Search

The terrestrial water cycle links the soil and atmosphere moisture reservoirs through four fluxes: precipitation, evaporation, runoff, and atmospheric moisture convergence (net import of water vapor to balance runoff). Each of these processes is essential for sustaining human and ecosystem well-being. Predicting how the water cycle responds to changes in vegetation cover remains a challenge. Recently, changes in plant transpiration across the Amazon basin were shown to be associated disproportionately with changes in rainfall, suggesting that even small declines in transpiration (e.g., from deforestation) would lead to much larger declines in rainfall. Here, constraining these findings by the law of mass conservation, we show that in a sufficiently wet atmosphere, forest transpiration can control atmospheric moisture convergence such that increased transpiration enhances atmospheric moisture import and results in water yield. Conversely, in a sufficiently dry atmosphere increased transpiration reduces atmospheric moisture convergence and water yield. This previously unrecognized dichotomy can explain the otherwise mixed observations of how water yield responds to re-greening, as we illustrate with examples from China's Loess Plateau. Our analysis indicates that any additional precipitation recycling due to additional vegetation increases precipitation but decreases local water yield and steady-state runoff. Therefore, in the drier regions/periods and early stages of ecological restoration, the role of vegetation can be confined to precipitation recycling, while once a wetter stage is achieved, additional vegetation enhances atmospheric moisture convergence and water yield. Recent analyses indicate that the latter regime dominates the global response of the terrestrial water cycle to re-greening. Evaluating the transition between regimes, and recognizing the potential of vegetation for enhancing moisture convergence, are crucial for characterizing the consequences of deforestation as well as for motivating and guiding ecological restoration., (© 2023 The Authors. Global Change Biology published by John Wiley & Sons Ltd.)

Immune-mediated inflammatory diseases of the central nervous system (CNS) are a group of neurological disorders in which inflammation and/or demyelination are induced by cellular and humoral immune responses specific to CNS antigens. They include diseases such as multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSD), acute disseminated encephalomyelitis (ADEM) and anti-NMDA receptor encephalitis (NMDAR encephalitis). Over the years, many in vivo and in vitro models were used to study clinical, pathological, physiological and immunological features of these neuroimmunological disorders. Nevertheless, there are important aspects of human diseases that are not fully reproduced in the experimental models due to their technical limitations. In this review, we describe the preclinical models of neuroimmune disorders, and how they contributed to the understanding of these disorders and explore potential treatments. We also describe the purpose and limitation of each one, as well as the recent advances in this field., (Copyright © 2020 da Silva, Silva, Goi, Molina, Machado and Sato.)

