Comparing Avocado, Swamp Bay, and Camphortree as Hosts of Raffaelea lauricola Using a Green Fluorescent Protein (GFP)-Labeled Strain of the Pathogen.

Raffaelea lauricola, a fungal symbiont of the ambrosia beetle Xyleborus glabratus, causes laurel wilt in members of the Lauraceae plant family. North American species in the family, such as avocado (Persea americana) and swamp bay (P. palustris), are particularly susceptible to laurel wilt, whereas the Asian camphortree (Cinnamomum camphora) is relatively tolerant. To determine whether susceptibility is related to pathogen colonization, a green fluorescent protein-labeled strain of R. lauricola was generated and used to inoculate avocado, swamp bay, and camphortree. Trees were harvested 3, 10, and 30 days after inoculation (DAI), and disease severity was rated on a 1-to-10 scale. By 30 DAI, avocado and swamp bay developed significantly more severe disease than camphortree (mean severities of 6.8 and 5.5 versus 1.6, P < 0.003). The extent of xylem colonization was recorded as the percentage of lumena that were colonized by the pathogen. More xylem was colonized in avocado than camphortree (0.9% versus 0.1%, P < 0.03) but colonization in swamp bay (0.4%) did not differ significantly from either host. Although there were significant correlations between xylem colonization and laurel wilt severity in avocado (r = 0.74), swamp bay (r = 0.82), and camphortree (r = 0.87), even severely affected trees of all species were scarcely colonized by the pathogen.

Sudden expansion of a one-dimensional bose gas from power-law traps.

We analyze free expansion of a trapped one-dimensional Bose gas after a sudden release from the confining trap potential. By using the stationary phase and local density approximations, we show that the long-time asymptotic density profile and the momentum distribution of the gas are determined by the initial distribution of Bethe rapidities (quasimomenta) and hence can be obtained from the solutions to the Lieb-Liniger equations in the thermodynamic limit. For expansion from a harmonic trap, and in the limits of very weak and very strong interactions, we recover the self-similar scaling solutions known from the hydrodynamic approach. For all other power-law traps and arbitrary interaction strengths, the expansion is not self-similar and shows strong dependence of the density profile evolution on the trap anharmonicity. We also characterize dynamical fermionization of the expanding cloud in terms of correlation functions describing phase and density fluctuations.

Mediastinal shift secondary to a diaphragmatic hernia: a life-threatening combination.

An 85-year-old man was referred to our department, with a three-day history of increasing shortness of breath. Following clinical and radiological assessment, diaphragmatic herniation of bowel was identified to be causing mediastinal shift and respiratory distress. An emergency laparotomy identified a massive diaphragmatic defect which was not amenable to primary closure. A colopexy procedure was performed to comparmentalise the abdomen and obliterate the diaphragmatic defect. Despite aggressive treatment in the intensive care unit he died from multi-organ failure. This case highlights an extremely rare and life-threatening cause of mediastinal shift and respiratory distress.

How was it for you? Families' experiences of receiving Behavioural Family Therapy.

The benefits of family interventions for families having to cope with serious mental health problems are well documented but routine implementation of these interventions is often problematic. Despite a wealth of research on the clinical outcomes of such interventions, very little is known about families' subjective perceptions of receiving them. This study reports the findings of a phenomenological enquiry into the lived experience of 10 families who received Behavioural Family Therapy (BFT) as part of a training initiative in the West Midlands Health Region of the UK. The results show that families were very satisfied with the intervention. They reported reductions in the levels of stress within the family, reduction in levels of carer burden, enhanced communication skills and a positive sense of empowerment. They attributed these changes to receiving BFT. The majority of families viewed mental health professionals and services more favourably compared to their experiences before receiving BFT. This is an important finding for service providers, commissioners and mental heath workers.

Co-localization of macrophage inflammatory protein-3alpha (Mip-3alpha) and its receptor, CCR6, promotes pancreatic cancer cell invasion.

