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Biomedical subjects

E S Sears

Publications and source records attributed to E S Sears.

16 recordsLinked to original sources

Crop biomass leaching for nutrient recycling in a CELSS.

Leaching may be employed as a biomass conversion technique to minimize consumption of system resources in a CELSS. This study examined leaching rates and total leachability of Triticum aestivum L. Yecora Rojo residue. Total biomass reduction and phosphate concentration in the leachate were tested as a function of particle size, leaching time of solid, temperature, and sonication versus mechanical agitation. For modeling purposes, phosphate rate constants were determined experimentally via batch testing on 25-mm biomass. Simulation models were written to predict the effect of liquid flow rate on phosphate leaching in concurrent and countercurrent reactors.

Biodegradation, Environmental↗

The effects of intracanopy lighting on cowpea production.

Utilizing a combination of above-canopy and intracanopy lighting may prove highly beneficial in a Lunar Controlled Ecological Life Support System (LCELSS) as a means of increasing volumetric efficiency of plant growth. Intracanopy lighting was not found to be detrimental to plant tissue and production per plant when cowpeas were grown using sand culture. Specifically, intracanopy lighting did not adversely influence leaf area, dry mass, or wet mass production. Although no significant differences were found when 25% of the lighting was placed intracanopy, this is important because it indicates that there is potential in saving space for controlled growth systems. The use of intracanopy lighting would allow plant trays to be "stacked" closer, thereby increasing volumetric plant density.

Biomass↗

Serial immune evaluation of cyclosporine- and placebo-treated multiple sclerosis patients.

During an ongoing clinical trial of cyclosporine (CsA) immunosuppression therapy for chronic progressive multiple sclerosis (MS), a comparison was made of the immune responses of 18 CsA- and 18 placebo (P)-treated MS patients. Patients randomized to receive either CsA or P had identical entry immune profiles. However, these MS patients displayed significantly increased T-helper:T-suppressor (TH:TS) ratios (P less than 0.01), percentage (%) active-T (P less than 0.01), % Ia+-T (P less than 0.05) and % Ta1+-T (P less than 0.01) cell phenotypes when compared to age-matched normal controls. Further, the MS-P-treated patients displayed significant increases (all P less than 0.01) in % pan-T, % helper-T, % active-T and % Ta1+-T cell phenotypes as well as panel mixed lymphocyte culture (panel MLC) functional responsiveness from entry to cumulative 12-month study data. In contrast, the MS-CsA-treated patients only displayed an increased % pan-T cell phenotype. The cumulative 12-month follow-up data showed that the MS-P-treated patients displayed significantly higher immune parameters than the MS-CsA-treated patients for % pan-T (P less than 0.05), % helper-T (P less than 0.01), TH:TS ratio (P less than 0.05), % active-T (P less than 0.01), % Ta1+-T cells (P less than 0.01) and panel MLC stimulation index (P less than 0.01). Thus, MS-CsA-treated patients did not display the progressive immune activation seen on serial evaluation during the follow-up time period that characterized the placebo-treated MS group.

Acute Disease↗

Disruption of the blood-brain barrier in hyperammonemic coma and the pharmacologic effects of dexamethasone and difluoromethyl ornithine.

Both hyperammonemia and blood-brain barrier (BBB) breakdown have been implicated in the evolution of hepatic encephalopathy. To define a possible relationship, Swiss Albino mice were subjected to sublethal encephalopathic doses of ammonium acetate; the integrity of the BBB was determined grossly with Evans blue and quantitatively with [14C]-alpha-aminoisobutyrate (AIB). Some animals were injected with a dose of ammonium acetate sufficient to maintain coma for 1 hr (AC group). One group, termed stuporous (AS), received only enough ammonium acetate to interfere with grooming and exploratory activity; this dosage was insufficient to completely block the righting response, which was absent in the AC group. When compared to that of controls (CON) receiving normal saline instead of ammonium acetate, cerebral tissue from the AC group was stained blue and contained nearly double the amount of AIB; AS group brain tissue was unstained and the AIB content did not differ significantly from normal. Some of the AC group were pretreated with drugs known to retard BBB breakdown; one set received dexamethasone (AC-DXMN), another the ornithine decarboxylase inhibitor difluoromethyl ornithine (AC-DFMO), and a third L-ornithine (AC-ORN). Brain tissue from the AC-ORN group stained blue and AIB content did not differ significantly from that of the untreated AC group. Cerebral tissue of the AC-DXMN pretreatment group stained light blue; AIB content was significantly lower than in the AC group and greater than the CON group. The AC-DFMO brains were unstained and AIB content was significantly lower than in the AC group but did not differ significantly from CON. These results indicate that hyperammonemia may induce BBB breakdown but that the disruption of barrier integrity is not antecedent to the development of coma, although it seems to coincide with coma in time.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

Maximizing the harvest of contrast enhancing lesions in multiple sclerosis.

Transient contrast enhancing lesions can be seen with CT in patients with MS, particularly during acute exacerbations. Conventional 40 gm iodine enhancement technique followed by immediate postinfusion scanning was compared with high dose (80 gm iodine) enhancement technique followed by a 1-hour delayed CT scan; delayed high dose technique (DHD) in nine exacerbations. New lesions, totaling 36 in all, were observed in each case with the DHD technique. With time, the borders expanded in 98% of lesions, thus confirming in vivo that a defective blood-brain barrier (BBB) underlies this phenomenon.

