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The Starting Lineup: Celtics Keep The Streak Alive
In their first road test since Rajon Rondo's injury, the Celtics were able to come back from 10 down at the start of the fourth quarter to beat the Raptors 99-95 and extend their win streak to five games. The catalyst in the rally? LeAndro Barbosa, who scored 11 of his 14 points in the fourth. Barbosa's energy at both ends of the floor sparked a dramatic turnaround in which the Celtics went from being outscored 34-19 in the third to winning the fourth 30-16. The Raptors, who'd finished the third on a 10-2 run, suddenly looked atrocious to start the fourth. Their first four shots were ugly misses from beyond 21 feet, and as they continued to settle for jumpers their offense became more and more stagnant. It often seemed as though they didn't even cross halfcourt until there were just six or seven seconds on the shot clock, and their attack essentially consisted of everyone standing and watching as Kyle Lowry dribbled aimlessly. Quite honestly, I believe it was as poor an offensive quarter as I've seen played by any team this season.
Kevin Garnett had a fantastic outing, leading the Cs with 27 points and 10 boards. It's a damn good thing he did, too, because Paul Pierce, Jeff Green, and Jason Terry combined to go 5-20 from the floor. Along with Barbosa, Garnett was at his best when it mattered most, scoring 11 of his own in the fourth. While most of his teammates couldn't have fallen from a boat and hit water, The Big Ticket was executing complex maneuvers fit for an Olympic diving competition…
As you can see, Andrea Bargnani made his return from a 26-game absence. He did so to a smattering of boos, which upset Dwayne Casey but didn't appear to faze nor inspire Bargnani, who had a typical Bargs game of 13 points and 3 rebounds on 5-10.
LeBron's incredible play continued in a 114-108 Heat victory over the Rockets. James, who's been averaging 30 points on 60% from the floor and 40% from three over his last 12, posted his third consecutive 30-point game as he hogged the stats until he'd had his fill (32/6/5). In the stead of Chris Bosh (illness), who has also been playing exceptionally well as of late, Dwyane Wade stepped up to score 31 points of his own. This is just the second time all season that LeBron and Dwyane have each topped 30 in the same game.
Despite trailing by double figures for most of the third quarter and even part of the fourth quarter, the Rockets were able to get back in this thing. After having failed to score between the 11:38 and 7:22 marks of the fourth, Houston came surging back thanks mostly to James Harden, who scored 11 straight points to bring his squad to within three. From that point, though, Miami displayed their defensive prowess by drawing charges (legitimate charges, no flops) on consecutive possessions. It then became a free-throw shooting contest and the Heat sealed the deal.
James Harden, though. With 36 points, 12 rebounds, and 7 assists… he was pretty incredible. Observe his abuse of Ray Allen at :35, and his discarding of LeBron James at 1:30 and 3:00 (yes, he cooked LeBron twice)…
The Nets eked out much-needed victory in Detroit, where they defeated the Pistons 93-90. Both teams were pretty sketchy down the stretch as they each failed to score for stretches of more than two minutes, but a couple of big buckets by Deron Williams and Brook Lopez made the difference for the Nets — that and a missed free throw by Greg Monroe. Had he been able to deliver, Monroe's free throw would've tied the game with 33 seconds to play. So, instead of being down two after Monroe proceeded to allow Lopez to back him down and score a layup, the Pistons trailed by three and were ultimately forced to play the fouling game. What I'm getting at here is that Greg Monroe, despite his impressive line of 23 points and 10 rebounds, kind of blew it. Williams and Lopez, on the other hand, had just 12 and 17 points respectively, but were able to manufacture important hoops late in the fourth quarter.
Kyrie Irving, Dion Waiters, and Tristan Thompson combined for 58 points in an encouraging display of hope for Cleveland. The young core missed just 10 of their 34 attempts from the floor, though the whole thing ought to be taken with a grain of salt as the aforementioned floor was that of the Time Warner Cable arena, home of the Charlotte Bobkittens. This 122-95 defeat is the fifth in a row for the 'Cats, who've not beaten the Cavaliers since Boris Diaw went off for 26/11/7 on March 30th of 2011. Good times, relatively speaking (Charlotte won 34 games that season, which is nearly twice as many as the 18 they've won since).
The Golden State Warriors suffered their second blowout loss in as many nights, losing 119-98 in Oklahoma City. The Thunder, already out to avenge a hotly-contested, 104-99 loss (January 23rd, the one where Scotty Brooks thought it'd be a good idea to run a play for Kendrick Perkins), apparently drew some extra motivation from the demonstrative habits of the Warriors' bench. Said Kevin Martin, who contributed 21 points in the onslaught: "Coach Jackson should talk to a couple of his bench players and make sure they get wet behind the ears before they come barking at a couple of our players."
Mark Jackson and company sure aren't making any friends on this road trip. Not that they should care. Jackson is likely more concerned by the fact that his team has given up 259 points — nearly three games worth for a Memphis or an Indiana — in their last two outings. Looking like the Warriors of old, these Warriors are.
Sorry guys, but that's all I've got today. I allowed myself to go to sleep last night without doing two things — finishing this post and setting an alarm. Fatal mistake. I'll try not to let it happen again. As a sign of my regret, I give to you some Rubio magic. Please forgive me.


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MP 'Colonel' Nasheed blames Home Minister Jameel for evidence bill delay
Dhivehi Rayithunge Party (DRP) MP Mohamed 'Colonel' Nasheed has claimed that Home Minister Mohamed Jameel's failure to give a professional opinion on the pending Evidence Bill is the reason for the bill's delay.
The remark by the Nolhivaram constituency MP comes at a time where both the Home Minister and Commissioner of Police Abdulla Riyaz have expressed concern over parliament's delaying of the essential bill.
During a debate in parliament last Wednesday, MP Nasheed claimed that the committee currently reviewing the bill had on numerous occasions requested a professional opinion from the Home Minister.
"We were forced to park the bill because [Jameel] could not spare us time. We are waiting for an opinion from him. Therefore, before opening his mouth to condemn parliament, he must look back at his own actions," said MP Nasheed.
He contended that along with the evidence bill, other pivotal bills such as the criminal procedure code require professional opinions from the attorney general, the Supreme Court and other members of the judiciary, as well as the police and Home Ministry.
"They are not able to give time for any of this. Kulhudhufushi-South Constituency MP Mohamed 'Kutti' Nasheed has neatly carried out parliament's end of the bargain. He initiated the drafting and other relevant work required from parliament. But, we have to face the truth that [the delay] is due to the Home Minister's failure to give us his time," he said.
"We have given time for him on four different occasions, but every time for some reason he calls us and cancels the appointment in the nick of time. How can the evidence bill be passed?" Nasheed questioned.
He reiterated that even though the country was run under a presidential system with separated powers of state, it does not mean that two of those powers could not collaborate in running the affairs of the state.
Police Commissioner's concerns
Meanwhile, Commissioner of Police Abdulla Riyaz has said it was of utmost importance that a mechanism be set which would speed up the process of obtaining witness statements before the witness is "influenced".
In a video released on the police website following the Criminal Court's acquittal of six suspects arrested in connection with the stabbing murder of Ali Shifan, Commissioner Riyaz stated that many people are afraid to give witness to the courts because of threats they face afterwards.
"In several countries, there are mechanisms to protect witnesses. That can only be achieved through legislation. According to our information, a draft witness protection act is currently submitted to the parliament," he said.
He said such key bills should become law as soon as possible in order for police to continue curbing criminal activities.
"Laws should be made in such a fashion that they guarantee the safety and protection of the people. Importance should be given to that. We hope that the necessary bills are passed as soon as possible which will remove a lot of barriers we are currently facing. It would be a huge assistance," he said.
The commissioner of police added that it was important to know the extent to which the court would go to accept circumstantial evidences and forensic evidences such as DNA.
He stressed that the constitution clearly mentioned that investigations be carried on the basis of evidence collected, but said there was no evidence act currently in place.
"DNA is one of the most authentic forms of evidence. Another is the fingerprint. Similarly, video evidence id very authentic too. We are talking about the fact that there is no legislation that dictates as to how such evidences will be accepted by the court."
Following claims that the initial evidence bill proposed in 2009 "made no sense at all", a new draft of the bill was proposed to Parliament's Independent Institutions Oversight Committee on October 2012.
The bill was drafted by former Minister of Legal Reform during President Gayoom's presidency, the current MP for Kulhudhuffushi- South, MP Mohamed 'Kutti' Nasheed.
Home Minister Jameel was not responding to calls at time of press.
Parliament postpones no-confidence votes against Home, Defence Minister over issue of secret ballot
Proposed crime prevention legislation may sideline human rights
Parliament to hold no-confidence vote against Home Minister Jameel, Defence Minister Nazim, JSC member Gasim Ibrahim
"Translation errors" slow Evidence Bill
DRP condemns sacking of State Minister for Health Ali Shareef
Supreme Court accepts case to invalidate transfer of power to speaker
Posted on March 24, 2013 March 24, 2013 Author Mohamed NaaheeCategories PoliticsTags crime, evidence bill, Home Minister Mohamed Jameel Ahmed, maldives, maldives news, MP Mohamed 'Colonel' Nasheed, parliament
One thought on "MP 'Colonel' Nasheed blames Home Minister Jameel for evidence bill delay"
Manu says:
Jameel is full of anger and negativism like Anni and people around him. Nothing good can come out of him.
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And if that's not happened to you then imagine the experience.
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Q: CUstomized links in gsp I have some controllers in my grails application:-
LoginController
LogoutController
SearchableController
cirnele.SearchAllController
com.ten.cirnelle.domain.CustomerController
com.ten.cirnelle.domain.ProjectController
com.ten.cirnelle.domain.PurchaseOrderController
com.ten.cirnelle.domain.QuotationController
com.ten.cirnelle.domain.ResourceController

