Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Synthesis of Aromatic Glycidyl Esters. (1966)
    s.l. : American Chemical Society
    Journal of chemical & engineering data 11 (1966), S. 447-448 
    Details
    ISSN: 1520-5134
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/je60030a054
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effects of polydispersivity on the phase behavior of the aqueous two-phase polymer systems (1988)
    s.l. : American Chemical Society
    Macromolecules 21 (1988), S. 3088-3095 
    Details
    ISSN: 1520-5835
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ma00188a029
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Protection by dimethyl urea against hyperglycaemia, but not insulitis, in low-dose streptozotocin-induced diabetes in the mouse (1984)
    Springer
    Diabetologia 26 (1984), S. 386-388 
    Details
    ISSN: 1432-0428
    Keywords: Dimethyl urea ; C57BL/KsJ mice ; insulitis ; pancreatic islets ; streptozotocin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The protective effect of dimethyl urea, a hydroxyl radical scavenger, against low-dose streptozotocin-induced diabetes has been evaluated. Dimethyl urea was given to C57BL/KsJ mice before five daily injections of streptozotocin. The saline pre-treated control animals became gradually hyperglycaemic, whereas the dimethyl urea treated group remained normoglycaemic during the 11 week follow-up period. Two weeks after the first streptozotocin injection, six out of ten dimethyl urea-treated and 12 out of 15 saline-treated mice had insulitis. Four or 11 weeks after the streptozotocin treatment, insulitis was rare in both groups. Multiple injections of dimethyl urea only did not affect the serum glucose concentrations or the islet morphology. It is suggested that dimethyl urea protected against hyperglycaemia by reducing the β-cell cytotoxic effects of the low doses of streptozotocin. An increased number of cells would thus be preserved and the animals less prone to develop diabetes, despite the presence of an inflammatory process in the pancreatic gland.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00266042
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Partial pancreatectomy in rats causes an impairment of the glucose-induced stimulation of pancreatic islet blood flow (1991)
    Springer
    Cellular and molecular life sciences 47 (1991), S. 627-629 
    Details
    ISSN: 1420-9071
    Keywords: Pancreatic islets ; islet blood flow ; partial pancreatectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Adult rats were subjected to either a sham operation (S-rats) or a 60% partial pancreatectomy (P-rats). Both P- and S-rats were normoglycemic and normoinsulinemic after surgery. Four weeks later, the animals were injected i.v. with 1 ml of either 0.9% (w/v) saline or 30% (w/v) D-glucose, and after 5 min whole pancreatic blood flow (PBF) and islet blood flow (IBF) were measured, using a microsphere technique. In the saline-injected P-rats both PBF and IBF values were, higher than in S-rats (p〈0.001 for both values). Administration of glucose had no effects on PBF in either S- or P-rats when compared to saline-injected animals. IBF was, however, markedly increased (p〈0.01) by glucose in S-rats in comparison with saline-injected S-rats, whilst no difference in IBF was observed between glucose- and saline-injected P-rats. The fraction of PBF diverted through the islets (fIBF) was approximately 10% in S-rats and 20% in P-rats. Glucose increased fIBF in S-rats, but had no effect in P-rats. In conclusion, in S-rats a glucose-stimulated insulin release is accompanied by an increase in IBF, but this is not observed in P-rats.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01949892
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Human interleukin-1β induced stimulation of insulin release from rat pancreatic islets is accompanied by an increase in mitochondrial oxidative events (1989)
    Springer
    Diabetologia 32 (1989), S. 769-773 
    Details
    ISSN: 1432-0428
    Keywords: Pancreatic islets ; insulin release ; interleukin-1β ; glucose metabolism ; amino acid metabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Acute exposure of pancreatic islets to interleukinl-1β results in an increase in insulin release, while an extension of the exposure time induces a functional suppression and eventually, destruction of the B-cells. We have recently suggested that the interleukin-1β induced inhibition of islet function is mediated through an impairment in oxidative metabolism. The aim of the current study was to investigate if the acute, stimulatory effects of interleukin-1β on islet function could also be related to changes in the substrate metabolism. For this purpose, rat islets were exposed for 90–120 min to 30 pmol/l human recombinant interleukin-1β (biological activity of 2.5 U/ml) and their function and metabolism characterized during this period. The cytokine did not increase insulin release in the presence of 1.7 or 5.5 mmol/l glucose but in both the presence of 16.7 mmol/l glucose or 10 mmol/l leucine + 2 mmol/l glutamine there was a 50% increase in insulin release. Interleukin-1β exposure increased the oxidation of D-[U-14C]glucose at 5.5 mmol/l glucose by 25% and at 16.7 mmol/l glucose by 60%. Carbohydrate and amino acid metabolism were further examined in the presence of D-[5-3H] glucose, D-[6-14C]glucose, [1-14C]pyruvate, L-[U-14C]glutamine, L-[U-14C]leucine and L-[1-14C]leucine. There was no difference between control islets and interleukin-1β exposed islets in terms of D-[5-3H]glucose utilization or [1-14C]pyruvate decarboxylation, but the oxidation of D-[6-14C]glucose was increased by 64% in the interleukin-1β