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Biomedical subjects

J Hamann

Publications and source records attributed to J Hamann.

At least 55 records · Page 3Linked to original sources
PubMed1994

Effects on milk yield, somatic cell count and milk conductivity of short-term non-milking of lactating quarters of cows.

Compensatory changes in daily milk production between quarters within an udder were investigated, together with related changes in cell count and electrical conductivity of fore milk samples. Two quarters per cow were left unmilked for 2 d (Group 1, four cows) or for 4 d (Group 2, four cows), and then all quarters of all cows were milked twice daily for a further period of 16 d. The mean daily yield per cow fell 50% during the period of milking two quarters. Daily yield for cows in Group 1 decreased significantly only during the treatment period and the first post-treatment period of 4 d, whereas the daily yield for Group 2 was significantly reduced during the whole post-treatment period. The cell count for all continuously milked (control) quarters was stable during the experiment, but increased in the treated quarters during the first 4 d of the post-treatment period. Non-milking was accompanied by a significant increase in fore milk conductivity which persisted for an additional 4 d after the resumption of normal milking. Throughout the last 12 d of the post-treatment period milk from both control and treated quarters had significantly decreased conductivity levels compared with the pretreatment values.

Animals↗
PubMed1994

Autoantibodies to glutamate decarboxylase detected in diabetes-prone BB/OK rats do not distinguish onset of diabetes.

The diabetes syndrome of the BB rat resembles human Type 1 (insulin-dependent) diabetes including the prevalence of autoantibodies to the 64 kDa Beta-cell autoantigen, which has been identified as glutamate decarboxylase. This study aimed at detecting the prevalence and level of glutamate decarboxylase autoantibodies in 120-day-old diabetic and non-diabetic diabetes-prone BB/OK rats compared to those of sex- and age-matched diabetes-resistant LEW.1A rats. The antibodies were detected using semipurified glutamate decarboxylase from rat brain in two immunoassays, a direct and a sandwich enzyme-linked immunosorbent assay. For the last assay autoantibody-containing immunoglobulins of a serum from a patient with the stiff-man syndrome were used to bind specifically the enzyme as autoantigen in plastic wells. The antibody levels measured as optical density at 490 nm (x +/- SD)/prevalence of the diabetic group (120 +/- 29 days of age) of BB/OK rats 0.57 +/- 0.29 (n = 51)/88% as well as those of the nondiabetic group (121 +/- 26 days of age) with 0.51 +/- 0.29 (n = 32)/97% was significantly increased (p < 0.01) compared to those of the diabetes-resistant control group 0.15 +/- 0.06 (n = 29)/0%. Furthermore in a 209 +/- 27-day-old group (n = 21) of non-diabetic but diabetes-prone BB/OK rats the autoantibody levels of 1.21 +/- 0.39 vs 0.51 +/- 0.26 were further significantly enhanced (p < 0.01). These results were confirmed by a sandwich assay.(ABSTRACT TRUNCATED AT 250 WORDS)

Age of Onset↗
PubMed1994

Monoclonal antibodies specific to the glutamic acid decarboxylase 65 kDa isoform derived from a non-obese diabetic (NOD) mouse.

Two monoclonal antibodies specifically recognizing the 65 kDa isoform of the enzyme glutamic acid decarboxylase (GAD) were generated by fusion of spleen cells of a non-obese diabetic (NOD) mouse which had received a single intraperitoneal injection of 0.2 ml complete Freund's adjuvant followed three days later by one administration of a subdiabetogenic dose of streptozotocin (80 mg/kg body weight) three days before the fusion experiment was performed. Both monoclonals belong to the IgG1 isotype and were screened with an enzyme-linked immunosorbent assay using rat brain extract as a natural source of GAD and additionally with a capture assay by means of immunoglobulins of a patient with Stiff-man syndrome. The specific binding to the 65 kDa isoform of the enzyme was detected by a radioligand and an enzyme-linked immunosorbent assay using recombinant human glutamic acid decarboxylase specific for both the 67 and 65 kDa isoforms. Both monoclonal antibodies recognize the same antigenic epitope, which is located in the N-terminal region of the first 17 amino acids detected by fragments of human pancreatic 65 kDa GAD. Three out of 30 sera from Type 1 diabetic patients specifically displaced the binding of the monoclonals from 125I-labelled GAD65 measured by radio-immunoassay. A striking binding of both monoclonals M61/8F9 and M61/7E11 to the islets of cryosections of human, monkey, pig and rat pancreas but not to mouse pancreas was detectable. The antibodies failed to bind on the cell surface of viable rat islet cells. It is concluded that also in the diabetes-prone NOD mice GAD65 autoantibodies occur although GAD65 was not detectable in the mouse islets.

