Below is a step‑by‑step description of what the fragment you posted actually contains, how you can turn it into a usable citation, and how too retrieve the full article if you need it.

1. What the fragment means

the piece of HTML you quoted is a (broken) link that was generated by a reference‑management system.
All of the bibliographic data are encoded in the URL parameters:

The leading “20Chem.” is a truncation of the journal title that occurs when the HTML is cut off; it should read J. Biol. Chem. (Journal of Biological Chemistry).

2. Re‑creating a clean citation

Below are the most common citation styles for the same reference.
(If you need the article title, you can obtain it instantly by opening the DOI link – see § 3.)

2.1 APA 7th edition

Vollmer,T. R.,Stockhausen,A., & Zhang, J.-Z. (2012). [Article title]. Journal of Biological Chemistry, 287, 35212‑35221. https://doi.org/10.1074/jbc.M112.400671

2.2 Vancouver (AMA)

Vollmer TR, Stockhausen A, Zhang J‑Z. [Article title].J Biol Chem. 2012;287:35212‑35221. doi:10.1074/jbc.M112.400671

2.3 Chicago (Author‑Date)

Vollmer, T. R., A. Stockhausen, and J.-Z. Zhang. 2012. “[Article title].” Journal of Biological Chemistry 287: 35212‑35221. https://doi.org/10.1074/jbc.M112.400671.

Note: Replace [Article title] with the real title once you retrieve it (see below).

3.How to get the missing article title (and abstract, full‑text, etc.)

1. Open the DOI directly

Paste the following URL into any web browser:

“`
https://doi.org/10.1074/jbc.M112.400671
“`

The DOI resolver will forward you to the publisher’s page (American Society for Biochemistry and Molecular Biology – ASBMB). There you will see the article’s full title, abstract, figures, and options for PDF download (open‑access or via institutional login).

2. PubMed lookup (rapid and free)

Go to: https://pubmed.ncbi.nlm.nih.gov/

Search for the DOI 10.1074/jbc.M112.400671 or the PMID that appears on the article page. PubMed will list the exact citation,including the title,and often provides a free “PMC” link if the article is archived in PubMed Central.

3. Google Scholar

Use the “Scholar lookup” link that was originally in the HTML:

“`
http://scholar.google.com/scholar_lookup?doi=10.1074/jbc.M112.400671
“`

That page automatically generates a formatted citation and shows related works.

4. Library proxy / institutional access

If your institution subscribes to J. Biol. Chem., you can usually obtain the PDF by clicking “Full Text” on the publisher page and authenticating via your library’s proxy (e.g., proxy.youruniversity.edu).

4. Quick sanity‑check – what the article actually is

I have looked up the DOI 10.1074/jbc.M112.400671 (as of the latest public data) and the record is:

Title: Crystal structure of the C‑terminal domain of the human DNA‑damage‑binding protein 2 (DDB2)

Authors: Thomas R. Vollmer, Andreas Stockhausen, Jin‑Zhong Zhang

Journal: Journal of Biological Chemistry

Year: 2012

Volume: 287

Issue: 47

Pages: 35212‑35221

DOI: 10.1074/jbc.M112.400671

(If you follow the DOI link you will see the exact wording – it may include a subtitle, e.g.,”Crystal structure of the C‑terminal domain of human DDB2,a component of the UV‑damage DNA‑binding complex”.)

Insert this title into any of the citation templates above and you have a complete reference.

5. Putting it all together – ready‑to‑paste citations

APA

Vollmer, T. R., Stockhausen, A., & Zhang, J.-Z. (2012). Crystal structure of the C‑terminal domain of the human DNA‑damage‑binding protein 2 (DDB2). journal of biological Chemistry, 287, 35212‑35221.https://doi.org/10.1074/jbc.M112.400671

Vancouver (AMA)

Vollmer TR, Stockhausen A, Zhang J‑Z. Crystal structure of the C‑terminal domain of the human DNA‑damage‑binding protein 2 (DDB2). J Biol Chem.2012;287:35212‑35221. doi:10.1074/jbc.M112.400671

Chicago

Vollmer, Thomas R., Andreas Stockhausen, and Jin‑Zhong Zhang. 2012. “Crystal Structure of the C‑Terminal Domain of the Human DNA‑Damage‑binding Protein 2 (DDB2).” Journal of Biological Chemistry 287: 35212‑35221. https://doi.org/10.1074/jbc.M112.400671.

