Miracle-dz/UniFAR-FTUs huggingface dataset:
Cursed complexity. Computational properties of subcortical neuronal microcircuitry in sensorimotor control

One of the big obstacles for understanding the nervous system is its inherent complexity. It poses problems when interpreting both experimental and theoretical studies since we are currently forced to consider only reduced variants of the actual circuitry of the brain. Since there exist problems that do not appear until a system is sufficiently complex, there are no guarantees that the results stemming from such reduced studies can be extrapolated to actually apply to the real brain. The initial part of the thesis investigates the properties of the spinocerebellar circuitry of the nervous system, and its role in motor control. Especially the cerebellum has been shown to play an important role in the coordination of fast movements, such as reaching and pointing. Paper I uses theoretical reasoning based on previously found experimental studies to show that the cerebellar circuitry should not be studied in isolation if the aim is to explore cerebellar function. The inputs provided by the pre-cerebellar circuits in the spinal cord and brain stem can significantly reduce the complexity of the problem that the cerebellar circuitry needs to solve. Papers II, IV and V investigate the properties of the mossy fiber pathways. Both the spinal border cell neurons that ascend the ventral spinocerebellar tract with sensorimotor information related to locomotion and the neurons of the cuneate nucleus that process tactile information are studied using behavioral stimulation, either in vivo (Paper V) or through modeling (Paper IV). The results indicate both that the overall activity of the circuitry provides the cerebellum with an easy to interpret encoding, but the individual neurons can at the same time segregate underlying features and details of the stimulus. This result can be seen as a parallel to the found statistics of spike generation in Paper III. Even though the neurons have complex electrodynamic properties, their average activity, described by their firing statistics is surprisingly similar between neurons with vastly different morphology. Paper VI reviews the theoretical grounds for sparse coding, and compares them to recent experimental findings, both in the cerebellum and the neocortex. While there are beneficial properties of certain sparse codes, the experimental results rather indicate that the circuitry both in the cerebellum and the neocortex do not actively maintain a sparse population code. (Less)
An introduction to nonequilibrium plasmas at atmospheric pressure

1) It is easier to apply electromagnetic fields than to uniformly heat and confine a plasma. However, electromagnetic fields naturally transport charged species whose concentrations and energies therefore naturally vary in space, particularly, close to the walls of the container. Generically, the species in such a plasma are not in thermal equilibrium. 2) It is energy efficient to not feed energy equally into all degrees of freedom within a gas or plasma, such as into the thermal displacement, rotation, and vibration of neutral molecules, but only into those degrees of freedom that can efficiently create the desired final reaction products for the particular application. Therefore it is frequently preferable to accelerate only electrons to high velocities and let them excite and ionize molecules by impact while keeping the gas cold. If the electron energy distribution is appropriate, some reactions can be triggered very specifically.
Climate and the Emergence of Global Income Differences

The latitude gradient in comparative development is a striking fact: as one moves away from the equator, economic activity rises. While this regularity is well known, it is not well understood. Perhaps the strongest correlate of (absolute) latitude is the intensity of ultraviolet radiation (UV-R), which epidemiological research has shown to be a cause of a wide range of diseases. We establish that UV-R is strongly and negatively correlated with economic activity, both across and within countries. We propose and test a mechanism that links UV-R to current income differences via the impact of disease ecology on the timing of the take-off to sustained growth.
A Germ Cell-specific Gene, Prmt5, Works in Somatic Cell Reprogramming

