Disentangling functional trait variation and covariation in epiphytic lichens along a continent-wide latitudinal gradient.

Characterizing functional trait variation and covariation, and its drivers, is critical to understand the response of species to changing environmental conditions. Evolutionary and environmental factors determine how traits vary among and within species at multiple scales. However, disentangling their relative contribution is challenging and a comprehensive trait-environment framework addressing such questions is missing in lichens. We investigated the variation in nine traits related to photosynthetic performance, water use and nutrient acquisition applying phylogenetic comparative analyses in lichen epiphytic communities on beech across Europe. These poikilohydric organisms offer a valuable model owing to their inherent limitations to buffer contrasting environmental conditions. Photobiont type and growth form captured differences in certain physiological traits whose variation was largely determined by evolutionary processes (i.e. phylogenetic history), although the intraspecific component was non-negligible. Seasonal temperature fluctuations also had an impact on trait variation, while nitrogen content depended on photobiont type rather than nitrogen deposition. The inconsistency of trait covariation among and within species prevented establishing major resource use strategies in lichens. However, we did identify a general pattern related to the water-use strategy. Thus, to robustly unveil lichen responses under different climatic scenarios, it is necessary to incorporate both among and within-species trait variation and covariation.

Towards quantification of vibronic coupling in photosynthetic antenna complexes.

Photosynthetic antenna complexes harvest sunlight and efficiently transport energy to the reaction center where charge separation powers biochemical energy storage. The discovery of existence of long lived quantum coherence during energy transfer has sparked the discussion on the role of quantum coherence on the energy transfer efficiency. Early works assigned observed coherences to electronic states, and theoretical studies showed that electronic coherences could affect energy transfer efficiency--by either enhancing or suppressing transfer. However, the nature of coherences has been fiercely debated as coherences only report the energy gap between the states that generate coherence signals. Recent works have suggested that either the coherences observed in photosynthetic antenna complexes arise from vibrational wave packets on the ground state or, alternatively, coherences arise from mixed electronic and vibrational states. Understanding origin of coherences is important for designing molecules for efficient light harvesting. Here, we give a direct experimental observation from a mutant of LH2, which does not have B800 chromophores, to distinguish between electronic, vibrational, and vibronic coherence. We also present a minimal theoretical model to characterize the coherences both in the two limiting cases of purely vibrational and purely electronic coherence as well as in the intermediate, vibronic regime.

Occupational exposure to UV light and mortality from multiple sclerosis.

BACKGROUND: The etiology of multiple sclerosis (MS) is largely unknown; low exposure to ultraviolet (UV) light has been a suggested risk factor. The aim of this study was to investigate whether occupational exposure to UV light reduces the risk of death from MS. METHODS: The cohort was based on all individuals in the Swedish census in 1980. All MS-related deaths were identified in the national registry of causes of death. A job-exposure matrix was developed to classify the occupational exposure to UV light. RESULTS: MS was recorded as a cause of the death for 839 individuals. The risk of MS-related death decreased with increasing occupational exposure to UV light. The relative risk adjusted for age, sex, and socioeconomic status was 0.48 (95% CI 0.28-0.80) in the high-exposure group and 0.88 (95% CI 0.73-1.06) in the intermediate-exposure group. CONCLUSIONS: Occupational exposure to UV light was associated with a reduced risk of MS. Our findings are corroborated by previous observations that UV light has a preventive role in the development of MS, although the possibility of reversed causality cannot be completely ruled out.

Maternal nutrition and reproduction of daughters in wild house mice (Mus musculus).

Food deprivation after weaning often has greater effects on the reproductive success of females than of males. However, if animals are deprived prenatally (that is, through food deprivation of the mother during gestation), the reproductive success of males may be more adversely affected than that of females because of a disruption in the organizational effects of testosterone in neonatal male mice. The hypotheses that daughters of female mice deprived of food during gestation would have lower reproductive success than control daughters, but that the impact of maternal food deprivation would be lower for daughters than it would be for sons, was tested. There was no difference in the proportion of daughters of food-deprived and control mothers that produced one or two litters. However, the mean number of pups weaned in the second litters by daughters of control females (5.9 +/- 0.57 SEM) was greater than the number of pups weaned by daughters of food-deprived females (4.5 +/- 0.65 SEM). There were no differences in the mean birth or weaning body weights of offspring. Therefore, maternal food deprivation in mice may have a small but significant effect on the reproductive success of daughters. However, studies of sons born to females that were subjected to the same food deprivation protocol indicate that maternal food deprivation may have a much greater effect on the reproduction of sons than on that of daughters.

