury in spinal cord compression injury. The factors causing the disappearance and restitution of the antigen are unknown.

Animals↗
PubMed1998

Urinary excretion of phenol, catechol, hydroquinone, and muconic acid by workers occupationally exposed to benzene.

OBJECTIVES: Animal inhalation studies and theoretical models suggest that the pattern of formation of benzene metabolites changes as exposure to benzene increases. To determine if this occurs in humans, benzene metabolites in urine samples collected as part of a cross sectional study of occupationally exposed workers in Shanghai, China were measured. METHODS: With organic vapour monitoring badges, 38 subjects were monitored during their full workshift for inhalation exposure to benzene. The benzene urinary metabolites phenol, catechol, hydroquinone, and muconic acid were measured with an isotope dilution gas chromatography mass spectroscopy assay and strongly correlated with concentrations of benzene air. For the subgroup of workers (n = 27) with urinary phenol > 50 ng/g creatinine (above which phenol is considered to be a specific indicator of exposure to benzene), concentrations of each of the four metabolites were calculated as a ratio of the sum of the concentrations of all four metabolites (total metabolites) and were compared in workers exposed to > 25 ppm v < or = 25 ppm. RESULTS: The median, 8 hour time weighted average exposure to benzene was 25 ppm. Relative to the lower exposed workers, the ratio of phenol and catechol to total metabolites increased by 6.0% (p = 0.04) and 22.2% (p = 0.007), respectively, in the more highly exposed workers. By contrast, the ratio of hydroquinone and muconic acid to total metabolites decreased by 18.8% (p = 0.04) and 26.7% (p = 0.006), respectively. Similar patterns were found when metabolite ratios were analysed as a function of internal benzene dose (defined as total urinary benzene metabolites), although catechol showed a more complex, quadratic relation with increasing dose. CONCLUSIONS: These results, which are consistent with previous animal studies, show that the relative production of benzene metabolites is a function of exposure level. If the toxic benzene metabolites are assumed to be derived from hydroquinone, ring opened products, or both, these results suggests that the risk for adverse health outcomes due to exposure to benzene may have a supralinear relation with external dose, and that linear extrapolation of the toxic effects of benzene in highly exposed workers to lower levels of exposure may underestimate risk.

Air Pollutants, Occupational↗
PubMed1997

Validation of benzene exposure assessment.

We conducted a methodologic study to validate a quantitative retrospective exposure assessment method used in a follow-up study of workers exposed to benzene. Assessment of exposure to benzene was carried out in 672 factories in 12 cities in China. Historical exposure data were collected for 3179 unique job titles. The basic unit for exposure assessment was a factory/work-unit/job-title combination over seven periods between 1949 and 1987. A total of 18,435 exposure estimates was developed, using all available historical information, including 8477 monitoring data. Overall, 38% of the estimates were based on benzene monitoring data. The highest time-weighted average exposures occurred in the rubber industry (30.7 ppm), particularly for rubber glue applicators (52.6 ppm). Because of its recognized link with benzene exposure, the association between a clinical diagnosis of benzene poisoning (hematotoxicity) and benzene exposure was evaluated (412 cases and 614,509 person-years) to validate the exposure-assessment method. Relative risks of benzene hematotoxicity increased very sharply with increasing estimated intensity of benzene exposure. Odds ratios were 2.2 (95% CI: 1.7-2.9), 4.7 (95% CI: 3.4-6.5), and 7.2 (95% CI: 5.3-9.8) for the intensity levels of less than 5 ppm, 5-19 ppm, 20-39 ppm, and 40 and more ppm, respectively. This sharp trend between benzene hematotoxicity and estimated exposure to benzene indicated that the exposure-estimation method used in this cancer epidemiology study is reliable.

Benzene↗
PubMed1997

Benzene and the dose-related incidence of hematologic neoplasms in China. Chinese Academy of Preventive Medicine--National Cancer Institute Benzene Study Group.

