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Biomedical subjects

A Brand

Publications and source records attributed to A Brand.

At least 253 records · Page 14Linked to original sources
PubMed1989

Intramammary infections and risk factors for clinical mastitis in herds with low somatic cell counts in bulk milk.

Ten herds with low somatic cell counts in bulk milk had an incidence of clinical mastitis of only 2.2 per 100 cows whereas 10 other herds with similarly low cell counts had an incidence of 53.6 per 100 cows. The major pathogens in the herds with a high incidence were Escherichia coli, Streptococcus uberis, Staphylococcus aureus and the coagulase-negative staphylococci. The percentage of uninfected quarters in the herds with a high incidence of clinical mastitis was 21.4 per cent compared with 12.2 per cent in the herds with a low incidence of clinical mastitis. The prevalence of coagulase-negative staphylococci, Corynebacterium bovis and Micrococcus species was higher in the herds with a low incidence of clinical mastitis. There was a significant linear relationship between the percentage of uninfected quarters and the incidence of clinical mastitis in the herds with a high incidence of clinical mastitis. In herds with a low incidence of clinical mastitis significantly less teat disinfection after milking was practised. The results suggest that infections with minor pathogens tend to protect cows against mastitis, and that teat disinfection after milking may increase the percentage of uninfected quarters and lead to an increased risk of clinical mastitis in herds with low somatic cell counts in bulk milk.

Animals↗
PubMed1989

Incidence of clinical mastitis on farms with low somatic cell counts in bulk milk.

A total of 1140 clinical cases of mastitis, with at least one inflamed quarter, were reported on 125 farms with somatic cell counts in bulk milk less than 150,000/ml. The average annual incidence was 17.9 cases per 100 cows and ranged from none to 80 cases per 100 cows. The microorganisms most frequently isolated were Escherichia coli (16.2 per cent), coagulase negative staphylococci (13.0 per cent), Staphylococcus aureus (9.6 per cent) and Streptococcus uberis (8.0 per cent). Only two cases of Streptococcus agalactiae were found. As the incidence of clinical mastitis increased, the proportion of S aureus also increased, while the proportions of E coli, S uberis and Streptococcus dysgalactiae remained about the same. Most of the clinical cases of mastitis occurred in early lactation, in November, December and January. However, after correction for the number of calvings per month, the incidence of mastitis was highest in the early summer months.

Animals↗
PubMed1989

Flunixin meglumine and flurbiprofen in cows with experimental Escherichia coli mastitis.

The effect of flunixin meglumine and flurbiprofen on the course of experimental Escherichia coli mastitis was examined. Nine cows (within one month post partum) were inoculated intramammarily with 20 x 10(5) viable E coli in both rear quarters. Three cows remained untreated (controls); three cows received three injections of flunixin meglumine and three cows received flurbiprofen as two intravenous infusions. Flunixin meglumine and flurbiprofen were initially given before clinical signs were observed. Treatment was repeated if the cows' temperature increased by more than 1 degree C. In the untreated cows, rectal temperature and heart rate increased from three hours after infection, and rumen motility (both frequency and amplitude) decreased from four hours after infection. Treatment with flunixin meglumine or flurbiprofen almost completely abolished the febrile response during the first nine hours after infection, and the decrease in rumen motility was less pronounced in the treated animals. These results suggest that the decrease in rumen motility during E coli mastitis is at least partly due to a mechanism involving prostaglandin.

Animals↗
PubMed1989

Comparison between clonogenic and cytotoxic assays for measuring LAK cell activity.

The antiproliferative effect of lymphokine-activated killer (LAK) cells was studied using a clonogenic assay in an attempt to find a model for predicting this effect in vivo or ex vivo (in the case of purging) in cancer treatment. The results were compared with the standard 51Cr-release cytotoxic assay. Cells from clonogenic neoplastic cell lines (K562 and HL-60) were plated in methylcellulose with LAK cells obtained from ten different donors in various effector-to-target (E:T) ratios. At E:T ratios of 16:1, elimination of greater than 90% of the clonogenic cells was seen in 20 of 21 experiments, whereas such lysis was incidentally found in the 51Cr-release assay. In almost all paired combinations, clonogenic cells tested in a colony assay were more sensitive to kill by LAK cells than the whole tumor cell suspensions measured in the 51Cr-release assay.

