Diamond Stress View Radiograph for Thumb Metacarpophalangeal Hyperextension.

BACKGROUND: Successful surgical management of thumb carpometacarpal (CMC) arthritis requires treatment of coexisting metacarpophalangeal (MCP) hyperextension deformity when present. The surgeon's decision to offer thumb CMC arthritis patients the option of no additional treatment, MCP capsulodesis, or MCP arthrodesis relies on the severity of the MCP deformity measured in clinic. The authors present a novel patient-performed radiographic stress view to measure MCP hyperextension. METHODS: Fifty-seven thumbs in 30 consecutive patients offered thumb CMC arthroplasty were enrolled. Clinic goniometer measurements, patient-performed stress view radiographs, and intraoperative manual stress views of each MCP joint were documented for study. Paired samples t test was used to compare the differences between the preoperative measurements and intraoperative measurements of the right and left thumb groups. RESULTS: The clinic goniometer measurements were significantly different ( P = .0001) than the MCP stress view obtained while the patient was under anesthesia. The difference in the new patient-derived x-ray stress view was not statistically significant compared with the stress view under anesthesia in the left ( P = .91) or right ( P = .53) groups. CONCLUSIONS: This new patient-performed stress view of the MCP joint allows accurate, objective measurement of hyperextension to aide in the decision making and patient education for the need of additional MCP joint surgery when addressing thumb CMC arthritis.

Endogenous RGS proteins attenuate Galpha(i)-mediated lysophosphatidic acid signaling pathways in ovarian cancer cells.

Lysophosphatidic acid is a bioactive phospholipid that is produced by and stimulates ovarian cancer cells, promoting proliferation, migration, invasion, and survival. Effects of LPA are mediated by cell surface G-protein coupled receptors (GPCRs) that activate multiple heterotrimeric G-proteins. G-proteins are deactivated by Regulator of G-protein Signaling (RGS) proteins. This led us to hypothesize that RGS proteins may regulate G-protein signaling pathways initiated by LPA in ovarian cancer cells. To determine the effect of endogenous RGS proteins on LPA signaling in ovarian cancer cells, we compared LPA activity in SKOV-3 ovarian cancer cells expressing G(i) subunit constructs that are either insensitive to RGS protein regulation (RGSi) or their RGS wild-type (RGSwt) counterparts. Both forms of the G-protein contained a point mutation rendering them insensitive to inhibition with pertussis toxin, and cells were treated with pertussis toxin prior to experiments to eliminate endogenous G(i/o) signaling. The potency and efficacy of LPA-mediated inhibition of forskolin-stimulated adenylyl cyclase activity was enhanced in cells expressing RGSi G(i) proteins as compared to RGSwt G(i). We further showed that LPA signaling that is subject to RGS regulation terminates much faster than signaling thru RGS insensitive G-proteins. Finally, LPA-stimulated SKOV-3 cell migration, as measured in a wound-induced migration assay, was enhanced in cells expressing Galpha(i2) RGSi as compared to cells expressing Galpha(i2) RGSwt, suggesting that endogenous RGS proteins in ovarian cancer cells normally attenuate this LPA effect. These data establish RGS proteins as novel regulators of LPA signaling in ovarian cancer cells.