Antony van Leeuwenhoek: Creation “Magnified” Through His Magnificent Microscopes

Although van Leeuwenhoek was not the inventor of the microscope, he advanced it more than anyone else for seeing living things. Antony van Leeuwenhoek1 (Fig. 1) found great joy in God’s smallest creatures. He first discovered protozoans in his youth. The Dutch haberdasher retained a child-like joy of discovery from his youth until his death at age 90. He lived to see tiny microbes though his homemade microscopes. He loved to grind and focus a new lens in order to see the unseen world. Leeuwenhoek spent countless hours grinding tiny lenses and looking through them. This Christian lay biologist even used candlelight to see specimens at night. For Leeuwenhoek, the amazing diversity of tiny life forms revealed under his homemade microscopes glorified God as much as looking at stars through a telescope. Leeuwenhoek was born in South Holland in 1632. As a young adult, he became a cloth merchant (also called a draper, or haberdasher). In 1668, he started his biological study as a hobby after seeing beautiful microscopic pictures while making a visit to London. After years of careful study, Leeuwenhoek (Fig. 2) made the microscope famous. In his lifetime, he became the father of microbiology and opened mankind to the world of microorganisms

Robert Koch, Creation, and the Specificity of Germs

Microbiology is dominated by evolution today. Just look at any text, journal article, or the topics presented at professional scientific meetings. Darwin is dominant. Microbiology is dominated by evolution today. Just look at any text, journal article, or the topics presented at professional scientific meetings. Darwin is dominant. Many argue that “nothing in biology makes sense except in the light of evolution” (Dobzhansky 1973). But it was not always this way. In fact, a review of the major founders of microbiology has shown that they were creationists.1 We would argue that a better idea thanevolution and one of much more practical importance is the germ theory of disease, originally put forth primarily by non-Darwinian biologists (Gillen and Oliver 2009). In our previous article (Gillen and Oliver 2009), we documented these and many other creation and Christian contributions to germ theory. But only recently has it become known that another important microbiology founder, Robert Koch (Fig. 1) and his co-workers were Linnaean creationists in their classification.2 This is due, in part, to additional works of Robert Koch that were translated from German to English. The year 2010 marks the 100thanniversary of his death (died: May 27, 1910). Although Koch and other German microbiologists were fairly secular in their thinking, their acceptance of Darwinian evolution was minimal

Ancient Tahitian Society

“Tahiti is far famed yet too little known.” Thus wrote J. M. Orsmond in 1848, and the same assertion can be made in 1972. Thousands of pages had been published about Tahiti and its neighboring islands when Orsmond uttered his judgment, and tens of thousands have been published since that time, but a unified, comprehensive, and detailed description of the pre-European ways of life of the inhabitants of those Islands is yet to appear in print. The present work, lengthy as it is, makes no such claim to comprehensiveness; rather, it is concerned mainly with the social relations of those inhabitants, and it serves up only enough about their technology, their religion, their aesthetic expressions, and so forth to place descriptions of their social relations in context and render them more comprehensible. Volumes 1 and 2 of this work are a reconstruction of the Islanders’ way of life as it was believed to have been just before it began to be transformed by European influence—a period labeled the Late Indigenous Era. Volume 3 covers events in Tahiti and Mo‘orea from about 1767 to 1815—a period labeled the Early European Era

Origins of Glutamatergic Terminals in the Inferior Colliculus Identified by Retrograde Transport and Expression of VGLUT1 and VGLUT2 Genes

Terminals containing vesicular glutamate transporter (VGLUT) 2 make dense axosomatic synapses on tectothalamic GABAergic neurons. These are one of the three types of glutamatergic synapses in the inferior colliculus (IC) identified by one of three combinations of transporter protein: VGLUT1 only, VGLUT2 only, or both VGLUT1 and 2. To identify the source(s) of these three classes of glutamatergic terminals, we employed the injection of Fluorogold (FG) into the IC and retrograde transport in combination with in situ hybridization for VGLUT1 and VGLUT2 mRNA. The distribution of FG-positive soma was consistent with previous reports. In the auditory cortex, all FG-positive cells expressed only VGLUT1. In the IC, the majority of FG-positive cells expressed only VGLUT2. In the intermediate nucleus of the lateral lemniscus, most FG-positive cells expressed VGLUT2, and a few FG-positive cells expressed both VGLUT1 and 2. In the superior olivary complex (SOC), the majority of FG-positive cells expressing VGLUT2 were in the lateral superior olive, medial superior olive, and some periolivary nuclei. Fewer FG-positive cells expressed VGLUT1&2. In the ventral cochlear nucleus, almost all FG-positive cells expressed VGLUT1&2. On the other hand in the dorsal cochlear nucleus, the vast majority of FG-positive cells expressed only VGLUT2. Our data suggest that (1) the most likely sources of VGLUT2 terminals in the IC are the intermediate nucleus of the lateral lemniscus, the dorsal cochlear nucleus, the medial and lateral superior olive, and the IC itself, (2) VGLUT1 terminals in the IC originate only in the ipsilateral auditory cortex, and (3) VGLUT1&2 terminals in IC originate mainly from the VCN with minor contributions from the SOC and the lateral lemniscal nuclei

