THE DEVELOPMENT AND POSSIBLE RELATIONSHIPS OF A NEW ATKINSIELLA PARASITIC IN INSECT EGGS

Atkinsiella entomophaga is a holocarpic parasite in eggs of various midges and caddis flies. Primary zoospores escape through long discharge tubes and assume an abbreviated period of motility before encysting. Laterally biflagellate secondary zoospores subsequently emerge from the cysts. Coincident with discharge tube formation, the thallus undergoes strong vacuolization giving the protoplast a reticulate aspect with nuclei situated between the vacuoles and connected to one another by protoplasmic threads. Stages in zoosporogenesis resemble those of members of the Lagenidiales. It is proposed that Atkinsiella be included in the Eurychasmaceae along with Eurychasma and Eurychasmidium and that the family be transferred to the Lagenidiales. All members of this family have diplanetic zoospores.     

CELL STRUCTURE AND THE METABOLISM OF INSECT FLIGHT MUSCLE

The biochemical properties of insect flight muscle were investigated to ascertain the mechanisms whereby energy is made available for the contractile processes. It was found: 1. The endogenous respiration of muscle homogenates was diminished by starving the flies. The substrate for this respiration was probably glycogen. 2. To obtain the maximal rate of oxidation of glucose, the homogenate had to be fortified with inorganic phosphate, Mg ions, ATP, and cytochrome c. The nucleotides, AMP and ADP, were not as effective as ATP. The addition of DPN or TPN was not necessary for this system. 3. Flight muscle homogenates oxidized glycogen, some sugars, and amino acids, as well as the intermediates of the glycolytic and tricarboxylic acid cycles. Other evidence demonstrated the substrate specificity of the muscle. 4. By centrifugation, the muscle homogenate was divided into two fractions: one, a soluble fraction representing the sarcoplasm; the other, the particulate fraction which contained the fibrils and the sarcosomes. 5. The particulate fraction, alone, oxidized all the citric acid cycle intermediates, α-glycerophosphate, phosphopyruvate, and the amino acids, glutamic, proline, and cysteine. Regardless of the substrate, no oxygen uptake was found with the sarcoplasm by itself. 6. A recombination of the sarcoplasm and the particulate component was required for the oxidation of glycogen, the hexoses, and all the phosphorylated intermediates of glycolysis, except phosphopyruvate. 7. Isolated mitochondria accounted for all the enzymatic activity of the particulate fraction. These results demonstrate that the enzymes of intermediate metabolism are localized in the sarcoplasm or sarcosomes. The third cytological entity, the myofibrils, plays no role in the energy-providing scheme. From a functional viewpoint, the sarcoplasm and the mitochondria, in combination, furnish the energy for the actomyosin contraction. The results are discussed in relation to analogous findings in other insects and vertebrates.     

THE ROLE OF GABA METABOLISM IN THE CONVULSANT AND ANTICONVULSANT ACTIONS OF AMINOOXYACETIC ACID

Abstract— At high dosage levels AOAA acted as a convulsant agent in mice and rats but in lower amounts it was an effective anticonvulsant agent against INH-induced seizures, by tripling the time to the onset of the convulsions. AOAA elevated brain GABA levels as a result of a preferential inhibition of the GABA-T enzyme system but, contrary to previous reports, the activity of the GAD enzyme system was also inhibited, even by relatively low dosage levels of AOAA. The state of excitability of the brain following the administration of AOAA was related, within the limits of the present study, to changes in GAD activity and GABA levels, but additional data are required before the relationship can be properly evaluated.     

Ca~(2+)在粟酒裂殖酵母细胞周期时相中的作用

以粟酒裂殖酵母(Schizosaccharomyces pombe)为研究材料,研究了Ca~(2+)在细胞周期时相中的作用。当外源Ca~(2+)浓度在0.5-20 mmol/L范围内,随Ca~(2+)浓度增加,细胞增殖速度加快,延滞期逐渐缩短。但SD-Ca（CaCl2省略）并不能终止Sch. pombe的细胞周期。采用缺氮对群体细胞进行同步化,并以EGTA 螯合培养介质中低浓度的Ca~(2+),Sch. pombe 细胞增殖被完全抑制,细胞流式法测定结果表明：细胞周期被终止在G1期。分析认为Ca~(2+) 对Sch. pombe 细胞增殖是必不可少的,外源Ca~(2+)在G1期向S期转化过程中起着关键性的作用。     

