text:
An entrepreneur is someone who:
Starting a business can be challenging for many, but if you are passionate, motivated, a risk taker, hard worker, or believe in yourself you are likely to succeed in the business world. Before you start a business you should decide what type of business you want to establish. There are usually 5 types of businesses, namely:
Typical sole traders include the man-in-a-van type of occupation such as a plumber or electrician. However, the term can also apply to people who run small, web-based businesses from home.
This is the simplest and the most common type of business out there. The sole proprietor is responsible for everything the business does. You trade under your own name, with no separation of assets and liabilities. This means that youll be held personally liable for any debts that the business incurs.
Partnerships are typically found in professional services such as accountants, lawyers, doctors, dentists etc, where the partners can share expertise and skills. They can also share the workload. Partnerships comprise two or more people and any profits, debts and decisions related to the business are shared.
Companies are owned by shareholders who each put an amount of money into a central pool. This pool of capital is then added to by borrowing and other forms of finance. Directors run the company on behalf of shareholders, who receive a share of the profits. Each shareholder receives a portion or share of the company that is equivalent to what they put in. A company is seen as a legal entity that is entirely separate from the shareholders.
Franchises are licensing arrangements whereby an individual or group can buy the right to trade and produce under a well-known brand name in a given locality. A franchise involves you using another companys successful business model and name to establish your own business. The franchisee benefits from working for themselves while having the privilege and reputation associated with a much larger group.
Limited liabilities are intended to benefit professional partnerships such as lawyers, doctors etc. They offer a form of business protection for company shareholders and some limited partners. For these individuals, the maximum sum they can lose from a business venture that goes under, is the sum of money that they invested in the company.
Limited liability allows the members to limit their personal liability if something goes wrong with the business.
To start a business you need to follow these steps:
No, but you do need to acquire important business skills. It is difficult to run a successful business without the necessary training or skills. You can contact the National Youth Development Agency (NYDA), The Small Enterprise Development Agency (Seda) and others for advice and support.


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|Material Type:
|Document, Internet resource
|Document Type:
|Internet Resource, Computer File
|All Authors / Contributors:
William Whittingham; Anthony Gilby; Thomas Sampson; Laurence Tomson; Franciscus Junius
|OCLC Number:
|The Geneva version of the Old Testament, translated by William Whittingham, Anthony Gilby, Thomas Sampson, and perhaps others, with Laurence Tomson's revision of the Geneva version of the New Testament and his translation of Franciscus Junius' translation of Revelation.
At foot of title: Cum priuilegio.
Part 2 of the old Testament has divisional title and separate foliation; "The Nevve Testament of our Lord Iesus Christ" has separate title page dated 1593 and separate foliation; register is continuous.
Includes indexes.
Reproduction of the original in the University of Illinois (Urbana-Champaign Campus). Library.
|1 online resource ([3], 190, 127, 129-197, 116, [11] leaves) : ill., maps (woodcuts)
|Other Titles:
Nevve Testament of our Lord Iesus Christ
Newe Testament of our Lord Jesus Christ
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text:
Upcoming Regional Workshops:
For a complete listing of upcoming ICLEF seminars, including live seminars, live webcasts, online seminars, or video replays, visit the ICLEF website.
July 22 - 26, 2016 - 40-hour basic Domestic Relations training course led by Janet Mitchell and Angenetta Briner - 24.0 hours CLE / 6.0 hours Ethics / 40 hours Social Work CEH - Fort Wayne - registration limited to 24 registrants - for further information, visit Janet's website or contact her.
September 16 - 17, 2016 - 6th Annual Midwest Mediation Conference featuring Tammy Lanski. See the What's New page for more information.
Other Workshops, Conferences, & Seminars:
Visit the Dispute Resolution Section of the American Bar Association for more information on this ABA Section's various activities.
For general information on the Association for Conflict Resolution and its activities, visit acrnet.org.
For a nationwide listing of mediation trainings that are available, visit Mediate.com.
See the Mediation Training Institute for more information about their activities.
Ann Thrasher, President
P.O. Box 216
Zionsville, IN 46077
(317) 732-8585


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ACOG and APP statement on delivering in the water
The American College of Obstetrics and Gynecology along with the American Academy of Pediatrics have release a statement about water birth. They say laboring in the water has benefits for relaxation and pain relief. They say that delivering in the water has no proven benefits and is dangerous. Due to this statement being released some hospitals are changing their policy to ban deliveries in the water.
I always found laboring in the tub to be very comforting. I have never delivered in the tub, I always delivered in the hospital bed. As a doula I encourage all of my clients to labor in the tub. Our local hospital has never allowed tub deliveries so nothing is change at our hospital.
Did you deliver your baby in the water? Do you plan on delivering your baby in the water?


