rongsheng lee in stock

HONG KONG (Reuters) - Trading in shares of China Rongsheng Heavy Industries Group Holdings Ltd, China"s largest private shipbuilder, was suspended on Thursday in the wake of media reports that said it had laid off 8,000 workers in recent months.A view of the Rongsheng Heavy Industries shipyard is seen in Nantong, Jiangsu province, in this file photo taken May 21, 2012. REUTERS/Aly Song/Files

No further details were available and China Rongsheng declined to comment, but analysts said the company’s balance sheet was under pressure. On Wednesday, its shares closed down 10 percent at HK$1.06.

“Moreover, Rongsheng has been suffering due to a major receivables past due problem, thus liquidity is a major concern. I think they are being forced to slash their workforce due to the extreme circumstances the company finds itself in.”

The Wall Street Journal said the job cuts at China Rongsheng represented some 40 percent of the firm’s workforce. The cuts sparked protests by workers earlier this week, according to media reports.

China Rongsheng is a major supplier of bulk carriers that ship iron ore from producer nations such as Brazil to China. Brazil"s Valeis one of its customers.

“We expect a continuing deterioration in the balance sheet given weak overall demand growth for bulk vessels, Rongsheng’s core product,” Barclays analyst Jon Windham said in a report.

According to its December 2012 annual report, issued on March 26, China Rongsheng’s cash and cash equivalents fell to 2.1 billion yuan ($342.53 million) from 6.3 billion yuan a year ago. It had borrowings of 16.26 billion yuan that were due in less than a year, said the report, the latest financial statistics available on the company’s website.

China Rongsheng is the country’s largest private shipbuilder by accumulated order books. It is based in eastern Jiangsu province, near Shanghai, and went public in Hong Kong in 2010.

HONG KONG (Reuters) - Jiangsu Rongsheng Heavy Industries Co Ltd has appointed Morgan Stanleyand JP Morganto finalize plans for its long-awaited IPO in Hong Kong, aiming to raise up to $1.5 billion in the fourth quarter, sources told Reuters on Tuesday.

This is Rongsheng’s latest bid to go public after it failed to raise more than $2 billion from a planned IPO in Hong Kong in 2008, mainly as a result of the global financial crisis.

Rongsheng"s early main shareholders included an Asia investment arm of Goldman Sachs, U.S. hedge fund D.E. Shaw and New Horizon, a China fund founded by the son of Chinese Premier Wen Jiabao.

The three investors sold off their stakes in Rongsheng for a profit early this year, said the sources familiar with the situation. Representatives for the banks, funds and Rongsheng all declined to comment.

Rongsheng’s revived IPO plan comes at a challenging time. Smaller domestic rival, New Century Shipbuilding, slashed its Singapore IPO in half last week, planning to raise up to $560 million from the originally planned $1.24 billion due to weak market conditions.

Given uncertainty in the global shipbuilding business environment as well as growing concerns over a huge flow of fund-raising events in Hong Kong, investment bankers suggest the potential size for Rongsheng could be $1 billion to $1.5 billion, according to the sources.

Rongsheng is seeking to tap capital markets to fund fast growth and aims to catch up with bigger state-owned rivals such as Guangzhou Shipyard International Co Ltd.

Rongsheng won a $484 million deal to build four ships for Oman Shipping Co last year. The vessels would carry exports from an iron ore pellet plant in northern Oman which is expected to begin production in the second half of 2010.

The tender-barge order marks a breakthrough for Shanghai- based Rongsheng as it’s the company’s first in the offshore engineering sector, according to Barclays Plc. The shipbuilder has also hired Don Lee, a former Sembcorp Marine Ltd. executive, and formed a dedicated offshore unit in Singapore as it seeks orders from energy companies to offset waning demand for dry bulk ships.

“Don Lee is very well-known in the marketing and operations of offshore products,” said Shanghai-based UOB Kay Hian Holdings Ltd. analyst Lawrence Li. “The market is expecting that he’ll bring in more offshore orders.”

Lee has worked in the industry for 40 years, and was previously senior general manager at Sembcorp Marine’s Jurong Shipyard, Rongsheng said in a statement yesterday. Singapore-based Sembcorp is the world’s second-biggest oil-rig maker after Keppel Corp.

