Reliance Communications accused telecom gear maker Ericsson, which is an operational unsecured creditor of the company, of attempting media trial and sensationalising the issue of dues recovery, saying it might put interest of even secured lenders at risk.

The Anil Ambani-led telecom firm, however, said it remained committed to clear dues of Ercisson from spectrum realisation.

“It is deeply regrettable that Ericsson India Private Limited (Ericsson), an operational unsecured creditor, is attempting a trial by media and sensationalising issues, as evidenced in recent media reports,” RCom spokesperson said in a statement.

Ericsson India on Friday moved the Supreme Court seeking initiation of contempt proceedings for the second time against Anil Ambani for allegedly not complying with its order to clear dues of ₹550 crore.

Besides seeking contempt proceedings against the RCom chairman and two others, Ericsson has also sought that they be “detained in civil prison” unless they purge themselves by making the payment.

It also sought directions to the Ministry of Home Affairs to prevent Ambani, Reliance Telecom Ltd chairman Satish Seth and chairperson of Reliance Infratel Ltd. Chhaya Virani from leaving the country.

RCom spokesperson said no notice on recent contempt petition filed by Ericsson, as referred in media reports last week, has been served to it till date and alleged that the Swedish firm is widely sharing the matter with the media and distorting issues.

“Needless to say, the Hon’ble Supreme Court has not even considered the matter till date. Ericsson’s conduct as an unsecured creditor gravely endangers and is at the cost of secured lenders comprising 38 banks and secured creditors including 17 public sector banks and 13 foreign banks,” the spokesperson said.

The crisis-ridden telecom services firm has a debt of over ₹47,000 crore.

RCom said it has taken all required steps towards enabling the settlement and remains fully committed to make the payment to Ericsson from the proceeds of the spectrum sale.

“The Department of Telecom (DoT) approval is pending since August 7, 2018, for which RCom has moved a contempt petition against DoT before the Supreme Court which is listed on Monday, January 7, 2019,” RCom spokesperson said.

Last year, RCom signed a pact with Reliance Jio for the sale of wireless spectrum, tower, fibre and media convergence nodes assets — the proceeds of which were to be used to pare debt.

RCom expects to get ₹975 crore from sale of the spectrum which it has promised to pay dues of ₹550 crore to Ericsson and ₹230 crore to settle dues of minority stakeholder Reliance Infratel.

The DoT has put the spectrum trading between the two companies on hold after Reliance Jio refused to bear the burden on any past dues that RCom owes to the government.

Both RCom and Reliance Jio are learnt to have approached jointly the telecom ministry seeking clarification on the stand of the government over their spectrum trading deal.

In a letter to the DoT on January 3, Jio cited petition of RCom before telecom tribunal TDSAT showing that the petitioners, who are the sellers, have retained the liabilities upon themselves.


events-generated
onOpen: anObject
	"Triggered when the suggestion menu is opened."

	self optionAt: 'open' put: anObject asFunction


Q:

Elmah errorMail not working on production

I am using ELMAH in my MVC3 application and logging the errors to a SQL Database and sending emails.
Locally everything is working fine, and emails are being delivered (using casini). But on the production server (IIS7) no emails are being delivered. I am able however to send emails through code!
  <elmah>
  <errorLog type="Elmah.SqlErrorLog, Elmah" connectionStringName="Elmah.Sql" applicationName="qatar" />
  <errorMail from="errors@gmail.com"
    to="someone@gmail.com"
    subject="Error"
    async="true"
    smtpPort="587"
    smtpServer="smtp.gmail.com"
    enablessl ="true"
    userName="myuser@gmail.com"
    password="mypassword" />

Any clues or direction?

A:

I found the reason, but still can't understand why it works locally:
enablessl should be changed to useSsl


Transplanted human umbilical cord blood mononuclear cells improve left ventricular function through angiogenesis in myocardial infarction.
Human umbilical cord blood contains an abundance of immature stem/progenitor cells, which may participate in the repair of hearts that have been damaged by myocardial infarction (MI). This study aimed to evaluate the effects of human umbilical cord blood mononuclear cells (hUCBC) transplantation on cardiac function and left ventricular remodeling in rat model of MI. Forty-five male Wistar rats were randomized into three groups: MI or control group (n = 15), MI plus cell transplantation (n = 15), and sham group (n = 15). Acute myocardial infarction (AMI) was established by ligating the left anterior descending artery, thereafter, hUCBC were implanted into the marginal area of infarcted myocardium. In MI/control group, DMEM was injected instead of hUCBC following the same protocol. Left ventricular function assessment was carried out by echocardiography and invasive hemodynamic measurements one month post MI. All rats were sacrificed for histological and immunochemical examinations. The transplanted hUCBC survived and engaged in the process of myocardial repair in the host heart. Echocardiography demonstrated that left ventricular function improved significantly in the rats that underwent cell transplantation. Hemodynamic studies found a significantly decreased left ventricular end-diastolic pressure (LVEDP) [(21.08 +/- 8.10) mmHg vs (30.82 +/- 9.59) mmHg, P < 0.05], increase in +dp/dt(max) [(4.29 +/- 1.27) mmHg/ms vs (3.24 +/- 0.75) mmHg/ms, P < 0.05), and increase in -dp/dt(max) [(3.71 +/- 0.79) mmHg/ms vs (3.00 +/- 0.49) mmHg/ms, P < 0.05] among MI group with hUCBC transplantation when compared with MI/control group. Masson's trichrome staining revealed that the collagen density in the left ventricle was significantly lower in rats of transplantation group than that in the MI control groups [(6.33 +/- 2.69)% vs (11.10 +/- 3.75)%, P < 0.01]. Based on immunostaining of alpha-actin, the numbers of microvessels were significantly (P < 0.01) increased at the boundary of infarction site. Similarly higher mRNA expression of vascular endothelial growth factor (VEGF) 164 and VEGF188 were found at 7- and 28-day post cell transplantation in MI group with hUCBC transplantation when compared with MI/control group. Transplanted hUCBC can survive in host myocardium without immunorejection, significantly improve left ventricular remodeling after AMI and promote a higher level of angiogenesis in the infarct zones. All these factors beneficially affect cardiac repair in the setting of MI. Therefore human umbilical cord blood may be potential source for cell-based therapy for AMI.


1935 Alberta general election

The 1935 Alberta general election was the eighth general election for the Province of Alberta, Canada. It was held on August 22, 1935, to elect members of the Legislative Assembly of Alberta.  The newly founded Social Credit Party of Alberta won a sweeping victory, unseating the 14-year government of the United Farmers of Alberta. It was one of only four times that Alberta has changed governments.

Premier John E. Brownlee had resigned on July 10, 1934, when he was sued and found liable for the seduction of a young clerk working in the Attorney-General's office.  Although the verdict was immediately set aside by the presiding judge, the scandal seriously damaged the UFA's reputation among socially conservative Albertans. Provincial Treasurer Richard G. Reid succeeded him, but was unable to change the party's fortunes.

Social Credit won 56 of the 63 seats in the legislature, and over 50% of the popular vote, well beyond even the most optimistic Socred projections. Many of those gains came at the expense of the UFA, which lost all of its seats in one of the worst defeats ever suffered by a provincial government in Canada. Reid and Brownlee, for instance, were heavily defeated by Socred challengers, with Reid being pushed into third place.

The UFA's wipeout happened just a month after the Prince Edward Island Tories lost all 18 of their seats at that year's provincial election. A similar wipeout would not happen again until the 1987 New Brunswick general election, when the governing New Brunswick Tories lost all 39 of their seats.

The Alberta Liberals in this election ran with the tactically fatal slogan, the "rest of Canada can't be wrong"—referring to the popularity of the Liberal Party in the rest of the country. It did not work; they had their seat count cut in half. However, due to the UFA being swept from the legislature, the Liberals wound up as the Official Opposition. The Conservatives lost four of their six seats.

The Socreds' expectations for the election had been so low that they had not even named a formal leader for the campaign. When the newly elected Socred MLAs held their first caucus meeting, the first order of business was to select a leader and premier-designate. The obvious choice was the party's founder and guiding force, Calgary-based Baptist pastor William Aberhart. Persuaded to accept the mantle of leadership, Aberhart was sworn in as premier on September 3.

The turnout of the 1935 election topped 80%, and no election in Alberta has come close to this mark.

This election campaign is seen as the most negative in Alberta's history, with reports of Social Credit members, operating openly and on Aberhart's directives, defacing the campaign signs of opponents and drowning their speeches by honking car horns. Many campaign ads also focused mostly on attacking the opposing parties.

After the 1935 election results were in, newspapers across North America took notice, with the Boston Herald running the headline "Alberta Goes Crazy!".

This shift marked the first in Social Credit's nine consecutive election victories, for a total of 36 years in office–one of the longest unbroken runs in government in the Commonwealth. The UFA never recovered from this wipeout defeat, and withdrew from politics altogether in 1937.

Results
Overall voter turnout was 81.8%, the highest in Alberta history.

Members elected
For complete electoral history, see individual districts

References

See also
 List of Alberta political parties

Category:1935 elections in Canada
1935
Category:1935 in Alberta
Category:August 1935 events


# coding=utf-8
# --------------------------------------------------------------------------
# Copyright (c) Microsoft Corporation. All rights reserved.
# Licensed under the MIT License. See License.txt in the project root for
# license information.
#
# Code generated by Microsoft (R) AutoRest Code Generator.
# Changes may cause incorrect behavior and will be lost if the code is
# regenerated.
# --------------------------------------------------------------------------

from .resource import Resource

class IntegrationAccountMap(Resource):
    """The integration account map.

    Variables are only populated by the server, and will be ignored when
    sending a request.

    All required parameters must be populated in order to send to Azure.