Animals↗
PubMed1994

A monoclonal antibody based enzyme-linked immunosorbent assay for the determination of GAD65, the smaller isoform of glutamic acid decarboxylase.

An enzyme-linked immunosorbent assay for GAD65, the smaller form of glutamic acid decarboxylase and an important autoantigen related to Type 1 diabetes, is described. The competitive binding assay is based on a monoclonal antibody specifically reactive with GAD65. The assay is suitable for quantification of this enzyme between 40 and 300 pg/microliter. The intraassay coefficients of variation (cv) are between 5.6% and 8.9% and the interassay cvs lie between 9.4% and 17.3%. The covalent binding of the antigen to magnetic beads as the solid phase makes the assay also applicable for quantification of GAD65 in tissue homogenates with a high concentration of detergent. The GAD65 content of islets isolated from newborn Lewis rat was detected to be 310 pg/islet. However, GAD65 was not detectable in mouse islets.

Animals↗
PubMed1994

The detection of autoantibodies to pancreatic islet cells by immunoenzyme histochemistry.

Using horseradish peroxidase- or alkaline phosphatase-conjugated secondary antibodies, an immunohistochemical assay was established for the detection of islet cell cytoplasmic antibodies (ICA). Determination of end-point titers showed a significant correlation between the conventional immunofluorescence and either immunocytochemistry assay. The assays with the enzyme-conjugated antibodies were more sensitive than the indirect immunofluorescence assay. Because of its simplicity, specificity, and easy microscopic evaluation of the chromogenic reaction product at the site of ICA binding, the indirect immunoperoxidase technique proved to be most suitable. This technique detected frequencies of ICA positives among newly diagnosed insulin-dependent (IDDM), noninsulin-dependent, and at-risk subjects that were comparable with previous studies. Preabsorption of ICA-positive sera with either rat or porcine brain extracts, containing the glutamate decarboxylase antigen, differently blocked, reduced or did not affect ICA reactivity with human or porcine pancreas sections. Testing of sera on human, bovine, and porcine pancreas sections demonstrated heterogeneity in ICA-binding with a high proportion of ICA false-positives on bovine pancreas. The results demonstrated that immunohistochemical techniques for detecting ICA are, in several aspects, preferable to indirect immunofluorescence and that individual serum ICA identify various antigens on pancreas from different species. However, bovine or porcine pancreas could not substitute for human pancreas in the ICA assay.

Adolescent↗
PubMed1993

Expression cloning of the early activation antigen CD69, a type II integral membrane protein with a C-type lectin domain.

CD69 is a very early activation Ag of T lymphocytes. It is a cell surface glycoprotein that can only be detected after stimulation of lymphocytes. Despite extensive studies on its biologic activities, little is known about its molecular function. To investigate the latter in more detail, we have cloned a cDNA encoding CD69 on the basis of its expression in COS cells. The nucleotide sequence of clone CD69.13 is 1676 bp in length and contains a single open reading frame of 600 bp encoding a protein of 199 amino acids. The predicted molecular mass of 22,559 Da could be confirmed by in vitro translation. The protein contains a hydrophobic transmembrane region between amino acids 41 and 61 but no N-terminal signal peptide, which suggests that it is a type II membrane protein. It has one potential N-glycosylation site at amino acid 166. Two glycosylated forms of 26 to 28 kDa and 32 to 34 kDa were detected both in transfected COS cells and in in vitro translation in the presence of canine microsomes. Proteinase K degradation of the N-terminal part after in vitro protein synthesis supports the view of CD69 being a type II integral membrane protein with the N-terminal 40 amino acids in the cytoplasm, a transmembrane domain of 21 amino acids, and C-terminal 138 amino acids as the extracellular domain. Homology searches revealed sequence similarity with members of a supergene family of type II integral membrane proteins with a C-type lectin domain, indicating that CD69 is involved in signal transduction.

Amino Acid Sequence↗
PubMed1993

Regional sublocalization of the human CD69 gene to chromosome bands 12p12.3-p13.2, the predicted region of the human natural killer cell gene complex.

