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Alexander von Humboldt, 1769-1859, scientific explorer of the eighteenth and nineteenth centuries, wrote with a rational mind as well as a romantic spirit. Humboldt's Personal Narrative of a Journey to the Equinoctial Regions of the New Continent during the Years 1799-1804 is a blend of the objective/rational and subjective/romantic, so much so that this work can be considered an early form of science writing in the tradition of literary journalism. Personal Narrative reveals that Humboldt drew on and combined his empirical, rational, and romantic backgrounds to inform and inspire the public and his fellow researchers. The strongest case for Humboldt's work being considered an early form of literary journalism is his consistent use of the picturesque, of which his particular use in Personal Narrative operates at the crossroads between an Age of Reason and Romanticism. In so doing, Humboldt uses the picturesque to entertain as well as inform his audience. Analyses looking for only objectivity, or only subjectivity, in Humboldt's work fall short because he actively uses both in his writing. His scientific philosophy and epistemology create a dynamic feedback loop between objectivity and subjectivity. Further analysis of Humboldt's work as a literary journalistic piece will shed more light on the methodological holism of his epistemology. Recognizing Personal Narrative as an early form of literary journalism opens the door to the works of other authors who were inspired by Humboldt's work to write in ways that could also be considered forms of literary journalism. [ABSTRACT FROM AUTHOR]

Although glycine prevents renal tubular cell injury in vitro, its effect in vivo is not clear. The purpose of this study was to investigate whether a bolus injection of glycine given before reperfusion plus continuous dietary supplementation afterward would reduce renal injury caused by ischemia-reperfusion. Female Sprague-Dawley rats received a semisynthetic powdered diet containing 5% glycine and 15% casein (glycine group) or 20% casein (control group). Two days later, renal ischemia was produced by cross-clamping the left renal vessels for 15 min, followed by reperfusion. The right kidney was removed before reperfusion. The postischemic glomerular filtration rate (GFR) showed that renal function was less impaired and recovered more quickly in rats receiving glycine. For example, at day 7, GFR in controls (0.31 [+ or -] 0.03 ml * [min.sup.-1] * 100 [g.sup.-1]) was about one-half that of glycine-treated rats (0.61 [+ or -] 0.06 ml * [min.sup.-1] * 100 [g.sup.-1], P < 0.05). Furthermore, tubular injury and cast formation observed in controls was minimized by glycine (pathology score, 3.2 [+ or -] 0.4 vs. 1.0 [+ or -] 0.4, P < 0.05). Urinary lactate dehydrogenase (LDH) concentration was elevated by ischemia-reperfusion in the control group (260 [+ or -] 22 U/l), but values were significantly lower by about fourfold (60 [+ or -] 30 U/l) in glycine-fed rats. Similarly, free radical production in urine was significantly lower in glycine-treated animals. Importantly, on postischemic day 1, binding of pimonidazole, an in vivo hypoxia marker, was increased in the outer medulla in controls; however, this phenomenon was prevented by glycine. Two weeks later, mild leukocyte infiltration and interstitial fibrosis were still observed in controls, but not in kidneys from glycine-treated rats. In conclusion, these results indicate that administration of glycine indeed reduces mild ischemia-reperfusion injury in the kidney in vivo, in part by decreasing initial damage and preventing chronic hypoxia. kidney; hypoxia; rat

Intravenous infusion of glycine significantly improves survival in liver transplantation in rats. This was gleaned from the results of an experiment, which revealed that minimal dissection of the rat liver for 12 minutes plus 13 minutes without manipulation did not affect survival. Thus, pretreatment of donors with intravenous glycine minimizes reperfusion injury caused by organ manipulation during harvest and after transplantation.

The ability of glycine to minimize cyclosporin A-induced nephrotoxicity by preventing hypoxia-reperfusion injury in the kidney was investigated. It was determined that cyclosporin A can cause hypoxia via vasoconstriction during increased blood pressure. It was also observed that cyclosporin A can cause increases in free radical formation that can attack lipid components and result in lipid peroxidation. The production of free radicals and a hypoxic condition result in renal injuries such as proximal tubule cell swelling, necrosis and infiltration of macrophages.

