text:
Q: Header photo (above navbar) disappears when screen is minimized In normal window size, my website contains the header photo, with Welcome and Travel Recommendations written over the photo, and at the bottom of the header, the navbar. I want it to look the same in mobile phone view, but the writing and header photo disappears every time I minimize the screen and the navbar moves on top of the page followed by the rest of the body content. Everything else works just fine. I'm just trying to find a way to keep the header photo in mobile view and the navbar below it. Thanks!
My HTML code is:

.....

 Welcome

 Travel recommendations

                <button type="button" class="navbar-toggle" data-toggle="collapse" data-target="#bs-example-navbar-collapse-1">
                    Toggle navigation

                </button>
             ...

A: <meta name="viewport" content="width=device-width, initial-scale=1.0">

Try adding this to the top of the document. It should now scale the image. You shouldnt need the @mediascreen code in the css now.

A: Try to use a flex-box or a css grid it's easy , below there is a link to a demo that i make for you to get a scaled and responsive header and navigation bar hope this help you have a good day.
There is the demo :
Scaled header and nav-bar
And of course don't forget to add to your  this code :
<meta name="viewport" content="width=device-width, initial-scale=1">

A: By the looks of things, your image should not disappear. But there are some things that you are doing which may cause the header photo to look like it is not displaying properly.
I would say that you should start debugging at the media-query.  Maybe try adding display:block; to your .brand class and maybe giving it a set height.  I think that might clear up some of your problems.
Also try adding a viewport meta to your html head, like this:
<meta name="viewport" content="width=device-width, initial-scale=1.0">

This will tell the browser how to control the page's dimensions and scaling.
Also, that min-height: -10% you have on your .address-bar class is useless, that is not going to do anything.  a div cannot have a size smaller than 0.
But if you say that it works full screen, try removing the entire media query and see if you still get the undesired result.  If not, there there is your place to start.


This mini breakout board is designed to simplify prototyping and experimentation work with the popular 18-pin PIC16F series microcontrollers. It is small in size (1.95? X 0.75?) and is breadboard friendly.
It supports PIC16F84A, PIC16F628A, PIC16F88, PIC16F648A, PIC16F1827, PIC16F1847, and other 18-pin microcontrollers in the same series. This board you can buy from Tindie.


text:
Чемпиона́т Литовской ССР по футбо́лу 1951 го́да () — 30-й розыгрыш чемпионата Литвы по футболу.

Итоговая таблица

Литература
 Vytautas Saulis ir Gediminas Kalinauskas. "Lietuvos futbolas, 1922-1997 m.: istorinė apybraiža" // Vilnius, "Diemedis", 1997. 44 p.

Ссылки
 История чемпионатов Литвы по футболу на RSSSF

Футбол в СССР в 1951 году
1951 год в Литве
Чемпионат Литвы по футболу

redpajama_set_name: RedPajamaWikipedia


A few years ago, when hearing that Huawei is launching its flagship, most people were like 'meh', but lately, the Chinese manufacturer managed to join the 'big boys' club and we're eagerly waiting to see what they are up to most of the time!
As you probably know, they're getting ready to launch the Huawei P10, a high-end flagship able to compete with other top notch upcoming models, like the Samsung Galaxy S8 or LG G6. Well, today we found out that the handset is scheduled to make its debut on February 26, during a press conference held during the Mobile World Congress, in Barcelona.
The information is confirmed by the invitations the manufacturer sent yesterday to members of the press, inviting them to their event, but without giving too many details about what they should expect. Well, like it's not obvious.
Usually, Huawei launches their P-series flagships at separate events, a month or two after MWC, so this year's date comes a surprise, with them moving away from the usual annual release circle. On the other side, they definitely want to steal the show (just like LG), so the date makes sense.
But hey, you're here to find out more details about the specs of the Huawei P10, right? Thought so.
First of all, let's focus a bit on the design. The flagship is expected to feature a solid metal unibody, pretty much similar to last year's P9, but with a few differences, though. If a couple of images revealed a few weeks ago, claiming to picture a prototype of the handset, are accurate, it could feature a fingerprint scanner just under the display, unlike the P9, which had it on the back.
Moving on, another subtle design change will be brought by the display, expected to be curved and measure 5.5 inches, thus being bigger. As for the resolution, the IPS-NEO LCD panel, with 16 million colors, will rock 2560 x 1440 pixels, another important update!
Unlike other manufacturers, Huawei has been relying lately on its own chipsets, so no, we won't see a Snapdragon under the hood, but their latest HiSilicon Kirin 960, a high-end chip, with eight cores, four of them running at 2.4GHz and four at 1.8GHz, for less demanding tasks.
The processor will be aided by a Mali-G71 MP8 GPU, while the amount of RAM and storage will differ. To be more specific, you will be able to choose between a variant with 4GB of RAM and 64GB of space or a whooping 6GB of RAM and 128 gigs of storage.
We must admit that the Huawei P9 had an impressive camera setup and we don't expect anything to change this year. And it seems that they're planning to follow the same recipe, with two cameras on the back, placed exactly in the same spot as on the P9. And yes, they will once again be Leica-branded, so there's no doubt that this rear setup will be able to take some really crispy shots.
Finally, we also expect some interesting things from a software point of view. There's no doubt that this smartphone will have Android 7.0 Nougat on board, customized with Huawei's EMUI, but we're also expecting to see a digital assistant.
After all, Apple has one, the Pixel duo has one and even HTC's newly launched U Ultra has it. Why wouldn't Huawei do the same thing?
Last week, at CES, the Mate 9 received a very important update: Amazon's Alexa, one of the most powerful AI assistants of the moment. If the rumors turn out to be true, the P10 could also feature it!
Oh, and let's not forget about one more thing: the P10 will also come with a larger model, called P10 Plus. However, the size will be the only difference (5.5" display), since the specs and features will be kept. After the initial MWC 2017 unveiling, the two phones should start hitting the shelves somewhere in March or April.
And this is pretty much everything we know about the Huawei P10. What are your first impressions? Would you opt for it as your daily driver? Let us know, by dropping a few lines in the comments section below!
Previous articleIs 2017 the Year of Foldable Smartphones?