PURPOSE: Macrophage inflammatory protein-3alpha (Mip-3alpha) is par t of a family of chemotactic cytokines involved in recruiting inflammatory cells throughout the body. CCR6 is a G-protein-linked, seven-transmembrane receptor that is highly specific for Mip-3alpha. The role of Mip-3alpha has been well defined in several inflammatory conditions, but its role has not been well defined in neoplastic processes. Mip-3alpha has been shown to promote pancreatic cancer cell migration, but no studies have demonstrated the effect of Mip-3alpha on pancreatic cancer cell invasion. We hypothesize that Mip-3alpha and its CCR6 receptor promote pancreatic cancer cell invasion. MATERIALS AND METHODS: Immunohistochemical staining was per formed for Mip-3alpha and CCR6 in pancreatic cancer tissue and the human pancreatic cancer cell line PANC-1. RNA was isolated from PANC-1 cancer cells, and the presence of Mip-3alpha messenger RNA in PANC-1 cancer cells was determined by reverse transcriptase polymerase chain reaction. PANC-1 cancer cell invasion of type IV collagen was evaluated in the presence of Mip-3alpha and anti-CCR6 antibody with the use of a modified Boyden chamber invasion assay. RESULTS: Co-localization of Mip-3alpha and its CCR6 receptor in pancreatic cancer was confirmed using immunohistochemical staining for Mip-3alpha and its CCR6 receptor and reverse transcriptase polymerase chain reaction for Mip-3alpha. Immunohistochemical staining of pancreatic cancer tissue and the PANC-1 cancer cell line showed positive staining for Mip-3alpha and its CCR6 receptor within the cancer cells. Staining was also positive for Mip-3alpha within stromal cells adjacent to the cancer cells in pancreatic cancer tissue. Reverse transcriptase polymerase chain reaction demonstrated the presence of Mip-3alpha messenger RNA within PANC-1 cancer cells. Invasion studies showed that increasing concentrations of Mip-3alpha promoted a dose-dependent increase in pancreatic cancer cell invasion of type IV collagen. The addition of 100 ng/mL of Mip-3alpha promoted a threefold increase in pancreatic cancer cell invasion over that of the control group. Anti-CCR6 antibody inhibited Mip-3alpha-stimulated PANC-1 cancer cell invasion of type IV collagen by 63%. DISCUSSION: Co-localization of Mip-3alpha and its CCR6 receptor promotes pancreatic cancer cell invasion of type IV collagen. This finding continues to highlight the importance that inflammation plays in the progression of pancreatic cancer. As the relationship between the inflammatory and neoplastic processes involved with pancreatic cancer becomes better defined, therapies targeting the inflammatory process may help prevent pancreatic cancer invasion and metastasis.

CD1d-restricted immunoglobulin G formation to GPI-anchored antigens mediated by NKT cells.

Immunoglobulin G (IgG) responses require major histocompatibility complex (MHC)-restricted recognition of peptide fragments by conventional CD4(+) helper T cells. Immunoglobulin G responses to glycosylphosphatidylinositol (GPI)- anchored protein antigens, however, were found to be regulated in part through CD1d-restricted recognition of the GPI moiety by thymus-dependent, interleukin-4-producing CD4(+), natural killer cell antigen 1.1 [(NK1.1)+] helper T cells. The CD1-NKT cell pathway regulated immunogobulin G responses to the GPI-anchored surface antigens of Plasmodium and Trypanosoma and may be a general mechanism for rapid, MHC-unrestricted antibody responses to diverse pathogens.

Inhibition of phosphatidylinositol-specific phospholipase C: studies on synthetic substrates, inhibitors and a synthetic enzyme.

Enzyme inhibition studies on phosphatidylinositol-specific phospholipase C (PI-PLC) from B. Cereus were performed in order to gain an understanding of the mechanism of the PI-PLC family of enzymes and to aid inhibitor design. Inhibition studies on two synthetic cyclic phosphonate analogues (1,2) of inositol cyclic-1:2-monophosphate (cIP), glycerol-2-phosphate and vanadate were performed using natural phosphatidylinositol (PI) substrate in Triton X100 co-micelles and an NMR assay. Further inhibition studies on PI-PLC from B. Cereus were performed using a chromogenic, synthetic PI analogue (DPG-PI), an HPLC assay and Aerosol-OT (AOT), phytic acid and vanadate as inhibitors. For purposes of comparison, a model PI-PLC enzyme system was developed employing a synthetic Cu(II)-metallomicelle and a further synthetic PI analogue (IPP-PI). The studies employing natural PI substrate in Triton X100 co-micelles and synthetic DPG-PI in the absence of surfactant indicate three classes of PI-PLC inhibitors: (1) active-site directed inhibitors (e.g. 1,2); (2) water-soluble polyanions (e.g. tetravanadate, phytic acid); (3) surfactant anions (e.g. AOT). Three modes of molecular recognition are indicated to be important: (1) active site molecular recognition; (2) recognition at an anion-recognition site which may be the active site, and; (3) interfacial (or hydrophobic) recognition which may be exploited to increase affinity for the anion-recognition site in anionic surfactants such as AOT. The most potent inhibition of PI-PLC was observed by tetravanadate and AOT. The metallomicelle model system was observed to mimic PI-PLC in reproducing transesterification of the PI analogue substrate to yield cIP as product and in showing inhibition by phytic acid and AOT.

Recognising post-traumatic stress in intensive care patients.