    :ivar id: The resource id.
    :vartype id: str
    :ivar name: Gets the resource name.
    :vartype name: str
    :ivar type: Gets the resource type.
    :vartype type: str
    :param location: The resource location.
    :type location: str
    :param tags: The resource tags.
    :type tags: dict[str, str]
    :param map_type: Required. The map type. Possible values include:
     'NotSpecified', 'Xslt', 'Xslt20', 'Xslt30', 'Liquid'
    :type map_type: str or ~azure.mgmt.logic.models.MapType
    :param parameters_schema: The parameters schema of integration account
     map.
    :type parameters_schema:
     ~azure.mgmt.logic.models.IntegrationAccountMapPropertiesParametersSchema
    :ivar created_time: The created time.
    :vartype created_time: datetime
    :ivar changed_time: The changed time.
    :vartype changed_time: datetime
    :param content: The content.
    :type content: str
    :param content_type: The content type.
    :type content_type: str
    :ivar content_link: The content link.
    :vartype content_link: ~azure.mgmt.logic.models.ContentLink
    :param metadata: The metadata.
    :type metadata: object
    """

    _validation = {
        'id': {'readonly': True},
        'name': {'readonly': True},
        'type': {'readonly': True},
        'map_type': {'required': True},
        'created_time': {'readonly': True},
        'changed_time': {'readonly': True},
        'content_link': {'readonly': True},
    }

    _attribute_map = {
        'id': {'key': 'id', 'type': 'str'},
        'name': {'key': 'name', 'type': 'str'},
        'type': {'key': 'type', 'type': 'str'},
        'location': {'key': 'location', 'type': 'str'},
        'tags': {'key': 'tags', 'type': '{str}'},
        'map_type': {'key': 'properties.mapType', 'type': 'str'},
        'parameters_schema': {'key': 'properties.parametersSchema', 'type': 'IntegrationAccountMapPropertiesParametersSchema'},
        'created_time': {'key': 'properties.createdTime', 'type': 'iso-8601'},
        'changed_time': {'key': 'properties.changedTime', 'type': 'iso-8601'},
        'content': {'key': 'properties.content', 'type': 'str'},
        'content_type': {'key': 'properties.contentType', 'type': 'str'},
        'content_link': {'key': 'properties.contentLink', 'type': 'ContentLink'},
        'metadata': {'key': 'properties.metadata', 'type': 'object'},
    }

    def __init__(self, **kwargs):
        super(IntegrationAccountMap, self).__init__(**kwargs)
        self.map_type = kwargs.get('map_type', None)
        self.parameters_schema = kwargs.get('parameters_schema', None)
        self.created_time = None
        self.changed_time = None
        self.content = kwargs.get('content', None)
        self.content_type = kwargs.get('content_type', None)
        self.content_link = None
        self.metadata = kwargs.get('metadata', None)


Q:

std::move on the return value is causing extra temporary object creation

Why calling get_data2() results in additional c-tor call (g++ 4.7.1 -std=c++11 -O3)?
Code:
#include <iostream>

struct data {
    data(data&&){std::cout << "cted(&&): " << (void*) this << std::endl; }
    data(data const&){std::cout << "cted(c&): " << (void*) this << std::endl; }
    data(){std::cout << "cted(): " << (void*) this << std::endl; }
    ~data(){std::cout << "dted(): " << (void*) this << std::endl; }
};

data create_data() { return data(); }

// with this one the c-tor is called twice
data get_data2() { return std::move(create_data()); }

// with this one the c-tor is called once
data get_data1() { return create_data(); }
int main() { data var = get_data1(); return 0; }

Output with get_data2():
cted(): 0x7ffffb2cd3df
cted(&&): 0x7ffffb2cd40f
dted(): 0x7ffffb2cd3df
dted(): 0x7ffffb2cd40f

Output with get_data1():
cted(): 0x7ffffd7f230f
dted(): 0x7ffffd7f230f

A:

The problem is that the explicit std::move prohibits copy elision, see Why does std::move prevent RVO? Another problem is that the explicit move is also unnecessary because in data create_data() { return data(); } you are already returning an rvalue.
As a side note: A very similar question came up a while ago and it turned out that the way you are using to track object creation is very unreliable, partly because the object is empty, see RVO force compilation error on failure.
Long story short: use only the data create_data() { return data(); } version.


Q:

Less. Авто-компиляция файла less в css, ubuntu 16.04

Как сделать авто-компиляцию файла less в css, чтобы каждый раз не вводить в терминале команду? Ubuntu 16.04, sublime text 3

A:

-- Установите node.js
-- создайте папку в вашем проекте tools, перейдите в новую папку.
-- введите npm install gulp (в консоле, находясь в нужной папке)
вы получите файл package.json
куда пропишите примерно следующее:
{
  "devDependencies": {

    "gulp": "^3.9.1",
    "gulp-clean-css": "^2.0.8",
    "gulp-concat": "^2.6.0",
    "gulp-cssnano": "^2.1.2",
    "gulp-less": "^3.1.0",
    "gulp-minify-css": "^1.2.4",
    "gulp-notify": "^2.2.0",
    "gulp-plumber": "^1.1.0",
    "gulp-rename": "^1.2.2",
    "gulp-sass": "^2.3.1",
    "gulp-uglify": "^1.5.3",
    "gulp-uglifyjs": "^0.6.2",
    "less-plugin-autoprefix": "^1.5.1",
    "pump": "^1.0.1"
  },
  "dependencies": {
    "pageres": "^4.3.0"
  }
}

создайте файл gulpfile.js
туда поместите примерно следующее:
var gulp = require('gulp');
var minifyCss = require('gulp-minify-css');
var concat = require('gulp-concat');
var rename = require('gulp-rename');
var cleanCSS = require("gulp-clean-css");
var less = require("gulp-less");
var LessAutoprefix = require("less-plugin-autoprefix");
var path = require('path');
var plumber = require('gulp-plumber');
var uglify = require('gulp-uglify');
var pump = require('pump');

var autoprefix = new LessAutoprefix({
    browsers: ["last 2 versions"]
});

var path_src = "../где лежат исходники/";
var path_pub = "../../куда помещать готовое/";

var ps = {
    less: [path_src + "путь к лесс файлам/src/**/*.less"],
    less_main: [path_src + "путь к лесс файлам/src/less/main.less"],
    less_out: path_pub + "css/папка с готовыми css",

    less_second_all: [path_src + "custom/**/*.less"],
    //less_second:      [path_src+"custom/main.less"],
    less_second_out: path_pub + "css/custom",

    resetCSS_in: [
        path_src + "reset_css/reset.css",
        path_src + "reset_css/normalize.css"
    ],
    resetCSS_out: path_pub + "css/reset",

    scripts: [path_src + "js/**/*.js"],
    scripts_out: path_pub + "js"
};

gulp.task("minResetCss", function() {
    return gulp.src(ps.resetCSS_in)
        .pipe(concat("reset.css"))
        .pipe(cleanCSS())
        .pipe(rename({
            suffix: ".min"
        }))
        .pipe(gulp.dest(ps.resetCSS_out));
});

gulp.task("mainCssProcessor", function() {
    return gulp.src(ps.less_main)
        .pipe(plumber())
        .pipe(less({
            plugins: [autoprefix]
        }))
        .pipe(concat("main.css"))
        .pipe(cleanCSS({
            advanced: false
        }))
        .pipe(rename({
            suffix: ".min"
        }))
        .pipe(plumber.stop())
        .pipe(gulp.dest(ps.less_out));
});

gulp.task("secondCssProcessor", function() {
    return gulp.src(ps.less_second_all)
        .pipe(plumber())
        .pipe(less({
            plugins: [autoprefix]
        }))
        // .pipe(concat("custom.css"))
        .pipe(cleanCSS({
            advanced: false
        }))
        .pipe(rename({
            suffix: ".min"
        }))
        .pipe(plumber.stop())
        .pipe(gulp.dest(ps.less_second_out));
});

gulp.task("mainScriptProcessor", function(cb) {
    pump([
            gulp.src(ps.scripts),
            // uglify(),
            gulp.dest(ps.scripts_out)
        ],
        cb
    );
});

gulp.task("watcher", function() {
    console.log("====================");
    gulp.watch(ps.less, ["mainCssProcessor"]);
    gulp.watch(ps.less_second_all, ["secondCssProcessor"]);
    gulp.watch(ps.scripts, ["mainScriptProcessor"]);
});

gulp.task("default", ["watcher",
    "minResetCss",
    "mainCssProcessor",
    "secondCssProcessor",
    "mainScriptProcessor"
]);

введите в консоли npm install
после установки, введите gulp в консоле, после чего будут автоматически собираться лесс файлы в css.
В примере используются дополнительные тулзы для минификации и ренейма файлов. + плюс есть таск перекладывающий и могущий минифицировать js файлы. Настройте пути, чутка прочитайте про gulp, и я думаю у вас все получится.
теперь gulp следит за лесс файлами и если вы внесли изменения -- все будет перекомпилироваться автоматом. в случае с больши лесс файлами, на компиляцию может уходить более 5 секунд(css более полумегабайта), учитываете это, иногда вводит в замешательство. В некоторых случаях имеет смыл перезапустить gulp.
Если на этапе установки не вышло установить пакеты. -- удалите файл package.json -- и попробуйте ввести отдельно команды npm install имя_пакета, npm сам создаст этот файл и сам туда все запишет. по поводу npm -- я там далеко не мастер, просто использую эту схему из проекта в проект, и некоторые детали забыл.


1. Technical Field
The present invention relates to a method of generating images for a multi-projection theater and, more particularly, to a method of generating projection images for a multi-projection theater, wherein a source image is mapped to a sphere, virtual planes according to the structure of a multi-projection theater are generated, and the source image on the sphere is projected on the virtual planes.
2. Description of the Related Art
In order to provide audiences with a new three-dimensional effect and immersive experience, a so-called “multi-projection system” different from a known screening system based on a single screen is proposed.
The “multi-projection system” is a technology in which a plurality of projection surfaces is disposed on the periphery of stands (e.g., the front, the left, the right, the ceiling, and the bottom) and an image having a three-dimensional effect and immersive experience can be provided to audiences although a 3D technology is not applied to the image itself.
Such a multi-projection system may be constructed in different structures depending on the conditions of theaters because a plurality of projection surfaces is disposed in various directions around stands. More specifically, a plurality of projection surfaces disposed in each theater may have different disposition angles, different areas, etc. depending on the conditions of each theater. Accordingly, it is essential to taken into consideration the structural characteristics of each theater in a process of generating projection images (i.e., images projected on a plurality of projection surfaces) for such a multi-projection system.
However, there is no prior art capable of generating projection images by taking the structure of a theater into consideration. The reason for this is that a need to generate projection images by taking into consideration the structural characteristics of a theater is low because a conventional theater includes only a single projection surface disposed at the front as described above.
Accordingly, there is a need for a technology capable of generating projection images for a theater by taking into consideration the structural characteristics of the theater.
The present invention has been invented based on such a technical background and also has been invented to satisfy the aforementioned technical needs and to provide additional technical elements that may not be easily invented by those skilled in the art to which the present invention pertains. Accordingly, the present invention should not be construed as being limited by the technical background.