Alcohol ingestion results in increases in the release of endotoxin from gut bacteria or membrane permeability of the gut to endotoxin, or both. Female rats are more sensitive to these changes. Elevated levels of endotoxin activate Kupffer cells to release substances such as eicosanoids, tumor necrosis factor-[Alpha] and free radicals. Prostaglandins increase oxygen uptake and most likely are responsible for the hypermetabolic state in the liver. The increase in oxygen demand leads to hypoxia in the liver, and on reperfusion, [Alpha]-hydroxyethyl free radicals are formed that lead to tissue damage in oxygen-poor pericentral regions of the liver lobule. KEY WORDS: alcohol-induced liver injury endotoxin free radicals sex differences rats

Rats showed a marked increase in hepatic oxygen uptake and ethanol metabolism two to three hours after exposure to acute alcohol and treatment with pimonidazole. Pericentral regions of liver lobules also showed a significant accumulation of pimonidazole, a hypoxia marker, suggesting that exposure to alcohol causes hypoxia. Pimonidazole accumulation was blocked by treatment with a Kupferr cell-specific toxicant, indicating that the increase in oxygen uptake involved Kupffer cells.

We investigated the hypothesis that hypokalemia might induce renal injury via a mechanism that involves subtle renal injury and alterations in local vasoactive mediators that would favor sodium retention. To test this hypothesis, we conducted studies in rats with diet-induced [K.sup.+] deficiency. We also determined whether rats with hypokalemic nephropathy show salt sensitivity. Twelve weeks of hypokalemia resulted in a decrease in creatinine clearance, tubulointerstitial injury with macrophage infiltration, interstitial collagen type III deposition, and an increase in osteopontin expression (a tubular marker of injury). The renal injury was greatest in the outer medulla with radiation into the cortex, suggestive of an ischemic etiology. Consistent with this hypothesis, we found an increased uptake of a hypoxia marker, pimonidazole, in the cortex. The intrarenal injury was associated with increased cortical angiontensin-converting enzyme (ACE) expression and continued cortical angiotensin II generation despite systemic suppression of the renin-angiotensin system, an increase in renal endothelin-1, a decrease in renal kallikrein, and a decrease in urinary nitrite/nitrates and prostaglandin [E.sub.2] excretion. At 12 wk, hypokalemic rats were placed on a normal-[K.sup.+] diet with either high (4%)- or low (0.01%)-NaCl content. Despite correction of hypokalemia and normalization of renal function, previously hypokalemic rats showed an elevated blood pressure in response to a high-salt diet compared with normokalemic controls. Hypokalemia is associated with alterations in vasoactive mediators that favor intrarenal vasoconstriction and an ischemic pattern of renal injury. These alterations may predispose the animals to salt-sensitive hypertension that manifests despite normalization of the serum [K.sup.+]. angiotensin II; endothelin; kallikrein; hypertension

Harvesting trauma to the graft dramatically decreases survival after liver transplantation. Since activated Kupffer cells play a role in primary nonfunction, the purpose of this study was to test the hypothesis that organ manipulation activates Kupffer cells. To mimic what occurs with donor hepatectomy, livers from Sprague-Dawley rats underwent dissection with or without gentle organ manipulation in a standardized manner in situ. Perfused livers exhibited normal values for [0.sub.2] uptake (105 [+ or -] 5 [micro]mol [multiplied by] [g.sup.-1] [multipled by] [h.sup.-1]) measured polarigraphically; however, 2 h after organ manipulation, values increased significantly to 160 [+ or -] 8 [micro]mol [multipled by] [g.sup.-1].[h.sup.-1] and binding of pimonidazole, a hypoxia marker, increased about threefold (P [is less than] 0.05). Moreover, Kupffer cells from manipulated livers produced three- to fourfold more tumor necrosis factor-[Alpha], and [PGE.sub.2], whereas intracellular calcium concentration increased twofold after lipopolysaccharide compared with unmanipulated controls (P [is less than] 0.05). Gadolinium chloride and glycine prevented both activation of Kupffer cells and effects of organ manipulation. Furthermore, indomethacin given 1 h before manipulation prevented the hypermetabolic state, hypoxia, depletion of glycogen, and release of [PGE.sub.2] from Kupffer cells. These data indicate that gentle organ manipulation during surgery activates Kupffer cells, leading to metabolic changes dependent on [PGE.sub.2] from Kupffer cells, which most likely impairs liver function. Thus modulation of Kupffer cell function before organ harvest could be beneficial in human liver transplantation and surgery. organ harvest; liver transplantation; hypoxia; primary nonfunction

