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Biomedical subjects

R F Thomas

Publications and source records attributed to R F Thomas.

At least 19 recordsLinked to original sources
PubMed2004

Destruction of wetlands and waterbird populations by dams and irrigation on the Murrumbidgee River in arid Australia.

The Lowbidgee floodplain is the Murrumbidgee River's major wetland in southeastern Australia. From more than 300,000 ha in the early 1900s, at least 76.5% was destroyed (58%) or degraded (18%) by dams (26 major storages), subsequent diversions and floodplain development. Diversions of about 2,144,000 ML year(-1) from the Murrumbidgee River come from a natural median flow of about 3,380,000 ML year(-1) providing water for Australia's capital, hydroelectricity, and 273,000 ha of irrigation. Diversions have reduced the amount of water reaching the Lowbidgee floodplain by at least 60%, from 1888 to 1998. About 97,000 ha of Lowbidgee wetland was destroyed by development of the floodplain for an irrigation area (1975-1998), including building of 394 km of channels and 2,145 km of levee banks. Over 19 years (1983-2001), waterbird numbers estimated during annual aerial surveys collapsed by 90%, from an average of 139,939 (1983-1986) to 14,170 (1998-2001). Similar declines occurred across all functional groups: piscivores (82%), herbivores (87%), ducks and small grebe species (90%), large wading birds (91%), and small wading birds (95%), indicating a similar decline in the aquatic biota that formed their food base. Numbers of species also declined significantly by 21%. The Lowbidgee floodplain is an example of the ecological consequences of water resource development. Yanga Nature Reserve, within the Lowbidgee floodplain, conserved for its floodplain vegetation communities, will lose these communities because of insufficient water. Until conservation policies adequately protect river flows to important wetland areas, examples such as the Lowbidgee will continue to occur around the world.

Agriculture↗
PubMed2002

Use of satellite image analysis to track wetland loss on the Murrumbidgee River floodplain in arid Australia, 1975-1998.

Demonstrating the extent of wetland loss and its causes are essential for policy makers and managers. We used Landsat satellite imagery to show major wetland loss in the Lower Murrumbidgee floodplain on the Murrumbidgee River in arid Australia. Stratification of the floodplain according to hydrology, use of imagery from the same time of year and the separation of developed areas, using ancillary information were essential. There was considerable loss of floodplain area over a 23 year period (1975-1998), mainly in the Nimmie-Caira stratum (59% loss), as wetland areas were replaced by irrigation bays. There was also a significant increase in fragmentation. For floodplain areas distant from the river, flooding patterns were more difficult to identify because of infrequent flooding and primary reliance on rainfall. Landsat imagery provided a powerful tool for demonstrating long-term changes in wetland area, even in highly variable environments. Such information can demonstrate the ecological costs of water resource development on floodplains, forming a basis for policy and management of rivers.

Agriculture↗
PubMed1999

Brief 95% O2 exposure effects on surfactant protein and mRNA in rat alveolar and bronchiolar epithelium.

In acute lung injury, a disturbed surfactant system may impair gas exchange. Previous evaluations of hyperoxia effects on surfactant proteins (SPs) followed exposures >1-2 days. To evaluate the effects of brief exposure to hyperoxia on the SP system, we exposed adult male rats to 95% O2 or air for 12, 36, and 60 h. SP-A, -B, and -C mRNAs were analyzed by Northern blot and semiquantitative in situ hybridization (ISH). SP-A and -B were analyzed in whole lung homogenates, lung lavage fluid, and fixed tissue by semiquantitative immunohistochemistry (IHC). All SP mRNAs were diminished at 12 h and rose to or exceeded control by 60 h as determined by Northern blot and ISH. These effects were seen mainly in the intensity of ISH signal per cell in both type II and bronchiolar epithelial (Clara) cells and to a lesser extent on numbers of positively labeled cells. SP-B declined to 50% of control in lavage at 12 h, but no changes in total lung SP-A and -B were seen. The number of SP-A positively labeled cells did not change, but SP-A label intensity measured by IHC in type II cells showed parallel results to Northern blots and ISH. The response of SP-A in Clara cells was similar. SP-B immunolabeling intensity rose in both type II and Clara cells throughout the exposure. SP-C ISH intensity fell at 12 h and was increased to two times control by 60 h of hyperoxia. Sharp declines in SP expression occurred by 12 h of 95% O2 and may affect local alveolar stability.

