Multi role ChatGPT framework for transforming medical data analysis.

The application of ChatGPTin the medical field has sparked debate regarding its accuracy. To address this issue, we present a Multi-Role ChatGPT Framework (MRCF), designed to improve ChatGPT's performance in medical data analysis by optimizing prompt words, integrating real-world data, and implementing quality control protocols. Compared to the singular ChatGPT model, MRCF significantly outperforms traditional manual analysis in interpreting medical data, exhibiting fewer random errors, higher accuracy, and better identification of incorrect information. Notably, MRCF is over 600 times more time-efficient than conventional manual annotation methods and costs only one-tenth as much. Leveraging MRCF, we have established two user-friendly databases for efficient and straightforward drug repositioning analysis. This research not only enhances the accuracy and efficiency of ChatGPT in medical data science applications but also offers valuable insights for data analysis models across various professional domains.

Activation of the melanocortin-1 receptor attenuates neuronal apoptosis after traumatic brain injury by upregulating Merlin expression.

Traumatic brain injury (TBI) is a common disease worldwide with high mortality and disability rates. Besides the primary mechanical injury, the secondary injury associated with TBI can also induce numerous pathological changes, such as brain edema, nerve apoptosis, and neuroinflammation, which further aggravates neurological dysfunction and even causes the death due to the primary injury. Among them, neuronal apoptosis is a key link in the injury. Melanocortin-1 receptor (MC1R) is a G protein coupled receptor, belonging to the melanocortin receptor family. Studies have shown that activation of MC1R inhibits oxidative stress and apoptosis, and confers neuroprotective effects against various neurological diseases. Merlin is a protein product of the NF2 gene, which is widely expressed in the central nervous system (CNS) of mice, rats, and humans. Studies have indicated that Merlin is associated with MC1R. In this study, we explored the anti-apoptotic effects and potential mechanisms of MC1R. A rat model of TBI was established through controlled cortical impact. The MC1R-specific agonist Nle4-D-Phe7-α-Melanocyte (NDP-MSH) and the inhibitor MSG-606 were employed to explore the effects of MC1R and Merlin following TBI and investigated the associated mechanisms. The results showed that the expression levels of MC1R and Merlin were upregulated after TBI, and activation of MC1R promoted Merlin expression. Further, we found that MC1R activation significantly improved neurological dysfunction and reduced brain edema and neuronal apoptosis induced by TBI in rats. Mechanistically, its neuroprotective function and anti-apoptotic were partly associated with MC1R activation. In conclusion, we demonstrated that MC1R activation after TBI may inhibit apoptosis and confer neuroprotection by upregulating the expression of Merlin.

Guanine-rich RNA sequence binding factor 1 regulates neuronal ferroptosis after spinal cord injury in rats via the GPX4 signaling pathway.

Spinal cord injury (SCI) can trigger multiple forms of neuronal cell death. Among these, ferroptosis stands out as a particularly important style of cell death due to its iron overload-dependent lipid peroxidative regulatory mechanism. The guanine-rich RNA sequence binding factor 1 (GRSF1) is an RNA-binding protein that has been implicated in cellular senescence, mitochondrial function, oxidative stress, erythropoiesis, and embryonic brain development. However, the function of GRSF1 in neuronal ferroptosis after SCI remains unclear. Here, we established a SCI rat model in vivo and evaluated the function of GRSF1 on neuronal ferroptosis by inhibiting and overexpressing GRSF1. We firstly verified the protein expression of GRSF1 and GPX4 at different time points after SCI. According of changes in expression, we chose 3 d post SCI to assess the effect of GRSF1 on ferroptosis. We found that GRSF1 expression decreased after SCI. In addition, GRSF1 was mainly localized in the cytoplasm of neurons. The results also showed that overexpression of GRSF1 promoted recovery of neurological functional after SCI. Further investigation revealed that GRSF1 might attenuate neuronal ferroptosis by regulating the GPX4 protein expression levels. In summary, our findings indicate that GRSF1 attenuates injury in SCI and reduces neuron ferroptosis and promotes functional recovery via GPX4.

Identification of immunity-related lncRNAs and construction of a ceRNA network of potential prognostic biomarkers in acute myeloid leukemia.

