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  • Flood alert in Multan as authorities plan breach at Sher Shah embankment – samaa tv

    1. Flood alert in Multan as authorities plan breach at Sher Shah embankment  samaa tv
    2. Multan city at risk as floodwaters enter its tehsil  Dawn
    3. Town evacuated as south Punjab reels under floods  The Express Tribune
    4. Pakistan evacuates 25,000 people from eastern city as rivers threaten flooding  AP News
    5. Over 1,500 evacuated from Jalalpur Pirwala on CM Maryam Nawaz’s orders  The Nation (Pakistan )

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  • Tiger Shroff’s Baaghi 4 earns just Rs 35.5 crore in 4 days — franchise’s lowest ever

    Tiger Shroff’s Baaghi 4 earns just Rs 35.5 crore in 4 days — franchise’s lowest ever

    Tiger Shroff’s Baaghi franchise has been flying high… until now. Baaghi 4 has stumbled out of the gate, posting the lowest domestic collections in the franchise’s history. After a lackluster opening weekend, the Monday numbers made it official: a mere Rs 4.25 crore, down from Sunday’s Rs 10 crore and Saturday’s Rs 9.25 crore. Its best single-day haul remains the opening-day Rs 12 crore. Four days in, according to Sacnilk, Baaghi 4 has amassed Rs 35.5 crore, enough to barely edge past Shahid Kapoor’s cop thriller Deva (Rs 33.97 crore), but still lagging behind re-releases and dubbed hits like Sanam Teri Kasam, Coolie, and Maa.

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  • Heavy rain shuts down all schools in Hyderabad

    Heavy rain shuts down all schools in Hyderabad

    After the Meteorological Department predicted heavy rain in Hyderabad, the district administration announced that educational institutions will remain closed in the city today, reported 24NewsHD TV channel.

    In this regard, Deputy Commissioner of Hyderabad issued notification on Tuesday.

    According to the notification, all private and government educational institutions will remain closed today.

    Reporter: Muhammad Hassan 


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  • Asia Cup 2025: India’s Complete Schedule, Squad Without Kohli & Rohit, and Key Matches to Watch | News

    Asia Cup 2025: India’s Complete Schedule, Squad Without Kohli & Rohit, and Key Matches to Watch | News

    The Asia Cup 2025 begins on September 9, with India’s campaign starting against UAE on September 10 in Dubai. The most-awaited India vs Pakistan clash is scheduled for September 14, followed by India’s final group-stage game against Oman on September 19 in Abu Dhabi. Led by Suryakumar Yadav, India enter as defending champions and the most successful team in Asia Cup history with eight titles. With stars like Shubman Gill, Hardik Pandya, Jasprit Bumrah, and Kuldeep Yadav, India aim for their ninth crown. Fans can catch Asia Cup 2025 live streaming on Sony LIV and TV telecast on Sony Sports.

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  • 5 key takeaways from Tokyo Fashion Week SS26

    5 key takeaways from Tokyo Fashion Week SS26

    The lack of strong menswear talent on the schedule is a sticking point. “Tokyo’s designer fashion scene has traditionally been very strong in menswear, yet unlike other global cities, Tokyo does not have a dedicated men’s fashion week aligned with the international menswear calendar,” says Mami Osugi, a Tokyo-based editor who serves on the jury of the Tokyo Fashion Award. “As a result, Tokyo’s talented menswear designers often miss out on the global attention they deserve.”

    JFWO is currently working on solutions, says Imajo. “One thing we may do in February is try and get the [off-schedule] brands to show closer to each other, but stretching everything out is easier for the designers because they are able to get the models and the venues [they want],” he says. Staying in closer contact with visiting buyers and inviting them to off-schedule shows is also an option JFWO are considering, Imajo adds.

    A growing front row

    Another of Tokyo Fashion Week’s main challenges has been its lack of international buyers and press. JFWO is gradually addressing this, and this season, invited more influential figures from Asia and beyond. Returning attendees this time included Andreas Murkudis of the eponymous store in Berlin, and journalist Eugene Rabkin of Style Zeitgeist; new invitees included menswear and womenswear buyers from 10 Corso Como in Seoul and IT in Hong Kong.