The early activation antigen CD69 is a member of a supergene family of type II integral membrane proteins with a C-type lectin domain. In recent reports the genes encoding the natural killer (NK) cell-related molecules of this supergene family, NKR-P1, NK1.1 and Ly-49, were shown to be clustered in a chromosomal region in mouse, termed the NK gene complex. The human homologue of this complex is likely to reside on chromosome 12 near the PRP locus (12p13.2). By analyzing T cell hybrids, the CD69 gene was previously mapped to human chromosome 12. Here we report the regional sublocalization of the human CD69 gene to chromosome bands 12p12.3-p13.2, suggesting that CD69 belongs to one linkage group together with different cell surface molecules on NK cells.

Animals↗
PubMed1993

Teat tissue reactions to milking: effects of vacuum level.

Machine-induced changes in diameter, thickness, and compressibility of the teat apex and teat barrel were measured on all teats of four cows milked at vacuums of 25, 30, 40, and 50 kPa. Measurements were made with an electronic caliper instrument immediately before milking and then at .5, 15, and 30 min after milking. Teat length was also measured at these times. Immediately after milking, for the two higher levels, teats were significantly thicker (7 to 10% thicker at 40 kPa, 17 to 25% at 50 kPa), shorter (by 3 to 6 mm), smaller in diameter (by 2 to 4 mm for the apex, 3 to 6 mm for the barrel), and less compressible for all milking treatments compared with the premilking status for individual teats. Although teat thickness recovered to the premilking mean values 30 min after milking at 40 or 50 kPa, the barrel still was significantly thicker after 30 min compared with those at the lower vacuum treatments. We suggest that changes in teat length, diameter, thickness, and compressibility after milking at low vacuum levels mainly reflect tissue responses to udder evacuation. In contrast, increased teat wall thickness and reduced compressibility of teat tissue at higher vacuum levels likely result mainly from machine-induced edema.

Animals↗
PubMed1992

Machine-induced teat tissue reactions and infection risk in a dairy herd free from contagious mastitis pathogens.

Machine-induced changes in teat thickness were measured in a randomly selected group of 22 cows from a commercial dairy herd consisting of 110 cows during an experiment lasting 1 year. Half the cows used were free from mastitis whereas the remainder had at least one quarter infected by environmental pathogens. Teats were classified according to a threshold change in teat end thickness of 5%. The relationships between quarter infection or teat duct colonization and teat end thickness changes induced by machine milking were investigated. Teats with greater than 5% change in thickness had significantly increased teat duct colonization and a slight, non-significant, increase in quarter infection. We conclude that machine-induced changes in teat end thickness are predisposing factors for teat duct colonization by environmental pathogens. This may provide an increased new infection risk, especially when hygiene is poor.

Animals↗
PubMed1992

[New aspects in the diagnosis of herpes simplex virus encephalitis--case reports and virologic findings].

Herpes simplex virus (HSV) is one of the most common causes of severe necrotizing encephalitis in men. Without adequate acyclovir treatment it has a mortality rate of 70%. An early, reliable virological diagnosis is therefore essential. In this study, two newly-introduced diagnostic methods were assessed and compared: Polymerase Chain Reaction (PCR) for detection of HSV-genome in cerebrospinal fluid and HSV-specific isoelectric focusing (IEF) for detection of intrathecal virus specific antibody synthesis in HSV encephalitis (HSVE). PCR proved more effective for the early diagnosis of HSVE and HSVE relapses, whereas HSV-specific IEF was superior for the diagnosis of HSVE in post-acute stages of the disease.

Adolescent↗
PubMed1992

Detection of antibodies against both isoforms of glutamate decarboxylase in BB/OK rats by western blotting and immuno trapping enzyme activity assay.

