Quantitative trait loci mapping of leaf angle and leaf orientation value in maize (Zea mays L.).

A major limiting factor for high productivity of maize (Zea mays L.) in dense planting is light penetration through the canopy. Plant architecture with a narrower leaf angle (LA) and an optimum leaf orientation value (LOV) is desirable to increase light capture for photosynthesis and production per unit area. However, the genetic control of the plant architecture traits remains poorly understood in maize. In this study, QTL for LA, LOV, and related traits were mapped using a set of 229 F(2:3) families derived from the cross between compact and expanded inbred lines, evaluated in three environments. Twenty-five QTL were detected in total. Three of the QTL explained 37.4% and five of the QTL explained 53.9% of the phenotypic variance for LA and LOV, respectively. Two key genome regions controlling leaf angle and leaf orientation were identified. qLA1 and qLOV1 at nearest marker umc2226 on chromosome 1.02 accounted for 20.4 and 23.2% of the phenotypic variance, respectively; qLA5 and qLOV5 at nearest bnlg1287 on chromosome 5 accounted for 9.7 and 9.8% of the phenotypic variance, respectively. These QTL could provide useful information for marker-assisted selection in improving performance of plant architecture with regard to leaf angle and orientation.

Time of the first defaecation and urination in very low birth weight infants.

The time for passage of the first stool and urine was studied in 111 infants who weighed less than 1500 g at birth. Delayed passage of the first stool (greater than 24 h) was noted in 25 (22.5%) infants of this group, including 7 cases (6.3%) in whom the delay was greater than 48 h (4 on the 3rd day, 2 on the 4th day, 1 on the 6th day of life, respectively). Three (2.7%) cases had delayed passage of the first urine (at 25, 25, and 45 h of life, respectively). Significant differences between the two groups with delayed and nondelayed passage of the first stool were noted in both the gestational age and in the time of the first enteral feeding. In very low birth weight infants, delay in the passage of the first stool is a common occurrence. This delay is probably due to physiological immaturity of the motor mechanisms of the gut, and lack of triggering effect of enteral feeds on gut hormones. As far as passage of the first urine was concerned, there were no significant perinatal factors found between the delayed and nondelayed groups.

[Propionic acidemia: report of a case that is successfully managed by peritoneal dialysis and sodium benzoate therapy].

Propionic acidemia is a rare hereditary disease which is an autosomal recessive disorder. Defect of propionyl CoA carboxylase results in abnormal accumulation of propionate and its metabolites which interfere the pathway of glycine cleavage and the urea cycle. This organic acidemia is characterized by a wide spectrum of clinical and biochemical findings, including recurrent vomiting, difficult feeding, lethargy, hypotonia, metabolic ketoacidosis, hyperglycinemia and hyperammonemia during the acute episodes. We present a male newborn infant who sustained this disorder and was managed successfully with blood exchange transfusion, peritoneal dialysis, supplemented with sodium benzoate and sodium bicarbonate therapy. Urine gas chromatography disclosed significant elevation of propionate and its metabolites which subsided 2 days after peritoneal dialysis. Special designed formula was then given with restriction of protein intake and supplement with sodium benzoate and sodium carbonate. Prenatal genetic counseling is necessary in further pregnancy. Diagnosis can be obtained when propionyl CoA carboxylase activity is low in cultured amniotic fluid cells or chorion villi sample or when there is abnormally high methylcitrate level in amniotic fluid.

cis elements and trans-acting factors involved in dimer formation of murine leukemia virus RNA.

The genetic material of all retroviruses examined so far consists of two identical RNA molecules joined at their 5' ends by the dimer linkage structure (DLS). Since the precise location of the DLS as well as the mechanism and role(s) of RNA dimerization remain unclear, we analyzed the dimerization process of Moloney murine leukemia virus (MoMuLV) genomic RNA. For this purpose we derived an in vitro model for RNA dimerization. By using this model, murine leukemia virus RNA was shown to form dimeric molecules. Deletion mutagenesis in the 620-nucleotide leader of MoMuLV RNA showed that the dimer promoting sequences are located within the encapsidation element Psi between positions 215 and 420. Furthermore, hybridization assays in which DNA oligomers were used to probe monomer and dimer forms of MoMuLV RNA indicated that the DLS probably maps between positions 280 and 330 from the RNA 5' end. Also, retroviral nucleocapsid protein was shown to catalyze dimerization of MoMuLV RNA and to be tightly bound to genomic dimer RNA in virions. These results suggest that MoMuLV RNA dimerization and encapsidation are probably controlled by the same cis element, Psi, and trans-acting factor, nucleocapsid protein, and thus might be linked during virion formation.

[Duplication of the alimentary tract: report of three cases].

Three cases of duplications of the alimentary tract are presented. Case 1 was a 5-month-old male baby. He was admitted due to copiously painless rectal bleeding. Tc-99m pertechnetate scanning revealed unusual tubular and spherical lesions. Laparotomy findings were that a tubular ileal duplication m assured 100cm or so in length and communicated with ileal lumen by its distal orifice. Moreover, there were 2 spherical duplications like ping-pong ball in morphology located in neighboring mesentery. Case 2 was a 2-day-old male newborn. He was admitted because of persistent bilious vomiting on his second day of life. Plain film x-ray revealed dilated stomach and scanty bowel gas. Laparotomy finding was that a cystic duplication measured 1.5cm in length which located in and obstructed the lumen of proximal jejunum. Also there was a distal orifice of duplication in communication with jejunal lumen. Case 3 was a 4-year-and-4-month-old boy who admitted after intermittently non-projectile vomiting for a period of 1 1/2 year. Sonography showed a calcification lesion at right upper quadrant of abdomen. Panendoscopy saw a refraction at second part of duodenum. The findings of laparotomy were that 2 tumor masses laid upon gastrocolic ligament. One was ossified soft tissue (gastrocolic ligament) with 1.5 x 1 x 0.8cm3 in size, and the other was cystic duplication of transverse colon in contact with beneath mesocolon. All duplications of 3 cases were lined with ectopic gastric and small intestinal mucosa, and ulcerative lesion was found in case 3 only. All lesions were resected and removed with good results.