text:
About meResumeResearch
& IndustryPublicationsTeachingInterestsContact
David guennec's Personal Pages
I am a Ph.D. in computer science. Currently, I work as a teacher at ENSSAT and as a researcher with IRISA/EXPRESSION team. The team is located in Lannion and Vannes, Brittany, France. My primary topics of interest are TTS (Text-To-Speech) and ASR (Automatic Speech Recognition). My Ph.D. work focused on the study of unit selection algorithms in Text-To-Speech synthesis. After, that I worked as a Language Technology Scientist at Voysis in Dublin, Ireland. At Voysis, I worked on TTS, ASR, NLP (Natural Language Processing) and DSP (Digital Signal Processing). Then, I came back to IRISA to work on TTS again.
After my Baccalauréat scientifique (French degree), in 2007, I first obtained a DUT (Diplôme Universitaire de Technologie) in computer science in 2009. I then entered ENSSAT (École Nationale Supérieure des Sciences Appliquées et de Technologie) where I achieved a "diplôme d'ingénieur" as long as a master degree (from the university of Rennes) in 2012. Finally, I joined the IRISA/CORDIAL team (which became IRISA/EXPRESSION team) for my Phd. Between February and July 2015, I worked as an intern at IDIAP research center in Switzerland. I defended my Ph.D. on the 22nd of September in 2016.
Besides research, I have been teaching computer science at ENSSAT between 2013 and 2016. I was mainly (but not only) involved in the following courses: C and Java language, Web technologies (client side mostly), UNIX/Linux programming, distributed programming and artificial intelligence. I taught a total of 380h of courses.
You can download my full resume in PDF using the following links: in English; in French. (outdated, new links soon)
Qualification aux fonctions de maître de conférences
Qualifié pour les fonctions de maître de conférences en section 27 - Informatique (qualification obtenue lors de la campagne 2017).
Accès à mon dossier de qualification : dossier.
(outdated, new info soon)
Since Sept. 2022 - University Lecturer and Researcher at Université de Rennes 1, ENSSAT, France.
Teaching at ENSSAT Lannion. Working on speech production problematics with IRISA/Expression team.
Dec. 2020-Jul. 2022 - DataScientist Voice AI at ViaDialog, France
Working on TTS & ASR problems (mainly neural TTS).
2020-2021 (9 months) - Research Engineer at IRISA (ENSSAT Lannion), France
Building a new end-to-end neural Text-To-Speech Synthesis system and training pipeline for the Expression team of IRISA.
2017 - 2020 (3 years) - Language Technology Scientist at Voysis, Dublin, Ireland.
Work on User Simulation, Voice Activity Detection and Query Endpoint Detection, Text-To-Speech synthesis, Wakeword Detection, Audio Analysis & Processing and NLP tasks.
Feb. - Jul. 2015 (5 month) - Research visit at IDIAP research center, Martigny, Switzerland
Analysis and synthesis of prosody for expressive speech synthesis. Work on F0 modelling using Atom-based intonation decomposition.
2013-2016 (3 years) - Teaching at ENSSAT Lannion, France
Two "missions d'enseignement" in 2013-2015 (service limited to 64h a year) and one ATER mission in 2015-2016 (full service).
Intervention in several bachelor and master courses (UNIX, distributed programming, AI)
2012-2016 (4 years) - Ph.D. at IRISA (ENSSAT Lannion), France
Study of Unit Selection algorithms for Text-To-Speech Synthesis.
2012 (6 months) - Research master's degree internship at IRISA (ENSSAT Lannion)
Evaluation of Sandwich Units performances in Text-To-Speech Synthesis.
2011 (4 months) - Research on free time with Laurent Miclet
Work on analogical proportions and formal concept analysis. Creation of an analogy-finding algorithm in concept lattices.
2009 (3 months) - DUT degree Research internship at ENSSAT Lannion
Processing written symbols using analogy. Study of natural analogical proportions.
2008-2009 (7 months) - Student project IUT Lannion
Developping a rendering engine for a 2D game.
Research: Recently: Text-To-Speech Synthesis, Natural Language Processing, Voice Activity Detection, Query Endpoint Detection, Audio Analysis. Older experience: Analogy Relations, ConceptLattices.
Languages (computing): Recently: C/C++, Python, Bash, Latex. Older experience: Java, Perl, Php, HTML/CSS/Javascript, PROLOG, SQL.
OS: UNIX/Linux, macOS, Windows.
Analysis techniques: UML, MERISE.
- Head of staff for organizing the 2011 Festival des Langues (festival on world languages) in Lannion, France.
- Member of staff organizing Jap'And Trégor 2011 (cultural event on Japanese culture).
French: Native Speaker.
English: Cambridge CAE (Certificate of Advanced English) - European level C1. 3y living in the Republic of Ireland.
German: European level B1 (Estimated).
Italian: Basics.
2012-2016 - Ph.D. at ENSSAT - Doctoral school Matisse - University of Rennes 1.
2011-2012 - Master's degee of research in computer science at ISTIC, University of Rennes 1
2009-2012 - Diplôme d'ingénieur in computer science (Master's degree + management skills) at ENSSAT, Lannion.
2007-2009 - DUT in computer science (Foundation Degree) IUT of Lannion (Institute of Technology).
2007 - Baccalauréat S with honors (equivalent to A Levels).
My work at ViaDialog (2020 - 2022)
At ViaDialog, my main task was the development and maintenance of a TTS capability. I served as lead for all TTS-related work.This included developping a working prototype capable of performing fast speech synthesis with a level of quality in line with 2021 standards. The system, based on a neural end-to-end architecture required voice data in order to be trained. Hence, I worked on the recording and post-production of the data. Finally, I operated the transformation of the prototype into an usable product and worked on its maintenance and extension of its capabilities such as adding SSML support, adding security features and much more.
Here are a few key points:
Developed a new TTS product: Built a TTS prototype and pursued productization of the tool, performance enhancement, packaging and added security features.
Recording of TTS voices: creation of the recording script, coaching of voice talents, quality checks and review of advancement.
Voices post-production, model training and enhancement: Creation and continuous enhancement of the TTS voices with internal evaluation and feedback from users.
Interactions with clients: Presentations, technical discussions with our clients and talks at tech events.
Management of interns and annotators: Managed several masters level interns who helped with the TTS prototype as well as annotators performing TTS related tasks.
My work at Voysis (2017 - 2020)
At Voysis, I focused on a wide variety of tasks, across a large part of our stack. I worked on ASR, Voice activity detection (and query endpoint detection), wakeword detection, NLP, Audio Analysis and Processing and TTS. I ran several data collection (audio and text utterances) and several evaluation campaigns.
A few key points:
Developed tooling for core pipeline: Built a user simulator to generate initial corpus to bootstrap training of new token tagger, intent classifer, named entity recognizer and language model.
Worked on assessing audio quality of queries: Analyzed queries manually (waveform, spectrogram...) and designed tools to simulate and automatically detect common types of issues.
Established evaluation strategies and wrote tooling: Done for TTS, VAD (Voice Activity Detection), Query Endpointing, Wakeword Detection, ASR, etc.
Performed data collections, cleaning: Created new Text-To-Speech (TTS) voice, training, evaluation and complementary corpora.
Gained experience as a cross-functional team member: Experience on core projects and most of our stack. Moved between teams : teams recomposed based on needs and skill sets.
Image: My office at ENSSAT (10/2015).
I am working in the automatic speech synthesis field. The subject of my PhD has been the "Study of Unit Selection Text-To-Speech Synthesis Algorithms".
Two main strategy types are currently under consideration in this field. The first one relies on a statistical parametric approach where one tries to model speech signals. Models are then used in a generative way to produce speech utterances. It is called the Statistical Parametric Speech Synthesis approach (often shortened as "SPSS" though this conflicts with the name of IBM's statistics software). The second approach, which is an evolution of concatenation-based synthesis, consists in preserving and annotating a large speech corpus (usually several hours or even tens of hours), then extract fragments (called units) and paste them together to reproduce a the utterance that had to be synthesized (target utterance). The mechanism (not trivial) by which these fragments are selected is referred to as Unit Selection. The general technique is called Corpus-Based Speech Synthesis.
My thesis is to explore, diagnose Units Selection mechanism and suggest improvements. To meet these objectives, a corpus-based speech synthesis was needed. For reasons of independence, flexibility and to ensure a transversal control of the application, it was decided to build a completely new system rather than using and modifying an existing tool. So I spent a considerable time during my thesis in contributing to the implementation of the achieved engine within the team and adding features in it.
On the pure research part, I first took interest in evaluating the impact of the search algorithm on Unit Selection. In particular, the question was to identify whether or not optimality of the solution (ie. corpus units to be concatenated) was important and if not, what search strategy was the best. My conclusion was that the search algorithm sensibly impacts selection process only when searching for the optimal solution (or near optimal). Optimality of the solution is not necessary, however. Even a very pruned unit selection can be used with few sensible flaw.
I took also interest in the formulation of the cost function that allows the search algorithm to evaluate corpus units should have. Adapted preselection filtering method (i.e. Not consider the units deemed least useful) and Unit Selection influenced by a Vocalic Sandwich criterion (trying to avoid concatenation on points where they can degrade the signal) were tested. New target costs (judging the dissimilarity between a unit and it's desired characteristics) and concatenation (capacity of the unit to be pasted to the previous one without generating problems) have been implemented and tested. I am currently continuing my work it that direction, paying particular attention to Atom-based intonation decomposition technique which I discovered during my stay at IDIAP and it's possible applications to Target Costs.
Prior to working in the field of speech synthesis, I worked briefly on analogy relations, first trough an internship and then on my free time. In particular, I developed a search algorithm for analog proportions in concept lattice, which led to a publication. This work was a collaboration with Laurent Miclet and Henri Prade.
Keywords (thesis related): Unit Selection ; Corpus-Based Speech Synthesis ; Text-To-Speech Synthesis ; Cost Function ; Concatenation Cost ; Target Cost ; Neural Networks ; Deep Learning.
D. Guennec, "Study of Unit Selection Text-To-Speech Synthesis Algorithms" . Defended in September 2016 at L'université de Rennes 1 (university of Rennes 1), France. Obtained with the "European Label".
An enhanced version of the document is available as a book (ISBN: 978-3-639-56032-9).
International conferences with a reading committee
[1] L. Miclet, H. Prade and D. Guennec, "Looking for analogical proportions in a formal concept analysis setting" in 8th International Conference on Concept Lattices and Their Applications, 2011.
[2] D. Guennec and D. Lolive, "Unit Selection Cost Function Exploration Using an A* based Text-to-Speech System" in 17th International Conference on Text, Speech and Dialogue, 2014.
[3] D. Guennec, J. Chevelu and D. Lolive, "Defining a Global Adaptive Duration Target Cost for Unit Selection Speech Synthesis" in 18th International Conference on Text, Speech and Dialogue, 2015.
[4] J. Chevelu, D. Lolive, S. Le Maguer and D. Guennec, "How to Compare TTS Systems: A New Subjective Evaluation Methodology Focused on Differences" in 16th Interspeech Conference, 2015.
[5] P. Alain, J. Chevelu, D. Guennec, G. Lecorvé and D. Lolive, "The IRISA Text-To-Speech System for the Blizzard Challenge 2015" in Blizzard Challenge workshop, 2015.
[6] E. Delais-Roussarie, D. Lolive, H. Yoo and D. Guennec, "How to improve rhythmic patterns according to literary genre in synthesized speech" in 8th Speech Prosody Conference, 2016.
[7] M. Sečujski, B. Gerazov, T. G. Csapó, V. Delić, P. N. Garner, A. Gjoreski, D. Guennec, Z. Ivanovski, A. Melov, G. Németh, A. Stojković and G. Szaszák, "Design of a Speech Corpus for Research on Cross-Lingual Prosody Transfer" in 18th International Conference on Speech and Computer, 2016.
[8] D. Guennec and D. Lolive, "On the suitability of vocalic sandwiches in a corpus-based TTS engine" in 17th Interspeech Conference, 2016.
[10] D. Guennec, H. Hajipoor, G. Lecorvé, P. Lintanf, D. Lolive, A. Perquin, G. Vidal, "BreizhCorpus: A Large Breton Language Speech Corpus and Its Use for Text-to-Speech Synthesis" in Odyssey workshop, 2022.
International Conferences with a reading committee in french
[1] D. Guennec and D. Lolive, "Utilisation d'un algorithme A* pour l'analyse de la sélection d'unités en synthèse de la parole" in 30th Journées d'Études sur la Parole, 2014.
[2] D. Guennec and D. Lolive, "Une pénalité floue fondée phonologiquement pour améliorer la Sélection d'Unité" in 31th Journées d'Études sur la Parole, 2016.
[3] E. Delais-Roussarie, D. Lolive, H. Yoo and D. Guennec, "Patrons Rythmiques et Genres Littéraires en Synthèse de la Parole" in 31th Journées d'Études sur la Parole, 2016.
[4] J. Chevelu, D. Lolive, S. Le Maguer and D. Guennec,"Se concentrer sur les différences : une méthode d'évaluation subjective efficace pour la comparaison de systèmes de synthèse" in 31th Journées d'Études sur la Parole, 2016.
Recent Reviews for International Conferences and Journals
Interspeech 2018, 2019, 2020, 2021, 2022.
ICASSP 2021, 2022, 2023.
Speech Prosody 2018, 2020, 2022.
Machine Translation Journal.
Image: My teaching/research place, ENSSAT engineering school in Lannion, Brittany, France
Year 2013-2014: 60h
Courses I gave as part of a "Mission d'enseignement" (teaching mission) during my second year as a PhD student at ENSSAT engineering school.
Artificial Intelligence (Master's degree level): 8h + 12h Project
UNIX/Linux programming (Master's degree level): 20h
Distributed programming (Master's degree level): 14h Project
Introduction to Linux (Bachelor's degree level): 6h Labs
Courses I gave as part of a "Mission d'enseignement" during my third year as a PhD student at ENSSAT engineering school.
Several courses in Algorithmics, C language and UNIX/Linux programming (Bachelor's degree level): 8h + 34h Labs + 14h Project
Web programming (Bachelor's degree level): 4h + 10h Project
Year 2015-2016: 250h
Courses I gave as part of my ATER (Attaché Temporaire d'Enseignement et de Recherche) position at ENSSAT.
Algorithmics, C language (Bachelor's degree level): 16h + 42h Labs/Project
Object Oriented programming (Master's degree level): 22h Labs + 8h Project
Advanced Algorithmics and Complexity (Master's degree level): 14h + 16h Project
Datastructures (Bachelor's degree level) : 20h Labs
Web Programming (Introduction+Client side) (Bachelor's degree level): Head of course: 6h Lectures + 12h Labs + 16h Project. Here are the lecture slides: Course.
Web Technologies (Bachelor's degree level): Head of course: 8h Lectures + 18h Project
Specification, Validation, Test, Profiling and Debug (Master's degree level): 20h Labs
Distributed Computing (Master's degree level): 2h Lectures + 16h Project. Here is the project subject: Subject.
UNIX/Linux programming (Bachelor's degree level): 10h Labs + 4h Project
Year 2022-2023: 257h (Anticipated)
Courses I am in the process of giving at ENSSAT.
July 2015 - September 2015 • Travel
A few photos of places I visited & loved with a few comments.
December 2015 • Music
One of my favorite interests is music, but one cannot always go to concerts. So, to listen to music recordings, you need either speakers or headphones. Here are my impressions concerning the latter.
You can contact me direcly using the following form:
Name*: Email Address*: Message*:
Elsewhere on the web:
Google+: Profile
LinkedIn: Profile
Viadeo: Profile
Copyright 2022 © David Guennec

redpajama_set_name: RedPajamaCommonCrawl


text:
Q: Unique behavior of my program , Unable to identify There is some problem during the run time of my program and i am unable to get what the problem is.
what happens basically is , my program automatically closes and displays the following in Microsoft visual c++ 2010 express window

