Evidence map›Paper›PMID 19046214›Full record

ReviewDiabetic medicine : a journal of the British Diabetic Association2008

New potential treatments for protection of pancreatic B-cell function in Type 1 diabetes.

S Cernea, P Pozzilli

Abstract readReview
In one paragraph

Review in Diabetic medicine : a journal of the British Diabetic Association, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Teplizumab therapy for type 1 diabetes.Expert opinion on biological therapy · 2010
    Review
  6. Pancreatic duodenal homeobox 1 protein is a novel beta-cell-specific autoantigen for type I diabetes.Laboratory investigation; a journal of technical methods and pathology · 2010
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

S CerneaDepartment of Immunobiology, Yale University, New Haven, CT, USA.
P Pozzilli

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes mellitus results from the progressive and specific autoimmune destruction of insulin-secreting pancreatic B-cells, which develops over a period of years and continues after the initial clinical presentation. The ultimate goal of therapeutic intervention is prevention or reversal of the disease by the arrest of autoimmunity and by preservation/restoration of B-cell mass and function. Recent clinical trials of antigen-specific or non-specific immune therapies have proved that modulation of islet specific autoimmunity in humans and prevention of insulin secretion loss in the short term after the onset of disease is achievable. The identification of suitable candidates for therapy, appropriate dosage and timing, specificity of intervention and the side-effect profile are crucial for the success of any approach. Considering the complexity of the disease, it is likely that a rationally designed approach of combined immune-based therapies that target suppression of B-cell specific autoreactivity and maintenance of immune tolerance, coupled with islet regeneration or replacement of the destroyed B-cell mass, will prove to be most effective in causing remission/reversal of disease in a durable fashion.

Indexed as

AutoimmunityDiabetes Mellitus, Type 1Disease ProgressionFemaleHumansHypoglycemic AgentsImmunotherapyInsulin-Secreting CellsIslets of Langerhans TransplantationMalePancreatic Function TestsTime FactorsHypoglycemic Agents

Identifiers

PMID19046214
PMCPMC2701557

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.