BACKGROUND: Benzene is a widely distributed environmental contaminant known to cause leukemia, particularly acute nonlymphocytic leukemia, and perhaps other hematologic neoplasms and disorders. Few epidemiologic studies, however, have been able to address relationships between the extent of benzene exposure and the level of risk. PURPOSE: A large cohort study was carried out in China to evaluate the risks of developing specific hematologic neoplasms and selected related disorders in relationship to quantitative estimates of occupational benzene exposure. METHODS: A cohort of 74828 benzene-exposed and 35805 unexposed workers employed from 1972 through 1987 in 12 cities in China was identified and followed to determine the incidence of hematologic neoplasms and related disorders. Estimates of benzene exposure were derived from work histories and available historic benzene measurements. Existing pathologic material and supporting medical records were reviewed to establish diagnoses of disease. Relative risks (RRs) (i.e., ratios of incidence rates for specific hematologic neoplasms and related disorders in the benzene-exposed group to incidence rates in the unexposed group) were determined by use of Poisson regression analysis, with stratification by age and sex. RESULTS: For workers historically exposed to benzene at average levels of less than 10 parts per million (ppm), the RR for all hematologic neoplasm combined was 2.2 (95% confidence interval [CI] = 1.1-4.2), and, for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes, the RR was 3.2 (95% CI = 1.0-10.1). For individuals who were occupationally exposed to benzene at constant levels of 25 ppm or more, the RR for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes was 7.1 (95% CI = 2.1-23.7). Workers with 10 or more years of benzene exposure had an RR of developing non-Hodgkin's lymphoma of 4.2 (95% CI = 1.1-15.9), and the development of this neoplasm was linked most strongly to exposure that had occurred at least 10 years before diagnosis (i.e., distant exposure) (P for trend = .005, two-sided). In contrast, the risk for the combination of acute nonlymphocytic leukemia and related myelodysplastic syndromes was significantly increased among those with more recent benzene exposure (P for trend = .003, two-sided), but it was not linked to distant exposure (P for trend = .51, two-sided). CONCLUSIONS: The results of this study suggest that benzene exposure is associated with a spectrum of hematologic neoplasms and related disorders in humans. Risks for these conditions are elevated at average benzene-exposure levels of less than 10 ppm and show a tendency, although not a strong one, to rise with increasing levels of exposure. The temporal pattern of benzene exposure appears to be important in determining the risk of developing specific diseases.

Age Distribution↗
PubMed1997

Benzene poisoning, a risk factor for hematological malignancy, is associated with the NQO1 609C-->T mutation and rapid fractional excretion of chlorzoxazone.

Benzene is a ubiquitous occupational hematotoxin and leukemogen, but people vary in their response to this toxic agent. To evaluate the impact of interindividual variation in enzymes that activate (i.e., CYP2E1) and detoxify (i.e., NQO1) benzene and its metabolites, we carried out a case-control study in Shanghai, China, of occupational benzene poisoning (BP; i.e., hematotoxicity), which we show is itself strongly associated with subsequent development of acute nonlymphocytic leukemia and the related myelodysplastic syndromes (relative risk, 70.6; 95% confidence interval, 11.4-439.3). CYP2E1 and NQO1 genotypes were determined by PCR-RFLP, and CYP2E1 enzymatic activity was estimated by the fractional excretion of chlorzoxazone (fe(6-OH)) for 50 cases of BP and 50 controls. Subjects with both a rapid fe(6-OH). and two copies of the NQO1 609C-->T mutation had a 7.6-fold (95% confidence interval, 1.8-31.2) increased risk of BP compared to subjects with a slow fe(6-OH) who carried one or two wild-type NQO1 alleles. In contrast, the CYP2E1 PstI/RsaI polymorphism did not influence BP risk. This is the first report that provides evidence of human susceptibility to benzene-related disease. Further evaluation of susceptibility for hematotoxicity and hematological malignancy among workers with a history of occupational exposure to benzene is warranted.

Benzene↗
PubMed1997

Manuifolins D, E, and F: new isoflavonoids from Maackia tenuifolia.

Chemical examination of roots of Maackia tenuifolia yielded three new isoflavans, manuifolins D, E, and F, along with the known (6aR, 12aR)-pterocarpin and (6aR,12aR)-maackiain. The new compounds were established as (3R)-5'-(1,1-dimethyl-2-propenyl)-4'- O-(3-methyl-2-butenyl)- 7,2'-dihydroxyisoflavan (1), (3R)-6,5'-bis(1,1-dimethyl-2-propenyl)-7,2',4', -trihydroxyisoflavan (2), and (3R)-5'-(1-isopropylethenyl)-8-(3-methyl-2-butenyl)-7,2',4'- trihydroxyisoflavan (3), respectively, by spectroscopic methods.

