Qaasid News

Download Our App

Category: 3. Business

  • Sterling volatility expected around the budget; German economy stagnating – business live | Business

    Sterling volatility expected around the budget; German economy stagnating – business live | Business

    Introduction: Sterling volatility expected around the budget

    Good morning, and welcome to our rolling coverage of business, the financial markets and the world economy.

    The pound is in the spotlight as investors brace for tomorrow’s budget, fearful of a negative market reaction to Rachel Reeves’s plans.

    The pound has weakened over the last few months, down from $1.36 in mid-September to $1.31 today, having hit a seven-month around $1.30 at the start of this month.

    Traders are anxious as to whether the chancellor will manage to rebuild, or even increase, her headroom to hit the government’s fiscal targets in coming years.

    Matthew Ryan, head of market strategy at financial services firm Ebury, predicts the pound will be volatile this week:

    “It’s unclear if there will be enough room to raise taxes sufficiently to reach the required £25-30 billion shortfall, with the government reportedly ruling out hiking income tax rates and seemingly unable to cut fiscal expenditure.

    “We instead see a sort of patchwork of assorted and targeted tax increases, but the devil will be in the details, and if Reeves is unable to convince markets that she has a credible long-term plan for fiscal sustainability, then the pound could struggle on Wednesday. At any rate, brace for volatility in sterling this week.”

    According to the Financial Times this morning, traders have been “piling into bets” that the budget will push the pound lower against the dollar,

    They report that trading volumes in put options, used to speculate on or hedge against a fall in the pound, have outstripped those of bullish call options by more than four to one over the past week, according to derivatives firm CME Group.

    News yesterday that the UK’s growth forecasts will be downgraded has further dampened the mood:

    The flurry of reports of potential budget measures over recent weeks – with an income tax rise first on, then off, the agenda – hasn’t reassured the markets.

    Thomas Pugh, chief economist at audit, tax and consulting firm RSM UK, says this “chaos” is costly:

    “The flip-flopping, U-turning and general chaos of the last couple of months means we are much less certain of what to expect in this week’s budget than usual.

    “This raises three issues. First, chaos has a cost. The recent economic data make it clear that worries about the Budget is dragging on growth. Second, uncertainty raises the chances of an adverse reaction in gilt markets on the day if the budget disappoints. Third, the chances of additional rate cuts next year are falling quickly because it looks like the budget will be less deflationary and more backloaded.

    A tax-heavy budget is likely to weigh on growth, increasing the possibility that the Bank of England cuts interest rates in December and again in 2026.

    Ipek Ozkardeskaya, senior analyst at Swissquote, says tomorrow’s budget is “make-or-break’ for sterling, because…

    ..either the Bank of England steps in to prevent a gilt flare-up if investors dislike what they hear, or to cushion the economy if tax hikes bite hard.

    The agenda

    • 11am GMT: CBI distributive trades report on UK retail

    • 1.30pm GMT: US retail sales report

    • 2pm GMT: Case-Shiller US house price index

    • 3pm GMT: Pending US home sales report

    • 3pm GMT: US consumer confidence report

    Share

    Key events

    “How do you spell stagnation? G-E-R-M-A-N-Y.”

    We have confirmation this morning that Germany’s economy failed to grow in the last quarter.

    German GDP was unchanged in the July-September period, statistics body Destatis has reported, which matche the initial estimate last month.

    Ruth Brand, president of the Federal Statistical Office, says:

    “Economic activity was hampered in the third quarter by weak exports, while investments increased slightly.”

    The lack of growth is a blow to chancellor Friedrich Merz’s efforts to stimulate the economy with a major spending programme.

    Carsten Brzeski, global head of macro at ING, fears that Germamy is in a state of “apparently never-ending paralysis”, with tariffs, the stronger exchange rate, and political tensions and uncertainty all hurting its economy.

    Brzeski told clients:

    How do you spell stagnation? G-E-R-M-A-N-Y. In the past three years, the German economy has recorded only two quarters of positive growth. On average, the economy has shrunk by 0.1% quarter-on-quarter in every single quarter since the fourth quarter of 2022.

    The just-released second estimate of German GDP in the third quarter of 2025 has confirmed this sad record of yet another stagnating quarter. On the year, the economy grew by a meagre 0.3%.

    Share

    Continue Reading

  • Alphabet to omega in AI?

    Alphabet to omega in AI?

    A Google logo is at the announcement of Google’s biggest-ever investment in Germany on November 11, 2025 in Berlin, Germany.

    Sean Gallup | Getty Images News | Getty Images

    Alphabet on Monday resuscitated the artificial intelligence trade, which had been flagging the previous week. Its stock jumped 6.3%, lifting associated AI names such as Broadcom, Micron Technology and AMD. Major indexes rallied, with the Nasdaq Composite posting its best day in six months.

    Investors were particularly enthusiastic about Broadcom because it helps to design and manufacture Google-parent Alphabet's custom AI chips. In other words, the more market share Alphabet's AI offerings gain, the greater the benefit to Broadcom — rather like Nvidia and the broader AI sector at the moment. Broadcom shares surged 11.1% on this notion, making it the S&P 500's top gainer.

    But while investors may cheer Alphabet's leadership on Monday, not everyone wants it to have the last word.

    "Some investors are petrified that Alphabet will win the AI war due to huge improvements in its Gemini AI model and ongoing benefits from its custom TPU chip," Melius Research analyst Ben Reitzes wrote to clients in a Monday note. "GOOGL winning would actually hurt several stocks we cover — so prepare for volatility."

    Approaching the market's moves from another angle, Melissa Brown, managing director of investment decision research at SimCorp, said it's a concern when just one stock lifts the market. "That just doesn't seem to me to be a sustainable force behind driving the market higher over the next however many days," she added.

    Alphabet on Monday may have brought about alpha — in the sense of market outperformance and potentially beginning a new phase of AI enthusiasm — but letting it be the omega as well could pose problems for investors.

    What you need to know today

    U.S. tech stocks roar back. The Nasdaq Composite popped 2.69%, its best day since May 12, on investors enthusiasm over Alphabet. Other major indexes rose in tandem. Asia-Pacific markets were mostly Tuesday as AI-related stocks ticked up.

    Record outflows from BlackRock's bitcoin ETF. The iShares Bitcoin Trust ETF has seen an exodus of $2.2 billion this month as of Monday stateside, according to FactSet data. That's almost eight times more in losses than last October, or its second-worst month on record.

    Sandisk joins the S&P 500. The flash storage vendor will replace marketing company Interpublic Group in the index before trading begins on Nov. 28 stateside. Shares of Sandisk jumped 7% in extended trading on Monday.

    Trump has back-to-back calls with Xi and Takaichi. But the Beijing-Tokyo spat is unlikely to be resolved soon. U.S. President Donald Trump has stayed publicly silent, adding uncertainty for Japan and Taiwan at a tense moment. 

    [PRO] The S&P 500's dividend yield is looking dismal. For investors who are still looking to hold dividend-paying stocks, however, research firm Trivariate Research has a few suggestions on the top performers.

    And finally...

    MUMBAI, INDIA - OCTOBER 22: Executive chair at the South Korean automaker Hyundai Motor Group Euisun Chung and managing director and CEO at India's National Stock Exchange (NSE) Ashish Kumar Chauhan and Jaehoon Chang, Chief Executive Officer (CEO) and President of Hyundai Motor Company pose for a photo during the listing ceremony of Hyundai Motor India for its initial public offering (IPO) at the NSE in Mumbai, India on October 22, 2024.

    Anadolu | Anadolu | Getty Images


    Continue Reading

  • UK's easyJet exceeds annual profit expectations, raises target for holidays business – Reuters

    1. UK’s easyJet exceeds annual profit expectations, raises target for holidays business  Reuters
    2. Week 48 2025: Dubai’s big buys; EasyJet annual results  FlightGlobal
    3. EasyJet’s Q4 revenue at £3.6B, up 7%  breakingthenews.net
    4. FTSE 100 Live 25 November: Index lower despite US advance, B&Q owner lifts guidance  London Evening Standard
    5. Tuesday preview: EasyJet results, US retail sales in focus  Sharecast.com

    Continue Reading

  • Australia is bringing in ‘world first’ minimum pay for food delivery drivers – here’s how it will work | Gig economy

    Australia is bringing in ‘world first’ minimum pay for food delivery drivers – here’s how it will work | Gig economy

    Food delivery companies in Australia have teamed up with the Transport Workers’ Union to set new minimum standards for delivery drivers, including a minimum hourly wage and accident insurance for injuries sustained on the job.

    In a deal described as a “world first”, the country’s two largest food delivery services, DoorDash and Uber Eats, have submitted a joint application with the Transport Workers’ Union to the Fair Work Commission.

    The deal still requires approval from the industrial umpire, but here’s what we know so far.

    What is changing for delivery drivers and their pay?

    The application to the FWC comes after a wide range of workplace reforms was introduced by the Albanese government, which included empowering the industrial umpire to set minimum standards for gig workers.