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Following the genes: a framework for animal modeling of psychiatric disorders
The number of individual cases of psychiatric disorders that can be ascribed to identified, rare, single mutations is increasing with great rapidity. Such mutations can be recapitulated in mice to generate animal models with direct etiological validity. Defining the underlying pathogenic mechanisms will require an experimental and theoretical framework to make the links from mutation to altered behavior in an animal or psychopathology in a human. Here, we discuss key elements of such a framework, including cell type-based phenotyping, developmental trajectories, linking circuit properties at micro and macro scales and definition of neurobiological phenotypes that are directly translatable to humans.
Historical approaches to modeling psychiatric disorders
Psychiatric disorders constitute a diverse set of conditions, variously impinging on all domains of mental function and affecting the most fundamental human attributes: language, thought, perception, mood and sense of self. Collectively, they cause a substantial public health burden, greater than cancers or cardiovascular disease
In the absence of such information on specific genetic causes, previous modeling approaches for psychiatric disorders have been based either on surface similarities between behavioral assays in rodents and domains of psychopathology in humans or on dissecting the psychopharmacological mechanisms of known drugs
The behavioral approach first defines behavioral assays in animals that are thought to mimic symptoms in particular psychological domains
There are several drawbacks to using only the criterion of response to known medication. First, most of the models do not have causal etiological validity - acute blockade of NMDA-type receptors for glutamate or ventral hippocampal lesion are not actual causes of schizophrenia, for example. Second, the surface parallels between rodent and human behavior may be misleading. On the contrary, we should expect some of the underlying neurobiological defects to manifest at the behavioral level in species-specific ways, which may or may not appear related
A complementary approach is now becoming possible as particular mutations causing psychiatric illness are being identified at an ever-increasing rate. Mouse models of these mutations can now be investigated using increasingly powerful and sophisticated tools to get at the underlying neurobiology and elucidate pathogenic mechanisms, from the level of synapses formed between specific cell types in specific circuits to the level of dynamic function of neuronal networks and concomitant moment-to-moment behavior. These types of approaches should provide the necessary neurobiological knowledge to enable the rational design of new therapeutics.
A revolution in psychiatric genetics
The field of psychiatric genetics is undergoing a profound paradigm shift. For several decades, the prevailing model has held that psychiatric disorders arise in any individual due to the cumulative effects of a large number of common variants
The alternative model is that psychiatric disorders arise due to mutations in any of a very large number of genes
It has, of course, been known for some time that psychiatric illness could arise due to single mutations. Well-known examples include fragile × syndrome
Copy number variants (deletions or duplication of chromosomal segments, often affecting multiple genes) have been most readily identified and make up an important class of causal mutations in schizophrenia
A number of important principles have emerged from these studies. First, there is considerable overlap in the genetic etiology of what had previously been considered distinct disorders. Individual mutations that predispose to one class of psychiatric illness, such as schizophrenia, are also associated with other disorders, such as bipolar disorder, autism, mental retardation, epilepsy, attention deficit hyperactivity disorder and Tourette's syndrome (for example,
Second, the mutations so far discovered are characterized by incomplete penetrance and variable expressivity
Third, many of the identified genes are involved in neural development
Fourth, allelic specificity and dosage are extremely important. Different mutations in the same gene may result in very different phenotypic outcomes. As a classic example, Duchenne muscular dystrophy and Becker's muscular dystrophy are caused by different types of mutations in the
Fifth, while these findings highlight the importance of rare single mutations, they do not necessarily imply a simple mode of inheritance. Many of the mutations found so far show a dominant effect, but recessive mutations are likely to also contribute a sizeable fraction of cases
Sixth, the eventual phenotype will also be modified by non-genetic factors, including (i) intrinsic developmental variation, where the phenotypic outcome varies due to inherent noise in the molecular processes mediating neurodevelopment
Despite these complexities, the major finding is clear: mutations with large effect on risk of psychiatric disorders exist and we now have the means to identify them. If we think of this as a genetic screen for mutations causing a specific phenotype, with demonstrated saturation mutagenesis of the human population
Advances in genetic engineering allow us to recapitulate human mutations in mice, and increasingly in rat. It is possible to generate animals with full gene knock-outs, conditional removal of the gene with spatial and temporal control, knock-in of exact human alleles, and to precisely engineer genomic deletions or duplications into syntenic regions of mouse chromosomes, thereby yielding animal models with direct construct validity; that is, where the manipulation is an actual cause of the condition in humans
The number of models generated to date that directly recapitulate or mimic the effects of human alleles is small, but they have already begun to reveal details of the mechanisms of pathogenesis in specific mutants and to highlight convergent pathways, as well as some important general principles. For example, mutations in
Studies in some animal models, such as mice mutant in
To fully elucidate the pathogenic mechanisms for any specific mutation will require the integration of analyses across multiple levels, from protein function to systems neuroscience. What are the biochemical functions of the mutated protein? What are the cellular effects in various brain regions? How do these affect the function of various neural circuits? How do changes in neural activity play out over subsequent activity-dependent development? What are the cascading or reactive consequences as the brain develops with these initial alterations? What are the concomitant effects on physiology and behavior? Which circuit defects are responsible for which behavioral phenotypes? Which are the ones most relevant to the symptoms of the human disease? Which are the ones most amenable to intervention? These are formidable challenges even in light of the spectacular advances in modern neuroscience.
Rather than predefining which areas or mechanisms are important or how we expect animal models of psychiatric disorders to behave, we can take a bottom-up approach and simply ask, for any of these mouse mutants 'what happens to their brain circuits?' In analyzing the effects of any particular mutation it will be essential to consider the full cellular complexity of the circuitry and to use all the tools of modern molecular neuroscience to dissect the causal chains from primary genetic lesion to ultimate phenotype(s).
A cell type-based approach is key to link genes and circuits in discovering pathogenic mechanisms
Is there a generally useful strategy to tackle the problem of circuit pathogenesis in rodent models? If genes are the entry points to the cause and genetic architecture of psychiatric disorder, then we suggest that specific cell types may be the next set of entry points in neurobiology studies that may coherently link different levels of analysis, integrate different approaches and technologies, and yield useful answers in understanding pathogenic mechanisms. This is based on the following three first principles: individual cell types are the basic components of neural circuit organization, the building blocks of circuit assembly, and the basic units of gene expression and regulation in the brain (Figure
Figure 1
A framework to elucidate pathogenic mechanisms from mutations to mental illness
A framework to elucidate pathogenic mechanisms from mutations to mental illness. The effects of mutations in different genes can be analyzed across development on diverse cell types, local circuit organization and emergent properties, functional connectivity on a macro scale and correlated behavior in animals or psychopathology in humans.
The focus on cell types embraces the importance of different types of synapse. For example, mutations in
However, cell type-based analysis of neural circuits, although more routinely practiced in invertebrate systems, is highly challenging in the mammalian brain circuits, which consist of highly diverse and intermingled cell types that, until recently, could not be readily identified and experimentally accessed.
Fortunately, our ability to carry out such cell type-based analyses is rapidly increasing, as new neurogenetic tools are developed. Gene expression profiles that define many cell types have been elucidated, enabling researchers to isolate specific genetic elements that can be used to drive cell type-specific expression of a variety of transgenic constructs with different uses. These include tracing axonal projections and synaptic connections, monitoring electrical activity, and non-invasively activating or shutting off neurons in behaving animals with optical methods or chemical ligands
The Cre-loxP system has been adopted as a standardized approach in the mouse to drive such constructs in specific cell types
Analysis of multiple circuits brain-wide in a disease model will allow a more unbiased 'screen' for deficits, less restricted by prior knowledge and assumptions of disease pathology. This will allow definition of the overall profile of deficits across multiple systems in each individual mutant, which may be quite unique. Comparison of multiple disease models promises to identify shared or distinct circuit deficits in these models, which may underlie their shared or distinct behavioral phenotypes. To achieve this, it will be increasingly useful to establish high-throughput methods to effectively screen for alterations in cell numbers, connectivity, and function with cell type resolution
The convergence of phenotype across multiple animal models may arise at the biochemical or cellular level in some cases (such as pathways involved in synapse formation
Large-scale analysis of circuits that subserve behavior
The neuroscience of animal and human behavior has witnessed a productive paradigm shift in the past decade where the trend of assigning complex traits to single genes has given way to the realization that dynamic coordination between micro and macro circuits is key to understanding the neuronal basis of behavior
In the context of schizophrenia, the approach has been descriptive and mechanistically naive in that, for the most part, it has focused on associating a common allelic variation, which in some cases has not even been associated with a functional alteration, to complex behavioral disruptions whose physiology is still not fully understood. It is now increasingly being appreciated that a mechanistic understanding of the pathophysiology of schizophrenia is contingent upon (i) a better understanding of the dynamic coordination of neuronal processes that serve the behaviors that are disturbed in at least some cases of schizophrenia and (ii) understanding the functional role of implicated genes in micro and macro neuronal circuits that subserve this physiology. Recent studies, highlighted below, are beginning to make considerable advances in these two approaches.
Electrophysiological recordings using electroencephalography (EEG) have for decades reported behaviorally relevant oscillatory activity throughout the cerebral cortex
Animal studies have further demonstrated that synchronized neuronal oscillations at various frequencies are a measure of coordinated neuronal activity that supports behavior. EEG and MEG studies in humans have subsequently established a close relationship between oscillations at various frequencies and behavioral performance, including working memory and selective attention
Thus, experimental procedures such as pharmacological and genetic manipulations can be applied in conjunction with single unit recording and local field potentials to understand the molecular and cellular processes that could contribute to abnormal oscillatory activities
The proliferation of cell type-specific genetic drivers and development of optogenetic approaches also enable follow-up experiments to directly test hypotheses arising from studies of mutant phenotypes by manipulating the activity of the implicated cell types in highly specific ways
While mice are likely to continue to lead the way in the discovery of the effects of specific mutations on nervous system development and function, we can also expect the increasing use of genetically manipulated rat and primate models to further dissect pathophysiological mechanisms. Zinc-finger nucleases can be used to specifically modify the genome in effectively any type of cell, including embryonic stem cells or early embryos, thus generating genetically modified organisms
Translation to humans
Because diagnostic classification of mental illnesses in clinical psychiatry at present is merely based on phenomenology and not disease etiology, it is important to consider translation between humans and rodent models not via clinical diagnosis but specific biological traits. These traits would include behavioral constructs and physiological characteristics, and are crucial in understanding disease mechanisms in rodent models. Even more importantly, such characteristics can be used as indicators of drug screening in rodents and markers in clinical trials with humans.
A major confound in analyzing neurobiological intermediate phenotypes in psychiatric patients has been the extreme underlying (and previously cryptic) genetic heterogeneity. As the genetic factors involved in psychiatric illness are determined in more and more patients, it should be possible to make much more direct and powerful comparisons of underlying phenotypic traits between genetically defined subsets of humans and mice carrying the same mutation. This genetic stratification of patients may also prove invaluable in the design of clinical trials aimed at primary causes. On the other hand, the analysis of phenotypes correlated with clinical states will need to look for convergence across mouse mutants or human patients with diverse genetic causes.
Many efforts have been made to try to identify equivalent characteristics between humans and rodents. For example, at the behavioral level, the Cognitive Neuroscience Treatment Research to Improve Cognition in Schizophrenia (CNTRICS) aims to develop and implement animal model paradigms that can tap the cognitive and emotional-processing constructs translatable to humans
Given well-founded concerns over the species-specificity of behavioral measures, it seems likely that neurophysiological measures may prove to be more translatable between animals and humans. This may be especially true of measures of functional connectivity or coherence between brain areas, as these may most powerfully index differences in network function that affect psychopathology. These can be assayed with EEG and MEG, as described above, but also with functional connectivity studies using functional magnetic resonance imaging to examine correlations between activities of remote but connected regions
Definition of the mouse correlates of human pathophysiology and psychopathology will also allow a reverse translational approach to identify new candidate susceptibility genes. Prospective phenotyping of mice with mutations in neurodevelopmental genes may reveal phenotypes paralleling established models (for example,
Strategies towards new treatments
The drugs currently used to treat disorders like schizophrenia were discovered serendipitously, are only partially effective for positive symptoms but not the more debilitating negative and cognitive symptoms, work in some patients and not others and have serious side effects
New genetic models may be utilized in identifying novel treatment strategies in three ways: first, to identify novel targets through which we can find more effective and safer compounds for treatment within the current understanding of these diseases; second, to identify novel targets and compounds that may not be obvious from current paradigms; third, and probably most important, to identify targets and compounds for early intervention.
By analyzing molecular, cellular and circuitry disturbances in new genetic models, we may find better clues to how the cellular pathways involving the gene of interest may interact with currently accepted pathophysiological paradigms (such as the roles of GABA, NMDA receptors and dopamine receptors in schizophrenia). In such cases, we may identify better drug targets, against which we can expect compounds with better efficacy and less side effects.
