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Biomedical subjects

S Nelson

Publications and source records attributed to S Nelson.

At least 181 records · Page 10Linked to original sources

Malocclusion in Labrador Inuit youth: a psychosocial, dental and cephalometric evaluation.

Epidemiological studies of malocclusion of world populations have been previously limited to dental parameters. This cross-sectional study examined the prevalence of malocclusion in the dentitions of Inuit (Eskimo) youth aged between 5-22 years from Labrador, Canada, using psychosocial, dental and skeletal (radiographic) parameters. Data were obtained from two communities, Nain (population 1079) and Hopedale (population 534). About 82% (n = 363) of the Inuit youth and 50% (n = 222) of their parents responded to the psychosocial questionnaires. In total, 78% (n = 348) of the Inuit youth were examined intraorally to determine the prevalence of malocclusion using the Treatment Priority Index (TPI), and 23% (n = 100) had cephalometric radiographs taken using a portable cephalometer. The results indicated that 95% of the Labrador Inuit youth examined had some degree of malocclusion, 10-16% were aware of their occlusal disharmonies, 55-65% wanted to have their teeth straightened, and 5% were teased by others because of their malocclusions. In addition, 63% of the parents seemed to be aware of their child's occlusal problems and 70% wished their children to wear orthodontic appliances if they were needed. Prevalence and awareness to malocclusion were positively correlated. According to the TPI, 18% had "severely handicapping" and 20% had "very severely handicapping" malocclusions. The TPI score increased with age from 5.25 in the young group to 8.05 in the older age group (mean 6.7). There were high prevalences of crowded anterior teeth, upper lingual posterior crossbites, and open or edge to edge bites. A prevalence of 35% Angle Class I, 49% Angle Class II and 16% Angle Class III molar relationships were observed. Cephalometric analysis demonstrated a mean wits measurement of -2.0 mm, a mean ANB angle of 4.7, a mean lower face height of 68.3 mm, a mean interincisal angle of 125 degrees and a mean frankfort mandibular plane angle of 31.3 degrees. A need for orthodontic care and further education were clearly indicated and highly recommended.

Adolescent↗

Pathophysiology of pneumonia.

The care and management of the pneumonia patient are formidable challenges to the physician. As long as the basic underlying host defense defects in these patients remain elusive, the clinician's approach will remain symptomatic and empirical. Further knowledge of the underlying pathophysiology of pneumonia will undoubtedly provide innovative approaches to both the prevention and the early and effective treatment of this infection. Clearly, the development of a multimodal approach, including components of immune modulation and immune restoration, is needed to improve the multiple defects in the host defense system; however, the normal host defense system operates in a delicate balance. Efforts to stimulate the immune system nonselectively may prove to be as deleterious to the patient as are the negative effects of their immunocompromised state.

Antibody Formation↗

Pathogenesis and host defense in pulmonary infections.

The development of pneumonia typically results from an overwhelming bacterial inoculum or a breakdown in the integrity of the host's pulmonary defense mechanisms. Augmentation of pulmonary defenses is one means of reducing the incidence, morbidity, and mortality from pneumonia. Strategies to enhance pulmonary or systemic defenses are actively being investigated. Selected established and investigational measures enhancing host defense mechanisms against various pathogens are reviewed.

Humans↗

Orientation selectivity of cortical neurons during intracellular blockade of inhibition.

Neurons in the primary visual cortex of the cat are selectively activated by stimuli with particular orientations. This selectivity can be disrupted by the application of antagonists of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) to a local region of the cortex. In order to determine whether inhibitory inputs are necessary for a single cortical neuron to show orientation selectivity, GABA receptors were blocked intracellularly during whole cell recording. Although the membrane potential, spontaneous activity, subfield antagonism, and directional selectivity of neurons were altered after they were perfused internally with the blocking solution, 18 out of 18 neurons remained selective for stimulus orientation. These results indicate that excitatory inputs are sufficient to generate orientation selectivity.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

Is there an energy conservation "system" in brain that protects against the consequences of energy depletion?

A poorly understood marked decrease (circa 50% of control) in local cerebral glucose utilization is caused by sublethal doses of NaCN. The decrease is global, occurring in essentially all brain regions and is entirely reversible within hours, leaving no obvious pathology. This event is not unique to NaCN in so far as a strikingly similar pattern of decreased glucose utilization occurs with some other toxins. Nor can it be attributed to a direct action of NaCN since local application by microdialysis to the striatum produces a global depression. These results imply that some widely distributed "system" or substance is involved. We speculate the existence of a "system" possibly related to the reticular activating system that senses a fall in energy production and acts globally to make cells quiescent and thus would give some protection from excitotoxic driven damage.

