All posts by admin

How to merge local and remote data in the browser

In a first step reconfigure your browser

Safari
Enable the develop menu using the preferences panel, under Advanced -> “Show develop menu in menu bar”.
Then from the safari “Develop” menu, select “Disable local file restrictions”.
Chrome
Close all running Chrome instances first. Then start the Chrome executable with a command line flag:
chrome –allow-file-access-from-files
On Mac OSX terminal you can do this with
open /Applications/Google\ Chrome.app –args –allow-file-access-from-files
Firefox
In the address bar, type about:config Find the security.fileuri.strict_origin_policy parameter and set it to false

 

Here is the script, loosedly based on https://www.html5rocks.com/en/tutorials/file/dndfiles and https://stackoverflow.com/questions/7346563/loading-local-json-file that loads json1 from the server, json2 from the local harddrive and merges both by id

<html>
<input type="file" id="files" name="files[]" />
<output id="list"></output>
</html>

<script src="jquery-1.11.1.min.js"></script>

<script>
// read local comma delimited file with id and name
function readTextFile(file) {
  var rawFile = new XMLHttpRequest();
  rawFile.open("GET", file, false);
  rawFile.onreadystatechange = function () {
    if(rawFile.readyState === 4) {
      if(rawFile.status === 200 || rawFile.status == 0) {
        rider = rawFile.responseText.split("\n");
        return rider;
      }
    }
  }
  rawFile.send(null);
}

// read server data in json format
var url = 'merge.json';
var json2;
$.ajax ({
    url: url,
    async: false,
    dataType: "json",
    cache: false,
    success: function(data) {
        json2 = data;
    },
    error: function(err) {
        console.log(JSON.stringify(err))
    }
});

// function to join by id
function joinObjects() {
  var idMap = {};
  for(var i = 0; i < arguments.length; i++) { 
    for(var j = 0; j < arguments[i].length; j++) {
       var currentID = arguments[i][j]['id'];
       if(!idMap[currentID]) {
          idMap[currentID] = {};
        }
      for(key in arguments[i][j]) {
          idMap[currentID][key] = arguments[i][j][key];
      }
    }
  }
  var newArray = [];
  for(property in idMap) {
    newArray.push(idMap[property]);
  }
  return newArray;
}

// selection of local fiel starts it all
function handleFileSelect(evt) {
  var files = evt.target.files; // FileList object
  // files is a FileList of File objects. List some properties.
  var output = [];
  for (var i = 0, f; f = files[i]; i++) {

  readTextFile( "file:///Users/wjst/Desktop/"+escape(f.name) );
  for(var i = 0; i < rider.length; i++) {
    rider[i] = rider[i].split(",");
  }
  json1 = rider.map(function(x) {
    return {    
      "id": Number(x[0]),
      "name": x[1]
    }
  })
  console.log(json1);
  console.log(json2);
  console.log( JSON.stringify( joinObjects(json1, json2) ));
 }
}

document.getElementById('files').addEventListener('change', handleFileSelect, false);
</script>

 

CC-BY-NC Science Surf accessed 20.01.2026

Wissenschaftsrat zu Peer Review

wissenschaftsrat.de schreibt

Das Begutachtungswesen (peer review) steht nach Ansicht des Wissenschaftsrates unter zunehmendem Druck. Sowohl die Erwartungen an die Leistungen von Gutachterinnen und Gutachtern als auch die Nachfrage nach Begutachtungen seien aus verschiedenen Gründen deutlich gewachsen, ohne dass die Gruppe der Gutachtenden systematisch vergrößert und Wissen über Begutachtungen strukturierter vermittelt wurden.

Positionspapier 23.10.2017

 

CC-BY-NC Science Surf accessed 20.01.2026

Treg and transplant rejection

Yesterday evening I heard an interesting talk here about lung transplant rejection where one of the best prognostic marker
was the (pre transplantation) Treg count.

I wonder if there are some preexisting patient conditions, like allergy, that are responsible for this phenomenon?
At least it is already known since 2008 that Treg function is important. Current Treg therapies are exploiting this. Another allergy hallmark the IL33/ST2 axis is actively tested at the moment in transplant rejection.

In contrast transplant acquired allergy is something different – a side effect of tacrolimus? Or any other ingredient of the cocktail of steroids, mycophenolate, and IL-2 receptor inhibitors such as basiliximab?

