Are allergies trying to protect us from ourselves?

This article is more than actual so I should repost it, again.  Sorry )


“I have a love/hate relationship with spring, thanks to the aggravating bouts of hay fever that transform me into a faucet for pretty much the entire season. So I’ll admit I was a little skeptical when my editor at Scientific American asked me last week if I wanted to write about a new paper coming out in Nature suggesting that allergies may actually be a good thing. But always curious, I said sure.

I have a love/hate relationship with spring, thanks to the aggravating bouts of hay fever that transform me into a faucet for pretty much the entire season. So I’ll admit I was a little skeptical when my editor at Scientific American asked me last week if I wanted to write about a new paper coming out in Nature suggesting that allergies may actually be a good thing. But always curious, I said sure.

Turns out it’s a fascinating—and pretty convincing—read. It’s dense, but the lead author, Yale immunobiologist Ruslan Medzhikov, was kind to take a good two hours out of his day on Monday to explain some of the gnarlier concepts to me. (Medzhikov is fascinating—you can read more about him in this profilepublished in Disease Models & Mechanisms.)

Medzhikov’s basic argument is that there is a convincing body of research suggesting that allergies have beneficial effects. They break down the toxic components of bee, snakescorpion and gila monster venom, for instance, and our allergic reactions to tick saliva prevent the parasites from feeding.

Ultimately, all allergic responses work towards a common goal: avoidance and expulsion, Medzhitov argues. As I explain in my piece,

More generally, hated allergic symptoms keep unhealthy environmental irritants out of the body, Medzhitov posits. “How do you defend against something you inhale that you don’t want? You make mucus. You make a runny nose, you sneeze, you cough, and so forth. Or if it’s on your skin, by inducing itching, you avoid it or you try to remove it by scratching it,” he explains. Likewise, if you’ve ingested something allergenic, your body might react with vomiting. Finally, if a particular place or circumstance ramps up your allergies, you’re likely to avoid it in the future. “The thing about allergies is that as soon as you stop exposure to an allergen, all the symptoms are gone,” he says.

Obviously, Medzhitov’s theory is just a theory, and it involves a lot of speculation (albeit informed speculation by a really smart guy). But some research suggests an association between allergy severity and cancer risk, in that people with more allergy symptoms are less likely to develop certain cancers. (One shouldn’t read too much into this though; some other factor may drive the association. Perhaps people who eat lots of eggs are more likely to have allergies but less likely to have cancer.) But all in all, I think Medzhitov’s idea does make sense and is well-supported, and most of the outside experts I spoke with agreed, though they did raise questions about some of the specifics.

One aspect of the theory that I didn’t mention in my piece is that it could explain a medical mystery: penicillin allergies. Medzhitov argues that in addition to protecting against venoms, vector-borne diseases and environmental irritants, allergies also evolved to protect against a class of toxins called haptens: proteins that bind to extracellular or membrane-bound proteins in the body, rendering them useless and ultimately causing all sorts of problems. As it turns out, in some people, the penicillin molecule undergoes transformation into a hapten. This transformation is very slow and inefficient—very few penicillin markers turn into haptens, which is a good thing because haptenated penicillin could be dangerous—but nevertheless, some people may develop allergic responses to these few haptenated penicillin molecules, and this can result in an allergic hypersensitivity to the drug, Medzhitov posits.

In the case of something like a penicillin allergy, management is fairly simple (though medically inconvenient): avoid penicillin. The problem today is that there may be millions of allergens in the form of environmental pollutants and irritants, and they may simply be unavoidable. This idea could help explain why allergic diseases have become more common in recent decades: We’re exposed to many more pollutants now than we were 50 years ago, and this chemical flurry could be dialing up our innate defense systems to a constant level of 11. An allergy may be protective, but “if it’s taken to an extreme, it is pathological,” Medzhitov says. I wonder, then, if we may have built ourselves a world that will forever make us sick.”


Palm, N., Rosenstein, R., & Medzhitov, R. (2012). Allergic host defences Nature, 484 (7395), 465-472 DOI: 10.1038/nature11047

Medzhitov, Ruslan (2011). Innovating immunology: an interview with Ruslan Medzhitov Disease Models & Mechanisms, 4 (4), 430-432 DOI:10.1242/dmm.008151

Akahoshi M, Song CH, Piliponsky AM, Metz M, Guzzetta A, Abrink M, Schlenner SM, Feyerabend TB, Rodewald HR, Pejler G, Tsai M, & Galli SJ (2011). Mast cell chymase reduces the toxicity of Gila monster venom, scorpion venom, and vasoactive intestinal polypeptide in mice. The Journal of clinical investigation, 121 (10), 4180-91 PMID: 21926462

Wada T, Ishiwata K, Koseki H, Ishikura T, Ugajin T, Ohnuma N, Obata K, Ishikawa R, Yoshikawa S, Mukai K, Kawano Y, Minegishi Y, Yokozeki H, Watanabe N, & Karasuyama H (2010). Selective ablation of basophils in mice reveals their nonredundant role in acquired immunity against ticks. The Journal of clinical investigation, 120 (8), 2867-75 PMID: 20664169

Sherman, P., Holland, E., & Sherman, J. (2008). Allergies: Their Role in Cancer Prevention The Quarterly Review of Biology, 83 (4), 339-362 DOI:10.1086/592850


#allergy, #conditions-and-diseases, #health, #research, #science, #theory

Our Oceans Have Their Own Kind Of Black Holes

I found this article really interesting – let’s check it :

Mild winters in Northern Europe are thanks to the Gulf Stream, which makes up part of those ocean currents spanning the globe that have always impacted the climate.

Yet our climate is also influenced by huge eddies, black holes of turbulence over 90 miles in diameter, that rotate and drift across the ocean. Their number is reportedly on the rise in the Southern Ocean, increasing the northward transport of warm and salty water. A good thing, because this could moderate the negative impact of melting sea ice in a warming climate.

Yet quantifying their impact so far has been difficult, because the exact boundaries of these swirling water bodies have remained undetectable.  A new paper has outlined a new mathematical technique, Coherent Lagrangian vortices, to find water-transporting eddies with coherent boundaries.

Mathematically speaking, ocean eddies are counterparts to the black holes in space. Credit: George Haller / ETH Zurich

George Haller, Professor of Nonlinear Dynamics at ETH Zurich, and Francisco Beron-Vera, Research Professor of Oceanography at the University of Miami, said the challenge in finding such eddies is to pinpoint coherent water islands in a turbulent ocean. The rotating and drifting fluid motion appears chaotic to the observer both inside and outside an eddy.

