Comparison of vegetable production, resource-use efficiency and environmental performance of high-technology and conventional farming systems for urban agriculture in the tropical city of Singapore.

Urban farming can improve cities' food security and resilience, but the performance of different farming systems with respect to land and investment constraints has not been systematically investigated. Here, we compared conventional soil-based farming, vertical farming with natural lighting (Vnat), and indoor vertical farming. This study aimed to compare (1) the dynamic production of leafy vegetables over time given the same amount of investment and land constraints, (2) the associated water and energy use, and (3) the global warming potential (GWP) of the urban farming sector if each of the three farming systems was solely used in the tropical city-state of Singapore. A system dynamics (SD) model was constructed to map the potential quantity of leafy vegetables produced, together with the water and energy use of each farming system. The land and monetary investment constraints were set at an additional 0.3% of the total land area of Singapore and an annual investment of SGD 10-20 million (0.001-0.005% of Singapore's annual GDP). Vnat farming was predicted to have the highest production level (110,000 t) and self-sufficiency (76.9% of total demand) by 2050 based on the SD model. This would be >3 times the self-sufficiency level achieved by indoor and soil-based farming systems given the same investment and land constraints. Indoor farming was simulated to use <14% the land area of Vnat while soil-based farming exhausted the additional 0.3% of the land allocated. Indoor farming was also the most energy intensive system, requiring 100 times more than Vnat farming. Comparison of the GHG emission rates showed that indoor farming had the greatest GWP-at 2.51 kg CO2-eq per kg of lettuce produced. Our results suggest that Vnat farming may be the best form of urban farming system to provide large amounts of food in Singapore, considering the production level, the amount of resources used, and the environmental impacts.

Empirical food webs of 12 tropical reservoirs in Singapore.

Background: Food webs summarise trophic interactions of the biotic components within an ecosystem, which can influence nutrient dynamics and energy flows, ultimately affecting ecosystem functions and services. Food webs represent the hypothesised trophic links between predators and prey and can be presented as empirical food webs, in which the relative strength/importance of the respective links are quantified. Some common methods used in food web research include gut content analysis (GCA) and stable isotope analysis (SIA). We combine both methods to construct empirical food web models as a basis for monitoring and studying ecosystem-level outcomes of natural (e.g. species turnover in fish assemblage) and intentional environmental change (e.g. biomanipulation). New information: We present 12 food webs from tropical reservoir communities in Singapore and summarise the topology of each with widely-used network indices (e.g. connectance, link density). Each reservoir was surveyed over 4-6 sampling occasions, during which, representative animal groups (i.e. fish species and taxonomic/functional groups of zooplankton and benthic macroinvertebrates) and all likely sources of primary production (i.e. macrophytes, periphyton, phytoplankton and riparian terrestrial plants) were collected. We analysed gut content in fishes and bulk isotope (d13C and d15N) profiles of all animals (i.e. fishes and invertebrates) and plants collected. Both sets of information were used to estimate the relative strength of trophic relationships using Bayesian mixing models. We document our protocol here, alongside a script in the R programming language for executing data management/analyses/visualisation procedures used in our study. These data can be used to glean insights into trends in inter- and intra-specific or guild interactions in analogous freshwater lake habitats.

Calcium: a mediator of the cellular response to chronic Na+/K(+)-ATPase inhibition.

Chronic reduction of Na+/K(+)-ATPase activity has been demonstrated in a number of cell systems to elicit a cellular homeostatic response. Over the course of this response, there is initially a transient stimulation of synthesis of new Na+/K(+)-ATPase molecules, followed by a delayed decrease in its degradation rate, eliciting an effective increase in the number of active pumps in the membrane. The resultant enhancement of pumping capacity promotes the extrusion of accumulated Na+ ions and restores the intracellular electrolyte milieu to preinsult conditions. No cellular mediators of either component of this response have previously been described. We therefore tested the possibility that changes in [Ca2+]i might contribute to the transient stimulation of synthesis observed. Indeed, an effective synthetic response to the inhibition of Na+/K(+)-ATPase by treatment with ouabain required elevated [Ca2+]i levels.

Juxtaglomerular cells cultured on a reconstituted basement membrane.