 

CC-BY-NC Science Surf accessed 20.01.2026

Exports OSX ratings to XMP ratings

for FILE in *.jpg
do
  FN=$(echo $FILE | sed -e "s/jpg/xmp/")
  RATE=$(mdls "$FILE" | awk '/kMDItemStarRating/' |  awk '{print $NF}' )
  OR=$(mdls "$FILE" | awk '/kMDItemOrientation/' |  awk '{print $NF}' )
  exiftool "$FILE" -xmp:rating=$RATE -n -xmp:orientation=$OR -o "$FN"
done

 

CC-BY-NC Science Surf accessed 20.01.2026

Keep your Excelsheet updated ;-) or how to bind Kendo UI for jquery on a Synology to websocket

This is not really about Excel but about Kendo Grid’s ability to update grid data in the browser.  This is already my second attempt as a Mosquitto based MQTT solution did not work properly.

Demo Grid

Installing node.js on the Synology is straightforward – just use the package manager. We also need some local packages. Change into the target directory and type

npm install express
npm install typescript
npm install ws

Copy also app.js from https://github.com/telerik/kendoui-ws-demo into that directory. Unfortunately app.js breaks in line 5 (we need another port as 5000 is already occupied in the Synology). It also crashes in line 6, as the node.js V4 version needs full extension. So use the following lines

var WebSocketServer = require("ws").Server;
var http = require("http");
var express = require("express");
var app = express();
var port = process.env.PORT || 5050;
var products = require("./products.js");

Then start the server by

/usr/local/bin/node /volume1/web/kendoui-ws-demo-master/app.js &

Get the client script in kendoui.for.jquery.2017.3.1018.trial/examples/grid/web-socket.html and change the host. Take care to use ws (Websocket), not wss (Websocket secure) unless you know what you are doing.

//var host = "wss://kendoui-ws-demo.herokuapp.com";
var host = "ws://myserver:5050";

That’s it.

 

CC-BY-NC Science Surf accessed 20.01.2026

First allergy cell found

A phenotypically and functionally distinct human TH2 cell subpopulation is associated with allergic disorders

Allergen-specific type 2 helper T (TH2) cells play a central role in initiating and orchestrating the allergic and asth-matic inflammatory response pathways. One major factor limiting the use of such atopic disease-causing T cells as both therapeutic targets and clinically useful biomarkers is the lack of an accepted methodology to identify and differentiate these cells from overall nonpathogenic TH2 cell types. We have described a subset of human memory TH2 cells confined to atopic individuals that includes all allergen-specific TH2 cells. These cells are terminally differ-entiated CD4+ T cells (CD27− and CD45RB−) characterized by coexpression of CRTH2, CD49d, and CD161 and exhibit numerous functional attributes distinct from conventional TH2 cells. Hence, we have denoted these cells with this stable allergic disease-related phenotype as the TH2A cell subset.

Sounds promising…

 

CC-BY-NC Science Surf accessed 20.01.2026

Hygiene hypothesis should be death but is still alive

There is a new paper today “The Hygiene Hypothesis in the Age of the Microbiome“. Fortunately there is a strong paywall…

An impressive illustration of the hygiene hypothesis was found in the consistent farm effect on asthma and allergies, which has partly been attributed to immunomodulatory properties of endotoxin as emitted by livestock.

which is not aware of “Time to abandon the hygiene hypothesis: new perspectives on allergic disease, the human microbiome, infectious disease prevention and the role of targeted hygiene

Although evidence supports the concept of immune regulation driven by microbe–host interactions, the term ‘hygiene hypothesis’ is a misleading misnomer.

see also “News Feature: Cleaning up the hygiene hypothesis

Still, the catchy hygiene hypothesis continues to be widely embraced by the public, the media, and even scientists: Uses of the term in the scientific literature rose threefold over the past 10 years compared with the decade prior, according to a search on Thomson Reuters Web of Science. “In science, when something has been propagated for so long, it can be hard to change,” says Marsha Wills-Karp, chair of environmental health and engineering at Johns Hopkins Bloomberg School of Public Health.

 

CC-BY-NC Science Surf accessed 20.01.2026

Timeline asthma / allergy genetics

First Genetic Study
1923 AF. Coca.J Immunol 8:163-171

First Linkage Study (AB0 blood group)
1936. I. Zieve, Ann Hum Gen 7:4074, 163-178

First Molecular Study (HLA)
1973 D. Marsh, Science 179:4074, 691-3

Second Linkage Study (SLC14A1)
1985, H. Eiberg, Cytogenet Cell Genet 40: 622 -journal discontinued, no online archive-

Third Linkage Study (11q31)  – questionable results
1989 W. Cookson, Lancet 1:8650, 1292-5

