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Biomedical subjects

C Holmberg

Publications and source records attributed to C Holmberg.

At least 145 records · Page 8Linked to original sources
PubMed1990

Fine-needle aspiration biopsy in the monitoring of liver allografts. Different cellular findings during rejection and cytomegalovirus infection.

Fine-needle aspiration biopsies were used for clinical monitoring of liver allografts; 21 patients with an inflammatory episode of acute rejection (12.0 +/- 3.3 CIU at the peak) were studied; all episodes were reversible. The inflammatory infiltrate consisted mainly of lymphoid cells, including lymphoid blasts, with increased numbers of class II and IL-2-receptor expressing lymphocytes. No lymphoid activation was seen in corresponding blood specimens. A rapid response to antirejection therapy with high-dose steroids was recorded by FNAB. Another group of 7 recipients without rejection developed a severe CMV disease. The CMV disease was associated with mild inflammation in the FNAB (3.2 +/- 0.9 CIU at the peak), but fewer blast cells and activated cell types were recorded in the graft, and blast cells and lymphocyte activation were seen in the blood specimens, as well. The inflammation disappeared from the FNABs during successful antiviral treatment. The cellular findings of rejection and CMV infection were significantly different, and the presence or absence of rejection could be firmly established by FNAB.

Biomarkers↗
PubMed1990

Glycerol catabolism in Bacillus subtilis: nucleotide sequence of the genes encoding glycerol kinase (glpK) and glycerol-3-phosphate dehydrogenase (glpD).

The glpPKD region of the Bacillus subtilis chromosome was cloned in its natural host in plasmid pHP13. The glpPKD region contains genes required for glycerol catabolism: glpK coding for glycerol kinase, glpD coding for glycerol-3-phosphate (G3P) dehydrogenase and glpP, proposed to code for a positively acting regulatory protein. The cloned 7 kb fragment carries wild-type alleles of glpK, glpD and glpP. It can also complement a strain deleted for the entire glpPKD region. The wild-type alleles were mapped to different subfragments, establishing the gene order glpP-glpK-glpD. The nucleotide sequence of glpK and glpD was determined. Immediately upstream of glpK, an additional open reading frame was found, possibly being part of the same operon. Putative transcription terminators were found in the region between glpK and glpD and downstream of glpD. In a coupled in vitro transcription/translation system, two proteins were found, corresponding in size to those predicted from the deduced amino acid sequences of glycerol kinase and G3P dehydrogenase (54 kDa and 63 kDa, respectively).

Alleles↗
PubMed1990

Recombinant human growth hormone treatment in short children with chronic renal disease, before transplantation or with functioning renal transplants: an interim report on five European studies.

Growth retardation is common in children with chronic renal disease. Final adult height is often reduced, even in children with a functioning renal transplant. The five European studies considered here aim to investigate the efficacy and safety of recombinant human growth hormone therapy (rhGH) in two groups of short children with chronic renal disease. The first group comprises 29 prepubertal children with preterminal chronic renal failure (i.e. before renal transplantation), and the second group comprises 39 prepubertal and pubertal children with functioning renal transplants. The median bone age retardation in the groups at the start of treatment was between 2.2 and 3.7 years; this did not change during the first year of treatment. This interim report concentrates on patients who have been treated for at least 1 year (i.e. 22 children from the first group, and 28 children from the transplant group (15 prepubertal and 13 pubertal children). The median height velocity increased from 4.8 cm/year to 10.0 cm/year in the first group (the chronic renal failure group), from 2.6 cm/year to 6.2 cm/year in prepubertal children with renal transplants and from 3.8 cm/year to 6.7 cm/year in pubertal children with renal transplants. The corresponding changes in height velocity SDS were from -1.3 to 5.1 for the chronic renal failure group and -2.8 to 2.3 for the prepubertal children with renal transplants. Renal function declined in the chronic renal failure group but this decline corresponded to expected progression of the disease. Some of the children with renal transplants showed a decreased renal function, which in most cases was explained by non-compliance or chronic rejection.

Adolescent↗
PubMed1990

Recommendation for collection of venous blood from children, with special reference to production reference values.

Reference values should be produced under standardized conditions. To enable comparison it is desirable to use the same procedure also in other clinical situations. A procedure for the collection of venous blood from children with special reference to production of reference values is recommended. It deals with five items: preparation of the child before specimen collection, preparation of the blood collection site, equipment for specimen collection, the specimen collection itself, and handling and storage of the specimen. Alternative methods are described since no single method is suitable for all paediatric age groups. The problem of adhering to a proposed procedure during routine clinical work is also commented upon. The recommendation has been produced as a joint effort of the Scandinavian Committee on Reference Values and a working group set up by the National Paediatric Societies in the Nordic countries.