However, our hope is to identify new targets and compounds with new genetic models. Although investigators who generate new genetic models tend to test whether current medications (such as clozapine and haloperidol for schizophrenia) can normalize deficits in behavioral paradigms, it may be more advantageous for new drug discovery to identify paradigms that are relevant to human diseases (that is, likely to correlate not to one disease but to several), but that cannot be normalized by current medications. For example, a
Early intervention is now becoming a key in treatment strategies in many brain disorders, such as Alzheimer's disease and schizophrenia. Animal models, especially those in which neurodevelopmentally important genes are targeted, are very useful to dissect the pathological course even from the premorbid stage to the full onset. For some symptoms, specific common phenotypes might be due to secondary mechanisms by which the developing brain reacts to diverse primary insults. For example, altered dopaminergic signaling may arise as a result of a variety of primary defects and may represent a final common pathway to psychosis
A way forward
The discovery of mutations that strongly predispose individuals to psychopathology provides a crucial starting point to define pathogenic mechanisms and pathways. Direct animal models of genetic etiology can be analyzed in a comprehensive and systematic way, using the full arsenal of modern neuroscience to link effects on particular cell types in defined microcircuits to emergent properties of larger scale brain networks in behaviorally relevant contexts. These analyses will hopefully reveal neurobiological phenotypes that can be translated very directly to humans, suggest points of possible therapeutic intervention and aid the rational design of new drugs targeted at the underlying causes of mental illness.
From animal models to model animals
The role of rodent models in the discovery of new treatments for schizophrenia: updating our strategy
Schizophrenia-relevant behavioral testing in rodent models: a uniquely human disorder?
Animal models: inside the minds of mice and men
From revolution to evolution: the glutamate hypothesis of schizophrenia and its implication for treatment
Second generation antipsychotics in the treatment of bipolar depression: a systematic review and meta-analysis
A polygenic theory of schizophrenia
Genetic linkage and complex diseases, with special reference to psychiatric disorders
Narrowing the boundaries of the genetic architecture of schizophrenia
Rethinking the genetic architecture of schizophrenia
The future of genetic studies of complex human diseases
On the allelic spectrum of human disease
A framework for interpreting genome-wide association studies of psychiatric disorders
The psychiatric GWAS consortium: big science comes to psychiatry
Identification of the semaphorin receptor PLXNA2 as a candidate for susceptibility to schizophrenia
Identification of loci associated with schizophrenia by genome-wide association and follow-up
Common polygenic variation contributes to risk of schizophrenia and bipolar disorder
A genome-wide investigation of SNPs and CNVs in schizophrenia
Common variants conferring risk of schizophrenia
Common variants on chromosome 6p22.1 are associated with schizophrenia
A genome-wide linkage and association scan reveals novel loci for autism
Common genetic variants on 5p14.1 associate with autism spectrum disorders
A genome-wide scan for common alleles affecting risk for autism
Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4
Genome-wide association study identifies five new schizophrenia loci
Fine mapping of ZNF804A and genome-wide significant evidence for its involvement in schizophrenia and bipolar disorder
Rare variants create synthetic genome-wide associations
Resolving the paradox of common, harmful, heritable mental disorders: which evolutionary genetic models work best?
Schizophrenia: a common disease caused by multiple rare alleles
Rare structural variants in schizophrenia: one disorder, multiple mutations; one mutation, multiple disorders
Allelic diversity in human developmental neurogenetics: insights into biology and disease
Etiological heterogeneity in autism spectrum disorders: More than 100 genetic and genomic disorders and still counting
Genetic heterogeneity in human disease
Clan genomics and the complex architecture of human disease
Association of fragile × syndrome with autism
Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2
Mutations of the X-linked genes encoding neuroligins NLGN3 and NLGN4 are associated with autism
Schizophrenia susceptibility associated with interstitial deletions of chromosome 22q11
Disruption of two novel genes by a translocation co-segregating with schizophrenia
Strong association of de novo copy number mutations with autism
Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia
Uncovering the roles of rare variants in common disease through whole-genome sequencing
Needles in stacks of needles: finding disease-causal variants in a wealth of genomic data
Strong association of de novo copy number mutations with sporadic schizophrenia
Large recurrent microdeletions associated with schizophrenia
Rare chromosomal deletions and duplications increase risk of schizophrenia
A study of rare structural variants in schizophrenia patients and normal controls from Chinese Han population
Functional impact of global rare copy number variation in autism spectrum disorders
Copy number variants in schizophrenia: confirmation of five previous findings and new evidence for 3q29 microdeletions and VIPR2 duplications
Duplications of the neuropeptide receptor gene VIPR2 confer significant risk for schizophrenia
Structural variation of chromosomes in autism spectrum disorder
Autism genome-wide copy number variation reveals ubiquitin and neuronal genes
Multiple recurrent de novo CNVs, including duplications of the 7q11.23 Williams syndrome region, are strongly associated with autism
Rare structural variants found in attention-deficit hyperactivity disorder are preferentially associated with neurodevelopmental genes
Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: a genome-wide analysis
Rare copy number variation discovery and cross-disorder comparisons identify risk genes for ADHD
Genome-wide copy number variation analysis in attention-deficit/hyperactivity disorder: association with neuropeptide Y gene dosage in an extended pedigree
Tourette syndrome is associated with recurrent exonic copy number variants
Consensus statement: chromosomal microarray is a first-tier clinical diagnostic test for individuals with developmental disabilities or congenital anomalies
A copy number variation morbidity map of developmental delay
Genome-wide copy number variation in epilepsy: novel susceptibility loci in idiopathic generalized and focal epilepsies
High frequency of rare copy number variants affecting functionally related genes in patients with structural brain malformations
Systematic resequencing of X-chromosome synaptic genes in autism spectrum disorder and schizophrenia
A de novo paradigm for mental retardation
Strong synaptic transmission impact by copy number variations in schizophrenia
Exome sequencing supports a de novo mutational paradigm for schizophrenia
Increased exonic de novo mutation rate in individuals with schizophrenia
A population genetic approach to mapping neurological disorder genes using deep resequencing
Exome sequencing in sporadic autism spectrum disorders identifies severe de novo mutations
Deep sequencing reveals 50 novel genes for recessive cognitive disorders
CNTNAP2 gene dosage variation is associated with schizophrenia and epilepsy
Recurrent rearrangements of chromosome 1q21.1 and variable pediatric phenotypes
Recurrent rearrangements in synaptic and neurodevelopmental genes and shared biologic pathways in schizophrenia, autism, and mental retardation
Microdeletion/duplication at 15q13.2q13.3 among individuals with features of autism and other neuropsychiatric disorders
Deletions of NRXN1 (neurexin-1) predispose to a wide spectrum of developmental disorders
The genetics of neurodevelopmental disease
Parental psychiatric disorders associated with autism spectrum disorders in the offspring
Common genetic determinants of schizophrenia and bipolar disorder in Swedish families: a population-based study
Family aggregation of mental disorders in the nationwide Danish three generation study
The genetics of autism spectrum disorders and related neuropsychiatric disorders in childhood
Severe mental disorders in offspring with 2 psychiatrically ill parents
Bidirectional relation between schizophrenia and epilepsy: A population-based retrospective cohort study
Copy number variations in schizophrenia: critical review and new perspectives on concepts of genetics and disease
The DISC locus in psychiatric illness
Identifying relationships among genomic disease regions: predicting genes at pathogenic SNP associations and rare deletions
The emerging role of synaptic cell-adhesion pathways in the pathogenesis of autism spectrum disorders
Disturbed synaptic connectivity in schizophrenia: convergence of genetic risk factors during neurodevelopment
Rare de novo variants associated with autism implicate a large functional network of genes involved in formation and function of synapses
Dystrophinopathies: clarification and complication
TCF4, schizophrenia, and Pitt-Hopkins syndrome
Identifying autism loci and genes by tracing recent shared ancestry
Genetic modifiers of neurological disease
A recurrent 16p12.1 microdeletion supports a two-hit model for severe developmental delay
Exome sequencing of ion channel genes reveals complex profiles confounding personal risk assessment in epilepsy
Oligogenic heterozygosity in individuals with high-functioning autism spectrum disorders
The genetics of brain wiring: from molecule to mind
Schizophrenia, "just the facts" what we know in 2008. 2. Epidemiology and etiology
Mouse chromosome engineering for modeling human disease
A conditional knockout resource for the genome-wide study of mouse gene function
A neuroligin-3 mutation implicated in autism increases inhibitory synaptic transmission in mice
Autism-linked neuroligin-3 R451C mutation differentially alters hippocampal and cortical synaptic function
Enhanced polyubiquitination of Shank3 and NMDA receptor in a mouse model of autism
Abnormal behavior in a chromosome-engineered mouse model for human 15q11-13 duplication seen in autism
Impaired hippocampal-prefrontal synchrony in a genetic mouse model of schizophrenia
Dosage-dependent phenotypes in models of 16p11.2 lesions found in autism
22q11.2 microdeletions: linking DNA structural variation to brain dysfunction and schizophrenia
Increased gene dosage of ube3a results in autism traits and decreased glutamate synaptic transmission in mice
Mouse neurexin-1alpha deletion causes correlated electrophysiological and behavioral changes consistent with cognitive impairments
Haploinsufficiency of the autism-associated Shank3 gene leads to deficits in synaptic function, social interaction, and social communication
Shank3 mutant mice display autistic-like behaviours and striatal dysfunction
Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism-related deficits
A mutation in mouse Disc1 that models a schizophrenia risk allele leads to specific alterations in neuronal architecture and cognition
Disc1 point mutations in mice affect development of the cerebral cortex
Genetic and functional analyses identify DISC1 as a novel callosal agenesis candidate gene
Parvalbumin neurons and gamma rhythms enhance cortical circuit performance
Optogenetics in neural systems
Neocortical excitation/inhibition balance in information processing and social dysfunction
Correction of fragile × syndrome in mice
Reversing neurodevelopmental disorders in adults
Partial reversal of Rett Syndrome-like symptoms in MeCP2 mutant mice
Altered neocortical rhythmic activity states in Fmr1 KO mice are due to enhanced mGluR5 signaling and involve changes in excitatory circuitry
Activity-dependent validation of excitatory versus inhibitory synapses by neuroligin-1 versus neuroligin-2
Neuroligin-1 deletion results in impaired spatial memory and increased repetitive behavior
Increased dentate gyrus excitability in neuroligin-2-deficient mice in vivo
Neuroligin-2 deletion selectively decreases inhibitory synaptic transmission originating from fast-spiking but not from somatostatin-positive interneurons
Control of cortical GABA circuitry development by Nrg1 and ErbB4 signalling
Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia
The dopamine hypothesis of schizophrenia: version III--the final common pathway
Dopamine system dysregulation by the ventral subiculum as the common pathophysiological basis for schizophrenia psychosis, psychostimulant abuse, and stress
GABA neuron alterations, cortical circuit dysfunction and cognitive deficits in schizophrenia
Genetic dissection of neural circuits
Molecular genetics and imaging technologies for circuit-based neuroanatomy
A proposal for a coordinated effort for the determination of brainwide neuroanatomical connectivity in model organisms at a mesoscopic scale
Reverse engineering the mouse brain
Conditional gene expression and targeting in neuroscience research
Targeting Cre recombinase to specific neuron populations with bacterial artificial chromosome constructs
A resource of cre driver lines for genetic targeting of GABAergic neurons in cerebral cortex
DISC1 and PDE4B are interacting genetic factors in schizophrenia that regulate cAMP signaling
All roads to schizophrenia lead to dopamine supersensitivity and elevated dopamine D2(high) receptors
Parsing the genetics of behavior
Development and plasticity of cortical processing architectures
Magnetoencephalography in neuropsychiatry: ready for application?
Modulation of oscillatory neuronal synchronization by selective visual attention
Large-scale recording of neuronal ensembles
Neural synchrony and the development of cortical networks
Abnormal neural synchrony in schizophrenia
Dysfunctional long-range coordination of neural activity during Gestalt perception in schizophrenia
Abnormal neural oscillations and synchrony in schizophrenia
Dissociative symptoms and interregional EEG cross-correlations in paranoid schizophrenia
Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes
NMDA receptor hypofunction leads to generalized and persistent aberrant gamma oscillations independent of hyperlocomotion and the state of consciousness
Entrainment of neocortical neurons and gamma oscillations by the hippocampal theta rhythm
Driving fast-spiking cells induces gamma rhythm and controls sensory responses
Neuronal gamma-band synchronization as a fundamental process in cortical computation
NMDA receptor ablation on parvalbumin-positive interneurons impairs hippocampal synchrony, spatial representations, and working memory
Oscillations and hippocampal-prefrontal synchrony
Complementary roles of cholecystokinin- and parvalbumin-expressing GABAergic neurons in hippocampal network oscillations
Ivy cells: a population of nitric-oxide-producing, slow-spiking GABAergic neurons and their involvement in hippocampal network activity
Distinct firing patterns of identified basket and dendrite-targeting interneurons in the prefrontal cortex during hippocampal theta and local spindle oscillations
How inhibition shapes cortical activity
Amygdala circuitry mediating reversible and bidirectional control of anxiety
Genome engineering with zinc-finger nucleases
Knockout rats via embryo microinjection of zinc-finger nucleases
Targeted integration in rat and mouse embryos with zinc-finger nucleases
Genetic manipulations in the rat: progress and prospects
Adeno-associated viral vectors for mapping, monitoring, and manipulating neural circuits
Millisecond-timescale optical control of neural dynamics in the nonhuman primate brain
The dawning of primate optogenetics
Cognitive neuroscience-based approaches to measuring and improving treatment effects on cognition in schizophrenia: the CNTRICS initiative
Evidence for abnormal cortical functional connectivity during working memory in schizophrenia
Prefrontal-hippocampal coupling during memory processing is modulated by COMT val158met genotype
Exploring the brain network: a review on resting-state fMRI functional connectivity
Inter-regional brain communication and its disturbance in autism
Constitutive genetic deletion of the growth regulator Nogo-A induces schizophrenia-related endophenotypes
Association of mouse Dlg4 (PSD-95) gene deletion and human DLG4 gene variation with phenotypes relevant to autism spectrum disorders and Williams' syndrome
Mutation of semaphorin-6A disrupts limbic and cortical connectivity and models neurodevelopmental psychopathology
Slitrk5 deficiency impairs corticostriatal circuitry and leads to obsessive-compulsive-like behaviors in mice
World Psychiatric Association Pharmacopsychiatry Section statement on comparative effectiveness of antipsychotics in the treatment of schizophrenia
Autism spectrum disorders: early detection, intervention, education, and psychopharmacological management
Effects of antipsychotics on the behavioral deficits in human dominant-negative DISC1 transgenic mice with neonatal polyI:C treatment


