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BACKGROUND: The pathogenesis of diabetic peripheral neuropathy has not yet been clarified, and TAM (Tyro3, Axl, and MerTK) receptor tyrosine kinases can control apoptotic cells and suppress inflammatory responses in the central nervous system. OBJECTIVE: To investigate the difference of Mer receptor tyrosine kinase (MerTK) levels in plasma and sciatic nerve tissue of Sprague-Dawley rats with type 2 diabetes and diabetic peripheral neuropathy, and to study the correlation between MerTK and diabetic peripheral neuropathy. METHODS: Forty male Sprague-Dawley were randomly divided into control group with 15 rats, type 2 diabetes group with 10 rats, and diabetic peripheral neuropathy group with 15 rats. The control group was fed with ordinary diet, while the experimental groups were fed with high-fat and high-sugar diet. After 6 weeks, intraperitoneal injection of streptozotocin at the minimum dose of 35 mg/kg was administered in the two experimental groups. After 14 days, tail vein blood was collected to detect blood glucose. If blood glucose ≥ 16.7 mmol/L, the model of type 2 diabetes was successfully established. Rats in the diabetic peripheral neuropathy group continued to be fed with a high-sugar and high-fat diet for 8 weeks. The sciatic nerve conduction velocity of rats was detected through live isolation under anesthesia. Blood samples were collected from the abdominal aorta, and the sciatic nerve tissue was collected. Histological changes of nerve fibers in each group were observed under a light microscope to confirm the success of diabetic peripheral neuropathy modeling. ELISA was used to detect peripheral blood glucose, blood lipids and serum MerTK levels in rats; hematoxylin-eosin staining was used to observe the histological changes in the sciatic nerve; immunofluorescence, immunohistochemistry and western blot were used to detect the expression of MerTK in the sciatic nerve tissue. RESULTS AND CONCLUSION: The Sprague-Dawley rat models of type 2 diabetes and type 2 diabetes peripheral neuropathy were successfully constructed, and the modeling rate of diabetic peripheral neuropathy was 80%. Compared with the control group, the blood glucose levels of rats in the type 2 diabetes and diabetic peripheral neuropathy groups were significantly higher (P < 0.000 1), while the blood glucose level in the diabetic peripheral neuropathy group was higher than that in the type 2 diabetes group; and the sciatic nerve conduction velocity was significantly decreased (P < 0.05), which was lower in the diabetic peripheral neuropathy group than the type 2 diabetes group. Histological examination: Compared with the control group, the sciatic nerve nuclei were reduced in the type 2 diabetes group, with some vacuolar degeneration and phagocytosis; in the diabetic peripheral neuropathy group, the cell body was swollen, the nuclear spacing was increased, vacuolar degeneration was observed, and the myelin sheath was partitioned and unsmooth, and lattice-like axons appeared. Serum MerTK levels were significantly higher in the diabetic peripheral neuropathy group than the control group. Expression of MerTK in the sciatic nerve tissue was significantly upregulated in the diabetic peripheral neuropathy group compared with the control group (P < 0.05). To conclude, elevated levels of MerTK in plasma and sciatic nerve tissue of rats with diabetic peripheral neuropathy are presumably related to its anti-inflammatory and immunomodulatory effects. [ABSTRACT FROM AUTHOR]

Objective To investigate the expression levels and clinical significance of long non DLX6-AS1 (IncRNA DLX6-ASI) in tissues and serum exosomes of cervical cancer patients. Methods coding RNA Eighty - two cervical cancer patients admitted between April 2022 and April 2023 at the Department of Gynecology, Hainan West Central Hospital were included as the study group, and 82 women with uterine fibroids were selected as the control group. Cervical cancer tissues and serum exosomes were collected postoperatively from the patients. The expression levels of IncRNA DLX6-AS1 in tissue samples and serum exosomes were quantified using real-time quantitative PCR (qRT-PCR). The clinical diagnostic value of IncRNA DLX6-AS1 for cervical cancer was evaluated using receiver operating characteristic (ROC) curve analysis. Results The relative expression levels of IncRNA DLX6 AS1 in both cervical cancer tissues and serum exosomes were significantly higher in the study group compared to the control group (P<0.05). Statistical differences in IncRNA DLX6 - AS1 expression were observed in cervical cancer tissues and serum exosomes among patients at different FIGO stages and with lymph node metastasis or not (P<0.05). The area under the ROC curve (AUC) for diagnosing cervical cancer using IncRNA DLX6-AS1 alone in tissue, alone in serum exosomes, and in combination were 0. 740, 0.692, and 0.781, respectively. Conclusion Elevated expression levels of IncRNA DLX6 AS1 in both tissues and serum exosomes are associated with cervical cancer and its severity. IncRNA DLX6ASI may serve as a potential biomarker for the diagnosis and prognosis of cervical cancer. [ABSTRACT FROM AUTHOR]

With the increasing maturity of neonatal intensive care technology， the survival rate of premature infants has been increased significantly. At the same time， the incidence of brain injury has also been elevated year by year， and most of the affected children are complicated with early clinical manifestations and long-term sequelae of nervous system injury. Therefore， finding a simple and effective diagnostic method to improve the quality of life of premature infants has become a key problem to be solved urgently in the current field. In recent years， more and more biological markers of brain injury have been studied and applied to the early diagnosis and prognosis assessment of brain injury in premature infants. This article reviews the domestic and international research progress on these biological markers， aiming to provide reference for the early diagnosis and prognosis assessment of brain injury in premature infants.

