No abstract

The intent of this study was to develop a technique for weight and ripeness estimation of oil palm (Elaeis guieensis Jacq. var. tenera) bunches from hyperspectral and RGB color images. In the experiments, color and hyperspectral images of the bunch were acquired from four different angles, each differing by 90 degrees. Acquired RGB color images were converted to HSI and L*a*b color space. Gray-scale thresholds were used to identify the area of the bunch and the area of space between the fruits. The total number of pixels in the bunch and the space were counted, respectively. In the hyperspectral images, the total number of pixels in the bunch was also counted from an image composed of three wavelengths (560 nm, 680 nm, and 740 nm), while the total number of pixels of space between fruits was obtained at a wavelength of 910 nm. From these sets of data, weight-estimation equations were determined by linear regression (LR) or multiple linear regression (MLR). As a result, the coefficient of determination (R 2 ) of actual weight and estimated weight were at a level of 0.989 and 0.992 for color and hyperspectral images, respectively. Estimation of oil palm bunch ripeness was also tested. Bunches belonging to 4 classes of ripeness (overripe, ripe, underripe, and unripe) were used for this study. Since ripeness estimation from overall data from a bunch was quite difficult, we focused on the difference in colors or reflectivity of the portion concealed and not-concealed with fronds. Euclidean distances between the test sample and the standard 4 classes of ripeness were calculated, and the test sample was classified into the ripeness class that had the shortest distance from the sample. In the classification based on color image, average RGB values of concealed and not-concealed areas were used, while in hyperspectral images the average intensity values of fruits pixels from the concealed area were used. The results of validation experiments with the developed estimation methods indicated acceptable estimation accuracy, and a possibility for practical use to estimate the ripeness of oil palm bunches.

The phytotoxic activities of the crude extract from the cyanobacterium, Hapalosiphon sp., on the initial growth and root cell division of several plant species were investigated. Although the germination percentages of the plants were not affected by the extract, their root and shoot growth were remarkably suppressed, depending on the extract concentrations. Roots were more sensitive to the extract than shoots and the sensitivity, determined by the I 50 concentrations between the susceptible and tolerant species, differed by 5 and 11 times in dicotyledonous and monocotyledonous plants, respectively. The mitotic index for wheat (Triticum aestivum L. cv. Norin 61) root cells was not affected, but the mitotic index for onion (Allium cepa L. cv. Raputa II) was reduced with the increasing concentration of the extract. In the onion root meristem, the number of cells in prophase, metaphase, anaphase, and telophase were decreased significantly with 6 g DW L −1 (g dry weight of algae L −1 ). This suggests that the extract might inhibit the processes regulating the entry of cells into mitosis.

The extracts of wood, bark, and leaves of Haldina cordifolia were evaluated for their phytotoxicity on seed germination, seedling growth, and root cell viability in two weeds (Mimosa pigra and Cenchrus echinatus) and two crop plants (Vigna radiata and Oryza sativa cv. Khao Dawk Mali 105). Seeds were grown in petri dishes and treated with 5 ml of extracts at various concentrations: 0.5, 1.0, 5.0, and 10.0 mg/ml. The inhibitory effect on seed germination increased with increasing concentration of the extract treatment. Bark extract was the most toxic at the highest concentration, causing total inhibition of germination in all tested seeds except in V. radiata. Low concentrations (0.5 and 1.0 mg/ml) of wood extract inhibited shoot and root growth in C. echinatus by 31.0%-56.0% and 67.0%-71.0%, respectively. Interestingly, it promoted root growth in M. pigra by 106.9%-108.8% (at low concentrations) and in V. radiata (at all concentrations) by 108.1%-108.9% (shoot) and 108.8%-120.1% (root). Bark extract inhibited seedling growth in all tested plants at different levels. Strong inhibition was found in roots of O. sativa (3.0%-4.0%). The result from Evans blue uptake study suggested that the H. cordifolia extract did not directly affect the root cell viability. Surprisingly, we found that M. pigra and V. radiata treated with the extracts at low concentrations had increasing number of lateral roots, suggesting that H. cordifolia extract could act as a plant growth regulator (PGR) and an herbicide at the same time, depending on concentration and target plant.

Crude extract-induced oxidative damage using the cyanobacterium, Hapalosiphon sp., was investigated in wheat seedlings (Triticum aestivum L. cv. Norin 61) and onion seedlings (Allium cepa L. cv. Raputa II).The analysis of root cell viability or cell death using Evans blue uptake showed that the root-tip cells of wheat and onion lost viability after 24 h and 48 h treatment with 3 g dry weight (DW) L -1 of the crude extract, respectively. Lipid peroxidation was induced in the roots of both species and the shoots of onion, whereas no increase in lipid peroxide formation was observed in the wheat shoots. In onion, the degree of random DNA fragmentation increased with the increasing concentration of the extract and laddering of the DNA was observed with 6 g DW L -1 of the extract, but no apparent DNA ladder formation occurred in the wheat. Pretreatment for 1 h with the NADPH oxidase inhibitors, diphenyleneidonium or imidazole, reduced the crude extract-induced root cell death in both species. From the results, we suggest that the Hapalosiphon sp. crude extract might enhance reactive oxygen species (ROS) production, which causes membrane lipid damage and fragmentation of the DNA of plant cells, resulting in cell death and growth inhibition. The crude extractmediated phytotoxic damage might be caused by ROS, triggered by NADPH oxidase.