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The Last Hurrah – We Can Hear the Fat Lady Singing
(Caravan Parks are Terrible for this Kind of Thing) - Mt Gambier to Home
We've been a bit slack with our blog, so grab a cuppa before you start reading our final tome.
Mt Gambier was a big hit. We saw many things that we have never seen, including climbing Mt Schank, a probably extinct volcano, and visiting Blue Lake, the water being the most incredible blue colour.
After seeing much of it already in pictures, the Great Ocean Road was better in real life and we all enjoyed visiting the great array of places. There was a good variety of scenery from out-of-the-way places to the tourist-swarmed Twelve Apostles. We spent a long while exploring Loch Ard Gorge, especially playing in the sand at the beach. Port Campbell was interesting – from the boy who screamed maniacally at sea gulls, so much so that people right at the other end of the beach were talking about him, to waking up one morning to watch a digger demolishing a large building from our beds.
When we reached Anglesea we decided to slow down and smell the roses a bit before Christmas hit. There was plenty to do just in the caravan park itself – from the pool, to mini golf, to the beach / river, a gym, a few games of bocce to go-kart bikes. We explored the surrounding areas, including the famous Bells Beach and the beautiful Lorne. The kids have become skate park fans and we are spending quite a bit of time hanging out with the local teenage boys, who don't seem to put our kids off from performing their tricks. Both the teenagers and our kids watch each other with sideways glances to see if they have impressed. They are learning that concrete is hard and can remove and bruise skin very well, but they have also learnt that risk-taking is a buzz when you can pull off a new stunt.
We stayed in a posh caravan park (sounds like an oxymoron) in Queenscliff, on the Bellarine Peninsula. The park had an indoor heated pool, kids club and a movie room, which was a big plus for our TV-starved kids. Standing at Point Lonsdale, one of the heads to Port Phillip Bay, watching the big cargo ships sail past the narrow gap was great fun. One beautiful day was spent exploring Queenscliff on hired bikes. We found some really interesting international markets – shipping containers full of crazy antique furniture and stuff (like an old ship's door and an old bike with an Asian-style trailer, old-fashioned ride-on shopping centre toys, weird Japanese poker machines, etc.).
From here on in it was all about catching up with family. We spent an enjoyable weekend with Jo's brother Kev and Janette and their daughter Kate, camping in their front yard in Melbourne. They showed us a few local sites but we pretty much just hung around and chewed the fat, which was a nice break from caravan park small talk.
In Ballarat we caught up with Jo's Mum and Dad, her brother Paul and Ros, with their kids Eloise, Alex and Olivia, and Kev, Janette and Kate joined us too. The place we stayed was amazing – it was an historic site, formerly a wealthy family's home, turned into an orphanage, then a school. It is now a very fancy resort with tastefully restored self-contained apartments (and a welcome step-up from what we've stayed in for the last 6 months). We felt very spoiled to stay in such a fancy place – thanks Mum and Dad! This was living it up and we tried everything on offer: paddle boats, pool, giant outdoor snakes & ladders and chess, beautiful gardens and lake, gym, table tennis, etc. Ballarat is a beautiful old town and we enjoyed exploring the area, but more so catching up with family. It's great being away from the hustle and bustle of commercialised Christmas and spending it with people you love.
Heading back to Melbourne, it was time to catch up with Andy's family. We stayed with Andy's brother Geoff, Katrina, and their kids Josh and Aaron who pampered us all. Andy's mum was there too so it was great to spend Christmas and New Year together. There was enough time to hang out lots and to explore places we hadn't been to before. Day trips to Phillip Island, Mornington Peninsula and a ride on the Puffing Billy in the Dandenongs were all lots of fun.
We are now back in the camper in Corowa, on the Murray River and are feeling close to home – a neighbouring Victorian asked about local NSW rules, a strange feeling after so long away. It's so stinking hot here that we had to go to the RSL for dinner tonight, just so we could sit in the air conditioning. We have been in the pool about 5 times today. Despite this, we are enjoying our last time together as a family before home. Every time we cross the Murray River the kids are confused about what state we are in. We have visited local towns like Rutherglen and Glenrowan, and have tasted local wines. Today the kids made giant chocolate freckles (organic, so it must be healthy), we went to Yarrawonga, where we thought we would linger longer (Slim Dusty fans will know what we're talking about – we listened to the song as we drove into town) and we watched the kids on a waterslide.
This is our final stop before returning home and back to reality, and we have mixed feelings – getting back to the comforts and friends will be nice, but to be honest, we could keep going for a good while yet. This lifestyle seems to suit us well and we're not looking forward to the business of daily life again. You'll have to all be nice to us so we don't get the blues. We have met many interesting people, caught up with good friends and family, seen lots of beautiful things, learned a great deal about our wonderful country and ourselves, covered over 25 000 kms (please don't count the carbon footprint), read well over 20 books each, put the camper trailer up and down exactly 60 times, not worked for 6 months (although as someone wisely said, 'It's not a holiday, it's an adventure' – there's plenty of work to do, just a different type), grown immeasurably closer as a family and experienced amazing things together – all with big thanks to God. Thanks for tuning in, we hope you enjoyed sharing our adventure with us. If you want to sit through a slide show of about 4 000 photos, let us know. This is our final blog, so with a tear in our eye and plenty of memories in the bank, we sign off.
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We had a great time working with the uber talented Stanley Chow http://www.stanleychowillustration.com on this charming 3D version of his popular Woody Allen tribute caricature. the figure was sculpted digitally then printed on the Objet Geometries Eden printer, hand molded, cast and painted. Available soon in a very limited quantity
Thank You!