    DoorDash, Uber Eats and the TWU have agreed on new protections for delivery drivers after years of talks. The deal is likely to have involved concessions from either side of the negotiating table, including the union agreeing to call the workers “employee-like”.

    Among the protections that would be legally enforceable under the new standards is a minimum “safety net” rate of pay of at least $31.30 an hour which would come into effect from 1 July 2026 and increase slightly from 1 January 2027.

    The safety net would apply to all modes of transport used by delivery drivers, with the rate varying slightly depending on the type of vehicle used.

    The protections also include new dispute resolution processes, new engagement and feedback mechanisms, representation rights and accident insurance for injured workers.

    Eric Ireland, a driver in Melbourne who has worked for several platforms, believes the new standards will result in an increase in pay because it means he and his colleagues will get paid even if they have to wait for a restaurant to finish preparing the food.

    “The peace of mind that you are actually getting paid while you’re on the job … can only be a good thing,” he says.

    Ireland says while some working conditions have improved since he started delivering food six years ago, pay has not kept up with the cost of living.

    “I sort of worked out on average I get about $22 an hour before I pay for petrol,” he says. “Sometimes you can earn a lot more than that if you do what they call a ‘quest’, which is doing 10 jobs in a weekend or something.”

    However, as the workplace relations expert Prof Alex Veen points out, the safety net is different to a “minimum wage” in the way you may typically think of one.

    The deal does not include penalty rates for things such as working late at night and, Veen says, the minimum hourly rate does not apply to time spent waiting between delivery jobs.

    “What it materially means for gig workers is that when they’re working in periods of low demand they are unlikely to make that as their hourly pay,” Veen, a lecturer at the University of Sydney’s business school, says.

    But he says there are many positives to the deal, including clarifying who is responsible for insuring both vehicles and the workers themselves.

    How will the accident insurance work?

    The application to the FWC states that workers are responsible for maintaining third-party insurances on the vehicles they use for deliveries, so if they get in an accident and damage another vehicle the delivery platform will not be liable for the cost.

    On the other hand, Uber Eats and DoorDash will have to organise and pay for personal accident insurance that “provides a reasonable minimum level of cover” for their delivery workers. As Veen points out, that is “obviously open to interpretation”.

    The TWU says 23 gig workers have been killed in Australia since 2017 and the figure could be higher because some are never reported as workplace deaths.

    Will customers pay more for food delivery?

    While Uber Eats and DoorDash are yet to confirm how they plan to fund an increase in operating costs, Veen says the platforms are most likely to pass them on to consumers.

    “They may try to pass some of the costs on to restaurants and they could take a smaller [profit] margin themselves, although that’s not in their interests to do so,” he says.

    Dr Michael Rawling, an associate professor who teaches workplace law at the University of Technology Sydney, says there may be a small increase in the price of a takeaway ordered through a third-party delivery app.

    “In Australia we like to see workers treated fairly and if the consumer knows that then I think they’ll cop a small increase,” he says.

    Is it really a world first?

    Rawling agrees the deal is “world leading” and “very significant”.

    He says while the deal hasn’t been ratified by the FWC, the “major players” who will be affected by the new standard have agreed on its content, which the industrial umpire will factor into its decision.

    “[Typically] what the parties have actually consented to is a preferred direction for the FWC to go into for that particular matter,” he says.

    What comes next?

    The FWC needs to approve the deal before it can come into effect.

    Prof Andrew Stewart, a workplace relations expert at the Queensland University of Technology, says it is “not a done deal”, especially as the FWC will have to consult with other stakeholders – including other delivery platforms.

    “Potentially a huge fly in the ointment is that the FWC is going to have to come to a view as to whether the workers are eligible for a minimum standards order,” he says. “Because there’s a perfectly credible argument that the workers are already employees [and not employee-like].”

    Stewart says if the FWC ruled that food delivery drivers were employees and not “employee-like” this would be a landmark ruling that would likely result in a challenge from the delivery platforms that could go all the way to the high court.

    He is not ruling out this outcome, even though he says it is more likely the FWC will accept the application as it stands.

    “I do not want to understate the significance of this deal,” he says. “It is a really important agreement that makes it much more likely we will get a minimum standards order much more quickly than we would if the TWU and the platforms were fighting over the details.”

    What does this mean for the gig economy more broadly?

    Overall, Stewart says the agreement on the application brings Australia a lot closer to having a safety net for at least one part of the gig economy.

    It could also influence future FWC decisions relating to minimum standards. At the moment, the commission is considering similar gig workers in other sectors including package delivery. And the TWU has previously flagged it will submit an application to cover ride-share drivers.

    Continue Reading

  • Asian shares advance after Wall Street gets a lift from hopes for a Fed rate cut

    Asian shares advance after Wall Street gets a lift from hopes for a Fed rate cut

    BANGKOK — Asian shares mostly gained on Tuesday after U.S. stocks rallied on hopes the Federal Reserve will cut interest rates soon.

    U.S. futures edged lower and oil prices also declined.

    Tokyo’s Nikkei 225 was nearly unchanged at 48,628.85, after reopening from a holiday.

    A plunge in technology giant SoftBank’s shares weighed on the market. It fell 10.3% on concerns that returns from its heavy investments in OpenAI may be threatened by the next generation Gemini artificial intelligenc e model that Google launched last week.

    In South Korea, the Kospi gained 0.3% to 3,859.12. Taiwan’s Taiex jumped 1.5%.

    Chinese markets also advanced. In Hong Kong, the Hang Seng climbed 0.4% to 25,821.47, while the Shanghai Composite index jumped 0.9% to 3,872.45.

    E-commerce giant Alibaba, which was due to report its earnings late Tuesday, gained 1.6%.

    Australia’s S&P/ASX rebounded to edge 0.1% higher, closing at 8,537.00.

    U.S. markets will be closed on Thursday for the Thanksgiving holiday. A day later, it’s on to the rush of Black Friday and Cyber Monday.

    The U.S. stock market rallied on Monday, at the start of a week with shortened trading because of the Thanksgiving holiday.

    The S&P 500 climbed 1.5% to 6,705.12 in one of its best days since the summer. The Dow Jones Industrial Average rose 0.4% to 46,448.27, and the Nasdaq composite jumped 2.7% to 22,872.01.

    Stocks got a lift from rising hopes that the Fed will cut its main interest rate again at its next meeting in December, a move that could boost the economy and investment prices.

    The market also benefited from strength for stocks caught up in the artificial-intelligence frenzy. Alphabet, which has been getting praise for its newest Gemini AI model, rallied 6.3% and was one of the strongest forces lifting the S&P 500. Nvidia rose 2.1%.

    Monday’s gains followed sharp swings in recent weeks, not just day to day but also hour to hour, caused by uncertainty about what the Fed will do with interest rates and whether too much money is pouring into AI and creating a bubble. All the worries are creating the biggest test for investors since an April sell-off, when President Donald Trump shocked the world with his “Liberation Day” tariffs.

    Despite all the recent fear, the S&P 500 remains within 2.7% of its record set last month.

    Several tests for the market lie ahead this week. One of the biggest will arrive Tuesday when the U.S. government will deliver data on inflation at the wholesale level in September.

    Economists expect it to show a 2.6% rise in prices from a year earlier, the same as in August. A higher-than-expected reading could deter the Fed from cutting its main interest rate in December for a third time this year, because lower rates can worsen inflation. Some Fed officials have already argued against a December cut in part because inflation has stubbornly remained above their 2% target.

    Traders are nevertheless betting on a nearly 85% probability that the Fed will cut rates next month, up from 71% on Friday and from less than a coin flip’s chance seen a week ago, according to data from CME Group.

    In other dealings early Tuesday, U.S. benchmark crude oil lost 25 cents to $58.59 per barrel. Brent crude, the international standard, shed 30 cents to $62.42 per barrel.

    The dollar fell to 156.70 Japanese yen from 156.91 yen. The euro slipped to $1.1517 from $1.1521.

    Bitcoin fell 1.1% to $88,100. It was near $125,000 last month.

    Continue Reading

  • Progress on share buyback programme

    Progress on share buyback programme

    Amsterdam,

    ING announced today that, as part of our €1.1 billion share buyback programme announced on 30 October 2025, in total 2,767,892 shares were repurchased during the week of 17 November up to and including 21 November 2025.

    The shares were repurchased at an average price of €21.60 for a total amount of €59,777,931.11.

    In line with the purpose of the programme to reduce the share capital of ING, the total number of shares repurchased under this programme to date is 7,899,202 at an average price of €22.02 for a total consideration of €173,950,206.98. To date approximately 15.81% of the maximum total value of the share buyback programme has been completed.

    For detailed information on the daily repurchased shares, individual share purchase transactions and weekly reports, see share buy back programme.

    Note for editors

    More on investor information, go to the investor relations section on this site.

    For news updates, go to the newsroom on this site or via X (@ING_news feed).

    For ING photos such as board members, buildings, go to Flickr.

