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Nitrogen (N) deposition is increasingly aggravating and has significant impact on the processes of forest soil carbon (C) cycling. However, how N deposition affects forest soil C cycling processes in the scenario of future drought-frequent climate is still unclear. Therefore, we conducted a 2.5-year experiment at two levels of N addition treatments (control and N addition) and three levels of moisture (well-watered: ca. 80% of field capacity, moderate drought: ca. 60% of field capacity, severe drought: ca. 40% of field capacity) to investigate the impact of N addition, drought, and their interaction on soil respiration (Rs) and soil organic carbon (SOC) content. The results showed that N addition significantly increased Rs and SOC content, and severe drought decreased Rs and SOC content. In a well-watered condition, N addition significantly increased annual mean Rs, but in moderate drought and severe drought condition, N addition did not obviously affect Rs. In the control group, severe drought significantly decreased annual mean Rs by 61.5%, and decreased SOC content in 0–10 cm and in 10–20 cm by 3.0% and 1.6%, respectively. However, in the N addition group, moderate drought and severe drought significantly decreased annual mean Rs by 27.6% and 70.5%, respectively. Meanwhile, compared to the well-watered condition, severe drought significantly decreased SOC content in 0–10 cm and in 10–20 cm by 12.4% and 11.9% in the N addition group, respectively. Severe drought also decreased aboveground and belowground biomass, fine root biomass, MBC, and specific respiration in N addition group. The Rs and SOC content were positively correlated with aboveground biomass, belowground biomass, and fine root biomass. These results suggest that under future global change scenarios, severe drought might offset the promotive effects of N deposition on soil respiration and C sequestration in the young subtropical forest. Moreover, the N deposition may enhance the suppressive effect of drought on soil respiration and C sequestration in the future.

BACKGROUND Glycated hemoglobin (Hb) (HbA1c) is an indicator that is used to diagnose and monitor the treatment of diabetes. Many factors can affect the detection of HbA1c. One of the most important of these factors is the Hb variant. Here, we report a rare Hb variant and evaluate its effect on HbA1c. CASE SUMMARY A 35-year-old man was suspected of harboring an Hb variant following the measurement of HbA1c with the Variant II Turbo 2.0 Hb detection system during a routine examination. Subsequently, we used the Arkray HA-8160 and ARCHITECT c4000 system to reanalyze HbA1c. Finally, the Hb variant was detected with a Capillary2FP analyzer that operates on the principle of capillary electrophoresis. We also used gene sequencing to investigate the mutation site. The value of HbA1c detected with the Variant II Turbo 2.0 system was 52.7%. However, the Arkray HA-8160 system did not display a result while the ARCHITECT c16000 system showed a result of 5.4%. The Capillary2FP analyzer did not reveal any abnormal Hb zones. However, gene sequencing identified the presence of a mutation in the Hb β2 chain [CD2(CAC>TAC), His>Tyr, HBB: c.7C>T]; the genotype was Hb Fukuoka. CONCLUSION Hb variants could cause abnormal HbA1c results. For patients with Hb variants, different methods should be used to detect HbA1c.

