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J J Miller

Publications and source records attributed to J J Miller.

At least 19 recordsLinked to original sources
PubMed2001

Preischemic hyperglycemia-aggravated damage: evidence that lactate utilization is beneficial and glucose-induced corticosterone release is detrimental.

Aerobic lactate utilization is crucial for recovery of neuronal function posthypoxia in vitro. In vivo models of cerebral ischemia pose a conceptual challenge when compared to in vitro models. First, the glucose paradox of cerebral ischemia, namely, the aggravation of delayed neuronal damage by preischemic hyperglycemia, cannot be reproduced in vitro. Second, in vitro elevated glucose levels protect against ischemic (hypoxic) damage, an outcome that has seldom been reproduced in vivo. Employing a rat model of cardiac-arrest-induced transient global cerebral ischemia (TGI), we found that hyperglycemic conditions, when induced 120-240 min pre-TGI, significantly reduced post-TGI neuronal damage as compared to normoglycemic conditions. In contrast, hyperglycemia, when induced 15-60 min pre-TGI, significantly aggravated post-TGI neuronal damage. Brain lactate levels in rats loaded with glucose either 15 min or 120 min pre-TGI were significantly and equally higher than those of control, saline-injected rats. The beneficial effect of 120 min pre-TGI glucose loading was abolished by lactate transport inhibition. A significant increase in blood corticosterone (CT) levels was observed upon glucose loading that peaked at 15-30 min and returned to baseline levels by 60-120 min. When rats loaded with glucose 15 min pre-TGI were treated with metyrapone, a CT synthesis inhibitor, a significantly lower degree of delayed neuronal damage in comparison to both untreated, 15 min glucose-loaded rats and normoglycemic, control rats was observed. Thus, although elevated levels of brain lactate cannot explain the glucose paradox of cerebral ischemia, hyperglycemia-induced, short-lived elevation in CT blood levels could. More importantly, lactate appears to play a crucial role in improving postischemic outcome.

Adenosine Diphosphate↗
PubMed2001

Blockade of lactate transport exacerbates delayed neuronal damage in a rat model of cerebral ischemia.

Studies over the past decade have demonstrated that lactate is produced aerobically during brain activation and it has been suggested to be an obligatory aerobic energy substrate postischemia. It has been also hypothesized, based on in vitro studies, that lactate, produced by glia in large amounts during activation and/or ischemia/hypoxia, is transported via specific glial and neuronal monocarboxylate transporters into neurons for aerobic utilization. To test the role of lactate as an aerobic energy substrate postischemia in vivo, we employed the cardiac-arrest-induced transient global cerebral ischemia (TGI) rat model and the monocarboxylate transporter inhibitor alpha-cyano-4-hydroxycinnamate (4-CIN). Once 4-CIN was establish to cross the blood--brain barrier, rats were treated with the inhibitor 60 min prior to a 5-min TGI. These rats exhibited a significantly greater degree of delayed neuronal damage in the hippocampus than control, untreated rats, as measured 7 days post-TGI. We concluded that intra-ischemically-accumulated lactate is utilized aerobically as the main energy substrate immediately postischemia. Blockade of lactate transport into neurons prevents its utilization and, consequently, exacerbates delayed ischemic neuronal damage.

Animals↗
PubMed2001

Sleep disorders: a risk factor for pseudotumor cerebri?

OBJECTIVE: To determine whether sleep-related breathing disorders are common in patients with idiopathic intracranial hypertension. MATERIALS AND METHODS: Medical records of 53 patients with idiopathic intracranial hypertension from a tertiary center neuroophthalmology practice were reviewed. Thirty-seven patients were identified who had a history of snoring, difficulty sleeping, or daytime somnolence. The data from polysomnograms were tabulated to determine the frequency of apneas, hypopneas, and arousals. RESULTS: Fourteen of 37 patients with idiopathic intracranial hypertension and symptoms of sleep disturbance underwent polysomnography. There were two men and 12 women varying in age from 24 to 58 years (mean, 39.4 +/- 11.9). These patients were obese with body mass indexes varying from 33.0 to 63.2 (mean, 46.0 +/- 9.5). A diagnosis of sleep apnea was made in six and upper airway resistance syndrome in seven patients. CONCLUSIONS: Sleep-related breathing problems were common in our patients with idiopathic intracranial hypertension. Obesity was common in these patients and may be playing a causative role in sleep apnea and idiopathic intracranial hypertension. It is suggested that idiopathic intracranial hypertension patients who have symptoms of sleep disturbance should be further evaluated for the presence of sleep-related breathing problems.

Adult↗
PubMed2001

Sleep disorders: a risk factor for normal-tension glaucoma?

