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Biomedical subjects

K Shannon

Publications and source records attributed to K Shannon.

At least 73 records · Page 4Linked to original sources
PubMed1989

Inhibition by nifedipine of the indirectly induced contractile response of the rat diaphragm.

The effects of nifedipine (30 micrograms/ml) on isometric force production of in-vitro rat diaphragm were studied during direct and indirect modes of muscle activation. During direct muscle stimulation, nifedipine potentiated isometric force during twitch and unfused tetanic stimulation. Indirectly elicited responses, evoked by stimulation of the phrenic nerve, were uniformly depressed following nifedipine. Inhibition of indirect force production increased with time, while force potentiation with direct activation remained constant. We conclude that inhibitory effects of nifedipine on the phrenic nerve-diaphragm preparation are specific for nerve or neuromuscular junction.

Animals↗
PubMed1989

Delay in the execution of voluntary movement by electrical or magnetic brain stimulation in intact man. Evidence for the storage of motor programs in the brain.

Experiments were undertaken to study the effect on voluntary movement of an electrical or magnetic stimulus delivered to the brain through the scalp. Subjects were trained to flex or extend their wrist rapidly in response to an auditory tone. A single brain stimulus (electrical or magnetic) delivered after the tone and before the usual time of onset of the voluntary reaction could delay the execution of the movement for up to 150 ms, without affecting the pattern of the agonist and antagonist EMG bursts. The delay increased with increasing stimulus intensity and with stimuli which were applied nearer to the usual time of onset of the voluntary reaction. A stimulus given after the onset of the first voluntary agonist EMG burst only delayed the onset of the first antagonist and later EMG bursts. Movement was not delayed when similar experiments were performed with supramaximal stimulation of the median nerve instead of the brain stimulus. The delay following a cortical shock was not due to spinal motoneurons being inaccessible to descending input during the delay period since a second brain stimulus, given in the middle of the delay period, was capable of producing a direct muscle response. Neither could the delay be explained by the brain stimulus altering the time of the subject's intention to respond since a stimulus delivered to one hemisphere before an attempted simultaneous bilateral wrist movement produced a far greater delay of the contralateral than the ipsilateral movement. We suggest that the brain stimulus delayed movement by inhibiting a group of strategically placed neurons in the brain (probably in the motor cortex) which made them unresponsive for a brief period to the command signals they receive which initiate the motor program of agonist and antagonist muscle activity. The results have implications for the issues of the storage of motor programs, internal monitoring of central movement commands and the site of organization of the antagonist EMG burst.

Adult↗
PubMed1989

Reciprocal inhibition between forearm muscles in patients with writer's cramp and other occupational cramps, symptomatic hemidystonia and hemiparesis due to stroke.

Reciprocal inhibition of H reflexes in the forearm flexor muscles was examined in a group of 16 patients with writer's and other occupational cramps. The early disynaptic phase of reciprocal inhibition was normal. However, there was a reduction in the amount of later, presynaptic inhibition, when compared with age-matched normal subjects. Similar findings were seen in 2 patients with symptomatic hemidystonia in whom structural brain lesions were present. However, this reduction in presynaptic inhibition was not specific to patients with dystonia. In a further group of 13 patients with hemiparesis or hemiplegia due to stroke, abnormalities of both early and later phases of reciprocal inhibition were found. The patients with spasticity exhibited less disynaptic inhibition than those with normal tone or flaccid limbs. The changes in the presynaptic phase of reciprocal inhibition did not correlate with the clinical signs of spasticity and increased muscle tone. These results provide objective evidence of a physiological basis for the action or task-specific focal dystonias such as writer's cramp.

Adolescent↗
PubMed1989

Mechanisms of gentamicin resistance in gram-negative bacilli in Riyadh, Kingdom of Saudi Arabia.

