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A local Wilson' Disease Chapter Meeting was held in s Long Beach, CA on January 17, 1999. Many thanks goes to Stefanie F. Kaplan, a new WDA member, who initiated and organized the event, and to each person who participated. Twenty-two people were in attendance. Dr. Brewer was the guest speaker in the morning while the afternoon was used for an open discussion session. Some key points which some members would like to share with everyone in the WDA are: * Diet does not really need to be altered with Wilson' s patients. Liver and shell fish are the only foods that should be limited. * Vegetarians accumulate copper more slowly and thus may be older during a diagnosis. * Children of WD patients should be tested at ages 5 and 15. * There are over 70 different mutations of WD genes. * Detection of WD carriers is still very difficult. * There are 3 Centers of Excellence for Wilson' s Disease. Please see Resource Corner for names of centers ; . This was an excellent opportunity for WD patients and families to meet. Plans were tentatively made for future meetings.
Lengthy silences, a self-conscious avoidance of all overt performance demands, and spontaneous empathic self-disclosure by the therapist of his or her intersubjective experience of the dyadic relationship with the patient from moment to moment. Such efforts might or might not yield relevant material about a patient's inner mental life and the possible symbolic meaning of the catatonic behaviors. In turn, such knowledge, even if true and relevant, might or might not be useful in developing effective therapeutic interventions. More often, such a patient's mental life becomes known only after the remission of the catatonia, when the patient can verbalize more spontaneously. Occasionally a patient is then able to relate both awareness of the efforts of others to communicate with him or her during the catatonia, as well as the often delusional ; reasons why the patient felt unable to respond. However, it is just as likely that the patient may recall little of the catatonia, with the whole episode essentially lost to rational consciousness, perhaps because of some sort of state-dependent learning. The notion that the patient is somehow to blame, as when the outpatient psychiatrist suggested that this was a "voluntary" psychosis, is an unfortunate but understandable attribution that reflects more the therapist's own sense of helplessness than anything about the nature of catatonia. To be sure, these patients do, to some extent, turn their catatonia on and off, and one can at times even make informed predictions about the patient's improvement or worsening on the basis of an understanding of the psychodynamic processes at work. For example, another case involved a nearly stuporous catatonic patient who was maintained drug free for many months on a research unit. He allowed himself to be moved about passively by his father when his father visited him. The father would say proudly and without insight at family therapy sessions, "Chuck loves me so much, he'll do anything for me. If I say, `Chuck, stand on your head, ' by golly, that's just what he'll do!" After the father left the unit, the patient would regress into an even more severe state of catatonic negativism, from which the nursing staff was unable to budge him for the subsequent 24 hours. Examples such as these, however, in no way detract from the primarily biological origins of catatonia, and no one would have dreamed of withholding medication from that patient once the research was over. In an.