What could be the reasons for this ? I have no idea why this is happening.
Let me tell that in my program i have used pointers too often and have used character arrays which i write to the disc
The program is too large to display
This is the function called after which my program stops :
void display_databases()
{

 struct info_of_trains
 {
int train_no;
char train_name[25];
char boarding_pt[25];
char destination[25];
int first_seats;
int fare_first;
int second_seats;
int fare_second;
char  date[20];
    };

    info_of_trains e;

  cout<<"TRno.  TRname     B.pt    D.pt    F.seats    F.fare   S.seats   F.second   Date\n";
  FILE *fp;
  fp=fopen("database","r");
  if(fp==NULL)
  {
cout<<"failure";
  }
  else
  {
  while(fread(&e,sizeof(e),1,fp)==1)
  {

printf(e.train_no,e.train_name,e.boarding_pt,e.destination,e.first_seats,e.fare_first,e.second_seats,e.fare_second,e.date);
  cout<<"-------------------------------------------------------------------------------\n";
   }
   fclose(fp);
   }
   }

This is where execution stops :!

A: You seem to have hit a breakpoint, or your program had an access violation (reading an illegal pointer). You also seem to have maximized/detached the debugging panels. You can reattach the panel by dragging the yellow bar at the top to the lower part of the screen.
Did you recieve a warning message before it happened? Otherwise, did you define a breakpoint (clicking in the left margin of the code editor, so a red circle appears there)
EDIT: As pointed out in the comments, the error occurs because you use printf the wrong way. Use cout instead, as you did above:
cout << e.train_no <<" " <<  e.train_name << " " << e.boarding_pt << " " << e.destination << " " << e.first_seats << " " << e.fare_first << " " << e.second_seats << " " << e.fare_second << " " << e.date << endl;

redpajama_set_name: RedPajamaStackExchange


Capcom is a Japanese manufacturer and distributor of electronic games machine founded in 1979. Since then it has grown into an international concern with offices in Tokyo, Osaka, California, England, Hong Kong and Germany. It has dual headquarters in Osaka, Japan and San Mateo County, California. Capcom is the creator of a number of well-known and established games such as Resident Evil, Street Fighter and Devil May Cry games across a number of platforms. Their games are supported by a wide variety of gaming consoles and machines including but not limited to Dreamcast, Game Boy, Nintendo, PlayStation, Wii and Xbox.