The identification of autoantibodies in central nervous system (CNS) inflammatory disorders improves diagnostic accuracy and the identification of patients with a relapsing disease. Usual methods to detect autoantibodies are usually divided into 3 categories: tissue-based assays, protein-based assays and cell-based assays (CBA). Tissue-based assays are commonly used for initial identification of autoantibodies based on staining patterns and co-localization. Once the antigen is known, autoantibodies can be detected using other antigen-specific methods based on recombinant proteins and CBA using transfected cells expressing the protein in their cell membranes. Compared to traditional methods using recombinant proteins such as ELISA and western blot, the CBA have advantage of detecting conformational sensitive antibodies using natively folded proteins in the cell membrane. This article reviews the utility of CBA into the clinical practice., Competing Interests: Declaration of Competing Interest The authors declare that this research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. RDM has received a scholarship from CAPES/Brazil. LPC has nothing to disclosure. APBS has received a scholarship from CNPq/Brazil. LDSG has received a scholarship from CAPES/Brazil. BKC has received a scholarship from CNPq/Brazil and speaker honoraria from Libbs. DCM has nothing to disclosure. DKS has received a scholarship from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan; a Grants-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (KAKENHI 15K19472); research support from CNPq/Brazil (425331/2016-4), FAPERGS/MS/CNPq/SESRS (17/2551-0001391-3) PPSUS/Brazil, TEVA (research grant for EMOCEMP Investigator Initiated Study), and Euroimmun AG (Neuroimmunological Complications associated with Arboviruses); and speaker honoraria from Biogen, Novartis, Genzyme, TEVA, Merck-Serono, Roche, and Bayer and has participated in advisory boards for Shire, Roche, TEVA, Merck-Serono and Quest/Athena Diagnostics., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: Neuroimaging studies suggest that acute sleep deprivation can lead to adaptations, such as compensatory recruitment of cerebral structures, to maintain cognitive performance despite sleep loss. However, the understanding of the neurochemical alterations related to these adaptations remains incomplete., Objective: Investigate BDNF levels, cognitive performance and their relations in healthy subjects after acute sleep deprivation., Methods: Nineteen sleep deprived (22.11±3.21years) and twenty control (25.10±4.42years) subjects completed depression, anxiety and sleep quality questionnaires. Sleep deprived group spent a full night awake performing different playful activities to keep themselves from sleeping. Attention, response inhibition capacity and working memory (prefrontal cortex-dependent) were assessed with Stroop and Digit Span tests. Declarative memory (hippocampus-dependent) was assessed with Logical Memory test. Serum BDNF was measured by sandwich ELISA. Data were analyzed with independent samples T-test, ANOVA, ANCOVA and curve estimation regressions. p<0.05 was deemed statistically significant., Results: The sleep deprived group showed higher BDNF levels and normal performance on attention, response inhibition capacity and working memory. However, declarative memory was impaired. A sigmoidal relation between BDNF and Stroop Test scores was found., Conclusions: Increased BDNF could be related, at least in part, to the maintenance of normal prefrontal cognitive functions after sleep deprivation. This potential relation should be further investigated., (Copyright © 2015 Elsevier B.V. All rights reserved.)

Quantification of the expectation of craniofacial growth during the pubertal growth spurt (PGS) is helpful in orthodontic diagnosis and treatment planning. Thus, this study investigated whether the stages of the vertebral maturation index (VMI) would be valid for estimating cranial and mandibular growth during the initial stages of PGS, testing the null hypothesis that these structures do not demonstrate differential growth dependent on the maturation stage. A study population of 45 patients of both genders with 2 lateral cephalometric radiographs, taken at a 12-month interval, was selected from files. All patients should not have been previously submitted to orthodontic treatment and should be before or during the peak stage of PGS. The S-N and Co-Gn cephalometric measurements were traced on both radiographs of each patient, by computed cephalometric tracings, for evaluation of skull and mandible, respectively. The growth of these structures was established by the difference between the measurements obtained on both tracings. The VMI stage was also estimated on the radiographs, determining the position of patients on the PGS curve at two periods, baseline and after 12 months. Cephalometric tracings and VMI estimates were performed by two calibrated examiners. Descriptive statistics revealed that both cephalometric measurements increased during the study period, especially Co-Gn, which demonstrated (ANOVA and Tukey's test; 5% significance level), a statistically significant peak of development (p = 0.001), when the patient was in the VMI stage representing the PGS peak. It was concluded that the VMI stages were valid for the analysis of cranial growth and especially of mandibular growth at the initial stages of PGS, thus rejecting the null hypothesis.

Compared with fetuses near term, midgestation fetal sheep at about 75 d of gestation have higher weight-specific glucose uptake rates, higher plasma glucose concentrations, lower plasma insulin concentrations, higher red blood cell insulin receptor concentrations and affinity, and a lower proportion of body weight accounted for by potentially insulin-sensitive skeletal muscle. Based on these observations, we measured the net rate of glucose uptake by the fetus from the uteroplacenta under basal and hyperinsulinemic conditions in eight fetal sheep at 76 d of gestation and eight fetal sheep at 132 d of gestation (term approximately 150 d). Hyperinsulinemia (414 +/- 90 pM) in the 76-d fetal sheep decreased plasma glucose concentration by 0.20 +/- 0.03 mM (-13%, p < 0.01) and increased the net rate of glucose uptake (8.4 +/- 2.2 mumol/min/kg, +21.3%, p < 0.05) and glucose clearance (11.4 +/- 2.6 mL/min/kg, +39%, p < 0.01). In the 132-d fetuses, a comparable hyperinsulinemia (306 +/- 36 pM) decreased plasma glucose concentration (-0.31 +/- 0.02 mM, -26%, p < 0.05) and increased glucose clearance (16.7 +/- 1.8 mL/min/kg, +73.6%, p < 0.05) to a greater extent than in the 76-d fetuses (p < 0.05 and p < 0.01, respectively). Net glucose uptake rate increased significantly in the 132-d fetuses (6.7 +/- 1.1 mumol/min/kg, +27.5%, p < 0.05), but not differently from the 76-d fetuses (p = 0.21). These data define brisk and significant effects of insulin on glucose metabolism in fetal sheep, even as early as approximately 50% of gestation. The midgestation fetal sheep, particularly in relation to its larger fractional content of body water and smaller fractional content of insulin-sensitive tissues, demonstrates glucose metabolic responses to insulin at least as great as those that occur near term.