Fabaceae↗
PubMed1997

Expression of the ubiquitin carboxyl-terminal hydrolase PGP 9.5 in axons following spinal cord compression trauma. An immunohistochemical study in the rat.

Protein gene product 9.5 (PGP 9.5) is a neuron-specific protein which acts as a ubiquitin carboxyl-terminal hydrolase. It facilitates the conversion of polyubiquitin to monoubiquitin, which can be reused for another catalytic cycle. Monoubiquitin plays an important role in degrading abnormal and denatured proteins. Previously, we have reported that ubiquitin-like immunoreactivity is expressed in axonal swellings following compression trauma to the rat thoracic cord. It was characterized by fast occurrence, progressive increase and gradual disappearance over a period of 9 days. The expression of PGP 9.5 has now been studied in the same material. Control rats showed a weak PGP 9.5 immunoreactivity in the nerve cell bodies of the cord. Except for the corticospinal tracts, the axons of other longitudinal tracts were weakly stained. Accumulation of PGP 9.5 immunoreactivity occurred in expanded axons at the site of compression already 4 h after trauma. They became more frequent in number 1 and 4 days after injury and remained so over the entire observation period of 9 days. The labelled axons were randomly distributed in the longitudinal tracts, but were never found in the corticospinal tracts. The extent of immunoreactivity was related to the degree of impact on the cord. Compression injury thus induces accumulation of both ubiquitin and PGP 9.5 immunoreactivity in axonal expansions. The injured axons may have a mechanism for degradation of proteins by the ubiquitin-mediated proteolytic pathway and another mechanism for effective ubiquitin regenerative cycling by the action of PGP 9.5.

Animals↗
PubMed1997

Effects of alpha-phenyl-N-tert-butyl nitrone (PBN) on compression injury of rat spinal cord.

alpha-Phenyl-N-tert-butyl Nitrone (PBN) is a free radical scavenger which recently has proved to be neuroprotective in experimental studies on focal cerebral ischemia and infarction. We therefore studied the effect of this drug in a model of moderate compression injury to rat spinal cord at the midthoracic level. The compound was given intraperitoneally 0.5 h before (100 mg/kg b.w) and at 1.5 h (50 mg/kg b.w) and 3.5 h (50 mg/kg b.w) after compression. Treated animals and controls (vehicle alone) were allowed to survive for 1 or 9 days following trauma. The functional outcome was tested by the inclined plane method and the motor performance score. By using MAP2 immunostaining the number of nerve cell bodies in the ventral horn and the ratio of MAP2 immunostained area to area of whole section of the cord were assessed to detect loss of neurons and loss of dendrites in the compressed segment. beta APP and PGP9.5 immunostaining was used to demonstrate axonal lesions. Treated and control rats showed at day 1 when tested with the inclined plane method a marked reduction of the capacity angle. This abnormality recovered gradually over the following days and was normalized at day 9. The motor performance score showed a marked reduction at day 1 which almost normalized at day 9. There was no difference regarding the functional outcome between rats given PBN and controls in none one of these functional tests. The spinal cord of normal rats presented immunoreactivity to MAP2 in nerve cell bodies and dendrites but not in axons and other structures. Following compression there was at day 1 and 9 a marked loss of MAP2 immunoreactivity in dendrites and nerve cell bodies. We could not detect any difference between the PBN and the control rats regarding the degree of cell loss or degree of reduction of dendrite staining. No difference between the two groups was seen with the axonal immunostainings (beta APP and PGP9.5). In conclusion, our study did not reveal any neuroprotective effect of PBN on the functional outcome and morphology (immunostaining to MAP2, beta APP and PGP9.5) in this model of moderate compression trauma to rat spinal cord.

Amyloid beta-Protein Precursor↗
PubMed1997

[The isolation and identification of four new 2, 2-dimethylchromenes].