Adolescent↗
PubMed1989

Combined immunodeficiency in a calf.

Combined immunodeficiency was documented in a 6-week-old Angus calf. The calf had lymphopenia, undetectable serum IgM or IgA, and low concentrations of serum IgG (420 mg/dl). The calf was treated for diarrhea, pneumonia, and shock, and was given antimicrobial drugs, fluids, and plasma. The calf died of systemic candidiasis and Escherichia coli bacteremia. Aggregated lymphatic folliculi (Peyer patches), lymph nodes, and thymic and splenic lymphoid tissue could not be identified at necropsy.

Animals↗
PubMed1989

Cloning of the glycerol kinase gene of Bacillus subtilis.

A 3.5 kb fragment of Bacillus subtilis DNA which contains wild type alleles of mutations in glpK (glycerol kinase) and glpD (glycerol-3-phosphate [G3P] dehydrogenase) was cloned in plasmid pHV32 in Escherichia coli. The cloned fragment expresses glycerol kinase in B. subtilis mutants carrying the mutations glpK11 and recE4 after induction with glycerol or G3P whereas it does not express G3P dehydrogenase. The cloned fragment thus contains the complete glpK but probably only part of glpD.

Alleles↗
PubMed1989

Risk of progressive kidney damage after acute leukemia.

In order to evaluate potential long-term renal sequelae of childhood leukemia, we studied 62 consecutive patients successfully treated for acute leukemia in 1971-83. At the time of this follow-up study they had been off therapy for 1-9 years and they were all in complete remission. Relative renal length was measured from X-ray films of intravenous pyelograms. Median relative renal length prior to the start of chemotherapy was +1.0 SD (range -1.5 to +4.0, n = 35), at discontinuation of therapy +0.5 SD (range -1.5 to +2.2, n = 22), and at follow-up -0.3 SD (range -3.9 to +2.6, n = 61). The mean calculated decrease in relative kidney size was 0.1 SD unit per year during the follow-up time. The median glomerular filtration rate was 110 ml/min/1.73 m2 (range 70 to 164). Six of 60 patients had glomerular filtration rates below 85 ml/min/1.73 m2. Three patients had some evidence of tubular dysfunction documented by increased excretion of urinary amino acids and/or beta-2-microglobulin or by reduced concentrating capacity. In spite of these abnormalities, we conclude that in most long-term survivors of childhood leukemia renal size and function are relatively well preserved. However, slightly reduced glomerular filtration rates in some patients indicated renal damage. A longer follow-up time is needed to find out whether the decrease in relative renal length is still continuing.

Acute Disease↗
PubMed1986

C-reactive protein--an indicator of generalized bacterial infection in children with nephrotic syndrome.

The usefulness of C-reactive protein for detecting bacterial infections in children with nephrotic syndrome was studied in 12 children who had a total of 29 episodes of infection. Four episodes were septic, with CRP values of 127-270 mg/l and 25 superficial or focal with all CRP values below 47 mg/l; 13 were below 10 mg/l. CRP thus discriminated the invasive bacterial diseases from other infections. It was not affected by the nephrotic syndrome activity.

Bacterial Infections↗
PubMed1986

Genetic control of serum neutralizing-antibody response to rabies vaccination and survival after a rabies challenge infection in mice.

Quantitative differences in serum neutralizing-antibody (SNAb) responses to rabies vaccination and survival after a rabies challenge infection between two inbred mice strains, C3H/J and C57BL/6J, were shown to be under genetic control. A 99% confidence limit calculated from the SNAb response titers of 14 C57BL/6J mice resulted in an upper limit for the SNAb response titer of C57BL/6J mice at 50.63. A SNAb titer less than or equal to 50.63 in response to rabies vaccination was assigned the phenotype of hyporesponder, and a SNAb titer greater than 50.63 in response to rabies vaccination was assigned the phenotype of hyperresponder in this study. The hyper-SNAb response to rabies vaccination and the higher frequency of survival after rabies challenge infection behave as Mendelian dominant alleles in F1 hybrids (C3H/J X C57BL/6J) and backcross (BC) (F1 [C3H/J X C57BL/6J] X C57BL/6J) progeny. Both a relatively hyper-SNAb response and a higher frequency of vaccine-inducible survival phenotypes occur in C3H/J mice. On the other hand, both the relatively hypo-SNAb response and a lower frequency of vaccine-inducible survival phenotypes behave as Mendelian recessive alleles and occur in C57BL/6J mice. C3H/J mice are H-2 Kk, and C57BL/6J mice are H-2 Kb. All three phenotypic traits (H-2 type, SNAb response, and survival after rabies challenge infection) segregate as independent (unlinked) monogenic traits in BC progeny (F1 [C3H/J X C57BL/6J] X C57BL/6J). The genetically controlled survival trait is inducible by rabies vaccination, but SNAb response is not a parameter that measures successful vaccine induction of preexposure protection from a rabies challenge infection in the BC progeny. The essential role of vaccination in developing preexposure protection in genetically responsive mice is confirmed, but indicates that in vitro measurements other than SNAb titers need to be developed to identify mice that have failed to achieve preexposure protection by rabies vaccination. This study confirms Lodmell's findings (D. L. Lodmell and B. Chesebro, J. Virol. 50:359-362, 1984; D. L. Lodmell, J. Exp. Med. 157:451-460, 1983) that susceptibility to rabies infection is genetically controlled in some mice strains. Additionally, this study indicates that conventional rabies vaccination even with more potent vaccines may not induce protection from infection in some genetically susceptible individuals.