Cell Line↗
PubMed1989

Twinning in dairy cattle: A study of risk factors and effects.

Twin calvings on Dutch dairy farms were studied using data collected through a routine herd health and production management program. Over a period of 6.5 yr, 381 twin calvings (762 calves) of a total of 11,951 calvings were recorded on 33 farms. The 381 twin calvings were compared with a referent group of 1,536 calvings that was randomly selected from the orginal 11,951 calvings. Risk factors for twin calvings were parity, season, herd and previous twinning. High cumulative milk production was associated with cows conceiving twins. Treatment for infertility in the preceding lactation was an equivocal risk factor. Twin calvings increased the risk of abortion, retained placenta, fertility-related treatment, as well as the number of days open and the number of inseminations per conception. Although twin calvings resulted in more calves born per dam, the number of available replacement heifers did not increase. After twin calving, cows produced slightly less milk and were culled more often than single calving cows. To adapt appropriate management practices for cows carrying twins, an early and reliable method for detecting twin pregnancies is needed.

Journal Article↗
PubMed1989

Long-term follow-up of severe aplastic anaemia patients treated with antithymocyte globulin. Severe Aplastic Anaemia Working Party of the European Cooperative Group for Bone Marrow Transplantation (EBMT).

468 severe aplastic anaemia (SAA) patients registered in the EBMT-SAA registry who did not undergo bone marrow transplantation and were treated with immunosuppressive therapy (IS; 96% of patients received ATG) were evaluated. Their median age was 23 years (range 1-73) at initial IS therapy, 59% were males; in 69% the aetiology of SAA was idiopathic. Of these 468 patients, 245 had a follow-up of less than 2 years after IS 166/245 died, 71/245 are still alive, 8/245 are lost to follow-up. Of 223 patients who survived greater than or equal to 2 years (LTS long-term survivors), 191 are alive, 21 died greater than 2 years and 11 are lost. Median follow-up of 223 LTS was 4.1 years (range 2.0-10.9). Comparison of 166 patients who died less than 2 years and 223 LTS revealed no difference at time of initial IS therapy as regards sex, duration of AA, or its aetiology, but the age distribution and, in particular, severity of SAA differed significantly: more LTS were between 21 and 40 years old (44% v. 32%, P less than 0.02), less LTS had reticulocytes less than 20 x 10(9)/l (63% v. 80%, P less than 0.001), polymorphonuclear granulocytes (PMN) less than 0.2 x 10(9)/l (30% v. 57%, P less than 0.001), haemorrhages (58% v. 79%, P less than 0.002) and infection (30% v. 49%, P less than 0.005) at time of IS. A gradual improvement of blood counts was seen in patients alive greater than or equal to 2 years after IS. At 2 years after IS 80% had a normal haemoglobin and PMN greater than 0.5 x 10(9)/l, but only after 5 years 80% of cases had platelets greater than 50 x 10(9)/l. Development of clonal disease was reported of 31 LTS: 19 developed paroxysmal nocturnal haemoglobinuria (PNH), one acute leukaemia, 11 myelodysplastic syndromes and of these 11 five subsequently acute leukaemia. The majority of these patients (23/31) are still alive. Actuarial mortality of LTS is 22% at 8 years, but so far no plateau was achieved. It is concluded that SAA patients who become LTS following IS, show an improvement in haematological status but are probably not cured and are prone to develop clonal (malignant) disease.

Adolescent↗
PubMed1989

Haematopoietic and immunologic abnormalities in severe aplastic anaemia patients treated with anti-thymocyte globulin.