Rongsheng won the tender-barge order from a Norwegian customer, it said without elaboration. The unit will have a maximum working depth of 2,000 meters and a drilling depth of 6,000 meters, according to the statement.

A company controlled by Rongsheng Chairman Zhang Zhi Rong, Wells Advantage Ltd., also last week agreed to pay $14 million to resolve U.S. regulatory claims that it profited from illegal trades before Cnooc Ltd. announced plans to buy Nexen Inc.

China Huarong Energy Company Limited, an investment holding company, engages in the energy exploration and production businesses. It explores for, produces, and sells crude oil. The company operates five oilfields in the Fergana Valley of the Republic of Kyrgyzstan; and sells petroleum products. It is also involved in commodity trading business; and oil and gas wholesale and distribution activities. The company was formerly known as China Rongsheng Heavy Industries Group Holdings Limited and changed its name to China Huarong Energy Company Limited in April 2015. China Huarong Energy Company Limited was founded in 2004 and is headquartered in Wan Chai, Hong Kong.

The Board is pleased to announce that the English name of the Company has been changed from "China Rongsheng Heavy Industries Group Holdings Limited" to "China Huarong Energy Company Limited" and the Chinese name of the Company has been changed from

The stock short name of shares of the Company for trading on the Stock Exchange will be changed from "CH RONGSHENG" to "HUARONG ENERGY" in English and from "中國 熔盛重工" to "華榮能源" in Chinese with effect from 9:00 a.m. on 24 April 2015. The stock

Reference is made to the announcement of China Huarong Energy Company Limited (formerly known as China Rongsheng Heavy Industries Group Holdings Limited) (the "Company") dated 29 October 2014 and the circular of the Company dated 17 February

The Board is pleased to announce that the English name of the Company has been changed from "China Rongsheng Heavy Industries Group Holdings Limited" to "China Huarong Energy Company Limited" and the Chinese name of the Company has been changed from

The stock short name of shares of the Company for trading on the Stock Exchange will be changed from"CH RONGSHENG" to "HUARONG ENERGY" in English and from "中國熔 盛重工" to "華榮能源" in Chinese with effect from 9:00 a.m. on 24 April 2015. The stock

Hong Kong Exchanges and Clearing Limited and The Stock Exchange of Hong Kong Limited take no responsibility for the contents of this announcement, make no representation as to its accuracy or completeness and expressly disclaim any liability whatsoever for any loss howsoever arising from or in reliance upon the whole or any part of the contents of this announcement. CHINA RONGSHENG HEAVY INDUSTRIES GROUP HOLDINGS LIMITED

By Order of the Board China Rongsheng Heavy Industries Group Holdings Limited LEE Man Yee

“The government should have saved the market because it is mainly small and individual investors who suffered. We don’t have the information that many institutional investors have,” said Liu Rongsheng, 62, a stationery store owner who was following the trading action at Guo Yuan Securities in central Shanghai.

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In foodborne botulism, BoNT must cross intestinal epithelial barriers to enter the blood stream and reach target neurons. The mechanism of how the large BoNT holotoxin or its multi-subunit complexes traverse the polarized epithelial monolayer is not fully understood. The three-dimensional structure of the BoNT/A complex has recently been elucidated (Gu et al., 2012; Lee et al., 2013). Carbohydrate binding sites have been identified and recently shown to be involved in binding to intestinal epithelia. BoNT holotoxins are known to cross the intestinal epithelium from the apical side and relocate to the basolateral side via transcytosis (Maksymowych and Simpson, 1998; 2004,; Ahsan et al., 2005; Fujinaga et al., 2009; Fujinaga, 2010). Large BoNT complexes have been shown to increase oral toxicity in mice by about 20 times over that of purified holotoxin. Toxin complex size is directly proportional to oral toxicity: the larger the complex, the greater the oral toxicity (Ohishi et al., 1977; Sugii et al., 1977; Chen et al., 1998). Studies by others suggest an active role for the NAPs, such as HA33 binding to surface receptors followed by internalization and transcytosis. HA33 was shown to disrupt epithelial tight junctions from the basolateral side, promoting rapid toxin complex passage via a paracellular mechanism (Fujinaga et al., 2009; Jin et al., 2009).