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Since 2005, Verali has been creating affordable, on-trend, fashion footwear aimed at the Australian youth market craving the hottest looks, fast. Their evening shoes turn heads wherever they go and their daytime boots and sandals add a fresh urban vibe to any look. Add Verali to your shoe collection now!


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Hudson: Deadline for AV Chamber Sizzlin' Summer BBQ
August 8, 2011
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The AV Chamber Sizzlin' Summer Social & BBQ will be held Aug. 17 at the Hudson Elks Pavilion on Park Street, Hudson. Deadline to register: Aug. 8. Cost: $20/adults, $10/children 4-12, under 3 free. Includes Memphis ribs, BBQ dixie chicken, hamburgers, hot dogs, cornbread, BBQ beans, mac & cheese, salad & watermelon, as well as cash bar, music, children's activities, volleyball, horseshoes, and local business displays. Casual attire encouraged. Rain or shine. To register, call 1-978-568-0360 or e-mail email@example.com.


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Are you a visual person when it comes to decorating?
I am for sure.
I like to be able to see what something will look like before I spend the money to create it.
Here's a little trick I do that I wanted to pass along in hopes that it may help you too.
Many phones have collage apps. I use PicStitch on mine, but there are a lot.
If you don't want to do this on your phone, you can do it on your computer using a website like PicMonkey.
The example I will use for you today is our dining room cabinet.
There are many ways you can style the top of it.
Here is a picture of our hutch that I have saved on my phone.
{I didn't use this one, but a similar one}
Last night I was browsing through Pinterest and saw so many different cool vignettes.
So I saved the pictures to my phone and then using the PicStitch app, created these collages so I could see what these various vignettes might look like on top of our cabinet.
Mind you, these are not to scale, it's just for fun to be able to visualize different ways of styling.
What's your favorite?
And, I didn't limit myself to cabinet top styling in my Pinterest search.
I used photos from console tables as well as entry tables and fireplace mantles.
Hopefully you can use this handy tool also!


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Watch Violent Flash Flood Tear Through Hospital
Prepare to witness the fury of Mother Nature in all her rage.
Prepare to witness the fury of Mother Nature in all her rage.
Boy, oh, boy can this girl play baseball.
Getting a drink at a bar can be frustrating, but when you do get the bartender's attention, chances are it doesn't end like this.
A good umpire blends into the game as much as cleats in the batter's box. This umpire, though, wants to be remembered like a walkoff grand slam in the seventh game of the World Series.
The crane from 'The Karate Kid' is now officially the second coolest martial arts kick you've ever seen.
You might be a redneck if you help your daughter pull her tooth with a bow and arrow. That's what you might be saying after watching this video, in which a girl does indeed use a bow to pull out a tooth.
They say the customer is always right. This video would prove that may not be the case.
When we say everyone has World Cup fever, we mean EVERYONE.
With the possibility that a "supershark" is roaming around Australia, you'd think swimmers would be a wee bit more leery of taking a dip.
Some really relationships end amicably and some don't. It's safe to say this one didn't.
Most of us, when we find ourselves with a spot of time on our hands turn to our phones for company and Richard Dunn is no exception. But, what he did differently has ensured that at least for now, boredom and loneliness will be the LEAST of his problems!
There is simply no way this is for real. That's what you'll think after watching this commercial.


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"Every time my girlfriend and I go on a vacation, I ask for a picture of horse saying "Hello!" in the "Special Requests" section of the reservation form. Finally, a hotel delivers."
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Tags funny, horse, hotel, request, special
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VideoBash is your first and final stop for free funny videos, games and pictures guaranteed to brighten up your day. The funniest jokes and the most unbelievable pranks caught on tape have been collected in one spot for your viewing pleasure. This is entertainment at its best and no one does it better than VideoBash. These funny clips crackle with humor and they will definitely have you laughing till your sides hurt. Quality is our number one priority and the free funny vids here are the best of the best. There are no mediocre videos here. All the videos, jokes, pranks on VideoBash are the cream of the crop and you'll be hooked from the get go. The best part is you don't have to keep all this good stuff to yourself, you can share all the free entertainment videos with your friends.


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Hi Ayesha! Have a look on the list of scholarships on medical sciences in Singapore. You can apply to those colleges through Uniguru's Managed Application Services. All the Best!
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I am a Dental Graduate, passed BDS from Dhaka Dental College under Dhaka University. I am interested to do MDS in NUS. I aspire to have support from any person especially of the students and teachers who could help me obtaining a scholarship so that I could study my desired program in NSU. My email: email@example.com.
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5 Useful iTune Tips & Tricks for iPhone/iPad Beginners
Owning a new iPhone or an iPad is lot of fun. However, many of the new users are also equally frustrated with the functionalities in iTunes.
If you've been asking around on how to change your iPhone ringtone and exporting video to your iPad, you've found the right article. Here we will be covering the 5 most useful tips and quick tricks in using iTunes specially written for the beginners.
1. How to Change Your iPhone Ringtone
If you're one the voices out there who complaining to your colleagues/classmates on why using the same ringtone as yours or you've been terribly sick of the xylophone sound, afraid not. Read further.
- iPhone and iPad only support ringtones format in m4r. So, google the iPhone ringtones and download the ringtone file in m4r. Mobile9.com has many ringtones available for free.
- Next, you need to sync the file to your iPhone/iPad. Connect your device and launch the iTunes.
- At the iTunes, click on the Ringtones tab on the right. Drag and drop your ringtone file into the list on left.
- Then, click on your device (1), and go to the Ringtones tab on top (2). You should able to see the ringtone file which you exported earlier on (3). Click "Apply" button (4) will copy the ringtone to your iPhone.
- At your iPhone, go to Setting > Sounds > Ringtones > Select your custom ringtone
Test your ringtone in front of your friends and you can start to brag on how you did this in less than 5 minutes.
2. How to Customize iPhone Ringtone Using Your Favourite Songs
Now that you already know how to change the iPhone ringtone, let's bring it up one notch – to customize your iPhone ringtone using your favorite songs. We won't question you where did you get your mp3s but we will teach you how to use your favorite song as your ringtone. Did we just heard some glee girls screaming in joy?
- As you may or may not know, iPhone / iPad ringtone only supports format in m4r. So the first step is to convert the sound files into m4a then rename it to m4r. Drop your favorite song into iTunes under Music.
- In the playlist, right click on the music file and select "Get Info"
- A pop-up window will appear and then go to the Option tab. Input the "Start time" and also the "End time". If you love the chorus and you want to make it as your iPhone ringtone, you have to key in the specific start time and end time. Please note that iPhone ringtone has to be 30 second or less. So if you plan to have the whole Lady Gaga's Bad Romance song as your iPhone ringtone, just forget about it.
- Next you need to convert the file. Right click at the file and select "Create AAC version".
OK – Before you start panicking because you couldn't find that option, do this .. Go to iTunes menu bar > Edit >Preferences > General> Import Settings. A small popup window will appear, at the "Import Using" dropdown menu, select AAC Encoder. Below it at the Setting dropdown menu select High Quality. This will enable the option of "Create AAC version" when you right click at the file.
- You are almost done. At your list, there should be two files with identical file name. The one that below is your new AAC version in m4a format. Now you need to rename the format to m4r. Right click at the file again and select "Show in Window Explorer". This will save you time of locating the new file.
- Next, change your file name. That's it. Now you have your iPhone ringtone in m4r format and ready to sync to your iPhone. Please refer to first part on "How to change your iPhone ringtone".
3. How to import videos into your iPhone / iPad
Before you bought the iPhone or iPad, we bet you must be thinking about the memory size. True enough, many opt for bigger size like 32GB and 64GB. But after owning the iPhone and iPad for about a year or so, it seems like you'll never used up the memory space! Then must be missing.. yes.. the videos.
Videos usually will take up a huge chunk of your memory space. So if you would like to make your money worthwhile and wanted to use up all your available memory, here is the easy manual on importing videos into your iPhone / iPad.
- In the iTunes, go to File > Add File to Library.
Make sure your video selection is in either H.264 or MPEG-4 format. You can convert your video file with these free iPad video converters.
- Next, click on your device (1), go to the Movies tab on top (2), click to enable the Sync Movie (3). Your movie will imported earlier will appear at the Movies listing (4).
- Then all you have to do is click the Sync button. Next, get your popcorn & coke ready, you are all set for the movie!
4. How to sync your photos to your iPhone/iPad
Now you just came back from a holiday and you hundred or maybe thousands of vacation photos. So the question is how do you import all these photos into your iPhone / iPad to make your colleague or friends jealous of the great time you had?
- In iTunes, click on your device (1), and go to the Photos tab on top (2). You have to enable the Sync Photos (3) and select the folder where contains your photos (4).
- Once you click on the Sync button, your selected photos will be copied into your device. Now you can start to show-off.
5. How to download and read eBook in iPhone / iPad
If you want to download and read an eBook through 3rd party websites instead of using iBook, here's a quick start.
- In iTunes, click on your device (1), and go to the Books tab on top (2).
- In the iTunes, go to File > Add File to Library.
- You have to enable the Sync Books and choose either "All books" or "Selected books".
- Click the Sync button to start reading downloaded ebooks in your iPhone or iPad.
We hope you enjoyed this article and we welcome for any comments/questions that you have.
While you're at it:
- 25 iPhone & iPad Application Builders for Non-Programmer
- 90 Absolutely Gorgeous iPhone Wallpapers
- 15 Lighter and Faster iPhone Managers (iTune Alternatives)
- 5 iPhone Funny Apps You Might Never See Before
- A Good iPhone Resources – iPhone Toolbox
About Author
Alexander believes in outer space aliens and has passion in new technology. He is easily fascinated with new inventions which bring him contributing in this platform. Alexander enjoys sharing his knowledge as he knew; this is the only way to keep human form competitive with the fellow extra-terrestrials.
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One Response to 5 Useful iTune Tips & Tricks for iPhone/iPad Beginners
Howdy would you mind stating which blog platform you're working with?
I'm going to start my own blog soon but I'm having a difficult time
selecting between BlogEngine/Wordpress/B2evolution and Drupal.
The reason I ask is because your design and style seems different
then most blogs and I'm looking for something unique.
P.S Apologiess foor getting off-topic but I had tto
my site: Experience Perutravelerblog.com (english)
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Carrying on their dominance from the first session of play, the Indian bowlers finished off the New Zealand innings for 350 when Harbhajan Singh struck to remove Chris Martin for 3 in the 118th over. Bhajji and Zaheer Khan had been rewarded for the bowling efforts with 4 wickets a piece. Meanwhile, the Kiwis had amassed a healthy total, but would it be enough to intimidate India's long and powerful batting line-up?
In response, India got off to a positive start with Gambhir edging a four over slip in the second over itself. Sehwag was initially a little more circumspect, especially while playing Martin. But both batsmen helped themselves to 10 runs off Southee in the 8th over, including a Sehwag four which was crashed through the covers. In the 11th over, Sehwag got stuck into Martin, hitting him for two consecutive boundaries, taking India to 39/0.
Once the openers had worked off the sheen of the ball and had caused it to swing less, they were more comfortable picking runs. They reached the 50-run mark in the 15th over when Gambhir drove Southee through the covers for a boundary. In the next over, Sehwag went for a big shot but didn't connect properly. However, it wobbled to mid-on and fell well short of the fielder. By the end of the 18th over, the openers had safely carried India to Tea with the score at 62/0.


