Method of obtaining the empirical scattering parameters for the Fe-B pair from the extended x-ray-absorption fine-structure data of Fe2B: Possible limitations.
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Biomedical subjects
Publications and source records attributed to M Choi.
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We performed a retrospective review of an outbreak of Salmonella gastroenteritis that occurred in a community nursing home in 1987. Forty-four of 199 residents had a diarrheal illness; Salmonella heidelberg was isolated from the stool in 19 cases. Although the distribution of cases suggested a common source for the outbreak, no common source of infection could be demonstrated, despite extensive investigation. The clinical presentation of symptomatic individuals ranged from mild diarrhea to a severe gastrointestinal illness, and 26% of symptomatic, culture-positive patients required hospitalization. The median duration of pathogen excretion during convalescence in untreated residents was six weeks, but six patients who were treated with antibiotics shed S. heidelberg for a median duration of 14.5 weeks. We conclude that (1) the clinical spectrum of Salmonella gastroenteritis in nursing-home patients is variable, ranging from mild to severe illness; and (2) nursing-home Salmonella outbreaks impose a high economic burden because of expense of epidemiologic investigation, prolonged isolation measures, hospitalization for severely ill residents, and potential institutional closure.
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Twenty volunteers participated in a single-session experiment in which bi-directional heart rate (HR) control was assessed before and after brief unidirectional HR biofeedback. Subjects attempted to raise (INC) and lower (DEC) HR while performing mental arithmetic, as well as in no-task conditions. Biofeedback training was also carried out in the presence and absence of mental arithmetic. Subjects were divided into two groups on the basis of initial HR reactivity to mental arithmetic. Group U received feedback and instructions to raise HR during the training period, while group D attempted to lower HR. Significant differences in HR modifications during INC and DEC trials were observed prior to any biofeedback training in no-task conditions. Following training, however, ability to raise HR deteriorated in group D, while HR decelerations were impaired in group U. Unidirectional training in HR control thus handicapped subsequent attempts to modify HR in the reverse direction. The pattern of HR change was generally paralleled by respiration rate. Subjects were also able to influence the cardiac reactions to mental arithmetic even before the administration of biofeedback. The data nevertheless suggest that training affects the magnitude of HR reactions after the biofeedback is withdrawn. In the biofeedback phase itself, the HR increases and decreases produced by groups U and D, respectively, were diminished on simultaneous mental arithmetic performance.
On the basis of conformational analysis of the vitamin D side chain and studies using conformationally restricted synthetic vitamin D analogs, we have suggested the active space region concept of vitamin D: The vitamin D side-chain region was grouped into four regions (A, G, EA and EG) and the A and EA regions were suggested to be important for vitamin D actions. We extended our theory to known highly potent vitamin D analogs and found a new region F. The analogs which occupy the F region have such modifications as 22-oxa, 22-ene, 16-ene and 18-nor. Altogether, the following relationship between the space region and activity was found: Affinity for vitamin D receptor (VDR), EA > A> F > G > EG; Affinity for vitamin D binding protein (DBP), A >> G,EA,EG; Target gene transactivation, EA > F > A > EG > or = G; Cell differentiation, EA > F > A > EG > or = G; Bone calcium mobilization, EA > GA > F > or = EG; Intestinal calcium absorption, EA = A > or = G >> EG. We modeled the 3D structure of VDR-LBD (ligand binding domain) using hRARgamma as a template, to develop our structure-function theory into a theory involving VDR. 1alpha,25(OH)(2)D(3) was docked into the ligand binding pocket of the VDR with the side chain heading the wide cavity at the H-11 site, the A-ring toward the narrow beta-turn site, and the beta-face of the CD ring facing H3. Amino acid residues forming hydrogen bonds with the 1alpha- and 25-OH groups were specified: S237 and R274 forming a pincer type hydrogen-bond for the 1alpha-OH and H397 for the 25-OH. Mutants of several amino acid residues that are hydrogen-bond candidates were prepared and their biologic properties were evaluated. All of our mutation results together with known mutation data support our VDR model docked with the natural ligand.
The role of chloride ions in the regulation of steroidogenesis in rat Leydig cells and adrenal cells has been investigated. It was found that the chloride channel blocker 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) inhibited LH but not dibutyryl cAMP (dbcAMP)-stimulated steroidogenesis in the Leydig cells. This was found to be via an inhibition of cAMP production, because both LH- and forskolin-stimulated cAMP productions were inhibited by DIDS. The exclusion of chloride ions enhanced steroidogenesis during incubation of Leydig cells and adrenal cells with dbcAMP. The adrenal cells were found to be more sensitive to dbcAMP than Leydig cells and the enhancing effects of chloride removal were higher. In the presence of chloride ions, near maximum steroidogenesis was achieved with approximately 60 microM and 1 mM dbcAMP in the adrenal and Leydig cells, respectively. In the absence of chloride ions the concentrations required decreased approximately 50-fold and 10-fold, respectively. It is concluded that although LH may regulate DIDS sensitive chloride channels, the enhanced stimulation of cAMP-mediated steroidogenesis by chloride exclusion is not mediated via these channels. We propose a model based on the present and previous studies [1] with Leydig tumour (MA10) cells i.e. that intracellular chloride ion depletion enhances the action of cAMP on protein synthesis which results in increased synthesis of the Steroidogenic Acute Regulator (StAR) protein and consequently increased steroidogenesis.
The development of pleural effusions in ESRD patients is a relatively common occurrence. Uremia, currently a rare cause of effusion, can lead to the development of hemorrhagic pleural fluid collections in patients who are underdialyzed. Uremic pleural effusions should be considered when common etiologies of effusions such as volume overload, congestive heart failure (CHF), infection, and malignancy have been excluded. Uremia-associated serosal injury allows transudation of fluid into the pleural space, and defective platelet function contributes to the hemorrhagic nature of the effusion. Although uremic effusions may occur less frequently in peritoneal dialysis patients, we present a patient who developed this complication due to a peritoneal dialysis regimen that was inadequate by current Dialysis Outcomes Quality Initiative guidelines. The pleural effusion resolved with an intensified dialysis regimen in the absence of a change in the underlying volume status.
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Cytomegalovirus (CMV) infection of the gastrointestinal tract is an increasingly recognized cause of morbidity and mortality during the course of HIV infection and in association with immunosuppressive pharmacotherapy. Mycophenolate mofetil, a novel immunosuppressive drug, is currently used in renal transplant recipients and is under evaluation for a variety of disorders. There is preliminary evidence to suggest that CMV reactivation may be more common during treatment with mycophenolate than with other immunosuppressive drugs. We present the case of a 59-year-old male with Wegener's granulomatosis who received mycophenolate and presented with guaiac-positive diarrhea 8 weeks after recovery from Salmonella brandenburg infection. CMV serology and assays for CMV antigens were entirely negative. Colonoscopy demonstrated pancolitis and examination of the specimens disclosed CMV infection. Ganciclovir was administered and the patient made an uneventful recovery. We discuss aspects of gastrointestinal CMV infection with an emphasis on pitfalls in diagnosis and the association with mycophenolate mofetil treatment. We also speculate as to the potential role of previous Salmonella infection and proinflammatory cytokines in CMV reactivation. In summary, when using mycophenolate, clinicians should be more aware of CMV reactivation and disease.
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