Fifth dimension of life and the 4/5 allometric scaling law for human brain

Brain cells are not spherical. The basal metabolic rate (B) of a spherical cell scales as B approximately r2, where r is the radius of the cell; that of a brain cell scales as B approximately r(d), where r is the characteristic radius of the cell and d is the fractal dimensionality of its contour. The fractal geometry of the cell leads to a 4/5 allometric scaling law for human brain, uniquely endowing humans with a 5th dimension and successfully explains why the scaling exponent varies during rest and exercise. A striking analogy between Kleiber's 3/4 law and Newton's second law is heuristically illustrated. A physical explanation is given for the 4th dimension of life for three-dimensional organisms and the 5th dimension for human brain.     

Pitfalls and challenges of estimating population growth rate from empirical data: consequences for allometric scaling relations

The intrinsic rate of increase is a fundamental concept in population ecology, and a variety of problems require that estimates of population growth rate be obtained from empirical data. However, depending on the extent and type of data available (e.g. time series, life tables, life history traits), several alternative empirical estimators of population growth rate are possible. Because these estimators make different assumptions about the nature of age‐dependent mortality and density‐dependence of population dynamics, among other factors, these quantities capture fundamentally different aspects of population growth and are not interchangeable. Nevertheless, they have been routinely commingled in recent ecoinformatic analyses relating to allometry and conservation biology. Here we clarify some of the confusion regarding the empirical estimation of population growth rate and present separate analyses of the frequency distributions and allometric scaling of three alternative, non‐interchangeable measures of population growth. Studies of allometric scaling of population growth rate with body size are additionally sensitive to the statistical line fitting approach used, and we find that different approaches yield different allometric scaling slopes. Across the mix of population growth estimators and line fitting techniques, we find scattered and limited support for the key allometric prediction from the metabolic theory of ecology, namely that log₁₀(population growth rate) should scale as ?0.25 power of log₁₀(body mass). More importantly, we conclude that the question of allometric scaling of population growth rate with body size is highly sensitive to previously unexamined assumptions regarding both the appropriate population growth parameter to be compared and the line fitting approach used to examine the data. Finally, we suggest that the ultimate test of allometric scaling of maximum population growth rates with body size has not been done and, moreover, may require data that are not currently available.     

Testing metabolic ecology theory for allometric scaling of tree size, growth and mortality in tropical forests

The theory of metabolic ecology predicts specific relationships among tree stem diameter, biomass, height, growth and mortality. As demographic rates are important to estimates of carbon fluxes in forests, this theory might offer important insights into the global carbon budget, and deserves careful assessment. We assembled data from 10 old-growth tropical forests encompassing censuses of 367 ha and > 1.7 million trees to test the theory's predictions. We also developed a set of alternative predictions that retained some assumptions of metabolic ecology while also considering how availability of a key limiting resource, light, changes with tree size. Our results show that there are no universal scaling relationships of growth or mortality with size among trees in tropical forests. Observed patterns were consistent with our alternative model in the one site where we had the data necessary to evaluate it, and were inconsistent with the predictions of metabolic ecology in all forests.     

Simple and complex synapses shown by freeze-etching of rat cortical synaptosomes

The shape of the synaptic sites (specialized contact areas) was examined on the synaptic membrane fracture faces of freeze-etched rat cortical synaptosomes. Simple and complex synapses were differentiated on the basis of the absence or presence of unspecialized areas in the synaptic sites. The particle-free nature of these areas is discussed.     

Precision of allometric scaling equations for trees can be improved by including the effect of ecological interactions

Allometric scaling relationships of the form Y = aX ^b are widely utilized in many types of models and analyses of tree structure. They are often viewed as static relationships where both the scaling exponent (b) and the normalization constant (a) obtain empirical values that are fixed within a single set of data. Among different sets of data, their values can show environmental variability. However, there have been only few attempts to give a mechanistic interpretation for this variability. We used field data to demonstrate how the scaling relationships in trees can be modified by ecological interactions. Moreover, we show how such processes can be incorporated into the scaling models to improve the fit and the information content of the scaling equations. When fixed theoretical scaling exponents were used instead of empirical exponents and when the effect of competitive interactions between trees was described by separate submodels that predicted the value of the normalisation constant in the scaling equations, it was possible to obtain 4–10% improvement in the model fit of three different structural scaling relationships. Our results suggest that unexplained variation in the values of the scaling parameters can be substituted by an identified effect of ecological factors on the value of the normalisation constant. This agrees with recent theoretical suggestions stating that ecological factors can directly influence the value of normalisation constants.     