Cardiovascular adaptations to exercise, particularly at the individual level, remain poorly understood. Previous group level research suggests the relationship between cardiac output and oxygen consumption (-) is unaffected by training as submaximal is unchanged. We recently identified substantial inter-individual variation in the exercise - relationship that was correlated to stroke volume (SV) as opposed to arterial oxygen content. Therefore we explored the effects of sprint interval training (SIT) on modulating - given an individual’s specific - relationship. 22 (21±2 yrs) healthy, recreationally active males participated in a 4-week SIT (8, 20 second sprints; 4x/week, 170% of the work rate at peak) study with progressive exercise tests (PET) until exhaustion. Cardiac output ( L/min; inert gas rebreathe, Finometer Modelflow™), oxygen consumption ( L/min; breath-by-breath pulmonary gas exchange), quadriceps oxygenation (near infrared spectroscopy) and exercise tolerance (6–20; Borg Scale RPE) were measured throughout PET both before and after training. Data are mean Δ from bsl±SD. Higher () and lower () responders were identified post hoc (n = 8/group). SIT increased the - post-training in (3.8±0.2 vs. 4.7±0.2; P = 0.02) while was unaffected (5.8±0.1 vs. 5.3±0.6; P = 0.5). was elevated beyond 80 watts in due to a greater increase in SV (all P<0.04). Peak (ml/kg/min) was increased in (39.7±6.7 vs. 44.5±7.3; P = 0.015) and (47.2±4.4 vs. 52.4±6.0; P = 0.009) following SIT, with having a greater peak both pre (P = 0.02) and post (P = 0.03) training. Quadriceps muscle oxygenation and RPE were not different between groups (all P>0.1). In contrast to , responders are capable of improving submaximal - in response to SIT via increased SV. However, the increased submaximal exercise does not benefit exercising muscle oxygenation. [ABSTRACT FROM AUTHOR]

Summary: This study investigated whether VO2peak is reproducible across repeated tests before (PRE) and after (POST) training, and whether variability across tests impacts how individual responses are classified following 3 weeks of aerobic exercise training (cycle ergometry). Data from 45 young healthy adults (age: 20·1 ± 0·9 years; VO2peak, 42·0 ± 6·7 ml·min−1) from two previously published studies were utilized in the current analysis. Non‐responders were classified as individuals who failed to demonstrate an increase or decrease in VO2peak that was greater than 2·0 times the typical error of measurement (107 ml·min−1) away from zero, while responders and adverse responders were above and below this cut‐off, respectively. VO2peak tests at PRE (three total) and POST (three total) were highly reproducible (PRE and POST average and single measures ICCs: range 0·938–0·992), with low coefficients of variation (PRE:4·9 ± 3·1%, POST: 4·8 ± 2·7%). However, a potential learning effect was observed in the VO2peak tests prior to training, as the initial pretraining test was significantly lower than the third (p = 0·010, PRE 1: 2 946 ± 924 ml·min−1, PRE 3: 3 042 ± 919 ml·min−1). This resulted in fewer individuals classified as adverse responders for Test 3 compared to any combination of tests that included Test 1, suggesting that a single ramp test at baseline may not be sufficient to accurately classify the VO2peak response in young recreationally active individuals. Thus, it is our recommendation that the initial VO2peak test be used as a familiarization visit and not included for analysis. [ABSTRACT FROM AUTHOR]