In Config.groovy, I have provided one of my configration:-
cirnelleControllerExclusions =['Login','Search','Searchable','Resource']

and from main.gsp, I am using:-
<g:each var="c" in="${grailsApplication.controllerClasses.sort { it.fullName } }">

    <g:if test="${grailsApplication.config.cirnelleControllerExclusions.contains(c.naturalName.split()[0]) == false}">

<g:link controller="${c.logicalPropertyName}">${c.naturalName.split()[0]}</g:link>

    </g:if>
</g:each>

this code is used to provide a menu like structure at the top of every view page and it is excluding 4 cotrollers, that i specified in Config.groovy to be display as a link in view pages.
but i have many users with different roles like
ROLE_PM
ROLE_SALES/BDM
ROLE_TEAMMEMBER
ROLE_ADMIN

and my requirement is that if an user with admin role logins, then he can view all the controllers as a link(except the 4) but if a user with PM role logins, then he cannot view CustomerController link and QuotationCotroller link.
so how can i customized my main.gsp to show menu links based on the role of user.
thnks

A: Try to use spring security plugin. There are tags for doing exactly what you want.
<sec:ifNotLoggedIn>
  <g:link controller="login" action="auth">Login</g:link>
</sec:ifNotLoggedIn>
<sec:ifAllGranted roles="ROLE_USER">
  <g:link class="create" controller="post" action="timeline">My Timeline</g:link>
</sec:ifAllGranted>

redpajama_set_name: RedPajamaStackExchange


text:
Q: Python: lxml is not reading element text all time I want to load xml file with below structure into pandas dataframe
The size of xml could be between 1 GB to 6GB
Below xml sample just have 5 records but my acutal file will have around 100000 records as mention in the RECORDS attributes below (RECORDS="108881")
Also each and every element in this file will have some value.
None of the element is empty in the whole file.
<?xml version="1.0" encoding="UTF-8"?>
<ACADEMICS>
   <STUDENTS ASOF_DATE="11/21/2019" CREATE_DATE="11/22/2019" RECORDS="108881">
    <STUDENT>
        <NAME>JOHN</NAME>
        <REGNUM>1000</REGNUM>
        <COUNTRY>USA</COUNTRY>
        <ID>JH1</ID>
        <SHORT_STD_DESC>JOHN IS A GOOD STUDENT</SHORT_STD_DESC>
    </STUDENT>
    <STUDENT>
        <NAME>ADAM</NAME>
        <REGNUM>1001</REGNUM>
        <COUNTRY>FRANCE</COUNTRY>
        <ID>AD2</ID>
        <SHORT_STD_DESC>ADAM IS A GOOD STUDENT</SHORT_STD_DESC>
    </STUDENT>
    <STUDENT>
        <NAME>PETER</NAME>
        <REGNUM>1003</REGNUM>
        <COUNTRY>BELGIUM</COUNTRY>
        <ID>PE5</ID>
        <SHORT_STD_DESC>PETER IS A GOOD STUDENT</SHORT_STD_DESC>
    </STUDENT>
    <STUDENT>
        <NAME>ERIC</NAME>
        <REGNUM>1006</REGNUM>
        <COUNTRY>AUSTRALIA</COUNTRY>
        <ID>ER7</ID>
        <SHORT_STD_DESC>ERIC IS A GOOD STUDENT</SHORT_STD_DESC>
    </STUDENT>
    <STUDENT>
        <NAME>NICHOLAS</NAME>
        <REGNUM>1009</REGNUM>
        <COUNTRY>GREECE</COUNTRY>
        <ID>NI8</ID>
        <SHORT_STD_DESC>NICHOLAS IS A GOOD STUDENT</SHORT_STD_DESC>
    </STUDENT>
</STUDENTS>

i am trying to read these xmls with lxml as below functions
As you can see in below functions, i am just interested in reading specific tags from xml file which are ["ACADEMICS","STUDENDS","ID","SHORT_STD_DESC"]
def recursive_dict(self,element):
        return element.tag, \
            dict(map(self.recursive_dict, element)) or element.text

def ConvertFilePivot(self, inputfile):
        context = etree.iterparse(inputfile, events=('start','end'), tag=["ACADEMICS","STUDENDS","ID","SHORT_STD_DESC"])
        lstValues = []
        asOfDate = ""
        for event, elem in context:
            if elem.tag == "ACADEMICS" :
                asOfDate = elem[0].attrib['ASOF_DATE']
            else:
                for event, elem in context:
                    doc = self.recursive_dict(elem)
                    lstValues.append(doc)
                dfvalues = pd.DataFrame(lstValues,columns=["ColName","ColValue"])
                columns = dfvalues['ColName'].unique()
                data = {}
                for column in columns:
                    data[column] = list(dfvalues[dfvalues['ColName'] == column]['ColValue'])

        dfdata = pd.DataFrame(data)
        return dfdata

Now, the problem is when i load this xml into dataframe as shown in above function, for some records i get 'None' as a text for ID and  SHORT_STD_DESC elements.
But the actual xml file has that value.
So i am not sure why it is not reflected in my dataframe ?
Any input would be great help for me.

A: This may be more a comment than an answer, but I can't fit it in an actual comment...
Try changing
 else:
     for event, elem in context:
           doc = self.recursive_dict(elem)

to just:
 else:
     doc = self.recursive_dict(elem)

and see if it works.


Vijay Anand also known as 'Goldie' is an Indian filmmaker, producer, director, screenwriter and an actor who made some classic films to date. He is related to actor Dev Anand and directed many in-house films of 'Navketan Films' (owned by actor Dev Anand). He was born on 22 January 1934 in Punjab. As an actor, he acted opposite Jaya Bhaduri in ' Kora Kagaz' which was critically applauded and was a hit film. Later, he also acted with Shabana Azmi. But his contribution to Indian cinema is understood as a director where he crafted classic film such as Guide, behind the camera lens. It was Guide that made him an acclaimed director of Indian cinema. The film was based on R.K. Narayanan's novel and it had Waheeda Rehman and Dev Anand playing the lead roles. The film won him even international recognition. The other three films that he directed after Guide for Dev Anand are Johny Mera Naam (1970), Jewel Thief (1967) and Tere Mere Sapne(1971). All these three films were blockbusters in the box office. If Guide boosted Waheeda's career, so did 'Jewel Thief for Vyjayanthimala and 'Johny Mera Naam' did the same magic for Hema Malini.
Vijay Anand made his debut as a director with his film 'Nau Do Gyarah'(1957) which had Dev Anand being pitted against Kalpana Karthik for the first time. After this movie, Dev Anand married Kalpana Karthik. This film was also was a blockbuster.
Vijay Anand's directional venture 'Tere Mere Sapne' was remade In Bengali and Telugu languages too. In 1972, the film was made in Bengali as Jiban Saikate with Soumitra Chatterjee and Aparna Sen. In the year 1982, it was remade into Telugu as Madhura Swapnam. Vijay Anand is also known for shooting extraordinary dance sequences songs like ''O Haseena" ( Teesri Manzil ), "Kaaton Se Kheech" (Guide ) and "Honthon Mein Aisi Baat" (Jewel Thief), These songs were picturised on Asha Parkeh, Waheeda, and Vyjayanthimala.
Other than Navketan Banners (Dev Anand production house) Vijay Anand also directed some movies outside it. His first direction outside Navketan was 'Teesri Manzil' which was for producer Nasir Hussain. The film which had Shammi Kapoor and Asha Parekh in lead roles were a hit. R.D. Burman's musical score gave some foot-tapping numbers for audiences to enjoy.
In most of his films except 'Guide' and 'Teesri Manzil', Vijay Anand had been the screenwriter. In 1973, he directed 'Black Mail' which featured Raakhee and Dharmendra in lead roles. The film was declared a hit.
After this film, he produced, directed and penned the script for 'Chupa Rustom' which failed in the box-office. In 1980, he directed 'Ram Balram' which had Dharmendra and Amitabh Bachchan being paired together after Sholay. The film was produced by Tito and had Zeenat Aman and Rekha being cast opposite Dharmendra and Amitabh. The film received average box office response due to the fact it had Amitabh and Dharmendra together.
Vijay Anand is well known for his other two films that were 'Kala Bazar' and ' Tere Ghar Ke Samne' which had melodious music of S.D. Burman . The actor and director passed away on 23 February 2004 due to a heart attack.
10 Bollywood Old Retro Song Genres!!