Friday, October 14, 2011

If you hear actions to increase the capital base for French and German banks, expect Greek default soon.

When multinationals call East Asia home, they will invest enough to treat East Asian consumers like their western counterparts. The investment process will lift the salaries of the Asian workers to the western level. They then have the consumption power to make the investment pay off. This would be a gigantic project to build a new global economy.

2011-09-26 / Andy Xie

summary

------------

The global crisis has turned into a chronicle one. The eurozone's response to its recurring debt crisis is another bandaid that would ease the pain for the time being. So are the expected Fed's QE 3 and the Obama Administration's $447 billion fiscal stimulus proposal. The structural headwinds and debt hangover plague the global economy. Neither can be solved quickly.

The expectation that the eurozone debt crisis would be worse than the US's crisis is wrong. Eurozone's indebtedness and fiscal deficits are much lower than the US's. When the region's governments run out of resources to contain the crisis, they will allow the ECB to print money to ease the crisis. In short, the eurozone crisis lasts but doesn't explode like the US's subprime crisis.

The bandaid measures by the eurozone and the US may spark a rally in risk assets like stocks. Like the previous rallies, this one would be relatively short, possibly for three months. The recurring crisis will generate short cycles in asset markets.

The global economy is on a path of slow growth-1-2% in the developed world and 4-6% in the emerging world, while inflation would be 3-5% for the former and 5-10% for the later. This stagflation world may last for a decade.

Betting on inflation is likely the best investment approach in this decade. While gold is consolidating, its bull market isn't over. Energy and agriculture are similarly on bullish trends. Multinational companies that sell to consumers in emerging markets may do well too.

Greek tragedy

-------------------

'History always repeats itself twice: first time tragedy, second time farce', so said Karl Marx. What if it repeats the third time? It could only be described as a Greek tragedy.

The expectation of an imminent Greek default set off another round of turmoil in the world's financial markets. The fear was based on its contagion through the eurozone banking system. The eurozone banks, especially French and German ones, are loaded with Greek bonds. The fear manifests through (1) the banks' unwillingness to lend to each other and (2) their share prices plummeting. Their collasping share prices reminded investors of what occurred before the Lehman crash, which sent stocks falling everywhere.

The irony is that this is mainly about accounting. The Greek bond prices already predict a Greek default almost for sure. But, the accounting rules allow the banks not to account for the losses until Greece actually declares default. Hence, they don't have to raise capital yet, even though they may already be bankrupt. The dance around Greece's debt crisis by other European countries is really about this accounting fiction.

Greece is in a vicious cycle. As it cuts spending to decrease fiscal deficit, the economy shrinks, and the tax revenue falls even more. Hence, it cannot meet the deficit target spelled out in the second EU assistance package. The EU has postponed its decision on the next installment of €8 billion from the second aid package to next month. The money is necessary for Greece to avoid default. It is unlikely that Greece will be able to meet that. If not, the EU has to decide if to go easier on Greece or let it go.

The market is expecting default. Greece's default is inevitable. The debt hole is just too deep for Greece to climb out. I'm not sure that it would be next month. The European banks may not be ready for it yet. French and German governments have to take actions to strengthen their banks first. Otherwise, the resulting chaos would be too damaging for Europe. If you hear actions to increase the capital base for French and German banks, expect Greek default soon.

The lesson on debt trap

--------------------------------

A financial crisis results from a mistake by the financial markets before. In the case of Europe the bond market gave Germany's interest rate to Southern European economies in anticipation of and after the establishment of euro. It led to excessive demand fueled by credit in the later and supercharged Germany's exports. The circle was completed by recycling Germany's trade surpluses into the cash-short Southern European economies through London-centered financial markets. It is one more piece of evidence that today's financial markets, despite ample liquidity and 24 hour trading cycle, are highly inefficient and can cause calamity on a global scale and frequently.

The same markets are demanding clarity on how the Southern European economies could repay their mountains of debts. As they haven't responded fast enough to satisfy the markets, the interest rates on their bonds have surged. At a high enough interest rate, any debtor is bankrupt. The Southern European economies have been travelling down this path of self fulfilling bankruptcy.

For example, Italy's national debt is 120% of GDP. When interest rate is 3%, it seems bearable, and the market is not worried and willing to roll over the principal. When the interest rate is 6%, the interest burden becomes unbearable, and the market isn't willing to roll over the principal anymore. The vicious cycle could lead to bankruptcy quickly.

This is a lesson for any country that depends too much on financial markets. The money may come easy. But, when you need it most, they turn on you. The cost could be catastrophic. The persistent high interest rate could decapitalize an economy like Italy's and turn it into a developing country.

Chinese local governments have been travelling down the same path in the past few years. They have borrowed heavily on the expectation that ever rising land price would allow them to pay off the debts. Such expectation is alive despite the collapsing property markets around the world.

Most local governments in China may have trouble paying off their debts. Urbanization has economies of scale. Only a small number of cities are in a virtuous cycle of growing population, rising employment, and more financing for infrastructure investment. Many cities that are investing heavily and hoping to attract population and employment will be disappointed.

Structural headwinds

----------------------------

The mistake by the financial markets fueled the debt bubble in the developed world. It was tolerated because the developed economies were losing competitiveness against the developing world. The bubble conveniently filled an employment shortfall due to globalization. In a crisis our attention is focused on the past like the accumulated debt load. A more challenging issue is how the underlying structural problems could be resolved. Otherwise, the crisis will never end.

Europe and the United State face the same problem. Globalization is equalizing wages for similar jobs. In the past, where one was born would mostly decide his or her living standard. Information revolution and globalization now allow global companies to hire people from everywhere to do work for everywhere too. For the world as a whole this increases efficiency, i.e., the whole pie becomes bigger. The biggest fallout is how it affects the workers in the developed world who compete against their counterparts in the emerging world.

Southern European economies depended on labor intensive industries in the division of labor within Europe. It was all fine until globalization came along. The debt bubble allowed them to maintain living standard through debt financed bubble activities to turn debt into income. Greece's bubble was in government generated employment financed by government issued bonds. Spain's property bubble turned foreign liquidity into its labor income.

The uncertainty due to Europe's debt crisis has been with us for a year and a half and seems destined to last for a long time to come. When France and Germany decide to recapitalize their banks, the uncertainty will diminish for the time being. But, the need for lasting fiscal austerity will trigger political uncertainties for years to come, negatively affecting the global economy and financial markets.

Rising productivity in emerging economies and an aging population at home have sapped Europe's growth potential. It needs to be frugal to balance its books, i.e., Europeans must accept a significant reduction in living standard. The reduction needs to come from less welfare benefits, higher taxes, or rising retirement age. Germany has done that in the past decade. Other countries must follow. This seems extremely difficult to achieve. The populaces in many eurzone countries refuse to accept cutbacks and put pressure on their governments to find another way out. The alternative is more debt, if the market agrees. Otherwise, more crises.

The United States is similar to Europe. Part of its economy is like Southern Europe's. Its high unemployment rate reflects more the globalization reality than insufficient demand at home. The stimulus attempt by the Obama Administration won't solve the problem.

Sluggish growth and high unemployment rate are the twin phenomena to accompany the developed economies in this decade. Even Germany may not escape this fate. Austerity rather than stimulus is likely the policy direction for the developed economies.

The economic difficulties that the developed economies face in this decade may lead to social instability. What occurred in London could spread to other major western cities in this decade. It will make their policy response to fiscal deficits difficult. This is why the current crisis will last for a long time to come.

The world is still expecting the global economy to recover like before. It won't happen. If the global economy is to have another up cycle, it must be led by emerging economies. But, they have been growing on exports before. Unless they change their growth model, the global economy will remain sluggish.

The developed economies account for 70% of the global economy and the emerging economies 30% in current exchange rates. In purchasing power parity the two are about the same size. The export model for the emerging economies doesn't work like before because the emerging economies are so much bigger than before.

Emerging economies must shift from export to consumption-led for the global economy to regain momentum. But, the income level in the emerging economies is still too low to shift to the consumption model. One shortcut is to lift the income level quickly through attracting multinationals to invest massively. Multinational corporations have become unsettled in Europe and the US by the rising political risk and sluggish demand. They are incentivized to find a new home. East Asia, China in particular, is in a position to become the new home for multinationals.

Germany, East Asia, and oil exporters run large trade surpluses. I suspect that Germany's surplus will dwindle, as the European debt crisis saps the demand from its major trading partners. Oil export countries don't have the sophisticated economies to make multinationals root there. Only East Asia has the labor force, growth potential, and capital surplus to attract multinationals.

When multinationals call East Asia home, they will invest enough to treat East Asian consumers like their western counterparts. The investment process will lift the salaries of the Asian workers to the western level. They then have the consumption power to make the investment pay off. This would be a gigantic project to build a new global economy.

China must play a leading role in this process. As the second largest economy and the largest trading nation in the world, it has the ability and responsibility to do so. As I wrote in this page before, China must recycle its trade surplus into the global economy in the right way for it to function well. Attracting MNCs to China's capital market is a first and necessary step for the global economy to recover. It is in China's interest to take this critical step towards a new global economy.

1 comments:

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A playoff berth is more an expectation than a hope for the Maple Leafs this season, and more than anybody, it's coach Ron Wilson who is under the gun to produce.

Head coach Ron Wilson, pictured at practice on Wednesday, thinks the current group of Leaf players is the best he's had since arriving in Toronto. "This is the clearly the deepest team and most skilled team we’ve had,” he says. “It’s an entirely different feeling."

By:Kevin McGranSports Reporter, Published on Wed Oct 05 2011

Tyler Bozak was asked on Twitter the other day just how excited he was, on a scale of 1 to 10, to start the season.

His answer was simple and honest: “Those numbers aren’t high enough.”

It’s off the scale how much this team can’t wait to play Montreal on Thursday night to open the season.

“We’ve been waiting for this moment for a long time,” Bozak said after practice Wednesday. “It’s been too long since we’ve had a real game. Winning like we did at the end of the year, we kind of got the feel of what it’s like to win a lot of games.”

There hasn’t been a Maple Leafs season with this much anticipation in quite some time.

Coach Ron Wilson, when asked to compare this group of Leafs to the previous three teams he coached coming out of camp, believes it’s the best one yet.

“This is the clearly the deepest team and most skilled team we’ve had,” said Wilson. “It’s an entirely different feeling.

“We started well last year, the first four games. What makes us feel really good this year is we believe in our goaltending, probably more than we ever have. Our back end is much more mobile than it’s been since I got here.