Animals↗
PubMed1999

Brief exposure to 95% oxygen alters surfactant protein D and mRNA in adult rat alveolar and bronchiolar epithelium.

Surfactant protein D (SP-D), which has structural homology to C-type lectin binding regions, may play a role in host defense and has no known surfactant function. Because other surfactant proteins have been shown to be increased after prolonged periods of hyperoxia, we sought to evaluate the early effects of hyperoxia (95% O2) on expression of SP-D in the adult male rat lung. Animals were exposed to air or to 12, 36, or 60 h of 95% O2. Northern blot analysis of total lung RNA revealed marked SP-D mRNA increases at 12 h 95% O2 compared with air-exposed controls, with decreasing expression to near that of air-exposed animals by 60 h. Semiquantitative in situ RNA hybridization demonstrated parallel results, with increased numbers of labeled alveolar epithelial (AE) and bronchiolar epithelial (BE) cells at 12 h and increased intensity of labeled alveolar cells, compared with air-exposed controls. After 60 h of exposure to 95% O2, mRNA label intensity in AE and BE was decreased to levels near those seen in air-exposed animals. In contrast, Western blotting showed a decline in total lung SP-D with 95% O2 exposure, beginning at 12 h and continuing at 36 and 60 h, respectively. Semiquantitative immunohistochemistry demonstrated a decline in AE labeling parallel to the total lung Western blot results, but labeled total BE cell numbers increased (P = 0.10). Hyperoxia had differential effects on SP-D abundance in AE and BE cells, and therefore may influence the availability of SP-D to bind microbial pathogens in the airways depending on cell type and location.

Animals↗
PubMed1993

Lack of beta 3-adrenergic receptor mRNA expression in adipose and other metabolic tissues in the adult human.

The beta 3-adrenergic receptor (beta 3AR) has been purported to play important roles in a number of metabolic functions, suggesting that beta 3AR agonists might be useful as antidiabetic and antiobesity therapeutic agents. However, these assertions are based entirely on extensive metabolic studies with such agonists in rodents. To clarify the role that the beta 3AR might have in humans, we sought to define the tissue distribution of the beta 3AR in adult human tissue by the use of a highly specific and sensitive approach. Northern blots of selected tissues failed to reveal any beta 3AR mRNA, suggesting little or no expression. To detect minute amounts of transcripts, we developed a reverse transcriptase-polymerase chain reaction (RT-PCR) method that uses primers to amplify a region of the beta 3AR that has little homology with the closely related beta 1- and beta 2-AR genes, and we verified the specificity of this approach using plasmids containing the cloned human beta 1-, beta 2-, and beta 3AR genes. RT-PCR performed on as little as 20 ng of total RNA from 3T3-F442A cells, which expressed beta 3AR at very low levels (approximately 20 fmol/mg of protein), provided an easily detectable signal by ethidium bromide staining and Southern blotting of electrophoresed products. RT-PCR was performed on RNA obtained from 23 different human tissues, using primers for the beta 3AR, the beta 2AR, and beta-actin, which acted as a control. Whereas beta-actin and the beta 2AR were detected in virtually all tissues, RT-PCR using beta 3AR primers gave products from 13 tissues, including skeletal muscle, lung, adipose tissue, kidney, small intestine, pancreas, spleen, and adrenal gland. An end-labeled 50-nucleotide probe identical to an internal region of the expected beta 3AR product hybridized under low stringency conditions to seven of these products. However, sequencing of these products, which were somewhat smaller in molecular size than expected, did not reveal beta 3AR DNA sequence. Given the specificity and sensitivity of our approach, we conclude that the beta 3AR is not expressed to any significant degree in the adult human tissues studied, including adipose tissue and other metabolic sites.

