Acute arthritis of cats associated with feline calicivirus infection

Twelve specific pathogen-free cats were infected either by intra-articular inoculation or by contact exposure to one of two strains of feline calicivirus (FCV), either F65, a field strain originating from an outbreak of lameness in a group of cats, or a vaccine strain. Following either route of exposure, both strains induced signs typical of FCV infection including oral and nasal ulceration, conjunctivitis and ocular discharge. These signs were of equal severity for both virus strains, but overall, following either route of infection, F65 induced more severe disease than the vaccine strain, with marked pyrexia, lethargy and lameness. Vaccine virus only induced a relatively mild lameness following intra-articular inoculation. Gross pathological and histopathological lesions were seen in some of the joints, but again changes were more severe in the F65-exposed cats. Virus was isolated from both normal and affected joints from both groups of F65-exposed cats, and from a joint from each cat inoculated intra-articularly with vaccine virus. Mild transient lameness was also seen in one of two control cats inoculated intra-articularly, but no pathological changes were seen or virus isolated from joints. A cDNA probe used in RNA dot blot hybridisation experiments was found to be specific and more sensitive than virus isolation in detecting FCV in selected tissues. This may be useful in future studies on the pathogenesis of FCV disease and in studies on viral persistence in FCV carriers.     

BID: a novel BH3 domain-only death agonist

The BCL-2 family of proteins consists of both antagonists (e.g., BCL-2) and agonists (e.g., BAX) that regulate apoptosis and compete through dimerization. The BH1 and BH2 domains of BCL-2 are required to heterodimerize with BAX and to repress cell death; conversely, the BH3 domain of BAX is required to heterodimerize with BCL-2 and to promote cell death. To extend this pathway, we used interactive cloning to identify Bid, which encodes a novel death agonist that heterodimerizes with either agonists (BAX) or antagonists (BCL-2). BID possesses only the BH3 domain, lacks a carboxy-terminal signal-anchor segment, and is found in both cytosolic and membrane locations. BID counters the protective effect of BCL-2. Moreover, expression of BID, without another death stimulus, induces ICE-like proteases and apoptosis. Mutagenesis revealed that an intact BH3 domain of BID was required to bind the BH1 domain of either BCL-2 or BAX. A BH3 mutant of BID that still heterodimerized with BCL-2 failed to promote apoptosis, dissociating these activities. In contrast, the only BID BH3 mutant that retained death promoting activity interacted with BAX, but not BCL-2. This BH3-only molecule supports BH3 as a death domain and favors a model in which BID represents a death ligand for the membrane-bound receptor BAX.     

Aldosterone and dexamethasone stimulate calcineurin activity through a transcription-independent mechanism involving steroid receptor-associated heat shock proteins

1. PD 81,723 has been shown to enhance binding of adenosine to A1 receptors by stabilizing G protein-receptor coupling ('allosteric enhancement'). Evidence has been provided that in the perfused hearts and isolated atria PD 81,723 causes a sensitization to adenosine via this mechanism. 2. We have studied the effect of PD 81,723 in guinea-pig isolated atrial myocytes by use of whole-cell measurement of the muscarinic K+ current (I[K(ACh)]) activated by different Gi-coupled receptors (A1, M2, sphingolipid). PD 81,273 caused inhibition of I[K(ACh)] (IC50 approximately 5 microM) activated by either of the three receptors. Receptor-independent I[K(ACh)] in cells loaded with GTP-gamma-S and background I[K(ACh)], which contributes to the resting conductance of atrial myocytes, were equally sensitive to PD 81,723. At no combination of concentrations of adenosine and PD 81,723 could an enhancing effect be detected. 3. The compound was active from the outside only. Loading of the cells with PD 81,723 (50 microM) via the patch pipette did not affect either I[K(ACh)] or its sensitivity to adenosine. We suggest that PD 81,723 acts as an inhibitor of inward rectifying K+ channels; this is supported by the finding that ventricular I(K1), which shares a large degree of homology with the proteins (GIRK1/GIRK4) forming I[K(ACh)] but is not G protein-gated, was also blocked by this compound. 4. It is concluded that the functional effects of PD 81,723 described in the literature are not mediated by the A1 adenosine receptor-Gi-I[K(ACh)] pathway.     

