The hydrolysis of epoxides catalyzed by inorganic ammonium salts in water: kinetic evidence for hydrogen bond catalysis.

Naturally-occurring inorganic ammonium ions have been recently reported as efficient catalysts for some organic reactions in water, which contributes to the understanding of the chemistry in some natural environments (soils, seawater, atmospheric aerosols, …) and biological systems, and is also potentially interesting for green chemistry as many of their salts are cheap and non-toxic. In this work, the effect of NH4+ ions on the hydrolysis of small epoxides in water was studied kinetically. The presence of NH4+ increased the hydrolysis rate by a factor of 6 to 25 compared to pure water and these catalytic effects were shown not to result from other ions, counter-ions or from acid or base catalysis, general or specific. The small amounts of amino alcohols produced in the reactions were identified as the actual catalysts by obtaining a strong acceleration of the reactions when adding these compounds directly to the epoxides in water. Replacing the amino alcohols by other strong hydrogen-bond donors, such as trifluoroethanol (TFE) or hexafluoroisopropanol (HFIP) gave the same results, demonstrating that the kinetics of these reactions was driven by hydrogen-bond catalysis. Because of the presence of many hydrogen-bond donors in natural environments (for instance amines and hydroxy-containing compounds), hydrogen-bond catalysis is likely to contribute to many reaction rates in these environments.

Evaluation of adsorbents for volatile methyl siloxanes sampling based on the determination of their breakthrough volume.

Volatile methyl siloxanes (VMS) have been detected in many different atmospheres such as biogas, sewage sludge, landfill gas, gasoline and ambient air. In these different atmospheres, their presence can involve several contamination problems and negative effects in industrial processes, their identification and quantification become a real challenge. Up to now there is no standardized procedure for VMS quantification, the sampling step remaining the major obstacle. Sampling gas through sorbent tube followed by analysis on TD-GC-MS is one of the reliable possibilities. It gathers sampling and preconcentration in one step and allows discrimination between all VMS, despite the difficulty to choose the appropriate adsorbent in order to avoid loss of analytes during sampling. In this context, this work deals with the comparison of different types of adsorbents based on the determination of the VMS breakthrough volume (BV). Although Tenax TA is the most widely used adsorbent, experiments show low BV values for the lightest VMS. At 25°C, the BV of TMS and L2 are, respectively, 0.2 and 0.44 L g(-1) which can contribute to an underestimation in concentration during their quantification. Carbosieve SIII usually used for C2-C5, did not adsorb light VMS as it was expected, and breakthrough volume obtained for VMS are more than ten times less than the values obtained for Tenax. On other hand, Chromosorb 106 and Carboxen 1000 in association with Carbotrap C and Carbotrap proved to be appropriated for VMS sampling, due to the high breakthrough volumes obtained for the lightest compounds comparing to the other adsorbents. The BVs of TMS for Carboxen 1000 and Chromosorb 106 are 1.2 × 10(4) and 39 L g(-1), respectively, and 49 × 10(4) and 1142 L g(-1) for L2, respectively.

Hydrocarbon removal from bilgewater by a combination of air-stripping and photocatalysis.

In order to prevent hydrocarbon discharge at sea from the bilge of ships, the International Maritime Organization (IMO) enacted the MARPOL 73/78 convention in which effluents are now limited to those with maximum oil content of 15 ppmv. Thus, photocatalysis and air-stripping were combined for the hydrocarbon removal from a real oily bilgewater sample and an original monitoring of both aqueous and gaseous phases was performed by GC/MS to better understand the process. Our results show that the hydrocarbon oil index [HC] can be reduced to its maximum permissible value of 15 ppmv (MARPOL) in only 8.5h when photocatalysis and air-stripping are used together in a synergistic way, as against 17 h when photocatalysis is used alone. However, this air-assisted photocatalytic process emits a large quantity of volatile organic compounds (VOC) and, within the first four hours, ca. 10% of the hydrocarbon removal in the aqueous phase is actually just transferred into the gaseous one. Finally, we highlight that the n-alkanes with a number of carbon atoms higher than 15 (N(C)>15) are those which most decrease the rate of [HC] removal.

Stacking the deck for success in interprofessional collaboration.

The practice of interprofessional collaboration is increasingly being recognized as an important skill for educators, health professionals, and social service providers. Collaboration involves team building and developing integrated service delivery mechanisms to improve outcomes for recipients of health, education, and social services. The focus on health promotion and illness prevention has led to an increasing demand for health educators to become involved in these collaboratives as members and more often as facilitators. Key concepts associated with early stages of collaborative development are described, with a focus on forming a group identity and weathering the conflicts associated with task and personnel issues. Descriptions and instructions for facilitating activities to move the group successfully through these initial stages are described.