Analysis of Variance↗

Cimetidine does not impair pulmonary clearance of Pseudomonas aeruginosa in normal rats.

Histamine (H2)-receptor blockers are commonly used in critically ill patients to prevent gastric bleeding and have been implicated in the pathogenesis of gram-negative bacterial (GNB) nosocomial pneumonia. These experiments were undertaken to determine if cimetidine affects pulmonary GNB clearance. Groups of normal Sprague-Dawley rats were given cimetidine (75 mg/kg) or an equal volume of sterile buffer intraperitoneally every 6 hr for 24 hr prior to intratracheal challenge with 1.0 x 10(8) Pseudomonas aeruginosa. At 6 and 24 hr after challenge, animals were sacrificed and gastric pH, quantitative lung cultures, and total and differential [alveolar macrophages (AM) and polymorphonuclear leukocytes (PMN)] cell counts in bronchoalveolar lavage fluid were performed. Results showed that cimetidine therapy resulting in gastric pH greater than 4.0 has no effect on the pulmonary clearance of P. aeruginosa.

Animals↗

Permittivities of fresh fruits and vegetables at 0.2 to 20 GHz.

Permittivities, moisture contents, tissue densities, and total soluble solids data were determined for samples of twenty-three kinds of fresh fruits and vegetables at 23 degrees C. Permittivities were measured at 41 frequencies between 200 MHz and 20 GHz with an open-ended coaxial-line probe and a microwave network analyzer. Results of the permittivity measurements are presented graphically, and dielectric constant and loss factor values at six frequencies across the range are tabulated along with sample descriptions and moisture, density, and total soluble solids data. Although specific values differ, the dielectric constant decreases steadily with increasing frequency, dropping more rapidly at frequencies above 5 GHz. Values for the loss factor decrease as frequency increases above 200 MHz to a broad minimum in the 1- to 3-GHz region and then increase again as the frequency approaches 20 GHz. The dielectric behavior of the fruit and vegetable tissues appears to be influenced by ionic conductivity and bound water relaxations at the lower frequencies and by free water relaxation at the higher end of the frequency range.

Fruit↗

Role of granulocyte colony-stimulating factor in the immune response to acute bacterial infection in the nonneutropenic host: an overview.

Granulocyte colony-stimulating factor (G-CSF) regulates the production and potentiates the function of neutrophils. Studies of animals and patients have shown that levels of G-CSF increase in response to certain types of acute bacterial infection; for example, levels of this factor increase in the lungs and in serum during pneumonia. Investigations of several nonneutropenic animal models of severe bacterial infection have indicated that exogenous recombinant G-CSF--either alone or in combination with antibiotics--can significantly enhance host defenses and improve rates of survival. Trials of recombinant G-CSF for the prevention or treatment of serious infection in clinical settings have recently been initiated.

Acute Disease↗

Expression of tumor necrosis factor-alpha and interleukin-6 cell-surface receptors of the alveolar macrophage in alcohol-treated rats.

The hypothesis was tested that alcohol may modulate alveolar macrophage cytokine receptors, thus interfering in lung immune defense mechanisms. Male rats were treated with alcohol either acutely (7 hr continuous intravenous alcohol infusion at a rate of 30 mg/100 g body weight/hr after a priming dose of 175 mg/100 g body weight) or chronically (feeding an alcohol-containing liquid diet for 12-14 weeks). Three hr before killing, the rats received an intravenous injection of Gram-negative bacterial lipopolysaccharide (LPS; Escherichia coli, O26:B6, 100 micrograms/100 g body weight). After anesthesia with sodium pentobarbital, the trachea was cannulated, and the lungs excised and lavaged to obtain alveolar macrophages. The recovered cells were used to measure the binding of recombinant human [125I]tumor necrosis factor-alpha (TNF-alpha) and [125I]interleukin-6 (IL-6). Kd and Bmax were determined at 4 degrees C, thus reflecting only the cell-surface binding sites and their affinity. Two binding sites were detected for both cytokines: high-affinity (Kd1 in the range of 20-110 pM), low-capacity (Bmax1 in the range of 1-13 fmol/10(6) cells), and low-affinity (Kd2 in the range of 0.6-1.3 nM), high-capacity (Bmax2 in the range of 34-100 fmol/10(6) cells). Acute alcohol treatment significantly decreased Bmax1 (39%) and Bmax2 (79%) for TNF-alpha, whereas chronic alcohol feeding abrogated the Bmax1 (Bmax1 = 0), without affecting Bmax2. In the acute group, LPS had an effect similar to that of alcohol. Alcohol administration did not modify the LPS effects. The following changes were monitored for IL-6 binding. Acute alcohol treatment markedly reduced (86%) Bmax2.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcoholic Intoxication↗