There are at least two proposed mechanisms of BoNT translocation. The first purports that NAPs only protect BoNTs from the low pH and degradative effects of intestinal juices and play no role in holotoxin uptake. In this model, BoNT holotoxin alone is able to traverse the intestinal and lung epithelium and reach the bloodstream intact (Maksymowych et al., 1999; Ahsan et al., 2005; Al-Saleem et al., 2012; Couesnon et al., 2012; Simpson, 2013). In a second model, NAPs play a direct function in binding intestinal receptors, disrupting tight junctions in the intestinal epithelial cell barrier, and promoting the paracellular transport of BoNTs following initial transcytosis (Matsumura et al., 2008; Jin et al., 2009; Sugawara et al., 2010). However, most of the evidence supporting either hypothesis is derived from in vitro cultured intestinal cell models and limited ex vivo studies that do not provide a complete picture of how toxin complexes translocate across the intestinal epithelia.

Little is known regarding the fate of BoNT once ingested. Previous studies have used ex vivo models or ligated intestines to examine the effects of exposure to recombinant BoNT complexes or fragments of BoNTs (Couesnon et al., 2012; Lee et al., 2014). Here we used the mouse oral model of intoxication to study the translocation of the native BoNT/A holotoxin, the BoNT/A complex and the recombinant HA-C. Passages of BoNT and NAPs through the small intestine were tracked over 24 h (Figs 4 and ​and55 and Supporting Information Fig. S5). Similar to the in vitro findings, immunofluorescence-labelled intestinal villi from mice fed with BoNT/A complex showed initial binding of BoNT/A starting at 2 h and peaked at 6 h. However, by 8 h, there is a decrease in immunofluorescence signal suggesting BoNT/A holotoxin clearance into the lymph or blood (Figs 4A and ​and5A).5A). At the intestinal crypts, we found that BoNT/A complex started to appear at the crypts from 2 to 8 h and a decrease in toxin staining by 8 h (Supporting Information Fig. S6). The immunofluorescence signals for HA70 and NTNH showed initial binding that occurred at 2 h and plateaued after 6 h (Fig. 5A and Supporting Information Fig. S7), much like BoNT/A in the complex. Immunofluorescence-labelled intestinal villi from BoNT/A holotoxin fed with mice showed a significant binding that occurred at 4 h and peaked at 8 h. HA70 and NTNH were absent from BoNT/A holotoxin mice, as expected (Figs 4B and ​and5B).5B). We also evaluated intestinal crypts from these tissues. Immunofluorescence images showed that holotoxin appeared in the crypts from 4 to 8 h with a decrease in immunostaining at 24 h (Supporting Information Fig. S6). Treatment of mice with the recombinant HA-C showed similar HA70 immunofluorescence pattern to BoNT/A complex, binding at 2 h and plateaued after 6 h with a longer sustained staining of HA70 at 24 h, suggesting that large amounts of HA70 remained bound to the intestinal cells (Figs 4C and ​and5C).5C). Interestingly, the addition of BoNT/A holotoxin with HA-C did not enhance the time of BoNT/A appearance or binding in the small intestines to that seen in BoNT/A complex-treated mice (Fig. 5).

What role do NAPs play in translocation? Previous data suggested that NAPs, specifically HA33, can disrupt tight junctions, compromising the epithelial cell barrier and allowing BoNT complex to enter through a paracellular pathway (Fujinaga, 2010). The HA-C was also shown to bind E-cadherin, a cell adhesion protein that likely plays a major role in toxin cell surface binding (Sugawara et al., 2010; Lee et al., 2014). The HA-C was observed to disrupt membrane integrity (measured by TER) quickly after toxin or HA addition and much faster after addition of toxins or HA to the basolateral side. These data combined with the location of E-cadherin in the intercellular space suggested that the paracellular translocation pathway was the likely route for toxin complex entry (Lee et al., 2014). In contrast, our results from measuring TER of polarized membranes of Caco-2 cell showed a gradual and mild disruption of membrane beginning at about 4 h after BoNT/A complex or HA-C addition to the apical side (Fig. 3A). When toxins were added to the basolateral side, an even smaller degree of membrane disruption was observed with BoNT/A complex compared with BoNT/A holotoxin (Fig. 3B). We did not observe obvious intestinal membrane disruptions in our small intestinal cross sections (Fig. 5). When BoNT/A holotoxin and the HA-C were added at the same time, no increase in the timing of BoNT/A holotoxin translocation to Caco-2 or small intestinal villi was observed (Fig. 2D and Supporting Information Fig. S5). Thus, in the absence of the NTNH link between the HA-C and BoNT/A holotoxin, toxin entry was not facilitated through a paracellular pathway of transport. The slight membrane disruption observed in TER reductions probably led to some paracellular translocation of the toxin but was likely not the main contributor to BoNT/A translocation. However, despite our results, we believe both models (paracellular vs. receptor-mediated internalization) are possible depending on the amount of toxins present. In the previous TER model, when in the presence of high levels of BoNT toxins, the predominant mode of transport is the likely paracellular pathway mediated by E-cadherin disruption of tight junctions. Our TER assays use substantially less toxin or HA protein than other assays and thus we do not observe the obvious effect of tight junction disruption.