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The waterways of Interior Alaska brought the first modern settlers to Fairbanks and remain just as important as roads and skyways in transporting goods and people across the state. They're also one of the most popular options for recreation and adventure.
Hop aboard a watercraft to experience Fairbanks from the riverbed. Choose Riverboat Discovery to learn all about local history, dog mushing, and native culture.
To continue lessons in local history, try your luck at Gold Dredge 8 and get a feel for what it was like to be an early pioneer hoping to strike it rich in such a harsh and remote environment.
The best way to glimpse the "real Alaska" of northern wilderness and bush villages is to book a trip with an operator of daily tours above the Arctic Circle. Warbelow's Air Adventures and Northern Alaska Tour Company are two good options. The companies offer tours for every schedule and interest, including rides on bush mail flights, multi-day excursions, and flying to a far-flung village to watch polar bears feasting on whale remains. Embark on an arctic tour and you are guaranteed to return home with more than a few Alaskan stories.
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Laboratory Investigations| July 2005
Pyruvate Modulates Hepatic Mitochondrial Functions and Reduces Apoptosis Indicators during Hemorrhagic Shock in Rats
Pushpa Sharma, Ph.D.;
Pushpa Sharma, Ph.D.
*Assistant Professor.
Kane T. Walsh, M.D.;
Kane T. Walsh, M.D.
†Staff Anesthesiologist.
Kimberly A. Kerr-Knott, M.D.;
Kimberly A. Kerr-Knott, M.D.
John E. Karaian, B.S.;
John E. Karaian, B.S.
‡Research Assistant.
Paul D. Mongan, M.D.
§Staff Anesthesiologist and Associate Professor.
Anesthesiology July 2005, Vol. 103, 65–73.
Pushpa Sharma, Kane T. Walsh, Kimberly A. Kerr-Knott, John E. Karaian, Paul D. Mongan; Pyruvate Modulates Hepatic Mitochondrial Functions and Reduces Apoptosis Indicators during Hemorrhagic Shock in Rats. Anesthesiology 2005; 103:65–73 doi: https://doi.org/10.1097/00000542-200507000-00013
Dysfunctional mitochondria have been widely accepted as one of the key targets and a mediator of secondary cell injury and organ failure during hemorrhagic shock (HS). The liver is known to be the first organ to display the signs of injury during HS. This report describes experiments to determine whether modulation of hepatic mitochondrial dysfunctions by pharmacologic agents could prevent liver injury in rats subjected to HS.
In this study, Sprague-Dawley rats were either treated as controls or subjected to computer-controlled arterial hemorrhage (40 mmHg) for 60 min followed by resuscitation with hypertonic saline, hypertonic beta-hydroxybutyrate, or hypertonic sodium pyruvate for the next 60 min before death. During the course of the experiment, animals were continuously monitored for hemodynamic and metabolic parameters. At the end of the experiment, the liver was excised and examined for oxidative injury, mitochondrial functions, expression of nitric oxide synthase, and indicators of apoptosis.
In comparison to hypertonic saline and hypertonic beta-hydroxybutyrate, pyruvate significantly protected the liver from oxidative injury, prevented the up-regulation of nitric oxide synthase, inhibited pyruvate dehydrogenase deactivation, and improved cellular energy charge and mitochondrial functions. In addition, pyruvate also reduced cleavage of poly-adenosine diphosphate ribose polymerase by preventing leakage of mitochondrial cytochrome c in the liver of HS animals.
These data suggest that modulation of mitochondrial metabolic functions is likely to be one of the important mechanisms by which pyruvate exerts its protective effects on the liver during HS and resuscitation in rats.
MULTIPLE organ failure in hemorrhagic shock (HS) has been commonly related to metabolic failure due to dysfunctional mitochondria. The liver is known to be the first organ to display the signs of injury during HS due to its high mitochondrial content, increased metabolic rate, lactic acid clearance, and increased production of oxygen and nitrogen species in comparison with other organs.1–3A relation between mitochondrial dysfunction and the irreversibility of pathologic damage in liver has been reported.4–6Therefore, it is logical to hypothesize that the pharmacologic agents that can reduce reactive oxygen and nitrogen species and prevent mitochondrial damage may offer a promising treatment for HS.
To test our hypothesis, we examined and compared the effects of pyruvate with another pharmacologic agent, β-hydroxybutyrate (β-HOB), in resuscitative fluids of rats subjected to HS. The rationale for the use of pyruvate and β-HOB is that they are antioxidants, decrease membrane permeability, and produce acetyl coenzyme A as the immediate substrate of the Krebs cycle to generate mitochondrial matrix reduced adenine dinucleotide for oxidative phosphorylation.7The uptake of β-HOB by mitochondria is adenosine triphosphate (ATP) dependent, whereas pyruvate requires the activity of the mitochondrial enzyme pyruvate dehydrogenase, which is regulated by the content of its E-1α subunit.8However, it is not known whether pharmacologic activation of pyruvate dehydrogenase complex (PDH) and up-regulation of its E-1α subunit could be linked to the improved hepatococellular ATP, mitochondrial functions, and decreased apoptosis. In addition, the use of β-HOB in the treatment of HS has not been extensively studied in HS. On the other hand, recent work from our laboratory and those of others have shown the use of pyruvate administration in restoring the cellular metabolic functions in the brain and heart and also in enhancing the survival rates during HS or ischemia by preventing the loss of ATP.7,9–12Despite this, the mechanisms for these responses are not fully understood, and the role of pyruvate in restoring the mitochondrial energetic functions in one of the most important organs, the liver, is still unresolved. The use of pyruvate and β-HOB as alternate adjuvants to metabolic resuscitative fluids may therefore provide a rational approach for the development of an effective metabolic therapy for HS by maintaining the hepatocellular functions.
The protocol and experimental procedures were reviewed and approved by the Animal Care and Use Committee of the Uniformed Services University of the Health Sciences at Bethesda, Maryland, with adherence to the Guide for Care and Use of Laboratory Animals .13
Animal and Surgical Preparation
Male Sprague-Dawley rats (Taconic Farms, German Town, NY) weighing 225–250 g were used in this study. Rats were not fasted at the time of experiment. Animals were anesthetized by spontaneously breathing 1.6% halothane in room air through a nose cone. The femoral artery and vein were surgically cannulated with PE-50 polyethylene tubing for fluid administration, blood sampling, and continuous monitoring of blood pressure. The incision was closed with interrupted sutures. Core temperature (rectal) was maintained at 37°± 0.2°C with a heat lamp. The rats were continuously monitored for mean arterial blood pressure (MAP) by connecting the arterial catheter to a pressure transducer and computerized physiograph (LABVIEW 5; National Instruments, Austin, TX). The readings were recorded every 10 s and averaged per minute over the course of the experiment. The baseline MAP was stabilized by infusing normal saline. At this point, the concentration of halothane was reduced to 1% throughout the experiment.
Induction of HS.
Computer-controlled arterial hemorrhage to a target of MAP of 40 mmHg was achieved over 15 min by the withdrawal of blood from femoral arterial catheter using an Instech P720 peristaltic pump (Instech Laboratories Inc., Plymouth Meeting, PA). This MAP of 40 mmHg was maintained by either removal or infusion of blood for a 60-min (T60) shock period.
Resuscitation Groups.
The animals were randomly assigned to the four treatment groups (n = 6 animals/group). In group 1, instrumented time control rats were anesthetized and instrumented in the same manner as rats in the other group but did not undergo arterial hemorrhage except the withdrawal of blood for laboratory investigation. Vital signs were recorded for 120 min by infusing normal saline three times the volume of blood lost. Groups 2, 3, and 4 were subjected to hemorrhage and resuscitation, but these three groups differed in the composition of resuscitative fluids: Group 2 received 7.5% hypertonic saline (HTS) to match the osmolality effects of sodium pyruvate, group 3 received 256 mg/ml hypertonic β-HOB, and group 4 received 225 mg/ml hypertonic sodium pyruvate infused at a rate of 5 ml/kg for 1 h.
Analytical Sampling Procedures.
Immediately before hemorrhage (T0) and every 60 min thereafter, arterial blood was collected for the measurement of pH, base excess, and blood gases (IL 1610 Blood Gas Analyzer; Instrumentation Laboratories, Lexington, KY). Serum lactate and pyruvate from arterial blood samples were also measured with a CMA 600 Analyzer (CMA/Microdialysis, Acton, MA).
Tissue Sampling.
Before death at T120, the rats' livers were excised immediately. The left lobe was placed in ice-cold isotonic sucrose Tris EDTA buffer, pH 7.4, for isolation of mitochondrial and cytosolic fraction,10while the remaining tissue was quickly frozen in liquid nitrogen, pulverized, and stored in cryovials at −80°C for analysis of lipid peroxidation, energy metabolites, and Western blotting for the semiquantitation of nitric oxide synthase and poly–adenosine diphosphate (ADP) ribose polymerase (PARP) proteins. Animals were then killed by exsanguination.
Isolation of Mitochondrial and Cytosolic Fractions.
The duration from harvesting of liver to homogenization was kept as short as possible (< 5 min). Tissue was minced, washed, and homogenized in ice-cold mitochondrial isolation buffer consisting of 0.25 m sucrose, 10 mm HEPES buffer, pH 7.4, and 1 mm EGTA in a ratio of 1:10 (vol/vol). Mitochondria were isolated by differential centrifugation at −4°C. In brief, cell membranes and nuclei were separated by centrifugation of tissue homogenate at 1,000g . The first supernatant was centrifuged at 10,000g for 15 min to get a mitochondrial pellet (S1). The supernatant thus obtained was centrifuged at high speed, 100,000g , for 60 min in a Beckman Ultracentrifuge-TL100 (Scientific Surplus, LLC, Hills Borough, NJ) to obtain the cytosolic pellet. The mitochondrial pellet was washed three times in mitochondrial isolation buffer without EGTA to obtain relatively pure mitochondria for determining the respiratory rates, activation state of PDH, level of its E-1α subunit, and citrate synthase activities. The cytosolic fraction was used for Western analysis of cytochrome c. All measurements were performed in duplicate, and the average of the two from each of the six animals in each group was used for data analysis.
Analytical Procedures
Measurement of Liver Enzymes.
The serum contents of liver enzymes alanine aminotransferase and aspartate aminotransferase were determined in our clinical chemistry laboratory at the Uniformed Services University of the Health Sciences.
Measurement of Tissue Lipid Peroxidation Level.
Malondialdehyde, a degradation product of peroxidized phospholipids, was quantified as an indirect marker of oxidative stress using a colorimetric thiobarbituric acid assay kit from Calbiochem (La Jolla, CA). The Malondialdehyde concentrations were normalized to protein content and expressed as nmol/mg tissue protein.
Protein Assay.
Protein contents in tissue, mitochondrial, or cytosolic samples were determined according to Bradford assay using bovine serum albumin as a standard.14
Determination of Adenine Nucleotides and Energy Charge in Liver.
To determine the contents of cellular nucleotides, pulverized frozen T120 liver tissue was deproteinated by incubation in 1.5 m perchloric acid (3 ml/mg protein) for 10 min and then neutralized with 2 m KOH. Nucleotides ATP, ADP, and adenosine monophosphate (AMP) were determined as a measure of reduced adenine dinucleotide formation at 340 nm using hexokinase and glucose 6-phosphate dehydrogenase as substrates.15Energy charge was calculated as an indicator of cellular metabolic status in liver by using the equation Energy Charge =[ATP]+ 0.5[ADP]/([ATP]+[ADP]+[AMP])
Determination of Pyruvate Dehydrogenase Complex Activity.
The total PDH (PDHt) and the native PDH (PDHa) in their activated or dephosphorylated form at T120 were determined in mitochondrial samples. For the measurement of PDHtactivity, the inactive (phosphorylated) form of the enzyme was converted to the "active" (dephosphorylated) form by incubating 25 mg mitochondrial protein in 1.0 ml of 10 mm MgCl2and 10 mm CaCl2for 5 min at 25°C. The activities of PDHtand PDHawere determined spectrophotometrically after reduction of p -iodonitrotetrazolium violet by PDH-dependent reduced adenine dinucleotide production at 500 nm.16The PDH activity was calculated using the molar extinction coefficient of p -iodonitrotetrazolium violet (5.4 × 103cm−1) and expressed as μmol · min−1· mg−1protein. The fractional activity of PDHain PDHtwas calculated as (PDHa/PDHt) × 100. To examine the relation between the fraction of active PDH and its E-1α component, Western blot analysis was conducted using the same mitochondrial preparations.
Citrate Synthase Assay.
As a standard marker of mitochondrial content in the samples, citrate synthase activity was measured in the mitochondrial pellet. The assay buffer included 50 mm Tris (pH 8.0), 0.5 mm DTNB, 0.1 mm acetyl coenzyme A, 0.05% Triton X-100, and 20 μg mitochondrial protein. The reaction was started by the addition of 0.5 mm oxaloacetate, and absorbance at 412 nm followed for several minutes at 30°C. Citrate synthase activity was determined according to the method of Srere and Matsuoka,17which couples coenzyme A to DTNB.
Measurement of Mitochondrial Respiratory Activity.
The rate of oxygen consumption in freshly isolated liver mitochondria was measured at room temperature using three-channel titration-injection respirometers (StrathKelvin oxygen microelectrodes with Oxygraph [Glasgow, United Kingdom] for data acquisition and analysis). One hundred microliters of the respiratory buffer (250 mm sucrose, 10 mm HEPES, pH 7.2, 20 mm KCl, 5 mm potassium phosphate, and 2 mm MgCl2) was added to each electrode, stirred, and equilibrated for 30 min with air in the Oxygraph chambers until a stable baseline was obtained. The mitochondrial suspension was added to give a final concentration of 1 mg/ml protein in 100 μl incubation buffer consisting of respiratory buffer plus substrates/inhibitors. Oxygen flux at the resting state or state 4 respiration through various segments of the electron transport chain (ETC) was determined using (1) flux of electrons from complex I to the end of the ETC (10 mm glutamate and 5 mm malate); (2) flux of electrons from complex II to the end of the ETC (after inhibition of complex I with 5 μm rotenone; state 4 respiration was restored by adding 10 mm succinate as complex II substrate); (3) flux of electrons from complex III to the end of the ETC (inhibition of complex III with 5 mm antimycin A was followed by adding 0.5 mm TMPD and 2 mm ascorbate substrates for complex IV [cytochrome c oxidase, cyclooxygenase]). Oxygen consumption measured in the presence of added ADP (active) was defined as state 3 respiration, and that measured after consumption of ADP (resting) was defined as state 4 respiration.18Respiratory control ratio was calculated as ratio of state 3 respiration to state 4 respiration and was used as a marker of mitochondrial respiratory activity. Mitochondrial respiration was calculated as the nanomoles of oxygen per minute per milligram of protein.
Western Blot Analysis for E-1α Subunit of PDH, Nitric Oxide Synthase, and Indicators of Apoptosis.
Mitochondria were used for the immunodetection of E-1α protein, tissue homogenates for nitric oxide synthase and PARP, and cytosol was used for the detection of cytochrome c. The samples for Western blotting were prepared in ice-cold lysing buffer (1:10 [wt/vol]) consisting of phosphate-buffered saline at a pH of 7.4, 230 mg/ml PMSF, 1 μg/ml leupeptin, and 1 μg/ml aprotinin in 1% Triton X-100. After brief sonication and centrifugation (1,000g × 10 min), these samples were denatured in Laemmli sample buffer. Approximately 15 μg protein was resolved on 10% sodium dodecyl sulfate gel and transferred to the nitrocellulose membrane of 0.45-μm pore size. The membranes were probed with primary mouse monoclonal antibody to either anti E-1α (dilution, 1:1,000; Molecular Probes, Eugene, OR), anti–nitric oxide synthase (dilution, 1:500; BD Transduction Laboratories, Lexington, KY), anti–cytochrome c (dilution, 1:500; Trevigen, Gaithersburg, MD), or anti PARP (dilution, 1:2,000; Biomol Research Laboratories Inc., Plymouth Meeting, PA). Detection was accomplished using horseradish peroxidase–conjugated antibody and enhanced chemiluminescence reagents (Pierce, Rockford, IL). Ponceau staining of the membranes with transferred proteins showed an equal amount of protein loaded in each lane (data not shown). Negative controls were performed by omitting the primary antibodies. The regulation of nitric oxide synthase, PARP, and cytochrome c was also standardized against antibodies to antiactin as a housekeeping gene. Human heart mitochondria from Mito-sciences (Eugene, OR) were used as control/marker for E-1α protein. Quantitative determinations of signal intensity of the protein bands were performed by measuring the integrated optical density using the Scion image program from Scion Corporation (Frederick, MD).
All data are presented as mean ± SE or median and range between 25 and 75% distribution. Statistical inference was performed using Sigma-Stat 3.1 (Aspire Software International, Leesburg, VA). Differences between groups for nonrecurring measurements were assessed using one-way analysis of variance. Differences between and within groups for multiple independent samples were performed by Kruskal-Wallis one-way analysis of variance on ranks followed by the Student-Newman-Keuls method. The level of statistical significance was accepted at P < 0.05 after correction for multiple comparisons.
Hemodynamic and Physiologic Response to HS and Resuscitation
Hemodynamic parameters in the control group (group 1) were stable throughout the experiment (table 1). The volume of shed blood for the induction of shock (40 mmHg) did not differ significantly among the various shock groups (groups 2, 3, and 4; table 1; P > 0.05) and was in the range previously reported for the same level (40 mmHg) of HS.19Because this was a computer-controlled shock model, the volumes of resuscitative fluids infused in each shock group were also similar (table 1). In comparison to baseline values, all animals in the hemorrhaged group had a significant increase in arterial partial pressure of oxygen (Po2). All treatments were equally effective in decreasing Po2and increasing partial pressure of carbon dioxide (Pco2) (P > 0.05).
Table 1. Hemodynamic and Metabolic Parameters during the Experiments
Osmolality, Acid–Base Parameters, and Markers of Ischemic Injury
Serum osmolality values were similar in all resuscitated groups. The arterial base excess, a reliable indicator of the severity of HS, oxygen debt, and volume deficit, was negative at the end of the 60-min shock period. Pyruvate administration prevented the magnitude of changes in acid–base parameters that occurred in other treatment groups (P < 0.05). Also, in comparison to controls, hemorrhaged animals showed signs of ischemic conditions characterized by significant lactic acidosis, a low lactate/pyruvate ratio, and a decrease in pH (P < 0.05) at T60. However, pyruvate treatment was able to reduce these ischemic events when compared with HTS or β-HOB.
