Pumping Liquid Crystals.
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Biomedical subjects
Publications and source records attributed to N Clark.
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Le Fort defined the classic weak points of facial fractures. Fractures of the midface and mandible are believed to require management with standard rigid fixation. Recent work has allowed mini- and microplating of multiple fracture fragments into more manageable larger segments for reduction and subsequent plating with rigid fixation to peripheral buttresses. The technique and indications for use are outlined.
The management of nasoethmoidal orbital injuries can be difficult. Clinical recognition and options for correction are diverse. Recently we treated several patients with limited facial injuries in which the nasoethmoidal complex "greensticks." Treatment with limited exposure and rigid fixation allows for adequate reduction. Clinical recognition and an outline for treatment of these limited injuries is presented.
In the last 20 years, the management of pan-facial injuries has progressed to the point where immediate treatment using open reduction with rigid fixation is now the standard of care. After discussing the historical progression of treatments, the authors present a plan for treatment of craniofacial injuries based on the use of incisions that expose the four areas of the face: the frontal area, upper midface, lower midface and occlusion, and the basal mandibular area. According to the authors, five incisions permit access to the entire anterior craniofacial skeleton: the coronal, lower eyelid, upper and lower gingival-buccal-sulcus, and the preauricular-retromandibular. Through these incisions, the facial buttresses can be accessed to allow reduction and rigid fixation of facial fractures.
The human immunodeficiency virus (HIV) matrix protein, p17, forms the outer shell of the core of the virus, lining the inner surface of the viral membrane. The protein has several key functions. It orchestrates viral assembly via targeting signals that direct the gag precursor polyprotein, p55, to the host cell membrane and it interacts with the transmembrane protein, gp41, to retain the env-encoded proteins in the virus. In addition, p17 contains a nuclear localization signal that directs the preintegration complex to the nucleus of infected cells. This permits the virus to infect productively non-dividing cells, a distinguishing feature of HIV and other lentiviruses. We have determined the solution structure of p17 by nuclear magnetic resonance (NMR) with a root-mean square deviation for the backbone of the well-defined regions of 0.9 A. It consists of four helices connected by short loops and an irregular, mixed beta-sheet which provides a positively charged surface for interaction with the inner layer of the membrane. The helical topology is unusual; the Brookhaven protein database contains only one similar structure, that of the immune modulator interferon-gamma.
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The use of costochondral grafts in the acute trauma setting is controversial. This new technique has recently been utilized in two patients with severe condylar head fractures using a newly designed Synthes AO mesh plate with microscrews (0.8 mm) and 1.5-mm fixation. The technique provides superb rigid fixation. This fixation technique is multifaceted and can be used in all settings of acute and chronic costochondral graft replacement.
A patient is described in whom two consecutive relapses of autoimmune thrombocytopenic purpura (AITP) were associated with loss of red cell antigens of the Kell and Lutheran blood group systems respectively. During the second relapse the glycoprotein CD44 and to a lesser extent the LW antigen were also depressed. Both relapses were associated with concomitant production of IgG antibody recognizing high-frequency determinants on the corresponding antigen-carrying protein. Blocking of antigen sites by these antibodies was not the cause of reduced antigen expression, because immunoblotting studies showed absence of Kell protein during the first relapse, and Lutheran protein during the second. On both occasions the red cell changes reverted to normal with disappearance of the antibody as the AITP entered remission. There was no evidence of clonal lymphocyte expansion as demonstrated using immunoglobulin JH and T cell receptor beta chain probes.