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Insight out now: Tell us what you think and win
Published: Wednesday 4th March 2015
Insight issue 13 is out now. Pick up your copy to read about our current research projects, staff and student success stories, and ACU news and events.
We are always looking to improve Insight magazine, so you get the stories, news and events that you most want to read about.
We are conducting a short online survey to find out what we do well, and what we could do better.
It takes just three minutes, and you'll go into the draw to win a $500 Load&Go Visa Gift Card.
Take the survey here.
Survey closes 26 March 2015.


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Master of Science in drug sciences
The University of Basel MSc in Toxicology and the MSc in Pharmaceutical Sciences are being replaced by the new MSc in Drug Sciences. This new Master study programme provides theoretical and practical training in the discovery, development, efficacy and safety of substances with a main focus on drugs/medicines. It is focused on a future career in industrial or academic research, product development or regulatory affairs. The appropriate choice of elective subjects provides the theoretical basis for later certification as professional toxicologist.
The next MSc in Drug Sciences programme starts in September 2017
- The programme includes two semesters of theoretical and practical courses on fundamentals/general skills, drug discovery and development, pharmacology and toxicology.
- The 3rd and 4th semesters are dedicated to the master thesis.
- All courses are held in English.
- To be admitted, you must have completed a Bachelor in Pharmaceutical Sciences or equivalent discipline.
Further information
Applications for 2017 (autumn semester) can be submitted online February - April 2017.
For details on the admissions criteria and the proposed course programme please visit this website or contact the Student Advice Center (Tel. +41 (0)61 267 30 23) or the Study Coordination of the Department of Pharmaceutical Sciences (Tel. +41 (0)61 267 15 53).


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The coalition of Windward has long-dated been reasoned one of the utmost handy locations and a splendid lay to be a resident of in Alpharetta. The federation of Windward itself surrounds the beautiful, 195 area unit Lake Windward and residents are wanted to use the lagoon which is hearty near a docking facility. Among the some different livelihood enjoyed by residents of Windward homes are the nationwide recognized, Golf Club of Georgia, numerous parks and bubble fields, numerous tennis courts and an Olympic swimming tarn transistorised near an extremely large slide. Comprised of most 100 individualistic neighborhoods, Windward, is one of the greatest communities anyplace in Atlanta.
A digit of reasons form Windward specified a excessive slot to singing. Among the most high-status for residents is the refuge. Well best-known by the municipality of Alpharetta, the Windward locality keep under surveillance is among the top-quality anywhere. Another extremely main rationale that that Windward has been such as a super fix to bid warren is the strange municipal instruction net that the brood be.
The simple college is Creek View and is among the top-quality in the communicate of Georgia. Webb Bridge Middle School and Alpharetta High School are commonly rated. The price tag of homes in Windward scope from the mid to full $200,000's up to and past $5,000,000 for additional estates near optimum lake views. Another drive that Windward makes a very good lodge to dwell is the location. Windward and North Point Parkways have some go trunk employment centers and some centers are exactly around the alcove from Windward.Post ads:
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Communities in Windward lie of pleasure gated neighborhoods on the Golf Club of Georgia and Lake Windward as well as numerous minor enclaves that produce up the bulk of the neighborhoods. With an highly progressive and safety headed homeowners association, Windward residents can e'er discovery thing to do and the homeowners fellowship is very alert in the region of condition in Windward. Each locality primarily has a chief who looks out for the neighborhood and if any singular leisure is noticed, the entire homeowners attachment is notified. Because of this, are ever more than fashionable than some other areas of Atlanta when you relate activity statistics.
Many of the neighborhoods are inwardly close coolness of the watery and tennis facilities and the community is terribly active. Driving through Windward you are expected to see family jogging, walk-to or bicycling nigh on the sea and roughly enjoying the outside and pretty view. The Windward Lake Club is the intuition of the outdoor activity and consists of an 18 square measure facility next to swim, tennis, ball and tarn sword of state. Outdoor activity in Windward is at the suspicion of this vibrant village for adults and offspring alike. If you enjoy an outdoor lifestyle, buying a warren in Windward mightiness be a great verdict for you.Post ads:
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Mari Mari Cultural Village Half Day Tour (Product Code: 3937-177676)
Summary of The Day: This fantastic half day tour from Kota Kinabalu will lead you to through the traditions and cultures of the different tribes of Sabah. This enriching experience begins as we depart your hotel and head for a 25 minute drive to the Mari Mari Cultural Village. Enjoy the rich spectrum of greenery and gorgeous landscapes.
Upon arrival we'll teleport back in time to ancient Borneo and discover a magical display of unique architecture, simulated lives, and ritualistic ceremonies. You will be ushered into the warmth of different homes of the ethnicities of Sabah to learn about each tribe and experience their amazing culture.
You'll also be led tot eh demonstration huts where you can see daily routines o traditional Sabahan life come alive. See a blowpipe-making demonstration, bamboo fire-starting demonstration, tattoo-make demonstration, and an din-depth look at the mystical symbolism behind them.
Learn how tree hark is shaped into vests, experience the traditional dances, and jump for a prize on the built-in Lansaran, a traditional trampoline-like floor. Taste Sabahan delicacies from each ethnic group such as the Montoku (rice wine) and enjoy the cultural performances by each tribe alongside a traditional meal. You're bound to find this an enriching and entertaining experience
|* A Minimum of 2 travelers is required for this tour to depart.
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CEE Financial Literacy and Economic Education Conference
07 Oct, 2015
October 7, 2015 12:00 am-11:59 pm
St. Petersburg, FL
St. Petersburg, FL
NGPF will be running an exhibit booth at the Council for Economic Education's 54th annual national conference,which will bring together over 500 educators, including 250 K-12 educators (many of whom attended on scholarships). View the CEE event page here.
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Oil jumps 8 percent on prospects for big OPEC output cut
Oil prices jumped more than eight per cent today to a five-week high as some of the world's largest oil producers gathered in Vienna to try to agree a production cut that could be bigger than expected.
Brent crude futures for delivery in January were up $3.83, or 8.3 percent, at $50.21 a barrel, recovering from a drop of nearly 4 percent on Tuesday and on course for their biggest one-day move in nine months. Brent crude for delivery in February was up $3.76 at $51.08 a barrel.
U.S. West Texas Intermediate (WTI) crude futures were $3.63 higher at $48.86 a barrel, a one-week high.
The Organization of the Petroleum Exporting Countries is discussing terms of a potential deal to cut production in an effort to prop up prices that have fallen by more than half since 2014 due to oversupply.
A source told Reuters that delegates were now discussing a bigger than expected cut in production of 1.4 million barrels per day (bpd).
A preliminary agreement struck in Algiers in September set an output cap at around 32.5-33 million barrels per day compared with the current 33.64 million bpd.
"It does rather look as though OPEC is going to come to an agreement," said Colin Smith, director of oil and gas research at Panmure Gordon in London.
Heading into the meeting, Saudi Arabia's energy minister, Khalid al-Falih, said the market's fundamentals were moving in the right direction, but he believed the group was "getting close to a deal".
"The extent of the (price) move shows no one wants to miss the boat. There must be a general consensus that there will be a cut, whether it's going to be bullish, I don't know, but it's the domino effect," PVM Oil Associates analyst Tamas Varga said.
An Iraqi delegate said that some form of agreement would be reached and Iran's oil minister also said he was optimistic.
Traders said markets were jittery and prices could swing sharply in either direction depending on developments in Vienna.
Oil fell by nearly 4 percent on Tuesday on reports of disputes between Saudi Arabia, Iran and Iraq over details of the planned production cut.
Iran and Iraq have been resisting pressure from Saudi Arabia to curtail production, making it harder for the group to reach an agreement on output cuts.
Analysts at Goldman Sachs, Barclays, and ANZ said oil prices would quickly fall to the low $40s a barrel if OPEC fails to strike a deal to cut output.
See our Comments Policy Comments are submitted under the express understanding and condition that the editor may, and is authorised to, disclose any/all of the above personal information to any person or entity requesting the information for the purposes of legal action on grounds that such person or entity is aggrieved by any comment so submitted. Please allow some time for your comment to be moderated.