“Those two factors right there, keeping pucks out of your net and getting the puck out of the zone as quickly as possible, are huge.”

That said, Wilson declined to offer a guarantee of making the playoffs. Paul Maurice did in 2007. He was fired in 2008.

“I never make any guarantees,” said Wilson.

Nonetheless, in Year 2.5 of GM Brian Burke’s rebuild, a playoff berth is more an expectation than a hope. And more than anybody, it’s Wilson who is on the hot seat. He’s in the final year of his contract and Burke — quite on purpose — did not offer him an extension.

In Burke’s mind, he’s been loyal to his coach, friend and fellow Providence College alum. Burke has stuck with Wilson through losing streaks and bad times and repeated seasons of missing the playoffs.

Burke fired a warning shot across Wilson’s bow in the summer, forcing the coach to fire two of his assistants, Tim Hunter and Keith Acton. Wilson replaced them with Greg Cronin and Scott Gordon, himself a former NHL coach.

The team is likely to start the season with both Tim Connolly and Nazem Kadri on the injured reserve list. Either can come off at any time, but both were listed as IR on the team’s website Wednesday. And a roster move would be required to open up a spot.

The arrival of centre David Steckel forced the team to assign Joey Crabb to the Marlies.

A bad start for this team — say through the first 20 games —and the calls for Wilson’s ouster will begin.

“That’s the last thing on our mind,” said defenceman Luke Schenn. “If things were to go wrong, the guys in the room and on the ice are a lot more accountable than the coach.”

His players don’t want a coaching change.

“He’s done a good job here,” Bozak said of Wilson.

Schenn, who’s been a Leaf for as long as Wilson has been the team’s coach, disagrees that Wilson is under the gun.

“Maybe if we had a bad finish to the end of the year, maybe there’d be a lot more heat on him,” said Schenn. “But we finished off good and part of that is because of the coach.

“They’ve been teaching us lots. There has been a lot of turnover. Burke and the management have stressed to us and to the fans and the media that they’re loyal to the coach.”

All that turnover is another reason the heat is on. Burke has added the kind of players Wilson wants. Steckel, the best faceoff man in the league, is in to help the penalty kill. John-Michael Liles is in to help the power play.

Special teams — the coach’s forte with his former clubs — have been a perennial Leaf weakness under Wilson. It’s time for that to stop.

“We’re going to work on (special teams) all the time, every day, and try to make ourselves better,” said Wilson. “Your power play and your penalty kill have to be adjusting all the time. Other teams are seeing what you’re doing on the special teams all the time and you have to add a different wrinkle to negate their advanced scouting.”

A good start, say the players, will be beneficial to all.

“We owe it to the fans, and everyone, and to ourselves to get off to a good start,” said Schenn. “That’s one of the bonuses — he (Wilson) would get rewarded because of it. We’re all one big family, one big group and we all want to do well.”

More on thestar.com

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Hamburg Harbour Pilots, Elbe River Pilots and the Pilots of NOK I already pratice their manoevres here at MTC in Hamburg successfully since 2009. We are now offering the training course "S007 - Shiphandling for Pilots" for pilots all around the globe.

We are providing training for officers and engineers serving on ships, using state of the art equipment and simulators.

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VTS Simulator Training for Global Tech I

More and more wind farms uprise in the Baltic and North sea. It is one of the official stipulations by the authorities for the offshore operating companies to permanently monitor and observe these offshore wind farms and the traffic around it ...


Q:

Face Recognition in Videos with OpenCV3 gives Unhandled exception (opencv_core310.dll)

Below code used to recognize face which i got from the below link
http://docs.opencv.org/3.0-beta/modules/face/doc/facerec/tutorial/facerec_video_recognition.html.
The only modification I've done is: Instead of using command line arguments to provide CSV and Cascade classifier paths, I have given them directly in the code.
Problem
Exception thrown at 0x00007FFDD0C0E09B (opencv_core310.dll) in facerecognization.exe: 0xC0000005: Access violation reading location 0xFFFFFFFFFFFFFFFF.
i am getting access violation problem as shown .
To solve problem i tried to
1)to debug step by step i get the exception when code reaches this line
CascadeClassifier haar_cascade;  after model->train
2)i reinstalled twice everything ie opencv_contru but again i same problem
3) i initially used at&t database as at.txt and since it use .pgm file (windows doesnt recognize and when i ran same problem),so i created my own data base with .jpg ie facecsv.txt(my database with 10 sets) but same problem persist
4) i changed haarcascade_frontalface_default.xml to other .xml files but still the same problem
5)dll is not a problem as configured it twice
code
#include "opencv2/core.hpp"
#include "opencv2/face.hpp"
#include "opencv2/highgui.hpp"
#include "opencv2/imgproc.hpp"
#include "opencv2/objdetect.hpp"

#include <iostream>
#include <fstream>
#include <sstream>

using namespace cv;
using namespace cv::face;
using namespace std;
int abc;

static void read_csv(const string& filename, vector<Mat>& images, vector<int>& labels, char separator = ';') {
    std::ifstream file(filename.c_str(), ifstream::in);
    if (!file) {
        string error_message = "No valid input file was given, please check the given filename.";
        CV_Error(CV_StsBadArg, error_message);
    }
    string line, path, classlabel;
    while (getline(file, line)) {
        stringstream liness(line);
        getline(liness, path, separator);
        getline(liness, classlabel);
        if (!path.empty() && !classlabel.empty()) {
            images.push_back(imread(path, 0));
            labels.push_back(atoi(classlabel.c_str()));
        }
    }
}

int main(int argc, const char *argv[]) {

    // Get the path to your CSV:
    string fn_haar = "C:\\OpenCV-3.1.0\\opencv\\build2\\install\\etc\\haarcascades\\haarcascade_frontalface_default.xml";
    string fn_csv = "C:\\OpenCV-3.1.0\\facedata\\facecsv.txt";
    int deviceId = 0;
    // These vectors hold the images and corresponding labels:
    vector<Mat> images;
    vector<int> labels;
    // Read in the data (fails if no valid input filename is given, but you'll get an error message):
    try {
        read_csv(fn_csv, images, labels);
    }
    catch (cv::Exception& e) {
        cerr << "Error opening file \"" << fn_csv << "\". Reason: " << e.msg << endl;
        // nothing more we can do

        cin >> abc;
        exit(1);
    }
    // Get the height from the first image. We'll need this
    // later in code to reshape the images to their original
    // size AND we need to reshape incoming faces to this size:
    int im_width = images[0].cols;
    int im_height = images[0].rows;
    // Create a FaceRecognizer and train it on the given images:
    Ptr<FaceRecognizer> model = createFisherFaceRecognizer();
    model->train(images, labels);
    // That's it for learning the Face Recognition model. You now
    // need to create the classifier for the task of Face Detection.
    // We are going to use the haar cascade you have specified in the
    // command line arguments:
    //
    CascadeClassifier haar_cascade;
    haar_cascade.load(fn_haar);
    // Get a handle to the Video device:
    VideoCapture cap(deviceId);
    // Check if we can use this device at all:
    if (!cap.isOpened()) {
        cerr << "Capture Device ID " << deviceId << "cannot be opened." << endl;
        return -1;
    }
    // Holds the current frame from the Video device:
    Mat frame;
    for (;;) {
        cap >> frame;
        // Clone the current frame:
        Mat original = frame.clone();
        // Convert the current frame to grayscale:
        Mat gray;
        cvtColor(original, gray, CV_BGR2GRAY);
        // Find the faces in the frame:
        vector< Rect_<int> > faces;
        haar_cascade.detectMultiScale(gray, faces);
        // At this point you have the position of the faces in
        // faces. Now we'll get the faces, make a prediction and
        // annotate it in the video. Cool or what?
        for (int i = 0; i < faces.size(); i++) {
            // Process face by face:
            Rect face_i = faces[i];
            // Crop the face from the image. So simple with OpenCV C++:
            Mat face = gray(face_i);
            // Resizing the face is necessary for Eigenfaces and Fisherfaces. You can easily
            // verify this, by reading through the face recognition tutorial coming with OpenCV.
            // Resizing IS NOT NEEDED for Local Binary Patterns Histograms, so preparing the
            // input data really depends on the algorithm used.
            //
            // I strongly encourage you to play around with the algorithms. See which work best
            // in your scenario, LBPH should always be a contender for robust face recognition.
            //
            // Since I am showing the Fisherfaces algorithm here, I also show how to resize the
            // face you have just found:
            Mat face_resized;
            cv::resize(face, face_resized, Size(im_width, im_height), 1.0, 1.0, INTER_CUBIC);
            // Now perform the prediction, see how easy that is:
            int prediction = model->predict(face_resized);
            // And finally write all we've found out to the original image!
            // First of all draw a green rectangle around the detected face:
            rectangle(original, face_i, CV_RGB(0, 255, 0), 1);
            // Create the text we will annotate the box with:
            string box_text = format("Prediction = %d", prediction);
            // Calculate the position for annotated text (make sure we don't
            // put illegal values in there):
            int pos_x = std::max(face_i.tl().x - 10, 0);
            int pos_y = std::max(face_i.tl().y - 10, 0);
            // And now put it into the image:
            putText(original, box_text, Point(pos_x, pos_y), FONT_HERSHEY_PLAIN, 1.0, CV_RGB(0, 255, 0), 2.0);
        }
        // Show the result:
        imshow("face_recognizer", original);
        // And display it:
        char key = (char)waitKey(20);
        // Exit this loop on escape:
        if (key == 27)
            break;
    }
    return 0;
}