Pyruvate Effects the Release of Hepatic Enzymes and Lipid Peroxidation
The data presented in table 2indicate that after HS at T120, plasma concentrations of aspartate aminotransferase and alanine aminotransferase were significantly increased in the HTS and β-HOB groups, and infusion of pyruvate reduced their concentrations, which were similar to those of control operated animals. Also, in these animals, HTS or β-HOB treatment showed a significant increase in the accumulation of malondialdehyde concentrations in liver tissue when compared with pyruvate or control animals (P < 0.05).
Table 2. Effect of Various Treatments on Liver Dysfunction, Lipid Peroxidation, Adenine Nucleotides, and Energy Charge
Pyruvate Effects on Activation State of Mitochondrial Pyruvate Dehydrogenase and Up-regulation of the E-1α Subunit
The data depicted in figure 1show that in comparison to control operated animals, the activities of both PDHtand PDHawere significantly reduced in HTS and β-HOB groups and not in pyruvate-treated animals (P > 0.05). The protective effect of pyruvate on the recovery of PDH activities was also substantiated by the observations that PDHawas 57 ± 5.9, 23 ± 4.5, 42 ± 1.8, and 61 ± 2.9% of PDHtin control, HTS, β-HOB, and pyruvate groups, respectively (P < 0.05 between HTS and β-HOB). The citrate synthase activity in hepatic mitochondria (nmol · min−1· mg−1mitochondrial protein) was approximately similar in all treatment groups (mean ± SE: control, 121 ± 30.7; HTS, 129 ± 25.8; β-HOB, 123 ± 27.5; pyruvate, 133 ± 22.3). The Western blot analysis of 40-kd E-1α protein in figure 2also shows significantly darker protein bands in control and pyruvate groups when compared with HTS– or β-HOB–treated animals. The quantitative densitometric analysis of this protein also indicates that it was increased in pyruvate-treated animals by factors of approximately 5 and 3 in comparison with the HTS and β-HOB groups, respectively (P < 0.05).
Fig. 1. Effect of treatments on the activity of total and active pyruvate dehydrogenase complex in rat liver mitochondria. Data are presented as mean ± SEM of four to six experiments. The resuscitative fluids containing hypertonic saline (HTS), β-hydroxybutyrate (β-HOB), and pyruvate were started 60 min after the beginning of the hemorrhage procedure. The control group of animals (instrumented time control) received only normal saline. The liver was harvested at 120 min. The activities of native or total pyruvate dehydrogenase complex (total PDH) and the active form of pyruvate dehydrogenase complex (active PDH) were determined spectrophotometrically. UNHANDLED_ENTITY P < 0.05 comparing the pyruvate group with HTS or β-HOB for the total pyruvate dehydrogenase complex activity. * P < 0.05 comparing the pyruvate group with HTS and β-HOB for the active form of pyruvate dehydrogenase complex.
Fig. 2. A representative Western blot of rat liver mitochondria showing the expression of E-1α subunit of pyruvate dehydrogenase complex in various treatment groups. Mitochondrial samples obtained from liver tissues at T120 were subjected to electrophoresis and immunostaining with antibodies to anti–E-1α protein. The considerably darker protein band with significantly higher integrated optical density (IOD) in the pyruvate-treated group when compared with others indicates that pyruvate prevented the loss of pyruvate dehydrogenase E-1α subunit.
Pyruvate Effects on Hepatic Adenine Nucleotides Contents and Energy Charge
The changes in adenine nucleotides and purine catabolites reflecting energy metabolites in hepatic tissue after resuscitation are shown in table 2. Data suggests that pyruvate was significantly effective in preventing the loss of hepatocellular ATP in comparison with HTS or β-HOB treatments (percent of controls ATP in HTS, 17%; β-HOB, 33%; pyruvate, 72%, P < 0.05). A concomitant increase in ADP and decrease in AMP concentrations after pyruvate treatment in comparison with other groups resulted in a significantly higher ATP/ADP ratio and a higher energy charge, which was similar to that of the control group (P > 0.05). However, total adenine nucleotide content (ATP plus ADP plus AMP) remained unchanged in all treatment groups.
Pyruvate Effects on Hepatic Mitochondrial Respiration in HS
The capacity of the ETC to oxidize substrates at its various segments was examined by measuring the respiratory control ratio with complex specific substrates. Data presented in table 3indicate that in comparison to control animals, liver mitochondria from HTS– and β-HOB–treated animals showed significantly increased state 4 (resting) respiration. Treatment with pyruvate attenuated these mitochondrial respiratory dysfunctions after HS. Rotenone-sensitive decrease in respiratory control ratio with substrates for complex II and I was significantly low in the HTS and β-HOB groups when compared with pyruvate. In addition, the oxygen consumption was still decreased after complex III inhibition with antimycin (antimycin A plus substrates of complex IV). Our results also demonstrate that respiratory control ratios with complex IV substrates were significantly lower in comparison with the substrates for complex I and II in HTS and β-HOB treatment groups when compared with pyruvate.
Table 3. Effect of Resuscitation Medium on Hepatic Mitochondrial Respiration in Hemorrhagic Shock
Evidence of Decreased Nitric Oxide Synthase, Low Cytochrome c Release, and Decreased Poly-ADP Ribose Polymerase Fragmentation in Liver by Pyruvate in HS
To gain insight into the molecular mechanisms of the action of HTS, β-HOB, and pyruvate on mitochondrial dysfunctions and cell death, inducible nitric oxide synthase, cytosolic cytochrome c, and PARP fragmentation expression were examined in liver from each treatment group. The Western blotting data in figure 3show significantly lighter protein bands from the pyruvate treatment in comparison with HTS and β-HOB. The integrated optical density of inducible nitric oxide synthase (table 4) in pyruvate-treated animals was not significantly different from that of the control group (P > 0.05), but it was 25% and 43% of that of the HTS and β-HOB groups, respectively (P < 0.05). The release of cytochrome c from mitochondria into the cytosol is an initial step to trigger the apoptotic events leading to DNA damage and cell death. The middle panel of figure 3shows that cytochrome c release into the cytosol was significantly lower in the pyruvate group than the remaining other groups except the control group, confirmed by integrated optical density data. The bottom panel of figure 3shows that the intact PARP was abundant in all liver samples as a 116-kd protein. Examining the PARP cleavage pattern in these samples shows that a background apoptosis signal was detectable as the faint 85-kd fragments of PARP in the liver of pyruvate-treated animals, but 85-kd and 50-kd bands with higher integrated optical density were noticed in the HTS– and β-HOB–treated HS rats (table 4; P < 0.05, n = 3). The percentage of PARP fragmentation was calculated by using the formula (optical density of 85-kd fragmented PARP)/optical density of total PARP (116-kd intact PARP + 85-kd fragmented PARP) × 100. The percentage of total PARP fragmentation was 21 ± 5% in the control group, 73 ± 5% for HTS, 68 ± 6% for β-HOB, and 27 ± 4% for pyruvate (table 4; P < 0.05, n = 3). In addition, the total PARP was significantly increased in all HS groups when compared with controls (P < 0.05), indicating a trigger of DNA repair mechanism by the activation of PARP.
Fig. 3. Representative Western blot of rat liver showing the expression of inducible nitric oxide synthase (iNOS), poly–adenosine diphosphate ribose polymerase (PARP), cytochrome c, and actin in various treatment groups. β-HOB =β-hydroxybutyrate; HTS = hypertonic saline.
Table 4. Intensity of Nitric Oxide Synthase, Cytochrome c, and PARP Protein Bands in Response to Various Resuscitative Fluids in Hemorrhagic Shock Rat Liver
This study demonstrates the beneficial effects of pyruvate on liver function, hepatocellular injury, mitochondrial functions, and indicators of apoptosis when compared with another ketone body, β-HOB, or saline solutions. In terms of MAP (40 mmHg), amount of blood shed, base excess, pH, Po2, Pco2, and lactate, there were no differences among the various shock groups, indicating that variation in the intensity of HS was not likely the cause of differences in the outcome of various treatments.
Our data strongly suggest a role for pyruvate in preventing liver damage in HS as indicated by a significant decrease in plasma concentrations of liver enzymes aspartate aminotransferase and alanine aminotransferase in comparison to hypertonic saline or β-HOB treatments. This effect of pyruvate was not related to the osmotic effects of the resuscitative fluids because serum osmolality values at the end of the resuscitation period were similar in all animal groups. However, the protective effect of pyruvate in reducing liver injury could be attributed to its antioxidant properties, because free radical scavengers have shown beneficial effects on liver function after ischemia–reperfusion.20In addition, a significant decrease in lipid peroxidation (accumulation of malondialdehyde in liver) with pyruvate treatment reported in the current study raises the possibility that HS-mediated liver injury is associated with oxidative stress, which can be either a cause or a consequence of mitochondrial dysfunctions.
At low pyruvate concentrations, the availability of pyruvate controls its own decarboxylation, which is not affected by any component of PDH. However, at high pyruvate concentrations, the reaction is strictly controlled by all of the PDH components, especially E-1α.21The amount of pyruvate we have used in the perfusate is of supramaximal level, and it seems that PDH activity in HS is regulated by the content of E-1α protein. We have observed a threefold higher level of E-1α protein in the pyruvate-treated animals when compared with HTS and β-HOB treatment. These observations show either an increased expression or attenuation in loss of the E-1α protein. The activities of PDHtand percentage activation of PDHareported in the control group are comparatively lower than the values reported for controls in the literature. The underlying mechanisms may be the nutritional state of the animal, techniques of the PDH measurement, and the fact that in our study control group, animals were not totally controlled because they were subjected to the trauma of surgery and anesthesia. Although the results of these experiments cannot account for why these differences occurred, they do contribute toward our understanding of pyruvate utilization via regulation of PDH activity in the liver during HS.
In this study, we have reported a significant decrease of PDHtin HTS– and β-HOB–treated animals when compared with pyruvate. This difference in mitochondrial PDHtmay indicate oxidative damage of PDH components because citrate synthase (mitochondrial matrix protein), which is more resistant to oxidative stress, was not affected by control or shock treatments. Our in vivo studies have confirmed a positive relation between the decreased mitochondrial PDHtand the percentage of PARP fragmentation, an indicator of apoptosis, which can be due to increased oxidative stress during HS because pyruvate treatment was able to reverse these changes. In this study, we have provided evidence supporting the notion that increases in PDHaby pyruvate can enhance hepatic energy charge. Our results are in accord with those of Jope and Blass,22who reported that the proportion of PDH in the active form in both brain and liver mitochondria changed inversely with changes in mitochondrial energy charge. We found that inclusion of pyruvate into the resuscitation fluid can stimulate hepatic metabolism by increasing the pool of high-energy adenine nucleotides, and these pyruvate-mediated changes may have subtle effects on mitochondrial dysfunctions leading to cellular energy depletion. These observations can also explain why pyruvate is an effective protective agent and β-HOB is not, because the entry of β-HOB into the cell is controlled by the availability of cellular ATP, which is depleted in hemorrhagic shock, whereas pyruvate can enhance its own oxidation by stimulating PDH activity.23–25
Availability of mitochondrial substrate, oxygen, and an intact ETC are the key components for adequate ATP production. Our results suggest that in the liver, HS can cause poor flux of electrons from the segments after complex I and II, and also, the defect lies in the transfer of electrons at the terminal end of the ETC (complex IV or cytochrome oxidase). The precise mechanism of respiratory control ratio inhibition at complex IV is not known, but it has been suggested (1) that nitric oxide could inhibit the enzyme cytochrome oxidase by competing with oxygen that can result in the formation of harmful molecules ONOO− (nitrates) 26,27and (2) that the loss of cytochrome c is an important substrate for enzyme cytochrome c oxidase (complex IV).
Stimulation of nitric oxide by inducible nitric oxide synthase can also be viewed as a defense mechanism to abate oxidative stress28in HS because, in our control study, although nitric oxide synthase was slightly up-regulated, it did not trigger the apoptotic events such as release of cytochrome c and PARP fragmentation. The release of cytochrome c out of the intramitochondrial space into the cytosol is an important trigger for caspase activation, which leads to the events characteristic of apoptosis. Our data show that pyruvate treatment of HS inhibits cytochrome c release from the mitochondria, thereby preventing up-regulation of indicators of cell death such as PARP fragmentation. Rapid activation of this enzyme depletes the intracellular concentration of its substrate, nicotinamide adenine dinucleotide, thus slowing the rate of glycolysis, electron transport, and subsequently ATP formation. This process can result in cell dysfunction and cell death.29Because of the conflicting role of PARP in apoptosis and necrosis,30,31it is difficult to define the HS-mediated cell death by apoptosis or necrosis, but it is clear from our study that inhibition of PARP fragmentation attenuates liver injury and prevents loss of cellular ATP. Thus, pyruvate also mediates its pharmacologic effects, in part by preventing the cleavage of PARP.
In conclusion, the beneficial effects of pyruvate as an alternate substrate in preventing HS-mediated liver injury can be attributed to increases in cellular energetic levels through its antioxidant and antinitrosyl properties and prevention of mitochondrial damage.
The authors thank Mulchand S. Patel, Ph.D. (Department of Biochemistry, State University of New York at Buffalo, Buffalo, New York), for discussion with pyruvate dehydrogenase complex activity, Michael Graham Espey, Ph.D. (Radiation Biology Branch, National Institutes of Health/National Cancer Institute, Bethesda, Maryland), for discussion with inducible nitric oxide synthase study, and Michael J. Dymond, B.S. (Department of Anesthesiology, Uniformed Services University of the Health Sciences, Bethesda, Maryland), for technical help.
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Mongan PD, Capacchione J, West S, Karaian J, Dubois D, Keneally R, Sharma P: Pyruvate improves redox status and decreases indicators of hepatic apoptosis during hemorrhagic shock in swine. Am J Physiol Heart Circ Physiol 2002; 283:H1634–44
Mongan PD, Fontana JL, Chen R, Bunger R: Intravenous pyruvate prolongs survival during hemorrhagic shock in swine. Am J Physiol 1999; 277:H2253–63
Slovin PN, Huang CJ, Cade JR, Wood CE, Nasiroglu O, Privette M, Orbach P, Skimming JW: Sodium pyruvate is better than sodium chloride as a resuscitation solution in a rodent model of profound hemorrhagic shock. Resuscitation 2001; 50:109–15
Institute of Laboratory Animal Resources: Guide for the Care and Use of Laboratory Animals, 7th edition. Washington, D.C., National Academy Press, 1996
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Bradford MM: A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 1976; 72:248–54
Passonneau JV, Lowry OH: Enzymatic Analysis: A Practical Guide. Totowa, New Jersey, Humana Press, 1993, pp 112–6
Humana Press
Hinman LM, Blass JP: An NADH-linked spectrophotometric assay for pyruvate dehydrogenase complex in crude tissue homogenates. J Biol Chem 1981; 256:6583–6
Srere PA, Matsuoka Y: Inhibition of rat citrate synthase by acetoacetyl CoA and NADH. Biochem Med 1972; 6:262–6
Chance B, Williams GR: Respiratory enzymes in oxidative phosphorylation: VI. The effects of adenosine diphosphate on azide-treated mitochondria. J Biol Chem 1956; 221:477–89
Zhao KS, Junker D, Delano FA, Zweifach BW: Microvascular adjustments during irreversible hemorrhagic shock in rat skeletal muscle. Microvasc Res 1985; 30:143–53
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Modak J, Deckwer WD, Zeng AP: Metabolic control analysis of eucaryotic pyruvate dehydrogenase multienzyme complex. Biotechnol Prog 2002; 18:1157–69
Jope R, Blass JP: A comparison of the regulation of pyruvate dehydrogenase in mitochondria from rat brain and liver. Biochem J 1975; 150:397–403
Hiraide A, Katayama M, Sugimoto H, Yoshioka T, Sugimoto T: Effect of 3-hydroxybutyrate on posttraumatic metabolism in man. Surgery 1991; 109:176–81
Garland PB, Newsholme EA, Randle PJ: Effect of fatty acids, ketone bodies, diabetes and starvation on pyruvate metabolism in rat heart and diaphragm muscle. Nature 1962; 195:381–3
Newsholme EA, Randle PJ, Manchester KL: Inhibition of the phosphofructokinase reaction in perfused rat heart by respiration of ketone bodies, fatty acids and pyruvate. Nature 1962; 193:270–1
Brown GC: Regulation of mitochondrial respiration by nitric oxide inhibition of cytochrome c oxidase. Biochim Biophys Acta 2001; 1504:46–57
Lizasoain I, Moro MA, Knowles RG, Darley-Usmar V, Moncada S: Nitric oxide and peroxynitrite exert distinct effects on mitochondrial respiration which are differentially blocked by glutathione or glucose. Biochem J 1996; 314(pt 3):877–80
Liu TH, Robinson EK, Helmer KS, West SD, Castaneda AA, Chang L, Mercer DW: Does upregulation of inducible nitric oxide synthase play a role in hepatic injury? Shock 2002; 18:549–54
Szabo C, Dawson VL: Role of poly(ADP-ribose) synthetase in inflammation and ischaemia-reperfusion. Trends Pharmacol Sci 1998; 19:287–98
Jaeschke H, Lemasters JJ: Apoptosis versus oncotic necrosis in hepatic ischemia/reperfusion injury. Gastroenterology 2003; 125:1246–57
Leist M, Single B, Kunstle G, Volbracht C, Hentze H, Nicotera P: Apoptosis in the absence of poly-(ADP-ribose) polymerase. Biochem Biophys Res Commun 1997; 233:518–22
Effect of Equiosmolar Solutions of Mannitol versus Hypertonic Saline on Intraoperative Brain Relaxation and Electrolyte Balance
Anesthesiology (November 2007)
Comparison of Equivolume, Equiosmolar Solutions of Mannitol and Hypertonic Saline with or without Furosemide on Brain Water Content in Normal Rats
Anesthesiology (April 2013)
Metabolic Profiling of Hearts Exposed to Sevoflurane and Propofol Reveals Distinct Regulation of Fatty Acid and Glucose Oxidation: CD36 and Pyruvate Dehydrogenase as Key Regulators in Anesthetic-induced Fuel Shift
13 C NMR Metabolomic Evaluation of Immediate and Delayed Mild Hypothermia in Cerebrocortical Slices after Oxygen–Glucose Deprivation
Influence of Hypovolemia on the Pharmacokinetics and Electroencephalographic Effect of γ-Hydroxybutyrate in the Rat