OBJECTIVE: To study urinary oxalate excretion in infants fed human milk versus formula, and to compare urinary calcium oxalate and calcium phosphate saturation in premature infants with term infants and adults. METHODOLOGY: We measured urinary oxalate-to-creatinine ratio and urinary oxalate concentration in 15 premature infants fed human milk compared to 16 formula-fed premature infants, and in eight human milk-fed term infants compared to 17 formula-fed term infants. We then studied urinary calcium oxalate and calcium phosphate saturations based on our observations of elevated urinary oxalate excretion in premature infants. Urinary calcium oxalate and calcium phosphate saturations were calculated from urinary concentrations of oxalate, calcium, sodium, potassium, chloride, uric acid, magnesium, phosphorus, and urinary pH. We calculated urinary calcium oxalate and calcium phosphate saturations in nine healthy adults and nine formula-fed term infants to establish control values for urinary saturation. Urinary calcium oxalate and calcium phosphate saturations were determined in nine premature infants receiving a glucose and electrolyte solution, 11 premature infants receiving parenteral nutrition, nine formula-fed premature infants, and 11 human milk-fed premature infants. RESULTS: Urinary oxalate excretion was higher in formula-fed compared to human milk-fed premature infants whether expressed as oxalate-to-creatinine ratio (0.32 +/- 0.04 versus 0.18 +/- 0.03, P < .01) or urinary oxalate concentration (0.047 +/- 0.007 versus 0.022 +/- 0.002 mg/mL, P < .01). Urinary oxalate excretion was higher in formula-fed term infants than in human milk-fed term infants whether expressed as oxalate-to-creatinine ratio (0.14 +/- 0.01 versus 0.07 +/- 0.01, P < .01) or urinary oxalate concentration (0.022 +/- 0.002 versus 0.012 +/- 0.002 mg/mL, P < .01). The urinary calcium oxalate saturation in healthy adults was 2.84 +/- 0.79; the value in formula-fed term infants was 2.12 +/- 0.31. The urinary calcium oxalate saturation was significantly higher in premature infants receiving formula (15.68 +/- 3.15), human milk (15.02 +/- 2.27), or parenteral nutrition (11.38 +/- 2.56) compared to adults or term infants (P < .01). Urinary calcium oxalate saturation in premature infants receiving a glucose and electrolyte solution (2.45 +/- 0.36) was not significantly different from that in adults or term infants. In contrast, urinary calcium phosphate saturation in premature infants as well as term infants and adults was less than 1; precipitation of calcium phosphate is not likely to occur under these conditions. CONCLUSION: Formula-fed infants have higher urinary oxalate excretion than human milk-fed infants. Premature infants receiving standard nutritional regimens may have urinary calcium oxalate saturation levels at which dissolved calcium oxalate may form nuclei of its solid phase.
The use of an arteriovenous fistula (AVF) to afford vascular access for free tissue transfer is described in 11 consecutive patients from a 1 year period. The leg was the site of pathology in six cases, and a reversed saphenous AVF to the femoral vessels was created. In the remaining five cases, those in the head and neck and arm regions, the recipient vessels varied. The mean patient age was 37.7 years, and ten of 11 patients were male. Etiologies of defect were automobile accidents in six cases, neoplasm in three, and gunshot wound and electrical injury in one patient each. Mean ischemia time was 113 +/- 15 min. Mean length of AVF was 27.3 +/- 2.1 cm. All flaps survived. AVF was a useful technique in the current study. Several maneuvers were undertaken to minimize the risk of thrombosis. All patients were given aspirin prior to AVF creation. Patients received dextran 40 in the postanastomosis period for 5 days. Finally, every effort was made to create the AVF between large vessels, especially in the leg, to maximize blood flow.
Surveys suggest that 8 to 41% of athletes may struggle with binge/purge and bulimic eating behaviors. Many of these athletes with bulimia struggle alone, receiving no professional help for recovery. This article offers effective counseling strategies for nutrition professionals who want to help bulimic athletes. Through a case study of a triathlete who binges, and then purges through compulsive exercise, a nutrition care plan is discussed that addresses the food and weight concerns commonly expressed by athletes with bulimia. The priorities of the care plan are to reduce preoccupation with weight, establish a pattern of regular eating, and address the underlying causes of the binges. The case demonstrates that nutrition counseling is only one part of the treatment program, and emphasizes the importance of developing a team of health professionals to assist athletes with bulimia.
