An evolutionarily conserved gene, FUWA, plays a role in determining panicle architecture, grain shape and grain weight in rice.

Plant breeding relies on creation of novel allelic combinations for desired traits. Identification and utilization of beneficial alleles, rare alleles and evolutionarily conserved genes in the germplasm (referred to as 'hidden' genes) provide an effective approach to achieve this goal. Here we show that a chemically induced null mutation in an evolutionarily conserved gene, FUWA, alters multiple important agronomic traits in rice, including panicle architecture, grain shape and grain weight. FUWA encodes an NHL domain-containing protein, with preferential expression in the root meristem, shoot apical meristem and inflorescences, where it restricts excessive cell division. Sequence analysis revealed that FUWA has undergone a bottleneck effect, and become fixed in landraces and modern cultivars during domestication and breeding. We further confirm a highly conserved role of FUWA homologs in determining panicle architecture and grain development in rice, maize and sorghum through genetic transformation. Strikingly, knockdown of the FUWA transcription level by RNA interference results in an erect panicle and increased grain size in both indica and japonica genetic backgrounds. This study illustrates an approach to create new germplasm with improved agronomic traits for crop breeding by tapping into evolutionary conserved genes.

Phylogenetic and recombination analysis of rice black-streaked dwarf virus segment 9 in China.

Rice black-streaked dwarf virus (RBSDV) is an economically important virus that causes maize rough dwarf disease and rice black-streaked dwarf disease in East Asia. To study RBSDV variation and recombination, we examined the segment 9 (S9) sequences of 49 RBSDV isolates from maize and rice in China. Three S9 recombinants were detected in Baoding, Jinan, and Jining, China. Phylogenetic analysis showed that Chinese RBSDV isolates could be classified into two groups based on their S9 sequences, regardless of host or geographical origin. Further analysis suggested that S9 has undergone negative and purifying selection.

Usefulness of serum interleukin-33 as a prognostic marker of severe traumatic brain injury.

BACKGROUND: Interleukin-33 is recently identified as a brain injury biomarker. We determined whether serum interlerukin-33 concentrations are associated with inflammation, severity and prognosis after traumatic brain injury (TBI). METHODS: We detected serum interlerukin-33 concentrations of 102 healthy controls and 102 severe TBI patients, as well as serum concentrations of 3 inflammatory biomarkers (interleukin-6, tumor necrosis factor-alpha and C-reactive protein) and 7 cell-specific proteins (myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1) in 102 severe TBI patients. The recorded poor prognosis variables included acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury, posttraumatic cerebral infarction and six-month mortality and poor outcome (Glasgow score of 1-3). RESULTS: Median interlerukin-33 concentration of patients (692 pg/mL) was substantially raised, as compared to controls. Interlerukin-33 concentrations were significantly correlated with Glasgow coma scale (GCS) score and the preceding biomarkers concentrations. Interlerukin-33 concentration > 692 pg/mL emerged as an independent prognostic predictor and its discriminatory capability exceeded those of the above-mentioned inflammatory biomarkers concentrations and was in the range of GCS scores and the aforementioned cell-specific proteins concentrations. CONCLUSION: Ascending serum interlerukin-33 concentrations could reflect inflammation, severity and worse prognosis following TBI.

Prognostic significance of serum translocator protein in patients with traumatic brain injury.

BACKGROUND: Translocator protein (TP) is related to inflammation and is involved in brain injury. The objective of this study was to ascertain whether serum TP concentrations are associated with the severity and prognosis of traumatic brain injury (TBI). METHODS: We quantified the serum concentrations of TP in 106 healthy controls and 106 patients with severe TBI. Recorded prognostic variables included acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury, posttraumatic cerebral infarction, 6-month mortality and 6-month poor outcome (Glasgow Outcome Scale score of 1-3). Trauma severity was assessed by Glasgow coma scale (GCS) score. Extent of inflammatory response was indicated by serum interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-a) and C-reactive protein (CRP) concentrations. RESULTS: Patients had significantly higher serum TP concentrations than controls. Among patients, serum TP concentrations strongly and independently correlated with GCS score and serum IL-6, TNF-a and CRP concentrations. Serum TP was identified as an independent predictor for the preceding prognostic variables, its prognostic predictive ability was similar to that of GCS score and it also significantly improved prognostic predictive ability of GCS score. CONCLUSION: Serum TP may be intimately linked with in inflammation, disease progression and poor prognosis in TBI patients.

Serum ST2 as a potential prognostic biomarker for traumatic brain injury.