Thirty-five patients with severe aplastic anaemia (SAA) were extensively evaluated 0.3-12.4 years (median 3.8) after anti-thymocyte globulin (ATG) treatment. All but one were transfusion independent. Most patients revealed a normal Hb level and a granulocyte count over 1.5 x 10(9)/l but were still thrombocytopenic due to decreased platelet production. Lymphocytopenia and/or monocytopenia was found in about 30%. Two patients had a monocytosis. Although there was a great range in degree of recovery at various time intervals after ATG, patients tested more than 4 years after ATG tended to have higher cell counts. Lymphocyte counts correlated with the interval between ATG and evaluation, and with haematopoietic recovery. Qualitative abnormalities were found in all cell lines. Most patients showed a homogeneous macrocytic RBC population, and almost 50% a positive sucrose lysis test; only three patients showed evidence of haemolysis and only two of these showed a positive Ham test. Mean platelet volumes were reduced out of proportion to their number. Platelet function, determined by bleeding time and aggregometry, was impaired in over 30%. The granulocytic series showed a shift to the left in about 30%. Hypersegmentation and pseudo Pelger-Huet anomaly were seen in some patients. Lymphocyte subset distribution in blood and bone marrow was within the normal range but absolute blood levels of CD4 cells in particular were slightly decreased, and tended to increase gradually with time after ATG. IgG and IgA levels were significantly decreased. In only one patient cytogenetic analysis of unstimulated bone marrow cells revealed an abnormal karyotype, but in eight of eight patients an increased sensitivity of lymphocytes to X-rays was found. These data suggest impairment at the level of the very early haematopoietic progenitor cell in all patients up to 10 years after ATG. Since similar findings have been reported in clonal (pre-)malignant disease, SAA, improved after ATG treatment, might be prone to clonal (malignant) evolution.

Adolescent↗
PubMed1989

Acquired Zwa antigen on Zwa negative platelets demonstrated by western blotting.

Zwa-negative platelets that had been incubated in random donor AB plasma for several hours and subsequently cryopreserved, were found to be Zwa-positive when tested 3 years later by Western blotting. Following this serendipitous observation, we demonstrated that the Zwa antigen could be passively adsorbed onto the membrane of Zwa-negative platelets incubating for 4 h in the plasma from Zwa-positive donors. This observation supports the hypothesis that passive acquirement of Zwa antigens is a pathogenic mechanism for inducing post-tranfusion purpura, and suggests that Zwa-negative platelets should not be stored in Zwa-positive plasma before transfusion.

Adult↗
PubMed1989

The effect of fresh versus stored blood on post-operative bleeding after coronary bypass surgery: a prospective randomized study.

In a prospective study, 237 patients undergoing a primary coronary bypass operation were randomized to receive 2 units of fresh whole blood (study group) or stored (2-5 d) blood (control group) at the end of the extracorporeal circulation. Serious post-operative bleeding necessitating a re-thoracotomy occurred in 4.2% of all patients with an equal distribution over the two groups. Post-operative haemoglobin content and platelet counts were higher in the study group, but the differences were small and clinically not important. There were no differences in transfusion requirements, post-operative blood losses and haemostatic parameters between the trial groups. At low post-operative platelet counts (below 120 X 10(9) platelets/l) however, patients in the control group lost significantly more blood and had increased transfusion requirements compared with patients in the study group (7.1 versus 4.8 units). These differences must be attributed to qualitative platelet defects in the transfused units of stored blood. The small, clinically insignificant, differences in two laboratory parameters between the study and control groups, and the increased transfusion requirements of a subpopulation of patients with low platelet counts in the control group do not justify giving fresh blood or prophylactic platelet transfusions to coronary bypass patients.

Blood Preservation↗
PubMed1989

Bone marrow histopathology of patients with severe aplastic anaemia before treatment and at follow-up.