To investigate the distribution of Ret-He and RBC in thalassemia and the value of combining HbA2 in the detection of thalassemia among patients with microcytic or hypochromic.145 patients with microcytic or hypochromic outpatient or hospitalization in our hospital from May 2018 to December 2019 were selected and were divided into the thalassemia group(68 cases) and the non-thalassemia group (77 cases), and at the same time, the patients were divided into four groups of the non-anemia, mild anemia, moderate anemia and severe anemia group according to the degree of anemia. The Ret-He, RBC, RDW-CV and HbA2 in patients were detected, and the distribution of these parameters were compared, and the joint detection of Ret-He, RBC and HbA2 about its sensitivity, specific and other indicators of auxiliary diagnosis of thalassemia were analyzed.Among patients with microcytic or hypochromic, according to the anemia grade Ret-He gradually decreased from the non-anemia group to the severe anemia group (P0.05); while RDW-CV was increased gradually from the mild anemia group to the severe anemia group (P0.05); both RBC and Ret-He were increased in the thalassemia group as compared with the non- thalassemia group (P0.05); while RDW-CV was decreased in the thalassemia group as compared with the non-thalassemia group (P0.05); meanwhile Ret-He in the α-thalassemia group was higher than that in the β-thalassemia group. ROC curve analysis showed that combined with HbA2, the specificity was 93.51%, the sensitivity was 66.18%, the positive predictive value was 90% and the negative predictive value was 75.189% when Ret-He was truncated with 19.25 pg and RBC was truncated with 4.95×10Among patients with microcytic or hypochromic, the distribution of RBC, Ret-He and RDW-CV was different in the thalassemia group and the non-thalassemia group, and was also affected by the degree of anemia. Combined Ret-He and RBC could improve the diagnostic specificity for thalassemia, which were screened by HbA2 in patients with microcytic or hypochromic.RBC、Ret-He与HbA2联合检测对地中海贫血的临床价值.探讨小细胞或低色素人群中Ret-He和RBC在地中海贫血中的分布情况及联合HbA2对地中海贫血检测的价值.选取本院2018年5月-2019年12月门诊检测出或住院的小细胞或低色素患者145例，将其分为地贫组（68例）及非地贫组（77例），并同时按贫血程度将患者分为非贫血、轻度贫血、中度贫血及重度贫血共4组，对患者进行Ret-He、RBC、RDW-CV及HbA2检测，比较各项参数的分布情况，并分析RBC、Ret-He与HbA2联合检测以辅助诊断地中海贫血的灵敏度、特异度.在小细胞或低色素患者中，根据贫血程度分级，Ret-He从非贫血组至重度贫血组逐渐下降（P0.05）；而RDW-CV则从轻度贫血组至重度贫血组逐渐上升（P0.05）；RBC及Ret-He在地贫组患者中均较非地贫组明显升高（P0.05），而RDW-CV则在地贫组中较非地贫组明显降低（P0.05）；同时Ret-He在α-地贫中较β-地贫明显升高（P0.05）。进行ROC曲线分析，Ret-He以19.25 pg为截断值，RBC以4.95×10在小细胞或低色素患者中， RBC、Ret-He及RDW-CV在地贫组及非地贫组的分布存在差异，并受贫血程度影响。加入Ret-He及RBC可提高小细胞或低色素患者依靠HbA2进行地中海贫血初筛时的特异度.

Several studies indicated that tonsillectomy can improve the prognosis of patients with immunoglobulin A nephropathy (IgAN). However, the relationship between tonsillar immunity and IgAN is still unclear.A total of 14 IgAN patients were recruited in the current study from May 2015 to April 2016 in Tongji Hospital. B cells, dendritic cells (DCs), and IgA1 positive cells in human tonsils were detected using immunofluorescence and immunohistochemistry. Correlations between these cells and clinicopathologic features were evaluated.CD19CD19

Vegetation restoration can affect the process of soil organic carbon (SOC) decomposition, but how this effect is related to soil moisture and temperature remains uncertain. Thus, we performed an incubation of 120 days using soils of degraded land, plantation forest, and secondary natural forest, at two levels of temperature under two moisture levels. We found that the amount of cumulative SOC decomposition in the plantation and secondary natural forest soil was ca. 11.7 times higher than that in the soil from degraded land. Higher soil moisture and temperature treatment increased SOC decomposition in the plantation and secondary natural forest soils. However, in the soil from degraded land, higher soil moisture did not increase SOC decomposition, and higher temperature only increased SOC decomposition in the 60%WHC treatment. The amount of cumulative SOC decomposition was positively correlated with soil MBC and DOC content. The responses of SOC decomposition and the decomposability of DOC to moisture and temperature along the vegetation restoration gradient were highly consistent. Furthermore, in the 60%WHC treatment group, the temperature sensitivity (Q10) of SOC decomposition declined with vegetation restoration age increase. Higher soil moisture did not affect Q10 in the plantation and secondary natural forest soil, but increased Q10 in the soil from degraded land. Our results indicate that higher soil temperature and moisture would stimulate SOC decomposition, but it is highly dependent on labile carbon supply and microbial metabolic activity along the vegetation restoration gradient.