TNF Nco-I RFLP is not an independent risk factor in rheumatoid arthritis.

The human TNF genes are located within the MHC class-III region on chromosome 6. The presence or absence of an Nco-I restriction site in the 5' non-coding sequence of the TNF beta gene defines two alleles (TNFB*1 and TNFB*2). The segregation of these alleles has been associated with levels of TNF alpha or TNF beta production in systemic lupus erythematosis (SLE), insulin-dependent diabetes mellitus (IDDM) and in healthy control individuals. Rheumatoid arthritis (RA) is characterized by high levels of TNF alpha within the synovial fluid and to address the question of whether this could be brought about by a genetic predisposition to high TNF production by RA individuals, we examined the distribution of this Nco-I polymorphism in 98 healthy volunteers and 123 patients with active rheumatoid arthritis. No difference was observed between the normal and RA groups with respect to haplotype segregation or allelic frequency. Furthermore, no difference was observed between DR4+ or DR4- individuals in the control or RA groups. These data demonstrate that the high level of TNF alpha seen in the joints of RA patients is unlikely to be due to a genetic predisposition of these patients to high TNF alpha production, as defined by the TNF Nco-I restriction fragment length polymorphism (RFLP).

Alleles↗

Improved self-inactivating retroviral vectors derived from spleen necrosis virus.

Self-inactivating (SIN) retroviral vectors contain a deletion spanning most of the right long terminal repeat's (LTR's) U3 region. Reverse transcription copies this deletion to both LTRs. As a result, there is no transcription from the 5' LTR, preventing further replication. Many previously developed SIN vectors, however, had reduced titers or were genetically unstable. Earlier, we reported that certain SIN vectors derived from spleen necrosis virus (SNV) experienced reconstitution of the U3-deleted LTR at high frequencies. This reconstitution occurred on the DNA level and appeared to be dependent on defined vector sequences. To study this phenomenon in more detail, we developed an almost completely U3-free retroviral vector. The promoter and enhancer of the left LTR were replaced with those of the cytomegalovirus immediate-early genes. This promoter swap did not impair the level of transcription or alter its start site. Our data indicate that SNV contains a strong initiator which resembles that of human immunodeficiency virus. We show that the vectors replicate with efficiencies similar to those of vectors possessing two wild-type LTRs. U3-deleted vectors carrying the hygromycin B phosphotransferase gene did not observably undergo LTR reconstitution, even when replicated in helper cells containing SNV-LTR sequences. However, vectors carrying the neomycin resistance gene did undergo LTR reconstitution with the use of homologous helper cell LTR sequences as template. This supports our earlier finding that sequences within the neomycin resistance gene can trigger recombination.

Base Sequence↗

Tumor necrosis factor-alpha induces c-jun during the regenerative response to liver injury.

After liver injury, remaining hepatocytes proliferate to regenerate the liver. Although the precise mechanisms that initiate and localize regeneration are unknown, local induction of c-jun is a critical, early step in the response. Treatment of rats with antibodies to tumor necrosis factor-alpha (TNF-alpha), a mediator of liver injury, inhibits regenerative induction of jun nuclear kinase activity and nuclear c-jun expression and alters the DNA binding activity of the c-jun transcription factor, AP-1, in liver. Pretreatment with anti-TNF antibodies does not affect pulmonary or renal c-jun expression or AP-1 binding activity post-partial hepatectomy. In primary hepatocyte cultures, TNF-alpha directly promotes the proliferative actions of mitogens, supporting in vivo evidence that it sensitizes hepatocytes to mitogens. Thus local release of TNF may act in a paracrine fashion to initiate regeneration in the injured liver by promoting induction of critical growth-related genes, such as c-jun.

