Understanding teacher design practices for digital inquiry-based science learning: the case of Go-Lab.

Designing and implementing online or digital learning material is a demanding task for teachers. This is even more the case when this material is used for more engaged forms of learning, such as inquiry learning. In this article, we give an informed account of Go-Lab, an ecosystem that supports teachers in creating Inquiry Learning Spaces (ILSs). These ILSs are built around STEM-related online laboratories. Within the Go-Lab ecosystem, teachers can combine these online laboratories with multimedia material and learning apps, which are small applications that support learners in their inquiry learning process. The Go-Lab ecosystem offers teachers ready-made structures, such as a standard inquiry cycle, alternative scenarios or complete ILSs that can be used as they are, but it also allows teachers to configure these structures to create personalized ILSs. For this article, we analyzed data on the design process and structure of 2414 ILSs that were (co)created by teachers and that our usage data suggest have been used in classrooms. Our data show that teachers prefer to start their design from empty templates instead of more domain-related elements, that the makeup of the design team (a single teacher, a group of collaborating teachers, or a mix of teachers and project members) influences key design process characteristics such as time spent designing the ILS and number of actions involved, that the characteristics of the resulting ILSs also depend on the type of design team and that ILSs that are openly shared (i.e., published in a public repository) have different characteristics than those that are kept private.

Physical and virtual laboratories in science and engineering education.

The world needs young people who are skillful in and enthusiastic about science and who view science as their future career field. Ensuring that we will have such young people requires initiatives that engage students in interesting and motivating science experiences. Today, students can investigate scientific phenomena using the tools, data collection techniques, models, and theories of science in physical laboratories that support interactions with the material world or in virtual laboratories that take advantage of simulations. Here, we review a selection of the literature to contrast the value of physical and virtual investigations and to offer recommendations for combining the two to strengthen science learning.

Anatomy of the distal tibiofibular syndesmosis in adults: a pictorial essay with a multimodality approach.

A syndesmosis is defined as a fibrous joint in which two adjacent bones are linked by a strong membrane or ligaments.This definition also applies for the distal tibiofibular syndesmosis, which is a syndesmotic joint formed by two bones and four ligaments. The distal tibia and fibula form the osseous part of the syndesmosis and are linked by the distal anterior tibiofibular ligament, the distal posterior tibiofibular ligament, the transverse ligament and the interosseous ligament. Although the syndesmosis is a joint, in the literature the term syndesmotic injury is used to describe injury of the syndesmotic ligaments. In an estimated 1­11% of all ankle sprains, injury of the distal tibiofibular syndesmosis occurs. Forty percent of patients still have complaints of ankle instability 6 months after an ankle sprain. This could be due to widening of the ankle mortise as a result of increased length of the syndesmotic ligaments after acute ankle sprain. As widening of the ankle mortise by 1 mm decreases the contact area of the tibiotalar joint by 42%, this could lead to instability and hence early osteoarthritis of the tibiotalar joint. In fractures of the ankle, syndesmotic injury occurs in about 50% of type Weber B and in all of type Weber C fractures. However,in discussing syndesmotic injury, it seems the exact proximal and distal boundaries of the distal tibiofibular syndesmosis are not well defined. There is no clear statement in the Ashhurst and Bromer etiological, the Lauge-Hansen genetic or the Danis-Weber topographical fracture classification about the exact extent of the syndesmosis. This joint is also not clearly defined in anatomical textbooks, such as Lanz and Wachsmuth. Kelikian and Kelikian postulate that the distal tibiofibular joint begins at the level of origin of the tibiofibular ligaments from the tibia and ends where these ligaments insert into the fibular malleolus. As the syndesmosis of the ankle plays an important role in the stability of the talocrural joint, understanding of the exact anatomy of both the osseous and ligamentous structures is essential in interpreting plain radiographs, CT and MR images, in ankle arthroscopy and in therapeutic management. With this pictorial essay we try to fill the hiatus in anatomic knowledge and provide a detailed anatomic description of the syndesmotic bones with the incisura fibularis, the syndesmotic recess, synovial fold and tibiofibular contact zone and the four syndesmotic ligaments. Each section describes a separate syndesmotic structure, followed by its clinical relevance and discussion of remaining questions.