    Rabkin intends to continue attending Tokyo Fashion Week whenever possible, finding it more interesting than Europe. “There are a lot of designers that you can only see here in Tokyo,” he says. “There is more of a connection between the brands, the fashion shows, the shops and the people in the street. In Paris, I always feel like I’m in a circus, and I don’t get that feeling in Tokyo, because you actually see interesting kids in the street. There’s more congruence.” Kohei Hashimoto, a womenswear buyer at Isetan, echoes the sentiment. “Tokyo stands out for the depth of consumer understanding of clothing and the closeness of fashion to everyday life. I believe it surpasses any other city in this respect,” he says.

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    What is Japanese style today?

    Japanese fashion customers are becoming harder to define. They are also spending less. We asked industry insiders to explain how tastes and norms are shifting.

    June Moon, chief womenswear buyer for 10 Corso Como Seoul, served on the jury of the Tokyo Fashion Award and was invited to attend Tokyo Fashion Week for the first time. “Compared to Seoul, which is very trendy and changes very fast, Japan is more consistent,” she says. “Japanese designers have their core philosophy and build the brand around this story.”

    Legacy designers, new faces and breakthrough talent

    Even with its smaller size, the week offered a blend of newcomer debuts alongside the return of legacy designers. Tsumori Chisato, known for her pastel kawaii prints and bold silhouettes, joined the schedule for a show celebrating her brand’s 35th anniversary. “It was my first time showing in seven and a half years,” she told press after the show. “I put all the rainbows and colours in my clothes to show my appreciation for everyone, for supporting me for all these years.”

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  • Maison Francis Kurkdjian Launches $28,000 Limited Edition of Baccarat Rouge 540

    Maison Francis Kurkdjian Launches $28,000 Limited Edition of Baccarat Rouge 540

    Already at the high end of luxury fragrances, Maison Francis Kurkdjian’s hero Baccarat Rouge 540 is getting a five-figure upgrade.

    In mid-September, the perfume house will unveil a $28,000 special-edition offering of the scent, complete with a crystal case and exclusive refill membership. The brand joins a wider range of LVMH labels unveiling fragrances at prices once reserved for handbags and jewellery as collectors’ enthusiasm drives demand.

    The Baccarat Rouge 540 Édition Millésime will be released in 54-product batches over the next decade, for a total of 540. With permanent collection bottles at $695 for 6.8 ounces, its price premium comes partly from the addition of ambergris to its ingredient list. But its crystal packaging takes top billing. The brand’s original bottle designer Fred Rawyler was enlisted to design a red crystal vessel. A crystal-compatible spray function was added to its 24-carat-gold cap, while 19 Baccarat artisans created a crystal display for the bottle that took 500 hours. The fragrance comes in a leather and beveled mirror-lined spruce box and a hand-stitched lambskin sleeve by Paris leather workshop Atelier Renard.

    “When I create, I never begin by thinking about the client. I simply follow my creative vision, striving to bring beauty into the world through my fragrances,” said Kurkdjian, the brand’s perfumer and artistic director.

    While Kurkdjian has long offered pricier bespoke fragrances for VIP clients, the launch is the label’s first “exceptional piece” to be unveiled by the maison.

    Owners will have access to what CEO Marc Chaya describes as “the ultimate customer journey,” an exclusive members club called Les amis du Rouge, inclusive of up to five refill purchases a year. Club membership will also include curated brand experiences such as dinners, masterclasses with Kurkdjian, shows at the brand-partnered Vienna State Opera and a visit to the perfumer’s upcoming Palais de Tokyo solo exhibition.

    Ultra-high-end collectible fragrance launches, long a practice of fellow LVMH-owned perfumier Guerlain, have become more frequent at the luxury house as avid collectors have helped drive a high-end fragrance boom. Some of the most expensive perfumes have been Bulgari’s Opera Prima launched for $235,000 in 2014 and Dior’s J’adore L’or Prestige Edition for $75,000 in 2016.

    Learn more:

    The Fragrance Market’s Squeezed Middle

    Fragrance may be booming, but the premium category has cratered compared to high-end niche perfumes and affordable body and hair mists that have become an expansion focus for brands.

    Disclosure: LVMH is part of a group of investors who, together, hold a minority interest in The Business of Fashion. All investors have signed shareholders’ documentation guaranteeing BoF’s complete editorial independence.