Diagnosis of immunoglobulin A nephropathy (IgAN) requires the evaluation of renal biopsy specimens. However, renal biopsy is an invasive procedure and is not frequently performed for various reasons. Thus, recognized noninvasive biomarkers for predicting IgAN progression are urgently needed.In the present study, we included 86 IgAN patients with renal biopsy from June 2015 to May 2016 and had their plasma interleukin-7 (IL-7) level measured with ELISA. The association between the plasma IL-7 level and clinico-pathological characteristics was analyzed. Immunohistochemical staining was used to assay the in situ expression of IL-7 in vivo. Western blotting was performed to examine the production of extracellular matrix, p-mTOR and the markers of autophagy under the treatment of IL-7 after TGF-β1 stimulation in renal tubular epithelial cells.IL-7 was significantly decreased in patients with IgAN compared to healthy subjects (2.3077 vs. 8.6294 pg/mL, P0.0001). There was a significant difference in the plasma IL-7 level between tubular atrophy/interstitial fibrosis T0 and T2 classes (P=0.0064). A lower plasma IL-7 value in patients at the time of biopsy indicated a poor renal outcome. In addition, IL-7 was over-expressed in renal tubular epithelial cells and significantly attenuated transforming growth factor βl-induced extracellular matrix production by suppression of cellular autophagy via activation of mTOR1 signaling.These results suggested that IL-7 might be a noninvasive biomarker for predicating IgAN. It protected renal proximal tubular epithelial cells from cellular fibrosis by inhibiting autophagy via mTORl signaling.

Lung adenocarcinomas with gene rearrangement in the receptor tyrosine kinase ROS1 have emerged as a rare molecular subtype. Although these lung adenocarcinomas respond to ROS1tyrosine kinase inhibitors, many patients ultimately acquire resistance. ROS1gene rearrangement is generally mutually exclusive with other driver genomic alterations, such as those in EGFR, KRAS, or ALK, thus multiple genomic alterations are extremely rare. Herein, we report a case of a 42-year-old man diagnosed with lung adenocarcinoma positive for a SDC4-ROS1 fusion, who was treated with crizotinib followed by three cycles of chemotherapy. A biopsy acquired after disease progression revealed the original SDC4-ROS1 fusion along with a KRAS point mutation (p.G12D).We reviewed the related literature to determine the frequency of gene mutations in non-small cell lung cancer patients. A better understanding of the molecular biology of non-small cell lung cancer with multiple driver genomic aberrations will assist in determining optimal treatment.

Hemangiomas of the rib are extremely rare benign neoplasm. Here we present a case in a 47-year-old female, detected by chest X-ray and underwent a surgical resection. Histologically, the tumor was composed of a homogeneous conglomerate, irregular, thin walled and dilated blood vessels containing red blood cells, supported by fibrous stroma and intermingled to regular bone trabeculae. The postoperative courses were uneventful, and there was no recurrence during 64 months follow-up.

C-ros oncogene 1 receptor tyrosine kinase (ROS1) rearrangement forms a novel molecular subgroup of non-small cell lung cancer (NSCLC). The present study explored the clinicopathological features and clinical efficacy of crizotinib in patients with ROS1-positive NSCLC. A retrospective analysis of 2,617 cases of NSCLC diagnosed between January 2013 and December 2016 was performed. ROS1 fusion genes were detected by reverse transcription-quantitative polymerase chain reaction, fluorescence in situ hybridization or next-generation sequencing techniques, and patients positive for the ROS1 fusion gene received oral treatment with crizotinib. The ROS1 fusion was identified in 67 out of 2,617 cases (2.56%), including 21 cases that were male and 46 cases that were female. The median age was 68 years. Among these cases, 59 (88.06%) were adenocarcinoma and 8 were non-adenocarcinoma. According to Tumor-Node-Metastasis (TNM) staging, 4 cases were stage I–IIIa and 63 (94.02%) were stage IIIb–IV. The epidermal growth factor receptor (EGFR) gene status included 60 cases of wild-type, 1 case of co-mutation and 6 unknown cases. Statistically significant differences were identified for sex, TNM staging and EGFR gene status between ROS1 fusion gene-positive and -negative patients (P