Copyright of Journal of New Medicine is the property of Sun Yat Sen University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The development in diagnosis and treatment of myocardial infarction has significantly improved the prognosis of some patients, while the overall survival rate of patients remains much room for improvement. Further research of the mechanism of injury after myocardial ischemia and reperfusion may explore new directions of research. As a newly discovered form of regulated cell death, ferroptosis, an iron-dependent cell death caused by lipid peroxidation, which has been characterized by cell death involving the accumulation of lipid peroxides and reactive oxygen species. Ferroptosis, which has been acknowledged to play an important role in ischemia-reperfusion injury. Studies suggest that iron death-related marker changes after myocardial infarction (MI), including hiatus of mitochondrial ferritin (FtMt) in intracellular iron metabolism, decreased levels of glutathione peroxidase 4 (Gpx4), a terminal molecule of glutathione metabolism pathway, insufficient use of antiporter cystine/glutathione synthesis (SXc-) in glutathione synthesis, and overexpression of Acyl-CoA synthetase long-chain family member 4 (ACSL4) can lead to oxidative stress, inflammatory response, cardiomyocyte injury after myocardial infarction, and can aggravate the myocardial ischemia-reperfusion injury. The four biological markers mentioned above, FtMt, Gpx4, SXc- and ACSL4, are important research targets for the diagnosis and treatment of iron death after MI, which may deserve further study.

Copyright of Journal of Guangxi Normal University - Natural Science Edition is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Taking the 4th-instar larval Propsilocerus akamusi as test object, this paper studied the acute toxicity of phenol, and the body mass, pupation rate, protective enzyme activities, and detoxifying enzyme activities of the larvae under exposure to phenol. The LC50 value of phenol to the larvae after exposure for 6, 24, 48, 72, and 96 h was 222.52, 134.86, 67.74, 47.39, and 35.76 mg·L-1, respectively, and the dry mass, fresh mass, and pupation rate of the larvae decreased under the exposure of 0.4, 4, and 40 mg phenol·L-1. During 72 h exposure to phenol, the larval catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), and carboxylesterase (CarE) activities responded to phenol in concentration-and time-dependent way, while the acid phosphatase (ACP) and alkaline phosphatase (ALP) activities responded slowly and were only inhibited significantly under the exposure to 40 mg·L-1 of phenol for 48 and 72 h, respectively. It was suggested that the body mass, pupation rate, and CAT, SOD, GST, and CarE activities of 4th-instar larval P. akamusi could be used as the biological markers to monitor the phenol pollution of water body. [ABSTRACT FROM AUTHOR]

Objective To invesigate the expression of long non-coding RNA (lncRNA) PTV1 and its significance in the renal carcinoma tissues. Methods Fifty-four cases of renal cell carcinoma tissues were collected and the adjacent tissues of above 2 cm to tumor (no cancer cells were found under microscope) were used as the controls. Total RNA was isolated to get cDNA by performing reverse transcription. Then real-time quantitative PCR (RT-qPCR) was used to detect the expression of PTV1 in the renal cell carcinoma tissues and the adjacent tissues. Then the PTV1 expression level in the renal carcinoma tissues and the relationships between the expression of PTV1 and clinical characteristics and the prognosis were analyzed. The cell proliferation and apoptosis rate were tested by using MTT and flow cytometry, respectively. Results The relative expression levels of PVT1 in the renal carcinoma tissues and adjacent tissues were 6.22 ±0.71 and 2.26 ±0. 36, respectively, and the expression in the renal cell carcinoma tissues was significantly higher than that of the adjacent carcinoma tissues (P<0.05). The high expression of PVT1 in the renal carcinoma tissues was found in 39 cases of 54 cases, and 15 cases were low expression. The relative expression of PTV1 in renal carcinoma tissues was related with lymph node metastasis and TNM stage (all P<0.05), and was not related with sex, age and pathological types (all P>0.05). The overall survival time of patients with high expression and low expression of PVT1 in the renal carcinoma tissues was 47. 9 ±9.4 and 67.2 ±3.8 months, the overall survival time of patients with high PTV1 expression was significantly lower than that of patients with low PTV1 expression (P<0.05). Moreover, knockdown PVT1 expression in 786-0 cell line decreased the proliferation activity and enhanced the apoptosis rate (all P<0.05). Conclusion PVT1 may promote the occurrence and development of renal carcinoma by affecting the proliferation and apoptosis of renal cells, which can be used as a potential new target for renal cell carcinoma. [ABSTRACT FROM AUTHOR]