Pretreatment bone marrow biopsies of 63 patients with severe aplastic anaemia (SAA) who were not transplanted and of whom 55 received ATG, were evaluated according to the amount and character of residual haematopoiesis ('genuine' aplasia/intermediate/hypoplastic myelodysplasia (MD], inflammatory infiltrate (Te Velde & Haak, 1977, grade I/II/III), and number of mast cells (normal or slightly increased/increased). Of 61 evaluable biopsies, 47 were 'genuine' aplastic, 11 intermediate and three hypoplastic MD. Inflammatory infiltrates were graded as III in 36/60 evaluable biopsies, as II in 21 and I in three. A moderate to marked increase of mast cells was seen in 19/61. Of grade III patients, 86% had a less than 90 d interval between diagnosis and administration of ATG, versus 50% of grade I/II patients (P less than 0.01). No other correlations with pretreatment characteristics were found. No significant prognostic value for survival or response to ATG of any of these three criteria has been identified. More patients with grade III inflammation tended to show adequate recovery at 4 and 6 months after ATG. Stem cell damage, not identifiable morphologically, and/or impairment of accessory cells might play a major role in eventual outcome of SAA patients. Thirty-five patients are currently alive, median 3.8 years (up to 12.4) after ATG. Follow-up bone marrow aspirates and biopsies of 32 patients were evaluable and none showed normal haematopoiesis. One patient revealed persistent aplasia. Of the remaining 31, haematopoiesis was decreased in 14 and increased in eight. All had dyserythropoiesis, 28 dysplastic myelopoiesis and in 16/29 with evaluable megakaryocytes, dysmegakaryopoiesis was found. Sixteen patients had normo- to hypercellular bone marrows with two dysplastic cell lines (consistent with myelodysplastic syndrome (MDS) according to the FAB-group). The prognostic impact of the dysplastic abnormalities found in these patients needs longer follow-up. Close observation is indicated in view of the previously recognized, albeit uncommon, evolution of SAA to MDS/acute non-lymphocytic leukaemia.

Adolescent↗
PubMed1989

Regulation of autoantibodies in inflammatory demyelinating polyneuropathy: spontaneous and therapeutic.

We have analyzed the role and regulation of autoantibodies in inflammatory demyelinating polyneuropathy (GBS/CIDP). The clinical significance of pathogenic autoantibodies to peripheral nerve tissue is suggested by the beneficial response of many of these patients to plasmapheresis and treatment with high doses of polyspecific IVIgG. Recovery, whether spontaneous or therapeutically-induced, is associated with anti-idiotypic suppression of the antoantibodies. Preliminary results suggest that these autoantibodies share cross-reactive idiotypes or, alternatively, that the regulatory anti-idiotypic antibodies are multireactive.

Autoantibodies↗
PubMed1989

Effect of steroidal anti-inflammatory drugs on Escherichia coli endotoxin-induced mastitis in the cow.

Effects of intramammary infusion of prednisolone (40 mg) or intramuscular injection of dexamethasone (30 mg) or flumethasone (5 mg) on local and systemic signs in Escherichia coli endotoxin-induced mastitis were studied. The effect of varying intervals (0, 2, and 4 h) between intramammary infusion of endotoxin and prednisolone in the same quarter was determined. Intramammary infusion of endotoxin (.01 mg lipopolysaccharide of E. coli) produced inflammation of the infused quarter, fever, tachycardia, and leukopenia followed by a neutrophilic leukocytosis in the blood and a decrease in plasma zinc and iron concentrations. All corticosteroid treatments, except intramammary administration of prednisolone 4 h after endotoxin infusion, enhanced leukocytosis and diminished local signs of inflammation. Intramuscular injection of dexamethasone or flumethasone together with intramammary infusion of endotoxin and intramammary administration of prednisolone 2 h after lipopolysaccharide infusion completely abolished the febrile response. Abolishment of fever and attenuation of several hematologic and blood biochemical changes may be explained by diminished synthesis of endogenous mediators within the inflamed quarters due to glucocorticosteroid action.

Animals↗