Social dominance rank and accessory sex glands in wild adult male house mice born to food-deprived mothers.

Food deprivation after weaning often has greater effects on the reproduction of females than males. However, if animals are deprived prenatally (i.e., through deprivation of the mother during gestation), the reproduction of males may be more negatively impacted because it may decrease their ability to compete with other males and their attractiveness to females. We tested the predictions that adult sons of females that are food-deprived during gestation would tend to lose agonistic encounters with sons of well-nourished (control) females and would have smaller accessory sex glands as well. Sons of control mothers were more frequently dominant to sons of deprived mothers. They also had heavier vesicular-coagulating gland complexes and tended to have heavier preputial glands. However, among males that had not been tested for social dominance rank, there were no such differences in accessory gland weights. These data indicate that maternal food deprivation affects sons only if they engage in agonistic encounters. These effects may be due to a disruption of the organizational effects of testosterone that occur in neonatal male mice and they are likely to have a strong negative impact on the reproduction of the sons of deprived mothers.

Phase II study of amonafide in patients with recurrent glioma.

Amonafide, a novel imide derivative with broad preclinical antitumor activity, achieves significant cerebrospinal fluid levels in animal models. In order to test its antitumor activity in patients with recurrent diffuse infiltrative glioma of the astrocytic and oligodendroglial type, we performed a phase II clinical trial. Of the 22 eligible and evaluable patients treated, 2 (9%) experienced tumor regression lasting more than one year. No other patients experienced tumor regression; one remained stable more than six months. Toxicities consisted primarily of myelosuppression, vomiting, and venous irritation at the infusion site. We conclude that amonafide has minimal activity in recurrent glioma patients. Further investigations are not warranted in this study population.

Phase II evaluation of infusional etoposide and cisplatin in patients with recurrent astrocytoma.

The purpose of this study was to determine the efficacy of 24-hour concomitant infusions of etoposide (100 mg/m2/day, days 1-3) and cisplatin (45 mg/m2/day, days 2-3) in the treatment of patients with recurrent astrocytoma. All 36 patients entered on this trial had histologic proof of astrocytoma with CT scan evidence of tumor progression despite prior radiotherapy and nitrosourea chemotherapy. At initial diagnosis, three patients had low-grade astrocytoma, but 33 (92%) had high-grade astrocytomas. ECOG performance score was 0-1 in 20 patients and 2-3 in 16 patients. The median age of all patients was 45.5 years. Dose-limiting toxicity was myelosuppression with median leukocyte and platelet nadirs of 2,150/mcL and 56,500/mcL respectively. One life-threatening infection occurred, but there were no treatment-related deaths. Vomiting occurred in 78% of patients, but was severe in only 6%. Peripheral neuropathy occurred in 28% but was severe in only 6%. Six patients (17%; 1 CR, 5 REGR) responded to therapy with median time to progression of 6.0 months (range 1.5-17.7 months). Five additional patients (14%) remained stable greater than 6 months and 1 has not progressed at 17.0+ months. Median time to progression and survival in all patients were 2.7 and 5.8 months, respectively. In conclusion, etoposide and cisplatin at this dose and schedule have limited activity in the treatment of recurrent high grade astrocytomas, although durable responses or periods of stability occurred in some patients. Considering the extent of myelosuppression, near maximal doses of the drugs were given.

The priming effect of glucose on insulin release does not involve redistribution of secretory granules within the pancreatic B-cell.

Short-term stimulation of the pancreatic B-cell with glucose produces a time-dependent potentiation of this cell, which markedly enhances the insulin response to a renewed stimulation with the hexose. To study if a redistribution of the B-cell secretory granules to a location close to the B-cell plasma membrane could underlie the priming effect of glucose, an investigation by ultrastructural morphometry was performed. After exposure of perfused rat pancreas to non-priming or priming concentrations of glucose, pale and dark B-cell secretory granules were distinguished and analysed both within a central and a peripheral zone of the B-cell. The pale secretory granules comprised 30-40% of the total granule population in the B-cell. Whereas no difference in diameter of the granules was observed, there was evidence for a greater numerical density of dark granules in the central than in the peripheral part of the B-cell. This finding may be in line with observations implying that newly synthesized insulin is released preferentially to older insulin. The present experiments did, however, not reveal any significant priming effect of glucose on the intracellular distribution of secretory granules in the pancreatic B-cell. The lack of morphological changes in the B-cell by glucose priming of insulin release should, rather, direct increased attention to the biochemical aspects of the priming phenomenon.

