[Driving Factors Analyze of Phytoplankton Community by Comparison of Population and Functional Groups and Water Quality Evaluation in Dongting Lake].

Phytoplankton is the most important component of water ecosystems, which could indicate the state of the water environment owing to its sensitivity to water environment variation. However, its response to the environment is influenced by classification methods. To understand the phytoplankton population(phyla and genera) and functional groups(FG) for driving response characteristics and applicability to the environment in Dongting Lake, a total of four samples were collected from the lake from March to December 2019, and the distribution characteristics of the phytoplankton population and functional groups and their responses to environmental factors were compared and analyzed. Meanwhile, the applicability of the TLI index, Shannon-Wiener index, and Q index was compared in Dongting Lake. The results showed that a total of 61 genera belonging to six phyla of phytoplankton were detected in Dongting Lake, which could be divided into 23 functional groups and nine dominant functional groups. The succession trend of functional groups was P/MP/D(March)→MP/P/J(June)→MP/H1(September)→Y/P/MP(December). The results of hierarchical segmentation showed that the population distribution and change in phytoplankton were driven by environmental factors more than the area in Dongting Lake. The main environmental factors affecting phytoplankton population and functional groups were water temperature(WT), permanganate index, dissolved oxygen(DO), conductivity(Cond), water level(WL), and total phosphorus(TP). RDA analysis showed that phytoplankton functional groups identified phytoplankton response to environmental factors better than phytoplankton population. It was shown that using the Q index to evaluate water quality had better applicability in Dongting Lake.

Signaling pathways and intervention therapies in sepsis.

Sepsis is defined as life-threatening organ dysfunction caused by dysregulated host systemic inflammatory and immune response to infection. Over decades, advanced understanding of host-microorganism interaction has gradually unmasked the genuine nature of sepsis, guiding toward new definition and novel therapeutic approaches. Diverse clinical manifestations and outcomes among infectious patients have suggested the heterogeneity of immunopathology, while systemic inflammatory responses and deteriorating organ function observed in critically ill patients imply the extensively hyperactivated cascades by the host defense system. From focusing on microorganism pathogenicity, research interests have turned toward the molecular basis of host responses. Though progress has been made regarding recognition and management of clinical sepsis, incidence and mortality rate remain high. Furthermore, clinical trials of therapeutics have failed to obtain promising results. As far as we know, there was no systematic review addressing sepsis-related molecular signaling pathways and intervention therapy in literature. Increasing studies have succeeded to confirm novel functions of involved signaling pathways and comment on efficacy of intervention therapies amid sepsis. However, few of these studies attempt to elucidate the underlining mechanism in progression of sepsis, while other failed to integrate preliminary findings and describe in a broader view. This review focuses on the important signaling pathways, potential molecular mechanism, and pathway-associated therapy in sepsis. Host-derived molecules interacting with activated cells possess pivotal role for sepsis pathogenesis by dynamic regulation of signaling pathways. Cross-talk and functions of these molecules are also discussed in detail. Lastly, potential novel therapeutic strategies precisely targeting on signaling pathways and molecules are mentioned.

[Fine root biomass, production, and turnover rate in a temperate deciduous broadleaved forest in the Maoer Mountain, China]. / å¸½å„¿å±±æ¸©å¸¦è½å¶é˜”å¶æž—ç»†æ ¹ç”Ÿç‰©é‡ã€ç”Ÿäº§åŠ›å’Œå‘¨è½¬çŽ‡.