    ING PROFILE

    ING is a global financial institution with a strong European base, offering banking services through its operating company ING Bank. The purpose of ING Bank is: empowering people to stay a step ahead in life and in business. ING Bank’s more than 60,000 employees offer retail and wholesale banking services to customers in over 100 countries.

    ING Group shares are listed on the exchanges of Amsterdam (INGA NA, INGA.AS), Brussels and on the New York Stock Exchange (ADRs: ING US, ING.N).

    ING aims to put sustainability at the heart of what we do. Our policies and actions are assessed by independent research and ratings providers, which give updates on them annually. ING’s ESG rating by MSCI was reconfirmed by MSCI as ‘AA’ in August 2024 for the fifth year. As of December 2023, in Sustainalytics’ view, ING’s management of ESG material risk is ‘Strong’. Our current ESG Risk Rating, is 17.2 (Low Risk). ING Group shares are also included in major sustainability and ESG index products of leading providers. Here are some examples: Euronext, STOXX, Morningstar and FTSE Russell. Society is transitioning to a low-carbon economy. So are our clients, and so is ING. We finance a lot of sustainable activities, but we still finance more that’s not. Follow our progress on ing.com/climate.

    Important legal information

    Elements of this press release contain or may contain information about ING Groep N.V. and/ or ING Bank N.V. within the meaning of Article 7(1) to (4) of EU Regulation No 596/2014 (‘Market Abuse Regulation’).

    ING Group’s annual accounts are prepared in accordance with International Financial Reporting Standards as adopted by the European Union (‘IFRS- EU’). In preparing the financial information in this document, except as described otherwise, the same accounting principles are applied as in the 2024 ING Group consolidated annual accounts. All figures in this document are unaudited. Small differences are possible in the tables due to rounding.

    Certain of the statements contained herein are not historical facts, including, without limitation, certain statements made of future expectations and other forward-looking statements that are based on management’s current views and assumptions and involve known and unknown risks and uncertainties that could cause actual results, performance or events to differ materially from those expressed or implied in such statements. Actual results, performance or events may differ materially from those in such statements due to a number of factors, including, without limitation: (1) changes in general economic conditions and customer behaviour, in particular economic conditions in ING’s core markets, including changes affecting currency exchange rates and the regional and global economic impact of the invasion of Russia into Ukraine and related international response measures (2) changes affecting interest rate levels (3) any default of a major market participant and related market disruption (4) changes in performance of financial markets, including in Europe and developing markets (5) fiscal uncertainty in Europe and the United States (6) discontinuation of or changes in ‘benchmark’ indices (7) inflation and deflation in our principal markets (8) changes in conditions in the credit and capital markets generally, including changes in borrower and counterparty creditworthiness (9) failures of banks falling under the scope of state compensation schemes (10) non- compliance with or changes in laws and regulations, including those concerning financial services, financial economic crimes and tax laws, and the interpretation and application thereof (11) geopolitical risks, political instabilities and policies and actions of governmental and regulatory authorities, including in connection with the invasion of Russia into Ukraine and the related international response measures (12) legal and regulatory risks in certain countries with less developed legal and regulatory frameworks (13) prudential supervision and regulations, including in relation to stress tests and regulatory restrictions on dividends and distributions (also among members of the group) (14) ING’s ability to meet minimum capital and other prudential regulatory requirements (15) changes in regulation of US commodities and derivatives businesses of ING and its customers (16) application of bank recovery and resolution regimes, including write down and conversion powers in relation to our securities (17) outcome of current and future litigation, enforcement proceedings, investigations or other regulatory actions, including claims by customers or stakeholders who feel misled or treated unfairly, and other conduct issues (18) changes in tax laws and regulations and risks of non-compliance or investigation in connection with tax laws, including FATCA (19) operational and IT risks, such as system disruptions or failures, breaches of security, cyber-attacks, human error, changes in operational practices or inadequate controls including in respect of third parties with which we do business and including any risks as a result of incomplete, inaccurate, or otherwise flawed outputs from the algorithms and data sets utilized in artificial intelligence (20) risks and challenges related to cybercrime including the effects of cyberattacks and changes in legislation and regulation related to cybersecurity and data privacy, including such risks and challenges as a consequence of the use of emerging technologies, such as advanced forms of artificial intelligence and quantum computing (21) changes in general competitive factors, including ability to increase or maintain market share (22) inability to protect our intellectual property and infringement claims by third parties (23) inability of counterparties to meet financial obligations or ability to enforce rights against such counterparties (24) changes in credit ratings (25) business, operational, regulatory, reputation, transition and other risks and challenges in connection with climate change, diversity, equity and inclusion and other ESG-related matters, including data gathering and reporting and also including managing the conflicting laws and requirements of governments, regulators and authorities with respect to these topics (26) inability to attract and retain key personnel (27) future liabilities under defined benefit retirement plans (28) failure to manage business risks, including in connection with use of models, use of derivatives, or maintaining appropriate policies and guidelines (29) changes in capital and credit markets, including interbank funding, as well as customer deposits, which provide the liquidity and capital required to fund our operations, and (30) the other risks and uncertainties detailed in the most recent annual report of ING Groep N.V. (including the Risk Factors contained therein) and ING’s more recent disclosures, including press releases, which are available on www.ING.com.

    This document may contain ESG-related material that has been prepared by ING on the basis of publicly available information, internally developed data and other third-party sources believed to be reliable. ING has not sought to independently verify information obtained from public and third-party sources and makes no representations or warranties as to accuracy, completeness, reasonableness or reliability of such information. This document may also discuss one or more specific transactions and/or contain general statements about ING’s ESG approach. The approach and criteria referred to in this document are intended to be applied in accordance with applicable law. Due to the fact that there may be different or even conflicting laws, the approach, criteria or the application thereof, could be different.

    Materiality, as used in the context of ESG, is distinct from, and should not be confused with, such term as defined in the Market Abuse Regulation or as defined for Securities and Exchange Commission (‘SEC’) reporting purposes. Any issues identified as material for purposes of ESG in this document are therefore not necessarily material as defined in the Market Abuse Regulation or for SEC reporting purposes. In addition, there is currently no single, globally recognized set of accepted definitions in assessing whether activities are “green” or “sustainable.” Without limiting any of the statements contained herein, we make no representation or warranty as to whether any of our securities constitutes a green or sustainable security or conforms to present or future investor expectations or objectives for green or sustainable investing. For information on characteristics of a security, use of proceeds, a description of applicable project(s) and/or any other relevant information, please reference the offering documents for such security.

    This document may contain inactive textual addresses to internet websites operated by us and third parties. Reference to such websites is made for information purposes only, and information found at such websites is not incorporated by reference into this document. ING does not make any representation or warranty with respect to the accuracy or completeness of, or take any responsibility for, any information found at any websites operated by third parties. ING specifically disclaims any liability with respect to any information found at websites operated by third parties. ING cannot guarantee that websites operated by third parties remain available following the publication of this document, or that any information found at such websites will not change following the filing of this document. Many of those factors are beyond ING’s control.

    Any forward-looking statements made by or on behalf of ING speak only as of the date they are made, and ING assumes no obligation to publicly update or revise any forward-looking statements, whether as a result of new information or for any other reason.

    This document does not constitute an offer to sell, or a solicitation of an offer to purchase, any securities in the United States or any other jurisdiction.


    Continue Reading

  • Factors associated with the avoidance of glaucoma surgery in secondary glaucoma due to ocular inflammatory disease | Journal of Ophthalmic Inflammation and Infection

    Factors associated with the avoidance of glaucoma surgery in secondary glaucoma due to ocular inflammatory disease | Journal of Ophthalmic Inflammation and Infection

  • Siddique SS, Suelves AM, Baheti U, Foster CS (2013 Jan-Feb) Glaucoma and uveitis. Surv Ophthalmol. 58(1):1–10. https://doi.org/10.1016/j.survophthal.2012.04.006

  • Neri P, Azuara-Blanco A, Forrester JV (2004) Incidence of glaucoma in patients with uveitis. J Glaucoma 13(6):461–465. https://doi.org/10.1097/01.ijg.0000146391.77618.d0

    Google Scholar 

  • Merayo-Lloves J, Power WJ, Rodriguez A, Pedroza-Seres M, Foster CS (1999) Secondary glaucoma in patients with uveitis. Ophthalmologica 213(5):300–304. https://doi.org/10.1159/000027443

    Google Scholar 

  • Takahashi T, Ohtani S, Miyata K, Miyata N, Shirato S, Mochizuki M (2002 Sep-Oct) A clinical evaluation of uveitis-associated secondary glaucoma. Jpn J Ophthalmol 46(5):556–562. https://doi.org/10.1016/s0021-5155(02)00549-x

  • Heinz C, Koch JM, Zurek-Imhoff B, Heiligenhaus A (2009) Prevalence of uveitic secondary glaucoma and success of nonsurgical treatment in adults and children in a tertiary referral center. Ocul Immunol Inflamm 17(4):243–248. https://doi.org/10.1080/09273940902913035

  • Dick AD, Tundia N, Sorg R, Zhao C, Chao J, Joshi A, Skup M (2016) Risk of Ocular Complications in Patients with Noninfectious Intermediate Uveitis, Posterior Uveitis, or Panuveitis. Ophthalmology. ;123(3):655 – 62. https://doi.org/10.1016/j.ophtha.2015.10.028. Epub 2015 Dec 19. Erratum in: Ophthalmology. 2016;123(11):2439. https://doi.org/10.1016/j.ophtha.2016.09.006.