'We may not be able to prevent stress or distress, but we can alter the intensity and duration of stress-related trauma by naming our demons, daring to struggle with them, and by creating healing communities.' (Chandler 1992, p 88) In order to create an environment in which the above process can take place it is incumbent upon nurses to assess patients in need and to institute appropriate intervention at an early stage. Critical care nurses have a particular responsibility to identify the seeds of post-traumatic stress and implement supportive and preventive strategies, primarily because of the numbers of traumatised victims passing through their care. Even so, there appears to be a dearth of critical care literature which addresses either assessment or intervention strategies relevant to this important aspect of practice. The purpose of this paper is to highlight aspects of assessment specific to post-traumatic stress through a critical analysis and explanation of its theoretical base. This will act as a precursor to providing direction on possible practice developments.

Support studies for installing the phosphodiester residues of the Thy-1 glycoprotein membrane anchor.

Support studies for late-stage installation of the three different types of phosphodiesters found in the rat brain Thy-1 glycoprotein membrane anchor are described. The strategy is geared towards optimizing convergency and the development of chemoselective procedures including deprotection, phosphorylation, esterification and cysteinylation has been investigated. Some of these procedures are being designed for oligosaccharides containing several unprotected hydroxy groups.

Effect of morphine and beta-endorphin on human Fc receptor-dependent and natural killer cell functions.

Interactions between opiates and the human immune system have important clinical implications. To further evaluate these interactions, we studied in vitro and in vivo effects of morphine sulfate (morphine) and beta-endorphin (Bend) on antibody-dependent cell cytotoxicity (ADCC), natural killer cell cytotoxicity (NKCC), and effector cell expression of antibody Fc receptors. Morphine and Bend had no potent in vivo or in vitro effect on FcR expression nor did they have a significant in vitro effect on ADCC by monocytes or polymorphonuclear cells. Bend enhancement of NKCC in vitro was inhibited by coincubation of effector cells with morphine. After taking 90 to 150 mg of oral morphine, study volunteers demonstrated a significant decrease in ADCC by peripheral blood mononuclear cells. The same individuals demonstrated a consistent increase in NKCC and no change in the expression of Fc receptors. Effector cells from these individuals responded normally to in vitro incubation with interferon-gamma (IFN-gamma).

Monocytes and polymorphonuclear neutrophils of patients with streptococcal pharyngitis express increased numbers of type I IgG Fc receptors.

Studies using cultured cells have shown that gamma interferon (IFN-gamma) induces the expression of Fc gamma RI (the type I Fc receptor for IgG) on human polymorphonuclear neutrophils (PMN) and greatly increases the number of these receptors on human monocytes. Administration of rIFN-gamma in vivo also causes enhanced Fc gamma RI expression on these cell populations. Because streptococcal antigens are potent inducers of IFN-gamma in vitro, we postulated that IFN-gamma would be produced endogenously in vivo in patients with streptococcal infections. Such production of IFN-gamma in vivo, even at low levels, might be expected to induce the expression of Fc gamma RI on monocytes and neutrophils. To evaluate this possibility, we used monoclonal antibody 32 (mAb 32), which is specific for Fc gamma RI, to quantitate the expression of this receptor on human peripheral blood cells. We measured the binding of mAb 32 to monocytes and PMNs isolated from healthy donors and from patients with group A beta-hemolytic streptococcal (GABHS) pharyngitis. PMNs from healthy donors (n = 12) had 700 +/- 600 (mean +/- SD) mAb 32 binding sites. Patients with pharyngitis and negative throat culture for GABHS (n = 11) had 2,100 +/- 1,600 sites on their PMNs. In contrast, the PMNs from patients with documented GABHS pharyngitis (n = 12) had 11,600 +/- 7,500 mAb 32 binding sites on their surface. There was a similar change in the expression of Fc gamma RI on monocytes, with control monocytes having a mean of 19,900 +/- 3,200 mAb 32 binding sites per cell and the GABHS-positive monocytes having 47,500 +/- 21,400 sites. The GABHS-negative throat culture group had a slightly elevated number of Fc gamma RI with a mean of 28,200 +/- 8,400 sites. 10 patients with documented urinary tract infections and three patients with uncomplicated pyelonephritis had no elevation in Fc gamma RI expression. These studies demonstrate that a localized group A streptococcal infection can cause systemic activation of the entire circulating pool of phagocytes, and suggest that a similar level of activation is uncommon in localized gram-negative infections of the urinary tract.

Differential synthesis of beta-major and beta-minor globin proteins in murine erythroleukemia cells is regulated at the transcriptional level.

