Biomedical subjects

V C Cox

Publications and source records attributed to V C Cox.

At least 19 recordsLinked to original sources

PubMed2005

SU proteins from virulent and avirulent EIAV demonstrate distinct biological properties.

Biologic activity of equine infectious anemia virus (EIAV) surface (SU) glycoprotein was assayed in a mouse model. Recombinant SU from virulent EIAV17 (SU17), administered intraperitoneally to mouse pups, induced dose-dependent diarrheal responses similar to those reported for SIV SU (Virology 277 (2000) 250). SU17 caused fluid accumulation without histological lesions in mouse intestinal loops, induced chloride secretory currents in Ussing chambers and increased inositol 1,4,5 triphosphate (IP3) levels in HT29 cells. An SU17 peptide, SU17(299-330), provoked a dose-dependent diarrheal response akin to enterotoxic peptides from SIV. In contrast, SU from an avirulent EIAV strain failed to induce a dose response in mouse pups and produced lower levels of activity than SU17 in Ussing chambers and IP3 assays. These results demonstrate that a mouse pup model is useful to monitor EIAV SU biologic activity, showing clear differences between the activities of SU derived from virulent and avirulent viruses, and may provide a useful screen of EIAV virulence.

Amino Acid Sequence↗

PubMed2004

Successful treatment of multidrug-resistant tuberculosis following drug-induced hepatic necrosis requiring liver transplant.

A 28-year-old female developed multidrug-resistant (MDR) tuberculous lymphadenitis following a trip to India. She was initially treated with a four-drug regimen of first-line anti-tuberculosis medications, but when sensitivities indicated resistance to isoniazid and rifampin, her regimen was altered to ciprofloxacin (CFX), pyrazinamide (PZA) and ethambutol. She subsequently developed a rash, flu-like symptoms and fever, which progressed to acute hepatic necrosis despite discontinuation of medication. The clinical presentation and subsequent investigations suggested a hypersensitivity reaction, possibly related to the quinolone. The patient subsequently had an orthoptic liver transplant; second-line anti-tuberculosis medications were restarted to which she responded clinically and radiologically. Our findings raise the possibility that the CFX and PZA combination was responsible for the hepatic necrosis. The patient also illustrates that active, even MDR tuberculosis is not a contraindication to hepatic transplant.

Adult↗

PubMed1993

Habenula lesions attenuate lateral hypothalamic analgesia in the formalin test.

The purpose of the experiment was to determine the role of the habenula complex (Hb) in lateral hypothalamic (LH) analgesia for tonic pain. The results demonstrate that lesions of the Hb attenuated LH analgesia in the formalin test. The result of Hb lesions cannot be attributed to non-specific brain damage since bilateral caudate nucleus lesions of similar extent to the Hb complex damage failed to modify the analgesic effect of LH stimulation. The critical damage was probably to the lateral habenula nucleus since it receives a major input from the LH. In addition to the primary finding, we observed that lesions of the Hb had no effect on the baseline response to formalin.

Analgesia↗

PubMed1992

Analgesia for tonic pain by self-administered lateral hypothalamic stimulation.

The present study was designed to determine if analgesia for tonic pain could be induced with self-administered lateral hypothalamic (LH) stimulation. The majority of studies of LH stimulation employed behaviorally non-contingent stimulation. According to some investigators behaviorally non-contingent LH stimulation might be aversive and consequently yield stress-induced analgesia rather than a primary analgesic effect. Other investigators have reported that non-contingent LH stimulation can be rewarding. Our findings indicate that LH analgesia for tonic pain can be obtained with self-administered LH stimulation. These findings indicate that the analgesia we have obtained in previous work is a primary effect and not dependent on stress induced by behaviorally non-contingent LH stimulation.

Analgesia↗

PubMed1992

The differential effects of lateral midbrain lesions on the two phases of formalin pain.

Lesions were placed in the lateral midbrain (LM) to determine the effects of disruption of paleo- and neospinothalamic systems, at the level of the midbrain, on the biphasic tonic pain response induced by formalin. During the first phase of formalin pain, subjects with LM lesions exhibited significantly less pain responding than did unoperated controls or subjects with lesions at another site, the habenula. During the second phase, there were no significant differences in pain responding among the three groups. The results suggest that the two phases are mediated by different neural substrates and specifically that Phase 2 appears to involve either neural substrates caudal to our LM lesions or sites rostral to the lesions but accessible via a more medial path.

Animals↗

PubMed1991

Analgesia for formalin-induced pain by lateral hypothalamic stimulation.

Few studies of analgesia induced by electrical brain stimulation have examined the effects of brain stimulation on responses to tonic pain stimuli. Recent evidence suggests that analgesia for tonic and phasic pain may involve different neural substrates. The present study examined the effects of lateral hypothalamic (LH) stimulation on responses to tonic pain induced by subcutaneous formalin. Our findings demonstrate that LH stimulation produced analgesia for tonic pain and that the effect is primary and not related to stress-induced analgesia. The results are discussed in relation to hypotheses regarding the different neural substrates involved in analgesia for tonic and phasic pain.

Analgesia↗

PubMed1980