Fine roots play an important role in energy flow and substance cycling in forests. How-ever, the estimates of biomass, production and turnover of fine roots remain large uncertainties, and the mechanism underlying local-scale spatial variation in fine roots is still unclear. In a temperate secondary forest in the Maoer Mountain in Northeast China, we investigated the vertical distribution of fine root biomass and necromass at the 0-100 cm profile and the dynamics, production and turnover rate of fine root in 0-20 cm soil layer. The sequential coring (including the Decision Matrix and the Maximum-Minimum formula) and the ingrowth core (3 cm diameter and 5 cm diameter) were compared in estimating production and turnover rate of fine roots. Forest stand variables that might affect fine roots were also explored. The results showed that 76.8% of fine root biomass and 62.9% of necromass concentrated in the 0-20 cm soil layer, and that both decreased exponentially with increa-sing soil depth. The seasonal variation in both fine root biomass and necromass was not significant in 0-20 cm soil layer, which might be related to the negligible snowfall in winter and the extremely high precipitation in summer. There was no significant difference in the results of the estimated fine root production between two diameter ingrowth cores. After log-transformed, fine root production and turnover rate estimated by the Decision Matrix, the Maximum-Minimum formula and ingrowth cores were significantly different among methods. With the increases of soil nutrient concentrations, fine root biomass/fine root necromass ratio significantly increased, fine root necromass significantly decreased, whereas fine root biomass, productivity, and turnover rate were not related to soil nutrient. There was a significant positive correlation between fine root production and aboveground woody biomass increment in the previous-year but not current-year.

Peg-Asparaginase-Associated Pancreatitis in Chemotherapy-Treated Pediatric Patients: A 5-Year Retrospective Study.

BACKGROUND: Asparaginase-associated pancreatitis (AAP) is one of the most common complications occurring in patients with asparaginase-treated acute lymphoblastic leukemia (ALL). Peg-asparaginase (peg-asp), a chemically recombined asparaginase with lower hyposensitivity and better patient tolerance, is now approved as the first line asparaginase formulation in ALL chemotherapy regimens. Due to the differences in pharmacokinetic characteristics and administration procedure between l-asp and peg-asp, this study aimed to investigate the clinical manifestations of peg-asp-associated pancreatitis. METHOD: Patients with peg-asp-associated pancreatitis diagnosed within a 5-year period (July 2014 to July 2019) were identified and retrospectively studied. The clinical manifestations, laboratory findings, and imaging results of patients with AAP were analyzed. AAP patients were further classified into mild/moderate and severe groups based on criteria used in previous studies. Clinical outcomes were compared between groups. RESULTS: A total of 38 patients were enrolled in this study. The underlying disease included ALL (n=35) and lymphoma (n=3). The majority of patients developed AAP during the first phase, called remission induction (n=26, 68.4%), after a median of 2 peg-asp doses (range: 1-11). The DVLP regimen (n=23) is the most common peg-asp regimen used in AAP patients. Abdominal pain occurred after a median of 14.5 days (range: 1-50) from the last peg-asp administration, accompanied by abdominal distension (n=14), nausea (n=17), vomiting (n=21), and fever (n=19). Serum amylase elevation was reported in all AAP patients, of whom 65.8% (n=25) exhibited an elevation in the level of this enzyme three times the upper normal level, fulfilling the Atlanta criteria. The level of serum lipase (median days of elevation=23 days, range: 4-75) was significantly elevated compared with that of serum amylase (median days of elevation=9 days, range: 2-71) and persisted at a markedly high level after the level of serum amylase returned to normal. Common local complications included abdominal ascites (n=10) and peripancreatic fluid collection (n=8). Approximately 42.1% (n=16) of patients with severe AAP experienced systemic complications (septic shock or hypovolemic shock) or severe local complications (pseudocyst), among whom 5 failed to recover. Approximately 84.8% (n=28/33) of the remaining patients resumed chemotherapy; among them, peg-asp formulation in 30.3% (n=10/33) of these patients was adjusted, while asparaginase treatment in 39.4% (n=13/33) was permanently discontinued. Five patients experienced an AAP relapse in later stages of asparaginase treatment. Comparison between mild/moderate and severe AAP patients showed a statistically significant difference in the number of pediatric intensive care unit stays (p=0.047), survival rate (p=0.009), AAP prognosis (p=0.047), and impacts on chemotherapy (p=0.024), revealing a better clinical outcome in mild/moderate AAP patients. CONCLUSION: Early recognition and management of AAP is essential in reversing the severity of AAP. The existing AAP criteria had a low strength in determining the severity of pediatric AAP. A well-defined AAP definition could help distinguish patients with high anticipated risk for redeveloping AAP and ALL relapse, in order to prevent unnecessary withdrawal of asparaginase. Our study could serve as a basis for conducting future large cohort studies and for establishing an accurate definition of pediatric AAP.

