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Biomedical subjects

B Greulich

Publications and source records attributed to B Greulich.

12 recordsLinked to original sources
PubMed1992

Natural course of remission in IDDM during 1st yr after diagnosis.

OBJECTIVE: To describe the natural course of clinical remission in insulin-dependent diabetes mellitus (IDDM) when insulin dose is minimized without loss of target glycemia and to identify factors that predict clinical remission. RESEARCH DESIGN AND METHODS: Ninety-five patients, who were placebo-treated control subjects in the Canadian-European multicenter randomized trial of cyclosporin A in recent-onset IDDM, were studied. RESULTS: The mean insulin dose decreased during the first months after diagnosis, with a nadir at 3 mo, when 27% of the patients did not require insulin to maintain target glycemia. At 1 yr, 10% of patients still did not need insulin. Patients not receiving insulin who had glycosylated hemoglobin within the normal range were called remitters. Mean basal and glucagon-stimulated C-peptide values were significantly (P less than 0.025) higher in remitters than nonremitters at the start of the study. Therefore, all patients were divided into those with values above the mean stimulated C-peptide (0.4 nM) and those with values below the mean at entry. The probability of entering a remission with a stimulated C-peptide greater than 0.4 nM was 10 times as high (P less than 0.05) as for those with a stimulated C-peptide below this level. Surprisingly, the beginning and end of the remission were associated with neither major changes in C-peptide levels nor islet cell antibody and insulin-antibody titer. A more rapid loss of stimulated C-peptide occurred in patients who lacked HLA-DR3 and -DR4 (P less than 0.05 at mo 9). CONCLUSIONS: This study shows a higher spontaneous clinical remission rate than expected during the 1st yr after diagnosis. Preserved beta-cell function at entry predicts a greater chance of entering a remission, and a more rapid loss of beta-cell function was seen in patients without HLA-DR3 and -DR4.

Adult↗
PubMed1987

Analysis of 22 immunomodulatory substances for efficacy in low-dose streptozotocin-induced diabetes.

Of 22 immunomodulatory substances screened 12 were effective in modulating the course of hyperglycemia following low dose streptozotocin treatment. In this animal model diabetes is induced by administration of low doses of streptozotocin (30-40 mg/kg) body weight to male C57BL/6J/Bom, C57BL/KsJ and C3H/He/Bom mice on 5 consecutive days. Conventional immunosuppressants (azathioprine, cyclophosphamide) largely protected from diabetes development. Partial suppression of hyperglycemia was also seen after administration of B. pertussis, fetal tissue extracts, FTS, inosine pranobex, metronidazole and ADA 202-718. The majority of these substances, when applied with another regimen, and TP5 caused enhancement of diabetes. In conclusion, several substances with a therapeutic potential in experimental diabetes have been identified. Those with little risk of side-effects may deserve further analysis.

Adjuvants, Immunologic↗
PubMed1986

Suppression of low-dose streptozotocin-induced diabetes by immunomodulatory lectins.

The effect of immunomodulatory lectins on diabetes development following low-dose streptozotocin treatment in inbred mice was studied. All lectins administered had been shown previously to suppress immune reactivity. Among plant lectins concanavalin A but not Lens culinaris or wheat germ agglutinin partially suppressed hyperglycaemia following low-dose streptozotocin. A similar inhibitory effect was found for the staphylococcal enterotoxin B. Finally, administration of an immunomodulatory lectin from vertebrates, electrolectin, also had a beneficial effect on the course of the disease. These findings indicate that some lectins have a suppressive effect on Type 1 diabetes in an animal model.

Animals↗
PubMed1984

Correlation of islet cell antibodies and HLA-DR phenotypes with diabetes mellitus in adults.

In a cross-sectional study, sera of 81 adult diabetic in-patients were tested for the presence of pancreatic islet cell antibodies (ICA), both IgG and complement-fixing. All patients had been well controlled initially with oral hypoglycaemic agents and therefore had been classified as having Type 2 (non-insulin-dependent) diabetes. However, 14 were subsequently classified as Type 1 (insulin-dependent) because they became insulin-dependent within 2 months of diagnosis. Ten of these patients (71%) were ICA-positive. Sixty-seven patients had been non-insulin-dependent for at least 1 year after diagnosis. Circulating ICA were present in 18 patients and 16 of these (89%) required insulin therapy. Secondary oral hypoglycaemic agent failure developed within a mean period of 3.7 years after diagnosis. In contrast, in the ICA-negative sub-group (n = 49) insulin treatment became necessary in 29 patients. Secondary oral hypoglycaemic agent failure of these patients had developed after a mean period of 8.4 years, which was significantly longer than in the ICA-positive patients (p less than 0.01). Complement-fixing-ICA were detected only in sera with an ICA-IgG titre of at least 8, and its prevalence was similar in the sub-groups tested, i.e., the Type 1 diabetic patients and the patients with secondary oral hypoglycaemic agent failure. With HLA-DR typing, a significant excess of the DR3 antigen and heterozygous DR3/DR4 phenotypes was found in ICA-positive patients with secondary oral hypoglycaemic agent failure and in the Type 1 diabetic patients, which was comparable with the frequencies reported in juvenile-onset Type 1 diabetes.