Circulating renin levels are regulated by release from juxtaglomerular (JG) cells. Here, for the first time, we describe the primary culture of rat juxtaglomerular cells on a reconstituted basement membrane. In addition, primary cultures were transformed with a temperature-sensitive SV40 large T antigen gene to promote the development of a continuous JG cell line. Both primary cultures and transformed JG cells maintain a highly differentiated state and secrete active renin. These preparations now provide a system in which characterization of the cellular mechanisms of regulation of renin synthesis and release is possible.

[Ca2+]i regulates transcription rate of the Na+/K(+)-ATPase alpha 1 subunit.

The Na+/K(+)-ATPase enzyme is a pivotal regulator of intracellular electrolyte levels in animal cells. Changes in the rate of its synthesis have been demonstrated to mediate a number of physiological responses. The cellular mechanisms implicated in such regulatory responses though remain poorly defined. Specifically, no intracellular mediators have previously been established. We now describe for the first time, one putative mediator: [Ca2+]i. Elevations in [Ca2+]i stimulate levels of mRNA alpha 1 and mRNA beta 1, sequences which encode both the catalytic subunit of the enzyme, the alpha subunit, and the glycosylated subunit, the beta subunit. These results suggest that elevations in [Ca2+]i modulate the synthetic rate of the active enzyme, and consequently changes in [Ca2+]i may mediate the regulation of its synthetic rate in a range of physiological settings. The mRNA alpha 1 response to the elevation of [Ca2+]i appears, at least partly, to reflect an increase in transcription rate. However, no such increase in transcription rate of the beta 1 subunit gene was detectable. Thus the mRNA beta 1 response, under conditions of elevated [Ca2+]i, may be explained by a decrease in specific mRNA degradation rate.

Rates of synthesis and degradation of Na+-K+-ATPase during chronic ouabain treatment.

Chronic inhibition of Na+-K+-ATPase activity in outer medullary kidney tubules has previously been demonstrated to elicit a 60% increase in activity, measured under maximal velocity (Vmax) conditions (J. Biol. Chem. 260: 12740-12743, 1985). To investigate the cellular mechanism of this response, we measured the rates of Na+-K+-ATPase synthesis and degradation over its full time course. A transient increase in the rate of synthesis occurred after 12 h of ouabain treatment. After 24-h treatment, the rate of synthesis returned to a level not different from control levels. The relative degradation rate after 24-h treatment, however, was markedly lower in ouabain-treated cells than in control cells. Thus the augmentation of the number of Na+-K+-ATPase sites, elicited by the transient increase in synthesis described, was maintained under steady-state conditions by a reduction in apparent degradation rate constant.

Na+/K+-ATPase regulation in Dahl salt-sensitive and salt-resistant rats.

Circulating Na+/K+-ATPase inhibitors have been implicated in volume-expanded forms of hypertension. Inhibition of vascular smooth muscle cell Na+/K+-ATPase has been demonstrated to elevate intracellular Ca2+ levels and enhance contractility, thus providing a mechanism of raised peripheral resistance. In cells chronically subjected to Na+/K+-ATPase inhibition, however, new Na+/K+-ATPase molecules are synthesized, which then restore the intracellular milieu to preinsult conditions. Restoral of the preinsult intracellular milieu in vascular smooth muscle cells would then be expected to lead to the reduction of muscle cell contractility and peripheral resistance. Thus circulating Na+/K+-ATPase inhibitors may not be effective in eliciting chronic forms of hypertension unless the target cell "homeostatic response" is impaired. We demonstrate an apparent such impairment in Dahl salt-sensitive rats, a genetic model of salt-sensitive hypertension.

Steroids, intracellular sodium levels, and Na+/K+-ATPase regulation.