Delayed branching of endothelial capillary-like cords in glycated collagen I is mediated by early induction of PAI-1.

Development of micro- and macrovascular disease in diabetes mellitus (DM) warrants a thorough investigation into the repertoire of endothelial cell (EC) responses to diabetic environmental cues. Using human umbilical vein EC (HUVEC) cultured in three-dimensional (3-D) native collagen I (NC) or glycated collagen I (GC), we observed capillary cord formation that showed a significant reduction in branching when cells were cultured in GC. To gain insight into the molecular determinants of this phenomenon, HUVEC subjected to GC vs. NC were studied using a PCR-selected subtraction approach. Nine different genes were identified as up- or downregulated in response to GC; among those, plasminogen activator inhibitor-1 (PAI-1) mRNA was found to be upregulated by GC. Western blot analysis of HUVEC cultured on GC showed an increase in PAI-1 expression. The addition of a neutralizing anti-PAI-1 antibody to HUVEC cultured in GC restored the branching pattern of formed capillary cords. In contrast, supplementation of culture medium with the constitutively active PAI-1 reproduced defective branching patterns in HUVEC cultured in NC. Ex vivo capillary sprouting in GC was unaffected in PAI-1 knockout mice but was inhibited in wild-type mice. This difference persisted in diabetic mice. In conclusion, the PCR-selected subtraction technique identified PAI-1 as one of the genes characterizing an early response of HUVEC to the diabetic-like interstitial environment modeled by GC and responsible for the defective branching of endothelial cells. We propose that an upregulation of PAI-1 is causatively linked to the defective formation of capillary networks during wound healing and eventual vascular dropout characteristic of diabetic nephropathy.

Activin type II receptors in embryonic dorsal root ganglion neurons of the chicken.

Activin induces neuropeptide expression in chicken ciliary ganglion neurons. To determine if activin might also influence neuropeptide expression in developing sensory neurons, we examined whether type II activin receptors are expressed during embryonic development of the chicken dorsal root ganglia (DRG), and also examined the effects of activin on neuropeptide expression in cultured DRG neurons. Using reverse transcription polymerase chain reaction (rtPCR), we detected mRNAs for both the activin receptors type IIA (ActRIIA) and type IIB (ActRIIB) in DRG from embryonic day 7 through posthatch day 1. With in situ hybridization, we found that morphologically identifiable neurons express mRNAs for both ActRIIA and ActRIIB. With developmental age, a subset of neurons that hybridizes more intensely with riboprobes to these receptor mRNAs becomes evident. A similar pattern of expression is observed with immunocytochemical staining using antisera against activin type II receptors. To examine whether embryonic DRG cells respond to activin we treated dissociated cultures of DRG with activin A and assessed the expression of vasoactive intestinal peptide (VIP) and calcitonin gene related peptide (CGRP) mRNAs using semiquantitative rtPCR. Activin treatment results in an increase in VIP mRNA, but does not affect CGRP mRNA levels. These observations indicate that neurons in the embryonic chicken DRG can respond to activin and suggest that activin has the potential to play a role in the development and function of DRG sensory neurons.

Agreement between clinical examination and quantitative tests of neurologic function among 384 subjects.

BACKGROUND: Quantitative neurological tests are often cheaper and easier than clinical examinations, and provide continuous data which may discriminate between exposed and nonexposed groups with more sensitivity than dichotomous (normal/abnormal) examination data. METHODS: We compare clinical examinations and analogous quantitative tests for arm tremor, postural sway, and vibrotactile sensitivity (finger and toe), for 384 subjects. RESULTS: The "abnormal" clinical outcomes studied were relatively common (range, 3-36%), and did not result in impairment of daily activity for affected subjects. All the quantitative tests were reasonably good predictors of the corresponding clinical outcome. The most predictive test was for toe vibrotactile sensitivity. The probability of an abnormal clinical result for those in the worst quartile for the toe test was 0.63, compared with 0.36 for all subjects. CONCLUSIONS: Our results suggest that certain quantitative tests might be used in epidemiologic studies instead of a physical examination.

Optic disk edema associated with peripapillary serous retinal detachment: an early sign of systemic Bartonella henselae infection.