Germ cells possess the unique ability to acquire totipotency during development in vivo as well as give rise to pluripotent stem cells under the appropriate conditions in vitro. Recent studies in which somatic cells were experimentally converted into pluripotent stem cells revealed that genes expressed in primordial germ cells (PGCs), such as Oct3/4, Sox2, and Lin28, are involved in this reprogramming. These findings suggest that PGCs may be useful for identifying factors that successfully and efficiently reprogram somatic cells into toti- and/or pluripotent stem cells. Here, we show that Blimp-1, Prdm14, and Prmt5, each of which is crucial for PGC development, have the potential to reprogram somatic cells into pluripotent stem cells. Among them, Prmt5 exhibited remarkable reprogramming of mouse embryonic fibroblasts into which Prmt5, Klf4, and Oct3/4 were introduced. The resulting cells exhibited pluripotent gene expression, teratoma formation, and germline transmission in chimeric mice, all of which were indistinguishable from those induced with embryonic stem cells. These data indicate that some of the factors that play essential roles in germ cell development are also active in somatic cell reprogramming.
Profile of Abaloparatide and Its Potential in the Treatment of Postmenopausal Osteoporosis

Abaloparatide (previously known as BA058) is a synthetic 34-amino acid peptide and novel selective activator of parathyroid hormone receptor 1 (PTHR1) currently under development as a new anabolic agent in the management of osteoporosis. This paper reviews the profile and potential of abaloparatide in the treatment of postmenopausal osteoporosis. This paper is based on clinical trials and a PubMed search. Search terms used were “abaloparatide”, “BA058”, and “PTHrP”. This review outlines the effects of this anabolic PTHR1 activator, which increases bone mineral density in patients at high risk for osteoporosis. The potential adverse effects of abaloparatide are also summarized. Abaloparatide has 41% homology to parathyroid hormone (PTH) (1-34) and 76% homology to parathyroid hormone-related protein (PTHrP) (1-34). The molecule was meticulously selected to retain stability and potent bone anabolic activity, and it has a limited effect on bone resorption (hence, a low calcium-mobilizing potential). Abaloparatide has shown promising results in a reduction of new onset vertebral (approximately 86% reduction) and nonvertebral fractures (approximately 43% reduction). In clinical trials to date, abaloparatide appears to have a good safety and tolerability profile with a significantly lower degree of hypercalcemia compared to that of teriparatide. Based on the clinical trials, the optimum dose of abaloparatide is 80 mcg subcutaneous once daily.
Performance modeling of fully adaptive wormhole routing in 2D mesh-connected multiprocessors

Several models of deterministic routing have been proposed for wormhole-routed mesh networks while there is only one model, to the best of our knowledge, proposed for fully adaptive wormhole routing in mesh interconnection networks. The paper proposes a new analytical performance model of fully adaptive wormhole-routed mesh networks with high accuracy. Simulation results show that, unlike the previous model which was applicable in light traffic loads, this model can be used for performance analysis for almost all traffic loads.
Implications of radio fingerprinting on the security of sensor networks

We demonstrate the feasibility of finger-printing the radio of wireless sensor nodes (Chipcon 1000 radio, 433MHz). We show that, with this type of devices, a receiver can create device radio finger-prints and subsequently identify origins of messages exchanged between the devices, even if message contents and device identifiers are hidden. We further analyze the implications of device fingerprinting on the security of sensor networking protocols, specifically, we propose two new mechanisms for the detection of wormholes in sensor networks.
Short- and long-term changes in CA1 network excitability after kainate treatment in rats.

Neuron loss, axon sprouting, and the formation of new synaptic circuits have been hypothesized to contribute to seizures in temporal lobe epilepsy (TLE). Using the kainate-treated rat, we examined how alterations in the density of CA1 pyramidal cells and interneurons, and subsequent sprouting of CA1 pyramidal cell axons, were temporally associated with functional changes in the network properties of the CA1 area. Control rats were compared with animals during the first week after kainate treatment versus several weeks after treatment. The density of CA1 pyramidal cells and putative inhibitory neurons in stratum oriens was reduced within 8 days after kainate treatment. Axon branching of CA1 pyramidal cells was similar between controls and animals examined in the first week after kainate treatment but was increased several weeks after kainate treatment. Stimulation of afferent fibers in brain slices containing the isolated CA1 region produced graded responses in slices from controls and kainate-treated rats tested <8 days after treatment. In contrast, synchronous all-or-none bursts of spikes at low stimulus intensity (i.e., "network bursts") were only observed in the CA1 several weeks after kainate treatment. In the presence of bicuculline, the duration of evoked bursts was significantly longer in CA1 pyramidal cells weeks after kainate treatment than from controls or those examined in the first week posttreatment. Spontaneous network bursts were also observed in the isolated CA1 several weeks after kainate treatment in bicuculline-treated slices. The data suggest that the early loss of neurons directly associated with kainate-induced status epilepticus is followed by increased axon sprouting and new recurrent excitatory circuits in CA1 pyramidal cells. These changes characterize the transition from the initial acute effects of the kainate-induced insult to the eventual development of all-or-none epileptiform discharges in the CA1 area.
Towards Behavioral Reflexion Models