They sought to find order in chaos by isolating coherent water islands from a sequence of satellite observations. To their surprise, such coherent eddies turned out to be mathematically equivalent to black holes.

No escape from the vortex

Black holes are objects in space with a mass so great that they attract everything that comes within a certain distance of them. Nothing that comes too close can escape, not even light. But at a critical distance, a light beam no longer spirals into the black hole. Rather, it dramatically bends and comes back to its original position, forming a circular orbit. A barrier surface formed by closed light orbits is called a photon sphere in Einstein’s theory of relativity.
They discovered similar closed barriers around select ocean eddies. In these barriers, fluid particles move around in closed loops – similar to the path of light in a photon sphere. And as in a black hole, nothing can escape from the inside of these loops, not even water.

It is precisely these barriers that help to identify coherent ocean eddies in the vast amount of observational data available. According to Haller, the very fact that such coherent water orbits exist amidst complex ocean currents is surprising.

Eddies as water taxis

Because black-hole-type ocean eddies are stable, they function in the same way as a transportation vehicle – not only for micro-organisms such as plankton or foreign bodies like plastic waste or oil, but also for water with a heat and salt content that can differ from the surrounding water. Haller and Beron-Vera have verified this observation for the Agulhas Rings, a group of ocean eddies that emerge regularly in the Southern Ocean off the southern tip of Africa and transport warm, salty water northwest. The researchers identified seven Agulhas Rings of the black-hole type, which transported the same body of water without leaking for almost a

Haller points out that similar coherent vortices exist in other complex flows outside of the ocean. In this sense, many whirlwinds are likely to be similar to black holes as well. Even the Great Red Spot – a stationary storm – on the planet Jupiter could just be the most spectacular example of a black-hole type vortex . “Mathematicians have been trying to understand such peculiarly coherent vortices in turbulent flows for a very long time”, explains Haller.

Notably, the first person to describe ocean eddies as coherent water islands may well have been the American writer, Edgar Allan Poe. In his story «A Descent into the Maelstrom», he envisioned a stable belt of foam around a maelstrom. This served as inspiration for Haller and Beron-Vera, who went on to find these belts – the oceanic equivalent to photon spheres – using sophisticated mathematical formulas. Their results are expected to help in resolving a number of oceanic puzzles, ranging from climate-related questions to the spread of environmental pollution patterns.

Eddy in the Gulf of Mexico

Just after the publication of Haller’s and Beron-Vera’s results, Josefina Olascoaga, also a Professor of Oceanography in Miami, tested their new mathematical method. She unexpectedly found a large, black-hole type eddy in the Gulf of Mexico. Olascoaga now uses her finding to assess the coherent transport of contamination from a possible future oil spill.
Citation: G. Haller and F. J. Beron-Vera, ‘Coherent Lagrangian vortices: the black holes of turbulence’, Journal of Fluid Mechanics / Volume 731 / September 2013, R4 (10 pages)  DOI:

#black-hole, #research, #science, #science-news

Mice Infected with Low-Virulence Strains of Toxoplasma gondii Lose Their Innate Aversion to Cat Urine, Even after Extensive Parasite Clearance

Fount this interesing research news (from PlosONe):

Toxoplasma gondii chronic infection in rodent secondary hosts has been reported to lead to a loss of innate, hard-wired fear toward cats, its primary host. However the generality of this response across T. gondii strains and the underlying mechanism for this pathogen-mediated behavioral change remain unknown. To begin exploring these questions, we evaluated the effects of infection with two previously uninvestigated isolates from the three major North American clonal lineages of T. gondii, Type III and an attenuated strain of Type I. Using an hour-long open field activity assay optimized for this purpose, we measured mouse aversion toward predator and non-predator urines. We show that loss of innate aversion of cat urine is a general trait caused by infection with any of the three major clonal lineages of parasite. Surprisingly, we found that infection with the attenuated Type I parasite results in sustained loss of aversion at times post infection when neither parasite nor ongoing brain inflammation were detectable. This suggests that T. gondii-mediated interruption of mouse innate aversion toward cat urine may occur during early acute infection in a permanent manner, not requiring persistence of parasite cysts or continuing brain inflammation.

Toxoplasma gondii is a highly prevalent and successful neurotropic protozoan parasite that infects mammals and birds and is found nearly everywhere in the world [1][2]. However, the parasite can only sexually reproduce in the feline gut, defining cats as the primary host [3]. When T. gondii infects an intermediate host such as rodents or humans, it infiltrates the central nervous system and forms slow-growing cysts inside neurons where it can persist for the life of the host [4]. In order to complete the parasite’s life cycle, an infected secondary host must be eaten by a cat. Behavioral studies comparing infected and uninfected mice have suggested that rodents lose their innate, hard-wired fear of cat odors when chronically infected with T. gondii[5][6][7], presumably enhancing the transmission of the parasite to its primary host.

While intriguing, these studies had several limitations. Most T. gondii strains found in North America and Europe can be categorized into three well-defined clonal lineages called Type I, Type II, and Type III [8][9][10]. The majority of behavioral studies have used Type II strains, which are known to result in high parasite-cyst loads in the brains of mice and cause correspondingly high levels of immune-mediated brain inflammation [11][12][13]. This can result in general brain pathology causing extraneous motor and behavioral changes in infected mice, complicating the interpretation of predator aversion responses.

Type III parasites, in contrast, result in a lower cyst burden and cause less general brain inflammation [14][15]. Type I parasites are typically highly lethal in mice; however, the recent identification of ROP5 genes as the mediators of acute virulence and the generation of attenuated parasites lacking this locus [16][17] permits long-term Type I infection studies in mice, perhaps due to a non-persistent infection following Immunity Related GTPase-mediated clearance. Extending mouse innate avoidance studies to include the less virulent Type III and attenuated Type I parasites described above could lead to clearer behavioral results, free of mitigating pathology-related changes.

Results and Discussion

In order to evaluate the loss of aversion to cat urine in mice, we developed a rigorous high throughput behavioral assay. Mice were placed in a 15-inch by 7-inch enclosure with a small plastic dish affixed to one end. Either bobcat urine or rabbit urine was added to the dish and mice were allowed to explore the cage freely for one hour in the dark. The movements of each mouse were automatically recorded using Motor Monitor Smart Frames by Kinder Scientific, which are comprised of a grid of infrared beams and detectors. Each time the animal crosses a photobeam, the system records a ‘beam break,’ and provides the position and time spent in each designated area. The time spent close to the dish, defined as ‘Near Target’, or on the opposite end of the enclosure, the ‘Avoidance Area’, was assessed for up to 16 individually caged mice simultaneously (Figure 1A).