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  • Amnesty says Pakistan spying on millions through phone-tapping, firewall – Reuters

    1. Amnesty says Pakistan spying on millions through phone-tapping, firewall  Reuters
    2. Pakistan: Mass surveillance and censorship machine is fueled by Chinese, European, Emirati and North American companies  Amnesty International
    3. Pakistan’s Growing Surveillance: A Chilling Union of Technology and Authority  Devdiscourse

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  • What Is Cancer Cachexia? Causes, Symptoms, Diagnosis, and Treatment

    What Is Cancer Cachexia? Causes, Symptoms, Diagnosis, and Treatment

    Introduction
    Pathophysiology of cancer cachexia
    Clinical features and symptoms
    Prevalence and clinical impact
    Diagnosis and staging
    Management strategies
    Challenges and research directions
    Conclusions
    References
    Further reading

    Cancer cachexia is a multifactorial syndrome marked by muscle and fat loss, driven by inflammation and metabolic dysregulation beyond malnutrition. It worsens quality of life, limits treatment tolerance, and requires multimodal management strategies.

    Image Credit: Ground Picture / Shutterstock.com

    Introduction

    Cancer cachexia is a complex metabolic syndrome characterized by the ongoing loss of skeletal muscle mass, with or without fat loss, that cannot be reversed entirely by conventional nutritional support and results in progressive functional decline.1

    Unlike simple weight loss or malnutrition, which are often reversible and primarily due to inadequate intake, cachexia involves involuntary and irreversible muscle wasting due to metabolic dysregulation and inflammation. It is underpinned by a sustained negative protein and energy balance driven by reduced intake and abnormal metabolism, distinguishing it clinically and biologically from starvation or isolated malnutrition.1,2 

    This article examines the causes and clinical manifestations of cancer cachexia, as well as current management strategies aimed at improving patient outcomes.

    Pathophysiology of cancer cachexia

    Complex cross-talk between tumor-derived factors and host responses leads to metabolic alterations such as increased autophagy, nutrient sequestration, proteolysis, and mitochondrial dysfunction. Key signaling nodes include JAK/STAT (particularly STAT3), NF-κB, and FOXO transcription factors that upregulate muscle ubiquitin ligases (MuRF1/MAFbx), while myostatin/activin A–SMAD2/3 signaling via ActRIIB suppresses anabolism. Cancer cachexia also disrupts hormonal mediators, such as insulin-like growth factor-1 (IGF-1), transforming growth factor-beta (TGF-β), leptin, and ghrelin, which are present in the liver, bones, adipose tissue, and stomach, respectively, thus highlighting the systemic effects of this condition.

    Increased energy expenditure due to accelerated muscle and fat loss also contributes to symptoms of cachexia. Dysregulation in the ubiquitin-proteasome system, autophagy-lysosomal pathway, and calcium-dependent proteolytic processes leads to skeletal muscle wasting. Adipose tissue browning and lipolysis (e.g., PTHrP-driven thermogenesis) further amplify hypermetabolism, and mitochondrial uncoupling further impairs adenine triphosphate (ATP) production to promote hypermetabolism and inefficient energy use.3,5

    Cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-1β stimulate protein breakdown, suppress protein synthesis, and induce anorexia through the hypothalamus. Dysregulation of hypothalamic appetite circuits (e.g., melanocortin system) contributes to anorexia and early satiety. Tumor-derived mediators, including proteolysis-inducing factor and parathyroid hormone-related protein (PTHrP), also amplify catabolism and disrupt appetite, contributing to systemic inflammation. 2,3

    Cachexia suppresses anabolic signaling through the mechanistic target of rapamycin (mTOR) and IGF-1; however, catabolic pathways remain active. This imbalance results in negative nitrogen and energy balance, muscle atrophy, impaired function, reduced treatment tolerance, and higher mortality. Multi-organ effects (gut barrier dysfunction/microbiome changes, cardiac remodeling, and central neuroinflammation) further sustain the syndrome.3,4

    Cancer cachexia as a multi-organ syndrome. This scheme illustrates the interaction of major organs commonly associated with and affected by cachexia. Cancer cachexia that happens in the muscle (center) is dependent on the alterations in other organs, such as adipose tissue, brain, gut, cardiac muscle, and immune cells. Cachexia-inducing tumors secrete many factors, such as cytokines, PTHrP, and other mediators, to induce muscle wasting directly, as well as affecting other organs such as the brain, cardiac muscle, gut, and adipocyte tissue, which aggravates cachexia syndrome. WAT, white adipocyte tissue; PTHrP, parathyroid hormone-related protein; TNF-α, tumor necrosis factor-α; IL-1, interleukin-1; IL-6, interleukin 6; IL-8, interleukin-8; IL-10, interleukin 10; and NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells.3