  • Daniel E, Pistilli M, Kothari S, Khachatryan N, Kaçmaz RO, Gangaputra SS, Sen HN, Suhler EB, Thorne JE, Foster CS, Jabs DA, Nussenblatt RB, Rosenbaum JT, Levy-Clarke GA, Bhatt NP, Kempen JH, Systemic Immunosuppressive Therapy for Eye Diseases Research Group (2017) Risk of ocular hypertension in adults with noninfectious uveitis. Ophthalmology 124(8):1196–1208. https://doi.org/10.1016/j.ophtha.2017.03.041Epub 2017 Apr 19

    Google Scholar 

  • Niederer RL, Wong ABC, Ma T, Chew S, Sims J (2023) Predictors of glaucoma in patients with uveitis and scleritis. Eye (Lond) 37(6):1254–1257. https://doi.org/10.1038/s41433-022-02101-7Epub 2022 May 24

    Google Scholar 

  • Ma T, Sims JL, Bennett S, Chew S, Niederer RL (2022) High rate of conversion from ocular hypertension to glaucoma in subjects with uveitis. Br J Ophthalmol 106(11):1520–1523. https://doi.org/10.1136/bjophthalmol-2021-318809Epub 2021 May 21

    Google Scholar 

  • Liu X, Kelly SR, Montesano G, Bryan SR, Barry RJ, Keane PA, Denniston AK, Crabb DP (2019) Evaluating the impact of uveitis on visual field progression using Large-Scale Real-World data. Am J Ophthalmol 207:144–150 Epub 2019 Jun 26

    Google Scholar 

  • Carreño E, Villarón S, Portero A, Herreras JM, Maquet JA, Calonge M (2011) Surgical outcomes of uveitic glaucoma. J Ophthalmic Inflamm Infect 1(2):43–53. https://doi.org/10.1007/s12348-010-0012-8Epub 2010 Nov 18

    Google Scholar 

  • Halkiadakis I, Konstantopoulou K, Tzimis V, Papadopoulos N, Chatzistefanou K, Markomichelakis NN (2024) Update on diagnosis and treatment of uveitic glaucoma. J Clin Med 13(5):1185. https://doi.org/10.3390/jcm13051185

    Google Scholar 

  • Almobarak FA, Alharbi AH, Morales J, Aljadaan I (2018) The influence of mitomycin C concentration on the outcome of trabeculectomy in uveitic glaucoma. Int Ophthalmol 38(6):2371–2379. https://doi.org/10.1007/s10792-017-0737-6Epub 2017 Oct 14

    Google Scholar 

  • Iwao K, Inatani M, Seto T, Takihara Y, Ogata-Iwao M, Okinami S, Tanihara H (2014) Long-term outcomes and prognostic factors for trabeculectomy with mitomycin C in eyes with uveitic glaucoma: a retrospective cohort study. J Glaucoma 23(2):88–94. https://doi.org/10.1097/IJG.0b013e3182685167

    Google Scholar 

  • Hoffmann EM, Hengerer F, Klabe K, Schargus M, Thieme H, Voykov B (2021) Aktuelle Glaukomchirurgie [Glaucoma surgery today]. Ophthalmologe. ;118(3):239–247. German. https://doi.org/10.1007/s00347-020-01146-x. Erratum in: Ophthalmologe. 2021;118(Suppl 2):183. https://doi.org/10.1007/s00347-021-01457-7.

  • Almobarak FA, Alharbi AH, Aljadaan I, Aldhibi H (2021) Long-term outcomes of initial trabeculectomy in glaucoma associated with granulomatous and non-granulomatous uveitis. Int Ophthalmol 41(10):3459–3470. https://doi.org/10.1007/s10792-021-01910-1Epub 2021 Jun 7

    Google Scholar 

  • Bitossi A, Mattioli I, Bettiol A, Palermo A, Malandrino D, Bacherini D, Virgili G, Giansanti F, Vannozzi L, Silvestri E (2023) Non-anti TNFα biologic agents for noninfectious uveitis associated with systemic inflammatory diseases: a systematic review. Expert Rev Clin Immunol 19(5):549–560 Epub 2023 Mar 27

    Google Scholar 

  • Sonoda KH, Hasegawa E, Namba K, Okada AA, Ohguro N, Goto H, JOIS (Japanese Ocular Inflammation Society) Uveitis Survey Working Group (2021) Epidemiology of uveitis in japan: a 2016 retrospective nationwide survey. Jpn J Ophthalmol 65(2):184–190. https://doi.org/10.1007/s10384-020-00809-1Epub 2021 Mar 11

    Google Scholar 

  • Chauhan K, Tyagi M (2024) Update on non-infectious uveitis treatment: anti-TNF-alpha and beyond. Front Ophthalmol (Lausanne) 4:1412930. https://doi.org/10.3389/fopht.2024.1412930

    Google Scholar 

  • Kalogeropoulos D, Sung VC, Curr Glaucoma J Pract (2018) Sep-Dec ;12(3):125–138. https://doi.org/10.5005/jp-journals-10028-1257

  • Pillai MR, Balasubramaniam N, Wala N, Mathews AM, Tejeswi B, Krishna H, Ishrath D, Rathinam SR, Sithiq Uduman SM (2024) Glaucoma in uveitic eyes: long-term clinical course and management measures. Ocul Immunol Inflamm 32(6):1041–1047 Epub 2023 May 4

    Google Scholar 

  • Mosaed S (2020) Ab interno trabeculotomy in uveitic glaucoma: confirmation of original results with extended applications. Clin Exp Ophthalmol 48(1):12–13. https://doi.org/10.1111/ceo.13699

    Google Scholar 

  • Ikegawa W, Suzuki T, Namiguchi K, Mizoue S, Shiraishi A, Ohashi Y (2016) Changes in anterior segment morphology of Iris Bombe before and after laser peripheral iridotomy in patients with uveitic secondary glaucoma. J Ophthalmol 2016:8496201. https://doi.org/10.1155/2016/8496201

    Google Scholar 

  • Škrlová E, Svozílková P, Heissigerová J, Fichtl M (2023) Pathogenesis and current methods of treatment, of secondary uveitic glaucoma. a review. Cesk Slov Oftalmol 79(3):111–115 English. https://doi.org/10.31348/2023/7

  • Shrestha S, Thapa M, Shah DN (2014) Pattern of intraocular pressure fluctuation in uveitic eyes treated with corticosteroids. Ocul Immunol Inflamm 22(2):110–115. https://doi.org/10.3109/09273948.2013.824106

    Google Scholar 

  • Razeghinejad MR, Katz LJ (2012) Steroid-induced iatrogenic glaucoma. Ophthalmic Res 47(2):66–80. https://doi.org/10.1159/000328630

    Google Scholar 

  • Alaghband P, Baneke AJ, Galvis E, Madekurozwa M, Chu B, Stanford M, Overby D, Lim KS (2019) Aqueous humor dynamics in uveitic eyes. Am J Ophthalmol 208:347–355 Epub 2019 Aug 30

    Google Scholar 

  • Yorio T, Patel GC, Clark AF (2020) Glucocorticoid-induced ocular hypertension: origins and new approaches to minimize. Expert Rev Ophthalmol 15(3):145–157 Epub 2020 May 14

    Google Scholar 

  • Chang SM, St Peter DM, Im LT, Munir WM, Schocket LS (2022) Dexamethasone implant migration in an eye with congenital glaucoma: a case report and review of the literature. Eur J Ophthalmol 32(5):NP46–NP50. Epub 2021 Mar 29 https://doi.org/10.1177/11206721211005696

    Google Scholar 

  • Nguyen QD, Merrill PT, Jaffe GJ, Dick AD, Kurup SK, Sheppard J, Schlaen A, Pavesio C, Cimino L, Van Calster J, Camez AA, Kwatra NV, Song AP, Kron M, Tari S, Brézin AP (2016) Adalimumab for prevention of uveitic flare in patients with inactive non-infectious uveitis controlled by corticosteroids (VISUAL II): a multicentre, double-masked, randomised, placebo-controlled phase 3 trial. Lancet. ;388(10050):1183-92. https://doi.org/10.1016/S0140-6736(16)31339-3. Epub 2016 Aug 16. Erratum in: Lancet. 2016;388(10050):1160. doi: 10.1016/S0140-6736(16)31538-0