Role of neutrophils in lung vascular injury and edema after premature birth in lambs

Carlton, David P., Kurt H. Albertine, Soo Chul Cho, MennoLont, and Richard D. Bland. Role of neutrophils in lung vascular injury and edema after premature birth in lambs. J. Appl. Physiol. 83(4): 1307-1317, 1997.Toinvestigate the role of neutrophils in the pathogenesis of respiratorydistress after premature birth, we assessed the relationship betweencirculating neutrophil concentration and neutrophil accumulation in thelung, lung lymph and pleural liquid flow, and extravascular lungwater in 10 chronically catheterized preterm lambs (127 ± 1 days gestation) that were mechanically ventilated for 8 h afterbirth. Circulating neutrophil concentration transiently decreasedwithin 2 h after birth and then returned to prenatal values by 6-8h. The decrease in circulating neutrophil concentration was relateddirectly to the accumulation of neutrophils in the air spaces, drainageof liquid and protein from the lung 6-8 h after delivery, andpostmortem extravascular lung water. In additional studies, weintravenously administered mechlorethamine to 5 fetal lambs to reducecirculating neutrophils before delivery (neutrophil concentrationbefore birth: 9 ± 11 cells/µl). Compared with control lambs,neutrophil-depleted lambs had significantly less drainage of liquid(7.8 ± 5.9 vs. 2.6 ± 1.9 ml/h, respectively) and protein (116 ± 74 vs. 42 ± 27 mg/h, respectively) from the lung 6-8 hafter birth and significantly less extravascular lung water atpostmortem (6.5 ± 0.8 vs. 4.8 0.6 g/g dry lung,respectively). Thus neutrophils contribute to thepathogenesis of respiratory distress after premature birth byincreasing lung vascular protein permeability and promoting lung edema.

     

Complement inhibition and statins prevent fetal brain cortical abnormalities in a mouse model of preterm birth

Premature babies are particularly vulnerable to brain injury. In this study we focus on cortical brain damage associated with long-term cognitive, behavioral, attentional or socialization deficits in children born preterm. Using a mouse model of preterm birth (PTB), we demonstrated that complement component C5a contributes to fetal cortical brain injury. Disruption of cortical dendritic and axonal cytoarchitecture was observed in PTB-mice. Fetuses deficient in C5aR (−/−) did not show cortical brain damage. Treatment with antibody anti-C5, that prevents generation of C5a, also prevented cortical fetal brain injury in PTB-mice. C5a also showed a detrimental effect on fetal cortical neuron development and survival in vitro. Increased glutamate release was observed in cortical neurons in culture exposed to C5a. Blockade of C5aR prevented glutamate increase and restored neurons dendritic and axonal growth and survival. Similarly, increased glutamate levels – measured by ¹HMRS – were observed in vivo in PTB-fetuses compared to age-matched controls. The blockade of glutamate receptors prevented C5a-induced abnormal growth and increased cell death in isolated fetal cortical neurons. Simvastatin and pravastatin prevented cortical fetal brain developmental and metabolic abnormalities -in vivo and in vitro. Neuroprotective effects of statins were mediated by Akt/PKB signaling pathways. This study shows that complement activation plays a crucial role in cortical fetal brain injury in PTL and suggests that complement inhibitors and statins might be good therapeutic options to improve neonatal outcomes in preterm birth.     

The permissive effect of cortical steroids on the induction of brain ornithine decarboxylase by nerve growth factor

The intraventricular administration of nerve growth factor causes a marked increase in the activity of ornithine decarboxylase in rat brain. This increase is much smaller in adrenalectomized rats. Dexamethasone and corticosterone, administered either systemically or intraventricularly, are able to restore the ability of nerve growth factor to induce ornithine decarboxylase. The steroids must be given at least three hours before the nerve growth factor to be fully effective.     

Histological studies on the development of porcine tonsils after birth

Tonsils form the topographically first immune barrier of an organism against the invasion of pathogens. We used histology to study the development of tonsils of pigs after birth. At birth, the tonsils consist of diffuse lymphoid tissue without any lymphoid follicle aggregations. At the age of 7 days, lymphoid follicles appeared in the soft palate tonsil. The lymphoid layer of the nasopharyngeal tonsil, soft palate tonsil, and lingual tonsil became thicker, and lymphoid follicles in the lamina propria were clearly visible at the age of 21 days. Secondary lymphoid follicles were present in the nasopharyngeal tonsil at the age of 50 days, and in the soft palate tonsil at the age of 120 days. Dendritic cells (DCs), CD3⁺ T cells and IgA⁺ B cells in the soft palate tonsil, nasopharyngeal tonsil and lingual tonsil increased continuously, especially during the first 21 days. The results suggested that tonsils have an important role in local immune defense against invading antigens after birth and will be beneficial for understanding the mechanisms of immunity in these animals after nasal and oral vaccination.     

