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Chlorophyll a concentration [ρ(Chla)] in phytoplankton is used to understand algal biomass and the primary productivity of a water body. To investigate the seasonal dynamics of [ρ(Chla)] and their relationship with environmental factors Tiegang Reservoir at Guangdong China, continuous observation and analysis was carried out from April 2013 to June 2014. The distribution of algae had an obvious spatial heterogeneity, and the ρ(Chla) gradual increased from the southeast to the northwest of the reservoir. From April to early December 2013 and from late April to June 2014, the dominant algae was cyanobacteria. In other months, bacillariophyta were dominant. Chlorophyta were at a low level throughout the year. Multivariate analysis showed that water temperature (WT) was the primary driving factor of the spatio-temporal distribution of algae. The main environmental factors of cyanobacteria, bacillariophyta and chlorophyta were greatly different. Single environmental factors such as WT, total organic carbon (TOC), nitrate nitrogen (NO3--N), and chemical oxygen demand (COD) were significantly related to the competitiveness of cyanobacteria and bacillariophyta. And they can be used as early warning indexs for cyanobacteria and diatom blooms. The dual synergistic effects of WT and other environmental factors on the competitiveness of cyanobacteria and bacillariophyta were analyzed. A combination of environmental factors at high risk for cyanobacteria or diatoms were found. [ABSTRACT FROM AUTHOR]

Background: Mutations in 6 genes have been identified as being part of the etiology of amelogenesis imperfecta (AI) with various phenotypes in an isolated condition. Among them the FAM83H gene is the major contributor to the etiology of AI with unknown function. Objective: This study aims to determine the phenotypic and molecular characterization of Chinese AI patients and to analyze the structure and function of the FAM83H protein. Methods: We enrolled 6 hypocalcified AI and 3 hypoplastic AI families from the Chinese population. Mutation analysis was performed by amplifying and sequencing all exons including intron-exon borders for FAM83H and ENAM genes. Structural modeling and function analysis on the FAM83H protein were carried out by bioinformatic processing. Results: No obvious anterior open bite was observed in all the investigated individuals. Five mutations (c.906T>G, c.924dupT, c.973C>T, c.1354C>T and c.2029C>T) in the C-terminal of the FAM83H gene were revealed, respectively, in 5 out of 6 hypocalcified AI families, and a splicing mutation c.534 + 1G>A in the ENAM gene was identified in 1 out of 3 hypoplastic AI families. Structural models of the N- and C-terminal regions of FAM83H were generated by homology modeling. The predicted structure of the FAM83H N-terminal shows resemblance to that of glycosyltransferases with GT-A folds, and the predicted structure of the FAM83H C-terminal possesses similarity to type I collagen protein. Conclusions: To our knowledge, this is the first report of AI with specific molecular variations in families of Chinese descent. Our study provides new insights into the structure and function of the FAM83H protein. [ABSTRACT FROM AUTHOR]

SFTS virus ( SFTSV) is a novel bunyavirus that causes severe fever with thrombocytopenia syndrome ( SFTS), an emerging infectious disease that occurred in China in recent years, with an average case fatality rate of 10-12%. Intervention in the early clinical stage is the most effective measure to reduce the mortality rate of disease. To elucidate the natural course of and immune mechanisms associated with the pathogenesis of SFTSV, 59 laboratory-confirmed SFTS patients in the acute phase, who were hospitalized between October 2010 and September 2011, were enrolled in this study, and the patients sera were dynamically collected and tested for SFTSV viral RNA load, 34 cytokines or chemokines and other related laboratory parameters. All clinical diagnostic factors in the acute phase of SFTS were evaluated and assessed. The study showed that the severity of the disease in 11 (18.6%) patients was associated with abdominal pain (p 0.007; OR = 21.95; 95% CI, 2.32-208.11) and gingival bleeding (p 0.001; OR = 122.11; 95% CI, 6.41-2328). The IP-10, TNF- α, IL-6, IL-10, granzyme B and HSP70 levels were higher over the 7-8 days in severe cases, accompanied by altered AST, CK and LDH levels. HSP70 (p 0.012; OR = 8.29; 95% CI, 1.58-43.40) was independently correlated with the severity of the early acute phase of SFTSV infection. The severity of SFTS can be predicted based on the presence of symptoms such as abdominal pain and gingival bleeding and on the level of HSP70 in the acute phase of the disease. [ABSTRACT FROM AUTHOR]