Figure 1. Assessment of aversion demonstrates loss of fear toward cat urine in Type I- and Type III-infected mice.

[A] Overhead representation of behavioral arena where a small dish containing the ‘target’ solution (yellow disk) is affixed at one end of the behavioral arena. ‘Near Target’ is defined as the area of the arena (white) proximal to the target. ‘Avoidance’ is defined as the most distal region (dark grey) of the enclosure relative to the target. [B] Representative heat maps of mouse place preference during a 60-minute trial of (i) uninfected mice exposed to rabbit urine, and (ii) uninfected, (iii) attenuated Type I-infected, and (iv) low-virulence Type III-infected mice exposed to bobcat urine from trials conducted at 2 months post infection. [C] Aversion ratio, the avoidance time to near target time, of uninfected (red circles), Type I-infected (green triangles), and Type III-infected (blue squares) animals when exposed to bobcat urine (filled shapes) or rabbit urine (open shapes) at 3 weeks, 2 months, and 4 months post infection (n = 10 for each group). Error bars are the Standard Error of the Mean (SEM).


In the process of optimizing our behavioral assay, we confirmed the loss of aversion to cat urine in mice previously reported by others [6][18]. In preliminary experiments with male and female Balb/c mice, chronic infection with two Type II parasite strains (Pru and ME49) caused loss of innate aversion to bobcat urine (unpublished data). Due to slightly higher variability in female mouse behavior, likely due to higher levels of pathology [19], we performed all other experiments exclusively with males.

As anticipated, mice infected with Type II parasites succumbed to infection during both the acute and chronic phase. Surviving mice tended to have more complications associated with the progress of the infection as well as more ‘sickness’ behavior characterized in part by lower activity levels. Due to the variety of generalized pathology and since detailed studies of Type II infection as it relates to mouse behavior exist elsewhere, we did not continue investigations with Type II parasites.

To better characterize T. gondii’s ability to cause loss of innate aversion to cat urine in mice, we compared two additional parasite strains: an attenuated Type I and a low-virulence Type III. Male mice were assayed at three time points: three weeks, two months, and four months post infection. Uninfected mice showed no place preference when exposed to non-predator control rabbit urine (Figure 1Bi), spending close to equal time in the Near Target Area and the Avoidance Area. When exposed to bobcat urine, these same animals exhibited marked aversion, spending more time in the Avoidance Area than in the Near Target Area (Figure 1Bii). Type I- and Type III-infected animals behaved similarly to uninfected animals when exposed to rabbit urine, including total movements made, proportion of time spent in the periphery (unpublished data), and lack of aversion (Figure 1C). Additionally, we performed a Hidden Cookie Test to evaluate general olfaction and observed no difference between uninfected and infected animals (Uninfected, Type I-, and Type III-infected animals found the cookie on average within 96±14, 109±18, and 123±31 seconds, respectively where variance indicates Standard Error of the Mean). Infection with either attenuated Type I or Type III parasites resulted in complete loss of aversion to bobcat urine (Figure 1Biii and 1Biv). This effect was observed at all three time points and appears to be an all-or-nothing effect (Figure 1C). There were no ‘non-responders’ in either infection group, nor did the effect diminish with time. These data show that the ability of T. gondii to disrupt innate predator aversion extends to all three major parasite clonotypes types.

We next investigated the parasite load and the immune response in the brains of mice infected with attenuated Type I and Type III parasites during chronic infection. Following the final behavior experiment, we sacrificed the cohort over the course of 4 weeks. We carefully perfused each animal with 20 mL of ice cold sterile PBS and then harvested the brains and skull cap meninges from each animal and assessed 10% of homogenated brain and meninges for parasite load using semi-quantitative polymerase chain reaction (qPCR) targeting an abundant T. gondii gene family, B1 [20]. Type III-infected mice all had readily detectable parasite load, well above uninfected controls (Figure 2Ai). In contrast, Type I-infected mice all had undetectable levels of brain-resident parasites (Figure 2Aii).


Figure 2. Persistent inflammation during chronic infection with Type III but not Type I parasites.

[A] Quantitative PCR of genomic DNA prepared from 10% of brain homogenate reveals that parasite DNA was readily detectable in Type III-infected animals (i) but undetectable in attenuated Type I-infected animals (ii). [B] Brain leukocytes were percoll purified from the remaining brain and meningeal homogenate, stained for surface markers CD4, CD8, CD19, CD11b, and Ly6G, and assayed using flow cytometry. Total numbers of cells positive for any of these markers are reported for uninfected, Type I-infected, and Type III-infected animals at 4 to 5 mpi. Average percentages of brain leukocyte populations for uninfected, Type I, and Type III animals are displayed in pie charts below each group. [C] Blood serum was collected following the final behavior experiment 4 months post infection (4 mpi). T. gondii specific antibodies were detected using ELISA. Relative absorbance at 405 nm (sample 1:10 dilution absorbance – HRP no serum control absorbance) is reported for uninfected, Type I, and Type III. Each dot signifies one mouse. Significance was determined by Student’s T-test for [A] and 1 way ANOVA for [B] and [C] where ns indicates p>0.05 and **** indicates p<0.0001 (n = 9 for each group).


The brain is generally considered an immune-privileged environment and immune cell leukocyte infiltration is known to be tightly regulated [21][22]. Thus, only during an ongoing infection would we expect to find a large number of brain-resident leukocytes such as CD4 and CD8 positive T cells, required to control toxoplasmosis [23][24]. We isolated and compared brain leukocytes isolated from the combined parenchyma and meninges of each animal. Purified cells were surface stained for a variety of leukocyte markers and analyzed using flow cytometry. Type III-infected animals had elevated total brain leukocyte numbers, whereas attenuated Type I-infected animals had equivalent brain leukocyte numbers to uninfected animals (Figure 2B). The average proportion of CD4 and CD8 positive T cells in Type III-, but not Type I-, infected animals were much higher than uninfected controls, reflecting ongoing brain inflammation. Brain leukocytes from uninfected controls and Type I-infected animals show a lower proportion of T cells, B cells, and neutrophils and likely correspond to meningeal leukocytes. We assayed blood serum for antibodies specific for T. gondii using an enzyme-linked immunosorbent assay (ELISA) and confirmed that both attenuated Type I and Type III parasites had established infection in our mice (Figure 2C). Together these data show that permanent loss of aversion to predator urine may not depend on persistent brain infection.