text:
More History (6247)
Books > History > The Economic Life of Northern India (C. A.D 700 - 1200 )
The Economic Life of Northern India (C. A.D 700 - 1200 )
by Lallanji Gopal
The topics dealt with are of as varied nature as those in his other Studies. The approach of most writers to the problems relating to Indian religions is based on literary sources; but in respect of the majority of topics discussed in the volume with the exception of the first few chapters, Prof. Sircar depends primarily on inscriptions and supplements epigraphic evidence by the testimony of literary and numismatic records wherever necessary. A few of the studies incorporated in the volume exhibit the author's search for truth spread over a number of years. Thus his investigation relating to the god Purusottamajaganna.tha of Puri began when he noticed the dominions of Gafiga Anarigabhima III (1211-39 A.D.) described as Purusottama's empire' in an inscription, in 1939. In the course of its progress, he found out, in 1946, how Bharru II (1305-27 A.D.) is represented in his records as a feudatory of the god Purusottama-Jagannatha and, in 1953, how a literary work speaks of the dedication of the Ganga kingdom to the god by king Anatigabhima. Finally in 1963, Prof. Sircar traced in a tenth century epigraph of the Satna District, Madhya Pradesh, how the god of Puri attracted pilgrims from distant regions. The chapter on Purusottamajagannatha in the volume is thus the result of a study of about quarter of a century.
D.C. SIRCAR (1907-1984) was an epigraphist, historian, numismatist and folklorist, known particularly for his work deciphering inscriptions in India and Bangladesh. He was the Chief Epigraphist, Archaeological Survey of India (1949-1962); Carmichael Professor of Ancient Indian History and Culture, University of Calcutta, (1962-1972) and the General President of the Indian History Congress. In 1972, Sircar was awarded the Sir William Jones Memorial Plaque.
Socio-economic history represents a relatively recent develop-ment especially in the world of Indian historiography. It is noticeable, however, that in the post-Independence era increasing attention has been devoted in this direction. It would not be too much to connect this tendency with the current emphasis and preoccupation with the problems of socio-economic planning and growth. A study of the past inevitably sheds light on the present. It was with this view of investigating the past to illumine the present and the future that a scheme of research on the social and economic history of ancient India was planned at the University of Allahabad many years ago and I had the privilege of helping several brilliant young scholars in producing a series of dissertations which also included Dr. Gopal's effort on the earlier economic development of ancient India. Seeking to continue his research, he later proceeded to England and the present work is the outcome of that effort. I welcome the present publication with particular happiness as it represents for me the beginning of a fulfillment of hope entertained for some time from one of my most brilliant pupils and colleagues at Allahabad.
Despite its increasing vogue significant socio-economic history is exceedingly difficult to write and remains a tricky business. Conceptual and methodological problems abound and are hardly susceptible of general and standardized answers. The researcher either tends to produce an inventory of well-known or little-known facts from documents or, if ambitious, tends to use a conceptual and interpretational framework derived from some standard work on western social history. It has, however, to be remembered that social being and consciousness, external relations and values, are inextricably mixed up and the genuine economic historian must be able to penetrate the hardened film of a long process of 'reification'-ancient and modern-to be able to communicate a socio-economic awareness without disturbing its inbuilt articulations so that it should scintillate with vital significance.
The unique importance of the period under study consists in the fact that it links ancient to medieval India and sheds light on both by a sort of debali-difiaka-gayal. It represents the cul-mination and degeneration of the classical traditions of ancient Indian culture and thus its study is important for determining the causes which sapped the vitality of Indians and rendered their resistance to the Muslim invaders surprisingly weak. On the other side, in order to have a proper understanding of the origins and true nature of the polity under the Turko-Afghan Sultans one cannot ignore the institutions of the early medieval period. The Turko-Afghan rulers had as a matter of necessity to use much of the machinery of administration already in existence.
But the attention which this period has received from scholars of Indian history has not been proportionate to its importance. Like a man with two wives it has to face the scornful neglect of the historians alike of ancient and medieval periods of Indian history. Many historians of ancient India have not bothered to follow the course of events after the decline of the Guptas or in any case after the reign of Harsa. On the other hand historians of medieval India have often concentrated on the period beginning with the establishment of the power of the Mamluk Sultans and have paid little attention to Sanskrit sources, which most of them were not competent to handle.
Ignorance as to the true historical details of the period ex-plains the misconceptions which can be seen in earlier works on the period. Thus V. A. Smith described Harp as the last emperor in the history of ancient India, after whom it is only a confased story of "a medley of petty states, with ever-varying boundaries and engaged in unceasing internecine war"2. Such a view implies an utter misunderstanding of the history of the early medieval period, the imperial ambitions of the important dynasties and, above all, the extent of the Pratihara kingdom, which at its height covered a larger area than could possibly be claimed by an eulogist of Harsal.
With a view to appraise correctly any aspect of social life we have to keep in mind the frame-work of the political history of the period. We can easily trace two dominant threads in the fabric of the political history. The period can be studied from the view-point either of the attempt of the native powers to achieve imperial glory, or of the gradual establishment of the political power of Islam. The death of Harsa created a temporary vacuum on the political stage and there followed several attempts on the part of different kings and dynasties to establish their political supremacy. In the earlier part of the period Kanauj had come to acquire an imperial halo and was the most coveted prize for those participating in the contest for imperial supremacy. At the beginning of our period we find Yaovarman ruling over Kanauj. With Lalicaditya Kashmir also entered into the arena ,of the politics of north India. Tibet also seems to have attempted to gain hegemony over some parts of north India. It is not un-likely that the activities of Kashmir and Tibet reflect the greater struggle for the control of the trade between the East and West fought on a larger scale in Central Asia2.
But soon north Indian politics came to be dominated by the tripartite struggle for supremacy among the Rastrakutas, the Pallas and the Pratiharas. Though both the Pallas and the Prati-haras had alternate moments of rejoicing, the Palas established their dominance over almost the whole of north India only under Dharmapala and Devapala. The Pratiharas no doubt achieved the zenith of their power during the reigns of Bhoja and Mahendra-pala, but they long enjoyed the position of the chief imperial power in north India. The struggle between the Pratiharas and the Palas was intercepted by the occasional outburst of the military might of the Rastrakutas, whose armies at least on three occasions, under Dhruva, Govinda III and Indra III, overran northern India. But they do not seem to have attempted a serious and lasting occupation of the conquered areas, and were satisfied merely to force the defeated kings to accept their temporary subjugation. The attempted thrust of the Arabs of Sind towards Gujarat, the victories over the Arabs claimed for some of the Pratihara kings, the feeling of animosity towards Islam which the Arab geographers ascribe to the Pratihara kings and the sympathetic and patronising attitude of the Rastrakuta kings towards the Arabs make a good case for the view that the struggle in northern India may well be described as a quadrangular one. Obviously the desire for martial glory and imperial supremacy was the dominant motive force behind this struggle. But the participation of the Arabs would suggest that the concern for economic gains was also to some extent an important reason.
About the middle of the tenth century the Pratihara empire disintegrated and gradually came to be confined to Kanauj and its neighborhood. The history of the eleventh century is do-minated by a number of states which had started their careers as the feudatories of the Pratiharas. These include the Caharn5nas in Rajasthan, the Caulukyas in Gujarat and the Paramaras in Malwa. Other important dynasties which participated in the imperial game were the Gahadavdlas, the Candellas and the Kalacuris. The history of the period is a record of continuous rivalry among these kingdoms, without any lasting success for any one of them. Be-sides these there were other smaller states. This political fragmen-tation sapped the vitality of the country and rendered it incapable of putting up an effective and combined resistance to the Muslim invaders.
The period under study can be described as forming the necessary background for the establishment of Muslim power in Here also we can point out several stages in this process. Arabs conquered Sind in 712 A.D. but their attempts to -Dv other interior areas were utterly unsuccessful. The Muslim state in Sind had a precarious existence, often threatened by the might of the Pratiharas. The Arab occupation was only an epi-sode, of no importance to other parts of the country ; for the narrative of the establishment of Muslim authority it is equally without much real value. The final conquest of northern India was effected by Muslim armies that came through the north-western frontiers. The period roughly before 1000 A.D. was one of successful resistance to Muslim invaders. The Muslims, however, never gave up the idea of extending their victorious arms to India. For over two hundred years they had continuously to hammer against the petty states of Kabul and Zabul, which offered stubborn and heroic resistance before they went down to the greatest military power of their times. The slow progress of the arms of Islam, which had brought under its mantle a con-siderable part of three continents, redounds to the credit of these two states. The next stage in this connection is marked by the date 997, when Mahmad, son of Sabuktigin, captured Ghazni and turned his attention to India. His conquests established Muslim power over Punjab, which thus served as the spring-board for the complete success of the Muslims. Even then the Muslims had to wait for some two hundred years until in 1193 A.D. Mu'izz-ud-din Ghari defeated Prthviraja Uhamana in the battle of Tarain. Now there was nothing to stop the onrush of the Muslims and the year 1206 witnessed the establishment of the Mamlak dynasty.
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India From Within (A Guide to India's History, Religion, Arts, Culture and Society)
by Alvaro Enterria, Preface by Mark Tully
Item Code: IHJ044
Neotectonic and Isoseismal Atlas of North India (Geological Survey of India)
by K. C. Joshi
Controller of Publications
Angkor Vat: India's Contribution Conservation (1986-1993) - A Rare Book
by B. Narasimhahiah
Item Code: NAC341
Prehistory and Protohistory of India-An India (Palaeolithic-Non-Harappan Chalcolithic Cultures)
by V.K. Jain
D. K. Printworld Pvt. Ltd.
Item Code: IDL191
Revealing India's Past (A Co-operative Record of Archaeological Conservation and Exploration in India and Beyond)
by Sir John Cumming, Foreword by Alfred Foucher
Pilgrims Books Pvt. Ltd.
India's China War
by Neville Maxwell
Natraj Publishers
The Making Of Modern India: The Cultural Heritage of India (1765-1947) (Volume VIII )
by Dr. Sukumar Bhattacharyya and Dr. Uma Das Gupta
Ramakrishna Mission Institute of Culture
Prehistory of India: A Comprehensive History of India (Vol. 1, Part 1)
by M. K. Dhavalikar
Manohar Publishers and Distributors