my database looks like
facecsv.txt
C:\OpenCV-3.1.0\facedata\Angelina Jolie/Angelina_1.jpg;0
C:\OpenCV-3.1.0\facedata\Angelina Jolie/Angelina_2.jpg;0
C:\OpenCV-3.1.0\facedata\Angelina Jolie/angelina_3.jpg;0
C:\OpenCV-3.1.0\facedata\Arnold Schwarzenegger/Arnold_1.jpg;1
C:\OpenCV-3.1.0\facedata\Arnold Schwarzenegger/Arnold_2.jpg;1
C:\OpenCV-3.1.0\facedata\Arnold Schwarzenegger/Arnold_3.jpg;1
C:\OpenCV-3.1.0\facedata\Brad Pitt/Brad_1.jpg;2
C:\OpenCV-3.1.0\facedata\Brad Pitt/Brad_2.jpg;2
C:\OpenCV-3.1.0\facedata\Brad Pitt/Brad_3.jpg;2
C:\OpenCV-3.1.0\facedata\Emma Watson/Emma_1.jpg;3
C:\OpenCV-3.1.0\facedata\Emma Watson/Emma_2.jpg;3
C:\OpenCV-3.1.0\facedata\Emma Watson/Emma_3.jpg;3
C:\OpenCV-3.1.0\facedata\Justin Timberlake/Justin_1.jpg;4
C:\OpenCV-3.1.0\facedata\Justin Timberlake/Justin_2.jpg;4
C:\OpenCV-3.1.0\facedata\Justin Timberlake/Justin_3.jpg;4
C:\OpenCV-3.1.0\facedata\Katy Perry/Katy_1.jpg;5
C:\OpenCV-3.1.0\facedata\Katy Perry/Katy_2.jpg;5
C:\OpenCV-3.1.0\facedata\Katy Perry/Katy_3.jpg;5
C:\OpenCV-3.1.0\facedata\Keanu Reeves/Keanu_1.jpg;6
C:\OpenCV-3.1.0\facedata\Keanu Reeves/Keanu_2.jpg;6
C:\OpenCV-3.1.0\facedata\Keanu Reeves/Keanu_3.jpg;6
C:\OpenCV-3.1.0\facedata\Nisarg/Nisarg_1.jpg;7
C:\OpenCV-3.1.0\facedata\Nisarg/Nisarg_2.jpg;7
C:\OpenCV-3.1.0\facedata\Nisarg/Nisarg_3.jpg;7
C:\OpenCV-3.1.0\facedata\Nisarg/Nisarg_4.jpg;7
C:\OpenCV-3.1.0\facedata\Nisarg/Nisarg_5.jpg;7
C:\OpenCV-3.1.0\facedata\Tom Cruise/Tom_1.jpg;8
C:\OpenCV-3.1.0\facedata\Tom Cruise/Tom_2.jpg;8
C:\OpenCV-3.1.0\facedata\Tom Cruise/Tom_3.jpg;8

and at&t database
C:\OpenCV-3.1.0\att_faces (1)\database\s1/1.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/10.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/2.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/3.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/4.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/5.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/6.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/7.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/8.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s1/9.pgm;0
C:\OpenCV-3.1.0\att_faces (1)\database\s10/1.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/10.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/2.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/3.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/4.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/5.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/6.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/7.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/8.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s10/9.pgm;1
C:\OpenCV-3.1.0\att_faces (1)\database\s11/1.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/10.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/2.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/3.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/4.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/5.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/6.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/7.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/8.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s11/9.pgm;2
C:\OpenCV-3.1.0\att_faces (1)\database\s12/1.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/10.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/2.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/3.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/4.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/5.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/6.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/7.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/8.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s12/9.pgm;3
C:\OpenCV-3.1.0\att_faces (1)\database\s13/1.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/10.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/2.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/3.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/4.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/5.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/6.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/7.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/8.pgm;4
C:\OpenCV-3.1.0\att_faces (1)\database\s13/9.pgm;4
and it goes upto 40 test sample s1 to s40

Problem
Exception thrown at 0x00007FFDD0C0E09B (opencv_core310.dll) in facerecognization.exe: 0xC0000005: Access violation reading location 0xFFFFFFFFFFFFFFFF.

I am using Windows 10 64-bit with Visual Studio 2015 and OpenCV 3.1.0 and opencv_contrib-master (Build Configuration: x64-Debug)
Their is similar question here Face Recognition in Video using OpenCV gives unhandled exception
but he used only one 1 label but i use more than 8 that didn't solved my problem

A:

I am using Windows 10 64-bit with Visual Studio 2015 and OpenCV 3.1.0 and opencv_contrib-master (Build Configuration: x64-Debug)

You're linking to release libraries, but you're in debug mode.
In debug you need to link to OpenCV libraries with the trailing "d": opencv_<module><version>d.lib.
So in your case to: opencv_core310d.lib, etc...


Mycobacteria: the global disease burden {#S001}
=======================================

Mycobacteria belong to the genus *Mycobacterium*, which is the only genus representing the *Mycobacteriaceae* family (order: *Actinomycetales*; class: *Actinobacteria*). The genus was proposed in 1896, to include two species namely tubercle bacillus (now known as *Mycobacterium tuberculosis*) and leprosy bacillus (*Mycobacterium leprae*) \[[@CIT0001]\]. Currently, there are \>190 distinct species of *Mycobacterium* genus, some of which are economically and clinically important pathogens of humans or animals \[[@CIT0002]\].

Among the human mycobacterial infections, those caused by *M. tuberculosis* (tuberculosis), *M. leprae* (leprosy) and *Mycobacterium abscessus* (chronic pulmonary infections) pose a public health concern. Mycobacterial infections affect ∼11--14 million people each year globally and tuberculosis (TB) alone is responsible for ∼1.3 million deaths each year, of which 374,000 were people living with HIV/AIDS. In 2016, 10.4 million people living with HIV/AIDS, were diagnosed with TB \[[@CIT0003]\].

In case of *M. leprae* infections, the World Health Organization (WHO) reported ∼200,000 new cases of leprosy each year (<http://www.who.int/wer/2017/wer9235/en/>). In 2016, 214,783 new cases of leprosy were reported globally. India reported the highest number (135,485) and Brazil 25,218 cases. Lack of effective early diagnostic tool(s), vaccines and limited understanding of the patterns of transmission contribute to the ongoing incidence.

In addition to TB and leprosy, Non-Tuberculous Mycobacteria (NTM), such as *M. abscessus complex,* are emerging worldwide as the cause of chronic pulmonary infections \[[@CIT0004],[@CIT0005]\]. Incidence rates of pulmonary infections due to NTM, vary greatly with geographical regions. The global incidence remained 1.0--1.8 in a population of 100,000, however, these rates are much higher in the US, Western Pacific and Canada \[[@CIT0005]\]. The prevalence of NTMs has increased from 1.3% \[[@CIT0006]\] to 32.7% in Colorado, in cystic fibrosis patients \[[@CIT0007]\].

The growing challenge of antimicrobial resistance {#S001-S2001}
-------------------------------------------------

The past few decades have seen a "discovery void" pertaining to antibacterial drug development, where very few new molecules have been patented or approved for clinical use \[[@CIT0008]\]. This is particularly true for drug discovery against mycobacteria, where no new drugs that were specifically developed for this purpose reached the clinic after the early 1960s until recently \[[@CIT0009]\]. Importantly, the emergence of resistance towards first-line and second-line drugs poses additional challenges to the development of suitable drugs in each of *M. tuberculosis*, *M. leprae* and *M. abscessus*. The approval of drugs and causes of resistance have been systematically reviewed for *M. tuberculosis* \[[@CIT0010],[@CIT0011]\], *M. abscessus* \[[@CIT0012]\] and *M. leprae* \[[@CIT0013]\]. Antibiotic resistance can arise due to physiological, intrinsic or acquired factors \[[@CIT0010],[@CIT0014]\]. The intrinsic resistance is attributed to cell-wall permeability, drug efflux systems, drug targets with low affinity and enzymes that neutralize drugs in the cytoplasm. The acquired resistance is conferred by chromosomal mutations.

Although the TB mortality rate is falling at ∼3% per year globally, drug-resistant TB remains a continuing threat \[[@CIT0003]\]. The spread of drug-resistant strains of TB (mono-resistant, multidrug-resistant, extensively drug-resistant and totally drug-resistant) is alarmingly high and accounted for 490,000 cases of multidrug-resistant TB (MDR-TB) in 2016. Around 47% of the MDR-TB cases are reported in Southeast Asia \[[@CIT0015]\]. Increase in isoniazid-susceptible rifampin resistance was also noted in 2016, with 110,000 cases globally. The global burden of MDR-TB has recently increased by \>20% annually \[[@CIT0016]\] and the treatment is successful in only 50% of the MDR-TB cases. With the ongoing transmission of the drug-resistant strains of *M. tuberculosis* in communities, it is increasingly important to research novel drug targets and identify potential leads that can be expanded to new drugs.

Drug resistance in leprosy is diagnosed by the mouse footpad method, which is time and labour-intensive. Alternatively, mutations can be detected in drug-resistance-determining regions of *M. leprae* drug targets such as dihydropteroate synthase (for the drug: dapsone), β subunit of RNA polymerase (rifampin) and subunit A of DNA gyrase (ofloxacin). As drug resistance has been suspected only in cases that self-report at the hospital as a result of reactivation or relapse in leprosy, the numbers are currently low; however, these may increase if a field-based surveillance system is implemented.

*M. abscessus* is naturally resistant to many first-line antimicrobials, including all the current TB drugs. The acquired resistance to aminoglycosides is known to be due to mutations in genes such as *rrs* \[[@CIT0012]\]. Likewise, mutations in 23S rRNA and genes such as *erm(41)* and *rrl* are known to cause macrolide resistance in *M. abscessus* \[[@CIT0017]\].

Thus, emergence of antibiotic-resistant strains and rapid spread due to globalization poses a serious challenge to the global health \[[@CIT0018]\]. Genomics has served as an important milestone in bacterial drug discovery \[[@CIT0019],[@CIT0020]\]. It is now possible to understand causes of emergence of antibiotic-resistant strains and to identify potential drug targets through combinatorial approaches involving comparative genomics, metabolomics, phylogenomics, evolutionary and structural biology/bioinformatics ([Figure 1](#F0001){ref-type="fig"}). Here we discuss the current status of drug discovery research in each area, focusing on the scope and applicability of computational approaches. Figure 1.From mycobacterial genomes to drug discovery. Post-genomic application areas in mycobacterial drug discovery such as comparative genomics and structural biology/bioinformatics are shown.

Availability of genome sequences and annotation data: applications of comparative genomic approaches to drug discovery research {#S002}
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Comprehensive understanding of the organization of mycobacterial genomes began in 1998 with the elucidation of the complete genome sequence of *M. tuberculosis* \[[@CIT0021],[@CIT0022]\]. The *M. tuberculosis* reference genome (H37Rv strain) is 4.41 Mbp in length and comprises 4081 protein genes, 13 pseudogenes, 45 tRNA genes, 30 ncRNA, 3 rRNA genes and 2 miscRNA genes (<http://svitsrv8.epfl.ch/tuberculist/>).

The genome of *M. leprae* was first sequenced in 2001 \[[@CIT0023]\]. This 3.2 Mbp genome has significant sequence similarity with that of *M. tuberculosis*; however, *M. leprae* reductively evolved to survive with 1614 protein genes, 1310 pseudogenes, 45 tRNA genes, 3 rRNA genes and 2 stable RNA genes (<http://svitsrv8.epfl.ch/mycobrowser/leprosy.html>).