Software architecture has become essential in the struggle to manage today’s increasingly large and complex systems. Software architecture views are created to capture important system characteristics on an abstract and, thus, comprehensible level. As the system is implemented and later maintained, it often deviates from the original design specification. Such deviations can have implication for the quality of the system, such as reliability, security, and maintainability. Software architecture compliance checking approaches, such as the reflexion model technique, have been proposed to address this issue by comparing the implementation to a model of the systems’ architecture design. However, architecture compliance checking approaches focus solely on structural characteristics and ignore behavioral conformance. This is especially an issue in Systems-of-Systems. Systems-of-Systems (SoS) are decompositions of large systems, into smaller systems for the sake of flexibility. Deviations of the implementation to its behavioral design often reduce the reliability of the entire SoS. An approach is needed that supports the reasoning about behavioral conformance on architecture level.In order to address this issue, we have developed an approach for comparing the implementation of a SoS to an architecture model of its behavioral design. The approach follows the idea of reflexion models and adopts it to support the compliance checking of behaviors. In this paper, we focus on sequencing properties as they play an important role in many SoS. Sequencing deviations potentially have a severe impact on the SoS’ correctness and qualities. The desired behavioral specification is defined in UML sequence diagram notation and behaviors are extracted from the SoS implementation. The behaviors are then mapped to the model of the desired behavior and the two are compared. Finally, a reflexion model is constructed that shows the deviations between behavioral design and implementation. This paper discusses the approach and shows how it can be applied to investigate reliability issues in SoS.
Group I mGluR-dependent depotentiation in the lateral amygdala does not require the removal of calcium-permeable AMPA receptors

There is conflicting evidence regarding whether calcium-permeable receptors are removed during group I mGluR-mediated synaptic depression. In support of this hypothesis, AMPAR rectification, a correlative index of the synaptic expression of GluA2-lacking calcium–permeable AMPARs (CP-AMPARs), is known to decrease after the induction of several types of group I mGluR-mediated long-term depression (LTD), suggesting that a significant proportion of synaptic CP-AMPARs is removed during synaptic depression. We have previously demonstrated that fear conditioning-induced synaptic potentiation in the lateral amygdala is reversed by group 1 mGluR-mediated depotentiation. Here, we examined whether CP-AMPARs are removed by mGluR1-mediated depotentiation of fear conditioning-induced synaptic potentiation. The synaptic expression of CP-AMPARs was negligible before, increased significantly 12 h after, and returned to baseline 48 h after fear conditioning, as evidenced by the changes in the sensitivity of lateral amygdala synaptic responses to NASPM. Importantly, the sensitivity to NASPM was not altered after induction of depotentiation. Our findings, together with previous results, suggest that the removal of CP-AMPARs is not required for the depotentiation of fear conditioning-induced synaptic potentiation at lateral amygdala synapses.
The strength of phyllosilicate-rich fault zones

