SURALP is a 29 degrees-of-freedom full-body walking humanoid robot designed and constructed at Sabanci University - Turkey. The human-sized robot is actuated by DC motors, belt and pulley systems and Harmonic Drive reduction gears. The sensory equipment consists of joint encoders, force/torque sensors, inertial measurement systems and cameras. The control hardware is based on a dSpace digital signal processor. This paper reviews the design of this robot and presents experimental walking results. A posture zeroing procedure is followed after manual zeroing of the robot joints. Controllers for landing impact reduction, early landing trajectory modification, foot-ground orientation compliance, body inclination and Zero Moment Point (ZMP) regulation, and independent joint position controllers are used in zeroing and walking. A smooth walking trajectory is employed. Experimental results indicate that the reference generation and control algorithms are successful in achieving a stable and continuous walk.

In bilateral control applications, time delays in the communication channel have destabilizing effects and cause degradations in the performance of the system. In this paper, a sliding mode observer is used in conjunction with a disturbance observer to predict states of the slave system. Predicted states are then used in control formulation. Simulation and experimental results show that the proposed method avoids instability due to time delays in bilateral operation and provides satisfactory performance.

A total of 75,206 blood serum samples from dairy cattle and quarantined heifers was collected between 2001 and 2007 and analyzed for bovine leptospirosis by the microscopic agglutination test (MAT). Serovar Hardjo was used for testing of all sera, with the addition of 2 or 3 randomly chosen other serovars (Grippotyphosa, Icterohaemorrhagiae, Pomona, Bataviae, Canicola, and/or Saxcoebing). From the total number of sera tested, 1197 (1.59%) were serologically positive, with a decreasing tendency over the years of research. The most prevalent serovar was Pomona (1.32%), followed by Hardjo (0.52%) and Grippotyphosa (0.37%). The differences among the studied regions in terms of the distribution of serovars and seroprevalence values may be attributed to different farm management approaches and climatic conditions. It is believed that the decrease in seroprevalence toward the last years of investigation may be due to the application of permanent control strategies against leptospirosis and antibiotic therapy for all seropositive animals with an antibody titer equal to or higher than 1:100.

There is no doubt that the development of diagnostic criteria has contributed greatly to epidemiological research in prion diseases, and Heath and colleagues emphasize this in surveillance studies of variant Creutzfeldt-Jakob disease (vCJD). We caution, however, against a more broad application in clinical practice, particularly in governing decisions about clinical diagnosis, communication with patients/caregivers, and access to experimental therapies. The physician looking after a young patient with an unexplained rapidly progressive neuropsychiatric syndrome, dementia, or ataxia needs to make prompt clinical decisions. There are treatable alternative diagnoses, and an early firm diagnosis is essential. The pulvinar sign on magnetic resonance imaging is often not identified when patients are first imaged, and a requirement for a clinical duration of 6 months or greater makes a probable diagnosis impossible in the early stages of disease. Physicians who have cared for families affected by vCJD are aware of the complicated psychological issues generated by the perceived mismanagement of the bovine spongiform encephalopathy epidemic, which are often exacerbated by a delay or equivocation about diagnosis. Several families also choose experimental intracerebroventricular pentosan polysulfate therapy, which requires neurosurgery. In the context of these issues, the role of tonsillar biopsy is underemphasized by Heath et al and the criteria. In our experience of 60 biopsies, by far the largest series worldwide, tonsillar biopsy has 100% sensitivity and specificity, at any stage of the disease. Prion protein deposition in the tonsil can be patchy, and at least 20 germinal centers need to be examined. The number examined in 1 French case reported by Heath et al may not have been adequate to avoid a false-negative result. It is notable that of the 6 most recent patients suspected clinically of having vCJD in the United Kingdom, 3 did not meet epidemiological criteria for probable vCJD while alive. Two of these patients would have been misdiagnosed as sporadic CJD according to the updated clinical diagnostic criteria for sporadic Creutzfeldt-Jakob Disease criteria; typical vCJD was diagnosed at autopsy in both. In a third patient, with a heterozygous codon 129 genotype reported by Kaski et al, the pulvinar sign was not thought to be present by all neuroradiologists, and no tissue was examined. It is reasonable to expect that tonsillar biopsy may have made the correct diagnosis in each of these cases. Given experience with transfusion-associated secondary vCJD, vCJD prions are likely to be present in significant titer in human blood, a diagnostic blood test based on detection of the infectious agent is clearly possible in principle, and if technologically achieved, will necessitate a complete revision of how we approach diagnosis in this disease.

Cancer is caused by multiple genetic alterations leading to uncontrolled cell proliferation through multiple pathways. Malignant cells arise from a variety of genetic factors, such as mutations in tumor suppressor genes (TSGs) that are involved in regulating the cell cycle, apoptosis, or cell differentiation, or maintenance of genomic integrity. Tumor suppressor mouse models are the most frequently used animal models in cancer research. The anti-tumorigenic functions of TSGs, and their role in development and differentiation, and inhibition of oncogenes are discussed. In this review, we summarize some of the important transgenic and knockout mouse models for TSGs, including Rb, p53, Ink4a/Arf, Brca1/2, and their related genes.