In outer medullary kidney tubules, both specific mineralocorticoid, and specific glucocorticoid Na+/K+-ATPase activation in vitro were inhibitable by amiloride, an inhibitor of a number of Na+-transporting mechanisms (Bentley, P.J. (1968) J. Physiol. (Lond.) 195, 317-330; Kinsella, J. L., and Aronson, P. S. (1980) Am. J. Physiol. 238, F461-F469). In addition, dexamethasone raised, whereas amiloride reduced, intracellular Na+ levels. These observations are consistent with the possibility that the steroidal responses are mediated by changes in intracellular Na+ ion activity. However, when intracellular Na+ levels were increased by the incubation of tubule segments in medium containing ouabain (10(-4) M), no Na+/K+-ATPase activation was observed, over incubation periods of up to 6 h. As mineralocorticoid and glucocorticoid effects are maximal within 2 h (Rayson, B.M., and Lowther, S.O. (1984) Am. J. Physiol. 246, F656-F662), these results suggest that the Na+ ion per se does not mediate the steroidal effects observed, directly. Incubation of tubule segments in medium containing 10(-4) M ouabain, at 37 degrees C, for longer periods (18 h), however, did indeed increase Na+/K+-ATPase activity, markedly. Thus, a potential homeostatic mechanism was demonstrable, where a chronic increase in intracellular Na+ level, measured after 2-4 h of treatment, resulted in an increase in Na+/K+-ATPase activity, such that the intracellular Na+ level was restored after 18-20 h of incubation to one not significantly different from the control value. This mechanism, however, appears to be clearly distinguishable from that which mediates steroidal Na+/K+-ATPase activation.

23Na NMR studies of rat outer medullary kidney tubules.

Two reservations have previously made interpretation of biological 23Na NMR measurements difficult: the "size" of the extracellular space penetrated by the shift reagent and the possibility of a 60% reduction in the intensity of the NMR-visible 23Na signal due to quadrupolar interactions (Berendsen, H. J. C., and Edzes, H. T. (1973) Ann. N. Y. Acad. Sci. 204, 459-485; Civan, M. M., Degani, H., Margalit, Y., and Shporer, M. (1983) Am. J. Physiol. 245, C213-C219; Gupta, R. K., and Gupta, P. (1982) J. Magn. Reson. 47, 344-350). We have addressed both these issues using a suspension of rat outer medullary kidney tubules, nephron segments responsible for the fine control of total body volume and electrolyte balance. First, the extracellular space penetrated by the shift reagent dysprosium tripolyphosphate, as defined by the extracellular 23Na resonance, revealed a space similar to that which contained extracellular 35Cl- ions. Measurement of an extracellular 35Cl- space using 35Cl NMR was possible because the intracellular 35Cl- resonance was broadened beyond detection in the cells studied. Second, to characterize the reduction of the 23Na signal by quadrupolar interactions, the intracellular 23Na level was raised artificially by simultaneously inhibiting Na+ efflux and increasing the ion permeability of the plasma membrane. Under these conditions, NMR-observable intracellular Na+ reached a level which was approximately 81% of that in the medium, a level determined using chemical techniques. This observation would suggest that the resonance of the intracellular 23Na pool was not subject to a 60% reduction in signal intensity, as a result of nuclear quadrupolar interaction. The intracellular 23Na level measured, under basal conditions, was 23 +/- 2 mumol/ml of cell water (37 degrees C) (n = 3, S.D.) and was demonstrated to be responsive to a number of physiological stimuli. The level was temperature-sensitive. It was reduced by inhibitors of apical Na+ transport, furosemide and amiloride, and it was raised with (Na+ + K+)-ATPase inhibition. The furosemide and amiloride actions described would suggest that the Na+-transporting mechanisms sensitive to these agents (e.g. Na+/K+/Cl- cotransport system, Na+:H+ exchange system) contribute to the regulation of the intracellular Na+ level in the kidney tubular preparation studied.

A common 43 K protein induced by glucocorticoids in a variety of cells and tissues.

We have investigated the domain of adrenal steroid action in a variety of mammalian cells and tissue by high resolution two-dimensional gel electrophoresis and autoradiography. Following in vivo or in vitro treatment with steroids, minced tissue or cells were pulsed with [35S]methionine, and they newly synthesized polypeptides compared with controls by visual inspection of partial protein maps. We have found a similar protein (Mr approximately 41-44K, pI approximately 6.3-6.5) to be consistently increased by dexamethasone in 3 rat tissues and 9 human, bovine and rat cell lines. The protein was constitutively synthesized in all targets; quantitative measurements on the magnitude of response show a 2-fold induction by dexamethasone in all systems, in vivo and in vitro. Glucocorticoid-specific hormones but not sex steroids increase the rate of synthesis; deoxycorticosterone has agonist or antagonist effects on 43K synthesis in different systems studied. Co-electrophoresis experiments indicated that 43K proteins co-migrate in at least 3 rat cell lines from tissues with diverse functions. The functional significance of this common glucocorticoid-induced protein is unknown; its ubiquity and electrophoretic properties suggest a highly conserved, common indicator of glucocorticoid action in diverse target cells and tissues, rather than a tissue-specific response.