The Genesis of Pathogenic E. coli

Even though some strains are pathogenic, most E. coli strains still show evidence of being one of God’s “very good” creations. Fig. 1. E. coli Gram stain (Wiki commons image). E. coli are Gram-negative bacteria, thus red or pink colored. The red color is due to a counterstain, called safranin. Escherichia coli is frequently in the news (Fig. 1). E. coli often gets “bad press” for contaminating drinking water or causing a food-borne infection (via hamburgers, apple juice, spinach, or other foods). Recently a new strain (E. coli O145) has been implicated in contaminating lettuce in the U.S., while another strain (E. coliO157:H7) is apparently in tons of beef and other foods. Pathogenic (disease-causing) E. coli is becoming so common in foods that the government is likely to “beef up” its regulation on the food industry (Dininny 2010). Even though some strains are pathogenic, most E. coli strains still show evidence of being one of God’s “very good” creations. E. coli is also a common experimental organism (a laboratory “pet”) of biologists, and is valuable for studying genetics and variation in living things. Newspapers, biology texts and the popular media increasingly discuss “evolution in action.” Evidence to support this concept includes emerging diseases, antibiotic resistance, and changes in characteristics of bacteria, especially the work of Richard Lenski’s lab. Lenski and his coworkers have shown that bacteria can change rapidly in phenotype (outward appearance) and evolutionists have seized upon this rapid phenotypic change as alleged powerful evidence for Darwinian evolution. Thus, E. coliand “evolution in action” is an important two-fold issue involving empirical (or observational/operational) science and its relationship to the theoretical (or historical) origins issue. Carl Zimmer (2008), in his book, Microcosm: E. coli and the New Science of Life, uses emerging diseases caused by E. coli to bolster his arguments for molecules-to-man evolution. Zimmer’s book popularizes the work of Lenski on emerging (i.e., newly appearing) diseases and increases the appeal of his research as seen in news magazines, general biology and microbiology texts, and at many scientific conferences. Zimmer states that scientists are investigating phenotypic changes in E. coli to demonstrate their ability to undergo “rapid bursts of evolution” (p. 97). Many biologists argue that the wide variation in pathogenicity found in E. coli as support for Darwinian evolution. The typical explanation for the origin of E. coli is that it has been around for billions of years and man only a few millions years. For the mutualistic relationship to have begun between man and microbe, animals and E. coli had to co-evolve in both E. coli and man. The human body had to allow a bacteria to pass through the stomach and reach the intestine (a rapid turnover rate) to become one of the most successful bacteria on the planet (i.e., it\u27s found in every mammal known and even extends to fish). Increasingly reoccurring themes (examples) are being declared about pathogenic E. coli and its “evolution in action”: primarily how new and emerging diseases arise. The origins of new diseases within the same species are really examples of variation and adaptation. We seek to provide an “answer” and alternative to the Darwinian paradigm through investigation of the origin of E. coli and its role in examples of “evolution in action.” The purpose of this article is to discuss the possible origin of E. coli from the time of Creation; and its modification since the Edenic Curse. The specific objectives of this article are to provide reasonable explanations for: (1) the origin and purpose of E. coli in the human body; (2) the genesis of new pathogenic E. coli strains; and (3) a reasonable alternative to evolution in regard to past changes in E. coli and similar bacteria. Finally, we discuss how E. coli fits into the historic, biblical worldview stages of Creation, Curse, Corruption, and Contagion.3 It will integrate the topics of modification and displacement for emerging diseases

