Bibliographic record
Abstract
Many growth factors have been proven that have neuroprotective effects after cerebral ischemia, including transforming growth factor β-I, insulin-like growth factor-I, and vascular endothelial growth factor. Recently, granulocyte colony-stimulating factor (G-CSF) is under investigation for the same purpose. In this study, we are going to evaluate its beneficial role in neuroprotection following experimental cerebral ischemia. Hypoxia-ischemia was induced in 3-month-old CD1 mice by using the Vannucci procedure. We randomly assigned 30 mice to the following groups: control group, NMDA antagonist group, and G-CSF group. Animals were anesthetized. Then animals were exposed to 30 minutes of hypoxia (6% oxygen, 94% N2). Following hypoxia, the blindly coded, prepared vials were administered. Following recovery, after 24 hours, the surviving animals were reanesthetized and the brain sections were examined for infarction. After acquiring the data, the randomization code was broken and results were statistically evaluated. Mean infarct volume in G-CSF-treated animals was 92.1 ± 20 (n = 10) vs 87.58 ± 20 (n = 12) in the NMDA antagonist group vs 92.51 ± 20 mm3 (n = 8) in the control group. Our results showed there was a trend of lower level of infarction following the NMDA antagonist (P = .055) There was no significant difference in mortality or physiologic parameters in different groups. Our results show that the G-CSF did not achieve a potent neuroprotective effect after focal cerebral ischemia. G-CSF is a cytokine that stimulates the differentiation and proliferation of blood cells. G-CSF, through specific receptors on endothelial cells, induces angiogenesis by stimulation of proliferation, migration, and release of proteolytic enzymes by endothelial cells. Even though there are few reports that mention that G-CSF maybe has some protective effect on neural cells, patients with cerebrovascular disease have not yet profited from treatments based on the angiogenic effect of G-CSF. We strongly advise more studies to be done to reach a discrete result on the effect of G-CSF. Category: Molecular Pathology
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.001 |
| Scholarly communication | 0.001 | 0.001 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.002 | 0.001 |
| Insufficient payload (model declined to judge) | 0.002 | 0.001 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".