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Christian Boar..Christian Boarding Schools f..
OrlandoOrlando
Why Should Parents...Why Should Parents Choose a...Why Should Parents Choose a...Why Should Parents Choose a Christian...
Christian Boarding Schools for Troubled Girls Near Orlando, FL
Like near-countless other families all over the country, Christian parents from the Orlando, FL area are seeking therapeutic treatment for their troubled teenage girl in unprecedented numbers.
Whether it be substance abuse, mental health disorders, and/or an unhealthy lack of motivation to achieve, the number of troubled teenage girls from Orlando, FL has grown and probably will continue to grow - but we have HOPE and SOLUTIONS.
Fortunately, for parents of out-of-control girls from Orlando, FL (and beyond), there are highly effective treatment facilities known as, Christian Boarding Schools for troubled girls that specialize in rehabilitating the overall psychological, behavioral, and (in some cases, like that of Elk Mountain Academy) spiritual state of struggling young women.
In addition to treating behavioral and emotional issues, Christian Boarding Schools for troubled girls also present young women with a unique educational opportunity that they would otherwise not have been granted, including (but not limited to):
Fully individualized academic curriculum: An accredited middle or high school education that allows students to go at their own pace rather than being held back or left behind like they most likely would at traditional public or private school.
Grade restoration: an invaluable educational opportunity for those who underperformed or have lacking grades from earlier in their schooling to go back and repair their initial marks, thus improving their overall GPA.
College-preparatory courses: classes that help prepare high school students for the day-to-day rigors and increased workload they will experience in college. In addition to gaining invaluable experience, some college preparatory classes also count as college credits.
More one-on-one attention with teachers: Due to their relatively small classroom sizes, Christian Boarding Schools for troubled teens allow students to have more one-on-one attention with teachers than they would at a traditional school. Having more face-to-face communication with teachers greatly increases a student's ability and overall chances to meet their full educational potential.
Christian Boarding Schools for Troubled Girls from the Orlando, FL Area
As a Christ-centered therapeutic boarding school, it is our pleasure to introduce every Elk Mountain Girls Academy (EMGA) student to Jesus Christ.
While there is no shortage of parents of a troubled girl from Orlando, FL to choose from, Christian families from the Orlando, FL area will find that it is much more difficult to find faith-based programs that align with their own, spiritual beliefs.
Fortunately for Christ-centered families from Orlando, FL, there is Elk Mountain Girls Academy.
EMGA is a Christian-based boarding school for troubled girls from the Orlando, FL area who also struggle with out-of-control behaviors and other life-controlling issues that may stunt and even eventually even threaten their future.
What makes our residential school unique is our dynamic balanced approach to treating troubled girls.
Rather than solely focus on one area of rehabilitation, At Elk Mountain Girls Academy, we proudly offer troubled girls from Orlando, FL a diverse treatment program that emphasizes therapy (sessions with a licensed therapist), education (a nationally accredited academic curriculum), and Christ-centered religious/church services (including youth group, Sunday school, and bible study).
Find a Top Christian Boarding School for Troubled Girls from Orlando, FL
Elk Mountain Girls Academy is one of the longest-running therapeutic boarding schools in the Pacific Northwest with over 24+ years of serving struggling teens and their families in need.
At EMGA troubled girls find lasting transformation...
"And we all, who with unveiled faces contemplate the Lord's glory, are being transformed into his image with ever-increasing glory, which comes from the Lord, who is the Spirit." 2 Corinthians 3:18
If you are seeking a Christian boarding school for troubled girls from Orlando, FL that is accredited by the Joint Commission and designed to help young women solve difficult emotional issues such, look no further.
If your troubled daughter needs therapeutic help for attachment disorders, attention deficit, eating disorders, anxiety, depression, self-destructive or antisocial behavior, and issues involved with their adoption, we can help. Like so many other girls we believe we can help your daughter get past her emotional struggles and trauma. Please inquire online or call us.
For more information regarding Elk Mountain Girls Academy, please call us today at Call (208) 266-1122.
Mental Health Guidance in Orlando, FL for Troubled Teens
Families from Orlando, FL have made Elk Mountain Academy their first choice for child change and guidance. Parents, looking for help for their child, can expect a team of compassionate, expert practitioners and leaders here at EMA. EMA operates from the understanding that "change" must come from the inside-out, not from the outside-in. We are devoted to the life skills development and experiential education for all adolescents, who may be struggling with depressive disorder, technology addiction (social media, cell phone), or divorce reaction problems, but also the entire family; with the guidance they need for lasting change.
Our practitioners are devoted to not only giving guidance to our clients in need, but also the whole family; with the care and commitment required for full change. It is our desire to assist, guide, and coach parents from Orlando, FL, with a troubled child, through a very difficult time. EMA is here to serve! There is hope... and you are not alone. The vision of EMA is to bring forth peace while rehabilitating emotional health for at-risk teen girls from Orlando, FL.
In short, the practitioners at EMA are skilled at supporting troubled adolescents from Orlando, FL with lasting change. As a premier therapeutic boarding school, we offer a variety of relevant residential treatment strategies (equine, life training, behavioral therapy), outdoor recreation and adventure therapy, and life skills development and experiential education; leading our clients to a healthy, balanced life. If you feel you may benefit from our therapeutic boarding school, we encourage you to contact our intake counselors as the first step to creating lasting change in your at-risk child's life. We provide guidance to vulnerable teenage girls from Orlando, FL. Call us at (208) 266-1122 to speak with one of our knowledgeable intake counselors today!
Additional Authorities in Orlando, FL
ALCOHOLICS ANONYMOUS (AA): Giving a global institution for anyone who has problems with alcohol, Alcoholics Anonymous (AA) operates in Orlando, FL, and across the globe. The resource is based on the principles set out in the twelve step program described in the iconic Alcoholics Anonymous book, published in the late 1930s. AA is self-financing and has no political, religious or racial bias. It is open to all who have drinking issues that they want to address. Over the past few decades, AA has been supporting millions of troubled adolescents and young adults nationally, internationally, and in Orlando, FL; to maintain a sober lifestyle.
Residential Treatment Centers for Troubled Girls
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All peace operations are political. Ian Martin wrote an essay with that title in CIC's first Review of Political Missions in 2010. It is unsurprising, then, that the report of the High-Level Panel on Peace Operations of which he has been a prominent member has the same starting point.
One month before launching the High-Level Independent Panel on Peace Operations to examine the state of UN peacekeeping operations and political missions, UN Secretary-General Ban Ki-Moon remarked the time had come to take stock of the lessons we have learned. "The world is changing and our support to peacekeeping, and indeed all peace operations, must keep pace."
Author(s) / Contributor(s): Alischa Kugel
A number of European countries are considering playing a greater military role in UN peacekeeping. However, they have many concerns about the UN's systems for managing missions, which differ markedly from NATO and EU standards. In this paper, based on in-depth interviews with Irish officers and policy-makers and UN officials, Edward Burke and Jonathan Marley give detailed insights into their experiences and lessons.
Author(s) / Contributor(s): Edward Burke, Jonathan Marley
Our Common Agenda: A Quick Scan
Bridging the Silos: Integrating Strategies across Armed Conflict, Violent Crime, and Violent Extremism to Advance the UN's Prevention Agenda
Strengthening Approaches to Conflict Prevention and Peacebuilding at the UN and IFIs: Key Ideas and Recommendations
L'ONU sous Trump/sous Guterres
Antonio Guterres : l'homme qui veut réformer l'ONU
Sustaining Peace in Security Transitions: The Liberian Opportunity


It's a great thing to own a boy puppy, and you have to choose a suitable name for your male dog. There are lots of good male dog names, and many boy dog names have great meanings and sounding. But please keep in mind that the name you chose need to fit the personality and characteristics of your boy puppy, so you need to watch your dog and see what special appearance and personality she has. Check out our collection of male dog names for your boy puppies.


