The main objective of this research was to examine the feasibility of Multi-GNSS precise point positioning (PPP) in precision agriculture (PA) through a series of experiments with different working modes (i.e. stationary and moving) under different observation conditions (e.g. open sky, with buildings or with canopy). For the stationary test carried out in open space in the UK, the positioning accuracy achieved was 13.9 mm in one dimension by a PPP approach, and the repeatability of positioning results was improved from 19.0 to 6.0 mm by using Multi-GNSS with respect to GPS only. For the moving test carried out in similar location in the UK, almost the same performance was achieved by GPS-only and by Multi-GNSS PPP. However, for a moving experiment carried out in China with obstruction conditions, Multi-GNSS improved the accuracy of baseline length from 126.0 to 35.0 mm and the repeatability from 110.0 mm to 49.0 mm, The results suggested that the addition of the BeiDou, Galileo and GLONASS systems to the standard GPS-only processing improved the positioning repeatability, while a positioning accuracy was achieved at about 20 mm level in the horizontal direction with an improvement against the GPS-only PPP results. In space-constrained and harsh environments (e.g. farms surrounded with dense trees), the availability and reliability of precise positioning decreased dramatically for the GPS-only PPP results, but limited impacts were observed for Multi-GNSS PPP. In addition, compared to real time kinematic (RTK) GNSS, which is currently most commonly used for high precision PA applications, similar accuracy has been achieved by PPP. In contrast to RTK GNSS, PPP can provide high accuracy positioning with higher flexibility and potentially lower capital and running costs. Hence, PPP might be a great opportunity for agriculture to meet the high accuracy requirements of PA in the near future.

Cyclin D3 promotes cell cycle progression but its expression and prognostic significance in human colorectal cancer is unknown. This study assayed cyclin D3 expression against cell cycle phase fraction and Duke’s stage in 35 fresh human primary colorectal cancers. DNA content, cell cycle phase fraction and cyclin D3 expression were assessed by flow cytometry in disaggregated tumors. Cyclin D3 expression and S-phase fraction were independently related to Duke’s stage. In Duke’s stage C tumors, a higher proportion of cells expressed cyclin D3 (14.4 vs. 8.8%, mean; p < 0.05 by Mann-Whitney U test) and were in DNA synthesis (S) phase (21.1 vs. 9.7%, mean; p < 0.05 by Mann-Whitney U test). Neoplastic deregulation of cyclin D3 expression may provide a selective growth advantage which is related to stage in human colorectal cancer.

p53 accumulation is common in colorectal cancer, but effects on growth homeostasis are unclear. In this study, DNA content, cell cycle phase fractions and DNA strand-breaks consistent with apoptosis were assessed by flow cytometry in 42 fresh primary colorectal tumours and matched normal mucosa. p53 accumulation was assessed in 37 fixed tumour sections, by immunohistochemistry. In normal mucosa, 10.3 ± 6.6% (mean ± s.d.) cells were in DNA synthesis phase while 28.7 ± 17.9% showed apoptosis. A relationship suggestive of growth homeostasis, was observed between these parameters ( r = 0.8; P < 0.05). In cancers, a greater number of cells were in DNA synthesis phase (15.6 ± 12.9% tumour vs mucosa 10.3 ± 6.6%; P < 0.02) while fewer showed apoptosis than normal mucosa (18.5 ± 17.0% tumour vs mucosa 28.7 ± 17.9%; P < 0.01). DNA synthesis and apoptosis fractions were unrelated in cancers, suggesting growth dysequilibrium. p53 accumulation was detected in 59% (22/37) tumours and was associated with reduced apoptosis compared to p53-negative tumours or mucosa (14.8 ± 15% p53 accumulation vs 26.3 ± 18% p53-negative; P < 0.05; vs 28.7 ± 17.9% mucosa; P < 0.05). p53 accumulation was unrelated to DNA synthesis phase fractions. p53 accumulation is accompanied by reduced apoptosis which may accentuate growth dysequilibrium in colorectal cancer. © 1999 Cancer Research Campaign