PURPOSE: To determine the prevalence of sleep-related symptoms and sleep-related breathing disorders by polysomnography in patients with normal-tension glaucoma (NTG). PATIENTS AND METHODS: This comparative case series included 23 patients with NTG, 14 NTG suspects, and 30 comparison patients without NTG. A sleep history was obtained and determined to be positive or negative. Polysomnography was offered for patients with a positive sleep history. Prevalence of a positive sleep history and prevalence of sleep disorders were the main outcome measures. RESULTS: The NTG, NTG suspect, and comparison groups did not differ with respect to age, body mass index, systemic disease, gender, or race. Thirteen (57%) of 23 patients with NTG, 6 (43%) of 14 NTG suspects, and 1 (3%) of 30 comparison patients had a positive sleep history (P = 0.001). Nine of 13 patients with NTG and four of six NTG suspects with a positive sleep history chose to undergo polysomnography. Seven (78%) of nine patients with NTG and all four NTG suspects undergoing polysomnography were diagnosed with a sleep disorder. Five patients with NTG had sleep apnea and two had sleep hypopnea. Two NTG suspects had sleep apnea; one had sleep hypopnea; and one had upper airway resistance syndrome. The one comparison patient with a positive sleep history had upper airway resistance syndrome by polysomnography. CONCLUSIONS: Sleep-disturbed breathing may be a risk factor for NTG. Although we do not provide evidence for a cause-and-effect relationship, various physiologic factors produced by sleep-disturbed breathing may play a significant role in the pathogenesis of this optic neuropathy. We recommend obtaining a sleep history from patients with NTG and performing polysomnography in those patients with sleep disturbance symptoms.

Adult↗
PubMed2001

Intracranial surgery: to shave or not to shave?

OBJECTIVE: In an effort to improve patient confidentiality as well as cosmesis, the authors have stopped shaving for all intracranial procedures. The objective was to determine whether this lack of shaving increased the postoperative infection rate. DESIGN: A retrospective study was performed comparing all intracranial surgical procedures performed in the last 2(1/2) years, when hair was not shaved, with the infection rate in patients who did have their hair shaved in the preceding 3(1/2) years. SETTING: An academic tertiary care referral center. PATIENTS: Every patient (children and adults) who underwent an intracranial procedure by the skull base surgery team was included. Similar patient demographics were used for the hair-shaved group. INTERVENTION(S): Intracranial procedures consisted of acoustic tumor removal, vestibular nerve sections, skull base surgery procedures, vascular decompressions, and craniotomies for benign and malignant tumors. MAIN OUTCOME MEASURES: The most essential criterion was to determine whether postoperative wound infection developed in a patient. This was documented as either minor (stitch abscess or wound dehiscence), moderate (wound breakdown requiring inpatient or outpatient therapy, such as oral or intravenous antibiotics), or severe (significant wound breakdown that required hospitalization, with surgical debridement and antibiotics). RESULTS: In all, 150 patients were not shaved for their intracranial procedures; postoperative wound infections developed in 11 (7%). The infections were minor (6), moderate (5), and severe (0). By comparison, 100 patients undergoing intracranial procedures had their hair shaved. In this group, the number of infections noted was 6 (6%). Their categorization into mild, moderate, and severe was 4, 2, and 0, respectively. Statistical analysis did not reveal any significant difference between the two infection rates. CONCLUSIONS: The rate of postoperative wound infection was statistically no greater when the hair was shaved than when it was not. Thus, for patient confidentiality as well as patient esteem, we recommend not shaving hair for intracranial procedures.

Adult↗
PubMed2001

Black tongue.

Explore the source record for details and available documents.

Asthma↗
PubMed1999

An increase in lactate output by brain tissue serves to meet the energy needs of glutamate-activated neurons.

Aerobic energy metabolism uses glucose and oxygen to produce all the energy needs of the brain. Several studies published over the last 13 years challenged the assumption that the activated brain increases its oxidative glucose metabolism to meet the increased energy demands. Neuronal function in rat hippocampal slices supplied with 4 mM glucose could tolerate a 15 min activation by a 5 mM concentration of the excitatory neurotransmitter glutamate (Glu), whereas slices supplied with 10 mM glucose could tolerate a 15 min activation by 20 mM Glu. However, in slices in which neuronal lactate use was inhibited by the lactate transporter inhibitor a-cyano-4-hydroxycinnamate (4-CIN), activation by Glu elicited a permanent loss of neuronal function, with a twofold to threefold increase in tissue lactate content. Inhibition of glycolysis with the glucose analog 2-deoxy-D-glucose (2DG) during the period of exposure to Glu diminished normal neuronal function in the majority of slices and significantly reduced the number of slices that exhibited neuronal function after activation. However, when lactate was added with 2DG, the majority of the slices were neuronally functional after activation by Glu. NMDA, a nontransportable Glu analog by the glial glutamate transporter, could not induce a significant increase in slice lactate level when administered in the presence of 4-CIN. It is suggested that the heightened energy demands of activated neurons are met through increased glial glycolytic flux. The lactate thus formed is a crucial aerobic energy substrate that enables neurons to endure activation.