The purpose of this randomized, double-blind study was to evaluate the efficacy and safety of a new controlled-release hydrogel pessary for ripening the cervix and initiating labor. Subjects had an entry Bishop score of 4 or less and gestational age of 37 or more weeks. One hundred fourteen women received a placebo pessary and 101 received the hydrogel pessary, containing 10 mg of prostaglandin (PG) E2. Compared with the placebo group, those given the PGE2 pessary were more likely to have an increase in Bishop score of 3 or more (60 or 59% versus 21 or 18%; P less than .0001), change to a Bishop score of 6 or higher (59 or 58% versus 18 or 16%; P less than .0001), and active labor (68 or 67% versus 15 or 13%; P less than .0001). Including the crossover study, uterine hyperstimulation (28 of 182, 15%) and fetal heart rate abnormalities (18 of 182, 10%) in PGE2-treated subjects were reversed on removal of the pessary with no apparent harm to the mother or fetus. These temporary adverse effects appeared while the pessary was in place and after the onset of active labor. Oxytocin was unnecessary in 89 of 182 (49%) of the PGE2-treated cases and was used more often to augment than to induce labor. We conclude that the described controlled-release PGE2 vaginal pessary induces appreciable cervical ripening and frequently initiates active labor with little or no need for oxytocin. The pessary may cause uterine hyperstimulation or fetal heart rate abnormalities, but these would be expected to reverse on removal of the pessary.

The net transfer rate of glucose to the fetus from the placenta (Rf,up) increases approximately 10-fold over the second half of pregnancy. To examine the mechanism underlying this increase, we measured Rf,up at different glucose concentration gradients between maternal arterial (GA) and umbilical arterial (Ga) glucose and at three fetal ages: midgestation (76.0 +/- 0.6 days, n = 6), late gestation (131.5 +/- 2.1 days, n = 8), and an intermediate age (103.3 +/- 1.9 days, n = 4). The GA -- Ga gradient was varied by changing Ga below and above control values with fetal insulin and glucose infusions, respectively, while GA was kept constant at 70 +/- 2 mg/dl by a glucose clamp procedure. The slope of the line relating Rf,up to GA -- Ga increased from 0.15 to 1.01 dl/min in the 76- to 131.5-day period, while the intercept in the GA -- Ga axis remained approximately constant at 34 mg/dl. This indicates a fivefold increase in the ability of the placenta to supply glucose to the fetus at fixed values of maternal and fetal glucose concentration (placental glucose transfer capacity). Concomitant with this increase, there was a significant (P less than 0.001) decrease in control Ga from 26.7 +/- 1.3 to 20.3 +/- 0.3 mg/dl, leading to a significant increase in the GA -- Ga gradient and an 11-fold increase in control Rf,up (from 1.53 to 16.77 mg/min). We conclude that, in the second half of pregnancy, fetal glucose demand grows much more rapidly than placental glucose transfer capacity and requires a decrease in fetal glucose concentration to balance glucose supply and demand.