Background The death-domain-associated protein (DAXX) was originally identified as a protein that binds to the transmembrane death receptor FAS and enhances both FAS-induced and transforming growth factor-β-dependent apoptosis. In a previous study, we found that nude mice injected with DAXX-overexpressing cells (ES-2-DAXX) accumulated large concentrations of first-generation ascites cells (I ascites cells). The role of DAXX in the development of ascites is unknown. The aim of this study was to analyze the effect of DAXX on proliferation and migration of ascites cells in ovarian cancer in vitro and in vivo. Methods Nude mice were housed in cages with a 14:10 h light:dark cycle; water and food were provided ad libitum. ES-2-DAXX cells (1×106) were injected intraperitoneally into athymic nude mice (8-week-old female mice). After 4 weeks, I ascites cells were collected. The I ascites cells were injected intraperitoneally into athymic nude mice (8-week-old female mice). After 4 weeks, II ascites cells were collected and cultured. Ascites cell survival, migration, and colony formation were measured using colony formation and cell growth assays. Immunofluorescent staining revealed the co-localization of DAXX and promyelocytic leukemia protein (PML) in ascites cell nuclei. Western blotting and immunohistochemistry showed that extracellular signal-related kinase (p-ERK) 1/2 and CEBP-β were highly expressed in tumor tissues formed by II ascites cells. Through immunoprecipitation, we also found that DAXX can interact with CEBP-β. Results DAXX enhanced ascites cell survival, migration, and colony formation. DAXX and PML nuclear foci dramatically increased in a passage-dependent manner in ascites cells, DAXX promoted the tumor growth of ascites cells in vivo, increased ascites cell proliferation in vivo, and enhanced ascites cell survival and migration by activating the ERK signalling pathway and integrating with CEBP-β. Conclusions DAXX can interact with CEBP-β. DAXX can induce ovarian cancer ascites formation by activating the ERK signal pathway and binding to CEBP-β.

Accumulating evidences have indicated that BIM expression largely decides the development of lung cancer and outcome of EGFR-mutant lung cancers after TKI treatments. BIM polymorphism is a 2,903-bp deletion in the second exon. To clarify the relationship between this BIM polymorphism and clinical outcomes of lung cancers, we conducted this meta-analysis and observed the survival and responses to TKIs. Sixteen cohort studies, covering 4393 WT and 916 BIM deletion patients were included. Overall, BIM deletion polymorphism was associated with significantly shorter progression-free survival (PFS) and slightly shorter overall survival (OS), compared to the WT group. Moreover, patients with BIM deletion polymorphism showed significantly inferior response to EGFR TKIs. In conclusion, our analysis confirmed that lung cancer patients harboring the BIM deletion have inferior survival and TKI responses. Examination of the novel biomarker BIM deletion in lung cancer patients, especially for the EGFR mutant cohort, could provide some prognostic utility.

Lung adenocarcinomas with gene rearrangement in the receptor tyrosine kinase ROS1 have emerged as a rare molecular subtype. Although these lung adenocarcinomas respond to ROS1tyrosine kinase inhibitors, many patients ultimately acquire resistance. ROS1gene rearrangement is generally mutually exclusive with other driver genomic alterations, such as those in EGFR, KRAS, or ALK, thus multiple genomic alterations are extremely rare. Herein, we report a case of a 42‐year‐old man diagnosed with lung adenocarcinoma positive for a SDC4‐ROS1 fusion, who was treated with crizotinib followed by three cycles of chemotherapy. A biopsy acquired after disease progression revealed the original SDC4‐ROS1 fusion along with a KRAS point mutation (p.G12D).We reviewed the related literature to determine the frequency of gene mutations in non‐small cell lung cancer patients. A better understanding of the molecular biology of non‐small cell lung cancer with multiple driver genomic aberrations will assist in determining optimal treatment.

The deposition thickness is one of the most important parameters of debris flow . How to define the deposition shape along the viscous debris flow gully and how to calculate deposition thickness rationally were rarely studied in previous researches. This paper discussed the calculation method of deposition thickness of viscous debris flow based on theoretical deduction. Firstly, force analysis was carried out for a debris flow cell selected from the deposition . Then, the formula for calculating the deposition thickness of viscous debris flow was constructed based on deduction from the viewpoint of theoretical mechanics. At last, the deposition thickness under different slope gradients, yield stresses and densities was calculated based on the deduced formula. The results showed that the deposition thickness decreases with the increasing of the slope gradient and density, and increases with the increasing of the yield stress before the deposition thickness reaches to the maximum value