It is possible that T. gondii causes a permanent change in the brain during acute infection, thereby not requiring continued parasite presence and an ongoing immune response. To address this possibility, we performed time course experiments, first infecting mice with Type III parasites. As expected, both parasite load and brain leukocyte numbers increased and remained well above uninfected levels (Figure 3A and 3B). We also infected mice with attenuated Type I parasites and detected parasites in the brain and meningeal homogenate in a number of mice between 5 and 20 days post infection (Figure 3D). At later time points, qPCR assays resulted in undetectable levels of these parasites. This early appearance of parasites in the brain and meninges may be related to the greater motility of Type I parasites in comparison to other strains [25], or may reflect more rapid dissemination within host cells. Early infection with attenuated Type I parasites was accompanied by a modest increase in total brain leukocytes (Figure 3E). While the Type I-infected animals had relatively low brain leukocyte numbers at day 13 post infection, the average percent of CD4 and CD8 positive T cells in these mice was similar to Type III-infected animals. Moreover, the increase in leukocyte infiltration is most striking when considering the total numbers of CD4 and CD8 T cells, providing further evidence for a T cell-mediated immune response in the brain and/or meninges following infection with attenuated Type I parasites (Figure 3F). Day 8 through day 20 post infection with attenuated Type I parasites from two separate experiments resulted in brain and meningeal T cell numbers all significantly above uninfected animals. This suggests that infection with attenuated Type I parasites does in fact elicit a transient inflammatory response in the brain and/or meninges following parasite presence.


Figure 3. Type I and Type III acute infection results in parasite and leukocyte infiltration of the brain region.

[A and D] Parasite presence was assessed using semi-quantitative PCR of genomic DNA prepared from 10% of each mouse brain and meninges at various times post infection. For reference, data from Figure 2A is included which was collected from animals that were used in behavior experiments 4 to 5 months post infection. [A] Type III-infected animals have detectable parasite in brain regions early during acute infection, which is sustained over time. [D] Some attenuated Type I-infected animals have detectable parasite in brain regions early during acute infection, decreasing to undetectable levels (average of uninfected indicated by black dashed line). [B and E] Brain leukocytes were percoll purified from the remaining brain and meningeal homogenate, stained for leukocyte surface markers CD4, CD8, CD19, CD11b, and Ly6G, and assayed using flow cytometry. [B] Type III-infected animals have brain leukocyte numbers above uninfected levels (black dashed line) 13 days following infection which continue to increase over time. [E] Average total cell numbers from Type I-infected animals. Average percentages of brain leukocyte populations for uninfected, Type I-, and Type III-infected animals at selected time points are represented in pie charts below the corresponding data in [B and E]. [C and F] Total brain and meningeal T cells (CD4 plus CD8), indicators of brain region inflammation, are reported for Type III- and attenuated Type I-infected animals. Each dot signifies one mouse. Significance was determined for [C and F] by Student’s T-test where * indicates p<0.02, and ** indicates p<0.002.


Combined with previously published studies, our data indicate that infection with all three major North American T. gondii clonal lineages results in loss of innate, hard-wired aversion to feline predator urine in mice. Immunological analysis of mice infected with attenuated Type I and low-virulence Type III strains demonstrates that this behavioral change is not directly correlated with parasite load or brain inflammation. Taken together, our studies suggest that permanent interruption of mouse innate aversion to feline urine is a general trait of T. gondii infection that occurs within the first three weeks, independent of parasite persistence and ongoing brain inflammation.

Some current models propose that cysts residing in neurons play an active role in mediating loss of predator aversion. For example, it has been posited that T. gondii cysts might actively modulate dopamine production [26][27][28][29], or directly interrupt neuronal activity [30],[31]. In line with this notion, some investigators report higher cyst density in amygdalar regions known to be involved in innate fear [6], although this has been challenged by others [32]. In contrast, our results suggest that cysts may not even be required for sustained fear disruption. Moreover, recent studies show that T. gondii can deliver effector proteins into cells that it does not invade [33][34], and that these proteins can manipulate host cells without active parasite replication [35]. Thus T. gondii may interact with and manipulate its intermediate hosts without the requirement of cyst formation or parasite persistence. In light of these findings and our data reported here, we believe that a new non-cyst-centric model of T. gondii-mediated behavior manipulation of the mouse intermediate host is warranted.

Materials and Methods

Ethics Statement

This study was carried out in strict accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Animal Care and Use Committee of UC Berkeley (Protocol #: R165-1212BCR).


All mice were bred and housed in specific pathogen-free conditions at the Association of Laboratory Care-approved animal facility at the Life Science Addition, University of California, Berkeley, CA. Preliminary experiments used male and female BALB/c mice bred in our facilities ranging in age from 5 to 16 weeks old. Females were housed 5 animals per cage while males were housed between 1 and 5 animals per cage. Males were separated and housed individually if they began to fight on a cage-by-cage basis. Behavior experiments reported here and time course experiments involved male BALB/c mice all 9 weeks old, ordered from The Jackson Laboratory, 10 mice per group. Animals were housed 5 per cage until they began to fight. Upon the first cage needing to be separated, all animals were housed individually. Mice were sacrificed between 5 days and 20 weeks post infection by transcardial perfusion with 20 mL ice-cold sterile phosphate buffered saline following anesthesia with 500 µL 2.5% avertin administered intraperitoneally (i.p.).

Behavior Studies

Mouse aversion was assayed using the MotorMonitor SmartFrame System (Kinder Scientific, Poway, CA; Build # 11011-16). We used 7×15 High-Density SmartFrames to record up to 16 individually caged animals simultaneously. Animal movement was evaluated in transparent (17 cm×38 cm) polycarbonate enclosures using the computerized photobeam system MotorMonitor. Animals were habituated for 1 hour the day before each trial in an empty enclosure. For the bobcat and rabbit urine exposure trials, a sterile cell culture dish (35 mm×10 mm, treated polystyrene) was affixed to one end of the enclosure using a small amount of Blu-Tack (Bostick). 400 µL of either bobcat urine (LegUp Enterprises, Lovell, ME) or rabbit urine (Pete Rickard’s, Fleming Outdoors, Ramer, AL) was added to the dish. One animal per cage was gently placed in the center of the enclosure and their activity monitored for 1 hour in the dark. The following day, we repeated the experiment with whichever urine sample was not used the previous day, the order of which was semi-randomized. Data was analyzed using MotorMonitor Software. User-defined Zone Maps were generated as described in Figure 1A. Recorded beam breaks were used by the software to quantify total movement and time spent in each zone. Heat maps were generated by MotorMonitor using the HotSpots Graphic Comparator for each animal trial (parameters: Time 1 hour, smoothing 0.1, Intensity Cube Rt, Minimum Visibility Normal). For the hidden cookie test, animals were food-deprived overnight (16–17 hours), during which time water was freely available. Testing performed on the following morning consisted of timing the latency for the animal to find an appetizing piece of food (1 Teddy Grahams cookie) buried 1 cm beneath fresh cage bedding.