In early ovine fetal development, the placenta grows more rapidly than the fetus so that at mid-gestation the aggregate weight of placental cotyledons exceeds fetal weight. The purpose of this study was to compare two separate methods of measuring uterine blood flow and glucose and oxygen uptakes in seven mid-gestation ewes, each carrying a single fetus. Uterine blood flow to both uterine horns was measured by microsphere and by tritiated water steady-state diffusion methodology. Calculations of tritiated water blood flows and oxygen and glucose uptakes were based on measurements of arteriovenous concentration differences across each uterine horn. The distribution of blood flow and oxygen uptake between the two uterine horns was strongly correlated with placental mass distribution. The two methods gave comparable results for uterine blood flow (457 +/- 35 vs 476 +/- 35 ml/min), oxygen uptake (457 +/- 35 vs 476 +/- 35 mumol/min), and glucose uptake (63 +/- 8 vs 64 +/- 6 mumol/min). Uterine blood flow was approximately 38% of the late gestation value and 56.1 +/- 1 times higher than umbilical blood flow. Uteroplacental oxygen consumption was about 58% of late gestation measurements and 3.9 +/- 0.5 times higher than fetal oxygen uptake. We confirm that the large placental mass of mid-gestation is associated with high levels of maternal placental blood flow and placental oxidative metabolism.

Penicillin allergy presents a major obstacle to the successful management of some antepartum infections. We studied 15 pregnant women with histories of penicillin allergy confirmed by positive immediate wheal-and-flare skin tests. Thirteen had syphilis, one listeria sepsis, and one Streptococcus viridans endocarditis. Each patient was desensitized over four to six hours by oral administration of increasing doses of penicillin V. At the completion of the procedure, full-dose parenteral therapy with penicillin G or ampicillin was instituted. No extracutaneous reactions were detected. Five of the subjects (33 per cent) experienced pruritus (three) or urticaria (two), but no interruption of desensitization or therapy was necessary. All clinically apparent maternal infections were cured. The pregnancy complicated by listeriosis aborted in the first trimester. The 11 neonates delivered to date are normal. These results indicate that oral desensitization is an acceptably safe approach to therapy in pregnant women who are allergic to penicillin and have infections that require beta-lactam drugs.

In order to determine whether insulin stimulates glucose uptake by the hindlimb tissue of the fetal lamb, we performed 7 paired, euglycemic glucose 'clamp' experiments in 7 chronically prepared fetal sheep. Four sample sets for oxygen content, glucose and lactate concentration were drawn from the external iliac artery and vein during a control period and repeated during a euglycemic, hyperinsulinemic 'clamp' period. Insulin was infused at constant rate (4 mU/min/kg) and the fetal arterial glucose concentration was maintained by variable glucose infusion. The glucose/oxygen quotient increased significantly: 1.05 +/- 0.07 (control) versus 2.02 +/- 0.16 (hyperinsulinemia). There was no change in lactate/oxygen quotient. The data demonstrate that with maximal insulin stimulation, fetal hindlimb tissues increase glucose uptake by 92% with no large change in lactate production, indicating a net accumulation of glucose carbon under these experimental conditions.

To study the effect of genetic differences in the maternal oxyhemoglobin dissociation curve on fetal O2 supply, we compared eight pregnant ewes homozygous for high O2 affinity hemoglobin (A) with eight pregnant ewes homozygous for low O2 affinity hemoglobin (B). Each ewe carried a single fetus. Fetal weights were not significantly different (A, 3,000 +/- 170 g; B, 3,070 +/- 270 g). The A ewes had significantly higher arterial O2 saturation (95 vs. 89.4%), uterine blood flow per kilogram of fetus (464 vs. 374 ml/min), uterine venous O2 saturation (78.1 vs. 67.5%), and placental-to-fetal weight ratio (0.107 vs. 0.085). Uterine venous PO2 was significantly less in A ewes (41.7 vs. 47.6 Torr), but umbilical venous and arterial PO2 and fetal O2 uptake were virtually equal in the two groups. We conclude that the difference in O2 affinity between A and B hemoglobins is fully compensated for by differences in arterial O2 saturation, in the rate of perfusion of the pregnant uterus, and in the degree of PO2 equilibration between the uterine and umbilical circulations so that the single fetuses of A and B hemoglobin carriers have equal levels of oxygenation.