Blood typing errors on U.S. Army identification cards and tags.
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Biomedical subjects
Publications and source records attributed to J M Henry.
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Recovery of D1- and D2-dopamine receptors in Wistar rat corpora striata were assessed following N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ blockade). Absolute recovery declines during senescence approximately 25 and 40% for the D1- and D2-subtypes, respectively. Net biosynthetic reductions are comparable to the overall age-related decreases in receptor concentrations for this rat strain. EEDQ administration also induces catalepsy behavior and impairs ability of animals to remain on an inclined screen. Recovery of inclined screen performance is also reduced with age, but is not strictly proportional to recovery of receptor concentrations.
Rat striatal membrane fluidity and dopamine receptor concentrations were modulated in vitro by ethanol or cholesterol hemisuccinate treatment. In general, available receptor levels are directly proportional to membrane fluidity. However, receptor concentrations remained higher in mature membranes at all levels of fluidity attained. These results suggest that apparent loss of striatal dopamine receptors during aging is not due to membrane sequestration.
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D-2 dopamine receptors from mature (3 to 6 months) and senescent (24 to 25 months) rat striatal membranes were solubilized with the detergent 3-(3-cholamidopropyl) dimethylammonio-2-hydroxy-1-propanesulfonate (CHAPSO). Essentially all of the receptors were recovered following CHAPSO treatment. Approximately 80 to 90% of the receptors were detected in the supernatant fraction under these conditions, with a small percentage remaining membrane bound in both age groups. A 10-fold reduction in binding affinity for [3H]spiperone was observed for solubilized receptors of both age groups. Ultra high speed centrifugation of untreated preparations (200,000 X g) revealed essentially no hidden D-2 dopamine receptors in the light membrane fraction from either mature or senescent rats. These results suggest that a decreased biosynthetic rate (Henry & Roth, 1984; Leff et al., 1984) rather than membrane sequestration accounts for loss of D-2 dopamine receptors with age.
Cerebral pilocytic astrocytoma is a known intracranial tumor, but its biological characteristics are less well documented. The authors report 30 patients with cerebral pilocytic astrocytoma who were accessioned by the Armed Forces Institute of Pathology between 1970 and 1980. Histological appearance of the tumor was correlated with clinical characteristics. Mean age of onset was 22.15 years, mean preoperative duration of symptoms was 3.77 years, and mean postoperative survival was 5.91 years, with 20 of 23 (87%) known to ultimately survive surgery. These cases of cerebral pilocytic astrocytoma exhibited histologic characteristics consistent with that of a low-grade tumor. Although several of these tumors were of guarded prognosis due to location, degree of infiltration or cyst recurrence, they generally demonstrated a natural course of a relatively low-grade neoplasm.
The recovery rate of striatal dopamine receptors following blockade by N-ethoxycarbonyl-2-ethoxy-1, 2-dihydroquinoline (EEDQ) in vivo is reduced by 25-35% in striata from senescent Wistar rats when compared to mature counterparts. No differences in binding affinity for [3H]-spiperone were observed for the different age groups at various times after EEDQ injection. These results suggest that loss of striatal dopamine receptors during aging may be due to a decreased biosynthetic rate.
An analysis of more than 18,000 primary central nervous system (CNS) tumors revealed only 18 cases (0.01%) in which dropped spinal metastases had caused the presenting symptoms. This group included 11 males and 7 females in whom there was no history of surgical intervention or irradiation. Primitive neuroectodermal tumors ( PNET , medulloblastoma), comprised the largest group (11 patients) followed by high-grade astrocytomas (anaplastic and glioblastoma) (5 patients). One case each of germinoma and ependymoma were also identified. The clinicopathologic data of these cases, and a brief review of the literature are presented.