T. gondii Infections

Tachyzoites were cultured on monolayers of human foreskin fibroblasts and prepared immediately before mouse infection as previously described [36]. All infections were administered i.p. in 200 µL volumes. Type I parasites used for infection were attenuated RHΔrop5 (dose: 5×105 parasites). Type II parasites used in preliminary studies were either Prugniaud expressing tandem dimeric tomato red fluorescent protein and OVA peptide [36](dose: 2500 parasites) or ME49 expressing luciferase [37] (dose: 300 parasites). Type III parasites used for infection were CEP expressing green fluorescent protein (dose: 5×105 parasites). All parasite strains were generously provided by John Boothroyd (Stanford, Palo Alto, CA).

Ex vivo Analysis of Tissue Samples

Brains and skull caps were harvested and placed in 10 mL ice cold PBS before being immediately processed. Brains were transferred to 2.5 mL cold RPMI medium 1640+ L-glutamine (Sigma) and meninges were dissected from the skullcaps as described elsewhere[38] and combined with the brain parenchyma. Brains and meninges were crushed using a 3 mL syringe plunger then homogenized by repeated passage through an 18-gauge needle. 10% of the homogenate was removed and stored at −20°C for future PCR analysis. The remaining homogenate was digested in 1 mg/mL Collagenase IA (Sigma) and 0.1 mg/mL DNase I (Roche) for 40 minutes at 37°C. The digested material was filtered through a 70 µm cell strainer and centrifuged at 800 g for 5 minutes. The brain and meningeal material was resuspended in room temperature 60% (vol/vol) Percoll (GE Healthcare)/RPMI and overlaid with 30% (vol/vol) Percoll/PBS and centrifuged with no acceleration or brakes for 20 minutes at 1000 g. Mononuclear cells were harvested from the gradient interface and washed twice in PBS before preparation for flow cytometric analysis.

Flow Cytometry

Antibodies to mouse CD4 (RM4–5), CD8α (53-6.7), CD19 (eBioID3), CD11b (M1/70), and CD11c (N418) were obtained from eBioscience. Anti-mouse Ly6G (1A8) was obtained from BD Biosciences. Cell viability was assayed using LIVE/DEAD® Fixable Aqua Dead Cell Stain Kits (Invitrogen). Surface staining with anti-mouse CD4, CD8, CD19, CD11b, CD11c, and Ly6G was performed at 4°C for 30 minutes. Cells were fixed and acquisitions were performed using a BD LSR II flow cytometer (BD) and data were analyzed with FlowJo software (Tree Star, Ashland, OR).

Parasite Load Assay

Whole genome DNA was isolated from brain and meningeal homogenate using DNeasy Blood and Tissue Kit (Qiagen). Parasite burden was assessed using semi-quantitative PCR as described elsewhere [39].

Serum ELISA for T. gondii

Blood was collected by mandibular vein bleed prior to animal sacrifice. Samples were incubated for 4 hours at room temperature to allow clot to form, then incubated at 4°C overnight. ELISA 96 well plates were coated with 1 µg/ml Soluble Tachyzoite Antigen (STAg). Plates were washed 3 times with PBS –0.05% TWEEN and blocked with 5% milk PBS-0.05% TWEEN, then washed 3 times more with PBS-0.05% TWEEN, and 54 µl of 5% milk PBS-0.05% TWEEN was applied to each well. Five serial dilutions, 6 µl each, of serum from each sample were incubated overnight at 4°C. Plates were washed three times with PBS-0.05% TWEEN, and once with PBS. Plates were then incubated with rabbit anti-mouse IgG (H+L)-HRP (Jackson Immuno Research) 1:1000 dilution for 2 hours at room temperature. H2O2 was added to ABTS substrate (Sigma) at 1:1000, mixed and applied to the plate. Enzymatic reaction times were recorded at 405 nm.

Statistical Analysis

Prism software (GraphPad) was used for statistical analysis. P values were calculated using two-tailed Student’s (non-parametric) t-test or 1 way ANOVA as indicated.


The authors would like to gratefully acknowledge John Boothroyd and Michael Reese (Stanford) for their generous gift of the attenuated Type I RHΔrop5 parasite, Shiao Chan and Kayleigh Taylor for technical assistance, and members of the E.A.R. and M.B.E. labs for helpful comments, support, and assistance.

Demolishing Darwin’s Tree: Eric Bapteste and the Network of Life

Eric Bapteste with ten other researchers across Europe and the United States are ready to provide a more “expansive” view of evolution that replaces Darwin’s tree with a “network” of life. Why is this necessary? Because “genetic data are not always tree-like.”

We’ve heard Bapteste criticize the tree of life before (see here and here). His new paper in Trends in Genetics, “Networks: Expanding Evolutionary Thinking” (see the summary at PhysOrg), seeks to “expand” evolutionary thinking by incorporating it within a larger “network” model. But if they replace the tree with a complex set of interconnections, what happens to the notion of universal common descent?

Down with Trees

The pro-network gang finds trees inadequate on several grounds. For one, a tree diagram is too simplistic:

“However, many patterns in these data cannot be represented accurately by a tree. The evolution of genes in viruses and prokaryotes, of genomes in all organisms, and the inevitable noise that creeps into phylogenetic estimations, will all create patterns far more complicated than those portrayed by a simple tree diagram. Genetic restructuring and non-vertical transmission are largely overlooked by a methodological preference for phylogenetic trees and a deep-rooted expectation of tree-like evolution.


Interesting: they still want “evolutionary thinking,” but what kind without trees? Another problem is that much of the genetic data is not tree-like:

Evolutionary networks today are most often used for population genetics, investigating hybridization in plants, or the lateral transmission of genes, especially in viruses and prokaryotes. However, the more we learn about genomes the less tree-like we find their evolutionary history to be, both in terms of the genetic components of species and occasionally of the species themselves.

Interesting: if “evolutionary history” is not tree-like, does universal common ancestry still hold? They explain that many patterns are mosaic-like rather than tree-like due to a number of non-vertical processes. What predominates are “reticulate” (net-like) relationships. Another problem is that tree diagrams are often inaccurate:

Tree-based genomic analysis is proving to be an accuracy challenge for the evolutionary biology community, and although genome-scale data carry the promise of fascinating insights into treelike processes, non-treelike processes are commonly observed.