The complete genome of *M. abscessus* strain ATCC 19977 was first sequenced in 2008 \[[@CIT0024]\]. The 5.06 Mbp genome consists of 4941 genes encoding 2886 proteins with functional assignments and 2055 hypothetical proteins (<https://www.patricbrc.org/view/Genome/36809.5>).

Rapid annotation of genomic data, leading to the development of general purpose as well as specialized resources, described in Supplementary Table 1, is providing important information pertinent to sequence, structure, function, metabolic pathway, taxonomy and drug resistance mutations.

Comparative genomics: understanding strain diversity and emergence of drug-resistant strains {#S002-S2001}
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Most pathogenic mycobacterium species including *M. tuberculosis* and *M. leprae* are slow growers taking \>7 days to form visible colonies on solid media. Comparative pan-genomic analyses indicate that the evolution of rapid and slow growers is attributed to a series of gene gain and gene loss events leading to adaptation to different environments \[[@CIT0025]\]. Classical methods for genotyping of mycobacterial strains include IS6110DNA fingerprinting, spoligotyping and 24 locus-MIRU (mycobacterial-interspersed repetitive units)-VNTR (variable number of tandem repeats) typing \[[@CIT0026]\]. With the availability of genome sequencing data, complete genome-based phylogenies are being used for genotyping and classification of mycobacteria \[[@CIT0027],[@CIT0028]\]. The classical *M. tuberculosis* complex is subdivided into seven distinct lineages with characteristic geographic distribution \[[@CIT0029]\]. Genomic analyses revealed three subspecies of *M. abscessus*, namely *M*. *abscessus*, *M. massiliense* and *M. bolleti* \[[@CIT0030]\]. Likewise, lineage diversity within distinct subtypes of *M. leprae* has been recently studied based on phylogenomic analyses of 154 genomes \[[@CIT0031]\].

Molecular phylogenetics and evolutionary dynamics methods allow study of epidemiology and links between genetic diversity and emergence of drug resistance in mycobacterial strains \[[@CIT0032]\]. Antibiotic-resistant genes are important markers for delineation of evolution and spread of drug resistance \[[@CIT0010],[@CIT0014],[@CIT0033]\]. Such computational studies have helped to answer specific questions such as: Whether a particular phylogenetic lineage is associated with drug resistance in an outbreak/epidemic? When and how the drug-resistant strains have emerged? What are the evolutionary factors that cause antimicrobial drug resistance in mycobacterium? Computational studies on mycobacterium addressing each of these questions are described below.

Recently, genomic studies focusing on population structure, origin and spread of MDR-TB have been undertaken across various parts of the world \[[@CIT0029],[@CIT0034]\]. A study \[[@CIT0034]\] on strain diversity and phylogeography using genomes of 340 *M. tuberculosis* strains (isolated during 2008--2013) from KwaZulu-Natal, helped to elucidate the timing of acquisitions of drug resistance mutations that confer XDR-TB, indicating that isoniazid-resistance evolved earlier than rifampicin-resistance^.^ Similarly, molecular epidemiology of MDR-TB in Ireland has been systematically examined using genomes of *M. tuberculosis* strains isolated during 2001--2014 from MDR-TB cases \[[@CIT0035]\]. Among seven lineages of MTB complex, Beijing lineage was observed to be associated with MDR \[[@CIT0035]\]. MDR-TB in Ireland was found to be introduced from other localities, as known for several European countries \[[@CIT0037]\].

In the case of *M. abscessus*, phylogenomic studies revealed the major role of recombination in causing lineage diversity \[[@CIT0030],[@CIT0038],[@CIT0039]\]. Population structure and recombination analyses provided significant evidence of gene flow and admixture among three lineages (*M. abscessus*, *M. massiliense*, and *M. bolleti*), and a correlation with pathogenicity and macrolide resistance in cystic fibrosis patients was found \[[@CIT0039]\]. Phylogenomic and genetic polymorphism analyses have also been carried out using *M. abscessus* isolates from US \[[@CIT0040]\]. A population genomic study \[[@CIT0041]\], based on the worldwide collection of clinical isolates of *M. abscessus,* has shown that the majority of *M. abscessus* infections are acquired through transmission (potentially via aerosols and fomites) of recently emerged circulating clones that have spread across the world. These clones are observed to be associated with increased virulence and worse clinical outcomes. This is a wake-up alarm! We are facing a pressing international infection challenge \[[@CIT0041]\].

In the case of *M. leprae*, a comprehensive study on phylogenomics and antibiotic resistance has been recently published \[[@CIT0031]\], which focuses on sequence and selection pressure analysis of wildtype as well as antibiotic-resistant genes. Several attempts have also been made to analyse the origin and spread of leprosy across various parts of the world \[[@CIT0042]\].

Thus, comparative genomics and phylogeographic studies are important in understanding the global spread and transmission dynamics of the mycobacterial infections. Strain diversity is shown to be one of the contributing factors to antibiotic resistance, linking transmission dynamics to medicine, across various geographic areas which are endemic for diseases such as TB \[[@CIT0043]\]. Furthermore, all these developments point to an increasing need for new and effective drugs to combat antibiotic resistance. Ideally, new drugs must have a novel mode of action to reduce events of cross-resistance, optimal dose-response, pharmacokinetic and toxicity profiles allowing safe and short duration of therapy either solely or in combination with other drugs. Comparative genomics of metabolic pathways provide a means to rapidly identify potential gene targets and thus could aid in drug discovery research (detailed in next section).

Comparative pathway analyses and identification of essential genes {#S002-S2002}
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*M. tuberculosis*, *M. abscessus* and *M. leprae* survive in distinct ecological niches with distinct evolving features that enable them to adapt to their specific environments. Malhotra et al. \[[@CIT0044]\] describe a 90% overlap of known and proposed drug targets against all mycobacterial species. The study identified the major pathways such as chorismate, purine/pyrimidine and amino acid biosynthetic pathways, essential for the survival of mycobacteria, as conserved in all these three species with minor differences in the carbon metabolism pathways.

*M. tuberculosis* is known for its peculiar ability to survive in the human macrophage despite varying stress conditions (redox, acidic, and nitrosamine) within the host. This has contributed to a very elaborate DNA repair and recombination system. The most up-to-date metabolic reconstruction for *M. tuberculosis* describes 1228 metabolic reactions, 1011 genes and 998 metabolites \[[@CIT0045]\], where 250 protein-coding genes present in the lipid biosynthetic pathways are responsible for the thick cell wall. Mutations in these pathways give rise to further changes in their metabolic pathways.

Draft metabolic reconstruction for *M. abscessus* exists in BioCyc \[[@CIT0046]\] and KEGG \[[@CIT0047]\] databases, with 110 pathways including biosynthesis, metabolism, biodegradation and information processing pathways. Evolutionary analyses showed that *M. abscessus* is more closely related to other NTMs such as *M. avium* complex and has a well-supported membrane transport system with a large number of efflux pumps, resulting in multidrug-resistant features \[[@CIT0048]\]. As an opportunistic bacterium, *M. abscessus* is able to survive outside its host and also contains metabolic pathways not associated with pathogenesis, which contribute to its larger genome size as compared to obligate pathogens.

In case of *M. leprae*, reductive evolution has led to the loss of common catabolic pathways such as lipolysis and impairment of the energy metabolism pathways \[[@CIT0023]\]. Moreover, the production of cognate and prosthetic groups from transport, biosynthetic and electron transfer pathways is also affected \[[@CIT0049]\]. With the loss of several functions, and the presence of a large number of conserved but unknown functions of pseudogenes, further studies to characterize the metabolic pathways in *M. leprae* are required.

Approaches to identify essential genes and prioritization of drug targets {#S002-S2003}
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The availability of genome sequences of mycobacteria, and annotations in sequence, structure and pathway databases facilitate systems-level analysis wherein comparative genomics and evolutionary bioinformatics approaches can be integrated to identify the minimal set of essential genes, leading to faster identification of putative drug targets. Essential genes that are necessary for the survival of the bacterium, and are critical components of metabolic and physico-chemical pathways, can be identified by gene knockouts, saturation transposon mutagenesis, RNA interference, etc. Essential genes have been characterized experimentally in the case of *M. tuberculosis* \[[@CIT0050]\]. However, limited studies have been carried out in *M. abscessus* and *M. leprae*. Specifically, *M. leprae* cannot be cultured *in vitro* and thus demands computational identification of essential genes.

Computational approaches for identification of essential genes, including machine learning, flux balance analyses and comparative genomics \[[@CIT0053]\], are faster and cheaper than experimental methods \[[@CIT0053]\]. Machine learning methods utilize unique genomic features of essential genes such as length of proteins, codon usage, GC content, sub-cellular localization, higher rate of evolutionary conservation, etc. Dedicated resources such as Database of Essential Genes \[[@CIT0054]\] and the database of Online Gene Essentiality \[[@CIT0055]\] have been developed, which serve as a platform for identification and prioritization of essential drug targets in various species including *M. leprae* \[[@CIT0056]\]. Advent of next-generation sequencing has enabled design of comparative genomics workflows to identify essential genes in case of *M. tuberculosis* \[[@CIT0057]\].

Upon identification of a set of essential genes, prioritization of drug targets can be achieved by further screening of essential genes based on computational predictions of ADMET (absorption, distribution, metabolism, excretion and toxicity) properties, sub-cellular localization, etc. In view of growing concern about drug resistance, attempts have been made to prioritize drug targets based on various analyses such as identification of uniqueness in metabolome and similarities to known druggable proteins, analysis of the protein-protein interactome, flux balance analysis of reactome and sequence-structural analysis of targetability of genes using integrative strategies \[[@CIT0058],[@CIT0059]\]. As most critical targets in a pathogenic organism are expected to be evolutionarily conserved, this has been applied to filter essential genes in *M. tuberculosis* \[[@CIT0058]\]. Likewise, convergent positive selection analyses were used to identify genes that possibly cause drug resistance in *M. tuberculosis* \[[@CIT0059]\]. Evolutionary rate has been proposed as a useful parameter for ranking and prioritizing antibacterial drug targets \[[@CIT0060]\]. Thus, understanding evolution of drug targets is one of the important aspects of the drug discovery, especially to tackle the problem of drug resistance.