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Integrin-Associated Protein Association With Src Homology 2 Domain Containing Tyrosine Phosphatase Substrate 1 Regulates IGF-I Signaling In Vivo
Laura A. Maile,
Byron E. Capps,
Emily C. Miller,
Ariel W. Aday and
David R. Clemmons
From the Division of Endocrinology, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina
Corresponding author: Laura A. Maile, laura_maile{at}med.unc.edu
Diabetes 2008 Oct; 57(10): 2637-2643. https://doi.org/10.2337/db08-0326
OBJECTIVE—Smooth muscle cell (SMC) maintained in medium containing normal levels of glucose do not proliferate in response to IGF-I, whereas cells maintained in medium containing 25 mmol/l glucose can respond. The aim of this study was to determine whether signaling events that have been shown to be required for stimulation of SMC growth were regulated by glucose concentrations in vivo.
RESEARCH DESIGN AND METHODS—We compared IGF-I–stimulated signaling events and growth in the aortic smooth muscle cells from normal and hyperglycemic mice.
RESULTS—We determined that, in mice, hyperglycemia was associated with an increase in formation of the integrin-associated protein (IAP)/Src homology 2 domaine containing tyrosine phosphatase substrate 1 (SHPS-1) complex. There was a corresponding increase in Shc recruitment to SHPS-1 and Shc phosphorylation in response to IGF-I. There was also an increase in mitogen-activated protein kinase activation and SMC proliferation. The increase in IAP association with SHPS-1 in hyperglycemia appeared to be due to the protection of IAP from cleavage that occurred during exposure to normal glucose. In addition, we demonstrated that the protease responsible for IAP cleavage was matrix metalloprotease-2. An anti-IAP antibody that disrupted the IAP–SHPS-1 association resulted in complete inhibition of IGF-I–stimulated proliferation.
CONCLUSIONS—Taken together, our results support a model in which hyperglycemia is associated with a reduction in IAP cleavage, thus allowing the formation of the IAP–SHPS-1 signaling complex that is required for IGF-I–stimulated proliferation of SMC.
Diabetes is an independent risk factor for atherosclerotic heart disease (1). Studies have shown a correlation between glucose levels and risk of developing atherosclerosis (2–4). Atherosclerosis is characterized by an increase in smooth muscle cell (SMC) migration and proliferation from the vessel wall into the lumen (5). Both in vitro and in vivo studies have demonstrated that IGF-I is a stimulator of SMC migration and proliferation (6–8). When SMCs grown in 5 mmol/l glucose are exposed to IGF-I, there is no increase in migration or proliferation (9). However, when glucose is increased to 25 mmol/l, IGF-I stimulates significant increases in migration and proliferation (10). Phosphorylation of Shc and subsequent activation of the mitogen-activated protein kinase (MAPK) pathway is absolutely required for the migration and proliferation of SMCs in response to IGF-I (11). When SMCs are grown in 25 mmol/l glucose and then exposed to IGF-I, Shc and MAPK phosphorylation are significantly increased. In contrast, when SMCs are grown in 5 mmol/l glucose, there is no increase in Shc or MAPK phosphorylation (10).
We have determined that in contrast to SMCs grown in 5 mmol/l glucose, when SMCs are exposed to 25 mmol/l glucose, Src homology 2 domain containing tyrosine phosphatase substrate 1 (SHPS-1) binds to the extracellular domain of IAP, via its extracellular domain. This interaction is required for IGF-I to stimulate SHPS-1 phosphorylation, which is required for recruitment and phosphorylation of Shc (12). The aims of this study were to determine whether IAP/SHPS-1 interacted in vivo, whether this interaction was regulated by changes in blood glucose levels, and whether this interaction regulated cellular responsiveness to IGF-I stimulation.
Human (endotoxin-free) IGF-I was a gift from Genentech (South San Francisco, CA). Polyvinyl difluoride membranes (Immobilon P) were from Millipore Corporation (Billerica, MA). Autoradiographic film was from Pierce (Rockford, IL). Fetal bovine serum, Dulbecco's modified medium, penicillin, and streptomycin were purchased from Life Technologies (Grand Island, NY). The monoclonal anti-phosphotyrosine (PY99) and the polyclonal anti–IGF-I receptor (IGF-IR) antibodies were from Santa Cruz (Santa Cruz, CA). The phospho/total extracellular signal–related kinase (ERK)1/2 and anti-Shc antibodies were purchased from BD Transduction Laboratories (Lexington, KY). The anti–SHPS-1 antibody was purchased from Upstate Cell Signaling Solutions (Charlottesville, VA). The β-actin was purchased from Chemicon (Temecula, CA). The matrix metalloprotease-2 (MMP-2) inhibitor IV (category number 444274) was purchased from EMD Biosciences (San Diego, CA). All other reagents were from Sigma (St. Louis, MO) unless stated.
Anti-IAP antibodies.
The anti-IAP monoclonal antibody, B6H12, was purified from a cell line derived from a B-cell hybridoma (13). The anti-IAP antibody (referred to as R569), which recognizes amino acids 41 and 61 in the extracellular domain of IAP, has been described previously (14).
Induction of hyperglycemia in mice.
Hyperglycemia was induced in C57/B6 mice (Taconic Hudson NY) using the low-dose streptozotocin (STZ) protocol (15). After a 4-h fast, mice were injected intraperitoneally with either STZ (50 mg/kg) in citrate buffer (pH 4.5) or citrate buffer alone daily for 5 days. The protocols used were derived from those published by the Animal Models of Diabetic Complications Consortium, which were developed to allow direct comparison of the studies from a large consortium of multiple investigators (15).
Blood glucose measurements.
Blood glucose levels were measured using a Freestyle Glucose monitor (Abbott Laboratories, Alameda CA). Blood was obtained from the cheek pouch using GoldenRod animal lancets (Medipoint International, Mineola, NY). Glucose levels were measured before the administration of IGF-I and after 15 min, 30 min, and 30 h.
Measurement of total cholesterol.
Total cholesterol levels were measured in whole blood using a Cardiocheck meter with cholesterol testing strips (Polymer Technology Systems, Indianapolis, IN).
Measurement of IGF-I levels.
An enzyme-linked immunoassay was used to measure IGF-I levels in the serum from mice obtained at necropsy by direct heart puncture (Diagnostic Systems Laboratories, Webster, TX). Samples were treated as described by the manufacturer. Absorbance was measured by a plate reader (measuring wavelength: 450 nm, background wavelength: 530 nm) Appropriate standards ranging in concentration from 0 to 4,000 ng/ml and internal controls (provided by the manufacturer) were used.
Treatment with IGF-I and assessment of SMC proliferation.
Fasted hyperglycemic and control mice were injected intraperitoneally with IGF-I (1 mg/kg), PBS alone, B6H12 (1 mg/kg), control IgG, or B6H12 plus IGF-I 30 h before death. Aortas were removed and fixed before embedding in paraffin. Serial sections (5 μm thick) were cut from the same region of aorta, and every 10th section (four sections/aorta) was incubated with an anti-Ki67 antibody (Abcam, Cambridge, MA) followed by a biotin-conjugated goat anti-rabbit secondary antibody. Staining was visualized using the ABC Elite kit (Vector Laboratories, Burlingame, MA). The number of SMCs staining positive for Ki67 was determined as a percentage of the total number of SMCs in each section. There were a total of six mice in each treatment group. The data shown are the mean percentages of Ki67+ cells from all four sections from each of the mice.
Treatment of mice with IGF-I for assessment of signaling events.
Fasted, hyperglycemic, and control mice were injected intraperitoneally with IGF-I (1 mg/kg) or PBS for 15 and 30 min before death Additional mice were injected with B6H12 (1 mg/kg) or IgG 30 h before death. Aortas were removed and immediately snap-frozen.
Homogenization of aorta samples for protein analysis.
The aortas were homogenized in ice-cold buffer, 20 mmol/l Tris, 150 mmol/l sodium chloride (pH 7.4), 2 mmol/l EDTA, and 0.05% Triton X100, using a glass tissue grinder. Protein levels were measured (bicinchoninic acid; Pierce), and equal amounts were either examined directly by Western immunoblotting after SDS-PAGE or after immunoprecipitation.
Proteins were separated by SDS-PAGE (under nonreducing conditions to visualize IAP; otherwise, reducing conditions were used) and then visualized by Western immunoblotting with appropriate antibodies (at concentrations between 1:500 and 1:1,000).
Analysis of MMP-2 gelatinase activity by zymography.
MMP-2 gelatinase activity was assessed in aorta homogenates and serum-free conditioned medium from murine aortic SMCs (mSMCs) by gelatin zymography (14).
Isolation of mSMCs.
mSMCs were isolated from the aorta of wild-type C57/B6 male mice and maintained in medium containing either 5 or 25 mmol/l glucose (16). Medium containing 5 mmol/l glucose was supplemented to 25 mmol/l with mannitol (the addition of mannitol does not affect IAP cleavage when SMCs are grown in 5 mmol/l glucose [14]). Both types of medium contained 1.0 mmol/l pyruvate.
Analysis of IAP from lysates of mSMCs.
mSMCs were plated in medium containing either 25 or 5 mmol/l glucose. The medium was changed after 3 days. After an additional 3 days, the monolayers were rinsed three times with SFM (5 mmol/l glucose supplemented to 25 mmol/l with mannitol) and incubated 16–17 h. The MMP-2 inhibitor (3 μg/ml) or an equivalent amount of vehicle (dimethylsulphoxide) was added for 4 h. Cells were lysed in modified radioimmunoassay buffer. After centrifugation, equal amounts of cellular protein were mixed with nonreducing gel-loading buffer, heated to 70°C for 10 min and separated by SDS-PAGE (8%). Proteins were visualized by immunoblotting (13).
Data quantification and statistical analysis.
For the biochemical analysis of aortic extracts, a representative Western immunoblot for each experiment is shown. Chemiluminescent images obtained from analysis of at least six mice from each treatment group (from at least three independent sets of mice analyzed over a period of 12 months) were scanned using a DuoScan T1200 (AGFA, Brussels, Belgium), and band intensities were analyzed using NIH Image, version 1.61. An unpaired t test and ANOVA were used to compare the differences in band intensities between the different groups.
Characterization of hyperglycemic mice compared with control mice.