We have demonstrated that stimulation of the human immunodeficiency virus type 2 (HIV-2) enhancer in T cells is dependent upon at least four cis-acting elements, including two purine-rich binding sites, PuB1 and PuB2, which are capable of binding members of the ets family of proto-oncogenes, the pets (peri-ets) site, which lies just upstream of the PuB2 site, and a single kappa B site (D. M. Markovitz, M. Smith, J. M. Hilfinger, M. C. Hannibal, B. Petryniak, and G. J. Nabel, J. Virol. 66:5479-5484, 1992). In this study, we examined the regulation of the HIV-2 enhancer in cells of monocytic lineage. We found that in immature monocytic cell lines, the HIV-2 enhancer is markedly induced by phorbol esters and that all four cis-acting elements are required for activation. In mature monocytic cells, constitutive activity is high, with only modest stimulation following phorbol ester treatment. Mutation of any of the four cis-acting elements resulted in greatly reduced basal expression in mature monocytes. This is in contrast to HIV-1, in which developmentally controlled expression of the enhancer in monocytes is mediated largely through the kappa B sites alone [G. E. Griffin, K. Leung, T. M. Folks, S. Kunkel, and G. J. Nabel, Nature (London) 339:70-73, 1989]. Further, we demonstrated that although both Elf-1, an ets family member with significant similarity to the drosophila developmental regulatory protein E74, and Pu.1, a monocyte- and B-cell-specific member of the ets family, bind the purine-rich enhancer region, Elf-1 is the protein which binds predominantly in vivo. A nuclear factor(s) which binds the pets site, an element which has been described only in HIV-2, was detected in extracts of all of the monocytic cells tested. These findings indicate that the mechanism by which cellular factors regulate HIV-2 enhancer function in monocytic cells differs significantly from that of HIV-1 and may offer a partial explanation for the differences in the biological and clinical characteristics of the two viruses.
The human immunodeficiency virus type 1 (HIV-1) and HIV-2 enhancers are induced differentially by physiologic T-cell activation signals. In contrast to that of HIV-1, HIV-2 transcription was quite responsive to stimulation of T cells by antigen presentation but weakly induced by tumor necrosis factor alpha. Like tumor necrosis factor alpha, expression of cloned NF-kappa B subunits strongly activated the HIV-1, but not the HIV-2, enhancer. The differences in response to these physiologic T-cell activation pathways may contribute to the differences in persistence of HIV-1 and HIV-2 infection.
Successful reconstruction of the severely injured foot and ankle remains a challenge for the surgeon. Frequently, bone and joint injuries to this area with overlying soft-tissue injuries or losses require the coordinate management by orthopedic and reconstructive specialists. Healthy, well-functioning feet are necessary to perform daily activities. Because of the dense packaging of the specialized interdependent structures of the feet, injuries to this area commonly cause significant (composite) wounds that, if not properly managed, can lead to progressive deformity and disability. Basic principles of wound management, especially those pertaining to open fracture management--wound evaluation, debridement, fracture reduction and fixation, preservation of viable tissues, prevention of infection, early soft-tissue reconstruction, and early bony reconstruction--are applicable in the management of foot and ankle wounds. The unique anatomy of the foot complicates reconstruction by limiting the availability of local tissues. Further reconstructive difficulties arise from the functional demands placed on feet and from the distal relationship of the feet to the rest of the body. Successful reconstruction of the foot is predicated on an intimate knowledge of the unique anatomy of the region, of the functional demands required of the feet, and of reconstructive methods. The simplest appropriate technique for the injured foot that is likely to produce the best outcome should be selected. Reconstructive options from the most simple to the complex include primary closure, healing by secondary intention, grafting, flaps (local and distant), and amputation. As typified by the authors' experience, reconstruction of the soft tissues of the foot and ankle frequently requires more complex methods. Seventy percent of our patients have required free-tissue transfer reconstructions, and an additional 5% have undergone other flap reconstructions.
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With the rising popularity of ultradistance sports events lasting from 6 to 24 hours or multiple days, athletes are consulting registered dietitians for specialized dietary advice. Many dietitians, however, lack experience with these types of events. This article provides basic guidelines ffor fueling the ultradistance athlete. The goals are to maintain normal hydration and blood glucose levels, which can be done by enforcing programmed drinking (approximately 250 to 500 mL/15 minutes, depending on the athlete's sweat rate and environmental temperature) and programmed eating (1 to 1.5 + g of carbohydrate per kilogram of body weight per hour, depending on the athlete's acceptance of and tolerance to solid and/or liquid foods during exercise). Athletes who compete longer than 6 to 8 hours should consume adequate electrolytes, particularly sodium (approximately 1 g/hour) through either sports drinks or foods. These guidelines are applied to a case study of the 1991 women's winner of the Race Across America, a 2,930-mile biking event.
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