Adult↗

Transient oculomotor paralysis in pseudotumor cerebri.

Transient oculomotor paralysis developed abruptly in a patient with well-documented pseudotumor cerebri. Other demonstrable causes of third-nerve palsy were excluded. Sixth-nerve palsy is known to occur in 10 to 40% of patients in most series of pseudotumor cerebri, but third-nerve palsy has not been reported previously. It may also be a nonspecific sign of raised intracranial pressure.

Adult↗

Active multiple sclerosis. Enhanced computerized tomographic imaging of lesions and the effect of corticosteroids.

Computerized axial transmission tomography (CT) of the brain is useful for imaging lesions in multiple sclerosis (MS). Active demyelination may be demonstrated with CT contrast enhancement (CTE) as regions of increased x-ray density. We report a series of patients with active MS who typify these changes. Corticosteroid therapy reduces the intensity of this phenomenon presumably by reestablishing the integrity of the blood-brain barrier; if corticosteroid therapy is instituted prior to the CT contrast study, the focal enhancement may be obscured. A transient vascular permeability defect is the basis for CTE during the acute exacerbation in MS. The possibility of MS must be kept in mind when one or more foci of increased density occur in the absence of mass effect during CTE. Appreciation of these features may prevent misdiagnosis.

Adult↗

Therapeutics of disordered movement.

Human motor behavior is organized around two major neurotransmitter systems in the basal ganglia--dopaminergic and cholinergic. Hypokinetic disease may result from hypofunction of the dopaminergic system or cholinergic hyperfunction. The reverse seems true for many hyperkinetic movement disorders. Drugs which facilitate dopaminergic neurotransmission or which block cholinergic transmission relieve many hypokinetic disorders; the opposite approach is useful in treating many hyperkinetic disorders.

Carbidopa↗

Nonkitotoc hyperosmolar hyperglycemia during glycerol therapy for cerebral edema.

Glycerol, an effective cerebral dehydrating agent, also has gluconeogenic properties, and can thereby elevate serum glucose to dangerously high levels in predisposed patients treated for cerebral edema. The nonketotic hyperosmolar hyperglycemic state usually occurs in cases of maturity onset diabetes or prediabetes, as in the two elderly patients discussed in this paper. The pathogenesis usually evolves through a constant diabetogenic stress that causes persistent hyperglycemia resulting in the exhaustion of ordinarily adequate insulin stores, ultimately allowing hyperglycemia to progress unchecked to metabolic coma. Precautions to recognize this development should be taken in appropriate patients.

Aged↗

Effects of synthetic buffers on reflexes in the isolated frog spinal cord.

Substitution of synthetic buffers (Tris, TES, HEPES, or 3,3-dimethylglutarate) for CO2-bicarbonate buffer in Ringer solution perfusing the isolated in vitro frog spinal cord preparation altered membrane properties and reflex activity. Perfusion with Ringer solution gassed with O2 and containing synthetic bu,fers consistently produced a depolarization of motoneurons and dorsal root fibers, decreased the amplitude (and usually the duration) of ventral and dorsal root potentials, and had variable effects on motoneuron and dorsal root reflex discharges. With Tris-Ringer these discharges decreased in amplitude; with Ringer containing one of the other synthetic buffers, these discharges were augmented. All changes were reversible when the cord was returned to bicarbonate-buffered Ringer aerated with 95% O2/5% CO2. The use of a combined buffer system-one containing a synthetic buffer and bicarbonate-induced smaller or minimal changes in bioelectric activity. At present the data are insufficient to allow firm conclusions concerning the mechanisms underlying these results; but it is evident 1) that changes in PCO2 and bicarbonate concentration and 2) that the pharmacological properties of synthetic buffers are important variables.

Animals↗

Inhibition of polyamine synthesis suppresses human lymphocyte proliferation without decreasing cytokine production or interleukin 2 receptor expression.

Difluoromethylornithine (DFMO) irreversibly inhibits ornithine decarboxylase (ODC), a crucial enzyme in polyamine synthesis, and impairs mitogen-induced lymphocyte proliferation. To examine the mechanism of action of DFMO, we studied the effect of this ODC inhibitor on lymphokine production and interleukin 2 (IL 2) receptor expression. DFMO decreased thymidine uptake of peripheral blood mononuclear cells stimulated by the mitogens phytohemagglutinin, concanavalin A, phorbol myristate acetate and ionomycin 60-70% compared with untreated cells, and the inhibition could be completely reversed by 10 mM spermidine. DFMO had no effect on IL 1 production by monocytes exposed to silica particles. Concentrations of IL 2 increased 7-fold in DFMO-treated, PHA-stimulated PBMC cultures, compared with untreated cells; whereas IL 2 receptor expression as measured by the anti-Tac monoclonal antibody was not affected by the inhibition of ODC. Mixing experiments using cells cultured with or without DFMO indicated that the inhibition by DFMO was not mediated by suppressor cells. Our results strongly support the concept that polyamines are required for a relatively late event in lymphocyte activation occurring after the interaction of IL 2 and its receptor.

Biogenic Polyamines↗