    Cancer cachexia as a multi-organ syndrome. This scheme illustrates the interaction of major organs commonly associated with and affected by cachexia. Cancer cachexia that happens in the muscle (center) is dependent on the alterations in other organs, such as adipose tissue, brain, gut, cardiac muscle, and immune cells. Cachexia-inducing tumors secrete many factors, such as cytokines, PTHrP, and other mediators, to induce muscle wasting directly, as well as affecting other organs such as the brain, cardiac muscle, gut, and adipocyte tissue, which aggravates cachexia syndrome. WAT, white adipocyte tissue; PTHrP, parathyroid hormone-related protein; TNF-α, tumor necrosis factor-α; IL-1, interleukin-1; IL-6, interleukin 6; IL-8, interleukin-8; IL-10, interleukin 10; and NF-kB, nuclear factor kappa-light-chain-enhancer of activated B cells.3

    Clinical features and symptoms

    Cancer cachexia is characterized by ongoing weight loss, which is primarily due to skeletal muscle, fat, and, in some cases, cardiac muscle loss. Unlike malnutrition, these changes reflect profound metabolic disturbances that cannot revert to normalcy through nutrition.5

    Muscle loss leads to weakness, fatigue, and lower physical performance. Patients often struggle with daily activities, which leads to more time spent in bed or seated, resulting in reduced mobility and independence. Reduced physical function also weakens social interactions and body image.2,3

    Appetite loss is common, and many patients experience altered taste or difficulty digesting and absorbing nutrients. Early satiety, dysphagia (in head and neck or upper GI cancers), and dysgeusia are frequent contributors to intake reduction, and caregivers may respond by encouraging repeated feeding, which can cause nausea, vomiting, regurgitation, or aspiration pneumonia.5

    Patients diagnosed with cancer cachexia may also experience emotional distress, frustration, and guilt over weight loss and poor appetite, whereas caregivers face emotional strain from multiple feeding challenges and complications. This dual burden intensifies the overall impact of this disease.4,5

    Prevalence and clinical impact

    Cancer cachexia affects up to 70% of patients with advanced malignancies and contributes to about 22% of cancer-related deaths. The prevalence of cancer cachexia varies by tumor type, with 80-87% of patients with pancreatic and gastric cancers diagnosed with this condition. Approximately 60% of patients are diagnosed with lung, colon, and prostate cancers, as well as non-Hodgkin lymphoma, whereas about 40% with breast cancer, sarcoma, leukemia, and Hodgkin lymphoma.5,6

    Cancer cachexia also leads to fatigue, muscular atrophy, and psychological discomfort, all of which significantly reduce patients’ quality of life. This condition may also reduce tolerance to cancer therapies like chemotherapy, radiation, and surgery, which can lead to treatment delays, dose reductions, or dose interruptions, as well as an increased risk of infection and poor wound healing. These effects collectively worsen morbidity, mortality, and healthcare utilization.5

    Cancer cachexia develops along a continuum, with pre-cachexia defined as ≤ 5% weight loss with anorexia and early metabolic changes, and cachexia is characterized by > 5% weight loss or sarcopenia with ongoing loss. Alternatively, diagnostic cut points include >2% weight loss with BMI <20 kg/m2, or sarcopenia with >2% loss, and refractory cachexia is often an advanced and treatment-resistant disease with poor performance status and a life expectancy of less than three months.1

    The severity of cancer cachexia also varies by tumor type, extent of inflammation, and treatment response, with earlier onset and more pronounced progression observed in lung and pancreatic cancers. In advanced disease, cachexia is often irreversible, which is typically managed with palliative care.7,8

    Diagnosis and staging

    The Evans criteria define cachexia as 5% or more weight loss in less than 12 months in the presence of chronic disease. Reduced muscle strength, fatigue, anorexia, low fat-free mass index, or abnormal biochemistry characterized by increased C-reactive protein (CRP) and IL-6 levels, as well as anemia and low serum albumin.5

    For cancer specifically, the 2011 international consensus (Fearon et al.) defines cachexia as: (i) >5% weight loss in the past 6 months (absent simple starvation), or (ii) BMI <20 kg/m2 with >2% weight loss, or (iii) sarcopenia with >2% weight loss, and recognizes a trajectory from pre-cachexia to cachexia to refractory cachexia.1 Other proposed clinical staging tools include CASCO/miniCASCO, the Cancer Cachexia Staging (CCS) system, and BMI-adjusted weight-loss grades to stratify severity and prognosis.4,7

    The Patient-Generated Subjective Global Assessment (PG-SGA), Mini Nutritional Assessment (MNA), and Nutritional Risk Screening (NRS-2002) can be used to assess nutritional status. Cross-sectional imaging (e.g., CT at L3) is widely used to quantify skeletal muscle; DXA and BIA are alternative methods when CT is unavailable.