Four new 2, 2-dimethylchromenes named leptol B (I), ethylleptol B (II), methylleptol B (III), leptene B (IV), along with a known chromene-methylevodionol (V) have been isolated from the aerial parts of Evodia lepta. Their structures were elucidated by spectroscopic analysis and chemical techniques.

Benzopyrans↗
PubMed1997

[Separation of pharmaceutical enantiomers on column and thin-layer plate of cellulose triacetate].

Microcrystalline cellulose triacetate (CTA) was prepared by heterogeneous acetylation of microcrystalline cellulose and used as liquid chromatographic chiral stationary phase and chiral thin layer plate to separate pharmaceutical enantiomers. The racemic Troegor's base, mathaqualone, chlormezanone and chloroquine were separated on the CTA chiral column and on the CTA chiral plate. 95% ethanol and the mixtures of 95% ethanol and water with different ratio and different pH values were used as mobile phase. The influences of eluent composition, pH and temperature on the chiral separation were discussed. The experimental results indicate that the CTA chiral plate was more sensitive to eluent composition and pH than chiral column possibly because the chiral adsorbent was not swollen on the plate.

Cellulose↗
PubMed1997

[The observation of the contained fluoride sealant on caries prevention for 3 years]

Pit and fissure sealant is an effective method for preventing pit and fissure caries,though it has less effect in smooth surface teeth.But the contained sealant is effective on caries prevention both in pit and fissure area and in smooth surface.The aim of the present search was observing the clinic results of the contained fluoride sealant on caries prevention.786 children aged 6-8 years old were divided into four groups.The first permanent molars in group 1 were sealed by the contained fluoride sealant and those in group 2 were used the conventional sealant.The same molars in group 3 were used the conventional sealant plus the APFI gel and those in group 4 were only used the APFI gel.APFI gel was used one time per half year.The results showed the caries preventive effect of the contained fluoride sealant was significant higher than the conventional sealant or the APFI gel in first molars which had been sealed for three years.The caries incidence of the unsealed teeth in group 1 was lower than that in the other groups.The results also indicated the caries preventive effect of all above methods was less in female than in male.

Journal Article↗
PubMed1996

Changes in microtubule-associated protein 2 and amyloid precursor protein immunoreactivity following traumatic brain injury in rat: influence of MK-801 treatment.

We investigated by immunohistochemistry dendritic and axonal changes occurring in the rat brain after mild focal cortical trauma produced by the weight drop technique. One and 3 days after injury, nerve cell bodies and dendrites in the perimeter of the impact site displayed decreased microtubule-associated protein 2 (MAP2) immunoreactivity. Some dendrites in the immediate adjacent region were more intensely stained and distorted. The dentate hilar region of the hippocampus showed a reduction of immunoreactive nerve cell bodies and dendrites. Twenty-one days after injury the strongly stained cortical dendrites and the reduction of immunoreactivity in the hippocampus remained, whereas the reduced staining in the perimeter of the lesion had normalised. These results indicate that there is a long-lasting disturbed dendritic organisation implicating impaired neurotransmission after this type of mild brain trauma. beta-Amyloid precursor protein (APP) immunohistochemistry revealed numerous stained axons in the ipsilateral subcortical white matter and thalamus indicating local and remote axonal injuries with disturbed axonal transport. Twenty-one days after injury, numerous small immunostained profiles appeared in the neuropil of the cortical impact site and in the ipsilateral thalamus. The axonal changes indicate disturbed connectivity between the site of the impact and other brain regions, chiefly the thalamus. The presence of beta-amyloid was investigated 21 days after trauma. There were no signs of beta-amyloid depositions in the brain after injury. Finally, we tested if the non-competitive NMDA receptor antagonist dizocilpine maleate (MK-801) could influence the observed MAP2 and APP changes. Pretreatment with this compound did not affect the early MAP2 and APP alterations. Instead, an increased expression of the APP antigen in the thalamus was observed 21 days after trauma in the MK-801-treated animals. The cause of this phenomenon is not known but may be related to a delayed neurotoxic action of MK-801 treatment.

Amyloid beta-Protein Precursor↗
PubMed1996

A cohort study of cancer among benzene-exposed workers in China: overall results.