The integrated strength of the lithosphere depends to a large degree on the brittle strength of the upper crust. Laboratory experiments at slow slip rates performed by Byerlee (Byerlee, 1978) have shown that, over a very large range of crustal stress conditions, the strength of faults as described by the coefficient of friction, only varies between 0.6 and 0.85, regardless of the material used in the experiments. This observed behaviour is termed Byerlee‟s rule. There are several lines of evidence that suggest that the strength of the brittle crust is dictated by Byerlee‟s rule. First, the angle between any fault plane and the principal tectonic driving stress component should be 25 to 30° if Byerlee‟s rule applies. Compilations of >M5.5 earthquakes has shown angles in that range, albeit with quite a lot of scatter (Collettini & Sibson, 2001; Sibson & Xie, 1998). Importantly, no earthquakes were recorded that show an angle greater than the predicted frictional lock-up angle (where it should be more favourable to create a new fault than to reactivate slip on the severely mis-oriented fault). Second, crustal stress measurements made in various boreholes show a variation in differential stress with depth that is entirely consistent with slip on faults with friction coefficients commensurate with those predicted by Byerlee (Townend & Zoback, 2000). Consequently, the inference has been made that crust strength is controlled by faults obeying Byerlee‟s rule.
Cancer-related anemia: its causes and characteristics.

Under normal circumstances, the circulating red blood cell mass is maintained at a level that is constant in each individual, although that level may vary by more than 10% among individuals of the same age and gender. At normal ambient oxygen tension, two factors determine the circulating red blood cell mass: red blood cell life span, which is finite and in humans approximates 120 days; and the rate of effective red blood cell production. To maintain a constant red blood cell mass, therefore, approximately 20 mL of red blood cells must be produced each day to replace those red blood cells lost from the circulation through senescence. Anemia, which may be defined functionally as lack of sufficient red blood cells to maintain adequate tissue oxygenation, develops when the demand for new red blood cells exceeds the capacity of the bone marrow to produce them. This may be due to excessive red blood cell destruction, impaired red blood cell production, bleeding, or any combination of these. Acquired anemia is always a consequence of another disorder, which must be identified to ensure that the corrective therapy is appropriate. In patients with solid tumors, multiple mechanisms for causing anemia have been identified: blood loss that is either intrinsic or iatrogenic; nutritional deficiencies involving primarily iron or folic acid; hemolysis (autoimmune, traumatic, or drug-induced); bone marrow failure due to tumor encroachment, myelofibrosis, or marrow necrosis; infection; inflammation; or simply the presence of a cancer elsewhere in the body. The three noted causes of marrow failure share a common denominator: impaired production of erythropoietin. For any degree of anemia, a patient with cancer produces much less erythropoietin than expected and, therefore, cannot compensate for impaired red blood cell production. Inflammation or infection can exacerbate this situation. Indeed, anemia in patients with cancer appears to behave much like that in patients with chronic renal failure who become anemic because of the inability of the kidneys to produce erythropoietin adequately. The cause of impaired erythropoietin production in patients with cancer who have anemia is not entirely understood, but may be due in part to the production of inflammatory cytokines in response to the tumor. Such cytokines also would be expected to blunt the ability of the bone marrow to respond to the available circulating erythropoietin. (ABSTRACT TRUNCATED AT 400 WORDS)
Experimental Models of Aural Cholesteatomas in Mongolian Gerbils

Mongolian gerbils have a remarkable propensity for the development of aural cholesteatoma; canal cholesteatomas develop spontaneously in aged animals. In the present study, cholesteatomas were produced in a single species, Meriones unguiculatus, by three different methods of induction: 1) external canal ligation (ECL), 2) eustachian tube obstruction (ETO) by electrocautery, and 3) application of propylene glycol (PG) into the middle ear. Each method of induction resulted in cholesteatomas with characteristic features and success rates. With ECL, cholesteatomas could be induced in all ligated ears; stage III and IV cholesteatomas were seen in 4 of 12 ears after 8 weeks. With ETO, cholesteatomas were seen in 7 of 9 animals 8 weeks after induction. With PG, cholesteatomas developed in 2 of 7 animals 4 weeks after induction, although keratin accumulation in the external auditory canal could be found in all animals injected. Although epithelial hyperplasia of the external auditory canal was most prominent in the ECL group, it was also seen in the ETO and PG groups. Keratin accumulation in the ECL or PG group was much greater than that in the ETO group. Thickening of the tympanic membrane, which was most prominent in the PG group, was quite variable in the other groups. Adhesions of the tympanic membrane began at the prominence of the cochlea in the ECL group. In contrast, adhesions in the PG group usually began at the superior bulla, the area in which PG was applied. Each of the three methods of inducing cholesteatoma may be helpful in investigating different clinical aspects of this disease.
Bacterial biofilms associated with ocular prostheses