Structural biology and bioinformatics to combat mycobacterial infections {#S003}
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Early approaches to the discovery of new antibiotics relied almost entirely on whole-cell phenotypic screening of natural products, microbial extracts and fermentation broths. This approach has helped in the discovery of most antibiotics in use to date and recently led to the approval of two new drugs, bedaquiline and delamanid, for the treatment of drug-resistant strains of TB \[[@CIT0061]\]. Structure-guided drug discovery, pioneered in academia and some companies in the 1970s became central to the discovery of antihypertensives that targeted renin and AIDS antivirals that targeted HIV protease in the 1980s and 1990s \[[@CIT0062]\]. Opportunities for structure-guided drug discovery of mycobacterial targets became real only later when genome sequences became available. Understanding the structure and mechanism of the target allowed progress and optimization of hit-to-lead molecules, as well as a better understanding of resistance mechanisms, identifying causes of potential side effects and drug-drug interactions. This understanding led many research groups to perform high-throughput screening (HTS) and fragment-based screening campaigns of chemical libraries \[[@CIT0065]\] directly against carefully selected targets of interest. The applications of structure-guided drug discovery to mycobacteria have been reviewed earlier \[[@CIT0066]\].

Structural features can also be used to further refine target selection and validation including lack of structural homology to human host to avoid mechanism-based toxicity and ligandability leading to modulation of target activity. Where the target protein has not been structurally or functionally characterized, it's structural model can be built based on homologous proteins using programs like MODELLER \[[@CIT0069]\]. Important information regarding target protein function and properties can be obtained from databases such as TubercuList (<http://svitsrv8.epfl.ch/tuberculist/>) or CHOPIN \[[@CIT0070]\]. Further, druggability of targets can be predicted by analysing properties and depths of various pockets/hotspots (capable of small-molecule binding interactions), using several databases and programs \[[@CIT0071]\].

Fragment-based drug discovery (FBDD): a promising alternative to HTS approach {#S003-S2001}
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The principal advantage of the FBDD approach compared to HTS methods is that very small libraries (\<10^3^ fragments) of low molecular weight (\<300 Da) compounds can be used to obtain good starting points for lead discovery \[[@CIT0065]\]. Initial fragment hits usually exhibit lower potency than the more complex molecules found in typical HTS compound libraries, but can be chemically optimized into lead candidates, thereby more effectively exploring the chemical space available for binding to the target protein \[[@CIT0068]\]. [Figure 2](#F0002){ref-type="fig"} illustrates a typical fragment screening cascade employed in our lab. The details of these steps are summarized in Supplementary File 1. Figure 2.FBDD cascade. Various techniques involved in each of the four stages are shown.

FBDD approaches have been successfully applied to design inhibitors targeting various key *M. tuberculosis* enzymes such as pantothenate synthetase \[[@CIT0072]\], transcriptional repressor \[[@CIT0073]\], cytochrome P450 \[[@CIT0074]\], thymidylate kinase \[[@CIT0075]\] and malate synthase \[[@CIT0076]\]. Some of the lead molecules developed from such fragment-based campaigns showed promising inhibitory response against *M. tuberculosis*, as shown in the example in Supplementary Figure 1.

Virtual screening, hotspot mapping and pharmacophore modelling to aid structure-guided drug discovery {#S003-S2002}
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*In-silico* screening and docking of compound libraries often help to reduce the time and cost involved in experimental testing of large sets of compounds to identify potential hits. The effectiveness of such virtual screening exercises can be improved by complementing the analysis with fragment hotspot-mapping programs \[[@CIT0071]\], which identify regions within the protein that provide relatively large contribution towards ligand binding in addition to information on interactions governing the predicted regions. Several studies \[[@CIT0077],[@CIT0078]\] have used an energy-based pharmacophore modelling approach to complement virtual screening, followed by chemical optimization to identify inhibitors. We have collaborated with Maria Paola Costi at the University of Modena in a similar study involving a combination of virtual screening and molecular dynamics simulation methods to identify novel chemical scaffolds targeting *M. tuberculosis* thymidylate synthase X \[[@CIT0079]\].

Phenotypic screening along with advances in chemical genetics and bioinformatics has allowed target-guided compound identification and optimization \[[@CIT0080]\], by utilizing target mechanism-based whole-cell screening or by genetic manipulation of the target phenotype, or by finding targets directly from phenotypic hits \[[@CIT0081]\]. The latter approach can employ various techniques such as whole genome sequencing to identify resistant mutants \[[@CIT0082],[@CIT0083]\], transcriptional profiling \[[@CIT0084]\], chemical biology and metabolomics \[[@CIT0085]\] or in-silico methods \[[@CIT0086]\]. These advances in the field discussed above, coupled with a comprehensive understanding of the chemical space of mycobacterial drugs, hold promise of accelerating the process of mycobacterial drug discovery.

From genomes to proteomes: automated modelling of proteomes through structural genomics and bioinformatics {#S003-S2003}
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Methods to identify structures that are potentially similar to the protein in question (*templates*) have been developed in our laboratory \[[@CIT0087]\] and elsewhere (reviewed in \[[@CIT0088]\]), as well as methods such as MODELLER \[[@CIT0069]\] and Rosetta \[[@CIT0089]\] to leverage this similarity to build theoretical, comparative models based on target-template alignments. Community-wide efforts, such as Critical Assessment Structure Prediction \[[@CIT0090]\] have led to substantial improvements in the accuracy of these approaches, both in terms of template identification and alignment, as well as model building and refinement. However, most of these methods focus on producing a single, most likely structure of each protein.

Our group has developed a structural genomics resource for *M. tuberculosis* (H37Rv strain) called CHOPIN \[[@CIT0070]\] which provides an ensemble of predicted models in different conformational states. These models are generated through a homology modelling pipeline. Development of such structural resources is important to identify potential therapeutic targets \[[@CIT0091]\].

Moving beyond proteomes: understanding the impact of drug-resistant mutations in drug targets {#S003-S2004}
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Mutations are likely to confer drug resistance by altering the energy landscape of the target protein, affecting the protein-protein interactions or affecting the drug/ligand binding with the target protein. Computational approaches to predict the effects of mutations on the structure and function of proteins can prove helpful in understanding the mechanism of drug resistance. Our lab has developed two well-established methods, SDM (Site Directed Mutator), based on a statistical approach using Environment Specific Substitution Tables \[[@CIT0092]\] and mCSM (mutation Cutoff Scanning Matrix), a machine learning approach \[[@CIT0093]\] to predict the structural and functional effects of mutations on the target proteins. mCSM is available in different flavours to predict the effects of mutations on protein stability (mCSM-stability), protein-protein interactions (mCSM-PPI) and protein-ligand interactions (mCSM-lig) \[[@CIT0094]\]. Additionally, in order to determine the impact of mutations on flexible protein conformations, tools like EnCOM \[[@CIT0095]\] and FoldX \[[@CIT0096]\] have been developed. Such methods have been used by our group and others to gain insights into the mechanism of mutations in various genetic and mycobacterial diseases including leprosy \[[@CIT0097]\]. Such analyses of the structural and functional mechanism of drug resistance causing mutations using computational approaches are very helpful in the rapid assessment of many mutations not easily achieved using experimental methods.

Challenges and future perspectives {#S004}
==================================

This review has focused on the importance of advances in sequence and structure determination of genomes and their protein products in efforts to develop structure-guided drug discovery against three mycobacteria: *M. tuberculosis*, *M. abscessus* and *M. leprae*. Although *M. tuberculosis* is the most studied mycobacterium, 3D structures of only ∼16% of gene products have been determined experimentally. Sequence-structure homology recognition and comparative modelling have proved useful in providing clues about druggability. Furthermore, the more accurate models, based on structures of close homologues, can provide a basis for virtual screening and ligand design.

Metabolic reconstructions are providing insights into how *M*. *tuberculosis* has adapted within the host, and similar studies in *M. abscessus* and *M. leprae* are needed to provide better understanding of pathogenesis and design of new treatment regimes. The current focus in many laboratories is on providing user-friendly databases for the structural proteomes, and extending these not only to structures of homo- and hetero-oligomers, and complexes with natural and synthetic ligands, but also to incorporate data on metabolic pathways and epistasis, which are important in target selection.

The target-guided approach for antibiotic drug development has generally led to a low rate of translation of *in-vitro* inhibitory response to bactericidal/bacteriostatic activity. This challenge requires further study not only of physico-chemical properties of compounds affecting permeability of the thick waxy cell envelopes of mycobacteria, but also of drug efflux pumps and metabolic inactivation of compounds by bacterial/host cell enzymes that affect compound bioavailability. The emergence of drug resistance through mutations in the target is also a growing challenge. We have developed systematic mutagenesis studies using our software with a view to identify regions where drug design might be directed with a minimal chance of resistance. This is likely to be a key component in drug discovery in future, especially through structure-guided fragment-based approaches, where choices of fragment elaboration or cross-linking can be made in the light of such analyses of mutability.

Disclosure statement {#S005}
====================

No potential conflict of interest was reported by the authors.


Sarpa

The term Sarpa may refer to any of the following:
 Sarpa salpa—a species of bream (fish)
 SARPA—a charter airline
 Sarpa—the Sanskrit term for snake/serpent, from which is derived:
 Sarpa Kavu—a Hindu sacred place in South India
 Sarpa Samskara or Sarpa Dosha—a sacred Hindu rite (pooja) practiced in the Kukke Subramanya Temple
 Sarpa Satra—an attempt by Janamejaya to eliminate the Naga race
 Sarpa Satra—an English language poem written by the Hindu poet Arun Kolatkar
 Sarpa Lake—a lake in southwestern Russia
 Sarpa River—a river which flows into the Volga River and after which Old Sarepta is named
 Sarpa de Tigre—Mexican luchador who was defeated by Rey Cometa in 2003


The social economy has declined. Online users’ patterns are changing: they no longer use social networks to broadcast, connect and share their lives. Consumers now seek deeper online and offline experiences for fulfillment.

“People want better experiences from devices, applications, websites and the offline services they enable,” said Chris Dixon, CEO of Hunch.

They are looking for something less superficial than what they currently find on social media sites. They want meaning and understanding. They want to be challenged.


Beretta Model 38

The MAB 38 (Moschetto Automatico Beretta Modello 1938), Modello 38, or Model 38 and its variants were a series of official submachine guns of the Royal Italian Army introduced in 1938 and used during World War II. The guns were also used by the German, Romanian, and Argentine armies of the time.

