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Biomedical subjects

V Esmann

Publications and source records attributed to V Esmann.

At least 37 records · Page 2Linked to original sources
PubMed1981

Phosphorylation of glycogen synthase in a homogenate of human polymorphonuclear leukocytes.

Glycogen synthase I in a homogenate of human polymorphonuclear leukocytes was phosphorylated under imitated physiological conditions utilizing the endogenous protein kinases. At subsequent steps of phosphorylation the 32P-labelled synthase was purified and characterized. Limited tryptic hydrolysis of the 32P-labelled synthase released four phosphopeptides (t-A, t-B, t-C, t-D) and subsequent chymotrypsinization of the trypsin resistant core released three phosphopeptides (c-A, c-B, c-C). One Pi/subunit was incorporated within 8-10 min and 2.2 Pi/subunit within 60 min increasing the Kc for Glc-6-P to 4-6 mM. The initial phosphorylation up to 0.8 Pi/subunit occurred mainly in peptide c-A and a linear relation between ratio of independence (RI) of glycogen synthase in the interval RI 0.85 to RI 0.05 and phosphorylation of this peptide of 0.5 Pi was observed. Phosphorylation of this peptide is responsible for the decrease in ratio of independence. From experiments with inhibitors and activators, the initial phosphorylation was found predominantly catalysed by the endogenous cAMP independent synthase kinase, however, the endogenous cAMP dependent protein kinase and phosphorylase kinase also phosphorylate endogenous glycogen synthase I to a minor degree. Circumstantial evidence for a Ca-dependent synthase kinase different from phosphorylase kinase is presented. The endogenous Glc-6-P dependent glycogen synthase occurring in a homogenate of leukocytes disrupted in the presence of NaF incorporated 1.07 Pi/subunit and Kc for Glc-6 was increased from 6-8 mM to 20 mM. From the present and previous experiments [7] a total of 8 major phosphorylatable sites have been defined, one on each of the peptides t-A, t-B, c-B, c-C and two on peptide c-A, which in addition may contain a third site for phosphorylase kinase. Assuming identical subunits, only 13 out of 32 sites are thus covalently modified at maximum phosphorylation. The operational defined synthase R (Kc for Glc-6-P 0.5 mM) and D (Kc for Glc-6-P 2-8 mM) activities correspond to synthase with about 0.8 Pi and 1.8-2.3 Pi/subunit, respectively.

Enzyme Activation↗
PubMed1981

Treatment of trigeminal and thoracic zoster with idoxuridine.

A double-blind random selection comparison was made of the therapeutic effects in acute herpes zoster of 40% idoxuridine (IDU) dissolved in dimethyl sulphoxide (DMSO) compared with DMSO and saline flavoured with garlic. Thoracic (80 patients) and trigeminal (42 patients) zoster were investigated separately. The patients were evaluated daily until skin healing and then at 1, 3 and 6 months by registering pain, paraesthesia and sensitivity disturbances as well as by clinical and photographic evaluation of the skin lesions. Duration of pain was positively correlated to age, to delayed healing and to elevated temperature in the acute phase of zoster. The period of pain before skin eruption was considerably longer in thoracic than in trigeminal zoster, while the latter was associated with a more severe inflammatory reaction, more neurologic sequelae, but also by a faster healing of the skin lesions. IDU was highly effective in shortening the period of pain and improving skin healing in trigeminal zoster, while no effect of IDU was observed in thoracic zoster. The reason for this difference is presently not understood.

Aged↗
PubMed1980

Epstein-Barr-virus-induced lymphoproliferative disorder converting to fatal Burkitt-like lymphoma in a boy with interferon-inducible chromosomal defect.

A 6-year-old boy presenting with swelling of cervical and axillary lymph-nodes was diagnosed as having an Epstein-Barr virus infection because of EBV-nuclear-antigen-positive B-lymphocytes in blood and lymph nodes and high antibody titres to EBV antigens. The natural killer activity of blood-lymphocytes was low, and so was the percentage of T-lymphocytes with Fc receptors for IgG (T-gamma cells). Chromosomal studies revealed a defect in the long arms of one of the chromosomes in pair no. 16 (16q22). The defect only appeared after addition of interferon to the lymphocyte cultures and preferentially in T-gamma lymphocytes. The disease progressed despite attempts to restore the patient's immune reactivity by interferon, transfer factor, and blood transfusions. Necropsy showed that the severe hyperplasia of lymph nodes found during life had become a Burkitt-like lymphoma. The possible connection between an interferon-induced chromosomal defect (break at 16q22) and reduced level of natural killer activity, reduced T-gamma lymphocytes, and proliferation of EBV-positive B-lymphocytes is discussed.

Burkitt Lymphoma↗
PubMed1980

Cryptococcal meningitis: complications due to intrathecal treatment.