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Tropical species can hardly be cultivated in orchards of the temperate zones. An export crop from rural areas of Thailand, maybe in combination with longan fruit orchards, would be an interesting prospect. However, until we fully understand the nutritional requirements of the wild strains, it is an open question how to develop a commercial cultivation technique. ACKNOWLEDGEMENTS This research was supported by Thailand Research Fund BGJ4580023 and , Royal Golden Jubilee PhD Program 4BCM 42D ; . The Silviculture Research Center SRC ; in Chiang Mai supported the Pinus kesiya seeds. REFERENCES Danell E 994 ; Cantharellus cibarius: Mycorrhiza formation and ecology. Comprehensive summaries of Uppsala dissertations from the Faculty of Science and Technology No. 35, Acta Universitatis Uppsaliensis, Uppsala, Sweden. Danell E, Camacho FJ 997 ; Successful cultivation of the golden chanterelle. Nature 385: 303. Goncalves CR 940 ; Observacoes sobre Pseudococcus comstocki Kuw., 902 ; atacando Citrus na baixada fluminense. Rodriguesia 4: 79263. Hall IR, Lyon AJE, Wang Y, Sinclair L 998 ; Ectomycorrhizal fungi with edible fruiting bodies Boletus edulis. Economic botany 52: 4456!
Increases in serum creatinine concentration during treatment. In two, the peak concentration did not exceed 1.3 mg dl. In the third, it increased from 1.5 to 2.1 mg dl, but spontaneously declined to 1.4 mg dl by day 5 of therapy. The fourth patient experienced a moderate increase in serum creatinine concentration; however, at autopsy, this was attributed to intrarenal hemorrhage due to severe thrombocytopenia. Thus, no patient was believed to have amikacin-related nephrotoxicity. Among 37 subjects receiving netilmicin, three experienced increases in serum creatinine concentration. In one patient who was begun on therapy while recovering from acute tubular necrosis, the serum creatinine level fluctuated between 1 and 2 mg dl. Another person was diagnosed as having hepatorenal syndrome. Neither was considered to have antibiotic-related nephrotoxicity. A third patient, who was treated with netilmicin for 39 days, experienced a rise in serum creatinine concentration from 1.0 to 2.1 mg dl. He was given carbenicillin concurrently and exhibited signs of allergy to this drug. Nonetheless, his renal dysfunction was considered probably related to the netilnicin. He was the only subject in this study believed to have aminoglycoside-related nephrotoxicity. Auditory toxicity. Fifteen patients receiving amikacin and 19 receiving netilmicin could be adequately assessed for auditory toxicity. Five of the 15 amikacin recipients 33.33% ; experienced decreases of at least 15 dB on least one occasion; however, in patient 47, the abnormalities were only at low frequencies and were considered likely to be due to room noise. If that patient is excluded entirely, the rate of auditory toxicity with amikacin becomes 4 14 28.5% ; . Three patients receiving netilmicin 3 19 [15.8%] ; experienced audiographic changes. Salient features of patients with auditory toxicity are summarized in Table 4. The rates of audiographic decreases with amikacin and netilmicin were not significantly different Table 5 ; by the chi-square test using 2 x 2 contingency tables with Yates' correction xc ; whether the rate of amikacin-related toxicity was regarded as 4 14 15. None of the patients reported a decrease in hearing. However, two complained of tinnitus. One patient 89 ; is described in Table 4. The other, a 58-year-old man treated with netilmicin for 7 days, noted intermittent tinnitus during treatment. Because he had no change in his audiograms, which showed stable high-frequency sensorineural loss throughout his course of therapy, he was not considered to have netilmicin-related cochlear damage. Vestibular toxicity. Sixteen patients receiv.

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Wrever, "Securitization." 52.54 and 63. 56. Though W ~ v does not specificdly dcd with the recognition of the r roblem. it underlies his entire discussion of security and security problerns. Barry Buan. "Environment as a Security Issue." in Pau1 Painchaud ed. ; , Geopolitical Perspectives on Environmental Sccuritv. Cahier du GERPE. No. 92-05, Universit Laval, Quebec. 1992 ; . 1 and 2 J f Were incorporated into Diagnostic Sensitivity Test Agar, held at 45C, dispensed in 20-ml volumes in plastic petri dishes, and used within 24 h. Inoculum was prepared by suspending in 1 ml saline a single colony from a PIA plate incubated for 24 h at 37C. This suspension was diluted 1 100 to give approximately 104 organisms per ml. The inoculum was applied with a Mast multipoint inoculator. After the plates had been incubated at 37C for 18 h, the minimum inhibitory concentration was calculated as the minimum concentration of antibiotic which inhibited growth of the organism. Susceptibility to carbenicillin was also investigated with a broth dilution technique. The inoculum used contained 104 cells cultured as described below for the extraction of bacterial exo and carboplatin. Pancreatic islet, gut enteroendocrine, parathyroid chief, and thyroid parafollicular C-cells ; with appropriately tissue-selective secretagogues results in measurable release of the usual resident hormone e.g., glucose causing pancreatic P cell insulin and Cpeptide release ; , but only adrenal medullary stimulation also elevates plasma chromogranin A51-53-55 consistent with the finding that the adrenal medulla is the quantitatively major normal tissue source of chromogranin A.13 The predominant source or sources of basal or unstimulated plasma chromogranin A in humans are still a matter of investigation. Human chromogranin A exhibits a significant ultradian or pulsatile rhythm, peaking on average every 51 minutes.56 Somatostatin infusion in humans suppresses basal circulating levels of chromogranin A and diminishes the frequency and amplitude of pulsatile peaks of plasma chromogranin A57; however, plasma catecholamines are unchanged, suggesting that somatostatin either inhibits chromogranin A release from nonsympathoadrenal sources or interferes with transport of chromogranin A to the circulation. In experimental animals, released adrenal medullary chromogranin A arrives in the circulation in part via a route involving the lymphatics.58 In renal insufficiency, plasma chromogranin A as immunoreactive fragments ; is elevated in proportion to the degree of uremia.59 This suggests that the kidney is involved in chromogranin A removal from circulation. Consequently, assessment of renal function is required for proper interpretation of elevations in plasma chromogranin A. On the other hand, chromogranin A is elevated to a lesser degree in patients with even severe liver disease, 55 precluding a quantitatively major role for the liver in chromogranin A disposition. Adults with uncomplicated diabetes mellitus have normal circulating chromogranin A, 60 arguing against an important role for systemic chromogranin A a precursor of pancreastatin19'20 ; in the altered insulin release seen in this disorder.