Creation and the Germ Theory: How a Biblical Worldview Encouraged the Concept that Germs Make Us Sick

The news media writes frequently that germs cause disease. Infectious diseases such as swine flu, Salmonella, Escherichia coli, MRSA, multi-drug resistant tuberculosis, and AIDS have captured the national headlines in recent months. With each passing year, these headlines reveal that some new disease outbreak or plague threatens thousands of lives. For example, in 2009 the news flash “Swine Flu Threatens the Globe” was broadcast across the nation, alarming many people. The emergence of a new strain of flu (H1N1) was said to place millions at risk

High Resolution Crystal Structures of the Wild Type and Cys-55 right-arrow Ser and Cys-59 right-arrow Ser Variants of the Thioredoxin-like [2Fe-2S] Ferredoxin from Aquifex aeolicus

The [2Fe-2S] ferredoxin (Fd4) from Aquifex aeolicus adopts a thioredoxin-like polypeptide fold that is distinct from other [2Fe-2S] ferredoxins. Crystal structures of the Cys-55 right-arrow Ser (C55S) and Cys-59 right-arrow Ser (C59S) variants of this protein have been determined to 1.25 Å and 1.05 Å resolution, respectively, whereas the resolution of the wild type (WT) has been extended to 1.5 Å. The improved WT structure provides a detailed description of the [2Fe-2S] cluster, including two features that have not been noted previously in any [2Fe-2S] cluster-containing protein, namely, pronounced distortions in the cysteine coordination to the cluster and a Calpha -H-Sgamma hydrogen bond between cluster ligands Cys-55 and Cys-9. These features may contribute to the unusual electronic and magnetic properties of the [2Fe-2S] clusters in WT and variants of this ferredoxin. The structures of the two variants of Fd4, in which single cysteine ligands to the [2Fe-2S] cluster are replaced by serine, establish the metric details of serine-ligated Fe-S active sites with unprecedented accuracy. Both the cluster and its surrounding protein matrix change in subtle ways to accommodate this ligand substitution, particularly in terms of distortions of the Fe2S2 inorganic core from planarity and displacements of the polypeptide chain. These high resolution structures illustrate how the interactions between polypeptide chains and Fe-S active sites reflect combinations of flexibility and rigidity on the part of both partners; these themes are also evident in more complex systems, as exemplified by changes associated with serine ligation of the nitrogenase P cluster

Assignment of Individual Metal Redox States in a Metalloprotein by Crystallographic Refinement at Multiple X-ray Wavelengths

A method is presented to derive anomalous scattering contributions for individual atoms within a protein crystal by collecting several sets of diffraction data at energies spread along an X-ray absorption edge of the element in question. The method has been applied to a [2Fe:2S] ferredoxin model system with localized charges in the reduced state of the iron−sulfur cluster. The analysis shows that upon reduction the electron resides at the iron atom closer to the protein surface. The technique should be sufficiently sensitive for more complex clusters with noninteger redox states and is generally applicable given that crystals are available

Quantitative assessment of damage during MCET: a parametric study in a rodent model

Abstract Background Myocardial cavitation-enabled therapy (MCET) has been proposed as a means to achieve minimally invasive myocardial reduction using ultrasound to produce scattered microlesions by cavitating contrast agent microbubbles. Methods Rats were treated using burst mode focused ultrasound at 1.5 MHz center frequency and varying envelope and pressure amplitudes. Evans blue staining indicated lethal cardiomyocytic injury. A previously developed quantitative scheme, evaluating the histologic treatment results, provides an insightful analysis for MCET treatment parameters. Such include ultrasound exposure amplitude and pulse modulation, contrast agent dose, and infusion rate. Results The quantitative method overcomes the limitation of visual scoring and works for a large dynamic range of treatment impact. Macrolesions are generated as an accumulation of probability driven microlesion formations. Macrolesions grow radially with radii from 0.1 to 1.6 mm as the ultrasound exposure amplitude (peak negative) increases from 2 to 4 MPa. To shorten treatment time, a swept beam was investigated and found to generate an acceptable macrolesion volume of about 40 μL for a single beam position. Conclusions Ultrasound parameters and administration of microbubbles directly influence lesion characteristics such as microlesion density and macrolesion dimension. For lesion generation planning, control of MCET is crucial, especially when targeting larger pre-clinical models.http://deepblue.lib.umich.edu/bitstream/2027.42/115462/1/40349_2015_Article_39.pd