The mean fasting glucose concentration of mice treated with STZ was 285 ± 47 mg/dl compared with 118 ± 17 mg/dl in control mice (mean ± SD, n = 25). Treatment with IGF-I for 30 h had no significant effect on the glucose levels in either the STZ or control mice. After 15 min, there was a transient 66 ± 7% decrease that returned to pretreatment levels by 20 min. There was no significant difference in the body weight between the mice treated with STZ (31 ± 2 g) and controls (29 ± 2 g). Cholesterol levels in the control and STZ-treated mice showed no significant difference (e.g., STZ-treated, 104 ± 3 mg/dl; control, 104 ± 6 mg/dl; NS). There was no significant difference in the levels of IGF-I (STZ-treated, 130 ± 7 ng/ml; control, 130 ± 5 ng/ml; NS). Administration of IGF-I resulted in a 5 ± 0.1-fold increase in serum IGF-I at 15 min; however, after 30 h, it had returned to baseline.
Shc phosphorylation, Shc recruitment to SHPS-1, and SHPS-1 phosphorylation are increased in aorta from hyperglycemic mice.
The proliferative response of cultured SMCs to IGF-I is determined by the extent of Shc phosphorylation (11). The aortic homogenates from the hyperglycemic mice showed a significant 2.8-fold increase in phosphorylated p52 Shc compared with the control mice (scanning units 34,570 ± 16,048 [hyperglycemic], 12,160 ± 2,459 [control], mean ± SD [n = 12, P < 0.005]) (Fig. 1A).
There was a fourfold increase in the amount of Shc associated with SHPS-1 in the hyperglycemic mice compared with the control mice (Fig. 1B, top panel). The scanning units for the hyperglycemic mice were 29,779 ± 14,414 compared with control (7,619 ± 5,848 [mean ± SD, n = 12, P < 0.005]).
Shc recruitment to SHPS-1 requires SHPS-1 phosphorylation (11). When SHPS-1 phosphorylation in aorta homogenates from hyperglycemic and control mice were compared, there was a sevenfold increase in SHPS-1 phosphorylation (Fig. 1B, middle panel). The scanning units for the hyperglycemic mice were 27,466 ± 14,652 compared with control (4,146 ± 3,305 [mean ± SD, n = 8, P < 0.005]).
Hyperglycemia regulates IAP cleavage.
In order for SHPS-1 to be phosphorylated, it must be associated with IAP (12). Our recent in vitro studies have determined that in SMCs cultured in 5 mmol/l glucose, SHPS-1 phosphorylation and formation of the SHPS-1–SHP-2–c-Src–Shc signaling complex (which is required for cellular replication) is impaired because of constitutive cleavage of IAP, which disrupts SHPS-1 binding (14). When the status of IAP in the aortic homogenates was determined, there was a significant (fivefold) increase in intact IAP detected in the homogenates from the hyperglycemic mice compared with controls. The samples were immunoblotted using an anti-IAP antibody (R569) that is specific for intact IAP (Fig. 2A, upper panel). The homogenates were also immunoblotted with an anti-IAP antibody that can detect both intact and fragmented IAP (Fig. 2A, lower panel). In the aortas obtained from the hyperglycemic mice, 82 ± 13.9% (mean ± SD, n = 10) of the total IAP was intact. This was significantly greater than the 20 ± 11.52% (mean ± SD, n = 10, P < 0.005) of the total IAP that was intact in aortas from the control mice. Our previous studies determined that in SMCs cultured in normal glucose, IAP cleavage is mediated by an increase in MMP-2 protease activity (14). Analysis of the aorta homogenates from the STZ mice using gelatin zymography showed that there was a 68.5 ± 0.05% decrease in the amount of protease activity associated with the pro-form of MMP-2 and a similar 59.3 ± 3% decrease in the amount of protease activity associated with the active form of MMP-2 compared with the control mice (Fig. 2, bottom panel; mean ± SD, n = 3, P < 0.05).
Hyperglycemia is associated with an increase in thrombospondin-1 and enhanced IAP–thrombospondin-1 binding.
The IAP ligand thrombospondin (TS)-1 enhances the response of SMC to IGF-I, in part through its binding to IAP (13). There is significantly more TS-1 associated with IAP in SMCs maintained in 25 mmol/l glucose compared with 5 mmol/l glucose (9). Therefore, we determined if the increase in intact IAP in hyperglycemic mice was associated with an increase in TS-1 binding to IAP. There was a sixfold increase in the amount of TS-1 in the aortas of the hyperglycemic mice. The scanning units were 21,968 ± 12,948 (hyperglycemic) and 3,715 ± 3,059 (control) (mean ± SD, n = 8, P < 0.005). Furthermore, there was a significant 3.8 ± 1.3-fold (mean ± SD, n = 8, P < 0.005) increase in the amount of TS-1 that could be coprecipitated with IAP (Fig. 2B).
IAP–SHPS-1 association regulates IGF-I–stimulated signaling events in hyperglycemic mice.
Consistent with the increase in intact IAP in the hyperglycemic mice, we detected a fourfold increase in the amount of IAP that could be coprecipitated with SHPS-1 in the aorta homogenates from hyperglycemic mice compared with controls (Fig. 3A). The scanning units were 27,463 ± 6,453 (hyperglycemic) and 960 ± 7,046 (control) (mean ± SD, n = 6, P < 0.05).
The anti-IAP antibody B6H12 disrupts the association between the two proteins and consequently it inhibits IGF-I signaling (12). To determine whether IAP–SHPS-1 association was required for IGF-I signaling in vivo, we treated the hyperglycemic mice with IGF-I with or without the systemic administration of B6H12. Treatment with B6H12 induced an eightfold decrease between IAP and SHPS-1 association (Fig. 3A) (scanning units 5,517 ± 550 [B6H12] and 27,463 ± 6,453 [hyperglycemic control] [mean ± SD, n = 6, P < 0.05]). Basal SHPS-1 phosphorylation was higher in the hyperglycemic mice compared with controls. After IGF-I, there was a 10-fold increase in SHPS-1 phosphorylation (Fig. 3B, top panel). Administration of B6H12 significantly decreased SHPS-1 phosphorylation in both the hyperglycemic (a twofold decrease) and the hyperglycemic mice treated with IGF-I (a fourfold decrease) (Fig. 3B, top panel). The scanning units were as follows: control mice: 1,725 ± 980, hyperglycemic mice: 13,751 ± 7,117, the hyperglycemic mice treated with IGF-I: 17,162 ± 6,704, hyperglycemic mice treated with B6H12: 7,041 ± 2,931, and hyperglycemic mice treated with IGF-I and B6H12: 6,539 ± 4,653 (mean ± SD, n = 6, P < 0.05).
Our previous studies have shown that activation of MAPK and stimulation of SMC proliferation in response to IGF-I requires formation of an IAP–SHPS-1–Shc signaling complex and Shc phosphorylation. Immunoblotting showed an eightfold increase in ERK1/2 phosphorylation in hyperglycemic mice compared with control mice (Fig. 3B, middle panel). Treatment of the hyperglycemic mice with IGF-I resulted in a 9.8-fold increase in ERK1/2 phosphorylation (compared with no IGF-I treatment). Treatment with B6H12 significantly inhibited the increase in ERK1/2 phosphorylation both in the presence or absence of IGF-I in the hyperglycemic mice (Fig. 3B, middle panel).
Increased cell proliferation in response to IGF-I in hyperglycemic mice.
To demonstrate if these differences in signaling observed in the aortas from hyperglycemic mice resulted in a change in SMC proliferation, hyperglycemic and control mice were injected with IGF-I, and percentage of SMCs that were Ki67+ was quantified. Treatment of the control mice with IGF-I increased the percentage of SMCs positive for Ki67 from 3.6 ± 1.2% (PBS alone) to 9 ± 4.5% (mean ± SD, n = 6). Hyperglycemia alone increased the number to 5.9 ± 1% (mean ± SD, n = 6; P < 0.05). Treatment of hyperglycemic mice with IGF-I resulted in a significant increase in the percentage of Ki67+ cells to 19 ± 2.5% (mean ± SD, n = 6; P < 0.05 when compared with both control and hyperglycemic mice) (Fig. 4). Analysis of IGF-I receptor protein levels showed no difference between the control mice and STZ-treated mice. (STZ, 103 ± 3% of the levels in the control mice [mean ± SD, n = 12]). To determine whether the hyperglycemia-induced increase in IAP association with SHPS-1 was related to enhanced SMC proliferation, hyperglycemic mice were injected with the anti-IAP antibody (B6H12) to disrupt IAP and SHPS-1 association (Fig. 3). After B6H12, the increase in Ki67+ cells induced by either hyperglycemia alone or hyperglycemia plus IGF-I was completely inhibited (3 ± 0.9 and 3.5 ± 1% of cells, respectively, were Ki67+; mean ± SD, P < 0.01).
MMP-2 cleaves IAP in murine SMCs.
We determined previously, using both RNA interference and metalloprotease inhibitors, that the protease in porcine SMCs responsible for the cleavage of IAP is MMP-2 (14). Therefore, we analyzed the ability of the MMP-2 inhibitor (14) to protect IAP from cleavage in mSMCs grown in 5 mmol/l glucose. Basally, there was a significant (65 ± 5%) decrease in the amount of intact IAP compared with mSMCs grown in 25 mmol/l glucose. When SMCs were incubated with the MMP-2 inhibitor, the level of intact IAP in the SMCs grown in 5 mmol/l glucose increased to 113 ± 7% of the level of intact IAP in SMCs grown in 25 mmol/l glucose (Fig. 5A). To confirm that MMP-2 activation is regulated by changes in glucose, we compared the amount of active MMP-2 in the conditioned medium from murine SMCs grown in 5 and 25 mmol/l glucose. There was a significant (2.6-fold) increase in active MMP-2, as detected by gelatin zymography, in the conditioned medium from mSMCs in 5 mmol/l glucose compared with the conditioned medium from mSMCs in 25 mmol/l glucose (Fig. 5B).
SMCs grown in medium containing 5 mmol/l glucose do not proliferate or migrate in response to IGF-I (9). In contrast, SMCs grown in 25 mmol/l glucose show significant increases after IGF-I stimulation (9). This difference in the responsiveness of SMCs in vitro is due to impaired IAP association with SHPS-1, preventing the recruitment and phosphorylation of Shc (9). The results of this study show that IAP is cleaved constitutively in aortic extracts from normoglycemic animals and does not bind to SHPS-1. In contrast, the induction of hyperglycemia in mice is associated with inhibition of IAP cleavage. This allows SHPS-1 and Shc phosphorylation and stimulation of DNA synthesis in response to IGF-I. Although we cannot rule out the possibility that other changes induced by STZ also contribute to changes in IAP cleavage, our data strongly support our conclusion that hyperglycemia is a critical regulator of IAP cleavage and thus allows IGF-I signaling leading to increased SMC replication (Fig. 6).