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Although penetration and sequestration of drug will impact upon the amount of drug associated with the cellular compartment, the dynamic equilibrium between cell and plasma will also be influenced by drug efflux mechanisms. This involves transport across one or more biological barriers, which may be influenced by a number of factors. It is now recognized that processes such as membrane-bound transport systems are important. A number of transport proteins have been identified by biochemical and molecular cloning methodologies in organs of importance in drug disposition, such as the intestine, liver and kidney9 Table 1 ; . The proteins that have been most extensively studied in the context of lymphocyte efflux of PIs are P-gp and multi-drug resistance-associated protein 1 MRP1 and carmustine!
FIG. 2. In vitro susceptibility of 111 strains of Pseudomonas aeruginosa to carbenicillin as determined by the tube dilution method.

Questionnaires and record forms. Photograph of eye worm sample in the back of this manual ; . Up-to-date map of the region plus GPS data, where possible. Notebooks, pens, pencils, erasers at least two of each and carteolol.
As expected for an equilibrium geometry. The frequencies and the corresponding intensities are shown in Table 4. As observed for the zinc complex, only minor differences between the various basis sets and the metallic ECP used were detected. Larger variations were observed between the different computational methods electron correlation descriptions. For instance, the RHF results shown in Table 4, clearly overestimated all frequencies, with the largest difference found for the C C stretch 20% ; . Below 500 cm-1, most of the calculated frequencies were overestimated between 5 and 10%. In the DFT and MP2 calculations, all deviations were found to be smaller, e.g., deviations for the C C stretch were 8% and 5% from DFT-B3LYP and MP2 methods respectively. For the other modes above 300 cm-1, most were overestimated between 1 to 10%. However below 300 cm-1, much better agreement with experimental results were obtained, with discrepancies between 1 and 3%. Remarkable is the prefect match between the frequency ordering found among all calculations carried out and the experimental results. Two exceptions, also observed for the zinc-dmit complex, should be pointed: w SCtS ; out-of-plane bending between 450 and 430 cm-1, for the DFT-B3LYP and MP2 methods. This reordering was not observed for the corresponding RHF calculation between 510 and 480 cm-1. The calculations confirmed the assignments previously reported in the literature.10 The C C, C S and C-S stretches were recognized at 1435, 1028 and 881 cm-1, respectively. The bands at 522 and 463 cm-1 were assigned as breathing mode from the dmit ring and SC t S bending mode, respectively. Between 360 and 300 cm-1, a series of bands was assigned as SaCeSm bending mode slightly coupled to the Sb-S stretching mode. The bands at 295 and 283 cm-1 were assigned as symmetrical and asymmetrical Sb-S stretches coupled to C C out-of-plane twisting and SC S in-the-plane bending. These modes were assigned from their symmetry and spectroscopic activity. While the symmetric stretch is Raman-active, the asymmetrical stretch occurs in the infrared. The band at 274 cm-1 arises from the C C out-of-plane. The band at 222 cm-1 results from the Sb-S stretching coupled to the S CtS bending. Finally the 150 cm -1 band was assigned as the fivemembers-ring deformation formed by the metal coordination to the thiolate sulfur. [Bi dmit ; 2]-1 geometry optimizations The symmetry of the [Bi dmit ; 2 ] -1 anion in [NEt4][Bi dmit ; 2] is C2. Table 5 lists the results for the geometry optimization carried out with the SBKd basis set and ECP pseudopotential. As previously mentioned.

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Renal transplantation in the African-American population is often associated with poor clinical outcomes; reasons for which are not fully elucidated. African-Americans have dramatically lower rates of referral for renal transplantation than nonAfrican-Americans.1, 2 Evidence also shows that compared to non-African-Americans, African-Americans are significantly less likely to be placed on transplant waiting lists, 3 to identify a living donor, 4 or to receive a cadaver transplant once placed on the waiting list.5 Despite the advent of immunosuppressive agents and surgical techniques with corresponding improvements in graft and patient survival rates, African-Americans suffer from higher rates of acute rejection and reduced long-term allograft survival.6 Researchers continue to examine strategies to improve clinical outcomes in this population including optimizing immunosuppressive pharmacologic therapies. Long transplant waiting times and low living donation rates likely contribute to poor outcomes among African-American renal transplant recipients. Foster and colleagues reported evidence that medical institutions can improve waiting time and living donation rates by providing targeted education and modifying their living donor program protocols.6 Strategies to improve access to transplantation for African-Americans at the University of Maryland included a formal family education program implemented in 1994 ; , a laparoscopic living donation program implemented in 1996 ; and a hepatitis B vaccination program no formal date of implementation ; . To assess the impact of the first two of these strategies on live donor transplantation rates, the investigators compared rates in three time periods: 1991 to September 1994 neither strategy October 1994 to February 1996 education program implemented ; and March 1996 to November 2001 both strategies implemented ; . Nine hundred forty-four African-American patients and 1, 223 non-African-American patients underwent renal transplantation and cefazolin!