Further, tree diagrams are often contradictory:

There are long-standing controversies regarding the evolutionary history of many taxonomic groups, and it has been expected by the community that genome-scale data will end these debates. However, to date none of the controversies has been adequately resolved as an unambiguous tree-like genealogical history using genome data. This is because quantity of data has never been a satisfactory substitute for quality of analysis. Many of the underlying data patterns are not tree-like at all, and the use of a tree model for interpretation will oversimplify a complex reticulate evolutionary process.

Interesting: how does a “reticulate evolutionary process” square with universal common descent? They give examples: the yeast phylogenetic data can only be force-fit into a tree, but then, “a species tree becomes only a mathematical average estimate of evolutionary history, and even if it is supported it suppresses conflicting phylogenetic signals.” It’s misleading, in other words.

Another example is the tree of placental mammals: “a problem that has been difficult to resolve as a bifurcating process because different genetic datasets support different trees.” Wriggling out of the tree-thinking straitjacket can resolve these controversies: “the network provides biological explanations that go beyond what can be accommodated by a simple tree model.”

Up with Networks

The team believes that network theory has matured to the point where it can be a valuable tool for biologists. It also promises job opportunities: “The further improvement of networks for evolutionary biology offers many outstanding opportunities for mathematicians, statisticians, and computer scientists.”

A network can be both a more parsimonious description of the amount of discordance between genes, and a starting point for generating hypotheses to explain that discordance.

Trees, Networks, and Scientific Explanation

The authors recognize that network-thinking is not a panacea. Biologists will still need to “interpret” the findings correctly:

However, biologists must also keep in mind that networks are not yet free of interpretive challenges. One must knowledgeably select from the various types of network methods available to interpret properly such features as internal nodes and the meaning of taxon groupings, which differ in important ways among methods. Furthermore, community standards do not yet exist for network assessment and interpretation. As with tree methods, the responsibility remains with the researcher to understand network methodology, apply it correctly, and make valid inferences.

Philosophers could have fun with this paragraph. It has the potential for investigator bias at each stage. It sounds like Finagle’s First Law: “To study a subject best, understand it thoroughly before you start” — i.e., know what the valid inferences are before you infer anything; know the right methods before you choose which method is right; and if all else fails, trust the consensus (community standards). But that’s predictable; they are, after all, still Darwinian evolutionists. What matters is the extreme paradigm shift this represents.

Historic Juncture

Calling it “historic,” the authors recognize the extent of the shift they are proposing:

These challenges do not detract from the fact that networks represent an historic juncture in the development of evolutionary biology: it is a shift away from strict tree-thinking to a more expansive view of what is possible in the development of genes, genomes, and organisms through time.

They use “development… through time” as a synonym for evolution. But what kind of evolution? If it is not tree-like, what is it? In a network diagram, common descent gets scrambled if one accepts “random lateral gene transfer” and “hybridization” as key processes, as these authors do. In fact, they say nothing about natural selection. The new picture is of interconnected nodes, with no clear progression from simple to complex. After all, a gene has to already exist to be laterally transferred. Two species must already exist in order to hybridize. There’s nothing here about a beginning and a progression. It’s all about relationships between nodes that could have (avoiding tree-thinking) been in existence all along. The sample network diagram in the PhysOrg article shows lines going up, down, and sideways between nodes. It claims that “Moving from tree-like depictions of evolution to network diagrams is an effective way to amend the Tree of Life without dismissing it,” but the move turns the tree upside down and inside out. The focus is on nodes and relationships — not progression.

Even the strictest creationists allow for “change over time” in terms of new interconnections and horizontal modifications among existing kinds of organisms. There’s nothing really Darwinian about Bapteste’s proposal. It could even be considered ID-friendly: pre-existing intelligently designed organisms change their relationships through time, occasionally sharing genetic information. By “expanding” the tree of life, this team is demolishing it. Bifurcating trees within network diagrams vanish as artifacts, like imagined faces in a bumpy ceiling when one backs away and sees the whole.

Trees as Dogma

Back to the complaint of Bapteste et al. that tree-thinking is an “expectation” and a “preference” – i.e., a set of assumptions chosen before the data has a chance to speak. Their opening paragraph shows that Darwinian evolutionists produce trees because they are trained to produce them:

Ever since Darwin, a phylogenetic tree has been the principal tool for the presentation and study of evolutionary relationship among species. A familiar sight to biologists, the bifurcating tree has been used to provide evidence about the evolutionary history of individual genes as well as about the origin and diversification of many lineages of eukaryotic organisms. Community standards for the selection and assessment of phylogenetic trees are well developed and widely accepted. The tree diagram itself is ingrained in our research culture, our training, and our textbooks. It currently dominates the recognition and interpretation of patterns in genetic data.

What they are saying is that this dominant way of looking at the data is both ingrained as a method, and also used to provide evidence for evolution! That’s circular. They are trained to think in terms of evolutionary trees, and then use evolutionary trees as evidence for evolutionary trees.


One can only welcome this paper’s bold proposal to overturn entrenched dogma and offer a more “expansive” view of “development…through time.” For one thing, if trees are artifacts emerging from expectations, they should be exposed as such. For another, the “network” diagram seems conducive to ID research inasmuch as it calls into question universal common ancestry via natural selection (i.e., neo-Darwinism), and seeks to portray the evidence honestly.

Their paper is the product of a meeting in Leiden last October called “The Future of Phylogenetic Networks.” It’s too soon to tell if Darwin security forces will let this band of independent thinkers gather a following. If nothing else, it shows (notwithstanding the insistences of the National Center for Science Education) that insiders know about the fundamental controversies in evolutionary theory, and are calling for some of the same reforms that advocates of intelligent design do.

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I have found this article it could be…

I have found this article – it could be a good approach :

By: Stephen C. Meyer

When two groups of experts disagree about a controversial subject that intersects the public school curriculum students should learn about both perspectives.

In such cases teachers should not teach as true only one competing view, just the Republican or Democratic view of the New Deal in a history class, for example. Instead, teachers should describe competing views to students and explain the arguments for and against these views as made by their chief proponents. Educators call this “teaching the controversy.”

Recently, while speaking to the Ohio State Board of Education, I suggested this approach as a way forward for Ohio in its increasingly contentious dispute about how to teach theories of biological origin, and about whether or not to introduce the theory of intelligent design alongside Darwinism in the Ohio biology curriculum.

I also proposed a compromise involving three main provisions:

(1) First, I suggested–speaking as an advocate of the theory of intelligent design–that Ohio not require students to know the scientific evidence and arguments for the theory of intelligent design, at least not yet.