exposed islets. There was also an interleukin-1β induced 45–60% increase in the decarboxylation of L-[1-14C]leucine and oxidation of L-[U-14C]leucine and L-[U-14C]glutamine, all intramitochrondrial events. The stimulation of insulin release by interleukin-1β in the presence of 16.7 mmol/l glucose was abolished in islets incubated in Ca2+ depleted medium, but the rate of D-[6-14C] glucose oxidation remained elevated (47% increase at 16.7 mmol/l glucose). These data indicate an increase in substrate metabolism at the mitochondrial level during acute exposure of rat pancreatic islets to interleukin-1β. The increase in oxidative events can explain the observed interleukin-1β induced increase in insulin release during glucose stimulation. Furthermore, these findings raise the possibility that mitochondria are primary targets of interleukin-1β action in the B-cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00264905
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Long-term effects of cyclosporin A on cultured mouse pancreatic islets (1984)
    Springer
    Diabetologia 27 (1984), S. 66-69 
    Details
    ISSN: 1432-0428
    Keywords: Islet β cell ; cyclosporin A mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the light of recent attempts to treat newly-diagnosed Type 1 (insulin-dependent) diabetic patients with cyclosporin A, and reports suggesting an impaired glucose tolerance following immunosuppresion therapy with cyclosporin A, we investigated the long-term effects of cyclosporin A on islet β-cell morphology and function in vitro. Collagenase-isolated mouse pancreatic islets were cultured free-floating for 7 days in medium RPMI 1640 + 10% calf serum in the presence of cyclosporin A (0.1 or 1.0 mg/l). Islets cultured in the presence of the higher cyclosporin A concentration had impaired islet proinsulin biosynthesis and insulin release when challenged with high glucose concentration. Moreover, the insulin content of the drug-exposed islets was decreased and so was the rate of DNA synthesis. The glucose oxidation and respiratory rates, however, remained unaffected, suggesting that the impaired insulin production was not a result of defective oxidative metabolism. There were no changes in the ultrastructure or phospholipid biosynthesis of the islets after the drug treatment. These data indicate that cyclosporin A affects islets in culture, the clinical implications of which are so far difficult to assess. The inhibitory effect of cyclosporin A on islet cell DNA synthesis must nevertheless be considered in attempts to ameliorate Type 1 (insulin-dependent) diabetes, and when grafting islet cells in numbers primarily insufficient to cure the recipient.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00275649
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    An interleukin-1 receptor antagonist protein protects insulin-producing Beta cells against suppressive effects of interleukin-1β (1991)
    Springer
    Diabetologia 34 (1991), S. 445-448 
    Details
    ISSN: 1432-0428
    Keywords: Interleukin-1β ; interleukin 1 receptor ; insulin secretion ; pancreatic islets ; RINm5F cells ; insulin-dependent diabetes mellitus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cytokine interleukin-1β may have an important role in the autoimmune mediated damage of pancreatic Beta cells in insulin-dependent diabetes mellitus. In the present study we have investigated the effects of an interleukin-1 receptor antagonist protein, a blocker of the type I interleukin-1 receptor, on the suppressive actions of recombinant interleukin-1β on insulin-producing cells. Brief exposure (1–2 h) of rat and mouse pancreatic islets to 10 ng/ml recombinant interleukin-1β induced an 70–80% inhibition of insulin response to glucose after 12 h. These effects were completely counteracted by co-incubation with 100 ng/ml interleukin-1 receptor antagonist protein. When rat islets were cultured for 48 h in the presence of recombinant interleukin-1β (5 ng/ml) higher concentrations of interleukin-1 receptor antagonist protein (5000 ng/ml) were required to protect Beta-cell function. Interleukin-1 receptor antagonist protein also counteracted the inhibitory effects of recombinant interleukin-1β on the growth of the rat insulinoma cell line RINm5F. These data suggest that interleukin-1 receptor antagonist protein can protect insulin-producing cells from the deleterious effects of recombinant interleukin-1β, and that these cells possess type I interleukin-1 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403185
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Inhibition of insulin secretion, but normal peripheral insulin sensitivity, in a patient with a malignant endocrine pancreatic tumour producing high amounts of an islet amyloid polypeptide-like molecule (1993)
    Springer
    Diabetologia 36 (1993), S. 843-849 
    Details
    ISSN: 1432-0428