BACKGROUND: ST2, a receptor of interleukin-33, is involved in inflammation. We discerned the relationship between serum soluble ST2 (sST2) concentrations, inflammation, severity and prognosis following traumatic brain injury (TBI). METHODS: We measured serum sST2, interleukin-6, tumor necrosis factor-alpha, C-reactive protein, myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1 concentrations in 106 healthy controls and 106 severe TBI patients. We recorded long-term prognosis (i.e., 6-month mortality and functional outcome) and in-hospital major adverse events, including in-hospital mortality, acute lung injury, acute traumatic coagulopathy, progressive hemorrhagic injury and posttraumatic cerebral infarction. RESULTS: sST2 concentrations were significantly higher in patients than in controls and were significantly correlated with Glasgow coma scale (GCS) score and the preceding biomarkers concentrations. Serum sST2 was an independent prognostic predictor and its predictive ability significantly exceeded those of serum interleukin-6, tumor necrosis factor-alpha and C-reactive protein concentrations and was similar to those of GCS scores and serum concentrations of other remaining biomarkers. Moreover, sST2 concentrations significantly improved predictive ability of GCS score. CONCLUSION: Increased serum sST2 concentrations are significantly related to inflammation, severity and prognosis, substantialized ST2 as a potential prognostic biomarker for TBI.

Plasma visfatin, associated with a genetic polymorphism -1535C>T, is correlated with C-reactive protein in Chinese Han patients with traumatic brain injury.

Visfatin is a newly identified pro-inflammatory adipokine and a genetic polymorphism -1535 C>T located in the visfatin gene promoter has been suggested to be associated with the regulation of visfatin expression in some inflammatory illness. However, there were some conflicting results regarding whether this variant is functional or not. This study aimed to examine the relations of the -1535 C>T single nucleotide polymorphism (SNP) of visfatin gene to the plasma visfatin and C-reactive protein concentrations in traumatic brain injury (TBI). 318 Chinese Han patients with TBI were recruited in this study. Plasma visfatin and C-reactive protein levels were significantly different between the genotypes in the SNP-1535 C>T even after adjustment for age, sex and body mass index. The genotype C-C had the highest plasma visfatin and C-reactive protein concentrations. The plasma visfatin and C-reactive protein concentrations between the variant genotypes C-T and T-T did not differ significantly. Plasma visfatin level was significantly associated with plasma C-reactive protein level using multivariate linear regression. Thus, the SNP-1535 C>T of visfatin gene seemed to be potentially involved in the inflammatory component of TBI through a decreased production of visfatin.

Change in plasma visfatin level after severe traumatic brain injury.

Higher plasma visfatin concentration has been associated with ischemic stroke. Thus, we sought to investigate change in plasma visfatin level after traumatic brain injury and to evaluate its relation with disease outcome. Seventy-six healthy controls and 98 patients with acute severe traumatic brain injury were recruited. Twenty-seven patients (27.6%) died and 48 patients (49.0%) suffered from unfavorable outcome (Glasgow outcome scale score of 1-3) in 6 months. On admission, plasma visfatin level was increased in patients than in healthy controls and was highly correlated with Glasgow Coma Scale score. A multivariate analysis identified plasma visfatin level as an independent predictor for 6-month mortality and unfavorable outcome. According to receiver operating characteristic curve analysis, the predictive value of the plasma visfatin concentration was similar to Glasgow Coma Scale score's. In a combined logistic-regression model, visfatin did not improve the predictive value of Glasgow Coma Scale score. Thus, increased plasma visfatin level is associated with 6-month clinical outcomes after severe traumatic brain injury.

Clinical observation of gastric bypass in treatment of type 2 diabetes.

BACKGROUND: Roux-en-Y gastric bypass (GBP) is the main surgical procedure used in type 2 diabetes. The objective of this study was to evaluate the different types of GBP in treatment of type 2 diabetes. METHODS: Patients with type 2 diabetes were randomly divided into two groups: those who underwent gastrojejunal loop anastomosis bypass and those who underwent gastrojejunal Roux-en-Y bypass. Blood glucose alterations, operation time, and operation complications were observed. RESULTS: Gastrojejunal loop anastomosis bypass and gastrojejunal Roux-en-Y bypass were both effective in the treatment of selected patients with type 2 diabetes. Compared with gastrojejunal Roux-en-Y bypass, gastrojejunal loop anastomosis bypass had the advantages of easier implementation, shorter operation time, and fewer operation complications. CONCLUSIONS: Gastrojejunal loop anastomosis is effective in treatment of type 2 diabetes. It is safe, easy to implement, and worthy of clinical popularization.