Dauer pheromone and G-protein signaling modulate the coordination of intraflagellar transport kinesin motor proteins in C. elegans.

Cilia length and function are dynamically regulated by modulation of intraflagellar transport (IFT). The cilia of C. elegans amphid channel neurons provide an excellent model to study this process, since they use two different kinesins for anterograde transport: kinesin-II and OSM-3 kinesin together in the cilia middle segments, but only OSM-3 in the distal segments. To address whether sensory signaling modulates the coordination of the kinesins, we studied IFT protein motility in gpa-3 mutant animals, since dominant active mutation of this sensory Galpha protein GPA-3QL) affects cilia length. In addition, we examined animals exposed to dauer pheromone, since dauer formation, which involves gpa-3, induces changes in cilia morphology. Live imaging of fluorescently tagged IFT proteins showed that in gpa-3 mutants and in larvae exposed to dauer pheromone, kinesin-II speed is decreased and OSM-3 speed is increased, whereas structural IFT proteins move at an intermediate speed. These results indicate that mutation of gpa-3 and exposure to dauer pheromone partially uncouple the two kinesins. We propose a model in which GPA-3-regulated docking of kinesin-II and/or OSM-3 determines entry of IFT particles into the cilia subdomains, allowing structural and functional plasticity of cilia in response to environmental cues.

Correlation of in vitro and in vivo somatotropic adenoma responsiveness to somatostatin analogs and dopamine agonists with immunohistochemical evaluation of somatostatin and dopamine receptors and electron microscopy.

OBJECTIVE AND PATIENTS: Twenty-four pituitary adenomas from acromegalic patients (13 females, 11 males; age range 19-65 yr) were characterized for somatostatin receptor subtype 2A (sst(2A)), dopamine D(2) receptor (D(2)R), GH, and prolactin (PRL) expression by immunohistochemistry, and results correlated with the in vitro and in vivo hormone responses to octreotide and quinagolide. In nine cases, GH and PRL content was further studied by immunoelectron microscopy. RESULTS: Immunoreactivity was semiquantitatively scored as 2 (>50% stained cells), 1 (10-50% stained cells), and 0 (<10% stained cells). Sst(2A) was scored as 2 in 13 cases, 1 in 10, and 0 in one; D(2)R was scored as 2 in 13 cases, 1 in nine, and 0 in 2; GH was 2 in 15 cases and 1 in nine; PRL was 2 in six cases, 1 in 13, and 0 in 5. Sst(2A) was positively correlated with in vitro (P = 0.003) and in vivo (P = 0.006) percent GH suppression by octreotide and with the chronic suppression of IGF-I by somatostatin analogs (P =0.008). D(2)R was positively correlated with in vitro percent GH (P =0.000) and PRL (P =0.005) suppression by quinagolide. Electron microscopy revealed two pure somatotroph adenomas, five somatomammotrophs with a variable coexpression of GH and PRL in the same cells, and two tumors consisting of mixed cell types, which were less sensitive to quinagolide and octreotide. CONCLUSION: Sst(2A) and D(2)R are frequently coexpressed in adenomas from acromegalic patients, and immunohistochemistry may be helpful in characterizing receptor expression in pituitary adenomas to select patients responsive to different treatments.

Mutation of the MAP kinase DYF-5 affects docking and undocking of kinesin-2 motors and reduces their speed in the cilia of Caenorhabditis elegans.