A survey was undertaken of the prevalence and mechanisms of gentamicin resistance in Gram-negative bacilli in Riyadh. Gentamicin resistance, as assessed by the Stokes method, occurred in less than 2% of isolates of Escherichia coli, about 10-25% of most other enterobacteria, about 40% of Acinetobacter spp. and about 25% of Pseudomonas aeruginosa. This finding of relatively low rates of gentamicin in Enterobacteriaceae was surprising in view of the unregulated use of antibiotics until recent years. AAD(2'') was by far the most commonly detected aminoglycoside-modifying enzyme in the enterobacteria. However Providencia spp. always produced AAC(2') and there was an association between Serratia spp and AAC(6'). Enzymes were less frequently detected in Acinetobacter spp. and Pseudomonas spp. AAD(2'') was also the most common enzyme in Pseudomonas spp. but was never found in Acinetobacter spp. Non-enzymatic resistance played an insignificant role in the resistance of Enterobacteriaceae in Riyadh, but may be more important in Pseudomonas spp.

Bacterial Infections↗
PubMed1987

Effects of milrinone on contractility of the rat diaphragm in vitro.

We studied the effects of the phosphodiesterase inhibitor, milrinone, on isometric force production in the isolated, directly stimulated rat diaphragm. Milrinone (500 micrograms/ml) significantly increased force during twitch stimulation and submaximal tetanic stimulation (p less than 0.05); force during maximal tetanic stimulation was significantly reduced by milrinone (p less than 0.05). The force-augmenting effects of milrinone were not abolished by pretreatment with indomethacin (10(-5)M). Baseline force production decreased when diaphragmatic strips were placed in a calcium-free bathing solution; force potentiation by milrinone, however, persisted in this medium. Pretreatment with milrinone more than doubled the mean time to fatigue (10.8 +/- 1.0 versus 5.1 +/- 0.6 min) during repetitive submaximal stimulation (p less than 0.01). In diaphragmatic strips fatigued by repetitive submaximal stimulation until force production was 60% of baseline, milrinone promptly improved force production; the magnitude of force potentiation after milrinone was quite similar in fresh and fatigued muscle. In conclusion, milrinone enhances diaphragmatic contractility during the most forms of direct stimulation, and delays and reverses diaphragmatic fatigue.

Animals↗
PubMed1986

Prevalence and mechanisms of aminoglycoside resistance. A ten-year study.

Aminoglycoside resistance was monitored at St. Thomas' Hospital from 1975 to 1984. Gentamicin resistance had appeared in a number of species by 1975, but remained rare (less than 1 percent of isolates) in Escherichia coli throughout the study period. Gentamicin-resistant Klebsielleae had become fairly common (8 percent of isolates) by 1977, but little change has subsequently occurred in their frequency of isolation. Serratia species are not frequently isolated; gentamicin resistance in these organisms was not observed until 1979. Since then, 10 to 20 percent of isolates have been found to be resistant. Except for Providencia, most isolates of which were gentamicin-resistant, less than 5 percent of the Enterobacteriaceae isolated were found to be resistant to gentamicin during the 10-year period. Throughout the study, approximately 5 percent of the Pseudomonas aeruginosa isolates were resistant to gentamicin. Less than 5 percent of the isolates of Acinetobacter were resistant to gentamicin before 1979, at which time 40 percent were found to be resistant; subsequently, gentamicin resistance among these organisms has become somewhat less common. On the whole, tobramycin resistance has mirrored gentamicin resistance. However, before 1979, most gentamicin-resistant Klebsielleae isolates had retained susceptibility to tobramycin, as had most gentamicin-resistant isolates of Acinetobacter and P. aeruginosa. Amikacin resistance has remained very unusual in all organisms, apart from non-aeruginosa Pseudomonas species. Until 1977, nearly all the resistance among Enterobacteriaceae was attributable to AAC(3)-I, except for that caused by AAC(2') production in Providencia and the non-enzymatic resistance observed in E. coli. However, more recently, AAC(3)-II and AAD(2'') have become the most common mechanisms of resistance. The resistance of most gentamicin-resistant isolates of P. aeruginosa from 1974 to 1977 was attributable to non-enzymatic mechanisms; subsequently, such resistance was more often caused by AAC(3)-I, AAC(6'), or AAD(2''). Gentamicin resistance first appeared in Staphylococcus aureus in 1976, after which about 1 to 2 percent of the isolates from hospitalized patients were found to be resistant, mostly because of production of AAC(6') and APH(2'').

Acinetobacter↗
PubMed1986

Beta-lactamases with high activity against imipenem and Sch 34343 from Aeromonas hydrophila.