PURPOSE: To describe optic disk edema associated with peripapillary serous retinal detachment as an early sign of systemic Bartonella henselae infection. METHODS: Multicentered, retrospective case series. RESULTS: Five women and two men presented with optic disk edema producing peripapillary serous retinal detachment. Each patient had a markedly elevated serum anti-B. henselae antibody titer. Patient age ranged from 11 to 44 years, with a mean and median of 26.6 and 28 years, respectively. The time from the onset of systemic symptoms to the onset of visual symptoms varied from 3 days to 1 month. The peripapillary serous retinal detachment resolved within 1 to 3 weeks in each case, producing a macular star in four of seven patients. Initial vision was 20/200 or worse in five of seven patients and improved in four of these five patients to 20/30 or better. CONCLUSIONS: Systemic B. henselae infection should be considered in patients who develop optic disk edema associated with a peripapillary serous retinal detachment, even in the absence of classic neuroretinitis with a macular star.

Shoulder disorders and postural stress in automobile assembly work.

OBJECTIVES: A case-referent study was conducted in an automobile assembly plant to evaluate the risk of shoulder disorders associated with nonneutral postures. METHODS: The cases were workers who reported shoulder pain to the plant clinic during a 10-month period and met symptom criteria (pain frequency or duration in the past year) in an interview; more than one-half also had positive findings in a physical examination. The referents were randomly selected workers who were free of shoulder disorders according to the clinic records, the interview, and the physical examination. For each of the 79 cases and 124 referents, 1 job was analyzed for postural and biomechanical demands by an analyst blinded to the case-referent status. RESULTS: Forty-one percent of the subjects flexed or abducted the right arm "severely" (above 90 degrees) during the job cycle, and 35% did so with the left arm. The peak torques at the shoulder were rather low. Shoulder disorders were associated with severe flexion or abduction of the left [odds ratio (OR) 3.2, 95% confidence interval (95% CI) 1.5-6.5] and the right (OR 2.3, 95% CI 1.2-4.8) shoulder. The risk increased as the proportion of the work cycle exposed increased. The relationships were similar for the cases with and without physical findings. Use of hand-held tools increased the risk and also modified the association with postural stress, although the joint exposure distributions limited full analysis of this finding. CONCLUSIONS: The findings support the conclusion that severe shoulder flexion or abduction, especially for 10% or more of the work cycle, is predictive of chronic or recurrent shoulder disorders.

Is there a common mechanism for the progression of different types of renal diseases other than proteinuria? Towards the unifying theme of chronic hypoxia.

The question of why chronic renal diseases progress is a topic only recently investigated. Putative causes such as proteinuria do not account for all aspects of progressive renal disease. An alternative mechanism, chronic hypoxia, is proposed that might better explain certain elements of progressive renal disease, but elements of the hypothesis remain subject to further study.

Spontaneous central retinal artery occlusion in hemoglobin sickle cell disease.

PURPOSE: To describe a case of spontaneous central retinal artery occlusion in a young man with hemoglobin sickle cell disease. METHOD: Case report. RESULTS: A 31-year-old African-American man with a history of hemoglobin sickle cell disease developed sudden painless loss of vision in the right eye. Medical history was remarkable for the recent history of a mild painful crisis, but no other systemic illness or contributing factors. Central retinal artery occlusion was diagnosed with retinal whitening, cherry red spot, and delayed arteriovenous transit on fluorescein angiography. Over the ensuing week, the patient had visual recovery to 20/60 in the absence of therapeutic intervention. CONCLUSION: Central retinal artery occlusion has been reported in sickle cell hemoglobinopathies (ie, SS, S-thal, sickle trait, and sickle cell), but the association with sickle cell disease is rare. Most reports have described additional contributing factors, such as trauma or concomitant systemic illness, to help account for the central retinal artery occlusion. The present case suggests that sickle cell disease alone is sufficient for the development of central retinal artery occlusion.

Hypoxia-induced changes in extracellular matrix metabolism in renal cells.

The mechanisms underlying the progressive fibrosis that characterises end-stage renal disease in vivo remain to be established but hypoxia, as a result of microvascular injury and loss, has been suggested to play an important role. In support of this hypothesis, in vitro studies show that hypoxia (1% O(2)) induces a fibrogenic phenotype in human renal tubular endothelia, interstitial fibroblasts and microvascular endothelial cells, simultaneously increasing extracellular matrix (ECM) production and decreasing turnover via effectors on matrix-degrading enzymes and their inhibitors. The effects of hypoxia on ECM metabolism are independent of hypoxia-induced growth factors and are mediated by a haem-protein sensor and activation of both protein kinase C- and tyrosine kinase-mediated signal transduction pathways. De novo gene transcription is regulated by both hypoxia-inducible factor-1-dependent and -independent mechanisms. Further understanding of the molecular mechanisms by which decreased oxygen alters expression of genes involved in ECM metabolism in renal cells may provide new insights into the pathogenesis of fibrosis and identify novel avenues for intervention.