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iCare ic100
The ic100 tonometer is now even simpler to use. The new automatic sequence mode, new navigation interface and positioning assistant enhance usability and make IOP measurement easier for operator and patient.
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Keeler's primary goal in its redesign was to completely surpass it with an entirely new model that will provide even greater accuracy, patient comfort and speed of use.
In addition the development team singled out its weight and size as being in need of a slimming programme. Users are looking for as small a 'footprint' as possible and our distributors for even lower shipping charges.
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The Keeler Applanation Tonometer (KAT) is a perfect example of Keeler's skills; we have applied 21st Century design techniques to a 20th Century device to deliver a premium quality instrument.
The Goldmann applanation principle is widely acclaimed as the most common and direct method of assessing IOP.
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Compact and light-weight, well balanced and easy to handle by single
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Argh! is an esoteric programming language in the spirit of Befunge, Brainfuck, and friends. It is a nice and simple language with two dimensional code-flow, a combined code/data array, an infinite stack, regular characters for all instructions, no strange braces or symbols, no unnecessary arithmetic operators (add and sub are all you need), and countless other features it doesn't have. The distribution includes interpreters for Argh! and Aargh! (an extended Argh! that is most likely Turing complete), the official specification, editing modes for emacs and vim, and lots of examples.
|Software Development Interpreters Games/Entertainment
|Operating Systems
|C Emacs Lisp
A Fluent OpenStack client API for Java.
A TWiki appliance that is easy to use and lightweight.


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Kendra Wilkinson and Hank Baskett are 'totally healed' after cheating scandal
Kendra Wilkinson and Hank Baskett have "totally healed" after they were slapped with infidelity claims two years ago.
The 30-year-old reality TV star has admitted she and her husband went through "hell" when rumours surfaced in 2014 claiming the former American footballer had cheated on her with a transgender model, but the couple - who wed in 2009 - have finally managed to get their rocky marriage on track.
And, although the cheating scandal knocked the blonde beauty's confidence, Kendra no longer feels the need to steal her husband's phone and check up on him.
Speaking to Us Magazine, she said: "I now realise [checking Hank's phone] was a waste of time. Even before the drama, I used to be so jealous. I don't want to live my life in fear."
Meanwhile, the pair - who have tried to put on a united front since the crippling allegations emerged - are willing to tell their young children Hank IV, six, and Alijah, 22 months, about the alleged affair when they're a little older.
Kendra said recently: "We're trying to obviously beat all this to the punch and just teach our kids who we are and show them love and show them happy parents and be as open as we can."


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|Message view
|« Date » · « Thread »
|« Date » · « Thread »
|"Hiller, Dean" <Dean.Hil...@nrel.gov>
|Re: Insert v/s Update performance
|Tue, 26 Mar 2013 23:18:15 GMT
Most likely compaction kicks in as updates cause duplicated rows in STCS and compaction causes load that may not have been there before(check your logs). Also, you can increase the number of nodes in your cluster as well to better handle the load. Later, Dean From: Jay Svc <firstname.lastname@example.com<mailto:email@example.com>> Reply-To: "firstname.lastname@example.com<mailto:firstname.lastname@example.com>" <firstname.lastname@example.com<mailto:firstname.lastname@example.com>> Date: Tuesday, March 26, 2013 5:05 PM To: "firstname.lastname@example.com<mailto:firstname.lastname@example.com>" <email@example.com<mailto:email@example.com>> Subject: Insert v/s Update performance Hi Team, I have this 3 node cluster. I am writing data to these node at the rate of 2,000 records/second. What I observed that if I do inserts. (Means records for those keys does not exist, my column family has 0 records to start with) then I have better write performacne, low SSTable count, low pending compaction and write latency is acceptable and CPU utilization on each node between 35% to 85%. When I ran same test but for update this time (means records already exists in Column family with same key), I observed that my SSTable count gone high 3 times. Pending compactions gone high more than 2 times and write latency has gone high too and CPU utilization was almost 92% to 100%. What is a reason of deteriorating Update performance v/s Insert performance. Since this is critical you help is highly appriciated. P.S. I also observed that high number of pending Mutation Stage on my nodetool tpstats. Thanks, Jay
|View raw message


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Deleted Tweets From Judy Chu, D-Calif.
Judy Chu's accounts: RepJudyChu, JudyChuCampaign
Tracking Since: November 17, 2011
We need a full and independent investigation - including any tapes Trump claims to have - to discover if Trump atte… https://t.co/QtaHbtJOMT
50 yrs ago, MLK gave a speech linking civil rights to the Vietnam war. This morning, @repjohnlewis told us it was f… https://t.co/lHavYsIPYJ
50 yrs ago, MLK gave a speech linking civil rights to the Vietnam war. This morning, @repjohnlewis told us it was f… https://t.co/fI6aTFdSXI
ICE's arrest of a mom trying to reapply for DACA is a reminder that Trump's words matter less than his actions. https://t.co/KGWzNcjotX
Just cast a proud vote for @NancyPelosi for Speake, because the people's House should be ethically accountable and open to free debate
Looking forward to @Elaine_Quijano moderating tonight's #VPDebate!
Thank you @HillaryClinton for featuring women leaders like #PatsyMink who paved the way for all of us. #AAPI #ImWithHer
•Select Panel to Attack Women not only hinders access to repro health care but will also slow research on #ZikaVirus
Washington caucuses started at 9:30! Let's get out to support @HillaryClinton and help her get to the WH! #Imwithher https://t.co/2Sx9Rl9ihR
Today is the last day to enroll 4 health coverage w #CoveredCA! Enroll @ the Bowl in #Pasadena til midnight tonight! https://t.co/fXx2TFluVE
RT @AAAJ_LA: Take #immigrationaction and get help on 1/24! RSVP: http://t.co/8pPLqtdoEe @RepJudyChu @Carecen_LA @CHIRLA @AAAJ_LA http://t.co/hCdYjRRQra
Saying farewell to @Resp ectCreators co-chair Rep. Howard Coble and welcoming new co-chair @repdougcollins http://t.co/055v8Nkgkj
Extending thoughts of comfort and solidarity to our neighbors in #Canada after yesterday's horrible attack in Ottawa.
RT @JosephLoegering: @CAPAC @RepBarbaraLee Antisemitic USA that denies that their lying and violence against us is Antisemitism http://t.co/BnUhrOYYG5
RT @jacqklimas: .@RepJudyChu with pro-life protesters outside House hearing on using federal funds for abortions. http://t.co/72ee9DDzRV
Had so much fun distributing 160 turkeys for local needy residents. Great to help spread the warmth of #Thanksgiving! http://t.co/yebHsruM
Today is Election Day! Polls are open until 8PM here in California. Here's where you can find more information: http://t.co/0gxQsW7T
Romney: a politician with no foreign policy experience pretending to have the answers for peace on earth: http://t.co/cJO9Nr56
RT to fight #votersuppression! Use app @ http://t.co/OxGCvDV6 & defend your right to vote! #voterid = #epicfail http://t.co/rC8SFQ0e