A large cohort study of 74,828 benzene-exposed and 35,805 unexposed workers employed between 1972 and 1987 in 12 cities in China were followed to determine mortality from all causes and the incidence of lymphohematopoietic malignancies and other hematologic disorders. Benzene-exposed study subjects were employed in a variety of occupations, including painting, printing, and the manufacture of footwear, paint, and other chemicals. All-cause mortality was similar in the benzene-exposed and unexposed comparison group. Statistically significant excess deaths were noted among benzene-exposed subjects for leukemia (RR = 2.3, 95% CP 1.1-5.0), malignant lymphoma (RR = 4.5, 95% CI: 1.3-28.4), and nonneoplastic diseases of the blood (RR = 95% CP 2.5-infinity), and a marginally significant excess was noted for lung cancer (RR = 1.4, 95% CI: 1.0-2.0). Risk was significantly elevated for the incidence of all lymphohematopoietic malignancies (RR = 2.6, 95% CI: 1.5-5.0), malignant lymphoma (RR = 3.5, 95% CI: 1.2-14.9), and leukemia (RR = 2.6, 95% CI.. 1.3-5.7). Among the leukemia subtypes, only acute myelogenous leukemia (AML) incidence was significantly elevated (RR = 3.1, 95% CI: 1.2-10.7), although nonsignificant excesses were also noted for chronic myelogenous leukemia (CML) (RR = 2.6, 95% CI: 0.7-16.9) and lymphocytic leukemias (RR = 2.8, 95% CI.. 0.5-54.5). Significant excesses were found for aplastic anemia (RR = infinity, 95% CI: 2.2-co) and myelodysplastic syndrome (RR = infinity, 95% CI: 1.7-infinity). Employment in benzene-associated occupations in China is associated with a wide spectrum of myelogenous and lymphocytic malignant diseases and related disorders. Investigations continue to assess the nature of these associations.

Adult↗
PubMed1996

Hematotoxicity among Chinese workers heavily exposed to benzene.

Benzene is a well-established hematotoxin. However, reports of its effects on specific blood cells have been somewhat inconsistent and the relative toxicity of benzene metabolites on peripheral blood cells in humans has not been evaluated. We compared hematologic outcomes in a cross-sectional study of 44 workers heavily exposed to benzene (median: 31 parts permillion [ppm] as an 8-hr time-weighted average [TWA] and 44 age and gender-matched unexposed controls from Shanghai, China. All hematologic parameters (total white blood cells [WBC], absolute lymphocyte count, platelets, red blood cells, and hematocrit) were decreased among exposed workers compared to controls, with the exception of the red blood cell mean corpuscular volume (MCV), which was higher among exposed subjects. In a subgroup of workers who were not exposed to more than 31 ppm benzene on any of 5 sampling days (n = 11, median 8 hr TWA = 7.6 ppm, range = 1-20 ppm), only the absolute lymphocyte count was significantly different between exposed workers (mean [sd]1.6 [0.4] x 10(3) mu L) and controls (1.9 [0.4] x l0(3) uL, p = 0.03). Among exposed subjects, a dose response relationship with various measures of current benzene exposure (i.e., personal air monitoring, benzene metabolites in urine) was present only for the total WBC count, the absolute lymphocyte count, and the MCV. Correlations between benzene metabolites and hematologic parameters were generally similar, although hydroquinone was somewhat more strongly associated with a decrease in the absolute lymphocyte count, and catechol was more strongly associated with an increase in MCV. Morphologic review of peripheral blood slides demonstrated an excess of red blood cell abnormalities (i.e., stomatocytes and target cells) only in the most heavily exposed workers, with no differences in granulocyte, lymphocyte, or platelet morphology noted. Although benzene can affect all the major peripheral blood elements, our results support the use of the absolute lymphocyte count as the most sensitive indicator of benzene-induced hematotoxicity.

Adult↗
PubMed1996

Expression of ubiquitin-like immunoreactivity in axons after compression trauma to rat spinal cord.