Steroid regulation of Na+-K+-ATPase: differential sensitivities along the nephron.

Steroid hormonal activation of the Na+-K+-ATPase enzyme was examined in enriched preparations of outer medullary collecting tubules (MCT) and outer medullary thick ascending limbs of the loop of Henle (MAL), prepared by sedimentation through a discontinuous Ficoll gradient. Using morphological criteria, there was a 2.9-fold enrichment of MCT in fraction 1 when compared with fraction 2 and a 2.2-fold enrichment of MAL in fraction 2 when compared with fraction 1. This separation was further defined using biochemical markers. Na+-K+-ATPase activity, Mg2+-ATPase activity, and the adenylate cyclase response to a number of hormones each supported the morphologic definition of separation. The two preparations were challenged in vitro with both aldosterone and dexamethasone. In fraction 1, the fraction enriched in the MCT, 10(-8) M aldosterone stimulated Na+-K+-ATPase activity by 37%. The same concentration of dexamethasone was without effect. In contrast, 10(-8) M dexamethasone stimulated Na+-K+-ATPase activity by 27% in fraction 2, the fraction enriched in the MAL. In this fraction an equimolar concentration of aldosterone was without effect. Thus, the regulation of Na+-K+-ATPase activity by mineralocorticoids on the one hand and by glucocorticoids on the other would appear to be discontinuously localized along the length of the outer medullary distal nephron.

Rorschach norms for inner city children.

Rorschach data for 272 Black children are presented in age groups from 3 to 12. The Rorschach characteristics presented are F+%, A%, Fabulized Combinations, Perseverations, Color Naming, Rejections, Wholes, Details, Small Details (Dd), R, M, and P. Comparisons with Ames and Exner reveal a lower form accuracy level, and a lower percentage of Wholes, with a higher D level. Response rate, rate of development of the M response, rate of development of the P response, and of the Animal response are very similar to the other normative samples.

Glucocorticoid stimulation of Na-K-ATPase in superfused distal segments of kidney tubules in vitro.

The ability of glucocorticoids to regulate Na-K-ATPase activity directly was assessed in separated rat kidney tubules derived from the distal nephron. These tubules were superfused under sterile conditions and maintained in a viable condition for at least 24 h in a newly devised apparatus. Viability was assessed by measuring O2 consumption, protein/DNA ratios, and Na-K-ATPase and Mg-ATPase activities. At a concentration of 10(-8) M, dexamethasone elicited a 27% increase in tubular Na-K-ATPase activity in 6 h and a 32% increase in 24 h. In a separate series, assayed at 24 h, the maximal effect was obtained at a dexamethasone concentration of less than 10(-8) M, and by inspection half-maximal stimulation was obtained at approximately 10(-9) M. At a concentration of 10(-7) M, 17 beta-estradiol, testosterone, progesterone, and deoxycorticosterone acetate had no significant effect on tubular Na-K-ATPase activity. These results as well as the time-course and dose-response data imply that the response is mediated by the glucocorticoid receptor pathway. Since the magnitude of response in vitro was similar to the one obtained after injection of dexamethasone in vivo, much if not all of the action appears to be direct and independent of glucocorticoid-induced changes in the filtered Na+ load.

Effects of lead poisoning on cognitive test performance.

47 lead-poisoned children, treated and without encephalopathy, are compared with sibling controls on perceptual-verbal pattern comparisons of subtests of the Wechsler Intelligence Scale for Children to determine whether there has been brain damage. Both groups of children do not differ significantly from each other on comparisons of these patterns, and they appear to be similar to each other in WISC functioning. The conclusion is that lead-poisoning, treated, and without encephalopathy, does not result in detectable brain damage by means of these pattern analyses.

IQ following treatment of lead poisoning: a patient-sibling comparison.