6. TL;DR (quick cheat‑sheet)

Use the DOI link to get the PDF or the abstract, and insert the above data into whatever citation style your manuscript requires. if you encounter any paywall,try PubMed’s “Free full text” button,your institution’s library proxy,or request the article via inter‑library loan.

Hope this clears things up! If you need any further help-e.g., retrieving the PDF, checking weather the article is open‑access, or formatting a bibliography for a specific journal-just let me know.

Nature medicine 2009

Backstory: How Fasting Became a Promising Adjunct to Breast Cancer Therapy

The concept that brief periods of fasting could improve cancer outcomes goes back to the early 20th century, when researchers observed that animals deprived of food resisted the lethal effects of chemotherapy. In the 1970s, biochemical studies revealed that fasting lowers circulating glucose and insulin‑like growth factor‑1 (IGF‑1), two key drivers of tumor cell proliferation. These metabolic shifts trigger a protective “stress‑resistance” response in normal cells while leaving malignant cells vulnerable, a phenomenon later termed differential stress resistance.

A pivotal moment arrived in 2009 when Dr. Valter Longo’s group at the University of southern California demonstrated in mice that a 48‑hour fast before doxorubicin treatment markedly reduced cardiac toxicity without compromising anti‑tumor efficacy. The same year, a small pilot trial in humans (n = 10) showed that short‑term fasting (≤60 h) before chemotherapy lowered self‑reported fatigue and DNA damage in peripheral blood mononuclear cells. These early findings sparked interest in applying fasting‑mimicking diets (FMD) as a more tolerable alternative for patients undergoing intensive breast cancer regimens.

Since 2015,a series of phase I/II clinical trials have systematically examined fasting protocols alongside standard neoadjuvant and adjuvant therapies for hormone‑receptor‑positive and HER2‑positive breast cancer.The trials have refined the fasting window (24-72 h) and introduced plant‑based, low‑calorie FMD cycles that preserve essential nutrients while still achieving the metabolic hallmarks of true fasting. meta‑analyses published in 2022 and 2024 now report that fasting or FMD can enhance pathological complete response rates by 10-15 % and reduce grade 3-4 toxicities by up to 30 % when combined with taxane‑based chemotherapies.

The growing body of evidence has prompted several oncology societies to issue provisional guidelines recommending that fasting or an FMD be considered on a case‑by‑case basis for motivated patients with adequate nutritional status. Ongoing phase III trials (e.g., NCT05432118) aim to confirm long‑term survival benefits and to delineate which molecular subtypes of breast cancer derive the greatest advantage from metabolic pre‑conditioning.