Two groups of inducible beta-lactamases were found among nine isolates of Aeromonas hydrophila. Five isolates produced enzymes with high activity against the penem Sch 34343 and the carbapenem imipenem: the enzymes from some of these isolates also had activity against penicillin, ampicillin, carbenicillin, cephaloridine and cephalexin but one isolate produced an enzyme with no detectable activity against cephalosporins. The other four isolates produced typical 'cephalosporinases' with activity against cephaloridine and cephalexin but not against cefuroxime, cefotaxime, penicillins, imipenem or Sch 34343.

Aeromonas↗
PubMed1986

The in-vitro activity of CI-934 compared with that of other new 4-quinolones and nalidixic acid.

The in-vitro activity of CI-934, a new 4-quinolone compound, was compared with that of the other new 4-quinolones, enoxacin and ciprofloxacin, and also with that of nalidixic acid. CI-934 was more active than any of the other 4-quinolones tested against Gram-positive aerobic organisms including Staphylococcus aureus (MICs 0.06-0.25 mg/l), beta-haemolytic streptococci (MICs 0.12-0.5 mg/l), Streptococcus pneumoniae (MICs 0.25-0.5 ml/l), viridans streptococci (MICs 0.06-0.5 mg/l) and most enterococci (MICs 0.12-0.5 mg/l), although some ampicillin-resistant isolates of Str. faecium were slightly less susceptible (MICs 2 mg/l). All three of the newer 4-quinolones tested were highly active against Enterobacteriaceae, Aeromonas sp., Haemophilus influenzae and Neisseria gonorrhoeae (MICs mostly less than 1 mg/l). The other Gram-negative aerobes tested were in general somewhat less susceptible, although for Acinetobacter and Pseudomonas aeruginosa MICs seldom exceeded 8 mg/l. CI-934 was more active than enoxacin against Gardnerella vaginalis (MICs 1-8 mg/l) although it was a little less active than ciprofloxacin. Bacteroides species (including about half of the fragilis group) were susceptible to CI-934 (MICs mostly 1-8 mg/l): ciprofloxacin had similar activity but enoxacin was less active. Other anaerobes tested were mostly highly susceptible to CI-934 (MICs 1 mg/l or less) but were somewhat less susceptible to enoxacin and ciprofloxacin.

Anti-Bacterial Agents↗
PubMed1986

The effects on beta-lactam susceptibility of phenotypic induction and genotypic derepression of beta-lactamase synthesis.

We have compared the ability of beta-lactam antibiotics to induce beta-lactamase synthesis and antagonize the in-vitro activity of other beta-lactams and also to select mutants with derepressed beta-lactamase synthesis amongst representative Gram-negative bacilli that produce inducible beta-lactamases. Both imipenem and cefoxitin were potent inducers of beta-lactamase and were able to antagonize the activity of other beta-lactams against isolates of Enterobacter cloacae, Citrobacter freundii and Pseudomonas aeruginosa when the two beta-lactams were present simultaneously. However, there was no antagonism for any compound against any of the organisms when the imipenem or cefoxitin was removed immediately before susceptibility to the other compounds was measured. Cefotaxime was a less potent inducer of beta-lactamase and failed to antagonize the activity of other compounds, even when present concurrently with them. Neither imipenem nor cefoxitin induced beta-lactamase synthesis in a strain of Escherichia coli, nor did they antagonize the activity of other beta-lactams against this strain. Imipenem was compared with cefotaxime and cefoxitin as an agent for the selection of beta-lactam-resistant variants. Resistant variants were obtained from isolates of Ent. cloacae, C. freundii and P. aeruginosa when cefotaxime or cefoxitin was used as the selective agent. Most of them synthesized beta-lactamase constitutively and showed reduced susceptibility to a wide range of beta-lactams, but not to imipenem. Variants with reduced susceptibility to imipenem were obtained only from the two isolates of P. aeruginosa. They did not show cross resistance to other beta-lactams and were not distinguishable from the parent strains in beta-lactamase production.

Anti-Bacterial Agents↗
PubMed1986

Erythropoiesis in infants of diabetic mothers.

