University of Texas Medical Branch

About: University of Texas Medical Branch is a education organization based out in Galveston, Texas, United States. It is known for research contribution in the topics: Population & Virus. The organization has 22033 authors who have published 38268 publications receiving 1517502 citations. The organization is also known as: The University of Texas Medical Branch at Galveston & UTMB.

Trends in length of stay, living setting, functional outcome, and mortality following medical rehabilitation.

Abstract: ContextChanges in reimbursement have reduced length of stay (LOS) for patients receiving inpatient medical rehabilitation. The impact of decreased LOS on functional status, living setting, and mortality is not known.ObjectiveTo examine changes in LOS, functional status, living setting, and mortality in patients completing inpatient rehabilitation.DesignRetrospective cohort study from 1994 through 2001 using information submitted to the Uniform Data System for Medical Rehabilitation.Setting and ParticipantsData were analyzed from 744 inpatient medical rehabilitation hospitals and centers located in 48 US states. A total of 148 807 patient records from 5 impairment groups (stroke, brain dysfunction, spinal cord dysfunction, other neurologic conditions, and orthopedic conditions) were examined. Patients’ mean age was 67.8 (SD, 15.8) years; the sample was 59% female and 81% non-Hispanic white.Main Outcome MeasuresDischarge setting, follow-up living setting, change in functional status, and mortality.ResultsMedian LOS decreased from 20 to 12 days (P<.001) from 1994 to 2001. The proportional decrease in median LOS was greatest (42%) for patients with orthopedic conditions. Mean days to follow-up remained constant from 89 in 1994 to 90 in 2001. Functional status was clinically stable, while efficiency (functional status change divided by LOS) increased significantly (P<.001). Rates of discharge to home and living at home at follow-up remained stable, ranging from 81% to 93%. However, mortality at 80- to 180-day follow-up increased from less than 1% in 1994 to 4.7% in 2001.ConclusionsLength of stay for inpatient rehabilitation decreased substantially from 1994 to 2001. Effectiveness as measured by change in functional status did not change clinically, and living setting did not change. Efficiency for functional outcomes improved but mortality at follow-up increased.

Okadaic acid inhibition of KCl cotransport. Evidence that protein dephosphorylation is necessary for activation of transport by either cell swelling or N-ethylmaleimide.

Abstract: The mechanism of activation of KCl cotransport has been examined in rabbit red blood cells. Previous work has provided evidence that a net dephosphorylation is required for activation of transport by cell swelling. In the present study okadaic acid, an inhibitor of protein phosphatases, was used to test this idea in more detail. We find that okadaic acid strongly inhibits swelling-stimulated KCl cotransport. The IC50 for okadaic acid is approximately 40 nM, consistent with the involvement of type 1 protein phosphatase in transport activation. N-Ethylmaleimide (NEM) is well known to activate KCl cotransport in cells of normal volume. Okadaic acid, added before NEM, inhibits the activation of transport by NEM, indicating that a dephosphorylation is necessary for the NEM effect. Okadaic acid added after NEM inhibits transport only very slightly. After a brief exposure to NEM and rapid removal of unreacted NEM, KCl cotransport activates with a time delay that is similar to that for swelling activation. Okadaic acid causes a slight increase in the delay time. These findings are all consistent with the idea that NEM activates transport not by a direct action on the transport protein but by altering a phosphorylation-dephosphorylation cycle. The simplest hypothesis that is consistent with the data is that both cell swelling and NEM cause inhibition of a protein kinase. Kinase inhibition causes net dephosphorylation of some key substrate (not necessarily the transport protein); dephosphorylation of this substrate, probably by type 1 protein phosphatase, causes transport activation.

Adherence of diarrheagenic Escherichia coli strains to epithelial cells.

Abstract: An important early step in the colonization of the human gastrointestinal tract by bacteria is the adhesion of the organism to the host surface. Although adhesion is essential to maintain members of the normal microflora in the intestine, it is also the critical early phase in all diarrheal infections caused by pathogenic Escherichia coli strains. It is important, therefore, to fully understand the mechanisms underlying E. coli adhesion and in that way to be able to develop methods of maintaining the intestinal normal microflora and to prevent pathogenic E. coli from initiating an infectious process.

Activation of the Hedgehog Pathway in Human Hepatocellular Carcinomas

Abstract: Liver cancers, the majority of which are hepatocellular carcinomas (HCCs), rank as the fourth in cancer mortality worldwide and are the most rapidly increasing type of cancer in the United States. However, the molecular mechanisms underlying HCC development are not well understood. Activation of the hedgehog pathway is shown to be involved in several types of gastrointestinal cancers. Here, we provide evidence to indicate that hedgehog signaling activation occurs frequently in HCC. We detect expression of Shh, PTCH1 and Gli1 in 115 cases of HCC and in 44 liver tissues adjacent to the tumor. Expression of Shh is detectable in about 60% of HCCs examined. Consistent with this, hedgehog target genes PTCH1 and Gli1 are expressed in over 50% of the tumors, suggesting that the hedgehog pathway is frequently activated in HCCs. Of five cell lines screened, we found Hep3B, Huh7 and PLC/PRF/5 cells with detectable hedgehog target genes. Specific inhibition of hedgehog signaling in these three cell lines by smoothened (SMO) antagonist, KAAD-cyclopamine, or with Shh neutralizing antibodies decreases expression of hedgehog target genes, inhibits cell growth and results in apoptosis. In contrast, no effects are observed after these treatments in HCC36 and HepG2 cells, which do not have detectable hedgehog signaling. Thus, our data indicate that hedgehog signaling activation is an important event for development of human HCCs.