    Keywords: Amylin ; endocrine pancreatic tumour ; glucose tolerance ; insulin resistance ; islet amyloid polypeptide ; pancreatic islets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Islet amyloid polypeptide or amylin is a polypeptide secreted mainly from the pancreatic beta cells together with insulin upon stimulation. High levels of islet amyloid polypeptide have also been shown to increase the peripheral insulin resistance and consequently a role for islet amyloid polypeptide in the glucose homeostasis has been suggested. We have studied the glucose homeostasis in a patient with a malignant endocrine pancreatic tumour producing large amounts of an islet amyloid polypeptide-like molecule (about 400 times the upper reference level for islet amyloid polypeptide). This patient developed insulin-requiring diabetes mellitus shortly after the tumour diagnosis. Both intravenous and oral glucose tolerance tests revealed inhibited early responses in insulin and C-peptide release, but the insulin and C-peptide response to glucagon stimulation was less affected. Aneuglycaemic insulin clamp showed normal insulin-mediated glucose disposal. In vitro experiments, where isolated rat pancreatic islets were cultured with serum from the patient, showed a moderately decreased islet glucose oxidation rate and glucose-stimulated insulin release compared to islets cultured with serum from healthy subjects. However, culture of rat islets with normal human serum supplemented with synthetic rat islet amyloid polypeptide did not affect the glucose-stimulated insulin release. In conclusion, the observed effects show that the diabetic state in this patient was associated with an impaired glucose-stimulated insulin release but not with an increased peripheral insulin resistance. Thus, the results suggest that if islet amyloid polypeptide has diabetogenic effects they are more likely to be exerted at the level of insulin secretion than at the level of peripheral insulin sensitivity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400360
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Comparison of mRNA contents of interleukin-1 b and nitric oxide synthase in pancreatic islets isolated from female and male nonobese diabetic mice (1995)
    Springer
    Diabetologia 38 (1995), S. 153-160 
    Details
    ISSN: 1432-0428
    Keywords: Key words Autoimmunity ; diabetes mellitus ; interleukin-1 ; nitric oxide ; nitric oxide synthase ; NOD mice ; pancreatic islets ; polymerase chain reaction.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Interleukin-1 β (IL-1 β) has been suggested to mediate beta-cell destruction in insulin-dependent diabetes mellitus (IDDM) by inducing nitric oxide production. In this study, we assessed the levels of IL-1 β and the inducible form of nitric oxide synthase (iNOS), using a semi-quantitative polymerase chain reaction assay, and performed determinations of nitrite accumulation and IL-1 β bioactivity, on pancreatic islets isolated from 5- and 16-week-old female and male nonobese diabetic (NOD) mice and from non-diabetes prone NMRI mice. NOD mouse islets contained notable amounts of IL-1 β mRNA. At 5 weeks of age, but not at 16 weeks, the values were higher in islets isolated from NOD females compared to males. The IL-1 β bioactivity showed differences roughly reflecting the mRNA levels in the NOD mouse islets. In the NMRI mouse islets the IL-1 β bioactivity was very low. The expression of iNOS mRNA increased in both male and female islets between 5 and 16 weeks of age. Immunocytochemistry of pancreatic sections indicated the presence of macrophages especially in the peri-insular area of the NOD mice which suggests that IL-1 β was produced by macrophages. The levels of IL-1 β activity and mRNA in freshly isolated islets from NOD 5-week-old females did not correlate to the iNOS mRNA content or to the nitrite production. However, after incubation with IL-1 β in vitro, both NOD and NMRI islets responded with a marked increase in nitric oxide production. It is concluded that the presence of IL-1 β in isolated NOD mouse islets, via an induction of iNOS expression and nitric oxide production, cannot explain the gender difference in diabetes incidence in NOD mice. [Diabetologia (1995) 38: 153–160]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400089
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Comparison of mRNA contents of interleukin-1Β and nitric oxide synthase in pancreatic islets isolated from female and male nonobese diabetic mice (1995)
    Springer
    Diabetologia 38 (1995), S. 153-160 
    Details
    ISSN: 1432-0428
    Keywords: Autoimmunity ; diabetes mellitus ; interleukin-1 ; nitric oxide ; nitric oxide synthase ; NOD mice ; pancreatic islets ; polymerase chain reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Interleukin-1Β (IL-1Β) has been suggested to mediate beta-cell destruction in insulin-dependent diabetes mellitus (IDDM) by inducing nitric oxide production. In this study, we assessed the levels of IL-1Β and the inducible form of nitric oxide synthase (iNOS), using a semi-quantitative polymerase chain reaction assay, and performed determinations of nitrite accumulation and IL-1Β bioactivity, on pancreatic islets isolated from 5- and 16-week-old female and male nonobese diabetic (NOD) mice and from nondiabetes prone NMRI mice. NOD mouse islets contained notable amounts of IL-1Β mRNA. At 5 weeks of age, but not at 16 weeks, the values were higher in islets isolated from NOD females compared to males. The IL-1Β bioactivity showed differences roughly reflecting the mRNA levels in the NOD mouse islets. In the NMRI mouse islets the IL-1Β bioactivity was very low. The expression of iNOS mRNA increased in both male and female islets between 5 and 16 weeks of age. Immunocytochemistry of pancreatic sections indicated the presence of macrophages especially in the peri-insular area of the NOD mice which suggests that IL-1Β was produced by macrophages. The levels of IL-1Β activity and mRNA in freshly isolated islets from NOD 5-week-old females did not correlate to the iNOS mRNA content or to the nitrite production. However, after incubation with IL-1Β in vitro, both NOD and NMRI islets responded with a marked increase in nitric oxide production. It is concluded that the presence of IL-1Β in isolated NOD mouse islets, via an induction of iNOS expression and nitric oxide production, cannot explain the gender difference in diabetes incidence in NOD mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400089
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...