A 50-year-old woman with cryptococcal meningitis was treated with amphotericin B intrathecally through a Rickham reservoir and intravenously, together with flucytosine orally. After 4 months of treatment cryptococci and cryptococcal antigen were still present in cerebrospinal fluid from time to time. After removal of the Rickham reservoir the patient recovered completely within 6 weeks. The persistent infection was thus found to be due to the presence of the Rickham reservoir, a complication to intrathecal therapy which has not been reported before.

Amphotericin B↗
PubMed1979

Purification and properies of cAMP dependent and independent histone kinases from human leukocytes.

Histone kinase activity was purified from human polymorphonuclear leukocytes by ammonium sulphate precipitation of a 180 000 x g supernatant, followed by DEAE-cellulose chromatography and gelfiltration. On DEAE-cellulose cAMP dependent kinase activity eluted in two peaks, I and III, at 1.2 mmho and 6.5 mmho, respectively. Catalytic subunit (C) from both peaks had Mr 33 000, 3.0S. Regulatory subunit (R) from peak I and III both had Mr 33 000 upon gelfiltration, but sedimented at 2.8--3.0S and 3.0--3.2S, respectively. R2 and R4 subunits were identified. The R-C dimer from peak I and III sedimented at 4.8S and (4.8)--5.1S, respectively. The holoenzyme from peak I had Mr 165 000, 6.7S, which suggest a R2C2 structure, while that of peak III sedimented at 6.7S, but eluted at Mr 330 000 (2R2C2) by gelfiltration. The Kmapp for peak I and III enzymes were, respectively: histone IIA 0.5 mg/ml (both forms), ATP 18 microM and 23 microM, and cAMP 5 X 10(-8) M and 6.3 x 10(-8) M. Both enzymes had pH optimum 6.7--6.9 and were equally sensitive to Ca2+, temperature and protein kinase inhibitor. The substrate specificity was histone VS greater than histone IIA = histone VIS greater than casein greater than phosvitin. Peak I enzyme, but not peak III enzyme, was dissociated by histone and high ionic strength and reassociation of R and C subunits were facilitated by ATP-Mg. It is concluded that peak I and III enzymes represent type I and II cAMP dependent protein kinases, respectively. Type I comprises 20--30% of cAMP dependent protein kinase activity and is absent from the 180 000 x g supernatant of gently disrupted cells. Purified catalytic subunit had Kmapp (ATP) 20 microM with rabbit muscle glycogen synthease I as substrates. Synthase I from rabbit muscle and human leukocytes were phosphorylated by catalytic subunit to synthase D (ratio of independence less than 0.07). cAMP independent histone kinase activity eluted in one peak (Peak II) at3 mmho. The enzymatic activity sedimented at 3.4S and eluted from gelfiltration with Mr 78 000. Kmapp for ATP was 78 microM and for histone IIA 0.5 mg/ml. The enzyme was sensitive to temperature, but less sensitive than cAMP dependent protein kinase to Ca2+, and insensitive to protein kinase inhibitor. The substrate specificity was histone IIA greater than histone VS = histone VIS, while casein and phosvitin were poor substrates. Glycogen synthase I was not phosphorylated. The cAMP independent histone kinase activity comprised 15% of the total histone kinase activity in a crude homogenate of leukocytes. Its physiological substrate is unknown.

Chromatography, DEAE-Cellulose↗
PubMed1979

Treatment of herpes zoster with idoxuridine ointment, including a multivariate analysis of symptoms and signs.

A double-blind, random selection comparison was made of the therapeutic effects in acute herpes zoster of (A) 40% idoxuridine (IDU) dissolved in dimethyl sulphoxide (DMSO), or one of the following ointments: (B) a basis of polyethylene glycol, (C) a basis with 60% DMSO, (D) a basis with 5% IDU and 60% DMSO, and (E) a basis with 40% IDU and 60% DMSO. Each group comprised 20 patients. The patients were evaluated daily until skin healing and then at 1,3, and 6 months by registering 4 neurological signs, 5 clinical evaluations of skin pathology and 4 photographic evaluations of the skin lesions. A 'profile' of the effect of each treatment was computed by calculating normalized means for each of the 13 variables. A non-random distribution of the clinical and photographic variables indicated a statistically significant, but small therapeutic effect of treatment A on skin healing, whereas no convincing effect on pain or sensitivity disturbances was established. Treatments B-E were without positive effects. The information given by the highly interdependent variables were computed for each variable and for groups of variables after appropriate scoring. It was found that the photographic evaluation contributed evidence independent of the clinical evaluation of skin pathology. A multiple correlation analysis revealed that age was positively correlated to the duration of pain and to delayed healing, that rapid healing was intimately connected to no or short-lived pain, and surprisingly that zoster in the trigeminal area healed faster than in other locations without being correlated to less pain. Treatment A must necessarily be reevaluated taking into account proper controls as well as age and affected dermatomes.

Adolescent↗