Ontogenetic development,allometric growth patterns,and daily increment validation of larvae and juvenile Culter alburnus

Fish ontogeny, allometric growth patterns, and otolith microstructure are fundamental in aquaculture and essential for understanding the early-life ecology of fish. Culter alburnus is a commercially important fish species and an excellent breeding target for aquaculture. In this study, newly hatched C. alburnus larvae were reared to the juvenile stage in a hatchery. Three days post hatch, the eyes, mouth, and intestine had developed, and the larval yolk sac had been completely absorbed. Fin rays started to differentiate in the flexion stage and were fully developed by the postflexion stage. Pigmentations were well developed in the juveniles. Culter alburnus larvae were characterized by 39–43 myomeres and 23–25 anal fin rays, swim bladder shape, and pigmentation. Head length, height, and musculature height showed positive allometric growth patterns, suggesting that head and trunk growth was prioritized. Positive allometric growth of the tail was simultaneous with the formation of fins, suggesting that swimming mode transformation, diet changes, and habitat shifts occurred after the start of the postflexion stage. Otolith growth increments in both the sagittae and lapilli were deposited daily, with the first increment formed on day 1 on the sagittae and day 4 of yolk sac absorption on the lapilli. Increments were thin and faint during the early developmental stage, gradually increasing to reach the broadest widths and the strongest contrast at the postflexion stage, which may be related to habitat shifts. This information will assist in the breeding and hatchery production of C. alburnus and establish suitable methods for analyzing this species’ spatiotemporal distributions and early-life traits.

     

Facilitation of reactions of cortical neurons to cortical and peripheral stimulation after tetanization of the brain surface

The electrical activity of neurons of the sensomotor cortex of an unanesthetized rabbit was investigated. Conditioning tetanization of the cortex was carried out through surface electrodes located close to the site of the lead. Test stimuli were supplied through electrodes 2.5–12 mm more caudally on the cortical surface. In addition, peripheral test stimuli were applied. Impulse reactions to previously ineffective stimuli develop after conditioning tetanization and prolonged (up to 1 min) intensification of exciting postsynaptic potentials (EPSP) to cortical and peripheral test stimuli is observed. Facilitation of the reactions is especially clear during tetanization superthreshold for evoking epileptiform afterdischarges. It continued after the conclusion of these discharges and could also be observed during tetanization subthreshold for evoking afterdischarges. The time course of the facilitation was similar to the time course of the post-tetanic intensification of reactions of single stimuli applied with the electrodes used for tetanization. An analysis of the changes in intracellular activity makes it possible to assume that the mechanism of post-tetanic potentiation (PTP) lies at the basis of the described facilitation, which is considered as the "cellular analog" of the dominant focus which develops as a result of tetanization of the cortical surface.Institute of the Brain, Academy of Medical Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 3, No. 1, pp. 3–12, January–February, 1971.     

Harold Cummins--and the birth, growth and development of dermatoglyphics.

The work of Harold Cummins in dermatoglyphics is reviewed, in the areas of populational variability, twin studies, dermatoglyphics of non-human primates, and dermatoglyphic methodology.     

Genetic basis in epilepsies caused by malformations of cortical development and in those with structurally normal brain

Epilepsy is the most common neurological disorder affecting young people. The etiologies are multiple and most cases are sporadic. However, some rare families with Mendelian inheritance have provided evidence of genes’ important role in epilepsy. Two important but apparently different groups of disorders have been extensively studied: epilepsies associated with malformations of cortical development (MCDs) and epilepsies associated with a structurally normal brain (or with minimal abnormalities only). This review is focused on clinical and molecular aspects of focal cortical dysplasia, polymicrogyria, periventricular nodular heterotopia, subcortical band heterotopia, lissencephaly and schizencephaly as examples of MCDs. Juvenile myoclonic epilepsy, childhood absence epilepsy, some familial forms of focal epilepsy and epilepsies associated with febrile seizures are discussed as examples of epileptic conditions in (apparently) structurally normal brains.     

Alterations of CaMKII after hypoxia-ischemia during brain development

Transient brain hypoxia-ischemia (HI) in neonates leads to delayed neuronal death and long-term neurological deficits. However, the underlying mechanisms are incompletely understood. Calcium-calmodulin-dependent protein kinase II (CaMKII) is one of the most abundant protein kinases in neurons and plays crucial roles in synaptic development and plasticity. This study used a neonatal brain HI model to investigate whether and how CaMKII was altered after HI and how the changes were affected by brain development. Expression of CaMKII was markedly up-regulated during brain development. After HI, CaMKII was totally and permanently depleted from the cytosol and concomitantly deposited into a Triton-insoluble fraction in neurons that were undergoing delayed neuronal death. Autophosphorylation of CaMKII-Thr286 transiently increased at 30 min of reperfusion and declined thereafter. All these changes were mild in P7 pups but more dramatic in P26 rats, consistent with the development-dependent CaMKII expression in neurons. The results suggest that long-term CaMKII depletion from the cytosolic fraction and deposition into the Triton-insoluble fraction may disable synaptic development, damage synaptic plasticity, and contribute to delayed neuronal death and long-term synaptic deficits after transient HI.