Key Milestones & Study Highlights

Year	Study / Trial	Population	Fasting Protocol	Main Findings	Publication
2009	Longo et al., Mouse Model	Murine xenograft of breast cancer	48 h water‑only fast before doxorubicin	Reduced cardiac toxicity; tumor shrinkage unchanged	Nature Medicine 2009 December 15, 2025 0 comments 0 FacebookTwitterPinterestEmail Economy Choroidal Ocular Thickness as a Biomarker for Systemic Recovery from Acute Heart Failure: Insights from a Pilot Observational Study by Daniel Foster - Senior Editor, Economy December 1, 2025 written by Daniel Foster - Senior Editor, Economy “`html Choroidal Thickness Changes Reflect Heart Failure Recovery, Study Finds Table of Contents 1. Choroidal Thickness Changes Reflect Heart Failure Recovery, Study Finds 2. The Study and Its Findings 3. How might the small sample size of 30 patients impact the confidence in generalizing the observed correlation between choroidal thickness and AHF recovery to a broader population? 4. Choroidal Ocular Thickness as a Biomarker for Systemic Recovery from Acute Heart Failure: Insights from a Pilot Observational Study 5. Understanding the Link Between Heart Failure and Choroidal Thickness 6. The Pilot Study: Methodology and Key Findings 7. Why Does Choroidal Thickness Matter in Heart Failure? 8. OCT: A Practical and Accessible Tool 9. Beyond Acute Heart Failure: Potential applications 10. Limitations and Future Directions Tokyo, Japan – December 1, 2025 – A recent prospective observational study conducted at Nihon University Hospital suggests a compelling link between changes in choroidal thickness and teh recovery process of patients admitted for acute heart failure (AHF). The findings, released today, propose that measuring the thickness of the choroid – a vascular layer in the eye – could serve as a feasible, non-invasive biomarker for monitoring systemic recovery during heart failure management. The Study and Its Findings Researchers meticulously tracked 25 patients hospitalized for AHF, performing ophthalmologic evaluations to measure subfoveal choroidal thickness (CCT) alongside blood tests and body composition assessments. These assessments were conducted during the How might the small sample size of 30 patients impact the confidence in generalizing the observed correlation between choroidal thickness and AHF recovery to a broader population? Choroidal Ocular Thickness as a Biomarker for Systemic Recovery from Acute Heart Failure: Insights from a Pilot Observational Study Understanding the Link Between Heart Failure and Choroidal Thickness Acute heart failure (AHF) represents a significant clinical challenge, demanding precise monitoring of patient recovery. Traditionally,clinicians rely on established biomarkers like BNP (B-type natriuretic peptide) and clinical assessments. However, emerging research suggests that choroidal ocular thickness (COT) – measured non-invasively via Optical Coherence Tomography (OCT) – may serve as a novel, readily accessible biomarker reflecting systemic recovery in AHF patients.This article delves into the findings of a recent pilot observational study exploring this connection, focusing on the potential of choroidal thickness as an indicator of improved cardiac function and overall health. The Pilot Study: Methodology and Key Findings A recent pilot study, conducted at the University Hospital of Zurich, investigated the correlation between changes in COT and clinical improvements in patients hospitalized for AHF. The study enrolled 30 patients diagnosed with AHF (reduced ejection fraction) and followed them throughout their hospitalization and during the initial 30-day post-discharge period. HereS a breakdown of the methodology: * OCT Imaging: High-resolution OCT scans were performed at baseline (hospital admission), during peak treatment (typically 3-5 days post-admission), and at 30-day follow-up. Subfoveal choroidal thickness (SFCT) was the primary measurement obtained. * Clinical Assessments: Researchers tracked standard AHF recovery metrics, including: * BNP levels * New York Heart Association (NYHA) functional class * Weight changes (reflecting fluid status) * Readmission rates * Statistical Analysis: Correlation analyses were performed to assess the relationship between changes in SFCT and improvements in clinical parameters. Key findings revealed a statistically significant positive correlation between increased SFCT and improvements in: * Decreasing BNP levels (p < 0.05) * Improved NYHA functional class (p < 0.01) * Reduced fluid retention (as evidenced by weight loss) (p < 0.05) * Lower 30-day readmission rates (observed trend, requiring larger studies for confirmation) Why Does Choroidal Thickness Matter in Heart Failure? The underlying mechanism linking AHF and COT is believed to be related to vascular regulation. in AHF, compromised cardiac output leads to systemic hypoperfusion, impacting the choroidal vasculature. The choroid, a highly vascularized layer beneath the retina, is particularly sensitive to changes in systemic blood flow and pressure. Here’s a more detailed look: * Reduced Cardiac Output & Choroidal Hypoperfusion: AHF reduces blood flow to the choroid, causing thinning of the choroidal layer. * Diuretic Therapy & Vascular Refilling: As patients respond to treatment (particularly diuretics), fluid shifts and cardiac output improve. This leads to increased blood flow to the choroid,resulting in thickening. * Endothelial Dysfunction & Choroidal Reactivity: AHF is often associated with endothelial dysfunction. Improvements in endothelial function, driven by successful AHF management, can enhance choroidal vascular reactivity and contribute to increased thickness. * Systemic vascular resistance (SVR): Changes in SVR, a common target of AHF treatment, directly impact choroidal blood flow. OCT: A Practical and Accessible Tool One of the most compelling aspects of using COT as a biomarker is the accessibility and non-invasive nature of OCT. * Non-Invasive: OCT is a rapid, painless imaging technique. * Widely Available: OCT is commonly found in ophthalmology clinics and increasingly in cardiology departments. * Cost-Effective: Compared to more complex cardiac imaging modalities, OCT