Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Virginia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed2002

Tourism and the market revolution. [Review of: Lewis, CM. Ladies and gentlemen on display: planter society at the Virginia Springs, 1790-1860. Charlottesville: University Press of Virginia, 2001; Corbett, T. The Making of American resorts: Saratoga Springs, Ballston Spa, Lake George; Sterngass, J. First resorts: pursuing pleasure at Saratoga Springs, Newport, and Coney Island. Baltiremore: Johns Hopkins University Press, 2001].

Explore the source record for details and available documents.

Health Resorts↗
PubMed2000

Assessment of school-based health centers in a rural state: the West Virginia experience.

PURPOSE: To assess the capability of school-based health centers (SBHCs) to provide access to health care for rural youth. METHODS: Review of annual patient records from SBHCs in West Virginia. Ten of 24 SBHCs in West Virginia in operation from July 1994 to June 1997 were selected for the study. Enrollment and utilization rates were generated for each site. A comparison was made between rates of enrollment, utilization, and annual visits among youth with private insurance, those covered by Medicaid, and youth without insurance. Rural and urban SBHCs within West Virginia were compared based on enrollment, utilization, and visit rates. The diagnostic categories were analyzed. Finally, enrollment rates, utilization rates, and insurance status for the West Virginia SBHCs were compared with national norms. RESULTS: Enrollment rates rose steadily during the study period from 27% in Year 1 to 64% by the end of Year 3. The utilization rate was 67% in Year 3. The youth with either Medicaid or no insurance comprised 52% of enrollees, but they accounted for 63% of all visits. West Virginia SBHCs have a higher rate of Medicaid users than the national average for SBHCs, and the annual visit rate for West Virginia youth is higher than the national average for nonmetropolitan adolescents. The enrollment rate of 64% is slightly higher than the national average for SBHCs. Within West Virginia, the enrollment rate in rural schools was significantly higher, 86% compared to 46% (p < .001), and the utilization rate was 70% in rural centers compared to 63% in the urban centers (p < .001). CONCLUSION: When SBHCs are available in rural areas, students use them. In West Virginia, SBHCs have contributed to providing access to health care for rural youth.

Adolescent↗
PubMed1991

Hospital CEOs' priorities and perceptions regarding industry issues and the Virginia Hospital Association's activities.

Based on a survey of Virginia hospital CEOs, it was revealed that four industry issues are causing a high degree of concern, namely Medicare/Medicaid reimbursement policies, personnel shortages, indigent care, and increased operating expenses. Each of these issues will be discussed regarding the VHA's activities to devise possible solutions. Regarding Medicare, the VHA has worked closely with the American Hospital Association in their federal advocacy efforts encouraging members to write, call, and visit their Congressional representatives to persuade them to pass legislation increasing the Medicare budget. Regarding Medicaid, which is administered by each state and in Virginia involves a 50/50 sharing of the funding between the federal and state governments, the VHA has challenged what it believes to be an illegal hospital reimbursement system through the federal judicial system. While the process is continuing, the VHA is encouraged by the U.S. Supreme Court's decision (July 1990) affirming hospitals' and all other health care providers' right, to pursue via the judicial process their allegation that a state is violating federal law by setting inadequate and inequitable Medicaid reimbursement rates to hospitals. In order to address the personnel shortages issue, the VHA has actively addressed recruitment and retention challenges by establishing a Health Manpower Resource Center and hiring a full-time director. This office targets high school students, second-career adults, and current health care professionals through communication and education programs. The area of indigent care represents one of the VHA's most notable achievements to date. This entails the recent Virginia legislation creating the Indigent Care Trust Fund. This fund's initial amount is some $15 million and represents an approximate 60/40 contribution ratio involving both the State of Virginia and hospitals in Virginia. A formula has been developed for each hospital in Virginia to assess how sensitive they are to indigent care patients, which includes patients who are either in households whose annual income is below the federal poverty level and/or patients who do not have health care insurance. Those Virginia hospitals who are less sensitive to indigent care will contribute to this fund, while those who have more exposure to indigent care patients will be reimbursed from it. Legislation will be proposed to the state legislature to broaden the contributory base to the Indigent Care Trust Fund by requiring employers who do not currently offer health care insurance to their employees to also contribute to the fund. Reimbursements from the fund to Virginia hospitals are scheduled to begin in FY 1991.(ABSTRACT TRUNCATED AT 400 WORDS)

Attitude of Health Personnel↗
PubMed2003

Identification by gene deletion analysis of barB as a negative regulator controlling an early process of virginiamycin biosynthesis in Streptomyces virginiae.