  • Suhler EB, Adán A, Brézin AP, Fortin E, Goto H, Jaffe GJ, Kaburaki T, Kramer M, Lim LL, Muccioli C, Nguyen QD, Van Calster J, Cimino L, Kron M, Song AP, Liu J, Pathai S, Camez A, Schlaen A, van Velthoven MEJ, Vitale AT, Zierhut M, Tari S, Dick AD (2018) Safety and efficacy of adalimumab in patients with noninfectious uveitis in an ongoing Open-Label study: VISUAL III. Ophthalmology 125(7):1075–1087. https://doi.org/10.1016/j.ophtha.2017.12.039Epub 2018 Feb 9

    Google Scholar 

  • Inoue T (2017) [The science of glaucoma surgery -Filtration surgery and the role of Cytokines]. Nippon Ganka Gakkai Zasshi 121(3):314–334 Japanese

    Google Scholar 

  • Lee J, Choi JA, Ju HH, Kim JE, Paik SY, Rao PV (2021) Role of MCP-1 and IL-8 in viral anterior uveitis, and contractility and fibrogenic activity of trabecular meshwork cells. Sci Rep 11(1):14950. https://doi.org/10.1038/s41598-021-94391-2

    Google Scholar 

  • Suzuki K, Iwata D, Namba K, Hase K, Hiraoka M, Murata M, Kitaichi N, Foxton R, Ishida S (2023) Involvement of angiopoietin 2 and vascular endothelial growth factor in uveitis. PLoS ONE 18(11):e0294745. https://doi.org/10.1371/journal.pone.0294745

    Google Scholar 

  • Singh S, Anshita D, Ravichandiran V (2021) MCP-1: Function, regulation, and involvement in disease. Int Immunopharmacol. 101(Pt B):107598. https://doi.org/10.1016/j.intimp.2021.107598

Continue Reading

  • South African rand steady ahead of key indicator data – Reuters

    1. South African rand steady ahead of key indicator data  Reuters
    2. South African Markets – Factors to watch on November 25  TradingView
    3. South Africa Gears Up For Key Economic And Market Updates  Finimize
    4. USD/ZAR Analysis 24/11: Rally Loses Steam (Chart)  DailyForex
    5. Another R160 million circling the drain, and trouble for South Africa’s Afrikaans Uber  BusinessTech

    Continue Reading

  • Novartis data underscore pioneering scientific innovation in Hematology and Oncology at ASH and SABCS

    Novartis data underscore pioneering scientific innovation in Hematology and Oncology at ASH and SABCS

    • Positive results from ianalumab pivotal Phase III trial in ITP patients previously treated with corticosteroids to be presented as late-breaker
    • Scemblix data across clinical and real-world settings offer new evidence informing CML care amid evolving patient needs
    • 96-week pelabresib Phase III data represent longest follow-up of first-line myelofibrosis patients in randomized combination trial
    • Kisqali NATALEE and MONALEESA data add to evidence of long-term benefits for early and metastatic breast cancer patients

    Basel, November 25, 2025 – Novartis will present data from over 70 abstracts, including investigator-initiated trials at the 67th American Society of Hematology (ASH) Annual Meeting & Exposition and 2025 San Antonio Breast Cancer Symposium® (SABCS). Featured among these latest advances in hematology and oncology are 11 oral presentations, with the Phase III VAYHIT2 trial for ianalumab in immune thrombocytopenia (ITP) accepted as a late-breaker abstract.

    “For decades, Novartis has redefined the future of hematology and oncology, and we’re building on that foundation with compelling new data presented at ASH and SABCS,” said Mark Rutstein, M.D., Global Head, Oncology Development, Novartis. “These data underscore how we seek to set new standards for transformative care, with the aim of turning cutting-edge innovation into meaningful impact for patients.”

    Key highlights of data accepted by ASH include:

    Abstract Title Abstract Number/ Presentation Details
    Ianalumab (VAY736)
    Primary results from VAYHIT2, a randomized, double-blind, Phase 3 trial of ianalumab plus eltrombopag versus placebo plus eltrombopag in patients with primary immune thrombocytopenia (ITP) who failed first-line corticosteroid treatment Abstract #LBA-2
    Oral Presentation
    December 9, 7:45 – 8:00 am ET
    Secondary analysis results from VAYHIT3, a Phase 2 study of ianalumab in patients with primary immune thrombocytopenia previously treated with at least two lines of therapy Abstract #844
    Oral Presentation
    December 8, 3:30 – 3:45 pm ET
    Scemblix® (asciminib)
    Asciminib (ASC) demonstrates continued improvement in patient-reported outcomes (PROs) vs investigator-selected tyrosine kinase inhibitors (IS-TKIs) in newly diagnosed chronic myeloid leukemia (CML): ASC4FIRST week 96 analysis Abstract #1997
    Poster Presentation
    December 6, 5:30 – 7:30 pm ET
    Improved long-term tolerability with asciminib (ASC) vs investigator-selected (IS) tyrosine kinase inhibitors (TKIs) in patients (pts) with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): Week 96 exploratory analysis of the phase 3 ASC4FIRST trial Abstract #5549
    Poster Presentation
    December 8, 6:00 – 8:00 pm ET
    Asciminib (ASC) in chronic myeloid leukemia in chronic Phase (CML-CP): Efficacy and safety results of the Phase 2 ASC2ESCALATE trial in the cohort of patients (pts) with 1 prior tyrosine kinase inhibitor (TKI) Abstract #906
    Oral Presentation
    December 8, 4:00 – 4:15 pm ET
    A comparison of real-world outcomes of asciminib versus ATP-competitive tyrosine kinase inhibitors as second-line treatment in patients with chronic myeloid leukemia in chronic phase Abstract #724
    Oral Presentation
    December 7, 5:15 – 5:30 pm ET
    Pelabresib (DAK539)
    Durable efficacy and long-term safety with pelabresib plus ruxolitinib in JAK Inhibitor–Naive myelofibrosis: 96-week Results from the Phase III MANIFEST-2 study Abstract #910
    Oral Presentation
    December 8, 3:30 – 3:45pm ET
    Rapcabtagene autoleucel (YTB323)
    Rapcabtagene autoleucel (YTB323) for patients with first line high-risk large B-cell lymphoma: phase II interim results Abstract #670
    Oral Presentation
    December 7, 5:15 – 5:30 pm ET
    Fabhalta® (iptacopan)
    Oral iptacopan monotherapy demonstrates clinically meaningful hemoglobin increases in patients with paroxysmal nocturnal hemoglobinuria with baseline hemoglobin levels 10 to <12 g/dL on anti-C5 therapy: Subgroup analysis of the APPULSE-PNH Phase 3b trial Abstract #4981
    Poster Presentation
    December 8, 6:00 – 8:00 pm ET
    Long-term safety and efficacy of iptacopan in patients with paroxysmal nocturnal hemoglobinuria: 4- and 5-year follow-up of patients from phase 2 studies who entered the roll-over extension program Abstract #3198
    Poster Presentation
    December 7, 6:00 – 8:00 pm ET
    The 2-year efficacy and safety of iptacopan monotherapy in patients with paroxysmal nocturnal hemoglobinuria with a history of aplastic anemia on concomitant immunosuppressive therapy who entered the roll-over extension program Abstract #4978
    Poster Presentation
    December 8, 6:00 – 8:00 pm ET

    Key highlights of data accepted by SABCS include:

    Kisqali® (ribociclib)
    Pooled analysis of patients (pts) treated with 1st-line (1L) ribociclib (RIB) + endocrine therapy (ET) in the MONALEESA (ML) studies: long-term progression-free survival (PFS) Abstract # PD5-10
    Poster Spotlight Presentation
    December 11, 8:09 – 8:12 am CST
    Five-year analysis of distant disease-free survival (DDFS) across key subgroups from the phase 3 NATALEE trial of ribociclib (RIB) plus a nonsteroidal aromatase inhibitor (NSAI) in patients with HR+/HER2− early breast cancer (EBC) Abstract # PS3-09-08
    Poster Presentation
    December 11, 12:30 – 2:00 pm CST
    Progression-free survival (PFS) and overall survival (OS) results from the phase 3 MONALEESA-3 trial of postmenopausal patients with hormone receptor–positive (HR+)/HER2-negative (HER2−) advanced breast cancer (ABC) treated with ribociclib (RIB) + fulvestrant (FUL): A subgroup analysis of patients with invasive lobular carcinoma (ILC) Abstract # PS1-10-27
    Poster Presentation
    December 10, 12:30 – 2:00 pm CST
    Ribociclib drug-drug interaction and concomitant medication management in early and advanced breast cancer patients Abstract # PS3-09-15
    Poster Presentation
    December 11, 12:30 – 2:00 pm CST
    Real-world patient (pt) and caregiver experiences with breast cancer (BC) risk of recurrence (ROR) in the US: Results of an Online Survey and Social Media Analysis Abstract # PS1-04-17
    Poster Presentation
    December 10, 12:30 – 2:00 pm CST
    Repower: a real-world noninterventional study of outcomes and experiences in patients with hormone receptor-positive (HR+)/human epidermal growth fact receptor 2-negative (HER2−) early breast cancer (EBC) treated with an adjuvant cyclin-dependent kinase 4 and 6 inhibitor (CDK4/6i) plus endocrine therapy (ET) Abstract # PS3-08-27
    Poster Presentation
    December 11, 12:30 – 2:00 pm CST

    Product Information

    For full prescribing information, including approved indications and important safety information about marketed products, please visit https://www.novartis.com/about/products.