The ubiquitin-mediated proteolytic pathway is an important mode of protein degradation in various tissues. Since breakdown of proteins may occur in axons after injury we evaluated the presence of ubiquitin-like immunoreactive material in rat spinal cord following compression injury of mild, moderate and severe degrees at T8-9 level, resulting in no neurological deficit, reversible paraparesis and paraplegia of the hind limbs, respectively. Rats with mild to severe compression injury surviving 1-4 days showed numerous, intensely immunoreactive expanded axons at the site of compression. The labelled axons were randomly distributed in the longitudinal tracts but they were never found in the corticospinal tracts. No labelling was detected by 9 days after injury. In addition, the presence of labelled axons was investigated in the T7 and the T10 segments from rats with moderate compression. No labelling was seen in T7, but in T10 segments many immunoreactive axons were present. Control rats did not show immunoreactive axons in the spinal cord. Neurons of dorsal root ganglia, trigeminal ganglia and of the grey matter of the spinal cord were immunoreactive. Cerebral cortical neurons did not show ubiquitin expression. Thus, compression of the rat spinal cord causes a transient accumulation of ubiquitin-like immunoreactive material in axonal swellings. Even though the dynamics of ubiquitin conjugates are not fully understood, the observed axonal accumulation presumably reflects arrested anterograde axonal transport of protein chiefly derived from neurons of dorsal root ganglia and the local neurons of the spinal cord. The presence of ubiquitin in damaged axons is one prerequisite for degradation of abnormal proteins by the ubiquitin-mediated proteolytic pathway, which may be activated in reactive axonal swellings.

Animals↗
PubMed1996

Increased expression of growth-associated protein 43 immunoreactivity in axons following compression trauma to rat spinal cord.

Growth-associated protein 43 (GAP43) is one compound used to indicate growth of axonal endings during development and regeneration, particularly of peripheral neurons. Using immunohistochemistry, we have studied the expression of GAP43 in the spinal cord of rats subjected to mild, moderate or severe compression injury and used neurofilament immunostaining to demonstrate axonal injuries. Samples removed from the compressed T8-9, the cranial T7 and the caudal T10 segments were studied at 4 h, 24 h, 4 days and 9 days after injury. Control rats showed a moderate immunostaining of neurons in dorsal root ganglia, weak staining of ventral motor neurons and, with the exception of the corticospinal tracts, a weak staining in some axons of the longitudinal tracts of the cord. Injury in the compressed region led to increased GAP43 immunoreactivity in axons of normal and expanded size. This occurred particularly 1-4 days after injury and normalized 9 days thereafter. More marked immunostaining was present in the cranial and caudal segments. The corticospinal tracts never showed such staining. The increase of GAP43 immunostaining is presumably caused by disturbed axonal transport from neurons with the capacity to synthesize and transport the GAP43 antigen. Transported material may thus be available for regeneration of axons, but this source of material may vary between different classes of axons within the cord.

Animals↗
PubMed1996

Accumulation of beta-amyloid precursor protein and ubiquitin in axons after spinal cord trauma in humans: immunohistochemical observations on autopsy material.

We evaluated by immunohistochemistry the presence of beta-amyloid precursor protein (beta APP) and ubiquitin-like material which may accumulate in axons of the human spinal cord subjected to injury. Autopsy material was obtained from nine cases with different types of trauma: breech delivery with neonatal spinal injury, compression of the cord induced by fractures of the vertebral column, haematomas or intradural meningioma. The posttrauma period ranged from 10 days to several years. The spinal cord of six control cases without evidence of injury presented beta APP immunoreactivity in nerve cell bodies and in a few axonal profiles but not in dendrites. Seven of the nine cases with spinal cord trauma showed an accumulation of beta APP-immunoreactive material in axons of the longitudinal tracts at the site of the injury. Five cases presented similar axonal immunoreactivity in the grey matter of the cord. Ubiquitin-like immunoreactivity was present in expanded axons in cases with spinal cord injury. Cases with spinal cord trauma thus present beta APP-immunoreactive axons particularly of the longitudinal tracts in the same way as in trauma to rat spinal cord and in various brain injuries. The aggregation of beta APP-immunoreactive material indicates disturbed axonal transport of beta APP. Accumulation of ubiquitin-like immunoreactive material in expanded axons at the site of trauma may be one prerequisite for degradation of abnormal proteins by the ubiquitin-mediated proteolytic pathway.

Adolescent↗