First Modern Family Study
1992 S. Dold,  Arch Dis Child 67:8, 1018-22

First gene (Fc∈RI-β)
1993 A.J.Sandford,  The Lancet  341:8, 332-334

First true gene (IL4)
1994 D. Marsh, Science 264:5162, 1152-6

First Genomewide Linkage Scan
1996 S. Daniels, Nature 383:6597, 247-50

Transatlantic Airway Conference Key Biscayne FL
1997 N. Zamel (only reported later by Thompson  2003 and Duffy 2019)

Second Genomewide Linkage Scan
1997 CSGA  Nature Genetics 15:389-392

Third Genomewide Linkage Scan
1999 M. Wjst,  Genomics 58:1-8

First GWAS
2007 M. Moffatt, Nat Genet 15:389-392

Second GWAS
2008 C. Ober,  NEJM 358: 1682-91

then it is getting confusing

 

CC-BY-NC Science Surf accessed 20.01.2026

Phantom reference

There is an interesting story at harzing.com: A conference template with a dummy reference, that was supposed to be edited by abstract authors, was finally cited by 400 authors :) I find even more citations at Google Scholar, 703 to be exact. Low  quality, missing  control, careless editing, and fake journals, creepy…

 

CC-BY-NC Science Surf accessed 20.01.2026

Open letter to the Sente developer

Dear Michael J. Cinkosky,

this is an open letter regarding Sente academic library software.

Sente is used by tens of thousands of researchers in all academic fields at universities and research organizations around the world

I am using Sente nearly every day for many years to collect and annotate the literature.

It is useful to retrieve papers and insert references in my own papers.

It seems that Sente is not more supported.

A while ago, I could build up a bibliography only in exports from my text processor.

Then online sync stopped.

Most recently also Google Scholar reference recognition ended.

It is now a useless software. I paid for it, I used it, which was a fair deal.

But now am now lost, if Sente just drowns in the internet.

Could you sell it to a company that continues support?

Your customer base would really appreciate it.

Or write a final countdown Endnote export script that preserves PDF links.

Or just give us the code at Github, we will continue to develop it.

We all appreciate your work with Genbank and also with Sente.

But don’t leave us without saying good-bye.

All the best,

 

CC-BY-NC Science Surf accessed 20.01.2026

Ende der Debatte

aus dem DH Newsletter 11/2017

DHV sieht Debattenkultur in Gefahr
Der Präsident des Deutschen Hochschulverbandes (DHV), Professor Bernhard Kempen, hat vor einer Erosion der Debattenkultur an Universitäten gewarnt. “Das Klima der Political Correctness ist bedenklich”, führte er im Interview mit der “Welt” aus. “Die Sensibilitätsschwelle für andere Ansichten, andere Meinungen, für das Fremde ist erheblich gesunken.” Früher seien Universitäten Stätten vehementer und teils heftiger geistiger Auseinandersetzungen gewesen, heute werde versucht, niemandem eine Ansicht zuzumuten, die ihn verstören könnte.

 

CC-BY-NC Science Surf accessed 20.01.2026

Genfer Gelöbnis in der Oktober 2017 Version

AS A MEMBER OF THE MEDICAL PROFESSION:

I SOLEMNLY PLEDGE to dedicate my life to the service of humanity;

THE HEALTH AND WELL-BEING OF MY PATIENT will be my first consideration;

I WILL RESPECT the autonomy and dignity of my patient;

I WILL MAINTAIN the utmost respect for human life;

I WILL NOT PERMIT considerations of age, disease or disability, creed, ethnic origin, gender, nationality, political affiliation, race, sexual orientation, social standing, or any other factor to intervene between my duty and my patient;

I WILL RESPECT the secrets that are confided in me, even after the patient has died;

I WILL PRACTISE my profession with conscience and dignity and in accordance with good medical practice;

I WILL FOSTER the honour and noble traditions of the medical profession;

I WILL GIVE to my teachers, colleagues, and students the respect and gratitude that is their due;

I WILL SHARE my medical knowledge for the benefit of the patient and the advancement of healthcare;

I WILL ATTEND TO my own health, well-being, and abilities in order to provide care of the highest standard;

I WILL NOT USE my medical knowledge to violate human rights and civil liberties, even under threat;

I MAKE THESE PROMISES solemnly, freely, and upon my honour.