Animals↗
PubMed1986

Congenital chloride diarrhoea.

Congenital chloride diarrhoea is an autosomal recessive disease characterized by life-long watery diarrhoea of prenatal onset with high faecal Cl- concentration. Seventy-nine patients have so far been reported. The basic defect involves the active Cl-/HCO3- exchange mechanism of the distal ileum and colon. The defect causes impaired absorption of Cl-, acidity of intestinal contents because of impaired excretion of HCO3-, and, secondarily, impaired Na+ absorption. Intra-uterine diarrhoea leads to hydramnios and often to premature birth. Unless adequately treated, most patients will die of hypo-electrolytaemic dehydration within the 1st few months of life. Some infants will survive in such a state, with severe alkalosis, hypochloraemia, hypokalaemia, and retarded growth and development. Their plasma renin and aldosterone concentrations will become grossly elevated, and pathological changes will develop in the kidneys. The diagnosis is established when faecal Cl- concentration exceeds 90 mmol/l after water and electrolyte deficits have been corrected. Congenital chloride diarrhoea should be treated with full oral replacement of the faecal losses of Cl-, Na+, K+, and water. This therapy will abolish all the secondary disorders, provide for normal growth and development, and prevent renal disease. Though this therapy does not abolish the diarrhoea, most children will become toilet trained at a normal age, their social adjustment will be unimpaired, and they will live a perfectly normal life.

Bibliographies as Topic↗
PubMed1985

Congenital Na+ diarrhea: a new type of secretory diarrhea.

We report a new type of congenital "secretory diarrhea" in a 9-year-old girl that led to contraction and severe metabolic acidosis in the first weeks of life. Her fecal Na+ concentration was high and the pH alkaline. All known causes of secretory diarrhea were excluded. Our findings indicate a defect in the handling of Na+ and H+ in the distal ileum and colon. Treatment with orally administered Na-K-citrate supplementation has normalized her fluid and electrolyte status and allowed normal growth and psychomotor development, but the diarrhea has persisted.

Acidosis↗
PubMed1985

Fatal unresponsive villous atrophy of the jejunum, connective tissue disease and diabetes in a girl with intestinal epithelial cell antibody.

The patient presented with a diabetes at the age of 3 years. At the age of 5 years she got persistent diarrhoea, lost weight and showed symptoms or arthritis and pericarditis. She was found to have total villous atrophy of the jejunum, which did not respond to dietary treatment, total parental nutrition, prednisone and cyclophosphamide medication. She had high titres of antinuclear antibodies and elevated serum IgG, but antibodies to DNA and to ribonuclearprotein were negative. A low titre of antibodies to human intestinal epithelial cells was found. The patient died of overwhelming fungal sepsis. We propose that the intestinal damage is part of the autoimmune disease. Careful study of jejunal biopsy specimens is helpful in distinguishing this type of patient from patients with coeliac disease.

Antibodies↗
PubMed1985

Interstitial nephritis of acute onset.

Interstitial nephritis was diagnosed at renal biopsy in 10 previously healthy children. All had identical clinical symptoms: anaemia, raised sedimentation rate, low glomerular filtration rate, protein and leucocytes in the urine, but no bacteria; nine also had glycosuria. Six of the children had a history of recent ingestion of drugs or a serologically proved infection, or both. One child later developed uveitis. After the acute phase all made at least partial recovery, but after a mean follow up of two years and eight months only four were without any signs of disease, three had equivocal findings, two definite renal disease, and one renal failure. Interstitial nephritis, therefore, seems to be a clinical entity often occurring without known cause or triggering factor, its prognosis is variable, and some patients may develop chronic renal failure.

Acute Disease↗