Hyperglycemia has been associated with an increase in SMC proliferation in response to several growth factors, including IGF-I in vitro (9,17–19). While studies in experimental animal models show that manipulation of IGF-I levels in vascular tissue is related to changes in neointimal formation and SMC proliferation, those studies have not assessed the effect of hyperglycemia on vascular cell proliferation (7,8,20,21). Our results clearly demonstrate that the presence of hyperglycemia results in enhanced responsiveness of vascular SMC to IGF-I in mice. Importantly, they also demonstrate that the signaling mechanism that accounts for enhanced SMC responsiveness to IGF-I in vitro (14) is activated in this animal model, thus leading to the conclusion that it accounts for the increase in cell replication.
Shc phosphorylation was significantly increased in the aorta from hyperglycemic mice, clearly demonstrating that the effect of glucose concentration on Shc phosphorylation is not an artifact of culture conditions or an in vitro phenomenon. For Shc to be phosphorylated in response to IGF-I, it must be recruited to phosphorylated tyrosine residues within the cytoplasmic domain of SHPS-1 (11). In normoglycemic mice, there is minimal SHPS-1 phosphorylation, but in hyperglycemic animals, there is a marked increase in basal and IGF-I–stimulated SHPS-1 phosphorylation. The elevated basal levels presumably reflect enhanced tissue responsiveness to endogenous IGF-I. The increase in SHPS-1 phosphorylation results in enhanced Shc recruitment to SHPS-1 and Shc phosphorylation (11). That this enhanced IGF-I responsiveness in the hyperglycemic animals has important consequences was confirmed in the experiments that showed increased MAPK activation and SMC proliferation.
IAP cleavage results in loss of SHPS-1 association, which disrupts the ability of IGF-I to stimulate MAPK pathway activation and SMC proliferation. Our results show that, in normoglycemic mice, the extracellular domain of IAP is cleaved, resulting in impaired IAP–SHPS-1 association and SHPS-1 phosphorylation. The importance of this association for IGF-I actions is underscored by the result of the experiment in which we disrupted IAP/SHPS-1 using the anti-IAP antibody B6H12. This resulted in attenuation of SHPS-1 phosphorylation and downstream signaling basally and in response to IGF-I. More importantly, this disruption of IAP–SHPS-1 resulted in complete inhibition of the IGF-I–stimulated increase in cell proliferation. This strongly supports the conclusion that failure of IAP–SHPS-1 to associate in normoglycemic conditions leads to attenuation of IGF-I signaling events.
Sajid et al. (22) demonstrated that after balloon injury in baboons, there is a significant increase in IAP in the neointima and media, whereas in uninjured vessels, IAP is only detected in endothelium A significant increase in TS-1 was detected in the same areas after injury (22). Consistent with our findings TS-1 binding to IAP was associated with enhanced SMC proliferation in vitro. While the mechanism that resulted in the increase in detection of intact IAP in the injured vessel was not determined in that study, it seems reasonable to propose that increased cellular levels of IAP and TS-1 are common responses of vascular SMCs to stress (e.g., mechanical injury or hyperglycemia). The increase in IAP and its association with TS-1 leads to enhanced responsiveness of SMCs to IGF-I.
Our finding of increased TS-1 in aorta from hyperglycemic mice is consistent with prior studies that detected increased levels of TS-1 in blood vessels of diabetic Zucker rats (23). Other models of diabetes have also demonstrated increases in TS-1 in cardiac fibroblasts (24), myocytes (25,26), and SMCs (27). TS-1 binding to IAP enhances IGF-I signaling by its ability to modulate the association between IAP and SHPS-1 (13). Because the increase in TS-1 that was detected in the hyperglycemic mice was associated with an increase in the amount of TS-1 associated with the IAP, it seems likely that this change is related to the increase in IAP/SHPS-1 association. Thus, the increased expression of TS-1 in response to hyperglycemia and the associated enhancement of IGF-I signaling is likely to be an important contributor to increased cell proliferation.
In a prior study using MMP-2 RNAi, we determined that the protease responsible for IAP cleavage in porcine SMCs was MMP-2 (14). Our studies using SMCs isolated from murine aorta and an MMP-2 inhibitor strongly support our conclusion that MMP-2 is the protease responsible for IAP cleavage (14). In this study, we demonstrate that there is more MMP-2 activity associated with the aorta from hyperglycemic mice than from control mice. Taken together, these findings suggest that hyperglycemia is functioning to regulate the amount of active MMP-2 in the extracellular environment, thereby regulating IAP cleavage (Fig. 6).
Understanding the role of MMPs in atherosclerosis is complicated by evidence suggesting they play a dual role by regulating SMC migration, matrix deposition, and instability caused by matrix destruction (28). The role of MMPs is further complicated by the use of inhibitors that are not specific for just one MMP and by the possibility of compensatory function of another MMP when one is inhibited. In MMP-2/Apo E−/− mice fed a high-fat diet, lesion size was reduced compared with control mice, apparently as a result of decreased SMC migration (29). In another study, after balloon injury to rats, inhibition of MMP-2 and -9 resulted in decreased SMC migration and early lesion development, but the intimal lesions eventually increased to control levels because of an increased SMC replication rate in the rats treated with the MMP inhibitor (30,31). These findings are consistent with our results that suggest that inhibition of MMP-2 cleavage of IAP enhances SMC proliferation in response to IGF-I. It is interesting to note that Webb et al. (31) observed that, unlike the other MMPs, MMP-2 was produced constitutively in normal rat vessels, but that there was a decrease in levels immediately after injury, rebounding again over time. Other studies have demonstrated either a decrease in MMP-2 (32,33) or an increase in its inhibitor TIMP-1 (34) in cells or tissues from diabetic animals. Thus, our studies support the conclusion that disruption of the association between IAP and SHPS-1 by modulating MMP-2 activity may provide opportunities for delaying the progression of lesion formation that occurs in response to hyperglycemia.
A: Shc phosphorylation and Shc recruitment to SHPS-1 and SHPS-1 phosphorylation in aorta homogenates from hyperglycemic compared with control mice. A: Aortas from hyperglycemic (STZ) and control (CON) mice were homogenized. Shc phosphorylation was determined following immunoprecipitation (IP) with an anti-Shc antibody and immunoblotting (IB) with an anti-phosphotyrosine antibody (p-Tyr). Total Shc levels were determined by immunoblotting with an anti-Shc antibody after Shc immunoprecipitation. The graph shows the difference in Shc phosphorylation when the aortas from the STZ mice are compared with the CON mice expressed as arbitrary scanning units (mean ± SD, n = 12, ***P < 0.005). B: Aortas from hyperglycemic (STZ) and control (CON) mice were homogenized. Shc recruitment to SHPS-1 was determined after immunoprecipitation with an anti–SHPS-1 antibody and immunoblotting with an anti-Shc antibody (Shc) (top panel). SHPS-1 phosphorylation was determined from using the same homogenate by immunoprecipitation with the anti–SHPS-1 antibody and immunoblotting with an antiphosphotyrosine (p-Tyr) antibody (middle panel). Total SHPS-1 levels were determined after immunoprecipitation and immunoblotting with the anti–SHPS-1 antibody. The graph shows the difference in Shc recruitment to SHPS-1 between the aortas from the STZ compared with the CON mice expressed as arbitrary scanning units (mean ± SD, n = 12, ***P < 0.005).
Hyperglycemia regulates cleavage of IAP and TS-1 association with IAP. A: Homogenates from hyperglycemic (STZ) and control (CON) mice were separated by SDS-PAGE and IAP protein levels visualized by Western immunoblotting (IB) with the anti-IAP antibody that selectively recognizes intact IAP (R569) and the anti-IAP monoclonal antibody B6H12 that detects intact and fragmented IAP. MMP-2 activity in homogenates from both groups of mice was assessed by gelatin zymography. The graph shows the difference in the amount of intact IAP between the aortas from the STZ compared with the CON mice expressed as percent (mean ± SD, n = 10, ***P < 0.005). B: Homogenates from hyperglycemic (STZ) and control (CON) mice were either immunoblotted (IB) with an anti–TS-1 antibody (top panel), immunoprecipitated (IP) with the anti-IAP antibody B6H12 before immunoblotting with the anti–TS-1 antibody (middle panel), or immunoblotted with the anti–β-actin antibody. The graph shows the difference in the amount of TS-1 between the aortas from the STZ compared with the CON mice expressed as arbitrary scanning units (mean ± SD, n = 8, ***P < 0.005).
Disrupting the association between IAP and SHPS-1 inhibits SHPS-1 phosphorylation and downstream signaling in response to IGF-I. A: Homogenates from control (CON), hyperglycemic (STZ), and hyperglycemic mice that had been treated with the anti-IAP antibody (B6H12) in vivo were immunoprecipitated (IP) with the anti–SHPS-1 antibody, and IAP association with SHPS-1 was determined by immunoblotting for IAP (B6H12) (top panel). Equal quantities of homogenate from each sample were also immunoblotted with an anti–β-actin antibody (bottom panel). The graph shows the difference in IAP association with SHPS-1 between the aortas from the STZ (with or without injection with B6H12) compared with the CON mice, expressed as arbitrary scanning units (mean ± SD, n = 6, *P < 0.05). B: Homogenates from control, hyperglycemic (STZ), and hyperglycemic mice treated with the anti-IAP antibody B6H12 and/or IGF-I were immunoprecipitated with the anti–SHPS-1 antibody and immunoblotted with the anti-phosphotyrosine antibody (p-Tyr) (top panel). Homogenates were also immunoblotted directly with the anti-phospho ERK1/2 antibody. To demonstrate that there was no difference in the amount of protein in each sample, equal quantities of aortic homogenates were also immunoblotted with the anti–β-actin antibody (bottom panel). The graph shows the difference in SHPS-1 phosphorylation between the aortas from the different treatment groups expressed as arbitrary scanning units (mean ± SD, n = 6, **P < 0.01 when STZ-treated mice are compared with control, ##P < 0.01 when IGF-I treatment of STZ mice is compared with STZ-treated mice alone, and ++P < 0.05 when treatment with B6H12 is compared with STZ alone).
