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Biomedical subjects

K M Johnson

Publications and source records attributed to K M Johnson.

At least 325 records · Page 18Linked to original sources
PubMed1965

Chronic infection of rodents by Machupo virus.

Machupo virus, the etiologic agent of human hemorrhagic fever in Bolivia, induced chronic asymptomatic infection in laboratory hamsters and colonized individuals of the peridomestic, wild, South American rodent, Calomys callosus. Viruria was detected for more than 500 and 150 days, respectively, in the two species. Chronic viremia was shown only for Calomys. Virus-neutralizing substances were present in parenterally infected adult animals, but not in animals born to, and in contact with, an infected female. Chronic infection in wild rodents may be an important mechanism in the natural history of Machupo and related virus infections.

Animals↗
PubMedDate not supplied

Inhibition by phencyclidine of excitatory amino acid-stimulated release of neurotransmitter in the nucleus accumbens.

The effects of phencyclidine (PCP) on the release of acetylcholine and dopamine, stimulated by excitatory amino acid agonists was examined in slices of nucleus accumbens of the rat. In slices incubated in [3H]choline or [3H]dopamine, the amount of tritium efflux produced by 1 mM N-methyl-D-aspartate (NMDA), kainic acid (KA) or quisqualic acid (QA) was compared with that produced in the presence of varying concentrations of phencyclidine. N-Methyl-D-aspartate stimulated the calcium-dependent release of both ACh and DA, which was completely inhibited by physiological concentrations of magnesium and inhibited by 2-aminophosphonovalerate (2-APV). Kainic acid- and quisqualic acid-stimulated release of ACh and DA was partially inhibited by magnesium or by 2-APV. Phencyclidine inhibited NMDA-stimulated release of ACh and DA with IC50's around 100 nM. Phencyclidine (0.1 microM) also significantly inhibited kainic acid and quisqualic acid-induced release of ACh in magnesium-free but not magnesium-containing buffer, suggesting that the effect of PCP on kainic acid- and possibly quisqualic acid-stimulated release of ACh is on that part of the response which is mediated by NMDA receptors. The results suggest that the inhibition by PCP of the release of ACh and DA in the nucleus accumbens is selective for NMDA-type receptors.

Acetylcholine↗
PubMedDate not supplied

Cardiac arrest secondary to indomethacin-induced renal failure: a case report.

Acute renal failure secondary to nonsteroidal anti-inflammatory agents is an uncommon occurrence, but may have serious or even lethal consequences. We present one such reaction resulting in cardiac arrest in a 59-year-old diabetic treated with indomethacin. Since presenting symptoms may be vague and unimpressive, one must consider this potential complication to make an early diagnosis and intervene appropriately. In addition when prescribing anti-inflammatory drugs such as indomethacin, one should be cautious in patients who are predisposed to the development of acute renal failure. Risk factors that should be considered are preexistent hepatorenal dysfunction, extracellular fluid volume contraction, and concomitant use of nephrotoxic drugs.

Acute Kidney Injury↗
PubMedDate not supplied

Perinatal diazepam exposure: behavioral and neurochemical consequences.

In the present study the effects of perinatal diazepam (DZP) exposure on behavior and benzodiazepine binding site characteristics in offspring were investigated. Pregnant F344 rats were treated during the last trimester of gestation with vehicle or diazepam (3 mg/kg, 5 mg/kg, or 10 mg/kg). Lactating dams were similarly treated on postnatal days 1-7. Both prenatal and postnatal exposure to diazepam resulted in significant effects on the acquisition and extinction of active avoidance behavior measured postweaning. The number of trials to extinction of one-way active avoidance behavior was significantly greater in offspring exposed gestationally to 3 mg/kg and 10 mg/kg diazepam and postnatally to 10 mg/kg diazepam. The mean response latencies for all diazepam treated groups were significantly shorter than those of the vehicle treated rats during the first 15 trials under extinction conditions. In contrast, neither gestational nor postnatal diazepam exposure significantly affected either acquisition or retention of a passive avoidance task. In addition, the binding affinity between the benzodiazepine type I selective ligand, CL218,872, and cortical membranes, as well as the degree to which GABA potentiated 3H-flunitrazepam were significantly altered by perinatal diazepam exposure. No treatment altered the approximate number of benzodiazepine binding sites in either the cortex, hippocampus, or cerebellum. The results of this study further support diazepam as a behavioral teratogen and give new evidence for neurochemical effects following gestational as well as postnatal diazepam exposure.

Animals↗
PubMedDate not supplied

Upregulation of the phosphorylated form of CREB in spinothalamic tract cells following spinal cord injury: relation to central neuropathic pain.

Spinal cord injury (SCI) often leads to the generation of chronic intractable neuropathic pain. The mechanisms that lead to chronic central neuropathic pain (CNP) following SCI are not well understood, resulting in ineffective treatments for pain relief. Studies have demonstrated persistent hyperexcitability of dorsal horn neurons which may provide a substrate for CNP. We propose a number of similarities between CNP mechanisms and mechanisms that occur in long-term potentiation, in which hippocampal neurons are hyperexcitable. One biochemical similarity may be activation of the transcription factor, cyclic AMP response element-binding protein (CREB), via phosphorylation (pCREB). The current study was designed to examine whether tactile allodynia that develops in segments rostral to SCI (at-level pain) correlates with an increase in CREB phosphorylation in specific neurons known to be involved in allodynia, the spinothalamic tract (STT) cells. This study determined that, in animals experiencing at-level allodynia 35 days after SCI, pCREB was upregulated in the spinal cord segment rostral to the injury. In addition, pCREB was found to be upregulated specifically in STT cells in the rostral segment 35 days after SCI. These findings suggest one mechanism of maintained central neuropathic pain following SCI involves persistent upregulation of pCREB expression within STT cells.

Analysis of Variance↗