The GABA-producing enzyme glutamate decarboxylase (GAD) is a prominent autoantigen in insulin-dependent diabetes mellitus (IDDM). Autoantibodies against GAD were found with a high prevalence in IDDM patients and in animal models for IDDM. The aim of this study was to detect autoantibodies against both isoforms of GAD in diabetic and non-diabetic but diabetes-prone BB/OK rats by Western blotting and to test their specificity to GAD by an immuno-trapping enzyme activity assay. Eighteen diabetic and 18 non-diabetic BB/OK rats (age 121 +/- 20 days) were investigated. In 10/18 (56%) of the diabetic and 13/18 (72%) of the non-diabetic BB/OK rats autoantibodies against at least one GAD-isoform were detected by Western blotting. In the immunotrapping enzyme activity assay, the mean value of the diabetic (1151 +/- 552 cpm, n = 11) and nondiabetic BB/OK rats (1978 +/- 1213 cpm, n = 10) was significantly (p < 0.01) increased compared to the LEW. 1A control rats (581 +/- 274 cpm, n = 12). 7/10 (70%) individual sera of the non-diabetic and 5/11 (45%) of the diabetic BB/OK rats were positive in this test. In conclusion, the prevalence of GAD autoantibodies in BB/OK rat is connected with the genetic susceptibility to IDDM but is not a predictor for the onset of the disease in BB/OK rats.

Animals↗
PubMed1990

Compensatory milk production within the bovine udder: effects of short-term non-milking of single quarters.

Daily quarter-milk yields of eight high-yielding cows (24-28 kg/d) and eight heifers (14-24 kg/d) were measured to examined to examined compensatory changes in milk production between quarters within an udder. Either one, two or three quarters per cow were left unmilked for 12 d, in early or late lactation, and then all quarters of all cows were milked normally for a further period of 12 d. Concentrate feeding levels were constant throughout the experiment. The mean daily yield per cow fell to 26, 59, and 75% during the period of milking either one, two or three quarters respectively. Twelve days after resumption of normal milking the total daily yield per cow was the same for cows continuously milked in two, three or all four quarters. Daily yield in cows with only one quarter milked continuously recovered to only 78% of the level of the pretreatment period. During the treatment period, the mean daily yield of the continuously milked quarters increased by almost 14% for cows milked in one quarter only, by more than 10% for two quarters milked, and by 4% per quarter if three quarters were milked. Milk yields of these quarters remained above their pretreatment levels when milking was resumed in the adjacent quarters. There was no difference in the compensatory effect between cows and heifers in early lactation, but the compensatory effects were lower in the lower in late lactation heifers.

Animals↗
PubMed1990

Measurement of machine-induced changes in thickness of the bovine teat.

Machine milking induced repeatable, short-term changes in thickness of the teat apex. These changes were measured with a spring-loaded caliper instrument under milking conditions that imposed differing forces on the teat apex. The mean percentage changes in teat end thickness (relative to the premilking values for individual teats) varied from 10% decrease up to 20% or more increase depending on the particular milking system used. The overall decrease in teat end thickness associated with cannula milking, milking at very low vacuum levels or milking with positive pressure pulsation may result from: (i) decrease in the intramammary pressure; and/or (ii) small changes in tone of teat musculature; and/or (iii) changes in the distribution of interstitial fluids in the teat apex. The overall increase in teat thickness caused by conventional or PKME milking systems results mainly from oedema (the extravascular accumulation of fluid). It is likely that milking equipment can, and should, be designed to minimize circulatory impairment resulting in oedema of the teat.

Animals↗
PubMed1989

[Factors for the genesis of bovine subclinical mastitis].

The infection risk of the bovine mammary gland is determined by susceptibility of the cow and contamination and invasion by mastitis pathogens. Genetic (e.g. yield) and lactational physiologic (e.g. stage of lactation) factors support the genesis of subclinical mastitis. This paper considers new data on cow individual and milking related influences on defence mechanisms in the teat end tissue acting in prevention of penetration through the teat canal by mastitis pathogens.

Animals↗
PubMed1977

[Myoclonic encephalopathy in childhood (author's transl)].

Two new cases of infantile myoclonic encephalopathy are reported and a survey of literature is given. The disease is characterized by generalised myoclonic jerks in all striated muscles, by cerebellar ataxia and by fast, jerking, mostly conjugated irregular eye movements (opsoclonus). The disease develops mostly during late infancy and early childhood. The pathogenesis is unknown, probably it is caused by immunological reactions to various agents. Treatment with ACTH or corticosteroids leads to rapid remission of the initial neurological symptoms, but it is suggested that therapy does not prevent frequent sequelae of psychomotor retardation and speech distubances. Remarkably, there is the high coincidence of infantile myoclonic encephalopathy and neuroblastoma. Therefore it is necessary to keep in mind the possibility of a causative neuroblastoma in all children with myoclonic encephalopathy and to control repeatly radiological findings and urin-excretion of catecholamines as well as their metabolic products.

Adrenal Cortex Hormones↗