We compared the transcription and translation of globin genes in three mouse erythroleukemia cell lines under different conditions in which there is differential expression of beta-major (beta ma) and beta-minor (beta mi). Transcription was measured by pulse labeling of whole cell RNA with [3H]uridine, and translation by labeling whole cell protein synthesis with [3H]leucine. Induction with dimethyl sulfoxide led to increased transcription of alpha, beta ma, and beta mi genes, and the proportion of beta mi RNA synthesized was similar to the proportion of beta mi globin protein produced, whether the cells produced 30-40% beta mi (lines 745 and 9M) or greater than 80% beta mi (clone 25-66). Induction with hemin did not lead to increased globin gene transcription in any line, although globin protein synthesis did increase. Thus, the mechanism of beta globin chain induction depends on the inducing agent, and not on the cell line or the type of beta globin gene product. The relative proportion of beta mi and beta ma globin chain proteins reflects the relative transcription of the two beta genes, whether or not transcription increased following induction.

Hand injuries at leisure.

In a survey of 383 moderate and severe hand injuries in adults, 246 (64.4%) occurred outwith work. Falling (sixty-four patients) and punching (forty-eight patients) were the commonest mechanisms of blunt injury. Glass (eight), knives (seven) and "do-it-yourself" materials (eight) were most frequently implicated in sharp trauma. No outstandingly dangerous hobbies or social activities were identified.

Experimental study of chronic ambulatory peritoneal dialysis. I. Inhibition of protein and amino acid losses by single amino acids.

A successful dog model of the continuous ambulatory peritoneal dialysis patient was developed. These preparations were employed in initial studies of the effects of single amino acid-containing dialysis solutions on the losses of protein and amino acids into the dialysate. A decrease of about 40% in the loss of total amino acids into the dialysate was observed when DL-serine-containing dialysis solutions were employed. The addition of DL-serine, L-lysine, or DL-alanine to the dialysis solutions diminished protein loss into the dialysate by 27-55%. DL-Glutamic acid and DL-aspartic acid were ineffective in this regard.

Increased synthesis of mouse minor hemoglobin in erythroid colonies: a cellular model for hemoglobin regulation.

Globin synthesis was examined in mouse erythroid colonies. Bone marrow cells from DBA/2J adults were cultured in methylcellulose and labeled with 3H-leucine; globin synthesis ratios were determined following electrophoresis of lysates on polyacrylamide gels containing urea, acid, and Triton X-100. Colonies derived from the immature progenitor cells, BFU-E and CFU-E, produced close to 40% beta mi of total beta, while cluster-forming units, erythroblasts, and reticulocytes synthesized approximately 30% beta mi. Thus, beta mi synthesis decreased with increasing maturity of the erythroid compartment being examined, qualitatively resembling the decrease in fetal hemoglobin between BFU-E and erythrocytes in human adults. The mouse system described here thus provides a small animal model for studies of changes in hemoglobin expression during erythroid development.

Increased mouse minor hemoglobin during erythroid stress: a model for hemoglobin regulation.

In mice with "diffuse" hemoglobin (Hb), the decrease in the proportion of minor Hb during ontogeny qualitatively resembles the decline observed in human Hb F. Since Hb F reappears during some forms of erythroid stress, we investigated the effect of hematopoietic stress on minor Hb in DBA/2 mice. The stresses were acetlyphenylhydrazine-induced hemolysis, phlebotomy, or infection with Friend erythroleukemia virus. Recovery from anemia was associated with a transient increase in the synthesis of minor Hb similar to the reappearance of Hb F in man. Minor Hb synthesis also increased during the evolution of erythroleukemia induced by both the anemic and the polycythemic strains of virus. Thus, the mouse model can be used to study Hb regulation, since changes in the modulation of minor Hb synthesis occur under conditions which are associated with alterations in Hb F synthesis in humans.

Natural history of hereditary cancer of the breast and colon.

The natural history of 106 patients from eighteen families manifesting hereditary breast cancer syndromes, and 117 affected patients from twenty families manifesting nonpolyposis hereditary colon cancer were evaluated. Findings were compared with the American College of Surgeons (ACS) long-term audits for breast and colon cancer respectively. The cardinal features of hereditary cancer were observed within the study group, including: (1) a significant younger age of onset (49 years, breast; 46 years, colon); (2) an excess of proximal lesions in the hereditary colon series (49%); and (3) an excess of bilaterality in the hereditary breast cancer patients. The clinical stage at presentation was similar for the hereditary and ACS audit patients. Five-year survival was significantly improved (P less than .05) for both hereditary cancer populations as compared to the ACS audits (67% hereditary breast cancer and 52% nonpolyposis hereditary colon cancer). Improved survival in hereditary colon and breast cancer patients may have a bearing on the design of future clinical protocols.