The Streptomyces virginiae gamma-butyrolactone autoregulator virginiae butanolide is a low-molecular-weight Streptomyces hormone eliciting virginiamycin biosynthesis through its binding to the specific receptor protein, BarA. Immediately downstream of barA lies barB, the transcription of which is tightly repressed by BarA in the absence of virginiae butanolide and derepressed in its presence. Thus, BarB is next to BarA on the virginiae butanolide-BarA signaling cascade. An in-frame 279-bp deletion was introduced into the barB allele, which rendered it inactive by eliminating the majority of the coding region, including the helix-turn-helix DNA-binding motif. No significant change was observed with the Delta barB mutant with respect to the timing or amount of virginiae butanolide production, or the morphological differentiation on solid media, indicating that barB neither participates in virginiae butanolide biosynthesis nor in cytodifferentiation. In contrast, analysis of virginiamycin production in the Delta barB mutant revealed that production of both virginiamycin M(1) and virginiamycin S occurred immediately after virginiae butanolide production, 2-3 h earlier than in the wild-type strain, indicating that BarB participates in the temporal retardation of virginiamycin production after virginiae butanolide inactivates the repressor function of BarA. RT-PCR analysis of the transcription of several genes surrounding barA-barB by the Delta barB mutant indicated that BarB plays a negative regulatory role, directly or indirectly, in the transcription of barZ, vmsR, and orf5 located upstream of barB.

Amino Acid Sequence↗
PubMed1998

The detection of hemorrhagic proteins in snake venoms using monoclonal antibodies against Virginia opossum (Didelphis virginiana) serum.

Most snakes and a few warm-blooded animals have a resistance to snake venoms because of naturally occurring antihemorrhagins found in their sera. The antihemorrhagins in serum of Virginia opossum (Didelphis virginiana) neutralize hemorrhagic activity by binding to hemorrhagins in snake venoms. The binding characteristic of antihemorrhagins in D. virginiana serum was used to develop a five-step western blot. The detection of hemorrhagic proteins were measured indirectly with antihemorrhagins in Virginia opossum serum and with DV-2LD#2, a monoclonal antibody specific for Virginia opossum antihemorrhagins. Snake venoms were separated by native-PAGE, transferred to a Millipore Immobilon-P membrane and then incubated with crude Virginia opossum serum. The hemorrhagins in snake venom bind to antihemorrhagins in Virginia opossum serum which react with DV-2LD#2 a monoclonal antibody that is specific for Virginia opossum antihemorrhagins. DV-2LD#2 monoclonal antibody inhibits antihemorrhagic activity in Virginia opossum serum when mixed in equal amounts. The inhibition of antihemorrhagins by DV-2LD#2 monoclonal antibody suggests specificity. DV-2LD#2 monoclonal antibody does not recognize antihemorrhagins in gray woodrat (Neotoma micropus) serum. The five-step western blot reveals two well-defined bands which represent hemorrhagins found in Western diamondback rattlesnake (Crotalus atrox) venom. Venoms from 15 different snake species were examined to determine the usefulness of the five-step western blot. Other hemorrhagic venoms (Great Basin rattlesnake (C. viridis lutosus), Prairie rattlesnake (C. viridis viridis), Tancitaran dusky rattlesnake (C. pusillus), Northern Mojave rattlesnake (C. scutulatus scutulatus type B) and Northern Pacific rattlesnake (C. v. oreganus)) had one single band in the five-step western blot. DV-2LD#2 did not bind to the non-hemorrhagic venoms and reacted with 50% of the hemorrhagic venoms used in this study. The monoclonal antibody, CAH, reacted with all the hemorrhagic venoms except for the venom of the King cobra (Ophiophagus hannah) and did not react with the non-hemorrhagic venoms. The hemorrhagic binding site of CAH monoclonal antibody and the antihemorrhagin in Virginia opossum are different binding sites. The five-step western blot will be a very useful assay for determining hemorrhagic activity without using live animals.