Low-molecular-mass surfactant protein type 1. The primary structure of a hydrophobic 8-kDa polypeptide with eight half-cystine residues.

The low-molecular-mass surfactant protein fraction, soluble in chloroform/methanol, contains at least two separate polypeptide chains. The 8-kDa form (type I) was isolated, [14C]carboxymethylated after reduction, and submitted to structural analysis. Its highly hydrophobic nature complicated purification, proteolytic cleavages, and sequence analysis. Acid hydrolysis in 6 M HCl for 7 days was necessary for release of branched-chain residues in full yield. Pepsin was the only enzyme found to cleave the surfactant protein and was used to complement peptide generation by chemical cleavage with CNBr. The primary structure deduced consists of 79 residues with 8 half-cystine residues, and a total of 39% branched-chain hydrophobic residues. However, 11 residues are charged at physiological pH, and all properties of the primary structure are not entirely outstanding in relation to those of other proteins. Hydrophobic segments, coupled with a presumably tight folding from the presence of disulfide bridges, probably explain the unusual properties and the solubility in organic solvents.

Abnormal B-cell function in neonatally streptozotocin-diabetic rats: insensitivity to alloxan toxicity.

The apparent toxicity of alloxan was compared in nondiabetic rats and rats made diabetic by injection with streptozotocin during neonatal life (STZ). In the perfused pancreas of nondiabetic rats, 1 mM alloxan rapidly but evanescently stimulated insulin secretion; this effect was followed by pronounced inhibition of the insulin response to 27 mM glucose (94% inhibition) or 1 mM 3-isobutyl-1-methylxanthine (76% inhibition). Conversely, in STZ-diabetic rats the stimulatory effect of alloxan was reduced to 22% of that elicited in nondiabetic rats. In further contrast, the inhibitory effect of alloxan exposure was abolished with regard to subsequent glucose-induced insulin secretion and attenuated with regard to 3-isobutyl-1-methylxanthine-induced insulin secretion. A relative insensitivity to alloxan was also seen in collagenase-isolated islets, where alloxan completely abolished glucose-induced insulin secretion in islets from nondiabetic rats, but only nonsignificantly reduced secretion (by 37%) in islets from STZ-diabetic rats. Insensitivity to glucose in STZ diabetic rats is associated with insensitivity to alloxan. This implies a common defect in the initial recognition site of glucose and alloxan.

B cell insensitivity in a rat model of non-insulin-dependent diabetes. Evidence for a rapidly reversible effect of previous hyperglycemia.

In perfused pancreas of rats rendered diabetic by streptozotocin injection (STZ) during neonatal age the insulin response to 27 mM glucose was significant but impaired. It was unaffected by the alpha adrenergic blocker phentolamine. When 27 mM mannoheptulose was added simultaneously with 27 mM glucose, insulin release was inhibited, but less promptly than in pancreases from non-diabetic rats. When mannoheptulose was introduced 15 min after starting perfusion with 27 mM glucose, inhibition was apparent in non-diabetic rats, but not in STZ. In non-diabetic rats perfusion without glucose for 40 min failed to affect the subsequent response to 27 mM glucose. Conversely, in STZ, glucose omission enhanced 3.7-fold the response to 27 mM glucose. Insulin release in response to 3-isobutyl-1-methylxanthine (IBMX) was more marked in STZ than in non-diabetic rats. After glucose omission the IBMX-induced response was, however, reduced (67%) in STZ, but not significantly (7%) in non-diabetic rats. Thus, glucopenia in vitro sensitizes B cells of STZ to glucose, but desensitizes them to IBMX. Abnormal responsiveness may be linked to metabolic consequences of B cell fuel abundance.

Acute graft-versus-host disease resulting from normal donor blood transfusions.

2 fatal cases of graft-versus-host disease (GvHD) occurred following blood product transfusions given to patients receiving standard chemotherapy for Hodgkin's disease. GvHD was established by HLA typing, clinical course, and compatible skin biopsy. 23 cases of GvHD following transfusion of blood products from normal donors are also reviewed. It should be suspected when fever or rash appear 1-2 weeks after transfusion of unirradiated blood products into a compromised host or when pancytopenia following chemotherapy is prolonged or unexpectedly severe. Prevention of GvHD by irradiation of granulocytes, platelets and packed red blood cells given to immunosuppressed patients is recommended to prevent this often fatal disease.