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Biomedical subjects

M Baker

Publications and source records attributed to M Baker.

At least 199 records · Page 11Linked to original sources
PubMed1990

Interleukin 2-induced tyrosine phosphorylation. Interleukin 2 receptor beta is tyrosine phosphorylated.

Interaction of interleukin 2 (IL2) with its high affinity membrane receptor complex (IL2R) is sufficient to induce proliferation of T lymphocytes. However, the biochemical mechanisms by which IL2 induces this process remain unresolved. The IL2R complex consists of at least two distinct polypeptides that bind IL2, a 75-kDa intermediate affinity subunit (IL2R beta) and a 55-kDa low affinity subunit (IL2R alpha). As indicated by Western blotting with anti-phosphotyrosine-specific antibodies and confirmed by phosphoamino acid analysis, we now demonstrate that interaction of the T cell growth factor interleukin 2 (IL2) with its high affinity receptor on IL2-sensitive human peripheral blood lymphoblasts induces tyrosine phosphorylation of proteins of 92, 80, 78, 70-75, and 57 kDa. IL2 induced tyrosine phosphorylation in YT 2C2 cells which express only the 75-kDa intermediate affinity IL2 binding molecule (IL2R beta) but not in cells which either express only the 55-kDa low affinity IL2 receptor molecule (IL2R alpha) or no IL2-binding sites. Therefore, IL2R beta, in the absence of IL2R alpha, appears sufficient to transduce the transmembrane signal leading to tyrosine phosphorylation. Two different antibodies reactive with phosphotyrosine specifically immunoprecipitated IL2R beta cross-linked to radiolabeled IL2. These findings suggest that IL2R beta is a substrate for the tyrosine kinase which is activated by IL2 binding to its receptor. Thus, like several other growth factor receptors, activation of the IL2R results in an increase in tyrosine phosphorylation with the receptor itself serving as one substrate.

Amino Acids↗
PubMed1990

Clinical and electromyographic studies of postpoliomyelitis muscular atrophy.

Eleven patients with progressive weakness following polio (postpoliomyelitis muscular atrophy syndrome) were compared electromyographically with nine patients who had stable strength following polio. Abnormalities included (1) abnormal motor unit characteristics in many muscles indicating widespread loss of motor neurons and reinnervation in muscles, including many not clinically affected by the polio; (2) prevalent spontaneous denervation potentials; and (3) abnormal single-fiber electromyographic jitter. These electromyographic abnormalities were similar in progressive and stable postpoliomyelitis patients even when muscles were separated by strength, stability, age and duration of the postpoliomyelitis state. Postpoliomyelitis muscular atrophy appears to be the clinically apparent end of the spectrum of abnormalities existing in all postpoliomyelitis patients.

Action Potentials↗
PubMed1990

Activation of a late H2B histone gene in blastula-stage sea urchin embryos by an unusual enhancer element located 3' of the gene.

In the sea urchin embryo, late histone genes are transcribed at low levels during cleavage and blastula formation and at substantially higher levels in later stages of embryogenesis. To investigate the molecular basis of the stage-specific expression of a late H2B histone gene, we injected mutant genes lacking portions of 5'- and 3'-flanking regions into Lytechinus pictus embryos and monitored their expression by RNase protection. A 200-bp region located 489 bp downstream of the mRNA 3' terminus was necessary for the increase in transcription of the late H2B gene at the mid-blastula stage of development. DNase I and methylation interference footprint analyses located only one factor-binding site in this region, and gel mobility shift experiments showed that the DNA-binding activity of this factor (designated H2B abp 1) paralleled the transcriptional activity of the L1 H2B gene. Additional mutagenesis and microinjection experiments located the activator element to a 32-bp DNA segment that includes the H2B abp 1-binding site. These experiments also showed that the 32-bp fragment functions independently of position and orientation and therefore has the hallmarks of an enhancer. That this fragment contains most or all of the L1 H2B gene transcription-stimulatory activity makes it unusual among enhancerlike elements, which generally consist of several clustered factor-binding sites that act additively or cooperatively to affect transcription. The nucleotide sequence of the L1 H2B enhancer element suggests that the trans-acting factor that interacts with it is a member of the antennapedia or engrailed class of homeodomain proteins.

Animals↗
PubMed1990

Haemophilus infection in cystic fibrosis.

Twenty seven patients with cystic fibrosis under the age of 12 years and 27 matched patients with asthma were followed up in a prospective study for one year. The isolation rate of non-capsulated strains of Haemophilus influenzae from cough swabs and sputum specimens taken at routine clinic visits every two months was significantly greater in cystic fibrosis than in asthma. Haemophilus para-influenzae was equally common in both groups. During exacerbations the isolation rate of H influenzae in cystic fibrosis was significantly greater than at other times, whereas in asthma there was no significant difference. The distribution of biotypes of H influenzae and H parainfluenzae was similar in the two groups. In cystic fibrosis, biotype I was associated with exacerbations. Biotype V was more common than in previous studies, but was not associated with exacerbations.

Bacterial Typing Techniques↗
PubMed1989

Hemiballismus: study of a case using positron emission tomography with 18fluoro-2-deoxyglucose.