(2) Instead, I proposed that Ohio teachers teach the scientific controversy about Darwinian evolution. Teachers should teach students about the main scientific arguments for and against Darwinian theory. And Ohio should test students for their understanding of those arguments, not for their assent to a point of view.

(3) Finally, I argued that the state board should permit, but not require, teachers to tell students about the arguments of scientists, like Lehigh University biochemist Michael Behe, who advocate the competing theory of intelligent design.

There are many reasons for Ohio to adopt this approach.

First, honest science education requires it. While testifying before the state board, biologist Dr. Jonathan Wells and I, submitted an annotated bibliography of over 40 peer-reviewed scientific articles that raise significant challenges to key tenets of Darwinian evolution. If students are to be required to master the case for Darwinian evolution (as we think they should), shouldn’t they also know some of the difficulties described in such scientific literature?

Shouldn’t students know that many scientists doubt that the overall pattern of fossil evidence conforms to the Darwinian picture of the history of life? Shouldn’t they know that some scientists now question previously stock Darwinian arguments from embryology and homology? And shouldn’t they also know that many scientists now question the ability of natural selection to create fundamentally new structures, organisms and body plans? Last fall 100 scientists, including professors from institutions such as M.I.T, Yale and Rice, published a statement questioning the creative power of natural selection. Shouldn’t students know why?

Second, constitutional law permits “teaching the controversy” about scientific theories of origins. In the controlling Edwards v. Aguillard case, the Supreme Court made clear that state legislatures (and by extension state boards) already have the right to mandate teaching scientific critiques of prevailing theories. Interestingly, the court also made clear that teachers have the right to teach students about “a variety of scientific theories about origins . . . with the clear secular intent of enhancing science education.” Our compromise proposal requires teaching existing scientific critique of Darwinism, and permits discussion of competing theories, just as the Court allows.

Third, federal education policy calls for precisely this kind of approach. The report language accompanying the federal education act (“No Child Left Behind”) states that “where topics are taught that may generate controversy (such as biological evolution), the curriculum should help students to understand the full range of views that exist [and] why such topics may generate controversy.”

Some have dismissed this language as irrelevant to Ohio’s deliberations because it appears in the report accompanying the federal education act, not in the act itself. But report language typically articulates Congress’s interpretation of law and guides its implementation. As such, report language expresses federal policy and has the effect of law. In this case, as Ohio’s John Boehner, chair of the House education committee, has advised the Ohio Board, the report language makes clear that “science standards not be used to censor debate on controversial issues in science including Darwin’s theory of evolution.”

Fourth, voters overwhelmingly favor this approach. In a recent national Zogby poll, 71% of those polled stated their support for teaching evidence both for and against Darwin’s theory of evolution. Only 15% opposed this approach. An even greater majority favored exposing students to “evidence that points to an intelligent design of life.”

Finally, good pedagogy commends this approach. Teaching the controversy about Darwinism as it exists in the scientific community will engage student interest. It will motivate students to learn more about the biological evidence as they see why it matters to a big question. This is not only good teaching; it is good science. As Darwin wrote in the Origin of Species, “A fair result can be obtained only by fully stating and balancing the facts and arguments on both sides of each question.”

Yet, the modern Darwinist lobby continues to distract attention from their advocacy of censorship by reciting a litany of complaints about the emerging theory of intelligent design. But that theory is not the issue in Ohio. The issue is whether students will learn both sides of the real and growing scientific controversy about Darwinism,and whether a 19th century theory will be taught dogmatically to 21st century students.

#id, #science, #science-controversy

A Tale of Two Professors

It was September 2004. A conservative group calling itself Students for Academic Freedom sent a letter to President Jo Ann Gora of Ball State University (BSU) demanding an investigation into the university’s peace studies program led by Professor George Wolfe. The group alleged that Wolfe had violated student rights in class by excluding contrary views from his course readings, by offering extra credit to students who agreed to take part in a protest against the Iraq war (but not offering credit for students who might want to demonstrate in support of the war), by coercing students to volunteer for various ideologically driven peace programs or attend “Interfaith Fellowship” meetings, and by “creat[ing] the impression that he would lower students’ grades on papers when he disagreed with their views.” (See “Letter to the President of Ball State University,” September 13, 2004, in Indoctrination or Education?, pp. 20-23.) 


The current controversy over BSU physics professor Eric Hedin bears eerie similarities to the nearly decade-old controversy over Professor Wolfe. Just like the Wolfe case in 2004, the Hedin case erupted when an outside interest group — this time the atheist Freedom from Religion Foundation (FFRF) — sent a letter of complaint to BSU’s President Jo Ann Gora. In both cases, there was a prominent public activist lurking behind the complaint. In 2004, the activist was conservative firebrand David Horowitz, founder of Students for Academic Freedom. In 2013, the activist is atheist Darwinian biologist Jerry Coyne at the University of Chicago, who started to hurl anathemas against Hedin’s course on his blog before the FFRF issued its formal complaint.

Despite the striking similarities, there are also dramatic differences between the two academic freedom controversies, especially in how BSU administrators chose to respond. Those differences raise important questions about whether BSU is committed to protecting academic freedom in an equal and impartial manner.

In the current dispute, Professor Hedin has been left in an academic no man’s land, waiting while a potentially biased “review panel” investigates him and while BSU’s provost equivocates in public about whether academic freedom protects Professor Hedin’s right to teach his course.

The contrast with how BSU handled the complaint against Professor Wolfe couldn’t be more stark. Instead of appointing a review panel or launching an extensive investigation in 2004, BSU officials quickly circled the wagons around Professor Wolfe and defended him to the media, the state legislature, and the public at large. The minimal investigation of the complaint against Wolfe seems to have consisted of the provost talking to both Wolfe’s supervisor and Professor Wolfe and reading some letters. The provost apparently did not even bother to interview the student who had come forward to allege discriminatory treatment in class. As a result, the Wolfe complaint was quickly disposed of. The letter of complaint from Students for Academic Freedom was dated September 13. A mere ten days later, on September 23, the provost issued a response exonerating Wolfe. (See “Reply from Ball State Provost Beverly Pitts” and “Reply to Provost Pitts” in Indoctrination or Education?, pp. 23-28.)

Wolfe himself later recalled:

When contacted by Ball State provost Beverly Pitts shortly after the Horowitz attack, she asked me how she should respond to the accusations that had been made. Dr. Pitts let me know from the beginning that she wanted to take on this fight, that this was her job as provost. She only needed from me material to address the issues in the media, and more importantly, to the Ball State board of trustees and politicians at the Indiana State House. (emphasis added)

Read the part in bold again: “Dr. Pitts let me know from the beginning that she wanted to take on this fight, that this was her job as provost.” All the provost needed was material she could use to defend Wolfe in the media and to the legislature. In other words, her inquiry was primarily about how to best defend their professor and his academic freedom.