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You work for weeks, months, or years to build a business that is killing it. Then you get a huge new customer. You feel like you've been put on the map. But then the reality sets in. Maybe you won the business because you're innovative, less expensive, faster, etc. But now you start getting completely destroyed by the overhead of making those sweet, sweet dollars from that new customer. Wouldn't it have been great to have known about a few things to ask about? My response includes a few tips on how to work with them, that just might save you some serious margin!. Check it out at http://www.inc.com/charles-edge/how-to-work-with-big-companies-without-getting-caught-in-red-tape.html.
krypted November 18th, 2016
Posted In: Articles and Books
I've been thinking a lot about content strategy and the why and when of how articles are posted. I'll keep writing whatever I want, whenever, often times based on what I happen to be working on at that moment. In other words, I actually have no content strategy for krypted, and I don't feel the need to implement one. But at least I explored it, thought about it, and got a few notes down for friends who do want one, or are thinking about it. That article went up on Huffington Post yesterday at http://www.huffingtonpost.com/charles-edge/the-importance-of-having-_2_b_9563304.html. A snippet of the article:
Search engine optimization (SEO) involves strategies and techniques that, when used properly, increases the amount of people that come to your website via search engines, like Google, Yahoo, and Microsoft Bing. Getting enough content, and more importantly the right content, on your site is your content strategy. As a business owner you always need to try new, interesting, and interactive ways to promote your company. And one of the best things you can do is to create a good content strategy for your organization's website.
A business owner, or marketing employee in a small business is likely to wear a lot of hats. In large companies, there are often teams of people creating, editing, releasing, and strategizing what content to create on a website. How does a smaller organization compete for a similar audience? A good content strategy at a small business can help keep you focused and provide a unique experience to your readers. You can get material out faster than if articles have to pass through multiple layers of approval before going public. Timely pieces can mean getting to audiences before the competition can catch up. And having a personable and authentic voice can keep readers coming back to your site.
Not only does a good content strategy allow you to take your business to the next level, but it also offers a wide range of other benefits, as you can see below!
The one point I didn't think to make was once you have a good content strategy in place, it becomes much easier to outsource the creation of content. You can bring in professional content creators (writers). And then you can hopefully just edit their work. I've never had the greatest of luck with that, so I just keep writing stuffs. But I know a lot of people who have, and a lot of people that do this work, and do it really… really… well!
krypted March 30th, 2016
Posted In: Articles and Books, Interviewing, Mass Deployment, Product Management, public speaking, Small Business
Tags: blogging, content strategy, SEO, Writing
krypted May 19th, 2014
Posted In: Articles and Books, Consulting
Tags: technical documentation, Writing
My next book, coauthored with Mr. TJ Houston, is now available. The rough draft was mostly complete the week of MacSysAdmin in Sweden. I announced the book at the conference and was busy at work after to get as much as possible complete. And after many an hour and month spent editing this book (props to TJ for doing a lot of the editing), it's finally available on Packt Publishing. To quote the site, this is what the book is on:
The Apple Configurator is an incredible piece of software which grants full control in mobile device management, but on a larger scale. The popularity of people taking their own devices to work has grown tremendously. However, valued professional and personal information is at risk, through loss, theft, or hacking. Instant Apple iOS Configuration Utility How-to is a hands-on guide that eliminates any worries that are associated with the deployment and security of iOS devices. This book provides practical, quick win solutions to combat these issues, with clear, concise, and informative examples providing solutions to secure, remote wipe, and encrypt devices. The book will further explore how to personalize iOS devices for configuration and deployment.
With the Instant Apple iOS Configurator Utility Book How-to, learn to build profiles with customised control settings, with examples on how to capture device information and use console logs for added protection. You will become skilled at tracking and installing provisional profiles for greater security. We will also explore developing workflows for successful deployment, installing software and applications whilst managing files on iOS devices, and how to deploy enrolment profiles for mobile device management solutions en masse. If you are looking for a complete guide that provides simple solutions to complex problems, look no further.
To buy, visit this link: http://www.packtpub.com/apple-ios-configuration-utility/book
Note: I think the title is a little off, that's in progress for being fixed.
krypted February 20th, 2013
Posted In: iPhone, Mac OS X, Mac OS X Server
Tags: Apple, Apple Configurator, apple ios configuration utility, Apple TV, Book, ios, os x, Writing
In December of 2004, in response to a request from my publisher at the time, I started this site in its current form. I kept the domain from my personal tinkeration site, which was a glorified file service, some static html pages for me to remember things (I can be a bit forgetful at times) and some .htaccess files to keep parts of the site private. I'd been using the domain for awhile, but started tinkering around with a few blogging engines and eventually settled on the one I'm using now.
The total number of posts now sits a little over 2020, with a few being drafts on upcoming products currently in beta and a few written by other authors. This puts me at a little over 2,000 posts that I've written personally. Some have been very short and just little tidbits for me to remember. But over the years there have been many that were around the depth and size of chapters of books as well (in fact some have been chapters I cut out of books and others have ended up becoming rough parts of chapters for books later). I started out writing about whatever it was I was thinking about. During the fall that meant a little football here and there (the University of Georgia Bulldogs seem to always disappoint me). During the spring it occasionally turned to surfing or cooking. And sometimes I even meandered into business stuff. But overall, it's mostly been technical writing.
There have been sprinklings of humor (which I should clearly stay away from), pictures (again, something I should stay away from), I even dabbled with trying to branch into making it a bit more of a social type of thing. It almost feels like 2,000 posts flew by. During that span I have remained at 318 (where i've written around 500 posts on the company site), cobbled together 8 or so books for a few different publishers, written articles for magazines and other sites and authored tons of technical documentation for various vendors in the IT industry (most of which you wouldn't know I wrote unless a screenshot accidentally has a SSID or something in the sidebar, etc). There has been a lot of writing.
The site is steady at around 150,000 uniques per month, with a solid distribution of visitors from all over the world, comments from all over the world and the site is starting to get article submissions from around the United States. Hopefully the submissions will continue to increase, as nothing makes me happier than editing the content of others and seeing more than what I work with on a daily basis, which invariably ends up teaching me more – and connecting others to the community.
A lot of people ask me how I can write so much. The answer is pretty simple: I am surrounded by amazing people who are life long learners, whether it's in the communities (or circles) I am in, at home or in a very concentrated sense, at the office. Much of writing is figuring out how to do things. Occasionally you find a better way later or someone comments on an article and tells me a better/more efficient way to do something. In fact, hopefully you are always looking for a way to make things better. Writing is no different than making a script, the more you do it the more efficient you get at it. And when friends (or strangers) comment on the site for corrections, hopefully the more information becomes available to the community. With repetition, the pace of writing quickens. But the number one reason I write so much is because it obviously makes me happy.
As I've mentioned, I'd like to make krypted.com into more of an outlet for others as well. Given the amount of traffic that the site gets, I feel it's not a bad outlet for others. I'd also like to re-skin the site and move it to a better host at some point in the future. I can say that I'd like to make the site more charitable (which I honestly would like), to make it more "social"/community (I have mixed feelings on that, but whatever) or to make it more useful for non-technical tasks. But over the years, I've learned that the site is what it is: technical content. No one wants to read me yammer on and on about football, my various travels, the great food I eat (mostly because I tend to eat at Subway more than I should, which means notsomuch on the great food thing) or even news about this site (although you're reading some now, so maybe…). People want to see the titles in a news feed or a Google search and decide if they want to read an article. That's it. So that's what I'll keep doing, perhaps making it more of a 'we' than an 'I' moving forward!
So 2,000 posts. Hopefully the next 2,000 will be better. Thanks for reading and visiting and keeping me goin'!
krypted July 6th, 2012
Posted In: Articles and Books, personal, sites
Tags: 10.8, 10.9, articles, Charles Edge, krypted.com, Lion, Mac OS X, mountain lion, os x, technical writing, Writing
Strunk & White's Elements of Style is one of the best works explaining the rules of writing in the English language that has ever existed (and I'm pretty sure that sentence broke at least five of those rules). I've given this book to many a budding writer over the years. I've also recently noticed that it's now all over the Internet, for free. For example, Bartleby has posted the 1918 edition of Elements of Style here.
If you haven't read Elements of Style then I strongly recommend it. It's short, concise and explains why that apostrophe goes in that one spot as opposed to the other. If you want to be a writer, this is one of your first stops on your journey.
krypted January 11th, 2012
Posted In: Articles and Books
Tags: Bartleby, elements of style, Internet, tech writing 101, technical writing, Writing, xkcd
I write a lot. There are the meanderings that appear on this site, the writing on the 318 TechJournal, more structured prose that goes into books (sometimes regrettably only slightly more structured), writing for clients, freelance writing, writing for other websites and even a bit of ghost writing here and there. Sometimes the writing is short, sometimes long, but there is a pretty consistent amount of it. The reason is because I enjoy it.
Most of my writing is technical in nature. And like many who maybe learn a thing or two on my site I end up sharing tips or tricks from places that I no longer remember where they came from. Others do the same thing, whether on web sites or in books or in a different fashion, such as in classes, on mailing lists or in forums. All vehicles are equally as helpful to those that need it. For the most part, my information comes from toiling away in my lab reproducing what knowledge I glean from other sites, from books and from man pages. Over the years afp548.com, xsanity.com, Apple kbase articles, forums, mailing lists and other places have helped me in ways that I cannot even begin to describe. As have books from O'Reilly, Peachpit Press, Apress and other publishers.
The things that I have learned how to do are almost all from things that others have written. This can be in the form of a book, a web site or even a man page. The code itself that comprises the technical topics is even written by someone else. This is true for any of us not writing new stuff in low level languages. A lot goes on inside of our systems. And wrapping your head around it all is a cumulative understanding, often not one gained in a single source.
I consistently do not name the sources where I learned how to do some of this stuff. This is not intentional; in many cases, I simply do not remember where I figured out how to do something 6 months or even 5 years ago. These omissions though do not mean that I do not know that I stand on the shoulders of a long line of giants. I say that without making any claim that I am one of those giants. Some day I hope to do something worthy, but I make no illusions that I have done anything to date worth more than passing mention, if that…
So a big thanks to all those who I have learned a thing or two (or 50) from. Your contributions are a debt I hope to some day repay to the communities you tirelessly helped to build. I only hope that we can do you the justice you deserve!
krypted February 16th, 2010
Posted In: Articles and Books, personal, sites
Tags: Writing
If you're making a bulleted list and you end an item with a period then all items need to end with a period. Whether it's a presentation or a paper. Consistency folks… Just so I don't seem like I'm trying to be the smart one, my wife pointed it out awhile back in one of my presentations. Now it's a pet peeve…
krypted October 10th, 2007
Posted In: Articles and Books
Tags: Writing