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And T4 DNA ligase were purchased from Bethesda Research Laboratories, Bethesda, Md., or Pharmacia Canada and used as recommended by the suppliers. Small-scale isolation of E. coli and P. aeruginosa plasmid DNA was done as described previously 28 ; with the modification that P. aeruginosa DNA was phenol extracted prior to ethanol precipitation. Chromosomal DNA was isolated by the procedure described by Silhavy et al. 42 ; . Plasmid DNA was labeled with biotin-14-dATP, using the BioNick labeling kit Bethesda Research Laboratories ; and following the instructions of the supplier. DNA fragments were transferred from agarose gels to nylon membranes as described by Sambrook et al. 34 ; . After UV fixation, the membranes were treated and probed with biotinylated probes in accordance with the instructions provided with the PhotoGene nucleic acid detection system Bethesda Research Laboratories ; . DNA restriction fragments were eluted from low-gelling-temperature agarose gels as described by Wieslander 49 ; or electroeluted from regular agarose gels as described by Sambrook et al. 34 ; . E. coli cells were made competent and transformed by the CaCl2 procedure 34 ; with the following modifications. After the cells 40 ml ; were harvested, they were suspended in 20 ml ice-cold 0.1 M MgCl2 and immediately centrifuged at 4C. The cells were then resuspended in 10 ml medium 75 mM CaCl2, 6 mM MgCl2, 15% [wt vol] glycerol ; and kept on ice for 30 min. After centrifugation at 4C, the competent cells were suspended in 1 ml medium and either used directly or frozen in small aliquots at -70C. P. aeruginosa was transformed by the procedure of Olsen et al. 30 ; . An ordered set of nested exonuclease III ExoIII ; -S1 nuclease deletions was generated by the procedure of Henikoff 14 ; . Briefly, pPS102 DNA was digested to completion with BamHI leaving ExoIllsensitive 3' recessed ends ; and PstI leaving ExoIII-resistant 3' protruding ends ; . The restriction sites for both of these enzymes are located at the same junction of chromosomal and vector DNAs, with PstI cleaving closer to the vector than BamHI. Thus, the deletions will progress from the BamHI site into the cloned segment of chromosomal DNA. DNA sequence analysis by the dideoxy-chain termination method was performed on single-stranded M13mp18 19 DNA subclones, using a T7 DNA polymerase kit and the protocol provided by the supplier Bio Can Scientific, Mississauga, Ontario, Canada ; . Labeled DNA fragments were separated on electrolyte gradient gels as described previously 39 ; . The IBI MacVector program was used for computer-assisted sequence analyses. In vivo cloning of DNA complementing glpR. For the cloning of DNA fragments complementing the PAO glpR2 allele, the bacteriophage mini-D3112-based in vivo cloning method of Darzins and Casadaban 7 ; was used with'the following modifications. A phage D3112 lysate was prepared by heat induction from CD10 containing the pADD948 replicon. Cells of recipient strain PRP406 were grown overnight in LB medium. To each 0.15 ml of these cells, 0 control ; , 0.15, or 0.5 ml of lysate 4 x 108 PFU ml ; was added at room temperature. After addition of 3 ml LVM top agar to each sample, samples were spread on LVM plates containing glycerol and carbenicillin and incubated at 30C. Colonies growing on these plates after 48 to 60 were purified on VBMM-carbenicillin medium and analyzed for the presence of recombinant plasmids. Construction of LacZ gene fusions. AgmR'-'LacZ gene fusions were constructed as follows. First, a 2.3-kb EcoRVSstI fragment from pPS102 see Fig. 2 ; was subcloned into pUC12 26 ; to yield pUC12-2.2. Next, a 1, 364-bp fragment and cefprozil.

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3. The Group owns a treated effluent discharge pipeline with a cost of Rs. 9, 257 Previous year: Rs. 9, 257 ; and net book value of Rs. 1, 594 Previous year: Rs. 2, 551 ; in equal proportion jointly with a third party in Pydibheemavaram pursuant to a mutual agreement and ceftriaxone.
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