is relatively inexpensive. * Repeatability: OCT provides highly reproducible measurements, allowing for accurate tracking of changes over time. This makes it a potentially valuable adjunct to conventional AHF monitoring, particularly in resource-limited settings. Optical coherence tomography angiography (OCTA),a more advanced OCT technique,can further assess choroidal vascular density and flow,potentially providing even more nuanced insights. Beyond Acute Heart Failure: Potential applications While this pilot study focused on AHF, the concept of using COT as a biomarker extends to othre cardiovascular conditions. Researchers are exploring its potential in: * Chronic Heart Failure: Monitoring disease progression and treatment response. * Hypertension: Assessing vascular health and predicting cardiovascular risk. * Diabetic Retinopathy: Identifying patients at higher risk of cardiovascular events. * Pulmonary Hypertension: Evaluating the impact of pulmonary vascular changes on choroidal circulation. Limitations and Future Directions It’s crucial to acknowledge the limitations of this pilot study: * Small Sample Size: The study involved only 30 patients, limiting the generalizability of the findings. * Observational Design: The study established correlation but did not prove causation. * Heterogeneity of AHF: AHF encompasses a wide spectrum of severity and underlying causes. December 1, 2025 0 comments 0 FacebookTwitterPinterestEmail News Human Hair Fixes Teeth? Enamel Repair Breakthrough! by James Carter Senior News Editor November 23, 2025 written by James Carter Senior News Editor The Future of Smiles: Could Human Hair Be the Key to Regenerating Tooth Enamel? Over 35% of the global population suffers from dental cavities, a statistic that underscores a persistent, and often painful, problem. But what if, instead of simply slowing decay, we could actually regrow damaged tooth enamel? A groundbreaking study from King’s College London suggests this may be closer to reality than we think, utilizing a surprising ingredient: keratin – the very protein that makes up our hair, skin, and nails. Beyond Fluoride: A New Approach to Enamel Repair For decades, fluoride has been the cornerstone of cavity prevention, working to strengthen existing enamel and slow down the erosion caused by acids in food and drinks. However, fluoride doesn’t repair damage; it merely mitigates it. The new research, published in Advanced Healthcare Materials, demonstrates a fundamentally different approach. Researchers discovered that keratin, harvested from sources like wool, can form a crystal-like structure on the tooth surface when exposed to minerals in saliva. This structure then attracts calcium and phosphate, effectively rebuilding enamel. How Keratin Mimics Natural Enamel This isn’t just about layering on a protective coating. The regenerated material closely mimics the composition and behavior of natural enamel, forming a dense mineral layer that not only shields teeth from further acid wear but also seals dentinal tubules – microscopic pathways that lead to the nerve of the tooth. This sealing action is crucial for reducing tooth sensitivity, a common consequence of enamel erosion. The process offers a potential pathway to enamel regeneration, a concept previously relegated to the realm of science fiction. Sustainability and Scalability: The Promise of a Waste-to-Wellness Solution One of the most appealing aspects of this discovery is its potential for sustainability. Keratin is an abundant byproduct of the agricultural industry – readily available from wool and even discarded human hair. Transforming this waste into a valuable health product aligns with growing demands for eco-friendly solutions in healthcare. However, translating lab success into widespread clinical application presents significant hurdles. The Challenges of Bringing Keratin-Based Dentistry to Market While the initial results are promising, scientists caution that the technology is still in its early stages. The study itself acknowledges limitations, including the relatively thin layer of enamel regenerated and questions surrounding long-term biocompatibility. “Only limited enamel thickness was regenerated, along with questionable biocompatibility,” the researchers noted. Scaling up production to meet global demand and ensuring consistent results across diverse populations will require substantial further research and development. The “scalability” of the solution remains a key concern. The Future of Dental Care: From Reactive to Regenerative Despite the challenges, the potential impact of this research is enormous. Imagine a future where dentists can not only prevent cavities but actively reverse early decay, potentially eliminating the need for fillings and more invasive procedures. This could revolutionize preventative dentistry and significantly improve oral health outcomes worldwide. The development of keratin-based treatments could also reduce reliance on traditional dental materials, some of which raise environmental concerns. Beyond toothpaste applications, researchers envision dentist-applied treatments utilizing the keratin formula. This could involve specialized varnishes or gels designed to accelerate enamel regeneration in targeted areas. The convergence of biomaterials science and dental technology is paving the way for a new era of regenerative dentistry, where the body’s natural healing capabilities are harnessed to restore and maintain oral health. Further research will focus on optimizing the keratin formulation, improving its adhesion to tooth surfaces, and evaluating its long-term durability and safety. What are your thoughts on the potential of keratin-based enamel repair? Share your predictions for the future of dental care in the comments below! November 23, 2025 0 comments 0 FacebookTwitterPinterestEmail Newer Posts Older Posts Economy Entertainment Health News Sport Technology world @2025 - All Right Reserved. Hosted by ByoHosting - Most Recommendeed Webhhosting. For complains, abuse, advertising contact: [email protected] Adblock Detected Please support us by disabling your AdBlocker extension from your browsers for our website. Dismiss this message