Compare that approach to the Hedin case today. By any objective measure, the complaint submitted by the Freedom from Religion Foundation against Hedin was far less serious, and far less credible, than the allegations lodged against Professor Wolfe. In saying this, I am not taking sides about who was right in the Wolfe controversy. Professor Wolfe vigorously challenged the allegations made against him at the time, and David Horowitz has continued to defend his criticisms of Wolfe. My point is merely that the complaint originally leveled against Wolfe put forward much more serious allegations of misconduct than the complaint against Hedin. The complaint against Wolfe identified a student by name who made specific charges of discriminatory treatment and the intimidation of students. By contrast, the complaint against Hedin did not identify any student who was willing to complain on the record against Hedin. Instead, it merely highlighted a few anonymous (and ambiguous) comments from, a website that doesn’t even verify whether those posting comments are in fact college students, let alone whether they ever took courses from the professor in question.

More importantly, and unlike in the Wolfe case, the complaint against Hedin did not allege that Hedin had actually intimidated students or threatened to grade them down for holding different beliefs than himself.

Despite the fact that the allegations against Hedin were far less weighty than those against Wolfe, BSU’s current provost Terry King did not dispose of FFRF’s complaint quickly. Instead, he created a review panel that appears to be stacked with faculty with conflicts of interest who are likely to be hostile to Professor Hedin’s point of view. In the meantime, Professor Hedin has been left hanging without any clear support from the top officials at his university. It is now more than forty days (and counting) since FFRF’s complaint — a far cry from the ten days it took for the university to resolve the more serious complaint against Professor Wolfe.

In public, meanwhile, BSU provost Terry King has equivocated about whether academic freedom protects Professor Hedin’s right to cover the topics included in his previously approved honors course. While saying that he supports academic freedom, Provost King has repeatedly emphasized that teaching must be “appropriate,” without defining what that means. Moreover, according to the BSU student newspaper, King “said some confuse First Amendment freedom of speech with academic freedom in a course, but the two are different.” It’s unclear what King meant by that comment, but he certainly seemed to be trying to limit the reach of academic freedom by making the distinction. King went on to define academic freedom in an extremely ambiguous manner: “in the appropriate teaching of a course, one can bring in controversial concepts if it’s appropriate to the nature of the course… We are very much in support of faculty members appropriately teaching their courses or appropriately doing their research even if it takes them into unpopular areas.” (emphasis added) Provost King did not define “appropriate” for the newspaper, which is such an ambiguous and subjective term that it could easily be used as a pretext to completely silence any professor who holds views that disagree with the majority of his or her colleagues. Is this all the guidance the provost provided to his review panel — to determine whether Hedin’s course is “appropriate”? If so, it won’t be especially surprising if the panel doesn’t end up ensuring Hedin’s academic freedom to teach his course.

BSU’s current provost should look more deeply into his own institution’s Faculty and Professional Personnel Handbook, which offers guidance that is a lot more clear-cut than his vague standard that a professor must be “appropriate.” The Handbook asserts: “Academic freedom is essential… and applies to both teaching and research… Academic freedom in its teaching aspect is fundamental for the protection of the rights of the teacher in teaching and of the student to freedom in learning.” (p. 63) Furthermore, “[t]he teacher is entitled to freedom in the classroom in discussing the appointed subject, but should be careful not to introduce a controversial matter which has no relation to the subject.” (pp. 63-64) Given that the purpose of Hedin’s “Boundaries of Science” course was to examine the nature and limits of science, as well as the possible metaphysical implications of science, Hedin’s exploration of the relationship between faith and science clearly cannot be disqualified on grounds that it “has no relation to the subject.” Later in the Handbook, there is an explicit statement that “Academic freedom and freedom of expression include but are not limited to the expression of ideas, philosophies, or religious beliefs, however controversial, in classroom or other academic settings.” (p. 68) Has Provost King made sure that his review panel is aware of this language and takes care to follow it?

Once BSU duly hires a professor, and a course is officially approved, should an administrator be able to censor the professor’s class simply because the professor’s views are controversial, or even because the administrator thinks the course is not balanced? BSU professor George Wolfe certainly doesn’t seem to think so. As he stated when defending his own academic freedom:

Who decides the question of balance? Is it the Provost? Is it the Dean? Is it the Department Chair? Is it the Professor? Is it the student? It obviously is the professor who has structured the class, knows the most about the material, and has the most insight into what creates the best learning environment for the students and it is the professor that should determine what is balance. If you have one student out of 20 that complains about the class, does that one student provide reason for changing the course content, we have student evaluations and we obviously know how the majority of the students are feeling about the teacher. (emphasis added)

In another forum, Wolfe went on to provide this expansive statement of academic freedom:

Academic freedom has a long tradition and is meant to protect faculty who teach controversial subjects or conduct controversial research. It also prevents administrators, government officials, and yes, even students, from dictating what can or cannot be taught in a class, or what teaching strategies should be used to present educational material. Professors therefore are free to “profess,” to teach in their own way, to assemble and present course material according to their informed educated judgment regarding the research and subject matter in their respective fields. Keep in mind that if we take this protection away from liberal professors, we take it away from conservative professors as well. (emphasis added)

As BSU faculty and administrators consider the case of Eric Hedin, they should read and carefully ponder the words of George Wolfe. If they end up placing special restrictions on Hedin’s right to teach — restrictions not placed on any other professors at BSU — they will have opened the door to future efforts to restrict their own right to teach. Indeed, they will have ceded the moral high ground and undermined their ability to protect professors who hold views that they favor.

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Soil biodiversity and ecosystem function

Another interesting article re research :

DIANABUJA'S BLOG: Africa, The Middle East, Agriculture, History and Culture

It has long been recognised that organisms living in the soil are important for making nitrogen available to plants and for storing carbon in the soil but a new paper in PNAS by de Vries et al…


diana buja’s insight:

Comprehensive studies of soil, such as this one, are so labor and finance intensive that similar studies in developing countries may not be possible.  What are the next ‘best bet’ options?

In Sudan (el-Obeid area) we discovered local farmers identified a soil type that was not identified by researchers.  The farmer-identified soil type was linked to specific forms of cropping.  That, in itself, was reason enough to conduct our less intensive, but more farmer-centered study, of soils.

Similar findings here in Burundi, regarding micro-catchment soil types – identified by farmers – especially in wetland areas.

But the weakness of these studies relates to their less specific…

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#news, #research, #science