Animals↗
PubMed2000

Identification of an AfsA homologue (BarX) from Streptomyces virginiae as a pleiotropic regulator controlling autoregulator biosynthesis, virginiamycin biosynthesis and virginiamycin M1 resistance.

Virginiae butanolide (VB)-BarA of Streptomyces virginiae is one of the newly discovered pairs of a gamma-butyrolactone autoregulator and the corresponding receptor protein of the Streptomyces species, and has been shown to regulate the production of antibiotic virginiamycin (VM) in S. virginiae. A divergently transcribed barX gene is situated 259 bp upstream of the barA gene, and the BarX protein has been shown to be highly homologous (39.8% identity, 74. 6% similarity) to S. griseus AfsA. Although AfsA is thought to be a biosynthetic enzyme for A-factor, another member of the family of gamma-butyrolactone autoregulators, the in vivo function of S. virginiae BarX was investigated in this study by phenotypic and transcriptional comparison between wild-type S. virginiae and a barX deletion mutant. With the same growth rate as wild-type S. virginiae on both solid and liquid media, the barX mutant showed no apparent changes in its morphological behaviour, indicating that barX does not participate in morphological control in S. virginiae. However, the barX mutant became more sensitive to virginiamycin M1 than did the wild-type strain (minimum inhibitory concentration, 50 microgram ml-1 compared with > 200 microgram ml-1) and exhibited reduced VB and VM production. The VM production was not restored by exogenous addition of VB, suggesting that BarX per se is not a biosynthetic enzyme of VBs but a pleiotropic regulatory protein controlling VB biosynthesis. DNA sequencing of a 5.6 kbp downstream region of barX revealed the presence of five open reading frames (ORFs): barZ, encoding a BarB-like regulatory protein; orf2, encoding a Streptomyces coelicolor RedD-like pathway specific regulator; varM, encoding a homologue of ATP-dependent transporters for macrolide antibiotics; orf4, encoding a homologue of beta-ketoacyl ACP/CoA reductase; and orf5, encoding a homologue of dNDP-glucose dehydratase. Reverse transcription polymerase chain reaction (RT-PCR) analyses of the downstream five genes together with those of the three upstream genes (barA, barB, encoding a regulatory protein; and varS, encoding a virginiamycin S specific transporter) revealed that, in the barX mutant, the transcriptions of barZ, orf2, varM and orf5 were completely repressed and those of barB and varS were derepressed. Because free BarA (BarA in the absence of VB) in wild-type S. virginiae represses the transcription of bicistronic barB-varS operon through binding to a specific DNA sequence (BarA-responsive element, BARE) overlapping the barB transcriptional start site, the derepression of barB-varS transcription in the barX mutant suggested that the in vivo function of BarA was impaired by the lack of BarX protein. Gel-shift assays revealed that BarA easily lost its DNA-binding activity in the absence of BarX but that the defect was restored by the presence of recombinant BarX as a fusion with maltose-binding protein (MBP-BarX), whereas MBP-BarX itself showed no DNA-binding activity, indicating that BarX is likely to be a co-repressor of BarA, enforcing the DNA-binding activity of BarA through protein-protein interactions.

Bacterial Proteins↗
PubMed1999

Patterns of infestation by adult Dermacentor variabilis (Acari: Ixodidae) in a mark-recapture study of raccoons (Mammalia: Carnivora) and Virginia opossums (Mammalia: Didelphimorphia) in Tennessee.

A mark-recapture study of raccoons (Procyon lotor L.) and Virginia opossums (Didelphis virginiana Kerr) was conducted from February 1991 through April 1994 to determine host interactions with adult Dermacentor variabilis Say. We captured 1,293 raccoons and Virginia opossums during the 3-yr study (140 individual raccoons and 160 individual Virginia opossums) with 1,895 adult D. variabilis collected. Raccoons had a significantly higher mean intensity and higher prevalence of adult ticks than Virginia opossums (Mann-Whitney Z = 6.15, chi 2 = 51.9, P < 0.001). Mean intensity follows Margolis et al. (1982) as being the mean number of parasite species per infected host. Prevalence follows Margolis et al. (1982) as being the number of individuals of the host species infected with a parasite species divided by the number of hosts examined. The time required for a higher prevalence and mean intensity of ticks to occur on raccoons than Virginia opossums was < 7 d. No significant differences occurred between the mean intensity or prevalence of D. variabilis between sexes or among age classes of raccoons. Significant differences in prevalence and mean intensity of ticks occurred between sexes and among age classes of Virginia opposums. Infestation increased by 0.64 ticks per day on Virginia opossums and 1.77/d on raccoons during the first 7 d. The base host finding rate (ticks per host per day) of adult D. variabilis on Virginia opossums was 0.064 and 0.053 on raccoons. Tick interactions with hosts are quantified and may reflect behavioral differences between sexes and among age groups intraspecifically, and host preferences of adult D. variabilis interspecifically.

