Biomedical subjects
J Carmody
Publications and source records attributed to J Carmody.
We have moral authority to apologize for the past.
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Involvement of abscisic acid-dependent and -independent pathways in the upregulation of antioxidant enzyme activity during NaCl stress in cotton callus tissue.
The role of abscisic acid (ABA) in the signal transduction pathway associated with NaCl-induced up-regulation of antioxidant enzyme activity was examined in a NaCl-tolerant cotton callus cell line treated with NaCl, ABA, paraquat, or H2O2 in the presence and absence or fluridone, an inhibitor of terpene, and therefore, ABA synthesis. Treatment with NaCl resulted in a rapid increase (within 30 minutes) in the ABA levels of the callus tissue, and the NaCl, ABA, and paraquat treatments induced rapid increases in the activities of superoxide dismutase, catalase, peroxidase, and glutathione reductase. Pre-treatment with fluridone significantly suppressed the NaCl-induced increases, but only slightly delayed the increases in tissue subjected to exogenous ABA treatment. This implies that ABA is involved in the signal transduction pathway associated with the NaCl-induced up-regulation of these antioxidant enzymes. Pre-treatment with fluridone had no effect on the paraquat-induced increases, suggesting that these enzymes can also be up-regulated by a pathway other than the one mediated by ABA. Both the NaCl and paraquat treatments produced significant increases in the superoxide levels within the callus, but the increase resulting from the paraquat treatment was significantly higher than the increase resulting from the NaCl treatment. These data suggest that NaCl stress results in the production of reactive oxygen intermediates (ROI) which signals the induction of an ABA-dependent signaling pathway. The production of very high levels of ROI, such as those that occur with paraquat treatment or perhaps during periods of prolonged or extreme stress, may induce an ABA-independent signaling pathway.
Effect of gender on anti-inflammatory and analgesic actions of two kappa-opioids.
The higher incidence of inflammatory and painful disorders in women and recent reports that have emphasized the importance of gender in nociceptive sensitivity and responsiveness to analgesics prompted us to investigate gender as a factor in the variability in response to opioids. We studied the anti-inflammatory and antinociceptive effects of two kappa-opioid agonists in adjuvant-induced arthritis, one that acts both peripherally and centrally (PNU50488H; 20 mg/kg/day), the other which is peripherally selective (asimadoline; 5 mg/kg/day). Both drugs had equally powerful anti-inflammatory effects in both male and female rats (reducing measures by 60-80%). In contrast, there were gender-based heterogeneities in their analgesic actions, contingent on the method of stimulation (mechanical or thermal); males were insensitive to the analgesic effects of asimadoline with thermal but not mechanical nociceptive stimuli. We also sought evidence for gender influences on the joint content of Substance P (SP), a peptide suggested to have a role in producing inflammation and found that levels were higher in the untreated arthritic females, although there were no gender differences in disease sensitivity or nociception in arthritic animals receiving no drugs. Paradoxically, both drugs elevated SP concentrations in the joints, perhaps as a consequence of an action of kappa-opioids to suppress SP release from peripheral nerves, but the gender differences remained. Further experiments are required to determine exact mechanisms responsible for the gender distinction in analgesic response to kappa-opioids that may involve differential activation of primary afferents.
Home testing for human immunodeficiency virus.
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Lack of a role for substance P in the control of dural arterial flow.
The role of the neuropeptide substance P (SP) in the control of dural arterial blood flow was examined in barbiturate-anaesthetised rats. The parietal skull was trephinised and the blood flow in branches of the medial meningeal artery was monitored with a laser Doppler flowmeter. Electrical stimulation of the dura mater encephali at a parasagittal site with pulses of 0.5 ms (10-20 V, 5-10 Hz, 30 s) caused a transient increase in dural blood flow which was reproducible in size with repetitive stimulation. Neither the basal flow nor the stimulus-evoked flow was significantly changed by topical administration of SP, the SP analog septide, or the NK1 antagonist RP 67580. It is concluded that SP released from dural nerve fibres upon local stimulation does not play an important role in the regulation of dural arterial flow.
The case. Bad care, good care, and spiritual preservation.
A cancer patient learning to walk again finds that his relationships with his two physical therapists affect his recovery. One woman gives hope as well as instruction. He advises healers to meet their patients as equals, "to take down as many barriers as they can, give away as many distancing privileges as possible."
Correlating CBC profile and infectious outcome. A study of febrile infants evaluated for sepsis.
The cases of 1,009 febrile infants who were evaluated for sepsis as outpatients during a seven-year period were reviewed to correlate their complete blood count (CBC) profiles with the infectious outcomes. Eighty-one infants had serious bacterial infections (SBIs); the remainder (928) were culture-negative. The infants with SBIs had a significantly greater mean total white blood cell (WBC) count and absolute band count (ABC) than did those who were culture-negative, whereas the difference in mean percent of polymorphonuclear leukocytes was not significant. The sensitivity of the ABC was significantly superior to that of total WBC count in predicting the outcome of SBI. The diagnostic data provided by the ABC can aid physicians in determining the predictive value of CBC profiles for infectious outcome in febrile infants receiving outpatient sepsis evaluation.