    The characteristic weight loss of cancer cachexia can be ambiguous and resemble other conditions like malnutrition, sarcopenia, or anorexia. As compared to malnutrition, cachexia persists despite adequate nutrition.

    Although anorexia may also be present, it does not account for the widespread inflammation, metabolic dysfunction, or persistent catabolism that occurs in cancer cachexia. Thus, cancer cachexia is a distinct and multifactorial syndrome that requires targeted interventions to preserve muscle mass, mitigate metabolic disruption, and improve functional outcomes.9,10

    Management strategies

    Cancer cachexia management is achieved through nutritional therapy that emphasizes high-calorie, high-protein diets, omega-3 fatty acids, and oral dietary supplements such as eicosapentaenoic acid, β-hydroxy-β-methylbutyrate, and L-carnitine. However, nutrition alone rarely reverses cachexia and is most effective when combined with other interventions.3,10 Early, structured nutrition pathways integrated into oncology care improve identification and support but do not substitute for anti-catabolic therapy.6

    Appetite stimulants like megestrol acetate can improve appetite and weight gain but may increase the risk of thromboembolism, adrenal suppression, and fluid retention. Corticosteroids can also improve appetite and reduce the severity of common symptoms like nausea; however, these pharmaceutical agents cannot prevent muscle loss and are associated with numerous long-term effects such as osteoporosis, immunosuppression, and sleep disturbances that limit extended use.5

    Anti-inflammatory agents, such as IL-6 antagonists (ALD518), IL-6R inhibitors (tocilizumab), and dual-target agents (OHR/AVR118), have been shown to stabilize body weight and reduce inflammation. Anamorelin, a ghrelin receptor agonist, increased lean body mass and body weight in advanced NSCLC (ROMANA 1/2) but did not improve handgrip strength; regulatory availability varies by region.11 In preclinical models, myostatin/activin A inhibitors, including soluble activin type IIB receptor (sActRIIB), preserved muscle integrity.5

    Resistance and aerobic exercise support muscle maintenance, improve protein metabolism, and attenuate inflammation. Resistance training enhances strength and mobility, whereas aerobic exercise reduces muscle atrophy through the activation of adiponectin signaling.

    Previously, a randomized controlled trial reported improvements in elbow and knee flexor/extensor muscles among pancreatic cancer patients after resistance training. Exercise improved functional independence; however, weight changes were modest.12

    A multimodal approach combining nutrition, drugs, and exercise offers the best outcomes in cancer cachexia. These management strategies can preserve muscle, boost appetite, reduce inflammation, and improve quality of life, with psychosocial and supportive care further enhancing these benefits. Where feasible, early referral to rehabilitation, symptom control (pain, nausea), and management of tumor- or treatment-related contributors (e.g., dysphagia) should be embedded in care plans.5,10

    Challenges and research directions

    Cancer cachexia management remains challenging due to the limited efficacy associated with single interventions. Thus, there remains an urgent need for multimodal strategies that address both metabolic dysregulation and chronic inflammation.13

    Although organizations such as the American Society of Clinical Oncology (ASCO) provide recommendations, there remains a lack of standardized treatment guidelines. Implementation of existing guidance (e.g., ESPEN/ASCO) into routine oncology pathways is suboptimal, and consistent screening plus early-stage intervention are key gaps.6,13

    Hormonal and metabolic agents, such as selective androgen receptor modulators (SARMs) and β2-adrenergic agonists, like enobosarm and formoterol, have also been widely studied for their potential role in managing cancer cachexia. These therapies stimulate appetite, preserve lean mass, and improve function. However, confirmatory phase 3 evidence demonstrating durable functional benefit remains limited.