A Practical Cross-Layer Mechanism For Fairness in 802.11 Networks

Many companies, organizations and communities are providing wireless hotspots that provide networking access using 802.11b wireless networks. Since wireless networks are more sensitive to variations in bandwidth and environmental interference than wired networks, most networks support a number of transmission rates that have different error and bandwidth properties. Access points can communicate with multiple clients running at different rates, but this leads to unfair bandwidth allocation. If an access point communicates with a mix of clients using both 1 Mb/s and 11 Mb/s transmission rates, the faster clients are effectively throttled to 1 Mb/s as well. This happens because the 802.11 MAC protocol approximate “station fairness”, with each station given an equal chance to access the media. We provide a solution to provide “rate proportional fairness”, where the 11 Mb/s stations receive more bandwidth than the 1 Mb/s stations. Unlike previous solutions to this problem, our mechanism is easy to implement, works with common operating systems and requires no change to the MAC protocol or the stations. Joseph Dunn received an M.S. in computer science from the University of Colorado at Boulder in 2003, and B. S. in coputer science and mathematics from the University of Arizona in 2001. His research interests are in the general area of computer systems, primarily focusing on security and scalability in distributed systems. He is currently working on his Ph.D. in computer science from the University of Colorado at Boulder. Michael Neufeld received a Ph.D. in Computer Science from the University of Colorado at Boulder in December of 2004, having previously received an M.S. in Computer Science from the University of Colorado at Boulder in 2000 and an A.B. in Computer Science from Princeton University in 1993. His research interests are in the general area of computer system, specifically concentrating on wireless networking, software defind/cognitive radio, and streerable antennas. He is currently a postdoc in the Computer Science department at the University of Calorado at Boulder pursuing research related to software defined radio and new MAC protocols for steerable phase array antennas. Anmol Sheth is a Ph.D. student in Computer Science at the University of Colorado at Boulder. He received his B.S. in Computer Science from the University of Pune, India in 2001. He has been co-leading the development of the MANTIS operating system. He has co-authored three papers include MAC layer protocol design, energy-efficient wireless communication, and adapting communications to mobility. Dirk Grunwald received his Ph.D. from the University of Illinois in 1989 and joined the University of Colorado the same year. His work addresses research and teaching in the broad area of “computer systems”, which includes computer architecture, operating systems, networks, and storage systems. His interests also include issues in pervasive computing, novel computing models, and enjoying the mountains. He is currently an Associate Professor in the Department of Computer Science and in Electrical and Computer Engineering and is also the Director of the Colorado Center for Information Storage. John Bennett is a Professor of Computer Science with a joint appointment in Electrical and Computer Engineering at the University of Colorado at Boulder. He also serves as Associate Dean for Education in the College of Engineering and Applied Science. He joined the CU-Boulder faculty in 2000, after serving on the faculty of Rice University for 11 years. While at Rice, Bennett pioneered a course in engineering design for both engineering and non-engineering students that has been emulated at several universities and high schools. In addition to other teaching awards, Bennett received the Keck Foundation National Award for Engineering Teaching Excellence for his work on this course. Bennett received his Ph.D. in 1988 from the University of Washington. Prior to completing his doctoral studies, he was a U.S. Naval Officer for several years and founded and served as President of Pacific Mountain Research, Inc., where he supervised the design and development of a number of commercial computing systems. Bennett's primary research interests are broadly focused in the area of distributed systems, and more narrowly in distributed information management and distributed robotic macrosensors.     

Early and intensive physiotherapy accelerates recovery postarthroscopic meniscectomy: results of a randomized controlled study

The efficacy of an early, intensive, supervised rehabilitation program to accelerate knee strength recovery in the first 3 weeks postmeniscectomy by arthroscopy was evaluated using a randomized controlled trial design. The maximal voluntary isokinetic strength of 31 men, randomly allocated to either a treatment (EXP) or a control (CTL) group, was measured twice by a blind rater: preoperatively (pretest) and 3 weeks postsurgery (posttest), using a computer-controlled Kin-Com dynamometer (Chattecx Corporation, Chattanooga, TN). Strength deficits of the operated leg at the pretest and posttest were established in percent of the values obtained for the sound leg at the pretest. In the interval between the surgery and the posttest, the patients of the EXP group (n = 15) received nine supervised treatments combined to home exercises whereas patients of the control group (n = 16) had no specific physiotherapy treatment but were given instructions in postsurgical management and prescribed exercises by the orthopedic surgeons. Patients of the EXP group had better knee extensor strength recovery than patients of the CTL group (ANCOVA, p < 0.001). The size of the strength difference (3 weeks postsurgery) between EXP and CTL subgroups (n = 8) matched according to preoperative deficits was as large as 26% and the residual deficits of the untreated patients were two to three times larger than those of the treated patients. The results of this study highlight the importance of instituting an early intensive and supervised rehabilitation program, especially for workers returning to a strenuous job requiring good knee extensor muscle function.