 

CC-BY-NC Science Surf accessed 20.01.2026

Sommerschlussverkauf

academics.de zu Hochschule 4.0 online Nov 2017

Harvard und MIT gründeten 2012 gemeinsam die Plattform EdX, auf der hochrangige Universitäten aus der ganzen Welt MOOCs anbieten. Auf der Plattform udacity werden “nanodegrees” (Mini-Abschlüsse) angeboten, die von Unternehmen mitkonzipiert und -finanziert werden (z.B. “Ingenieur für künstliche Intelligenz” in Zusammenarbeit mit IBM Watson). Wie “Hochschule 4.0” und das Forschen, Lernen und Lehren letztendlich aussehen werden, in welchen Kurs- und Lernformaten und mit welchen Abschlüssen die Vermittlung von Wissen zukünftig gestaltet werden wird, ist eine offene Frage.

detailreicher, besser geschrieben, aber auch kritischer: “Kein Bock auf MOOC” Dirk Böttcher und Lea-Marie Kanzler.
Links: https://www.class-central.com https://www.edx.org https://de.udacity.com

 

CC-BY-NC Science Surf accessed 20.01.2026

An update of IL2 function

More than 7 years ago, I wrote a blog post that there is nothing new under the sun predicting the next asthma genetics study for 2020 to include 100K asthmatics.

Ok, I am wrong the paper appeared already a week ago with 360K  asthmatics while basically doubling the number to 136 independent risk variants. It’s not an asthma only study as the authors had a rather loose definition of asthma or rhinitis or eczema – is is more about the allergy/atopy complex.

It will be a long time reading and replicating the data while my first interest was to examine the affected gene list as shown in table ST15. Using the online Enrichr database I get the following result from the GO ontology

This is basically the same result as the authors see in their table ST20.

 

The highest combined score is with a negative regulation of IL-2. What does that mean? A genetically disturbed pathway predicted by a gene ontology network?

IL2 was discovered in 1976 by Robert Gallo by growing T-cells in culture for more than nine months by stimulating lymphocytes with phytohemagglutinin. ((IL1 was described back in 1972 by Charles Dinarello). Gallo identified T-cell growth factor (TCFG), now known as interleukin-2 (IL-2) as being absolutely important for a protective immune responses (Science 1976).

The next important paper was also published  in Science 1984 showing the following figure

 

So we have in allergy 2 hits on IL2: by genetics (as show in the new study) and by early vitamin D supplementation (as I reviewed earlier). Maybe we need more clinical studies like the Zhang 2016 study:

In a general population-derived birth cohort, we found that in infants who developed food allergy, cord blood displayed a higher monocyte to CD4(+) T cell ratio and a lower proportion of natural regulatory T cell (nT(reg)) in relation to duration of labor. CD14(+) monocytes of food-allergic infants secreted higher amounts of inflammatory cytokines (IL-1β, IL-6, and tumor necrosis factor-α) in response to lipopolysaccharide. In the presence of the mucosal cytokine transforming growth factor-β, these inflammatory cytokines suppressed IL-2 expression by CD4(+) T cells. In the absence of IL-2, inflammatory cytokines decreased the number of activated nT(reg) and diverted the differentiation of both nT(reg) and naïve CD4(+) T cells toward an IL-4-expressing nonclassical TH2 phenotype.

Suppressed IL2 is a key for allergy development shown also in experiments by Bonnet 2016:

We previously demonstrated that Tregs can be selectively expanded and activated by low doses of IL-2 (ld-IL-2) inducing immunoregulation without immunosuppression and established its protective effect in autoimmune diseases. In this study, we evaluated the ability of ld-IL-2 to control allergy in an experimental model of food allergy. Ld-IL-2 induced Treg expansion and activation that elicited protection against clinical manifestations of food allergy in two mouse models with OVA and peanut. This clinical effect was lost in Treg-depleted mice, demonstrating the major contribution of Tregs in ld-IL-2 efficacy. Mechanistic studies further indicated that protection from allergy could be explained by a Treg-dependent local modification of the Th1/Th2 balance and an inhibition of mast cell recruitment and activation. Preventive and therapeutic effects of ld-IL-2 were observed over a 7-mo-period, highlighting its long-term efficacy. This study demonstrated that ld-IL-2 is efficient to prevent and to treat allergic immune responses, and thus represents a promising therapeutic strategy for managing allergic diseases.

What we do need now for allergy prevention is a trials of newborns with low dose IL2 and also more trials refining the IL2 antagonist application of vitamin D.

 

CC-BY-NC Science Surf accessed 20.01.2026

Your last name determines your research success

What’s in a name? Liran Einav and Leeat Yariv 2006 write

Faculty with earlier surname initials are significantly more likely to receive tenure at top ten economics departments, are significantly more likely to become fellows of the Econometric Society, and, to a lesser extent, are more likely to receive the Clark Medal and the Nobel Prize. These statistically significant differences remain the same even after we control for country of origin, ethnicity, religion or departmental fixed effects.

Somebody should have told me that earlier!

 

CC-BY-NC Science Surf accessed 20.01.2026