Oxytricha nova is a hypotrichous ciliate containing a transcriptionally active macronucleus and a transcriptionally inactive micronucleus. Two-dimensional gel electrophoresis shows that macronuclei contain a normal complement of inner histones. However, despite extensive efforts, no classical H1-like protein has been detected. Micrococcal nuclease digestion indicates a nucleosome repeat length of approximately 220 bp for macronuclear chromatin. Thermal denaturation profiles of macronuclear chromatin in 0.2 mM EDTA display four transitions at about 46, 57, 64, and 79 degrees C. The lowest of these shifts to higher temperature as the ionic strength is raised to 3-5 mM Na phosphate. These results are consistent with the absence of H1 and a nucleosome repeat of 220-230 bp. Circular dichroism (CD) results agree with these findings. By contrast, micronuclear chromatin displays a much smaller premelt and a more suppressed DNA CD signal at 285 nm, consistent with a micronuclear chromatin repeat of 165-185 bp as determined by micrococcal nuclease digestion.
We have previously demonstrated a direct relationship between the activity of the arachidonic acid cascade in vivo and the extent of cellular damage following several types of experimental injury. Since phospholipase activity has been shown to regulate arachidonic acid availability, we tested the ability of circulating phospholipase A2 (PLA2) of pancreatic origin to stimulate prostanoid production or induce cellular injury in the isolated, perfused rabbit liver. Experimental conditions were similar to those present during pancreatitis or early splanchnic artery occlusion shock. The administration of PLA2 at a rate of 100 U/min for 10 min resulted in enhanced rates of thromboxane B2 and 6-ketoprostaglandin F1 alpha release between 1 and 5 min into the infusion period. No changes in hepatic perfusion pressure, vascular resistance, wet tissue weight, or release of lactic dehydrogenase or acid phosphatase into the effluent were observed in either vehicle or PLA2-treated livers. This indicates that cellular injury was not a factor in the prostanoid release. These data suggest that circulating PLA2 can directly stimulate de novo prostanoid synthesis in noninjured tissues. Thus, enhanced plasma prostanoid concentrations in intact animals during periods or regional cellular injury may be due in part to circulating PLA2 released from damaged tissues.
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The authors have designed an experiment to detect a hitherto unrecognized interaction between high doses of the glucocorticoid, dexamethasone, and brain irradiation. Eighteen juvenile male rhesus monkeys received 1800 rads to the whole brain in 8.5 minutes. For 1 1/2 days before and 10 1/2 days after the irradiation, nine animals received approximately 2.9 mg/kg/day of dexamethasone intramuscularly in addition to irradiation, while the remaining nine animals served as the control group and received saline. All animals eventually developed a progressive neurological syndrome, and died of delayed radiation necrosis of the brain. The two groups were compared with regard to latency to onset of clinical signs, survival time, and number, distribution, and location of lesions of radionecrosis. Large doses of desamethasone did not alter the susceptibility of the primate brain to delayed radiation necrosis. Detailed morphological study of the radionecrotic lesions supports the hypothesis that most, if not all, of the lesions develop as the consequence of injury to blood vessels.
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Pathologic studies of women with fatal cerebrovascular disease who have received oral contraceptives are infrequently found in the literature. Three cases of this type are reported here. The pathologic findings included an intrinsic vascular lesion in the form of intimal hyperplasia with and without associated thrombosis, found in arteries supplying the brain. Similar vascular lesions have been reported previously in other sites of the vascular system in association with exogenous or endogenous steroids. They have also been found in other species under the influence of steroids. This hyperplasia of vessel intima may be found in association with other clinicopathologic entities, but stigmata of other diseases were not found in these three patients.
The cases of six patients are presented to delineate the clinical profile of delayed radiation necrosis of the brain. In five the diagnosis was verified histologically. Symptoms most often begin 9 months to 2 years after radiotherapy. Progressive visual impairment and dementia are common following perisellar irradiation, while hemispheric signs predominate following irradiation of the cerebrum. Cerebrospinal fluid protein may be elevated. Focal delta slowing is usually present on electroencephalography. The necrotic brain may appear on radionuclide brain scan as an area of abnormal uptake and also act as an avascular space-occupying lesion. With computerized tomography, radiation necrosis appears as an intracerebral area with diminished absorption coefficient that is often enhanced with intravenous contrast medium. The syndrome may be sufficiently characteristic to eliminate the need for surgical exploration and biopsy in some cases. Cumulative experience suggests that the risk-to-benefit ratio of radiotherapy becomes increasingly unfavorable for most patients with benign intracranial neoplasms when the standard brain tumor dose of 5000 to 7000 rads is fractionated at greater than 200 rads per day.
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