Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple joint replacement is a viable option for rehabilitation of young polyarthritic patients with unsalvageable joints. Young polyarthritic patients in this part of the world suffer from chronic neglect because of ignorance, apathy and low socio-economic status. During the period of chronic neglect, these patients acquire extreme deformities of various joints either due to active disease (ankylosing spondylitis, rheumatoid arthritis) or irreversible changes in the joint configuration like ankylosis and soft-tissue contracture. Associated spine and thoracic cage affection create problems for anaesthesia and peri-operative positioning. We report 2 cases of multiple joint replacements for young polyarthritic patients who were bedridden for 6 to 11 years. Surgeries were performed in a phased manner and after extensive rehabilitation both patients were able to walk unaided. Various problems and difficulties encountered have been addressed so as to serve as a guide to surgeons who may have to deal with such unusual situations of chronic neglect. We also report a modified exposure technique without trochanteric osteotomy for total hip replacement, which is valuable in extreme external rotation ankylosis.
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PMID:Multiple joint replacement in chronically neglected polyarthritic patients: Two case reports. 1246 65

Normally, mice sleep during the day and are active at night. In Huntington's disease mice (R6/2 line) this circadian pattern disintegrates progressively over the course of their illness. Cognitive decline and apathy in R6/2 mice can be improved with sleeping drugs, suggesting that sleep disruption contributes to their neurological decline. We wondered if wakefulness was equally important. Here, we used two drugs to manage sleep/wake cycles in R6/2 mice, Alprazolam (to put them to sleep) and Modafinil (to wake them up). We found that both drugs improved cognitive function and apathy, but had a stronger effect when used in combination. Remarkably, beneficial effects on cognitive performance were also seen in vehicle-treated cage-mates of Alprazolam/Modafinil-treated mice, suggesting that behavioral intervention to regularize sleep/wake activity might be therapeutically useful. We suggest that focused management of sleep and wakefulness will slow the progression of cognitive decline and apathy in neurological conditions where sleep is disordered.
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PMID:Management of sleep/wake cycles improves cognitive function in a transgenic mouse model of Huntington's disease. 1945 May 69

Objective To observe the changes of expression of P-glycoprotein (PGP) in the brain of pentylenetetrazole (PTZ)-kindled epileptic mice after 2-chloride adenosine (2-CAdo) stimulation. Methods The C57BL/6 mice (n=40) were randomly divided into three groups: control group (n=8), PTZ group (n=16) and 2-CAdo group (n=16). The epileptic model was established by intraperitoneal injection of PTZ [30 mg/(kg.d)]. The control group were given the same amount of normal saline. The seizures were observed during PTZ kindling (kindling rate, latency time, start time and durations of seizures). After kindled, the 2-CAdo group was continuously injected with 2-CAdo [0.6 mg/(kg.d)] for 2 weeks. The other two groups were injected with normal saline instead. Then, all the mice of these three groups were sacrificed. HE staining was adopted to observe the histopathological changes of cerebral cortex and hippocampus of the mice, and the expression of PGP was detected by immunohistochemistry and Western blotting. Results At the time of seizures, the mice showed whole body tremor, hair erection, apathy, loss of appetite, cage offense and other abnormalities. HE staining showed that the damage of cerebral cortex and hippocampus of the 2-CAdo group was less than that of the PTZ group. Immunohistochemistry and Western blotting showed that the expression of PGP in the cerebral cortex of the 2-CAdo group was significantly lower than that in the control and PTZ groups. In the hippocampus, the expression of PGP in the 2-CAdo and PTZ groups was significantly higher than that in the control group, especially highest in the 2-CAdo group. Conclusion The 2-CAdo can reduce the damage of brain tissue, upregulate the expression of PGP in the hippocampus, and downregulate the expression of PGP in the cerebral cortex.
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PMID:[The 2-chloride adenosine alleviates the damage of brain tissues in pentylenetetrazole-kindled epileptic mice by regulating P-glycoprotein expression]. 2839 20