Analysis of High-Risk Clinical Factors of Early Death in Secondary Hemophagocytic Lymphohistiocytosis / 中国实验血液学杂志

OBJECTIVE@#To explore the high-risk clinical factors of early death in patients with secondary hemophagocytic lymphohistiocytosis (sHLH), and further identify the clinical factors related to the rapid progression of sHLH in the short term.@*METHODS@#The clinical manifestations, laboratory examination and prognosis of sHLH patients were retrospectively analyzed. Continuous variables were grouped by median, univariate and multivariate Cox regression analysis and Kaplan-Meier survival curve were used to explore the risk factors affecting early death of sHLH. Then, a nomogram model was established with independent risk factors, Bootstrap resampling method was used for verification, and consistency index (C-index) and calibration curve were used to detect the prediction accuracy.@*RESULTS@#A total of 126 sHLH patients were enrolled, with a median age of 48.5(16-88) years, including 74 males and 52 females. Fifty-five patients (43.6%) died within 30 days, including 39 males and 16 females. Univariate regression analysis showed that lymphocyte count <0.45×109/L, platelet count (PLT) <39.5×109/L, prothrombin time (PT)≥13.3 s, activated partial thromboplastin time (APTT)≥39.7 s, albumin (ALB) <25.9 g/L, lactate dehydrogenase (LDH)≥811 U/L, creatinine (Cr) ≥67 μmol/L and procalcitonin (PCT)≥0.61 ng/ml were risk factors for death within 30 days in sHLH patients. Multivariate regression analysis showed that lymphocyte count <0.45×109/L, APTT≥39.7 s and ALB <25.9 g/L were independent risk factors for death within 30 days in sHLH patients. A nomogram model was established based on the above three risk factors, its C-index was 0.683, and the calibration chart showed good agreement between the observed and predicted values of sHLH.@*CONCLUSIONS@#Lymphopenia, prolonged APTT, and hypoalbuminemia are risk factors for early death of sHLH patients. Early identification and positive intervention are expected to reduce early mortality in sHLH patients. The nomogram model based on the above risk factors provides a method for clinicians to evaluate sHLH.

Cloning and expression of LAR gene and its correlation with phloridzin content in Lithocarpus polystachyus / 中草药

Objective: To clone the leucoanthocyanidin reductase (LAR) gene of Lithocarpus polystachyus, and analyze the relationship between LAR gene expression level and phloridzin content. Methods: According to the results of L. polystachyus transcriptome sequencing (unigene: DN30711_c0_g1_i1), the full-length cDNA sequence of LAR gene was amplified by PCR and the bioinformatics analysis was carried out. Its expression was detected by quantitative Real-time PCR (qRT-PCR). The phloridzin content of L. polystachyus was measured by UPLC method and the correlation between LAR gene expression and phloridzin content was analyzed by SPSS 18.0 software. Results: The full-length cDNA of the LAR gene was 1 053 bp and contained a complete open reading frame that encoded 350 amino acids. This protein did not exist a transmembrane domain and was localized in the cytoplasm. The LAR protein of L. polystachyus was the number of PCBER_SDR_a family and had a high similarity (95%) to the LAR protein of Quercus suber and their genetic relationship was close. The phloridzin content of L. polystachyus was positively correlated with the expression of LAR gene (P < 0.05). Conclusion: The LAR gene of L. polystachyus was cloned for the first time. It was confirmed that the content of phloridzin was positively correlated with the expression of LAR gene of L. polystachyus, which laid a theoretical and technical basis for revealing the biosynthesis mechanism of phloridzin of L. polystachyus.

Mechanism study on leptin resistance in lung cancer cachexia rats treated by Xiaoyan Decoction / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To study the leptin resistance mechanism of Xiaoyan Decoction (XD) in lung cancer cachexia (LCC) rats.</p><p><b>METHODS</b>An LCC rat model was established. Totally 40 rats were randomly divided into the normal control group, the LCC model group, the XD group, and the positive control group, 10 in each group. After LCC model was set up, rats in the LCC model group were administered with normal saline, 2 mL each time. Rats in the XD group were administered with XD at the daily dose of 2 mL. Those in the positive control group were administered with Medroxyprogesterone Acetate suspension (20 mg/kg) by gastrogavage at the daily dose of 2 mL. All medication lasted for 14 days. The general condition and tumor growth were observed. Serum levels of leptin and leptin receptor in the hypothalamus were detected using enzyme-linked immunosorbent assay. Contents of neuropeptide Y (NPY) and anorexia for genomic POMC were detected using real-time PCR technique.</p><p><b>RESULTS</b>Serum leptin levels were lower in the LCC model group than in the normal control group with statistical significance (P < 0.05). Compared with the LCC model groups, serum leptin levels significantly increased in the XD group (P < 0.01). Leptin receptor levels in the hypothalamus increased significantly in the LCC model group (P < 0.01). Increased receptor levels in the LCC model group indicated that either XD or Medroxyprogesterone Acetate could effectively reduce levels of leptin receptor with statistical significance (P < 0.01). There was also statistical difference between the XD group and the positive control group (P < 0.05). Contents of NPY was higher in the LCC model group than in the other groups with statistical difference (P < 0.05). There was no statistical difference in NPY between the normal control group and the rest 2 treatment groups (P > 0.05). There was statistical difference in POMC between the normal control group and the LCC model group (P < 0.05). POMC could be decreased in the XD group and the positive control group with statistical significance (P < 0.05), and it was more obviously decreased in the XD group (P < 0.05).</p><p><b>CONCLUSIONS</b>Leptin resistance existed in LCC rats. XD could increase serum leptin levels and reduce leptin receptor levels in the hypothalamus. LCC could be improved by elevating NPY contents in the hypothalamus and reducing POMC contents, promoting the appetite, and increasing food intake from the periphery pathway and the central pathway.</p>