In the cilia of the nematode Caenorhabditis elegans, anterograde intraflagellar transport (IFT) is mediated by two kinesin-2 complexes, kinesin II and OSM-3 kinesin. These complexes function together in the cilia middle segments, whereas OSM-3 alone mediates transport in the distal segments. Not much is known about the mechanisms that compartmentalize the kinesin-2 complexes or how transport by both kinesins is coordinated. Here, we identify DYF-5, a conserved MAP kinase that plays a role in these processes. Fluorescence microscopy and EM revealed that the cilia of dyf-5 loss-of-function (lf) animals are elongated and are not properly aligned into the amphid channel. Some cilia do enter the amphid channel, but the distal ends of these cilia show accumulation of proteins. Consistent with these observations, we found that six IFT proteins accumulate in the cilia of dyf-5(lf) mutants. In addition, using genetic analyses and live imaging to measure the motility of IFT proteins, we show that dyf-5 is required to restrict kinesin II to the cilia middle segments. Finally, we show that, in dyf-5(lf) mutants, OSM-3 moves at a reduced speed and is not attached to IFT particles. We propose that DYF-5 plays a role in the undocking of kinesin II from IFT particles and in the docking of OSM-3 onto IFT particles.

Pegylated interferon-alpha protects type 1 pneumocytes against SARS coronavirus infection in macaques.

The primary cause of severe acute respiratory syndrome (SARS) is a newly discovered coronavirus. Replication of this SARS coronavirus (SCV) occurs mainly in the lower respiratory tract, and causes diffuse alveolar damage. Lack of understanding of the pathogenesis of SARS has prevented the rational development of a therapy against this disease. Here we show extensive SCV antigen expression in type 1 pneumocytes of experimentally infected cynomolgus macaques (Macaca fascicularis) at 4 d postinfection (d.p.i.), indicating that this cell type is the primary target for SCV infection early in the disease, and explaining the subsequent pulmonary damage. We also show that prophylactic treatment of SCV-infected macaques with the antiviral agent pegylated interferon-alpha (IFN-alpha) significantly reduces viral replication and excretion, viral antigen expression by type 1 pneumocytes and pulmonary damage, compared with untreated macaques. Postexposure treatment with pegylated IFN-alpha yielded intermediate results. We therefore suggest that pegylated IFN-alpha protects type 1 pneumocytes from SCV infection, and should be considered a candidate drug for SARS therapy.

Newly discovered coronavirus as the primary cause of severe acute respiratory syndrome.

BACKGROUND: The worldwide outbreak of severe acute respiratory syndrome (SARS) is associated with a newly discovered coronavirus, SARS-associated coronavirus (SARS-CoV). We did clinical and experimental studies to assess the role of this virus in the cause of SARS. METHODS: We tested clinical and postmortem samples from 436 SARS patients in six countries for infection with SARS-CoV, human metapneumovirus, and other respiratory pathogens. We infected four cynomolgus macaques (Macaca fascicularis) with SARS-CoV in an attempt to replicate SARS and did necropsies on day 6 after infection. FINDINGS: SARS-CoV infection was diagnosed in 329 (75%) of 436 patients fitting the case definition of SARS; human metapneumovirus was diagnosed in 41 (12%) of 335, and other respiratory pathogens were diagnosed only sporadically. SARS-CoV was, therefore, the most likely causal agent of SARS. The four SARS-CoV-infected macaques excreted SARS-CoV from nose, mouth, and pharynx from 2 days after infection. Three of four macaques developed diffuse alveolar damage, similar to that in SARS patients, and characterised by epithelial necrosis, serosanguineous exudate, formation of hyaline membranes, type 2 pneumocyte hyperplasia, and the presence of syncytia. SARS-CoV was detected in pneumonic areas by virus isolation and RT-PCR, and was localised to alveolar epithelial cells and syncytia by immunohistochemistry and transmission electron microscopy. INTERPRETATION: Replication in SARS-CoV-infected macaques of pneumonia similar to that in human beings with SARS, combined with the high prevalence of SARS-CoV infection in SARS patients, fulfill the criteria required to prove that SARS-CoV is the primary cause of SARS.