The biological samples of oral genetic diseases and rare diseases are extremely precious. Collecting and preserving these biological samples are helpful to elucidate the mechanisms and improve the level of diagnose and treatment of oral genetic diseases and rare diseases. The standardized construction of biobanks for oral genetic diseases and rare diseases is important for achieving these goals. At present, there is very little information on the construction of these biobanks, and the standards or suggestions for the classification and coding of biological samples from oral and maxillofacial sources, and this is not conducive to the standardization and information construction of biobanks for special oral diseases. This consensus summarizes the background, necessity, principles, and key points of constructing the biobank for oral genetic diseases and rare diseases. On the base of the group standard "Classification and Coding for Human Biomaterial" (GB/T 39768-2021) issued by the National Technical Committee for Standardization of Biological Samples, we suggest 76 new coding numbers for different of biological samples from oral and maxillofacial sources. We hope the consensus may promote the standardization, and smartization on the biobank construction as well as the overall research level of oral genetic diseases and rare diseases in China.

Fusarium graminearum is the primary causal agent of Fusarium head blight (FHB) of wheat. The phenylpyrrole fungicide fludioxonil is not currently registered for the management of FHB in China. The current study assessed the fludioxonil sensitivity of a total of 53 F. graminearum isolates collected from the six most important wheat-growing provinces of China during 2018 and 2019. The baseline fludioxonil sensitivity distribution indicated that all of the isolates were sensitive, exhibiting a unimodal cure with a mean effective concentration for 50% inhibition value of 0.13 ± 0.12 μg/ml (standard deviation). Five fludioxonil-resistant mutants were subsequently induced by exposure to fludioxonil under laboratory conditions. Ten successive rounds of subculture in the absence of the selection pressure indicated that the mutation was stably inherited. However, the fludioxonil-resistant mutants were found to have reduced pathogenicity, higher glycerol accumulation, and higher osmotic sensitivity than the parental wild-type isolates, indicating that there was a fitness cost associated with fludioxonil resistance. In addition, the study also found a positive cross resistance between fludioxonil, procymidone, and iprodione, but not with other fungicides such as boscalid, carbendazim, tebuconazole, and fluazinam. Sequence analysis of four candidate target genes ( FgOs1 , FgOs2 , FgOs4 , and FgOs5 ) revealed that the HBXT2R mutant contained two point mutations that resulted in amino acid changes at K223T and K415R in its FgOs1 protein, and one point mutation at residue 520 of its FgOs5 protein that resulted in a premature stop codon. Similarly, the three other mutants contained point mutations that resulted in changes at the K192R, K293R, and K411R residues of the FgOs5 protein but none in the FgOs2 and FgOs4 genes. However, it is important to point out that the FgOs2 and FgOs4 expression of all the fludioxonil-resistant mutants was significantly ( P < 0.05) downregulated compared with the sensitive isolates (except for the SQ1-2 isolate). It was also found that one of the resistant mutants did not have changes in any of the sequenced target genes, indicating that an alternative mechanism could also lead to fludioxonil resistance.

Objective: Hepatocellular carcinoma (HCC) is a hypervascularized tumor. Aberrant angiogenesis is the main cause, which results in cancer growth and progression. It has been showed that microRNA-302 cluster (miR-302) may be associated with angiogenesis. Here, we aimed to identify the role of miR-302a/b/c in the regulation of cell angiogenesis in HCC., Patients and Methods: MRNA expression of miR-302a/b/c and MACC1 was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The protein of MACC1 was measured using Western blot. Cells proliferation, migration, and invasion abilities were investigated via Cell Counting Kit-8 (CCK-8) assay or transwell assay, respectively. Tube formatting assays were used to explore the tube formation capacity. The interaction among miR-302a/b/c was analyzed by luciferase assay., Results: The expression of miR-302a/b/c was greatly reduced while MACC1 expression, whether mRNA or protein was conspicuously elevated in HCC tissues and cells. Then, functional experiment results showed miR-302a/b/c overexpression and MACC1 down-regulation inhibited the proliferation, migration, invasion ability, and tube formation capacity of HUVECs. In addition, we detected that miR-302a/b/c directly targeted MACC1 and suppressed MACC1 expression, and miR-302a/b/c could suppress tumor angiogenesis in HCC by targeting MACC1., Conclusions: MiR-302a/b/c may function as a potential suppressor of tumor angiogenesis in HCC by targeting MACC1, indicating a promising target for HCC therapy.