Animals↗
PubMed1992

Purification and molecular cloning of a butyrolactone autoregulator receptor from Streptomyces virginiae.

In streptomyces, low molecular weight compounds termed "autoregulators" have been isolated as primary signal molecules for triggering secondary metabolism and/or cytodifferentiation. Streptomyces virginiae produces a set of autoregulators termed virginiae butanolide A-E which trigger virginiamycin production, and possesses a high-affinity virginiae butanolide receptor (Kim, H.S., Nihira, T., Tada, H., Yanagimoto, M., and Yamada, Y. (1989) J. Antibiot. (Tokyo) 42, 769-778). The virginiae butanolide receptor has now been purified to apparent homogeneity with 14,000-fold purification and an 8.6% activity yield. The purified receptor showed a Mr of 36,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and a maximum ligand binding of 33.0 nmol/mg protein, indicating a 1:1 binding stoichiometry (1.18 mol of virginiae butanolide/36 kDa of protein) between virginiae butanolides and the receptor. Due to a blockage at the amino terminus, fragment peptides were generated by lysyl endopeptidase and five partial amino acid sequences were determined. The gene (vbrA) encoding the virginiae butanolide receptor was identified on a 5.0-kbp BamHI fragment by hybridization to synthetic oligonucleotide probes, cloned, and sequenced. Nucleotide-sequence analysis predicted a 319-amino acid open reading frame (vbrA) in which all the partial amino acid sequences of the receptor appeared, and 166 bp downstream from it another open reading frame for a 144-amino acid protein which was designated as a ribosomal protein L11 from its high homology (62-64%) to the amino acid sequences of ribosomal protein L11 of several origins, and thus denoted as rplK. The C-terminal half of VbrA showed 36% overall homology to the amino acid sequence of an essential protein (NusG) of Escherichia coli. Furthermore, the gene assembly of vbrA-rplk of S. virginiae closely resembled that of nusG-rplK of E. coli, suggesting that vbrA may constitute a part of an essential gene cluster encoding components of transcriptional and translational apparatuses.

Amino Acid Sequence↗
PubMedDate not supplied

Fatal traumatic brain injury, West Virginia, 1989-1998.

OBJECTIVE: The objective of this study was to describe fatal cases of traumatic brain injury (TBI) among West Virginia residents. METHODS: The authors analyzed data from the National Center for Health Statistics Multiple Cause of Death tapes for the period 1989-1998. They compared West Virginia's annualized average TBI death rate with the rates of other states and with the rate among U.S. residents for the same period. U.S. Bureau of Census population estimates were used as denominators. RESULTS: A total of 4,416 TBI deaths occurred in West Virginia in 1989-1998, for an annual average death rate of 23.6 per 100,000 population. From 1989 to 1998, TBI death rates declined 5% (p=0.4042). Seventy-five percent (n=3,315) of fatalities occurred among men. Adults > or =65 years of age accounted for the highest percentage of fatal injuries (n=1,135). The leading external causes of fatal TBI were: firearm-related (39% of reported fatalities), motor vehicles-related (34%), and fall-related (10%). Firearm-related TBI became the leading cause of TBI fatalities in 1991, surpassing motor vehicle-related TBI. Seventy-five percent of firearm-related TBI deaths were suicides (n=1,302). West Virginia's TBI death rate (23.6 per 100,000) was higher than the national rate (20.6 per 100,000). In 23 states, the average TBI death rates over the 10-year period were higher than West Virginia's. Whereas modest declines in TBI death rates occurred for motor vehicle-related and firearm-related causes in West Virginia, a concomitant 38% increase occurred in the fall-related TBI death rate during the decade. CONCLUSION: Data presented in this report can be used to develop targeted prevention programs in West Virginia.

Accidental Falls↗