The raphe nuclei (Latin: raphe = 'seam'; nuclei = cell 'clusters'; pronounced RAY-fee) are a moderate-size cluster of nuclei found in the pons part of the hindbrain portion of the brain stem.
Their main function is to release serotonin to the rest of the brain. Selective serotonin reuptake inhibitor (SSRI) antidepressants are believed to act in these nuclei, as well as at their targets.
The raphe nuclei are traditionally considered to be the medial portion of the reticular formation, and they appear as a ridge of cells in the center and most medial portion of the brain stem.
All of these nuclei have fascinating interactions with almost every pertinent portion of the brain, but only a few of them have specifically independent interaction worth exploring in their own right. These select nuclei are discussed as follows.
Overall, the caudal raphe nuclei, including the raphe magnus, pallidus and raphe obscurus, all project towards the spinal cord and brain stem. The more-rostral nuclei, including the raphe pontis, centralis (also called median), dorsal, tend to project towards the brain areas of higher function.
The 7 raphe nuclei receive afferent connections from some of the most fascinating spots in the brain, only to project back to them and alter their processes.
The raphe nuclei have a vast impact upon the central nervous system. The raphe nuclei can be of particular interest to neurologists and psychologists since many of the neurons in the nuclei (but not the majority) are serotonergic, i.e., contain serotonin - a type of monoamine neurotransmitter. Serotonin, also called 5-HT, seems to be the culprit in many of our modern psycho-pharmaceutical problems, such as anorexia, depression, and sleep disorders. It is not the sole culprit in the aforementioned disorders, but it is the area that the pharmacologists know how to affect in the best manner. It is important to note that pharmacology traditionally affects global serotonin levels, while the actions of the raphe nuclei are dependent on the complex interplay between nuclei.
Projections from the raphe nuclei also terminate in the dorsal horn of spinal gray matter where they regulate the release of enkephalins, which inhibit pain sensation.
Currie, David (2005). A Lecture, Higher Brain Function: Activation of the Brain and Levels of Consciousness. East Tennessee State University.
Sari, Youssef (October 2004). Serotonin1B receptors: from protein to physiological function and behavior. Neuroscience & Biobehavioral Reviews 28 (6): 565–582.
↑ (1999) "Understanding the neuroanatomical organization of serotonergic cells in brain provides insight into the functions of this neurotransmitter" George J. Siegel Basic Neurochemistry, Bernard W. Agranoff, Stephen K. Fisher, R. Wayne Albers, Michael D. Uhler, Sixth, Lippincott Williams and Wilkins. ISBN 0-397-51820-X. "In 1964, Dahlstrom and Fuxe (discussed in ), using the Falck-Hillarp technique of histofluorescence, observed that the majority of serotonergic soma are found in cell body groups, which previously had been designated as the raphe nuclei."
↑ Briley, M (October 1993). Neurobiological mechanisms involved in antidepressant therapies. Clin Neuropharmacol 16 (5): 387–400.
↑ BilZ0r, Erowid (2005). Figure 4. Diagram of the human brain showing the divergent serotonergic projections of the raphe nuclei to both cortical and subcortical locations throughout the brain.. (PNG) The Neuropharmacology of Hallucinogens: a technical overview. Erowid Pharmacology Vaults.