History

Originally designed by Beretta's chief engineer Tullio Marengoni in 1935, the Moschetto Automatico Beretta (Beretta Automatic Musket) 38, or MAB 38, was developed from the Beretta Modello 18 and 18/30, derived from the Villar Perosa light machine gun of World War I. It is widely acknowledged as the most successful and effective Italian small arm of World War II and was produced in large numbers in several variants. Italy's limited industrial base in World War II was no real barrier toward the development of advanced and effective small arms, since most weapons did require large amounts of artisan and semi-artisan man-hours to be fine-tuned and made reliable by default. Italian specialized workers excelled and the initial slow rate of production meant that the MAB 38 became available in large numbers only in 1943, when the fascist regime was toppled and Italy split between the Allied-aligned co-belligerent forces in the south and German collaborationists of the Italian Social Republic in the north.

The MAB 38 was developed by Beretta to compete in the rich market of machine and sub-machine guns; it was a well-made and sturdy weapon, introducing several advanced features and was suitable for police and special army units. Presented to Italian authorities in 1939, its first customer was the Italian Ministry of Colonies, which purchased several thousands MABs to be issued as standard firearm of the Polizia dell'Africa Italiana (Italian Africa Constabulary), the government colonial police force. Army orders were slow to come; although impressed by excellent qualities and firepower of the weapon, the Italian military did not feel the MAB was suitable for standard infantry combat. It was judged ideal for police and assault units and in the beginning of 1941 small orders were placed for Carabinieri (military and civilian police), Guardie di Pubblica Sicurezza (national state police), and paratroopers. The Italian Army requested minor changes to reduce production costs, notably the changed shape of the recoil compensator and the removal of the bayonet and catch as the MAB 38A. This was the standard army variant, used throughout the war and issued to elite Italian units, paratroopers, Alpini "Monte Cervino" assault battalion, 10th Arditi Regiment, "M" Battalions of Milizia Volontaria per la Sicurezza Nazionale (MVSN, Blackshirts) and military police.

The Italian Royal Navy also purchased the type and MAB 38A were given to the "San Marco" Marine Regiment and naval security troops; The Regia Aeronautica (Italian Royal Air Force) issued the MAB 38A to its crack A.D.R.A. Regiment. Orders were still small and the Carcano M1891 rifle remained the standard weapon even in elite units. Until 1943, MAB 38A (and since 1942, the MAB 38/42) was available almost exclusively to paratroopers, Blackshirts, tank crews and Carabinieri military police, given the need of all of the former to express high volumes of firepower in prolonged actions or to keep close-quarters combat superiority. The paratroopers of the 185th Airborne Division Folgore was armed exclusively with the weapon. Blackshirt legions (one per infantry division) were regarded and used as elite assault units both for their fanaticism and their Beretta 38s.

After the Italian armistice of September 8, 1943, the Italian armed forces melted away and an Italian army was reconstructed in northern Italy under German sponsorship, the Beretta MAB equipped many units. The Italian Social Republic (R.S.I.) army fought a guerrilla war against partisans from the start, as well as against the Allies. For assault and counterinsurgency units, where firepower at close range was a vital asset, it was the ideal weapon. Production of the MAB became priority and it was supplied in great numbers to R.S.I. formations, especially elite units and it became an iconic weapon, symbolizing the Italian soldier in popular culture. Later in the war, a simplified variant known as the MAB 38/44 was introduced. Regardless of the tables of organization and equipment of a unit, the Beretta 38 was a popular weapon that could eventually find its way into the hands of virtually any soldier, especially amongst officers and higher non-commissioned officers, in any type of unit.

A magazine-holding vest was designed for elite troops (Blackshirts, paratroopers) armed with the Beretta 38; these were dubbed "Samurai" due to the similarity of the stacked magazines with traditional Japanese armour. A special canvas holster was issued with the MAB with two magazine-carrier pouches sewn on, to be worn as a belt but only came into use during the brief life of the R.S.I. and by then could be seen in the employ of many different units whose "elite" status could have been reasonably questioned (such as Black Brigades and other militias). The Beretta MAB was highly praised by Italian resistance movement fighters as well, being far more accurate and powerful than the British Sten which was common issue in partisan units, although the smaller Sten was more suited for clandestine operations. German soldiers also liked the Beretta MAB, judging it large and heavy, but reliable and well made.

The 1938 series was extremely robust and proved very popular with Axis forces as well as Allied troops, who used captured examples. Many German soldiers, including elite forces such as the Waffen-SS and Fallschirmjäger forces, preferred the Beretta 38.Quarrie, Bruce, Fallschirmjäger: German Paratrooper, 1935-45, Osprey Publishing (2001), , , p. 59 Germany manufactured 231,193 Beretta M38s in 1944 and 1945. Firing a powerfully loaded Italian version of the widely distributed 9×19mm Parabellum cartridge, the Cartuccia 9 mm M38, the Beretta was accurate at longer ranges than most other submachine guns. The MAB could deliver an impressive firepower at close range and at longer distances its size and weight was an advantage, making the weapon stable and easy to control. In expert hands, the Beretta MAB allowed accurate short-bursts shooting up to  and its effective range with Italian M38 ammunition, was s, an impressive result for a 9 mm submachine gun.

Specifications
MAB 38, in its first variants, was a fine weapon by any standard, crafted with high quality materials, flawlessly finished and with carefully machined parts. Models 38/42 and 38/44 were easier and faster to build, the finish was sacrificed for speed of production but the quality remained high. The mechanism was a traditional simple blowback recoil but with a novel floating firing pin, an automatic safety on open bolt (both later removed to save production costs), a recoil compensator on the muzzle, a bolt cocking handle with sliding dust cover and a striking trigger gear with no fire selector but with two triggers instead; the fore trigger was for semi-automatic fire and rear trigger for full-auto. The user could shift quickly between methods without switching levers or safety catches, which proved useful in combat. The full-auto trigger had a safety catch on left side, which was eliminated from 1942 and the rear sight was adjustable up to  in the MAB 38 and 38A, the 38/42 and 38/44 variants had fixed rear sights. The MAB 38 had a wooden stock, was about  long and weighed about  when loaded, with an effective range of about .

Variants

The Model 1938 can be recognized by its machined steel receiver, fine craftsmanship and finish and by the perforated cooling jacket over the barrel. It was produced from 1938 to 1950 and fired 9×19mm Parabellum ammunition at 600 rounds per minute. It used 10, 20, 30 or 40-round magazines; the short 10-round magazine, when used in conjunction with the fixed bayonet, was popular with Allied and Axis forces for guarding prisoners or internal security.Smith, Joseph E., Small Arms of the World, 11th ed., Harrisburg, PA: The Stackpole Company (1969), pp. 481-482 In combat, the 30 round magazine was the most common. The original MAB 38, first issued to Italian police in 1939, had a bayonet mount and stock rest for the Carcano M91/38 folding bayonet.

In compliance with Italian army requirements, bayonet mount and rest were eliminated and the recoil compensator was redesigned, the two horizontal muzzle slots substituted by 4 transversal cuttings, judged more effective. This standard army variant was renamed MAB 38A and issued in 1941. Despite its undeniable effectiveness, the Beretta Model 38 proved too time-consuming and expensive to produce during wartime. Marengoni designed a simplified model made from sheet steel, in which the cooling jacket and bayonet mount were eliminated and the separate firing pin mechanism replaced by a fixed firing pin machined on the face of the bolt. The barrel and wooden stock were also shortened to save weight and cost.Small Arms of the World, pp. 482-483 This new model the Model 38/42 had a fluted barrel to aid cooling and save weight. It also had a slower rate of fire (550 rpm). The Model 38/43, was an intermediate production stage between the 42 and 44 patterns.  The 38/42 and 38/43 were adopted by the Wehrmacht as the Maschinenpistole 738(i), abbreviated as MP.738. Models produced for the German Army received German acceptance marks.

The Model 38/44 was a minor revision of the 38/43, in which the bolt was simplified and a large-diameter recoil spring used in place of the operating spring guide. It also eliminated the fluting to save time and increase production. The 38/44 was also adopted by the German army as the MP.739.  A variant of the Model 38/44 was fitted with an MP40-style under-folding stock as the Model 1.

After World War II, the 38/44 continued in production in slightly revised form as the 38/49 series: the Model 2 or MP 38/44 Special with an MP40-style under-folding stock and extended magazine well, the Model 3 with an extended magazine well and telescoping steel-wire buttstock and the Model 4 with a standard wooden rifle stock. All of these models have a push-button cross-bolt safety catch at the middle of the stock After Marengoni's death, Beretta engineer Domenico Salza revised the safety system of the Model 38/49 series as the Model 5, identified by a large rectangular grip-safety button located in the stock's finger groove. The Model 5 was produced for the Italian Army, police and the armed forces of several other nations until 1961, when production ceased in favor of the compact, modern Beretta M12.

Unusually, it ejectes to the left, because of the non'reciprocating
cocking/charging handle, slot cover, on the right, side, being in the way.

Users
 : captured by the Albanian Partisans in vast quantities during the war
 : Used by Armée de Libération Nationale
 :Used by Mukti Bahini.
 : Models 38/44 and 38/49
 : Model 38/49
 : 350 ordered and 50 delivered in 1943.
 : Models 38/42 and 38/49

 : Italian surplus MP38s bought in 1958.

 : MP38/49 (Model 4) and Model 5, identified as the MP1. Used by Bundeswehr (until 1959) and Bundesgrenzschutz (replaced at the end of the 1960s)
 : MP1938/49 variant. Deployed during the United Nations Operation in the Congo.

 : Model 38/44

  Italian Social Republic
  Italian Resistance

 : Used by Western Somali Liberation Front rebels during Ogaden War.
  Model 38/44
 : 5,000 ordered in 1941 and delivered during 1942. Received both Model 38A and Model 38/42.

 : Model 38/49
 : Model 38/49
 : Model 38/49
 : Captured in vast quantities.

See also
 List of Italian submachine guns

References

Further reading
 Dunlap, Roy F., Ordnance Went Up Front, Samworth Press, (1948)
 Hogg, Ian V. and Weeks, John, Military Small Arms of the 20th Century, 6th ed. DBI Books, Inc. (1991),
 Smith, Joseph E., Small Arms of the World, 11th ed., Harrisburg, PA: The Stackpole Company (1969),
 G. Rosignoli, RSI: uniformi, equipaggiamento ed armi, Albertelli Ed., 1985

Category:World War II submachine guns
Category:World War II infantry weapons of Italy
Model 38
Category:9mm Parabellum submachine guns
Category:Submachine guns of Italy