    Immunomodulatory approaches, including IL-6 antagonists, target inflammatory and catabolic pathways central to muscle wasting. Numerous preclinical studies have also confirmed the anti-inflammatory effects of natural compounds like resveratrol, curcumin, and ginsenoside derivatives; however, safety concerns remain with agents like cannabinoids and testosterone. Future trials should prioritize patient-centred endpoints (function, treatment tolerance, survival) and standardized definitions/staging to enable comparison across studies.3,14

    Conclusions

    Cancer cachexia is a complex and multifactorial syndrome that affects metabolic, immune, and neurological systems. Optimal management requires a multidisciplinary approach that combines nutritional support, pharmacologic therapy, and exercise to preserve muscle mass and physical function.

    Future research is needed to develop targeted anti-cachexia agents that enhance muscle growth, improve functional outcomes, and maintain quality of life. Understanding underlying mechanisms and identifying novel therapeutic targets will be pivotal for reducing morbidity, improving treatment tolerance, and ultimately extending survival in patients with cancer cachexia.

    References

      1. Fearon, K., Stasser, F., Anker, S. D., et al. (2011). Definition and classification of cancer cachexia: an international consensus. The Lancet Oncology 12(5); 489-495. DOI:10.1016/S1470-2045(10)70218-7, https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(10)70218-7/
      2. Donohoe, C. L., Ryan, A. M., & Reynolds, J. V. (2011). Cancer Cachexia: Mechanisms and Clinical Implications. Gastroenterology Research and Practice, 601434. DOI:10.1155/2011/601434, https://onlinelibrary.wiley.com/doi/10.1155/2011/601434
      3. Setiawan, T., Sari, I. N., Wijaya, Y. T., et al. (2023). Cancer cachexia: molecular mechanisms and treatment strategies. Journal of Hematology & Oncology 16; 54. DOI:10.1186/s13045-023-01454-0, https://jhoonline.biomedcentral.com/articles/10.1186/s13045-023-01454-0
      4. Yue, M., Qin, Z., Hu, L., & Ji, H. (2024). Understanding cachexia and its impact on lung cancer and beyond. Chinese Medical Journal Pulmonary and Critical Care Medicine 2(2); 95-105. DOI:10.1016/j.pccm.2024.02.003, https://www.sciencedirect.com/science/article/pii/S2772558824000045
      5. Ni, J., & Zhang, L. (2020). Cancer Cachexia: Definition, Staging, and Emerging Treatments. Cancer Management and Research 12, 5597. DOI:10.2147/CMAR.S261585, https://www.dovepress.com/cancer-cachexia-definition-staging-and-emerging-treatments-peer-reviewed-fulltext-article-CMAR
      6. Sadeghi, M., Keshavarz-Fathi, M., Baracos, V., et al. (2018). Cancer cachexia: Diagnosis, assessment, and treatment. Critical Reviews in Oncology/Hematology 127; 91-104. DOI:10.1016/j.critrevonc.2018.05.006, https://www.sciencedirect.com/science/article/pii/S1040842817302731
      7. Mariean, C. R., Tiucă, O. M., Mariean, A., & Cotoi, O. S. (2023). Cancer Cachexia: New Insights and Future Directions. Cancers 15(23), 5590. DOI:10.3390/cancers15235590, https://www.mdpi.com/2072-6694/15/23/5590
      8. Hariyanto, T. I., & Kurniawan, A. (2020). Cachexia in Cancer Patients: Systematic Literature Review. Asian Journal of Oncology 6(3);107-115. DOI:10.1055/s-0040-1713701, https://asjo.in/cachexia-in-cancer-patients-systematic-literature-review/
      9. Santos, J. M., & Medeiros, R. (2020). Cancer cachexia and its pathophysiology: Links with sarcopenia, anorexia, and asthenia. Journal of Cachexia, Sarcopenia and Muscle 11(3); 619. DOI:10.1002/jcsm.12528, https://onlinelibrary.wiley.com/doi/10.1002/jcsm.12528
      10. Muthanandam, S., & Muthu, J. (2021). Understanding Cachexia in Head and Neck Cancer. Asia-Pacific Journal of Oncology Nursing 8(5); 527. DOI:10.4103/apjon.apjon-2145, https://apjon.org/article/S2347-5625(21)00079-2/fulltext
      11. Temel, J. S., Abernethy, A. P., Currow, D. C., et al. (2016). Anamorelin in patients with non-small-cell lung cancer and cachexia (ROMANA 1 and ROMANA 2): results from two randomised, double-blind, phase 3 trials. Lancet Oncology 17(4);519–531. DOI:10.1016/S1470-2045(15)00558-6, https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(15)00558-6/abstract
      12. Wiskemann, J., Clauss, D., Tjaden, C., et al. (2019). Progressive resistance training to impact physical fitness and body weight in pancreatic cancer patients: a randomized controlled trial. Pancreas 48(2):257-266. DOI:10.1097/MPA.0000000000001221, https://journals.lww.com/pancreasjournal/abstract/2019/02000/progressive_resistance_training_to_impact_physical.18.aspx
      13. Arends, J., Musaritoli, M., Anker, S., et al. (2023). Overcoming barriers to timely recognition and treatment of cancer cachexia: Sharing Progress in Cancer Care Task Force Position Paper and Call to Action. Critical Reviews in Oncology/Hematology 185, 103965. DOI:10.1016/j.critrevonc.2023.103965, https://www.sciencedirect.com/science/article/pii/S1040842823000537
      14. Wijaya, Y. T., Setiawan, T., Sari, I. N., et al. (2022). Ginsenoside Rd ameliorates muscle wasting by suppressing the signal transducer and activator of transcription 3 pathway. J Cachexia Sarcopenia Muscle 13(6):3149-62. DOI:10.1002/jcsm.13084, https://onlinelibrary.wiley.com/doi/10.1002/jcsm.13084