Objective: Using bioinformatics analyses, this study aimed to identify lncRNAs related to the immune status of acute myeloid leukemia (AML) patients and ascertain the potential impact in immunity-related competing endogenous RNA (ceRNA) networks on AML prognosis. Methods: AML-related RNA-seq FPKM data, AML-related miRNA expression microarray data, and gene sets associated with immunity-related pathways were, respectively, obtained from the TCGA, GEO, and ImmReg databases. An immunity-related ceRNA network was then constructed according to the predicted interactions between AML-related mRNAs, lncRNAs, and miRNAs. After performing LASSO and multivariate Cox regression analyses, lncRNAs in the ceRNA network were used to establish an AML prognostic model. According to mutual regulatory relationships and consistent trends of expression among candidate ceRNAs, two ceRNA subnetworks related to the AML prognostic model were determined. Finally, the correlation between the expression levels of mRNAs, lncRNAs, and miRNAs in each ceRNA subnetwork and immune cell infiltration (assessed by combining the ESTIMATE and CIBERSORT methods and ssGSEA) was analyzed. Results: A total of 424 immunity-related differentially expressed (IR-DE) mRNAs (IR-DEmRNAs), 191 IR-DElncRNAs, and 69 IR-DEmiRNAs were obtained, and a ceRNA network of 20 IR-DElncRNAs, 6 IR-DEmRNAs, and 3 IR-DEmiRNAs was established. Univariate Cox regression analysis was conducted on 20 IR-DElncRNAs, and 7 of these were identified to be significantly correlated with the overall survival (OS) time in AML patients. Then, two IR-DElncRNAs (MEG3 and HCP5) were screened as independent OS-related factors by LASSO and multivariable Cox regression analyses, and a prognostic model was constructed to evaluate the survival risk in AML patients. Survival analyses indicated that the OS of patients was often poor in the high-risk group. Additionally, from this model, two ceRNA regulatory pathways, namely, MEG3/miR-125a-5p/SEMA4C and HCP5/miR-125b-5p/IL6R, which were potentially involved in the immune regulation of AML prognosis were identified. Conclusion: lncRNAs HCP5 and MEG3 may act as key ceRNAs in the pathogenesis in AML by regulating immune cell representation as part of the regulatory lncRNA-miRNA-mRNA axes. The candidate mRNAs, lncRNAs, and miRNAs included in the ceRNA network identified here may serve as useful prognostic biomarkers and immunotherapeutic targets for AML.

PTEN-knockdown disrupts the morphology, growth pattern and function of Nthy-Ori 3-1 cells by downregulating PAX8 expression.

The incidence of thyroid disorders, which are common endocrine diseases, has rapidly increased in recent years. However, the etiology and pathogenesis of these disorders remain unclear. Phosphatase and tension homolog (PTEN) is a dual-specific phosphatase that is associated with multiple thyroid disorders; however, the role of PTEN in thyroid disorders remains unknown. In the present study, the human thyroid follicular epithelial cell line Nthy-Ori 3-1 was used to determine the role of PTEN in thyroid disorders. PTEN expression was knocked down using a PTEN-specific short hairpin RNA. Western blotting was subsequently used to determine protein expression, the Matrigel tube formation assay and iodide uptake assay were applied for evaluating the morphology and function of thyroid cells. The results showed that PTEN knockdown decreased the protein expression of paired box 8 (PAX8). The morphology and tubular-like growth pattern of thyroid cells were therefore disrupted, and restoration of PAX8 expression reversed these effects. Furthermore, PTEN-knockdown decreased the expression of specific thyroid proteins (thyroglobulin, TG; thyroid peroxidase, TPO; and sodium/iodide symporter, NIS) and inhibited the iodide uptake ability of thyroid cells by downregulating PAX8, suggesting that PTEN deficiency may impair the function of thyroid cells. In conclusion, the present study reported an important function of PTEN in normal thyroid cells and identified the involvement of PAX8. These results may improve understanding of the role of PTEN in the pathogenesis of thyroid disorders.

Deficiency of PTEN leads to aberrant chromosome segregation through downregulation of MAD2.

Proper spindle formation and accurate chromosome segregation are essential for ensuring mitotic fidelity. Phosphatase and tensin homolog (PTEN) is a multifunctional protein, which is able to maintain the stability of the genome and chromosomes. The present study described an essential role of PTEN in regulating chromosome segregation to prevent gross genomic instability via regulation of mitotic arrest deficient 2 (MAD2). PTEN knockdown induced cell cycle arrest and abnormal chromosome segregation, which manifested as the formation of anaphase bridges, lagging chromosomes and premature chromatid separation. In addition, MAD2 was identified as a potential target of PTEN. Furthermore, the present study revealed that PTEN knockdown resulted in MAD2 degradation via the ubiquitin­proteasomal pathway, while restoration of MAD2 expression partially ameliorated the mitotic defects induced by PTEN loss. The results from the present study proposed a novel mechanism by which PTEN maintains chromosome stability.

Arsenic trioxide inhibits angiogenesis in vitro and in vivo by upregulating FoxO3a.