Animals↗
PubMed1999

Study of cerebral energy metabolism using the rat hippocampal slice preparation.

This article describes methods and experimental paradigms used in combination with the rat hippocampal slice preparation in an attempt to better understand cerebral energy metabolism under the following conditions: normal resting conditions, conditions of oxygen and/or glucose deprivation, and conditions of activation (excitation). The outcome of this attempt, as described herewith, demonstrates the unmatched usefulness of the brain slice preparation as an in vitro tool in the field of neuroscience.

Animals↗
PubMed1999

Accentuated viral exanthems in areas of inflammation.

Types of lesions and patterns of distribution aid in the recognition of viral exanthems. Varicella and hand-foot-and-mouth disease can appear atypically in areas of inflammation. We describe 5 cases of morphologically altered exanthems that localized early and preferentially to areas of inflammation.

Chickenpox↗
PubMed1999

In vitro, animal, and human characterization of OPTISON infusions for myocardial contrast echocardiography.

UNLABELLED: Traditionally, performing myocardial contrast echocardiography with OPTISON required maximal bolus dosing. However, sustained and consistent opacification of the myocardium would be preferable for perfusion imaging. METHODS: Images of 5 anesthetized dogs and 6 human volunteers were obtained with a second harmonic ultrasound system during bolus administration of OPTISON and 2 infusion techniques. One infusion technique used diluted OPTISON, and the other used the buoyant properties of OPTISON microspheres by placing the contrast agent between an infusion source and the intravenous site in a vertically oriented extension line (ELT). Myocardial intensities and in vitro microsphere characteristics were analyzed to assess the consistency of microsphere delivery over time. RESULTS: In addition to providing higher myocardial opacification intensity than diluted infusions, ELT infusions provided consistent microsphere concentration, phantom enhancement, and near-peak bolus-level myocardial opacification for 7 to 15 minutes. The myocardial intensity at 3 and 5 minutes in human subjects during ELT infusions (30 mL/h; 2.5 mL) was lower (220 arbitrary units [au] and 165 au, respectively) but not significantly different (P =.3 and.1, respectively) than the peak myocardial intensity (265 au) after bolus administration. CONCLUSION: This new ELT infusion method provides an acceptable alternative to bolus administration of OPTISON for prolonged myocardial opacification.

Adult↗
PubMed1999

The glucose paradox in cerebral ischemia. New insights.

The present in vivo findings that lactate, accumulated during an ischemic episode, is an essential aerobic energy substrate during the initial postischemic period are in full agreement with out in vitro findings. Moreover, the beneficial effects of hyperglycemia are also in agreement with our and others' in vitro results that have demonstrated a neuroprotective effect of glucose against hypoxic change. The aggravation of ischemic delayed neuronal damage by glucose loading 15 min prior to the ischemic insult is likely the result of glucose induction of a short-acting (30 to 60 min) systemic factor (hormonal?) that, when combined with an ischemic insult, potentiates the ischemic damage.

Animals↗
PubMed1999

Failure to demonstrate therapeutic tachyphylaxis to topically applied steroids in patients with psoriasis.

BACKGROUND: Tachyphylaxis, defined as a rapidly decreasing response to a physiologically active agent after administration of a few doses, can be well demonstrated in the experimental setting. However, tachyphylaxis in the clinical setting lacks clear demonstration. OBJECTIVE: Our purpose was to identify dermatologists' perception of the clinical incidence of tachyphylaxis and then design a prospective study that would estimate the clinical incidence of tachyphylaxis. METHODS: Clinical and academic dermatologists completed a survey questionnaire about the incidence of tachyphylaxis and the time course to its occurrence. Subjects with plaque psoriasis applied topical corticosteroid twice daily for 12 weeks to their plaques, leaving an isolated plaque untreated for comparison. Plaques were evaluated every 2 weeks. By means of a 9-point scale, an end point for clinical detection of tachyphylaxis was defined as "an increase in plaque elevation of at least 2 occurring after a detectable decrease in plaque elevation with topical steroid." RESULTS: The survey found that 57% of dermatologists perceived that tachyphylaxis occurred after 8 weeks of therapy with topical corticosteroid. In the 12-week clinical study, none of 32 patients exhibited detectable signs of tachyphylaxis. CONCLUSION: What accounts for the commonly held belief of tachyphylaxis in the clinical setting may be related to the therapeutic efficacy of topical corticosteroids. Failure of topical corticosteroids to clear psoriasis after an initial improvement may give the impression of tachyphylaxis. The common clinical perception of tachyphylaxis may also be related to issues of compliance outside a study setting or a psoriasis flare unrelated to therapy.

Administration, Topical↗