Phew. Bit of a mouthful the title, but just look!
Keith Richard, Brian Jones & Charlie Watts. 'Tis a beautiful thing.
circa late 1963 or early '64.
of Stones autographs, then this is it.
We have a special M+ grading for items of this stature: i.e.


On Thu, Nov 01, 2018 at 05:20:57PM +0000, Jay McCanta wrote: > I have the snippets. May I mail them to you directly. I was trying to cleanse them, but I'm afraid I'm changing them too much. Yes, sure.
Sumit, thanks for your answer. Sumit Bose <sbose(a)redhat.com> wrote: > Michael Ströder wrote: >> I'm currently trouble-shooting performance issues on CentOS 6.10 running >> sssd 1.13.3 using sssd-ad as backend. >> >> Enumeration is already disabled. >> >> Also these options were set (DNS names obfuscated): >> ad_enabled_domains = ad1.example.com >> ad_server = dc1.ad1.example.com, dc2.ad1.example.com >> ad_enable_dns_sites = false >> >> Looking sssd still asks various naming contexts of the *many* other >> trusted domains. >> >> Any clue how to effectively disable all "foreign" lookups? > > ad_enabled_domains will ignore requests looking up users and groups from > domains not listed but I guess if a user from domain ad1.example.com is > a member of a group from ad2.example.com this group will still be looked > up. Fortunately every group needed should be in forest ad1.example.com. > Setting 'subdomain_provider = none' should disable all kind of domain > discovery. I couldn't find this in the man pages. Where is this parameter documented? Is it already available in package sssd-1.13.3-60.el6.x86_64 on RHEL/CentOS 6.10? Is it a global or a domain-specific parameter? We tried that (both global and domain), but no change. Still all domains are tried which are found beneath DC=DomainDnsZones,DC=ad1,DC=example,DC=com. My impression is also that this is done recursively leading to sssd contacting 70+ domains... > But depending on the other stetting you might e.g. have to > set ldap_idmap_default_domain_sid to tell SSSD about the domain SID of > the local domain to make automatic id-mapping work. No ID-mapping needed in this case. The MS AD entries contains uidNumber and gidNumber attributes. Ciao, Michael.
HI! I'm currently trouble-shooting performance issues on CentOS 6.10 running sssd 1.13.3 using sssd-ad as backend. Enumeration is already disabled. Also these options were set (DNS names obfuscated): ad_enabled_domains = ad1.example.com ad_server = dc1.ad1.example.com, dc2.ad1.example.com ad_enable_dns_sites = false Looking sssd still asks various naming contexts of the *many* other trusted domains. Any clue how to effectively disable all "foreign" lookups? Ciao, Michael.


text:
Read Next:	Sarah Wright Takes Charge of Sky Cinema After Management Shuffle
January 25, 2019 3:45PM PT
Film Review: 'The Farewell'
Less extroverted than she appeared in 'Crazy Rich Asians,' Awkwafina plays a Chinese-American woman who learns that her grandmother is dying but is forced to keep it a secret in this tragicomic true story from writer-director Lulu Wang.
By Peter Debruge
Chief Film Critic @https://twitter.com/askdebruge?lang=en	FOLLOW
Peter's Most Recent Stories
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CREDIT: Courtesy of Sundance Film Festival
Lulu Wang
Awkwafina, Tzi Ma, Diana Lin
In the past decade or so, film critics have been pressured to put a "spoiler alert" before sharing anything that might potentially undermine people's enjoyment of a movie. But how are people supposed to treat things that might be viewed as "spoilers" in real life? If you knew something that could potentially ruin the rest of someone's time on Earth — like, say, that they had Stage IV lung cancer and less than three months to live — would you be doing them a favor by keeping that information secret? Wouldn't they want to know?
Lulu Wang's "The Farewell" begins with the words "Based on an actual lie," which is a pretty funny way to present a true story about how the Chinese American filmmaker's family decided to spare their grandmother a terminal diagnosis. They don't want to spoil the limited time she has left, and so they conspire to carry on as if everything's normal — except that each of them is saddened by the news, and so they engineer a plan to throw a fake wedding celebration for one of her grandsons in China, allowing everyone to say their goodbyes together. And so, what began as a small lie — "a good lie," in the doctor's words — snowballs into a much more elaborate deception.
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Wang has publicly shared a version of this story before, on NPR's "This American Life" podcast, and here, she puts a tragicomic spin on it, casting Awkwafina (operating at a quarter her potential wattage) as a version of herself: a young woman caught between countries who doesn't seem to identify with American culture but also doesn't understand — or at least agree with — the Chinese custom of protecting relatives from realizing when they're ill. Awkwafina, as we know, is the vivacious "Crazy Rich Asians" co-star who nearly stole the show, and one hopes that the success of that film could spell a certain commercial interest in "The Farewell," even if it's destined to earn just a fraction of the audience.
It practically goes without saying that all families must grapple with versions of these questions when it comes to the illness and loss of loved ones, and what makes "The Farewell" so effective is that in delving into such a specific case, the film invites audiences to reflect on the passing of relatives close to them. Here, no one wants to trouble Nai Nai (Zhao Shuzhen), but that's hardly the only lie-by-omission in the air. Billi (Awkwafina) knows that she's been turned down for a Guggenheim Fellowship but keeps that news to herself. And when she visits her parents in New York City, they initially attempt to hide Nai Nai's diagnosis from her as well. It's only because Billi senses that something's wrong and demands an explanation — a forceful attempt to cut past the charade of propriety, which exists to protect other people's feelings.
Even then, her mom (Diana Lin) and dad (Tzi Ma) initially advise that she stay behind. "You can't hide your emotions," they warn — and they're right. When Billi arrives up at Nai Nai's unannounced (after charging the flight to her already precarious credit cards), her facial expression looks like she's shown up for a funeral, not a wedding — which was supposed to be her cover story. Then again, Nai Nai would have to be a pretty terrible poker player not to see through all the puffy-faced frowns at her table, and yet, she goes along with the charade.
Alternating between situational melancholy and wryly comedic observations, Wang's script spends plenty of time weighing the ethics of the family's collective deception, but never overtly questions whether Nai Nai knows quite how sick she is. And yet, having done the same thing to her late husband (she now shares her home with an elderly man, Mr. Li, who keeps his distance during the family's visit), there's a high likelihood that "the lie" in question is more a case of willful ignorance — the way spouses might overlook clues of their partner's infidelities, or old friends tactfully forget to mention the "work" you've had done. For all involved, the sham wedding ceremony serves to deflect from the depressing situation at hand while giving everyone the kind of closure they need — including Nai Nai, who interrupts an otherwise serious hospital visit to try matchmaking between Billi and her bilingual young doctor.
However universal its basic premise, as a window into another culture — or, for those with Chinese roots, a reflection of one's own — "The Farewell" presents without necessarily explaining behaviors that aren't always intuitive. As a result, mileage will vary according to viewers' personal frame of reference. First- and second-generation immigrant stand-ups love to riff on much of the behavior seen here, which may help white audiences navigate some of the nuances, like what it means to be called "skinny" by one's elders or Nai Nai's trust in tai chi and vitamins over modern medicine.
But "The Farewell" doesn't aim for the kind of big laughs a film such as "The Big Sick" strives to inspire, not does it lean quite so heavily into its more tear-jerky elements. Frankly, there are a hundred ways that Wang could have spun this into a more broadly appealing mainstream comedy, and yet she prefers to play it closer in tone to an independent drama like Ang Lee's "The Wedding Banquet" — which also involved staging a fake nuptial feast in order to keep relatives in the dark, albeit for far different reasons.
Ultimately, it's a smart move to keep things understated, easing us along with funny situations, while subtly weaving a second kind of sadness underneath: Ever so slowly, Wang allows us to realize that Billi's visit is about more than just saying goodbye to her grandmother; it's also a chance to reconnect with the China she left behind at age 3, the fond but hazy memory of which she's been clinging to all this time, never entirely letting herself acclimate to her new home in America. One could read the final scenes as a double farewell — to a woman she loves and a country that has been keeping a kind of secret from her as well: that it's not as perfect as she remembered it.
Film Review: 'The Farewell'
Reviewed at Sundance Film Festival (competing), Jan. 25, 2019. Running time: 100 MIN.
A Ray Prods., Big Beach, Kindred Spirit presentation, in association with Depth of Field, Seesaw. Producers: Daniele Melia, Peter Saraf, Marc Turtletaub, Andrew Miano, Chris Weitz, Jane Zheng, Lulu Wang, Anita Gou. Executive producer: Eddie Rubin. Co-producers: Josh Cohen, Dan Balgoyen.
Crew: Director, writer: Lulu Wang. Camera (color, widescreen): Anna Franquesa Solano. Editors: Michael Taylor, Matthew Friedman. Music: Alex Weston.
With: Awkwafina, Tzi Ma, Diana Lin, Zhao Shuzhen, Lu Hong, Jiang Yongbo, Chen Hanwei.
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Hollywood is heading down the California coast to San Diego because It's time for 2019 Comic-Con International. The annual cosplay celebration officially kicks off tomorrow, July 18, with a preview happening tonight. Here, Variety gives you a guide to this year's parties and activations. Make sure to check back for updates. More Reviews TV Review: [...]
Finance Forum Brings African WIP Into Focus at Durban FilmMart
The 10th edition of the Durban FilmMart, which unspools parallel to the 40th Durban Intl. Film Festival, will feature 10 fiction and 10 documentary works-in-progress taking part in its annual Finance Forum. The leading co-production market on the continent, the Forum brings together producers, distributors, sales agents, broadcasters, funding bodies, and other industry players from across the [...]
Hollywood just can't wait for "The Lion King" to hit theaters. That's because Disney's highly anticipated remake is expected to draw herds of moviegoers at a time when ticket sales are seriously struggling. Box office watchers predict that the studio's grand return to the Pride Lands could become one of this year's biggest hits. "The [...]