Arsenic trioxide (As2O3) has been used clinically for the treatment of acute promyelocytic leukemia and some solid tumors. However, the mechanisms of its anti-tumor effects are still elusive. Angiogenesis is a key process for tumor initiation, and increasing evidence has supported the role of anti-angiogenesis caused by arsenic in tumor suppression, although the detailed mechanism is not well understood. In the present study, we found that As2O3 significantly inhibited the angiogenesis of human umbilical vein endothelial cells (HUVECs) in vitro, and this was mediated by the upregulation of FoxO3a. Knockdown of FoxO3a could restore the angiogenic ability of HUVECs. Moreover, vascular endothelial cell-specific knockout of FoxO3a in mice could disrupt the anti-angiogenesis effect of As2O3 and endow the tumors with resistance to As2O3 treatments. Our results revealed a new mechanism by which As2O3 suppresses angiogenesis and tumor growth.

[Analysis of risk factors of intra-abdominal infection after surgery for colorectal cancer].

OBJECTIVE: To investigate the risk factors of intra-abdominal infection(IAI) after colorectal cancer surgery. METHODS: Clinical and follow-up data of 773 colorectal cancer patients undergoing operation in our hospital from October 2011 to December 2014 were retrospectively analyzed. Patients were divided into intra-abdominal cavity infection group (110 cases, IAI group) and non intra-abdominal infection group(663 cases, non-IAI group). All the patients administered prophylactic antibiotics 30 minutes to 2 hours before operation. Univariate and multivariate analysis were performed to evaluate the risk factors of IAI. RESULTS: Preoperative factors associated with postoperative IAI included hepatic cirrhosis, kidney diseases, diabetes or other basic diseases, prophylactic use of drugs, hypoalbuminemia, anemia, intestinal obstruction, and American Society of Anesthesiologists (ASA) anesthetic grading score (all P<0.05). Postoperative factors associated with postoperative IAI included use of laparoscopy or stapler, united exenteration, existence of anastomotic fistula, time of drainage tube placement, operation time and tumor staging (all P<0.05). Multivariate logistic regression analysis showed that preoperative diabetes(OR=2.36, 95% CI:1.45 to 4.76, P<0.01), combined exenteration (OR=2.02, 95% CI:1.02 to 4.00, P<0.01), anastomotic leak (OR=4.41, 95% CI:1.77 to 10.99, P=0.001), operation time≥140 minutes (OR=2.88, 95% CI:1.78 to 4.67, P<0.01) and period of postoperative drainage≥10 days(OR=4.57, 95% CI:2.78 to 7.52, P<0.01) were independent risk factors of postoperative IAI, while the use of stapler was protective factor (OR=0.37, 95% CI: 0.23 to 0.60, P<0.01). Compared with prophylactic use of cephamycins plus metronidazole, cefuroxime plus metronidazole had a higher rate of IAI(OR=2.10, 95% CI:1.23 to 3.58, P=0.007). CONCLUSIONS: Prevention of postoperative IAI is required for colorectal cancer patients, particularly in those with preoperative diabetes, combined exenteration, anastomotic leak, operation time longer than 140 minutes and postoperative drainage period longer than 10 days. Preoperative use of cephamycins plus metronidazole has better efficacy in prevention of postoperative IAI.

[Epidemiological characteristics and risk factors for patients with catheter-related bloodstream infections in intensive care unit].

OBJECTIVE: To explore the epidemiological characteristics, bacterial composition and risk factors for patients with catheter-related bloodstream infection (CRBSI) in intensive care unit (ICU). METHODS: A prospective survey was conduced for 2 605 ICU patients during January 2010 to December 2013. The clinical data of CRBSI and non-CRBSI patients were compared and their relevant risk factors analyzed. RESULTS: Among them, there were 1 773 cases of arteriovenous catheterization. And 94 cases (5.3%) had CRBSI. The 1 000-day catheter infection rate was 9.8. The mortality rates of CRBSI and non-CRBSI patients were 23.4% and 10.7% respectively. And the difference was statistically significant (χ² = 14.38, P < 0.01). The occurrence of CRBSI was a risk factor for mortality. Logistic regression analysis showed that the occurrence of CRBSI was 3.33 folds for venous catheterization time > 6 days over ≤ 6 days (95% CI: 2.04-5.56), 2.50 folds for trauma patients over non-trauma ones (95% CI: 1.49-4.17), 2.98 folds for malignant tumors patients over non-malignant tumors ones (95% CI: 1.61-5.51) and 4.32 folds for diabetics over non-diabetics (95% CI: 2.07-9.01). For different sites of arteriovenous catheterization, the occurrences of CRBSI were not statistically significant. For CRBSI patients with blood culture, the positive microorganisms were gram-negative bacteria (61.7%), gram-positive bacteria (26%) and fungi (12.3%). CONCLUSION: The occurrence of CRBSI is a risk factor for mortality. And diabetes, trauma and arteriovenous catheterization time > 6 days are risk factors for CRBSI. Comprehensive preventive measures should be taken to reduce the incidence of CRBSI.