Adipose Tissue↗
PubMed1992

Long-term agonist exposure induces upregulation of beta 3-adrenergic receptor expression via multiple cAMP response elements.

During continuous stimulation by agonist, beta 1- and beta 2-adrenergic receptors (ARs) undergo processes that lead to decreases in receptor expression. This receptor down-regulation serves to limit the cellular cAMP response during chronic agonist exposure. In the recently described third subtype of the beta AR, denoted beta 3AR, we found four potential cAMP response elements in the 5' flanking region, suggesting that expression of this receptor might be positively regulated by agonists. These elements were cloned into the vector pA10CAT2, which contains a chloramphenicol acetyltransferase reporter gene, and transiently expressed in VERO cells. Three of these elements, TGACTCCA, TGAGGTCT, and CGAGGTCA (located 518, 622, and 1125 bases upstream of the beta 3AR coding block, respectively) were found to increase transcription of the chloramphenicol acetyltransferase gene in response to cAMP analogues and agents that increase intracellular cAMP. 3T3-F442A cells, when differentiated into the adipocyte phenotype by insulin, expressed beta 3AR, and nuclear runoff studies from such cells confirmed cAMP enhancement of beta 3AR mRNA transcription. In these cells, beta 3AR mRNA increased in response to exposure to the beta 3AR agonist isoproterenol and remained elevated during exposures of up to 24-30 hr. During prolonged exposure to agonist, no downregulation of beta 3AR expression in 3T3-F442A cells occurred. Indeed, beta 3AR expression increased during agonist exposure to approximately 165% of basal expression. In marked contrast, beta 1AR expression declined by approximately 70% in response to chronic agonist exposure. These studies reveal a subtype-specific prolonged transcriptional regulation of a beta AR gene by the end product of its signal transduction pathway. Thus, the beta 3AR undergoes a paradoxical increase in receptor expression during chronic agonist exposure.

1-Methyl-3-isobutylxanthine↗
PubMed1979

Studies on tryptophan accumulation in brain during methiothepin-induced enhancement of 5-hydroxyindole synthesis.

The elevation of brain tryptophan, 5-hydroxytryptophan and 5-hydroxyindoles (serotonin + 5-hydroxyindole acetic acid) that results from a tryptophan load is potentiated by prior administration of methiothepin, a serotonin receptor antagonist. Co-administration of valine with tryptophan attenuates these effects even in animals receiving methiothepin pretreatment. Administration of methiothepin and tryptophan to rats with widespread reduction of brain 5-hydroxyindole levels resulting from raphe lesions or 5,7-dihydroxytryptamine pretreatment still enabled brain tryptophan levels to rise considerably above the sum of increases found in animals receiving one or the other. Following transection of the spinal cord, the cranial portion still exhibited enhanced uptake of tryptophan and 5-hydroxyindole synthesis following methiothepin plus tryptophan treatment, however, both these events were absent in the caudal segment. Apparently, enhanced tryptophan uptake can proceed in the presence of minimal neuronal activity; however, when nerve impulse flow is eliminated, both 5-hydroxyindole synthesis and tryptophan uptake is impaired.

Amino Acids↗
PubMed1975

Application of a lateral compression clamp in the management of mandibular fractures.

A lateral compression clamp system has been used in the treatment of fractures of the mandible. It provides rigid fixation and promotes earlier osteogenesis at the fracture site. Intermaxillary fixation can often be eliminated in edentulous persons and greatly reduced in duration when necessary as an adjunct to fixation in patients with teeth. These significant qualities make the compression clamp quite beneficial in the treatment plan and postoperative management of many otherwise difficult cases. Having evaluated our experiences with compression clamps, we believe that this approach deserves further attention and may contribute to a solution of the controversy that often exists regarding the management of mandibular fractures in both edentulous patients and those with a compromised complement of teeth.

Accidents, Traffic↗