text:
using System.Linq;
using QuantConnect.Util;
using System.Collections.Generic;
using QuantConnect.Securities.Option;
using QuantConnect.Securities.Option.StrategyMatcher;

namespace QuantConnect.Securities.Positions
{
    /// <summary>
    /// Class in charge of resolving option strategy groups which will use the <see cref="OptionStrategyPositionGroupBuyingPowerModel"/>
    /// </summary>
    public class OptionStrategyPositionGroupResolver : IPositionGroupResolver
    {
        private readonly SecurityManager _securities;
        private readonly OptionStrategyMatcher _strategyMatcher;

        /// <summary>
        /// Creates the default option strategy group resolver for <see cref="OptionStrategyDefinitions.AllDefinitions"/>
        /// </summary>
        public OptionStrategyPositionGroupResolver(SecurityManager securities)
            : this(securities, OptionStrategyMatcherOptions.ForDefinitions(OptionStrategyDefinitions.AllDefinitions))
        {
        }

        /// <summary>
        /// Creates a custom option strategy group resolver
        /// </summary>
        /// <param name="strategyMatcherOptions">The option strategy matcher options instance to use</param>
        /// <param name="securities">The algorithms securities</param>
        public OptionStrategyPositionGroupResolver(SecurityManager securities, OptionStrategyMatcherOptions strategyMatcherOptions)
        {
            _securities = securities;
            _strategyMatcher = new OptionStrategyMatcher(strategyMatcherOptions);
        }

        /// <summary>
        /// Attempts to group the specified positions into a new <see cref="IPositionGroup"/> using an
        /// appropriate <see cref="IPositionGroupBuyingPowerModel"/> for position groups created via this
        /// resolver.
        /// </summary>
        /// <param name="newPositions">The positions to be grouped</param>
        /// <param name="currentPositions">The currently grouped positions</param>
        /// <param name="group">The grouped positions when this resolver is able to, otherwise null</param>
        /// <returns>True if this resolver can group the specified positions, otherwise false</returns>
        public bool TryGroup(IReadOnlyCollection<IPosition> newPositions, PositionGroupCollection currentPositions, out IPositionGroup @group)
        {
            var impactedGroups = GetImpactedGroups(currentPositions, newPositions);
            var positionsToConsiderInNewGroup = impactedGroups.SelectMany(positionGroup => positionGroup.Positions);

            @group = GetPositionGroups(newPositions.Concat(positionsToConsiderInNewGroup)).Where(positionGroup =>
            {
                // from the resolved position groups we will take those which use our buying power model and which are related to the new positions to be executed
                if (positionGroup.BuyingPowerModel.GetType() == typeof(OptionStrategyPositionGroupBuyingPowerModel))
                {
                    return newPositions.Any(position => positionGroup.TryGetPosition(position.Symbol, out position));
                }
                return false;
            }).FirstOrDefault();

            return @group != null;
        }

        /// <summary>
        /// Resolves the position groups that exist within the specified collection of positions.
        /// </summary>
        /// <param name="positions">The collection of positions</param>
        /// <returns>An enumerable of position groups</returns>
        public PositionGroupCollection Resolve(PositionCollection positions)
        {
            var result = PositionGroupCollection.Empty;

            var groups = GetPositionGroups(positions).ToList();
            if (groups.Count != 0)
            {
                result = new PositionGroupCollection(groups);

                // we are expected to remove any positions which we resolved into a position group
                positions.Remove(result);
            }

            return result;
        }

        /// <summary>
        /// Determines the position groups that would be evaluated for grouping of the specified
        /// positions were passed into the <see cref="Resolve"/> method.
        /// </summary>
        /// <remarks>
        /// This function allows us to determine a set of impacted groups and run the resolver on just
        /// those groups in order to support what-if analysis
        /// </remarks>
        /// <param name="groups">The existing position groups</param>
        /// <param name="positions">The positions being changed</param>
        /// <returns>An enumerable containing the position groups that could be impacted by the specified position changes</returns>
        public IEnumerable<IPositionGroup> GetImpactedGroups(PositionGroupCollection groups, IReadOnlyCollection<IPosition> positions)
        {
            var symbolsSet = positions.Where(position => position.Symbol.SecurityType.HasOptions() || position.Symbol.SecurityType.IsOption())
                .SelectMany(position =>
                {
                    return position.Symbol.HasUnderlying ? new[] { position.Symbol, position.Symbol.Underlying } : new[] { position.Symbol };
                })
                .ToHashSet();

            if (symbolsSet.Count == 0)
            {
                return Enumerable.Empty<IPositionGroup>();
            }

            // will select groups for which we actually hold some security quantity and any of the changed symbols or underlying are in it if they are options
            return groups.Where(group => group.Quantity != 0
                && group.Positions.Any(position1 => symbolsSet.Contains(position1.Symbol)
                    || position1.Symbol.HasUnderlying && position1.Symbol.SecurityType.IsOption() && symbolsSet.Contains(position1.Symbol.Underlying)));
        }

        private IEnumerable<IPositionGroup> GetPositionGroups(IEnumerable<IPosition> positions)
        {
            foreach (var positionsByUnderlying in positions
                .Where(position => position.Symbol.SecurityType.HasOptions() || position.Symbol.SecurityType.IsOption())
                .GroupBy(position => position.Symbol.HasUnderlying? position.Symbol.Underlying : position.Symbol))
            {
                var optionPosition = positionsByUnderlying.FirstOrDefault(position => position.Symbol.SecurityType.IsOption());
                if (optionPosition == null)
                {
                    // if there isn't any option position we aren't really interested, can't create any option strategy!
                    continue;
                }
                var contractMultiplier = (_securities[optionPosition.Symbol].SymbolProperties as OptionSymbolProperties)?.ContractUnitOfTrade ?? 100;

                var optionPositionCollection = OptionPositionCollection.FromPositions(positionsByUnderlying, contractMultiplier);

                var matches = _strategyMatcher.MatchOnce(optionPositionCollection);
                if (matches.Strategies.Count == 0)
                {
                    continue;
                }

                foreach (var matchedStrategy in matches.Strategies)
                {
                    var positionsToGroup = matchedStrategy.OptionLegs
                        .Select(optionLeg => (IPosition)new Position(optionLeg.Symbol, optionLeg.Quantity, 1))
                        .Concat(matchedStrategy.UnderlyingLegs.Select(underlyingLeg => new Position(underlyingLeg.Symbol, underlyingLeg.Quantity * contractMultiplier, 1)))
                        .ToArray();

                    yield return new PositionGroup(new OptionStrategyPositionGroupBuyingPowerModel(matchedStrategy), positionsToGroup);
                }
            }
        }
    }
}

redpajama_set_name: RedPajamaGithub


26/10/2014�� Trailer for the How to Brew All Grain DVD featuring top brewing authors John Palmer and Brad Smith. Available from http://beersmith.com/dvd This video teaches you how... Brewing Fermenting Bottling - Just Brew It. brew pot or a digital kitchen model. How to brew beer A brief guide to get you started making your own home brew Source: How to Brew by John Palmer.
Introduces brewing in a easy step-by-step review that covers the essentials of making good beer. This book includes ingredients, methods, recipes and equipment information.
Water is an essential component for staying alive and one of the foundation elements in the brewing process. Written by How to Brew author John Palmer and professional brewer, Colin Kaminski, this second book in Brewers Publications Brewing Elements Series, Water, will take the mystery out of using water in brewing beer.


text:
UPDATE – Decatur graduation is on
Dan Whisenhunt May 28, 2014
The front steps of Decatur High School. Photo by Dan Whisenhunt
UPDATE: Principal Lauri McKain says graduation plans will proceed as planned. Here is her letter to students and parents:
Families and Guests of Class of 2014 Graduates,
We had a great graduation practice this morning, and I let the seniors know that we will proceed with the graduation ceremony tonight at 7pm. As I stated in earlier communication, if we have to move indoors, only TICKETED guests will get in. Our hope is that we can proceed with the ceremonies outside, but we won't make that call until later. We will look at the radar in the late afternoon and make the best call we can to ensure the safety and comfort of our guests.
Thanks for ensuring the graduates closest family members arrive with a ticket. Others are invited this evening, but will only be granted entry if we proceed in the stadium. Thanks for your understanding and cooperation.
Happy graduation!!
Lauri McKain
Decatur High School | Principal
Decatur High students were scheduled to hold their commencement ceremony on Thursday, May 29, but school officials are considering changing those plans if the weather doesn't cooperate.
Principal Lauri McKain, who is leaving the high school to become City Schools of Decatur's Director of Secondary Education, sent out a note to parents telling them there's a 40 percent chance of thunderstorms in the forecast.
"By tomorrow afternoon, no later than 2 pm, we will make a final call as to whether we will postpone graduation to Friday morning at 10 am," she wrote.
The commencement ceremonies are usually held in the high school's stadium.
"Currently, Friday's weather forecast looks beautiful, so if we postpone we will still be able to have graduation in the stadium," she said. "It's hard to predict when the forecast calls for scattered showers. We will use an abundance of caution and make a determination that errs on the side of our guests' comfort and safety."
Next year, Noel Maloof will become the next Decatur High School principal. Maloof currently is the principal at Dunwoody High.
The High School reports that there are 202 students enrolled in the class of 2014.
Decatur High has one of the highest graduation rates in the state. The school's grad rate in 2013 was 93.9 percent. The school reports that 81 percent of its 2013 graduates are attending a four-year college.
"Approximately 70 percent of students graduate having taken at least one AP course," the DHS website says.
Decatur High School


Comprised of small black basalt and white limestone cobbles Calçada Portuguesa, or Portuguese pavement can be found throughout Portugal's plazas and walkways. The mosaics often reflect their maritime history with stylized ships, waves and sea creatures. Originating in the Middle East and brought to ancient Greece and Rome, the craft was exported beyond Portugal's mainland. In the Azorean archipelago, the volcanic islands were rich with basalt but limestone had to be imported. This resulted in a black field with white pattern whereas on the mainland it was reversed. Examples of Calçada Portuguesa can also be found in the former colonies such as Brazil and Macau. The future of the art and existing mosaics is uncertain as very few calceteiros or craftsmen are left and materials are scarce.