The instability of the three-dimensional high-shear layer associated with a near-wall low-speed streak is investigated experimentally. A single low-speed streak, not unlike the near-wall low-speed streaks in transitional and turbulent flows, is produced in a laminar boundary layer by using a small piece of screen set normal to the wall. In order to excite symmetric and anti-symmetric modes separately, well-controlled external disturbances are introduced into the laminar low-speed streak through small holes drilled behind the screen. The growth of the excited symmetric varicose mode is essentially governed by the Kelvin–Helmholtz instability of the in ectional velocity profiles across the streak in the normal-to-wall direction and it can occur when the streak width is larger than the shear-layer thickness. The spatial growth rate of the symmetric mode is very sensitive to the streak width and is rapidly reduced as the velocity defect decreases flowing to the momentum transfer by viscous stresses. By contrast, the anti-symmetric sinuous mode that causes the streak meandering is dominated by the wake-type instability of spanwise velocity distributions across the streak. As far as the linear instability is concerned, the growth rate of the anti-symmetric mode is not so strongly affected by the decrease in the streak width, and its exponential growth may continue further downstream than that of the symmetric mode. As for the mode competition, it is important to note that when the streak width is narrow and comparable with the shear-layer thickness, the low-speed streak becomes more unstable to the anti-symmetric modes than to the symmetric modes. It is clearly demonstrated that the growth of the symmetric mode leads to the formation of hairpin vortices with a pair of counter-rotating streamwise vortices, while the anti-symmetric mode evolves into a train of quasi-streamwise vortices with vorticity of alternate sign.

These results suggest that determining F. nucleatum levels may help predict clinical outcomes in colorectal cancer patients. Further confirmatory studies using independent datasets are required to confirm our findings.

Stability experiments were made on plane Poiseuille flow generated in a long channel of a rectangular cross-section with a width-to-depth ratio of 27·4. By reducing the background turbulence down to a level of 0·05 %, we succeeded in maintaining the flow laminar at Reynolds numbers up to 8000, which is much larger than the critical Reynolds number of the linear theory, about 6000. The downstream development of the sinusoidal disturbance introduced by the vibrating ribbon technique was studied in detail at various frequencies in the range of Reynolds number from 3000 to 7500. This paper presents the experimental results and clarifies the linear stability, the nonlinear subcritical instability and the breakdown leading to the transition.

BACKGROUND: The canonical Wnt signalling pathway is activated in most sporadic colorectal cancers (CRCs). We previously reported that FZD7 functions as a receptor for the canonical Wnt signalling pathway in colon cancer cells. METHODS AND RESULTS: In this study, we examined the function of FZD7 in survival, invasion and metastatic capabilities of colon cancer cells. FZD7_siRNA transfection decreased cell viability of HT-29 and HCT-116 colon cancer cells. Expression of c-Jun, phosphorylation of JNK and c-Jun, and activation of RhoA were suppressed after FZD7_siRNA transfection into HCT-116 cells. In vitro invasion activity and Wnt target gene expression were also reduced in HCT-116 cells transfected with FZD7_siRNA. Liver metastasis of stable FZD7_siRNA HCT-116 cell transfectants in scid mice was decreased to 40 -50% compared to controls. The mRNA levels of FZD7 in 135 primary CRC tissues were examined by real-time PCR. FZD7 mRNA levels were significantly higher in stage II, III or IV tumours than in non-tumour tissues (Po0.005), and overall survival was shorter in those patients with higher FZD7 expression (Po0.001). CONCLUSION: These data suggest that FZD7 may be involved in enhancement of survival, invasion and metastatic capabilities of colon cancer cells through non-canonical Wnt signalling pathways as well as the canonical pathway.

Background Accumulating evidence shows an over-abundance of Fusobacterium nucleatum in colorectal tumour tissues. Although stool DNA testing of Fusobacterium nucleatum might be a potential marker for the detection of colorectal tumours, the difficulty in detecting Fusobacterium nucleatum in stool by conventional methods prevented further explorations. Therefore, we developed a droplet digital polymerase chain reaction (PCR) assay for detecting Fusobacterium nucleatum in stool and investigated its clinical utility in the management of colorectal tumours in a Japanese population. Methods Feces were collected from 60 healthy subjects (control group) and from 11 patients with colorectal non-advanced adenomas (non-advanced adenoma group), 19 patients with colorectal advanced adenoma/carcinoma in situ (advanced adenoma/carcinoma in situ (CIS) group) and 158 patients with colorectal cancer of stages I to IV (colorectal cancer group). Absolute copy numbers of Fusobacterium nucleatum were measured by droplet digital PCR. Results The median copy number of Fusobacterium nucleatum was 17.5 in the control group, 311 in the non-advanced adenoma group, 122 in the advanced adenoma/CIS group, and 317 in the colorectal cancer group. In comparison with that in the control group, the Fusobacterium nucleatum level was significantly higher in the non-advanced adenoma group, the advanced adenoma/CIS group and the colorectal cancer group. Conclusions This study illustrates the potential of stool DNA testing of Fusobacterium nucleatum by droplet digital PCR to detect individuals with colorectal tumours in a Japanese population.