    Novartis in hematology
    Our legacy in hematology runs deep, shaped by over 25 years of progress, partnerships and a commitment to keep asking questions, challenging norms and striving for better answers in a uniquely complex field. In the past two decades, we have delivered more than 10 medicines across more than 15 blood cancers and serious blood disorders including leading the era of targeted therapies in cancer and bringing the first CAR-T therapy to patients.

    Innovation in hematology has brought significant progress, yet patients and clinicians continue to face persistent challenges. We’re forging the future of hematology, powered by our foundation in scientific discovery to deliver meaningful change for patients with unmet needs.

    Novartis in breast cancer 
    For over 30 years, Novartis has been at the forefront of driving scientific advancements for individuals affected by breast cancer and enhancing clinical practice in collaboration with the global community. With one of the most comprehensive breast cancer portfolios and pipeline, Novartis leads the industry in discovery of new therapies and combinations in HR+/HER2- breast cancer, the most common form of the disease. 

    Disclaimer

    This press release contains forward-looking statements within the meaning of the United States Private Securities Litigation Reform Act of 1995. Forward-looking statements can generally be identified by words such as “potential,” “can,” “will,” “plan,” “may,” “could,” “would,” “expect,” “anticipate,” “look forward,” “believe,” “committed,” “investigational,” “pipeline,” “launch,” or similar terms, or by express or implied discussions regarding potential marketing approvals, new indications or labeling for the investigational or approved products described in this press release, or regarding potential future revenues from such products. You should not place undue reliance on these statements. Such forward-looking statements are based on our current beliefs and expectations regarding future events, and are subject to significant known and unknown risks and uncertainties. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those set forth in the forward-looking statements. There can be no guarantee that the investigational or approved products described in this press release will be submitted or approved for sale or for any additional indications or labeling in any market, or at any particular time. Nor can there be any guarantee that such products will be commercially successful in the future. In particular, our expectations regarding such products could be affected by, among other things, the uncertainties inherent in research and development, including clinical trial results and additional analysis of existing clinical data; regulatory actions or delays or government regulation generally; global trends toward health care cost containment, including government, payor and general public pricing and reimbursement pressures and requirements for increased pricing transparency; our ability to obtain or maintain proprietary intellectual property protection; the particular prescribing preferences of physicians and patients; general political, economic and business conditions, including the effects of and efforts to mitigate pandemic diseases; safety, quality, data integrity or manufacturing issues; potential or actual data security and data privacy breaches, or disruptions of our information technology systems, and other risks and factors referred to in Novartis AG’s current Form 20-F on file with the US Securities and Exchange Commission. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise.

    About Novartis 
    Novartis is an innovative medicines company. Every day, we work to reimagine medicine to improve and extend people’s lives so that patients, healthcare professionals and societies are empowered in the face of serious disease. Our medicines reach nearly 300 million people worldwide.

    Reimagine medicine with us: Visit us at https://www.novartis.com and connect with us on LinkedIn, Facebook, X/Twitter and Instagram.

    # # #


    Continue Reading

  • MIF/CD74 axis regulates alveolar epithelial type II cell apoptosis, autophagy, and transdifferentiation in bronchopulmonary dysplasia via the TGFβ1/SMAD4 pathway | Respiratory Research

    MIF/CD74 axis regulates alveolar epithelial type II cell apoptosis, autophagy, and transdifferentiation in bronchopulmonary dysplasia via the TGFβ1/SMAD4 pathway | Respiratory Research

  • Zhao ZW, Lin XX, Guo YZ, He X, Zhang XT, Huang Y. Irisin alleviates hyperoxia-induced bronchopulmonary dysplasia through activation of Nrf2/HO-1 pathway. Peptides. 2023;170:171109.

  • Sotiropoulos JX, Oei JL. The role of oxygen in the development and treatment of bronchopulmonary dysplasia. Semin Perinatol. 2023;47(6):151814.

  • Jain D, Feldman A, Sangam S. Predicting Long-Term respiratory outcomes in premature infants: is it time to move beyond bronchopulmonary dysplasia? Child (Basel). 2020;7(12):283.

  • Ala M, Mohammad Jafari R, Dehpour AR. Sildenafil beyond erectile dysfunction and pulmonary arterial hypertension: thinking about new indications. Fundam Clin Pharmacol. 2021;35:235–59.

    Google Scholar 

  • Principi N, Di Pietro GM, Esposito S. Bronchopulmonary dysplasia: clinical aspects and preventive and therapeutic strategies. J Transl Med. 2018;16:36.

    Google Scholar 

  • Choi CW, Kim BI, Hong JS, Kim EK, Kim HS, Choi JH. Bronchopulmonary dysplasia in a rat model induced by intra-amniotic inflammation and postnatal hyperoxia: morphometric aspects. Pediatr Res. 2009;65:323–7.

    Google Scholar 

  • Tang JR, Seedorf GJ, Muehlethaler V, Walker DL, Markham NE, Balasubramaniam V, et al. Moderate postnatal hyperoxia accelerates lung growth and attenuates pulmonary hypertension in infant rats after exposure to intra-amniotic endotoxin. Am J Physiol Lung Cell Mol Physiol. 2010;299:L735-748.

    Google Scholar 

  • Farr L, Ghosh S, Moonah S. Role of MIF cytokine/CD74 receptor pathway in protecting against injury and promoting repair. Front Immunol. 2020;11:1273.

    Google Scholar 

  • Marsh LM, Cakarova L, Kwapiszewska G, von Wulffen W, Herold S, Seeger W, Lohmeyer J. Surface expression of CD74 by type II alveolar epithelial cells: a potential mechanism for macrophage migration inhibitory factor-induced epithelial repair. Am J Physiol Lung Cell Mol Physiol. 2009;296:L442–452.

    Google Scholar 

  • Grieb G, Merk M, Bernhagen J, Bucala R. Macrophage migration inhibitory factor (MIF): a promising biomarker. Drug News Perspect. 2010;23:257–64.

    Google Scholar 

  • Sauler M, Leng L, Trentalange M, Haslip M, Shan P, Piecychna M, Zhang Y, Andrews N, Mannam P, Allore H, et al. Macrophage migration inhibitory factor deficiency in chronic obstructive pulmonary disease. Am J Physiol Lung Cell Mol Physiol. 2014;306:L487–496.

    Google Scholar 

  • Zhang C, Ramsey C, Berical A, Yu L, Leng L, McGinnis KA, Song Y, Michael H, McCormack MC, Allore H, et al. A functional macrophage migration inhibitory factor promoter polymorphism is associated with reduced diffusing capacity. Am J Physiol Lung Cell Mol Physiol. 2019;316:L400–5.

    Google Scholar 

  • Shi X, Leng L, Wang T, Wang W, Du X, Li J, et al. CD44 is the signaling component of the macrophage migration inhibitory factor-CD74 receptor complex. Immunity. 2006;25:595–606.

    Google Scholar 

  • Petre MA, Petrik J, Ellis R, Inman MD, Holloway AC, Labiris NR. Fetal and neonatal exposure to nicotine disrupts postnatal lung development in rats: role of VEGF and its receptors. Int J Toxicol. 2011;30:244–52.

    Google Scholar 

  • Yu S, Poe B, Schwarz M, Elliot SA, Albertine KH, Fenton S, et al. Fetal and postnatal lung defects reveal a novel and required role for Fgf8 in lung development. Dev Biol. 2010;347:92–108.

    Google Scholar 

  • Hoffman AM, Ingenito EP. Alveolar epithelial stem and progenitor cells: emerging evidence for their role in lung regeneration. Curr Med Chem. 2012;19:6003–8.

    Google Scholar 

  • Klasen C, Ziehm T, Huber M, Asare Y, Kapurniotu A, Shachar I, et al. LPS-mediated cell surface expression of CD74 promotes the proliferation of B cells in response to MIF. Cell Signal. 2018;46:32–42.

    Google Scholar 

  • Takahashi K, Koga K, Linge HM, Zhang Y, Lin X, Metz CN, et al. Macrophage CD74 contributes to MIF-induced pulmonary inflammation. Respir Res. 2009;10:33.

    Google Scholar 

  • Cao L, Wang X, Liu X, Meng W, Guo W, Duan C, et al. Tumor necrosis factor α-dependent lung inflammation promotes the progression of lung adenocarcinoma originating from alveolar type II cells by upregulating MIF-CD74. Lab Invest. 2023;103:100034.