      Further Reading

      Last Updated: Sep 9, 2025

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  • Japan's Nikkei crosses 44,000 for first time on trade, stimulus optimism – Reuters

    1. Japan’s Nikkei crosses 44,000 for first time on trade, stimulus optimism  Reuters
    2. Japan stocks higher at close of trade; Nikkei 225 up 1.62%  Investing.com
    3. Nikkei Hits New High As Stimulus Hopes Lift Market  Finimize
    4. Nikkei 225 Technical: Bullish trend remains intact despite Japan’s PM resignation  marketpulse.com
    5. Japan’s Nikkei rises to 44,000 for first time on trade, spending optimism  Yahoo Finance

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  • Prince Harry in UK for Queen Elizabeth’s death anniversary, seeks path to reconciliation

    Prince Harry in UK for Queen Elizabeth’s death anniversary, seeks path to reconciliation

    Prince Harry is in the United Kingdom this week for a packed schedule of charitable engagements, but behind the public appearances, there’s reportedly a personal goal, too — reconciliation with family.

    Britain’s Prince Harry, Duke of Sussex delivers a speech during the annual WellChild Awards in London on September 8.(AFP)

    According to close friends, Prince Harry wants to keep coming back to meet family and wants to bring his wife, Meghan Markle and children along, The Times report said.

    In May, Prince Harry openly expressed his intention to reconcile with his royal family. In an emotional interview with the BBC, he said he was “devastated” at losing a legal challenge over his security in the UK.

    “I would love reconciliation with my family. There’s no point continuing to fight any more, life is precious,” said Prince Harry, who said the dispute over his security had “always been the sticking point,” he said at the time.

    Another friend of Prince Harry told The Times that he made it “absolutely clear” that he wants to rebuild ties with the royal family. “It’s on them now,” he said.

    However, those in royal circles see it differently. His unwise choice of words about Charles’s health and repeated suggestion that the King should have intervened in his security battle — something the King would never consider, given his constitutional role may have only compunded the situation.

    Prince Harry’s first visit to the UK in months

    This week marks Harry’s first extended visit to the UK in months. He arrived in London ahead of the WellChild Awards on Monday, the third anniversary of Queen Elizabeth II’s death.

    On Tuesday, he travelled to Nottingham for an event focused on supporting young people affected by violence. The rest of the week will be spent in private meetings and receptions with several of his patronages, including the Invictus Foundation, Scotty’s Little Soldiers, and The Diana Award.

    His itinerary has been described as “jam-packed with hardly any downtime,” but amid reconciliatory efforts, there is one question left– Will Prince Harry meet with his father, King Charles III?

    The two have not seen each other since February 2024, when Harry made a brief visit following the King’s cancer diagnosis. While both sides are said to miss each other, no meeting is currently scheduled.

    In a recent BBC interview, Harry acknowledged the deep fractures within the family, especially with his father. “I don’t know how much longer my father has,” he said. “He won’t speak to me because of this security stuff. Of course, some members of my family will never forgive me for writing a book. But I would love a reconciliation.”

    If that happens, it would be the first time the two have met in more than 18 months. Royal biographer Tom Bower called it “a meeting full of peril.”

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