A 64-year-old man had right-sided persistent hemiballismus. Cerebral computed tomography (CT) and 0.5-T magnetic resonance imaging (MRI) showed no abnormalities, but 1.5-T MRI showed decreased signal intensity of the putamina, greater on the left than on the right. The subthalamic area was normal on CT and MRI. Positron emission tomography with 18fluoro2-deoxyglucose showed marked hypometabolism of the left putamen (60% of the right) and hypermetabolism of the left parietal lobe (138% of the right). The decreased metabolism of the left putamen may indicate a reduction in neuronal firing. The pathophysiology of the hemiballismus in this case may be loss of tonic inhibition of the lateral globus pallidus from the putamen, leading in turn to greater inhibition of the subthalamic nucleus, less excitation of the medial globus pallidus, and less inhibition of the thalamus and motor cortex, and thus allowing expression of the ballistic movements.

Adolescent↗
PubMed1989

Depolarization changes the mechanism of accommodation in rat and human motor axons.

1. We have previously studied accommodation in rat and human motor axons by testing excitability with combinations of long and short current pulses. We found that normally polarized axons accommodate slowly and partially (over about 50 ms) to subthreshold depolarizing currents, and that the principal mechanism is the activation of slow potassium channels (Bostock & Baker, 1988). To understand the response of human nerves to ischaemia, we have now extended these observations to axons already depolarized before the testing currents were applied. 2. Rat ventral root axons were depolarized by passing continuous currents or by raising the extracellular potassium concentration. Human forearm nerves were depolarized by ischaemia, induced by inflating a sphygmomanometer cuff on the upper arm. Depolarized rat and human motor axons accommodated much more rapidly and completely than normally polarized axons (e.g. accommodation in rat axons was 50% complete within 2 ms at about 15 mV depolarized to rest). 3. The fast component of accommodation in depolarized rat fibres was not blocked by tetraethylammonium ions or 4-aminopyridine, was not accompanied by a conductance or potential change, and had a time constant of 1.7 ms at 30 degrees C. It was attributed to inactivation of closed sodium channels. 4. In depolarized rat fibres exhibiting fast accommodation, a brief rise in excitability was seen at the break of an anodal current. Our prediction that human motor axons would show anode-break excitation during ischaemia was readily confirmed. 5. The results are discussed in relation to Hill's (1936) mathematical description of accommodation in nerve, and it is concluded that his description is only applicable to depolarized axons.

Action Potentials↗
PubMed1989

Altered expression of leucocyte sialoglycoprotein in Wiskott-Aldrich syndrome is associated with a specific defect in O-glycosylation.

The Wiskott-Aldrich syndrome (WAS) is an X-linked immune deficiency disorder characterized clinically by both lymphocyte and platelet dysfunction. Studies of WAS T lymphocytes have revealed deficient or defective cell surface expression of the highly O-glycosylated leucocyte sialoglycoprotein CD43. To further elucidate the basis for, and functional relevance of, CD43 modifications on WAS lymphocytes, we have studied lymphocytes from two WAS patients with regard to membrane glycoprotein profile and mitogen-induced proliferative responses. CD43 was found to be either absent or altered in size on peripheral blood lymphocytes and lectin-stimulated T cells from both patients. Compared with control cells, the WAS lymphocytes displayed reduced, but measurable proliferative responses to lectins and neuraminidase/galactose oxidase, and virtually no response to periodate, a mitogenic agent which targets sialic acid residues on membrane glycoproteins such as CD43. Analysis of activities of three glycosyltransferases involved in O-glycosylation revealed marked reduction in the level of activity of UDP-N-acetylglucosamine: Gal beta 1-3GalNAc-R beta-1,6-N-acetylglucosamine (beta-1,6-GlcNAc) transferase in one WAS patient and no detectable activity of this enzyme in a second. beta-1,6-GlcNAc transferase activity has recently been shown to increase during T cell activation coincident with changes in the O-linked glycans on CD43. A selective reduction of this glycosyltransferase in WAS lymphocytes suggests that O-linked oligosaccharides may be important to the structure of membrane glycoproteins involved in lymphocyte activation.

Cell Division↗
PubMed1988

Evidence for two types of potassium channel in human motor axons in vivo.

We have obtained evidence that human axons in vivo possess potassium channels similar to two types found in rat nerve, giving rise to a slowly activating potassium conductance and inward rectification. This was achieved non-invasively by tracking the thresholds of single motor axons in the forearm while applying polarizing currents. On average, human ulnar motor axons appear to have fewer outwardly rectifying potassium channels than rat nerves.

Adult↗
PubMed1988

Magnetic resonance imaging for monitoring relapse of acute myeloid leukemia.

Magnetic resonance provides a non-invasive tool for monitoring normal and leukemic bone marrow. Measurements of the T1 relaxation times are elevated in acute myelogenous leukemia. However, interpatient variability diminishes the usefulness of MR measurements for diagnosing leukemia. In following the time course of individual patients, T1 relaxation time measurements appear to give an early and sensitive indication of leukemic relapse after remission and this may serve a clinical role in the management of leukemia by reducing the regularity of necessary marrow aspirates and biopsies.

Bone Marrow↗