    Google Scholar 

  • Li R, Wang F, Wei J, Lin Y, Tang G, Rao L, et al. The role of macrophage migration inhibitory factor (MIF) in asthmatic airway remodeling. Allergy Asthma Immunol Res. 2021;13:88–105.

    Google Scholar 

  • Sauler M, Zhang Y, Min JN, Leng L, Shan P, Roberts S, et al. Endothelial CD74 mediates macrophage migration inhibitory factor protection in hyperoxic lung injury. FASEB J. 2015;29:1940–9.

    Google Scholar 

  • Chen XQ, Wu SH, Luo YY, Li BJ, Li SJ, Lu HY, et al. Lipoxin A(4) attenuates bronchopulmonary dysplasia via upregulation of Let-7c and downregulation of TGF-β(1) signaling pathway. Inflammation. 2017;40:2094–108.

    Google Scholar 

  • Kunzmann S, Ottensmeier B, Speer CP, Fehrholz M. Effect of progesterone on Smad signaling and TGF-β/Smad-regulated genes in lung epithelial cells. PLoS One. 2018;13:e0200661.

    Google Scholar 

  • Jin M, Lee J, Lee KY, Jin Z, Pak JH, Kim HS. Alteration of TGF-β-ALK-Smad signaling in hyperoxia-induced bronchopulmonary dysplasia model of newborn rats. Exp Lung Res. 2016;42:354–64.

    Google Scholar 

  • Lu J, Zhong Y, Lin Z, Lin X, Chen Z, Wu X, et al. Baicalin alleviates radiation-induced epithelial-mesenchymal transition of primary type II alveolar epithelial cells via TGF-β and ERK/GSK3β signaling pathways. Biomed Pharmacother. 2017;95:1219–24.

    Google Scholar 

  • Zhou Y, Hill C, Yao L, Li J, Hancock D, Downward J, et al. Quantitative proteomic analysis in alveolar type II cells reveals the different capacities of RAS and TGF-β to induce epithelial-mesenchymal transition. Front Mol Biosci. 2021;8:595712.

    Google Scholar 

  • Bhaskaran M, Kolliputi N, Wang Y, Gou D, Chintagari NR, Liu L. Trans-differentiation of alveolar epithelial type II cells to type I cells involves autocrine signaling by transforming growth factor beta 1 through the Smad pathway. J Biol Chem. 2007;282:3968–76.

    Google Scholar 

  • Faul F, Erdfelder E, Lang AG, Buchner A. G*power 3: a flexible statistical power analysis program for the social, behavioral, and biomedical sciences. Behav Res Methods. 2007;39:175–91.

    Google Scholar 

  • Serdar CC, Cihan M, Yücel D, Serdar MA. Sample size, power and effect size revisited: simplified and practical approaches in pre-clinical, clinical and laboratory studies. Biochem Med Zagreb. 2021;31:010502.

    Google Scholar 

  • Chou HC, Li YT, Chen CM. Human mesenchymal stem cells attenuate experimental bronchopulmonary dysplasia induced by perinatal inflammation and hyperoxia. Am J Transl Res. 2016;8:342–53.

    Google Scholar 

  • Lee HJ, Kim BI, Choi ES, Choi CW, Kim EK, Kim HS, et al. Effects of postnatal dexamethasone or hydrocortisone in a rat model of antenatal lipopolysaccharide and neonatal hyperoxia exposure. J Korean Med Sci. 2012;27:395–401.

    Google Scholar 

  • Ni W, Lin N, He H, Zhu J, Zhang Y. Lipopolysaccharide induces up-regulation of TGF-α through HDAC2 in a rat model of bronchopulmonary dysplasia. PLoS One. 2014;9:e91083.

    Google Scholar 

  • Zhang Q, Ran X, He Y, Ai Q, Shi Y. Acetate downregulates the activation of NLRP3 inflammasomes and attenuates lung injury in neonatal mice with bronchopulmonary dysplasia. Front Pediatr. 2020;8:595157.

    Google Scholar 

  • Sakurai R, Lee C, Shen H, Waring AJ, Walther FJ, Rehan VK. A combination of the aerosolized PPAR-γ agonist Pioglitazone and a synthetic surfactant protein B peptide mimic prevents hyperoxia-induced neonatal lung injury in rats. Neonatology. 2018;113:296–304.

    Google Scholar 

  • Deng J, Wang SH, Zheng XM, Tang ZM. Calcitonin gene-related peptide attenuates hyperoxia-induced oxidative damage in alveolar epithelial type II cells through regulating viability and transdifferentiation. Inflammation. 2022;45:863–75.

    Google Scholar 

  • Chen XY, Kao C, Peng SW, Chang JH, Lee YL, Laiman V, Chung KF, Bhavsar PK, Heriyanto DS, Chuang KJ, Chuang HC. Role of DCLK1/Hippo pathway in type II alveolar epithelial cells differentiation in acute respiratory distress syndrome. Mol Med. 2023;29:159.

    Google Scholar 

  • Dewor M, Steffens G, Krohn R, Weber C, Baron J, Bernhagen J. Macrophage migration inhibitory factor (MIF) promotes fibroblast migration in scratch-wounded monolayers in vitro. FEBS Lett. 2007;581:4734–42.

    Google Scholar 

  • Shin HN, Moon HH, Ku JL. Stromal cell-derived factor-1α and macrophage migration-inhibitory factor induce metastatic behavior in CXCR4-expressing colon cancer cells. Int J Mol Med. 2012;30:1537–43.

    Google Scholar 

  • Cao H, Tadros V, Hiramoto B, Leeper K, Hino C, Xiao J, et al. Targeting TKI-activated NFKB2-MIF/CXCLs-CXCR2 signaling pathways in FLT3 mutated acute myeloid leukemia reduced blast viability. Biomedicines. 2022. https://doi.org/10.3390/biomedicines10051038.

    Google Scholar 

  • Poulsen KL, Fan X, Kibler CD, Huang E, Wu X, McMullen MR, Leng L, Bucala R, Ventura-Cots M, Argemi J et al. Role of MIF in coordinated expression of hepatic chemokines in patients with alcohol-associated hepatitis. JCI Insight. 2021;6(11):e141420.

  • Li X, Wang L, Hao J, Zhu Q, Guo M, Wu C, et al. The role of autophagy in lamellar body formation and surfactant production in type 2 alveolar epithelial cells. Int J Biol Sci. 2022;18:1107–19.

    Google Scholar 

  • Serralha RS, Rodrigues IF, Bertolini A, Lima DY, Nascimento M, Mouro MG, Punaro GR, Visoná I, Rodrigues AM, Higa EMS. Esculin reduces P2X7 and reverses mitochondrial dysfunction in the renal cortex of diabetic rats. Life Sci. 2020;254:117787.

    Google Scholar 

  • Zeiner PS, Preusse C, Blank AE, Zachskorn C, Baumgarten P, Caspary L, et al. MIFReceptor CD74 is Restricted to Microglia/Macrophages, Associated with a M1‐Polarized Immune Milieu and Prolonged Patient Survival in Gliomas. Brain Pathol. 2015;25(4):491–504.

    Google Scholar 

  • Zhou DN, Li SJ, Ding JL, Yin TL, Yang J, Ye H. MIF may participate in pathogenesis of polycystic ovary syndrome in rats through MAPK signalling pathway. Curr Med Sci. 2018;38(5):853–60.

    Google Scholar 

  • Huang JM, Zhao N, Hao XN, Li SY, Wei D, Pu N, et al. CX3CL1/CX3CR1 signaling mediated neuroglia activation is implicated in the retinal degeneration: a potential therapeutic target to prevent photoreceptor death. Invest Ophthalmol Vis Sci. 2024;65:29.

    Google Scholar 

  • Shen J, Ma H, Wang C. Triptolide improves myocardial fibrosis in rats through inhibition of nuclear factor kappa B and NLR family pyrin domain containing 3 inflammasome pathway. Korean J Physiol Pharmacol. 2021;25:533–43.

    Google Scholar 

  • Zhou X, Xu W, Wang Y, Zhang H, Zhang L, Li C, et al. LncRNA DNM3OS regulates GREM2 via miR-127-5p to suppress early chondrogenic differentiation of rat mesenchymal stem cells under hypoxic conditions. Cell Mol Biol Lett. 2021;26:22.

    Google Scholar 

  • Zhang D, Wu Y, Li Z, Chen H, Huang S, Jian C, et al. MiR-144-5p, an exosomal miRNA from bone marrow-derived macrophage in type 2 diabetes, impairs bone fracture healing via targeting Smad1. J Nanobiotechnol. 2021;19:226.

    Google Scholar 

  • Shang P, Liu W, Liu T, Zhang Y, Mu F, Zhu Z, et al. Acetyl-11-keto-β-boswellic acid attenuates prooxidant and profibrotic mechanisms involving transforming growth factor-β1, and improves vascular remodeling in spontaneously hypertensive rats. Sci Rep. 2016;6:39809.