Forty-seven children treated for lead poisoning (PbB 50 to 365 microgram/dl) were compared to siblings next in age (PbB less than 40 microgram/dl) by a battery of psychologic tests. Symptoms were present in 18 but none had frank encephalopathy. Physical and neurologic examinations revealed no residual damage. Mean psychologic test scores showed no significant difference between patients and controls except in the arithmetic subtest, in which patients' scores were not related to lead concentration. Intelligence tests failed to distinguish children successfully treated from their sibling controls.

A study of the interaction of catecholamines and antidiuretic hormone on water permeability and the cyclic AMP system in isolated papillae of the rat.

The diffusional water permeability of collecting ducts in vitro and the cyclic A.M.P. content of isolated papillae were measured after exposure to different concentrations of antidiuretic hormone, isoproterenol and noradrenalin. Antidiuretic hormone 25 mu units/ml. caused a 25% increase in diffusional water permeability. This response was not affected by isoproterenol (10(-6) M) or noradrenalin (2 x 10(-6) M). Antidiuretic hormone 100 mu unit ml-1 caused a 50% increase in diffusional water permeability which likewise was not altered by isoproterenol or noradrenalin. Isoproterenol (10(-6) M) and noradrenalin (2 x 10(-6) M) had no significant effect on basal levels of diffusional water permeability. Isoproterenol had no significant effect on the tissue concentration of cyclic A.M.P. concentration induced by antidiuretic hormone. Noradrenalin (2 x 10(-6) and 10(-4)) had no significant effect on basal cyclic A.M.P. concentration. However, noradrenalin inhibited the stimulation of cyclic A.M.P. induced by antidiuretic hormone. This effect was inhibited by phentolamine. This study suggests that catecholamines do not alter water handling by a direct action on the water permeability of the kidney but probably exert their action through an effect of A.D.H. release.

The effects of sodium chloride, urea and mannitol on the permeability in vitro fo rat papillary collecting ducts to THO, 14C-urea and 22Na.

1. The diffusional permeabilities of collecting duct membranes to THO, 14C-urea and 22Na+ have been measured at different concentrations of urea, NaCl and mannitol. 2. In the absence of urea in perfusate and bath or in its presence in low concentrations, the diffusional permeability to urea was 2.0 (s.e.m. = 0.15, n = 58) micrometer s-1, compared with 0.87 (s.e.m. = 0.06, n = 29) microgram s-1 when 200 mmol/l urea was present. The permeability of the collecting ducts to THO or Na+ was not affected by the different urea concentrations. 3. High concentrations of sodium chloride increased the diffusional permeability of collecting ducts to water and urea but did not affect the diffusional permeability of the collecting duct to Na+. 4. Mannitol had effects similar to those of sodium chloride. 5. In all media tested there was an increase in THO and urea permeability when supramaximal amounts of antidiuretic hormone were added. The increases in the various media for each substance were similar, despite widely different starting permeabilities. 6. The results suggest that solutes and water move across collecting duct epithelium by several pathways that respond differently to various stimuli.

A study in vitro of the concentrating defect associated with hypokalaemia and hypercalcaemia.

The diffusional water permeabilities of collecting ducts in the presence and absence of antidiuretic hormone have been measured in isolated papillae from normal, hypokalaemic and hypercalcaemic rats. In a similar in vitro situation the effect of antidiuretic hormone on the papillary content of cyclic AMP has been measured. The diffusional water permeability of collecting ducts in the absence of antidiuretic hormone did not differ significantly in papillae taken from the different groups of rats. The diffusional water permeability in the presence of ADH was 7.4 +/- 0.2 (S.E.M.) mum s-1 in collecting ducts taken from normal rats. In collecting ducts taken from hypokalaemic or hypercalcaemic rats the corresponding values were 5.9 +/- 0.3 and 5.8 +/- 0.5 mum s-1 respectively. This significant decrease (P less than 0.01) in the response to antidiuretic hormone would shift the point at which distal tubule fluid first attains isotonicity with the interstitium. If this shifts from cortex to medulla a greater amount of water enters the interstitium of the medulla and produces an impairment of maximal urinary concentrating ability and this defect could explain most of the observed results in hypokalaemic and hypercalcaemic. Cyclic AMP content of the tissue after the addition of ADH was reduced in papillae taken from hypokalaemic rats. This reduced activation of adenyl cyclase could be the mechanism responsible for the impaired response in water permeability but it is also possible that there is interference, with the chain of reactions mediating permeability changes, at a separate site.