the lid tension by botulinum toxin injection in patients with blepharospasm. And Razeghinejad and Dehghani reported that with-the-rule astigmatism reduced after treatment of hypotony. Therefore, we considered that the pressure on the hypotonic eyeball exerted by the eyelids might have increased with-the-rule astigmatism during the persistent hypotony. In the present case, we have reported restoration of the axial length, anterior chamber depth, lens thickness and vitreous cavity length after treatment of the persistent hypotony (Table 1). Ikeda et al. reported that an anterior shift of the lens–iris diaphragm and thickening of the crystalline lens result in transient myopia, and the anterior chamber was shallower, the lens was thicker and the vitreous cavity was longer immediately after the injury than at day 17 after the injury. In our patient, however, we observed a decrease in the length of the vitreous cavity as well as shallowing of the anterior chamber and lens thickening compared with 7 months after the treatment. We assumed that the 5 months of persistent hypotony might have decreased the vitreous volume, unlike the two cases previously reported by Ikeda et al. Another possible explanation is the different measurement time points. We performed the biometric measurements 7 months after IOP restoration by the laser treatment, whereas Ikeda et al. performed the biometric measurements 17 days after the injury. Large numbers of cases and further analysis will be needed to prove this hypothesis. In conclusion, we have reported the changes in biometric measurements after trauma-induced persistent hypotony and the gradual changes in refraction during a period of persistent hypotony. For the first time, we showed that significant with-the-rule astigmatism gradually developed during the period of persistent traumatic hypotony.
Chronic Prenatal Ethanol Exposure Increases GABAAReceptor Subunit Protein Expression in the Adult Guinea Pig Cerebral Cortex

Excessive consumption of ethanol during pregnancy can produce teratogenic effects in offspring and is the leading cause of mental deficiency in the Western world. The objective of this study was to examine the effects of chronic prenatal ethanol exposure on the number of GABAA receptors and relative protein levels for GABAA receptor α1 and β2/3 subunits in the adult guinea pig cerebral cortex. Timed pregnant Dunkin-Hartley strain guinea pigs were given one of the following oral treatments daily throughout gestation: 4 gm of ethanol per kilogram of maternal body weight, isocaloric-sucrose with pair feeding, or isovolumetric water withad libitum access to food. The ethanol treatment resulted in a peak maternal blood ethanol concentration of 328 ± 55 mg/dl (71.3 ± 12.0 mm) on gestational day 57 (term, ∼68 d). Chronic prenatal exposure to ethanol resulted in increased spontaneous locomotor activity throughout development and decreased cerebral cortical weight in adult offspring. The number of cerebral cortical [3H]muscimol binding sites was increased in adult offspring from the ethanol treatment group, and there was a corresponding increase in the amount of GABAAreceptor α1 and β2/3 subunit proteins in these same animals. For individual offspring, there were correlations between locomotor activity and cerebral cortical weight, as well as between cerebral cortical weight and GABAA receptor neurochemistry. There was no effect of chronic prenatal ethanol exposure on [3H]MK-801 binding in this tissue. These data demonstrate that chronic prenatal ethanol exposure has long-term consequences on the regulation of GABAA receptor expression in the cerebral cortex.