    Google Scholar 

  • Wang H, Shi X, Guo Z, Zhao F, He W, Kang M, et al. Microrna-211-5p predicts the progression of postmenopausal osteoporosis and attenuates osteogenesis by targeting dual specific phosphatase 6. Bioengineered. 2022;13:5709–23.

    Google Scholar 

  • Tanguy J, Boutanquoi PM, Burgy O, Dondaine L, Beltramo G, Uyanik B, Garrido C, Bonniaud P, Bellaye PS, Goirand F. HSPB5 Inhibition by NCI-41356 reduces experimental lung fibrosis by blocking TGF-β1 signaling. Pharmaceuticals (Basel). 2023;16(2):177.

  • Shi Y, Jin Y, Liu F, Jiang J, Cao J, Lu Y, Yang J. Ceramide induces the apoptosis of non–small cell lung cancer cells through the Txnip/Trx1 complex. Int J Mol Med. 2021;47(5):85.

  • Bao T, Zhu H, Zheng Y, Hu J, Wang H, Cheng H, et al. Expression of long noncoding RNA uc.375 in bronchopulmonary dysplasia and its function in the proliferation and apoptosis of mouse alveolar epithelial cell line MLE 12. Front Physiol. 2022;13:971732.

    Google Scholar 

  • Xiong Y, Wang Q. STC1 regulates glioblastoma migration and invasion via the TGF–β/SMAD4 signaling pathway. Mol Med Rep. 2019;20:3055–64.

    Google Scholar 

  • Jiang Y, Liu Y, Xiao W, Zhang D, Liu X, Xiao H, et al. Xinmailong attenuates Doxorubicin-induced lysosomal dysfunction and oxidative stress in H9c2 cells via HO-1. Oxid Med Cell Longev. 2021;2021:5896931.

    Google Scholar 

  • Shen S, Ji C, Wei K. Cellular senescence and regulated cell death of tubular epithelial cells in diabetic kidney disease. Front Endocrinol (Lausanne). 2022;13:924299.

    Google Scholar 

  • Yu H, Li D, Zhao X, Fu J. Fetal origin of bronchopulmonary dysplasia: contribution of intrauterine inflammation. Mol Med. 2024;30:135.

    Google Scholar 

  • Parsons A, Netsanet A, Seedorf G, Abman SH, Taglauer ES. Understanding the role of placental pathophysiology in the development of bronchopulmonary dysplasia. Am J Physiol Lung Cell Mol Physiol. 2022;323:L651-8.

    Google Scholar 

  • Wei Y, Wang Y. Celastrol attenuates impairments associated with lipopolysaccharide-induced acute respiratory distress syndrome (ARDS) in rats. J Immunotoxicol. 2017;14:228–34.

    Google Scholar 

  • Roper JM, Mazzatti DJ, Watkins RH, Maniscalco WM, Keng PC, O’Reilly MA. In vivo exposure to hyperoxia induces DNA damage in a population of alveolar type II epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2004;286:L1045-1054.

    Google Scholar 

  • O’Reilly MA, Staversky RJ, Finkelstein JN, Keng PC. Activation of the G2 cell cycle checkpoint enhances survival of epithelial cells exposed to hyperoxia. Am J Physiol Lung Cell Mol Physiol. 2003;284:L368-375.

    Google Scholar 

  • Sureshbabu A, Syed M, Das P, Janér C, Pryhuber G, Rahman A, et al. Inhibition of regulatory-associated protein of mechanistic target of rapamycin prevents hyperoxia-induced lung injury by enhancing autophagy and reducing apoptosis in neonatal mice. Am J Respir Cell Mol Biol. 2016;55:722–35.

    Google Scholar 

  • Chen Y, Chang L, Li W, Rong Z, Liu W, Shan R, et al. Thioredoxin protects fetal type II epithelial cells from hyperoxia-induced injury. Pediatr Pulmonol. 2010;45:1192–200.

    Google Scholar 

  • Yee M, Buczynski BW, O’Reilly MA. Neonatal hyperoxia stimulates the expansion of alveolar epithelial type II cells. Am J Respir Cell Mol Biol. 2014;50:757–66.

    Google Scholar 

  • Hou A, Fu J, Shi Y, Qiao L, Li J, Xing Y, et al. Decreased ZONAB expression promotes excessive transdifferentiation of alveolar epithelial cells in hyperoxia-induced bronchopulmonary dysplasia. Int J Mol Med. 2018;41:2339–49.

    Google Scholar 

  • Roger T, Schlapbach LJ, Schneider A, Weier M, Wellmann S, Marquis P, et al. Plasma levels of macrophage migration inhibitory factor and d-dopachrome tautomerase show a highly specific profile in early life. Front Immunol. 2017;8:26.

    Google Scholar 

  • Sun H, Choo-Wing R, Fan J, Leng L, Syed MA, Hare AA, et al. Small molecular modulation of macrophage migration inhibitory factor in the hyperoxia-induced mouse model of bronchopulmonary dysplasia. Respir Res. 2013;14:27.

    Google Scholar 

  • Prencipe G, Auriti C, Inglese R, Devito R, Ronchetti MP, Seganti G, et al. A polymorphism in the macrophage migration inhibitory factor promoter is associated with bronchopulmonary dysplasia. Pediatr Res. 2011;69:142–7.

    Google Scholar 

  • Kevill KA, Bhandari V, Kettunen M, Leng L, Fan J, Mizue Y, et al. A role for macrophage migration inhibitory factor in the neonatal respiratory distress syndrome. J Immunol. 2008;180:601–8.

    Google Scholar 

  • Gao J, Wu M, Wang F, Jiang L, Tian R, Zhu X, et al. CD74, a novel predictor for bronchopulmonary dysplasia in preterm infants. Medicine. 2020;99:e23477.

    Google Scholar 

  • Yao HC, Zhu Y, Lu HY, Ju HM, Xu SQ, Qiao Y, et al. Type 2 innate lymphoid cell-derived amphiregulin regulates type II alveolar epithelial cell transdifferentiation in a mouse model of bronchopulmonary dysplasia. Int Immunopharmacol. 2023;122:110672.

    Google Scholar 

  • Hou A, Fu J, Yang H, Zhu Y, Pan Y, Xu S, et al. Hyperoxia stimulates the transdifferentiation of type II alveolar epithelial cells in newborn rats. Am J Physiol Lung Cell Mol Physiol. 2015;308:L861-872.

    Google Scholar 

  • du Bois RM. Strategies for treating idiopathic pulmonary fibrosis. Nat Rev Drug Discov. 2010;9:129–40.

    Google Scholar 

  • Bueno M, Calyeca J, Khaliullin T, Miller MP, Alvarez D, Rosas L, Brands J, Baker C, Nasser A, Shulkowski S et al. CYB5R3 in type II alveolar epithelial cells protects against lung fibrosis by suppressing TGF-β1 signaling. JCI Insight. 2023;8(5):e161487.

  • Bueno M, Zank D, Buendia-Roldán I, Fiedler K, Mays BG, Alvarez D, et al. PINK1 attenuates MtDNA release in alveolar epithelial cells and TLR9 mediated profibrotic responses. PLoS One. 2019;14:e0218003.

    Google Scholar 

  • Chilosi M, Carloni A, Rossi A, Poletti V. Premature lung aging and cellular senescence in the pathogenesis of idiopathic pulmonary fibrosis and COPD/emphysema. Transl Res. 2013;162:156–73.

    Google Scholar 

  • Chung EJ, Kwon S, Reedy JL, White AO, Song JS, Hwang I, et al. IGF-1 receptor signaling regulates type II pneumocyte senescence and resulting macrophage polarization in lung fibrosis. Int J Radiat Oncol Biol Phys. 2021;110:526–38.

    Google Scholar 

  • Chung EJ, Reedy JL, Kwon S, Patil S, Valle L, White AO, et al. 12-lipoxygenase is a critical mediator of type II pneumocyte senescence, macrophage polarization and pulmonary fibrosis after irradiation. Radiat Res. 2019;192:367–79.

    Google Scholar 

  • Citrin DE, Shankavaram U, Horton JA, Shield W 3rd, Zhao S, Asano H, et al. Role of type II pneumocyte senescence in radiation-induced lung fibrosis. J Natl Cancer Inst. 2013;105:1474–84.

    Google Scholar 

  • Zhang T, Zhang J, Lv C, Li H, Song X. Senescent AECⅡ and the implication for idiopathic pulmonary fibrosis treatment. Front Pharmacol. 2022;13:1059434.

    Google Scholar 

  • Wójcik-Pszczoła K, Chłoń-Rzepa G, Jankowska A, Ferreira B, Koczurkiewicz-Adamczyk P, Pękala E, Wyska E, Pociecha K, Gosens R. Pan-Phosphodiesterase inhibitors attenuate TGF-β-Induced Pro-Fibrotic phenotype in alveolar epithelial type II cells by downregulating Smad-2 phosphorylation. Pharmaceuticals (Basel). 2022;15(4):423.

    • Continue Reading