MITOCHONDRIA AND THE CONTROL OF INTRACELLULAR CALCIUM

1.Because the calcium (Ca) ion is intimately associated with so many biochemical and physiological phenomena, it is fundamental to understand how intracellular Ca is maintained and controlled. This review draws attention to the vital role played by mitochondria in controlling intracellular Ca and describes how transport of the ion into and out of mitochondria may itself be controlled. 2.The heterogeneous distribution of Ca is a property of most, if not all cells. This arises because the ion binds strongly to a variety of biological compounds, especially those containing oxyanions, which themselves have a heterogeneous distribution in cells, but mostly because of the existence in the cell of specific Ca-ion transport systems. 3.Although the concentration of total Ca in the cell may be quite high, a very large proportion of it is bound and non-diffusible; a small fraction is diffusible but unionized. The proportion of Ca that is ionized is probably much less than I% of the total 4.The mechanisms by which Ca is transported into and out of the mitochondrial matrix are discussed. Inward movement of the ion occurs in response to the membrane potential (negative inside) generated by respiration. The process is carrier-mediated and exhibits characteristics such as substrate specificity, high affinity for Ca, satur-ability, cooperativity, stimulation by permeant anions and is specifically inhibited by low concentrations of Ruthenium Red and lanthanum. The properties of the Ca carrier are geared therefore to facilitate rapid inward movement of Ca into the mitochondria. Such a carrier system is found in mitochondria isolated from a wide variety of tissues and species. 5.Ionized Ca appears not to be distributed across the inner mitochondrial membrane according to the Nernst equation, so the possibility exists that the ion is transported as Ca/H⁺ antiport or as Ca/anion symport. Alternatively, an efflux system coupled to inward movement of a cation may serve to prevent the [Ca ion]_in/[Ca ion]_out from attaining equilibrium. These components together contribute to a Ca-translocation cycle that permits Considerable flexibility in the overall control of Ca flux. 6.Evidence for Ca cycling in mitochondria is presented and the influence of physiological agents such as Mg, phosphoenolpyruvate, inorganic phosphate and adenine nucleotides, on the influx and efflux components are discussed in some detail. Moreover, various hormones administered in vivo are able to induce changes in mitochondrial Ca cycling. One important feature that emerges from this collection of data is that the ability of mitochondria to retain Ca is associated with their ability to retain also their adenine-nucleotide complement. 7.Various lines of research provide convincing evidence in support of the view that mitochondria play a major role in controlling cell Ca in vivo. Especially significant are the observations that the ‘activity’ of mitochondrial Ca transport can change during development in both insect and mammalian tissue, can depend on the hormonal status of the tissue and undergoes a permanent change in certain tumour cells. 8.Finally, consideration is given as to how the mitochondrial Ca transport system is able to modify Ca-sensitive enzyme activities by regulating the Ca concentration in specific environments. Some biological activities that might be susceptible to such control are discussed.     

THE ESSENTIAL ROLE OF CALCIUM ION IN POLLEN GERMINATION AND POLLEN TUBE GROWTH

Brewbaker, James L., and Beyoung H. Kwack. (U. Hawaii, Honolulu.) The essential role of calcium ion in pollen germination and pollen tube growth. Amer. Jour. Bot. 50(9): 859–865. Illus. 1963.—A pollen population effect occurs whenever pollen grains are grown in vitro. Small pollen populations germinate and grow poorly if at all, under conditions which support excellent growth of large pollen populations. The pollen population effect is overcome completely by a growth factor obtained in water extracts of many plant tissues. This factor is shown to be the calcium ion, and its action confirmed in 86 species representing 39 plant families. Other ions (K⁺, Mg⁺⁺, Na⁺) serve in supporting roles to the uptake or binding of calcium. The high requirement of calcium (300–5000 ppm, as Ca (NO₃)₂·4H₂O, for optimum growth) and low calcium content of most pollen may conspire to give calcium a governing role in the growth of pollen tubes both in vitro and in situ. It is suspected that ramifications of this role extend to the self-incompatibilities of plants and to the curious types of arrested tube growth distinguishing, for example, the orchids. A culture medium which proved its merit in a wide variety of pollen growth studies included, in distilled water, 10% sucrose, 100 ppm H₃BO₃, 300 ppm Ca (NO₃)₂·4H₂O, 200 ppm MgSO₄·7H₂O and 100 ppm KNO₃.     