Animals↗

Loss of compartmentalization of alveolar tumor necrosis factor after lung injury.

Tumor necrosis factor (TNF), a compartmentalized cytokine, is a key mediator in the systemic inflammatory response syndrome and may play a role in multiorgan failure. To assess whether compartmentalization of alveolar TNF is preserved following lung injury, isolated perfused lungs from Sprague-Dawley rats were given intratracheally 1 ml/kg of phosphate-buffered saline (PBS), 0.1 mg/kg of lipopolysaccharide (LPS), or 125,000 units of murine recombinant TNF (mrTNF). To induce lung leak, one group of rats was given 50 mg/kg of alpha-naphthylthiourea (ANTU) intraperitoneally. Then, 125,000 units mrTNF was given intratracheally to these lungs. Samples of perfusate were assayed for TNF by the L929 cytotoxicity assay before (0 min) and 180 min after the intratracheal challenge, and bronchoalveolar lavage (BAL) was performed for TNF assay. ANTU increased lung leak but intratracheal TNF and LPS did not. The isolated perfused lung preparation expressed small amounts of perfusate TNF and underwent minimal leak that was not caused by TNF release. Endogenous or exogenous intrapulmonary TNF remained predominantly compartmentalized, but following ANTU, TNF readily appeared in the perfusate. Compartmentalization of alveolar TNF is lost during alveolar-capillary injury, suggesting that the injured lung may contribute to a systemic inflammatory response and subsequent multiorgan failure.

Animals↗

Characterization of the functional properties and nuclear binding proteins of the rat luteinizing hormone/chorionic gonadotropin receptor promoter in Leydig cells.

The experiments presented herein were designed to study the molecular basis of the restricted cellular localization and transcriptional regulation of the LH/CG receptor in Leydig cells. Using luciferase fusion constructs transfected into Leydig and Sertoli cell lines, we show that the proximal 186 basepairs (relative to the translation start site) of the 5'-flanking region of the rat LH/CG receptor represent a basal promoter that accounts for the Leydig cell-specific expression of this receptor. A region that confers negative transcriptional regulation by cAMP maps to nucleotides -40 to -70 of this basal promoter. Using mobility shift and deoxyribonuclease footprinting assays, we also report the detection of Leydig cell-specific protein(s) that bind to the basal LH/CG receptor promoter. The binding of this protein(s) to the promoter involves an AP-2 consensus sequence beginning at nucleotide -59 as well as additional sequences that remain to be identified. In spite of the fact that the AP-2 site is involved, the protein-DNA complexes detected in Leydig cells are not recognized by an antibody to AP-2.

Animals↗

Rapid induction of messenger RNA for nitric oxide synthase II in rat neutrophils in vivo by endotoxin and its suppression by prednisolone.

Nitric oxide is believed to participate in nonspecific cellular immunity. Gram negative bacterial endotoxins increase the production of reactive nitrogen intermediates (RNI) in phagocytic cells by inducing the enzyme nitric oxide synthase II (NOS II). Anti-inflammatory glucocorticoids attenuate endotoxin-induced increases in RNI. This study evaluated the effect of in vivo administration of prednisolone on Escherichia coli lipopolysaccharide endotoxin (LPS)-induced increases in plasma RNI and neutrophil mRNA for NOS II and production of RNI in the rat. We show that LPS rapidly induces mRNA for NOS II and production of RNI (NO2- and NO3- anion) in rat neutrophils within 2 hr after in vivo administration of a sublethal dose of 0.5 mg/kg, i.v. A pharmacologic dose of prednisolone (50 micrograms/kg, im) given 15 min before LPS-attenuated production of NO2- and NO3- by neutrophils and suppressed LPS-stimulated mRNA for NOS II. 3-Amino, 1,2,4-triazine inhibited NO2- and NO3- production without affecting gene expression for NOS II. These data demonstrate that LPS rapidly induces functional gene expression for NOS II and prednisolone prevents induction of NOS II activity by inhibiting transcription of its mRNA.

Amino Acid Oxidoreductases↗

A deficit in care. The educational needs of thoracic patients.

1. There is a need for increased educational input for thoracic surgical patients. 2. Information and health education are important aspects of holistic care. 3. Care plans should aim to help the patient regain and maintain a level of independence. 4. Discharge planning should ideally begin prior to admission for surgery.

Humans↗