Adult↗
PubMed1984

Cell mediated immunity to islet cells: lessons from animal studies.

As a pathogenic factor of type I (insulin-dependent) diabetes cell mediated immunity to pancreatic islet cells, i.e. lymphocytic insulitis has been studied in mice with spontaneous lupus-like autoimmune disease, in mice with experimentally induced immune dysregulation and in mice treated with multiple low doses of streptozotocin or with alloxan. The following conclusions have been reached: Autoimmunity to B-islet cells requires a disturbed immune system. Autoimmune insulitis requires altered B-islet cells. Cellular immunity to B-islet cells apparently involves two different mechanisms: The intrainsular invasion of single lymphocytes and macrophages and the mostly periinsular/periductular infiltration of large numbers of lymphocytes and macrophages. Some observations indicate a primary role of helper and suppressor T lymphocytes as well as of macrophages in B-islet cell destruction. In this paper an attempt will be made to combine observations on the induction and course of insulitis in several animal models in a general scheme of pathological events. Several conclusions on the mechanism of islet autoimmunity have been reached. At the time being however, these "lessons" must be regarded as hypotheses, which may be helpful in understanding the pathogenesis of human type I diabetes.

Animals↗
PubMed1981

Induction of experimental autoimmune diabetes by low-dose streptozotocin treatment in genetically resistant mice.

We have studied the effect of suppressor cell elimination on the induction of experimental autoimmune diabetes in mouse strains which are normally low or intermediate responders to multiple low-dose streptozotocin treatment. BALB/c (low responder) and C57BL/6J (intermediate responder) mice received 70 mg cyclophosphamide/kg, 1 or 6 days before the onset of streptozotocin injections. Following cyclophosphamide treatment, BALB/c mice become susceptible to the diabetogenic effect of streptozotocin. Similarly the manifestation of diabetes in C57BL/6J mice is enhanced. Thus in both strains immunomodulation by cyclophosphamide treatment significantly increases the susceptibility towards the diabetogenic effect of streptozotocin. We therefore conclude that in mice of strains BALB/c and C57Bl/6J suppressor cells control the level of resistance towards the induction of experimental autoimmune diabetes by low-dose streptozotocin treatment.

Animals↗
PubMedDate not supplied

Twelve years and more than 30,000 nurse-midwife-attended births: the Los Angeles County + University of Southern California women's hospital birth center experience.

This article describes the setting, policies, practices, and outcomes of the nurse-managed in-hospital birth center at Los Angeles County + University of Southern California Women's Hospital, where women are selected upon admission for birth center care. A retrospective review of available data was made; when compared with hospital records, the primary data source was found to be 96% accurate. Results of the review indicated that from 1981 to 1992, there were 36,410 birth center admissions and 30,311 births, all attended by nurse-midwives; no intrapartum maternal or fetal deaths occurred among all admissions. The intrapartum transfer rate averaged 17%, and declined steadily from a high of 28% in 1982 to a low of 7% in 1990. More in-depth review showed an overall primary cesarean birthrate of 1.8% and an operative birthrate of 4% among the 25,890 admissions and 22,490 births from 1985 to 1992. Detailed postpartum and newborn outcomes from 1982 to 1986 showed a neonatal intensive care unit admission rate of 1.5% and a one-week newborn readmission rate of 1.3% among newborns discharged within 12 to 24 hours; 85% of all newborns returned for follow-up care. This large longitudinal experience demonstrates excellent outcomes that can be achieved when nurse-midwives, working cooperatively with a multidisciplinary health care team, provide in-hospital birth center care to a predominately low-income Hispanic population using a variety of less-traditional intrapartum management techniques. Broader implications for making alternative maternity care services available for low-income women with nurse-midwives and nurses playing a central role are discussed.

Adolescent↗