[Smoking and physicians].
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Effects on recovery of soleus and extensor digitorum longus muscles of prolonged wheel running during a period of repeated nerve damage.
The right sciatic nerve in NMRI mice was frozen under anaesthesia 13 times at three-week intervals for a total period of 8.5 months. During this period, but not afterwards, one sub-group of these mice had access to running wheels in which the animals ran several kilometres per night, thereby actively or passively training reinnervated or denervated leg muscles, as well as the intact contralateral muscles. A number of distinct effects persisted for as long as 14-18 weeks after the termination of this "endurance training". In reinnervated soleus muscle, tetanic force was significantly higher (37%) in the trained muscles as was muscle weight (36%); in general, negative effects of the nerve damage persisted. In the reinnervated extensor digitorum longus, tetanic force and muscle weight were significantly smaller in the trained animals (by 11 and 16%, respectively) which are considered typical effects of endurance training. The resistance of the soleus neuromuscular junction to block by both curare and Mg2+ was depressed on the damaged side but this property was not influenced by the training; in extensor digitorum longus the pattern was similar. It is concluded that training during the period of repeated cycles of denervation-reinnervation produced significant effects which impressively outlasted the training period. The possible nature of these effects is discussed.
Nimodipine reduces morbidity, mortality after disruption of cerebral blood flow.
Nimodipine is a 1,4 dihydropyridine with Ca++ channel blocking properties. It is more lipophilic than most calcium channel blockers, and thus has a greater volume of distribution within the brain. Many actions of nimodipine have been proposed from work done in animal models following induction of complete or partial cerebral ischemia for varying lengths of time. However, these experimental results have not been sufficiently documented in patient populations, and there exists conflicting data as to nimodipine's mechanism of action in the cerebral ischemic patient. Regardless of the exact mechanisms of action, studies suggest that nimodipine may significantly reduce morbidity and mortality in patients following disruption of cerebral blood flow.
Low temperature worsens mammalian oxygen toxicity.
Oxygen toxicity was assessed in mice exposed to 5 ATA of oxygen. Central nervous system toxicity was measured as the latent period before convulsions, and lung damage estimated by wet and dry weight measurements. Our results confirmed previous findings that hyperbaric oxygen induces hypothermia in animals, and this effect is profound in mice exposed to 5 ATA of oxygen at ambient temperatures of 15 degrees C and 5 degrees C. However, even marked hypothermia had very little effect on the latent times to convulsions in mice. Unexpectedly, the combination of hypothermia and hyperbaric oxygen produced much more severe lung damage than either treatment alone, with a 2.7-fold increase in weight in the 5 degrees C group (average rectal temperature of 16.1 degrees C). These results indicate that hyperoxic-induced hypothermia cannot be considered a protective mechanism against oxygen toxicity and indeed hypothermia can markedly potentiate hyperbaric oxygen toxicity.
Swim stress reduces chronic pain in mice through an opioid mechanism.
Chronic nociception has been studied in male mice by means of the formalin test in which forelimb motor behaviour is scored after subcutaneous formalin injection. The rating remained above 2.0 for 30 min after the injection (scale range 0-3). The magnitude of the nociception has been compared with that reported in other animal types. Mice are more sensitive than rats, cats and monkeys. The stress of a swim of 3 min has been found to reduce nociception by up to 25%. This analgesia is wholly opioid in nature, being abolished by a moderate dose of naloxone (1 mg/kg).
Endogenous opioids are not involved in the pathology induced by hyperbaric oxygen treatment.
In mice, oxygen at hyperbaric pressures (515 kPa; 5 ATA) induces convulsions and lung damage (edema and hemorrhage). Morphine treatment (15 mg X kg-1, i.p.) significantly protects against the development of this pathology. The protection is abolished by naloxone (1 mg X kg-1, i.p.). Electric footshock, which induces diverse opioid effects, affords no protection against hyperbaric oxygen damage. Possible mechanisms of the morphine action are discussed.
Opioid-independent hyperalgesia induced in mice by pentobarbitone at low dosage.
The abdominal constriction (writhing) test was used to investigate the effect of pentobarbitone on nociception in mice. At dosages of 10, 20 and 30 mg/kg, pentobarbitone produced marked increases in nociceptive scores. The extent of the enhancement of nociception was uninfluenced by naloxone or swim-stress. The swim-stress induced analgesia but, in contrast to previous results using other tests for nociception, the analgesia was wholly non-opioid with the abdominal constriction test.
Effects of electric footshock on barbiturate sensitivity, nociception and body temperature in mice.
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The characteristics of the opioid-related analgesia induced by the stress of swimming in the mouse.
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