Hyperglycemia enhances the proliferative response of SMCs to IGF-I in vivo. Control (PBS) and hyperglycemic mice (STZ) were treated with IGF-I for 30 h (in the presence of the anti-IAP antibody B6H12 or control IgG). The aortas were removed and paraffin sections prepared. After staining with an anti-Ki67 antibody, the number of proliferating cells in the layer was counted and expressed as the percentage of Ki67 cells. The mean data from six mice per treatment group (with four sections counted/mouse) is shown graphically, and representative images are also shown. *P < 0.05 when the number of Ki67 cells are compared with control mice. **P < 0.01 when Ki67 staining in the presence of B6H12 is compared with STZ or STZ plus IGF-I.
Hyperglycemia-regulated activation of MMP-2 regulates IAP cleavage in murine SMCs. A: Murine SMCs were grown in medium containing either 25 or 5 mmol/l glucose before overnight incubation in serum-free medium. mSMCs grown in both 25 and 5 mmol/l glucose were then exposed to either an MMP-2 inhibitor (MMP-2i) or vehicle alone before lysis. Intact IAP was visualized after immunoblotting with the anti-IAP antibody that recognizes intact IAP (R569). Blots were then stripped and reprobed with the anti–SHPS-1 antibody. The graph shows the amount of IAP expressed as arbitrary scanning units (mean ± SD, n = 3, **P < 0.01 when IAP levels in lysate from SMCs grown in 5 mmol/l glucose are compared with lysate from SMCs grown in 25 mmol/l glucose and ##P < 0.01 when IAP levels in SMCs grown in 5 mmol/l glucose are compared with lysates grown in 5 mmol/l glucose and treated with the MMP-2 inhibitor). The scanning units were as follows: 25 mmol/l glucose 27,321 ± 3,862, 25 mmol/l glucose plus MMP-2 inhibitor 28,052 ± 3,641, 5 mmol/l glucose 9,697 ± 2,516, 5 mmol/l glucose plus MMP-2 inhibitor 30,637 ± 2,117 (mean ± SD, n = 3, P < 0.01). B: Conditioned medium collected from mSMCs grown in 25 and 5 mmol/l glucose and incubated overnight in serum-free medium was analyzed by gelatin zymography (top panel). The graph shows the difference in MMP-2 gelatinase activity expressed as arbitrary scanning units (mean ± SD, n = 3, *P < 0.05). The scanning units for medium collected from mSMCs in 25 mmol/l glucose were 2,173 ± 576 and for mSMCs in 5 mmol/l glucose they were 5,593 ± 1,671 (mean ± SD, n = 3, P < 0.05).
Proposed model by which hyperglycemia enhances IGF-I signaling in SMCs in vivo. Hyperglycemia protects IAP from cleavage by downregulating MMP-2 protease activity that enhances IAP binding to both TS-1 and SHPS-1. This in turn enhances SHPS-1 phosphorylation in response to IGF-I, generating a high-affinity binding site to recruit the SHP-2–c-Src–Shc. Phosphorylation of Shc then leads to activation of downstream signaling pathways including MAPK, which in turn lead to SMC proliferation.
This work was funded by National Institutes of Health Grant HL56850 to D.R.C. and an American Heart Association Mid-Atlantic Affiliate Beginning Grant-in-Aid (0465462U) to L.A.M.
The authors thank the staff of the University of North Carolina (UNC) Michael Hooker Microscopy Facility and Dr. Kirk McNaughton and Carolyn Suitt of the UNC Cardiovascular Biology Histopathology Core Facility for expert histology and immunohistochemistry.
Published ahead of print at http://diabetes.diabetesjournals.org on 15 July 2008.
Accepted July 3, 2008.
Received March 6, 2008.
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October 2008, 57(10)
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Current Position of Political Parties in the 52nd Parliament which must be convened by within six weeks after the return of the Writ or November 23, 2017.
New Zealanders delivered the most frustrating verdict on their politicians as the results of the general elections came in last night.
National Party, which hoped to make its magic of 'Delivering for New Zealanders,' took 46% of the total votes counted thus far, making it the single largest Party in Parliament, three seats shy of majority to govern. With 58 seats in its kitty, the Party still needs three more to from a government. It is assured of one seat that it bequeathed to ACT Party (such support for one seat in the Epsom Constituency has been a part of its election strategy since 2008) but still insufficient to come into the Fourth Term.
Labour Party showed remarkable rebound, claiming 35.8% of the votes counted but its 45 seats would still keep it away from the Treasury benches. Jacinda Ardern has proved to be rejuvenator of her Party, and campaigned vigorously to excite her fellow MPs, electoral and List candidates and encourage people to vote. There were at least three opinion polls that placed Labour ahead of National, sending shockwaves across the Bill English camp. But just a week before elections, fortunes turned in favour of National.
The Green Party, which suffered its worst performance, has been able to obtain just 5.9% of the votes, translating to seven seats. But it is in no position to influence the formation of the next government, although it is very keen to be in the Treasury benches.
New Zealand First Party is in a unique position to decide whether National or Labour would govern over the next three years, with at least two of its MPs firmly obtaining at least two ministerial portfolios, albeit outside the Cabinet, as was the practice in the past.
However, Party Leader Winston Peters, who won in the Northland Constituency in the By-Election held on March 2, 2015, failed last night as the provisional results were announced. He received 12,394 votes, while his National Party opponent received 13 686 votes.
Nonetheless, as the Leader of the third largest Party as on date, he is in the position to decide who should be in the next government.
National Party supporters and some political commentators have said that the Party has the right to rule since it has won 58 seats- more importantly, 46% of New Zealanders have voted for the Party. This, according to them, is the 'Right of Legitimacy,' since technically, National can govern alone with 59 seats (with ACT's one seat) in Parliament.
However, in a democracy, a Party must demonstrate its ability with actual numbers. National must therefore get either National First or the Green Party as its coalition partner to form the next government.
The recent saga of accusations of 'leaked information over his Superannuation overpayments' have further damaged the relationship between the two.
But politics is a game of expediency and it is extremely rare that politicians remember their vows of the past.
But the political scene in New Zealand is not yet clear.
Jacinda Ardern is down but not out. She congratulated Bill English on the splendid performance of his National Party but did not concede defeat. "MMP would decide the next government and I cannot predict what other Leaders will decide," she said.
Labour and Greens enthusiasts would like to believe that if New Zealand First would come to their camp, the three Parties can form a coalition government as they would have the required number of seats – 61 as of now – the exact number required.
But there are several imponderables in this equation. New Zealand First may be able to work with Labour on important areas such as foreign ownership of land and property, housing and immigration (both parties share workable ideologies) but there are several other areas (taxation is one of them) in which there would be discord.
On the equation with the Greens, Mr Peters and his Party have serious differences.
And yet, three-party coalitions have worked in the past, in fact, in the Helen Clark government (which had the old Alliance Party, New Zealand First and UnitedFuture) and the John Key and Bill English governments (with ACT and UnitedFuture). There have been differences among these coalition partners but the respective governments were no threat, and they ran their full tenure.
Once again, our analysis has proved to be right in the case of electoral prospects of candidates of Indian origin. New Zealanders are not yet ready to elect them and their presence in Parliament can be only through the List.
Kanwaljit Singh Bakshi, who has been on National List since 2008 polled 3969 votes compared to 14,004 votes that went to Labour candidate, sitting MP Jenny Salesa. In general election 2014, their final tally was respectively 4422 votes and 17,676 votes.
Dr Parmjeet Parmar, another National Candidate, contesting from Mr Roskill, received 10,168 votes, while Labour's Michael Wood received 15,843 votes.
In the 2014 general election, at which she contested for the first time in Mt Roskill, she obtained 10,546 votes, compared to 18,637 votes won by Labour Candidate Phil Goff.
However, in the by-election (caused by the resignation of Mr Goff on his election as Mayor of Auckland) held on December 3, 2015, she won 4771 votes, compared to Labour Party candidate Michael Wood, who received 11,623 Votes. There are no Party votes in a by-election.
Priyanca Radhakrishnan, who stood for the first time as a Labour candidate in Maungakiekie, lost to National Candidate Denise Lee, polling 12,338 Votes. Ms Lee received 12,338 votes. Although she has not been successful at the electorate, Priyanca will be a Member of Parliament as she is well placed on the Labour Party List (11).
In 2014, Carol Beaumont of Labour had poled 13784 Votes, compared to Peseta Sam Lotu-liga, who won 16,132 Votes.
Bala (Venu) Beeram campaigned hard as National Party candidate in Kelston where his formidable opponent was Carmen Sepuloni of Labour Party. Bala ran a spirited campaign, visiting every household several times with more than 100 volunteers and supporters and yet success eluded him. He polled 7850 Votes, while Carmel retained the seat with 13,199 votes.
Chris Penk, who was National's candidate in Kelston in general election 2014, took 9724 votes, while Carmen received 15,091 votes. His Party nominated him to run in the Helensville electorate vacated by Sir John Key. There were no surprises. He took 18,417 votes, unmatched by Labour's Kurt Taogaga, with 5619 votes.
Bala is unlikely to make it to Parliament this time for his ranking on National List (57) is not favourable, given the Party's Listing system.
General Election 2017 is over but battle lines are still drawn. The outcome will be known over the next week or so. We will provide continue to keep you updated.


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