Botulinum neurotoxin serotype A holotoxin, BoNT/A complex and rabbit polyclonal antibodies against BoNT/A were purchased from Metabiologics. The median lethal dose of BoNT/A holotoxin and complex was estimated at 0.42 ng kg−1 or about 8 pg/mouse by intraperitoneal injection and 27 μg kg−1 or about 0.5 μg/mouse for BoNT/A complex via oral gavage (Cheng et al., 2008). Caco-2, a human epithelial colon adenocarcinoma cell line, was purchased from the American Type Culture Collection. Chemicals and reagents were purchased from Sigma-Aldrich and tissue culture supplies were from Life Technologies. Monoclonal antibodies (mAbs): a mAb against the NTNH complex protein, referred to as NTNH 84-27-7-5, was generated following immunization with a recombinant protein corresponding to aa 616-1193 of the NTNH molecule and prepared in Phosphate Buffered Saline (PBS) by the Stanker laboratory (unpublished results); the HA70 specific mAb, NAP80-7-2-1 (Stanker et al., 2013). The recombinant HA-C was obtained from the Jin lab and was prepared as described in Lee et al. 2013 (Gu et al., 2012; Lee et al., 2013).

Al-Saleem FH, Ancharski DM, Joshi SG, Elias M, Singh A, Nasser Z. Simpson LL. Analysis of the mechanisms that underlie absorption of botulinum toxin by the inhalation route. Infect Immun.2012;80:4133–4142. PubMed]

Lee K, Gu S, Jin L, Le TT, Cheng LW, Strotmeier J, et al. Structure of a bimodular botulinum neurotoxin complex provides insights into its oral toxicity. PLoS Pathog.2013;9:e1003690. PubMed]

Lee K, Zhong X, Gu S, Kruel AM, Dorner MB, Perry K, et al. Molecular basis for disruption of E-cadherin adhesion by botulinum neurotoxin A complex. Science.2014;344:1405–1410. PubMed]

Yao G, Lee K, Gu S, Lam KH. Jin R. Botulinum neurotoxin A complex recognizes host carbohydrates through its hemagglutinin component. Toxins.2014;6:624–635. PubMed]

China Rongsheng Heavy Industries Group <1101.HK>, the country"s largest private shipbuilder, said on Monday its chairman had stepped down just three months after the cash-strapped company posted its sharpest fall in half-year net profit.

Listed in November 2010, Rongsheng was hit by an insider dealing scandal involving a firm owned by Zhang ahead of the $15.1 billion bid for Canadian oil firm Nexen Inc by China offshore oil and gas producer CNOOC <0883.HK>.

In August, Rongsheng posted an 82 percent drop in half-year profit on a dearth of new orders and warned that economic uncertainties would continue to weigh on the global shipping market.

As part of the changes at China Rongsheng, the company said that Zhang De Huang was retiring and had resigned as an executive director and as vice chairman of the board.

Citation:Lee K, Gu S, Jin L, Le TTN, Cheng LW, Strotmeier J, et al. (2013) Structure of a Bimodular Botulinum Neurotoxin Complex Provides Insights into Its Oral Toxicity. PLoS Pathog 9(10):

Copyright: © 2013 Lee et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.