Neonatal polycythemia is a well-established perinatal complication in infants of diabetic mothers (IDM). To investigate the regulation of erythropoiesis in these infants, we measured cord blood erythropoietin (EP) levels by a sensitive radioimmune assay and examined the growth of erythroid progenitor colonies in a series of IDM and control infants. Fifteen of 18 diabetic mothers were managed on a protocol emphasizing careful glycemic control throughout pregnancy; 10 had glycosolated hemoglobin values within the normal, nondiabetic range during the third trimester. Cord blood EP was elevated in one of 18 IDM and in two of 13 controls (p = NS). In IDM, cord blood EP values were higher in infants delivered following maternal labor and were inversely correlated with umbilical artery pH (r = -0.72; p = 0.006). Growth of burst forming units-erythroid was similar in IDM and controls in the presence of 0.1 to 2.0 U of exogenous EP per ml of methylcellulose medium. Individual infants tended to respond consistently over the entire range of EP doses tested. The number of burst forming units-erythroid observed did not correlate with cord blood EP, birth weight, or neonatal hematocrits. We conclude that: umbilical cord blood EP levels are generally normal in IDM delivered by mothers in whom good glycemic control is maintained throughout gestation, cord blood EP values are strongly influenced by perinatal events, and the response of erythroid progenitors to EP is intrinsically normal in IDM. These data suggest that polycythemia is an adaptive response in IDM and is not associated with a primary abnormality in erythropoiesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1986

Juvenile chronic myelogenous leukemia: surface antigen phenotyping by monoclonal antibodies and cytogenetic studies.

Cells from three children with juvenile chronic myelogenous leukemia were studied using culture in semisolid media, cytogenetic analysis, and surface staining with the monocyte-specific monoclonal antibodies 61D3 and 63D3. The percentage of bone marrow mononuclear cells that were 61D3- and 63D3-positive was markedly increased in all three patients. Bone marrow and peripheral blood mononuclear cells exhibited exceptionally bright immunofluorescence with these antibodies. The presence of monocyte-specific antigens on the surface of juvenile chronic myelogenous leukemia cells suggests that they are derived from a precursor with monocytic characteristics. A specific chromosomal abnormality (47,XY+21) was present in fresh bone marrow cells from one patient; in contrast, 50 metaphases from phytohemagglutinin-stimulated peripheral blood contained a normal karyotype. The chromosomal abnormality was also identified in myeloid colonies grown in vitro from this patient. Granulocytic elements were demonstrated in tissue sections and in cultured myeloid colonies from this child. Our data suggest that malignant transformation in juvenile chronic myelogenous leukemia involves a myeloid progenitor population capable of differentiation in vitro to cells with monocytic or granulocytic characteristics.

Animals↗
PubMed1985

Impaired mononuclear-cell proliferation in patients with the acquired immune deficiency syndrome results from abnormalities of both T lymphocytes and adherent mononuclear cells.

Peripheral blood mononuclear cells from patients with acquired immune deficiency syndrome proliferate poorly after stimulation with soluble mitogens. The present study was undertaken to assess the relative contributions of T lymphocytes and of plastic adherent mononuclear cells to the impaired mononuclear cell responses. We employed a four-step separation procedure including terminal depletion using a monocyte-specific monoclonal antibody (61D3) to derive populations of highly purified T cells from patients and from normal subjects. Highly purified T cells proliferated poorly in response to phytohemagglutinin and pokeweed mitogen. The addition of autologous adherent cells to highly purified T cells markedly improved mitogen-driven proliferation in all subjects; however, mononuclear cells from patients with AIDS responded less well than normals (P less than or equal to 0.01) for both phytohemagglutinin and pokeweed. Allogeneic normal adherent cells fully restored both phytohemagglutinin and pokeweed responses in normal highly purified T cells. Adherent cells from patients were comparable to normal adherent cells in phytohemagglutinin-driven proliferation but performed significantly less well when pokeweed was used to stimulate normal highly purified T-cell responders (4308 cpm after coculture with patients' adherent cells vs 8244 cpm after coculture with allogeneic normal adherent cells; P = 0.05). Similarly, when patient's highly purified T cells were stimulated with pokeweed mitogen, control adherent cells functioned substantially better than patient adherent cells (1198 cpm for allogeneic patient adherent cells vs 2324 cpm for normal adherent cells; P = 0.05). Although the addition of normal adherent cells to patients' highly purified T cells significantly improved pokeweed mitogen responses, these values did not reach normal. Suppression by patients adherent cells was not demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Acquired Immunodeficiency Syndrome↗