THE CONTROL OF POPULATION-DENSITY THROUGH SOCIAL BEHAVIOUR: A HYPOTHESIS

Any given species of animal generally occurs at a higher population-density where food is more plentiful, and vice versa ; quantitative evidence points to a rather close correlation between the two. Such density differences arise from the activities of the animals themselves, and this implies that population-density is subject to effective internal control, i.e., it is self-regulating.
A theory is put forward that, for each species, population-densities are limited at a safe level, which will protect the food-supply from long-term depletion and assure its renewal for the future. Instead of competing directly for food, animals compete for conventional substitutes, e.g. territory or social position, which are capable of imposing a ceiling density at the optimum level, and can prevent it from rising to the starvation level which would endanger future resources.
Such limitation by conventional means requires the existence of a social organisation. Forms of social competition supplant direct competition for food; their intensity is density-dependent and provides the animals with an index of population-density. This index serves as the "feed-back" for the machinery of density-adjustment, which operates, very broadly, through (1) direct movement (emigration/immigration), and (2) varying the birth and survival rates.     

ROLE OF CALCIUM IN THE CALLOSE RESPONSE OF SELF-POLLINATED BRASSICA STIGMAS

In Brassica oleracea, sporophytic self-incompatibility prevents germination of self pollen, or normal growth of self pollen tubes. After self-pollination, the papillae of stigmas synthesize callose. The role of Ca⁺⁺ in the formation of stigmatic callose was tested by adding compounds that interact with Ca⁺⁺ to suspensions of pollen that were known to induce callose formation in self stigmas. The calcium channel antagonist, lanthanum, and the calcium chelating agent, EGTA, reduced or abolished the callose response to self-pollen suspensions. In the presence of Ca⁺⁺, the calcium ionophore, A23187, induced callose in stigmatic papillae when added to pollen suspensions, or alone. Therefore, callose deposition in response to incompatible pollinations appears to be a calcium-dependent process. Pretreatment of pistils with 100 μm 2-deoxy-D-glucose abolished the callose response to self-pollination, while self pollen remained inhibited and cross pollen grew normally in treated pistils. Thus, callose formation in the stigma is not an essential part of the self-incompatibility mechanism preventing the growth of self pollen in Brassica.     

THE ROLE OF STRESS HORMONES IN THE CONTROL OF GRANULOCYTE PRODUCTION

It has previously been indicated that the inhibitory power of the granulocytic chalone is not influenced by adrenalin. It is now shown that this is true both in absence and in presence of exogenous hydrocortisone. It is also shown that hydrocortisone itself does not cause significant inhibition of DNA synthesis in rat bone marrow cells in vitro, but that it does act to augment the inhibitory effect which the granulocytic chalone induces. It is suggested that the primary action of hydrocortisone may be on the cell membrane which changes the cell wall permeability to chalone, perhaps by reducing its rate of loss from the cells.     

ROLE OF FETAL AND INFANT GROWTH IN PROGRAMMING METABOLISM IN LATER LIFE

Fetal growth and development is dependent upon the nutritional, hormonal and metabolic environment provided by the mother. Any disturbance in this environment can modify early fetal development with possible long-term outcomes as demonstrated by extensive work on ‘programming’. Growth restriction resulting from a deficit in tissue/organ cell number (as measured by tissue DNA content) is irrecoverable. However, when the cell size (or cell protein content) is reduced, the effects on growth may not be permanent. Recent epidemiological studies using archival records of anthropometric measurements related to early growth in humans have shown strong statistical associations between these indices of early development and diseases in later life. It has been hypothesised that the processes explaining these associations involve adaptive changes in fetal organ development in response to maternal and fetal malnutrition. These adaptations may permanently alter adult metabolism in a way which is beneficial to survival under continued conditions of malnutrition but detrimental when nutrition is abundant. This hypothesis is being tested in a rat model which involves studying the growth and metabolism in the offspring of rat dams fed a low-protein diet during pregnancy and/or lactation. Using this rat model, it has been demonstrated that there is:

• (i) Permanent growth retardation in offspring nursed by dams fed a low-protein diet.
• (ii) Permanent and selective changes in organ growth. Essential organs like the brain and lungs are relatively protected from reduction in growth at the expense of visceral organs such as the liver, pancreas, muscle and spleen.
• (iii) Programming of liver metabolism as reflected by permanent changes in activities of key hepatic enzymes of glycolysis and gluconeogenesis (glucokinase and phosphoenolpyruvate carboxykinase) in a direction which would potentially bias the liver towards a ‘starved’ setting. We have speculated that these changes could be a result of altered periportal and perivenous regions of the liver which may also affect other aspects of hepatic function.
• (iv) Deterioration in glucose tolerance with age.
• (v) An increase in the life span of offspring exposed to maternal protein restriction only during the lactation period, and a decrease in life span when exposed to maternal protein restriction only during gestation.

These studies show that hepatic metabolism and even longevity can be programmed by events during early life.