The concept of glomerular self-defense.

The balance between local offense factors and defense machinery determines the fate of tissue injury: progression or resolution. In glomerular research, the most interest has been on the offensive side, for example, the roles of leukocytes, platelets, complement, cytokines, eicosanoids, and oxygen radical intermediates. There has been little focus on the defensive side, which is responsible for the attenuation and resolution of disease. The aim of this review is to address possible mechanisms of local defense that may be exerted during glomerular injury. Cytokine inhibitors, proteinase inhibitors, complement regulatory proteins, anti-inflammatory cytokines, anti-inflammatory eicosanoids, antithrombotic molecules, and extracellular matrix proteins can participate in the extracellular and/or cell surface defense. Heat shock proteins, antioxidants, protein phosphatases, and cyclin kinase inhibitors may contribute to the intracellular defense. This article outlines how the glomerulus, when faced with injurious cells or exposed to pathogenic mediators, defends itself via the intrinsic machinery that is brought into play in resident glomerular cells.

British contributions to renal physiology: Of dynasties and diuresis.

British contributions to renal physiology trace back to the seminal contribution of William Bowman, who defined the structure of mammalian nephron and its blood supply and pointed out its likely mode of function. A series of contributions followed, which stemmed from a distinguished lineage of physiologists based at University College London and which had, as its high point, the establishment by Ernest H. Starling, in 1899, of a method for measuring oncotic pressure and the subsequent demonstration that glomerular filtration requires a hydrostatic pressure in excess of oncotic pressure in the glomerular capillaries. Arthur Cushny published a monograph on renal function in 1917 which had wide influence. The homeostasis of water and sodium chloride were the subjects of important contributions by Verney and De Wardener, respectively. Little contribution was made by British renal physiologists to the understanding of single nephron function with the emphasis being largely on integrative physiology.

Inference of the existence of high blood pressure as a cause of renal disease in the mid-19th century: observations on vascular structures in the kidney.

Histological examination of the kidney was well under way by the mid-19th century. Pathological changes noted to be present in Bright's disease gave rise to considerable debate in the literature of the time. Toynbee was perhaps the first to note medial hypertrophy and intimal narrowing of blood vessels in the kidney, while Johnson, around the same time, thought that kidney disease was the cause of compressed vessels. Although he later proposed a causal relationship between contraction of vessels and hypertrophy, Johnson never went beyond the insights articulated by Bright himself and failed to make the link between hypertrophy of vessels and persistently raised blood pressure. Traube considered the possibility that cardiac and renal disease could be the consequences of the same unknown disease, but rejected hypertrophy per se as a causal factor. Gull and Sutton disagreed strongly with Johnson and proposed the presence of a general disease which leads to both cardiac hypertrophy and renal disease. But it was Ewald, writing in Germany, who was able to ascribe both cardiac and vascular hypertrophy to increasing tension in the arterial system and he was the first to articulate the effect of hypertension on the kidney.

Progressive renal disease: fibroblasts, extracellular matrix, and integrins.

Progressive renal disease is characterized by expansion of the tubulo-interstitium and accumulation of extracellular matrix within this tissue compartment. Interstitial fibroblasts are the primary producers of the interstitial matrix, and in the evolution of tubulo-interstitial fibrosis these cells undergo changes, namely increased proliferation, differentiation to myofibroblasts, and altered extracellular matrix metabolism, all of which, in other cell types, have been shown to be regulated by the major family of extracellular matrix receptors, the integrins. In the normal kidney, interstitial fibroblasts express alpha1, alpha4, alpha5, and beta1 integrins, and fibrosis is associated with increased expression of alpha1, alpha2, alpha5, alphav, and beta1 integrins. In particular, alpha5, beta1, and alphav are suggested to be linked with the fibrotic process. In vitro, renal fibroblasts express a similar range of integrins, and ligation of selected receptors is associated with specific functions. Ligation of alpha6 stimulates proliferation, while alpha5 promotes expression of myofibroblastic phenotype, and beta1 integrin has been implicated in cell contraction. Recent studies suggest that renal fibroblasts also express the non-integrin matrix receptors, discoidin domain receptors, and that changes in activation of these receptors may be associated with fibrogenic events. Thus the current, albeit limited, data suggest an important role for receptors for extracellular matrix molecules in the pathogenesis of progressive renal fibrosis.