[Effects of different manure nitrogen input ratio on rhizosphere soil microbial biomass carbon, nitrogen and microbial quotient in double-cropping rice field]. / æœ‰æœºè‚¥æ°®æŠ•å ¥æ¯”ä¾‹å¯¹åŒå­£ç¨»ç”°æ ¹é™ åœŸå£¤å¾®ç”Ÿç‰©ç”Ÿç‰©é‡ç¢³ã€æ°®å’Œå¾®ç”Ÿç‰©ç†µçš„å½±å“.

To explore the characteristics of rhizosphere soil microorganisms in paddy fields with different manure nitrogen (N) input ratios at different growth stages of early and late rice in double-cropping rice system, a field experiment was conducted with five different treatments: 1) 100% N of chemical fertilizer (M1), 2) 30% N of organic matter and 70% N of chemical fertilizer (M2), 3) 50% N of organic matter and 50% N of chemical fertilizer (M3), 4) 100% N of organic matter (M4), and 5) no N fertilizer input as a control (M0). The rhizosphere soil microbial biomass carbon (MBC), microbial biomass nitrogen (MBN), and microbial quotient (SQ) of the paddy fields were measured using the fumigation-extraction and chemical analysis methods. The results showed that the rhizosphere MBC, MBN, and SQ of the paddy fields at main different growth stages of early and late rice were increased by fertilization, which increased first and then decreased with the development of rice growth period, peaked at the heading stage, and reached the minimum value at the maturity stage. The effects of different fertilization treatments were in order of M4＞M3＞M2＞M1＞M0, with no significant difference among M2, M3 and M4, but being significantly higher than M0. Therefore, the application of organic matter, and combined application of chemical fertilizer with organic matter could significantly increase the rhizosphere MBC, MBN, and SQ of the paddy fields at early and late rice growth period, while chemical fertilizer alone had little effect.

Synergistic function of Smad4 and PTEN in suppressing forestomach squamous cell carcinoma in the mouse.

The genetic bases underlying esophageal tumorigenesis are poorly understood. Our previous studies have shown that coordinated deletion of the Smad4 and PTEN genes results in accelerated hair loss and skin tumor formation in mice. Herein, we exemplify that the concomitant inactivation of Smad4 and PTEN accelerates spontaneous forestomach carcinogenesis at complete penetrance during the first 2 months of age. All of the forestomach tumors were invasive squamous cell carcinomas (SCCs), which recapitulated the natural history and pathologic features of human esophageal SCCs. A small population of the SCC lesions was accompanied by adenocarcinomas at the adjacent submucosa region in the double mutant mice. The rapid progression of forestomach tumor formation in the Smad4 and PTEN double knockout mice corresponded to a dramatic increase in esophageal and forestomach epithelial proliferation. The decreased expression of p27, p21, and p16 together with the overexpression of cyclin D1 contributed cooperatively to the accelerated forestomach tumorigenesis in the double mutant mice. Our results point strongly to the crucial relevance of synergy between Smad4 and PTEN to suppress forestomach tumorigenesis through the cooperative induction of cell cycle inhibitors.