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Conventional floating bridge systems used during emergency repairs, such as during wartime or after natural disasters, typically rely on passive rubber bearings or semi-active control systems. These methods often limit traffic speed, stability, and safety under dynamic conditions, including varying vehicle loads and fluctuating water levels. To address these challenges, this study proposes a novel Hydraulic Self-Adaptive Bearing System (HABS). The system integrates real-time position closed-loop control and a flexible support compensation method to enhance stability and adaptability to environmental changes. A modified three-variable controller is introduced to optimise load response, while a multi-state observer control strategy effectively reduces vibrations and improves traffic smoothness. A 1:15 scale prototype was constructed, and a co-simulation model combining MATLAB/Simulink and MSC Adams was developed to simulate various operational conditions. Results from both experiments and simulations demonstrate the HABS's ability to adapt to varying loads and environmental disturbances, achieving a 72% reduction in displacement and a 54% reduction in acceleration. These improvements enhance traffic speed, stability, and safety, making the system a promising solution for emergency and floating bridges, providing superior performance under challenging and dynamic conditions.

The neutralising ability of rabbit anti-gastrin-17 (G17) antiserum raised by Gastrimmune, an immunogen constructed of the N-terminal portion of human G17 conjugated to diptheria toxoid (DT), was evaluated. The anti-serum (denoted anti-G17: DT) was shown to displace 125[I] G17 from the gastrin receptors on AR42J cells. The therapeutic effect of the rabbit anti-G17:DT anti-serum was evaluated on a freshly derived human colorectal cancer cell line, AP5, which was shown to express both gastrin receptors and gastrin immunoreactivity as assessed by immunocytochemistry. Rabbit anti-G17:DT anti-serum was shown to block basal in vitro growth of AP5 cells when used at an antigen binding capacity of 3.75 x 10(-9) M. The same dilution of anti-serum completely reversed growth stimulated by human G17 at concentrations of 1 x 10(-10) and 1 x 10(-9) M but did not inhibit growth at 1 x 10(-8) M G17. When AP5 was grown as a xenograft in nude mice, the sensitivity to the proliferative effect of human G17 was maintained. In addition, the basal growth of AP5 xenografts was significantly reduced by i.v. infusion of rabbit anti-G17:DT anti-serum when compared to treatment with rabbit anti:DT control anti-serum. Thus anti-G17:DT antibodies raised by Gastrimmune may be of clinical value in gastrin-sensitive tumours.

The gastrointestinal tumour cell lines, MKN45G and C146 possessed oestrogen receptors (ER) of affinities 1.8 x 10(-8) and 5.2 x 10(-9) M respectively. C146 and MKN45G had enhanced proliferation in the presence of oestradiol (10(-8) and 10(-10) M). Fifty-six percent (5/9) of primary gastric and colorectal tumours had their proliferation enhanced by oestradiol. The anti-steroidal drug, danazol, inhibited the basal growth of MKN45G (10 micrograms ml-1 45% of the untreated control), C146 (10 and 5 micrograms ml-1, 20 and 48% of control, respectively) and 3/9 GI primary tumours (10 micrograms ml-1). Danazol competed with 3 [H]-Oestradiol for binding to ER on MKN45G and C146, at concentrations from 10 to 1 micrograms ml-1.

A hepatic invasive human colorectal xenograft model was derived in nude mice by selection through the liver of the parental cell line, C170. Following intraperitoneal injection, tumours selectively grew on the liver in > 80% of the animals within 15-20 days. The liver-invading xenograft line, renamed C170HM2, had a significantly greater expression of the Lewisx antigen compared to C170 (mean linear fluorescence per cell > 1000 compared with 500 for C170, P < 0.02). C170HM2 had significantly elevated proliferation (when compared with C170) in the presence of epidermal (P < 0.001) and basic fibroblast growth factor (P < 0.001). C170HM2 also mitogenically responded to type I collagen (derived from rat tails), unlike C170. C170HM2 tumours when invading the liver expressed both interstitial collagenase and gelatinase activity at the invading edge.

The gastrin receptor antagonist, CR2093, competed with 125I-gastrin-17 (5 x 10(-10) M) for binding to gastrin receptors on the rat pancreatic adenocarcinoma, AR42J (CR2093 concentration inducing 50% of 125I-gastrin-17 binding (IC50) was 8 x 10(-5) M), on the human gastric adenocarcinoma, MKN45 (IC50 5.5 x 10(-5) M) and the human colo-rectal adenocarcinoma C523 (IC50 greater than 10(-4) M). Intravenous administration of CR2093 (40 mg kg-1 day-1) reduced the gastrin-17 stimulated growth of AR42J xenografts in nude mice to below that of the original basal growth (P = 0.0166 from basal and P = 0.0109 from gastrin stimulated growth). CR2093 administration also reduced the gastrin-stimulated growth of MKN45 xenografts (P = 0.045) but failed to inhibit the gastrin enhanced proliferation of C523 xenografts. This may be related to the affinity (Kd) of the gastrin receptors present on the xenograft lines as the Kds of the two xenografts inhibited by CR2093 were 4.6 x 10(-10) M (AR42J) and 1.2 x 10(-9) M (MKN45) respectively whereas the Kd of C523 was of higher affinity (2.2 x 10(-10) M). GR antagonists may be a viable therapeutic option for gastrin receptor positive, gastro-intestinal tumours.