The Comparative Immunological Characteristics of SARS-CoV, MERS-CoV, and SARS-CoV-2 Coronavirus Infections.

Immune dysfunction and aberrant cytokine storms often lead to rapid exacerbation of the disease during late infection stages in SARS-CoV and MERS-CoV patients. However, the underlying immunopathology mechanisms are not fully understood, and there has been little progress in research regarding the development of vaccines, anti-viral drugs, and immunotherapy. The newly discovered SARS-CoV-2 (2019-nCoV) is responsible for the third coronavirus pandemic in the human population, and this virus exhibits enhanced pathogenicity and transmissibility. SARS-CoV-2 is highly genetically homologous to SARS-CoV, and infection may result in a similar clinical disease (COVID-19). In this review, we provide detailed knowledge of the pathogenesis and immunological characteristics of SARS and MERS, and we present recent findings regarding the clinical features and potential immunopathogenesis of COVID-19. Host immunological characteristics of these three infections are summarised and compared. We aim to provide insights and scientific evidence regarding the pathogenesis of COVID-19 and therapeutic strategies targeting this disease.

[The influence of induced autophagy in vitro on proliferation of multiple myeloma cells].

OBJECTIVE: To investigate the influence of autophagy on the survival and proliferation of multiple myeloma (MM) cells. METHODS: Multiple myeloma (MM) cell line U266 cell autophagy was induced by serum-free culture condition, and adding rapamycin or 3-MA respectively. The cells proliferation was observed. U266 cells, lymphoma cell Jurket under normal culture condition, and serum-free cultured Jurket cell were used as control group. The proliferation and apoptosis of cells were determined by CCK8 and flow cytometry, respectively. MDC staining were employed to detect the autophagy. The mRNA expression of Mtor and Beclin1 gene of U266 cells were assayed by RT-PCR. Protein LC3I/LCII and LAMP1 was analyzed by western blot. RESULTS: There was low level of autophagy in U266 cells, sera starvation increased the level of autophagy. Rapamycin upregulated autophagy of the U266 cells and stimulated their proliferation. But the autophagy level of sera starvation and rapamycin group declined when culture for 96h.3-MA had the same effects on U266 cells, although it was on 24 h. But rapamycin and 3-MA could inhibit cell proliferation under normal culture condition. Compared with normal culture condition, apoptosis of U266 cells increased significantly after 24h incubation in medium without sera \[(1.33 ± 0.09)% and (17.90 ± 1.46)%, respectively\] (P < 0.01). Rapamycin and 3-MA could inhibit the serum-free induced apoptosis \[(6.23 ± 0.12)% and (6.97 ± 0.03)%, respectively\](P < 0.01), but cell apoptosis was at the same level after 72 hour incubation \[(30.37 ± 0.27)%, (30.13 ± 1.93)% and (28.57 ± 2.83)%, respectively\] (P > 0.05). However, apoptosis of U266 cells decreased to 18.7% and 12.6% after removal of rapamycin and 3-MA. CONCLUSION: There is basically level of autophagy in MM cells which is higher than those in the Jurkat cells. Both Rapamycin and 3-MA can inhibit the cells proliferation under normal culture condition. Up-regulated autophagy promotes survival and proliferation of MM cells under sera deletion. Rapamycin strengthens this effect with limited duration. 3-MA has dual effects on cell autophagy.