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1. Higher Post-operative Day 1 (POD1) pain scores were independently associated with increased 30-day infectious and non-infectious complications.

2. Infectious complications developed later (mean 6.5 days) than non-infectious complications (4.1 days).

Evidence Rating Level: 2 (Good)

Early postoperative pain is a significant concern following major abdominal surgery, with growing evidence linking its intensity to increased 30-day complication risks. This retrospective cohort study analyzed 1,000 patients undergoing cytoreductive surgery with hyperthermic intraperitoneal chemotherapy (HIPEC), esophageal, liver, or pancreatic surgery at Radboud University Medical Center (2014–2020). Pain scores on postoperative day 1 (POD1) were assessed using the Numeric Rating Scale (NRS), and complications were classified by Clavien-Dindo (CD) criteria. Results revealed 790 complications in 572 patients (36.7% infectious, 63.4% non-infectious), with infectious complications occurring later (mean 6.5 vs. 4.1 days, *p*<0.001). Logistic regression demonstrated that higher POD1 pain scores significantly predicted total complications (OR=1.132), CD severity (OR=1.131), infectious (OR=1.126), and non-infectious complications (OR=1.079). Covariates like age, ASA class, open surgery, and longer duration also contributed. The study highlights the role of early pain in impairing recovery (e.g., reduced mobility, immunosuppression) and underscores the need for optimized perioperative analgesia to mitigate complications.

Click to read the study in RAPM

Image: PD

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The search for new ways to treat malaria — a disease that kills some 600,000 people a year, most of them children in Sub-Saharan Africa — may have just gotten a boost.

Chemists at UC San Francisco have found a way to rearrange the atoms in a new generation of malaria drugs to make them easier to put into pill form without forfeiting their effectiveness against the malaria parasite.

New malaria drugs are desperately needed. The parasite that causes the disease has developed resistance to today’s best therapies and is spreading from Southeast Asia into Africa.

“Now that drug resistance is in Africa, many more lives are at risk,” said Adam Renslo, PhD, professor of pharmaceutical chemistry in the UCSF School of Pharmacy and senior author of the paper. “These new molecules could give us the upper hand we need to control this deadly disease.”

The work, which appears Aug. 8 in Science Advances, was funded by the National Institutes of Health.

The drawn-out battle against malaria

For centuries, malaria has been known for causing cyclical and sometimes deadly fevers. In the 1950s, chemists developed new and more potent malaria drugs based on quinine, an anti-malarial compound found in plants.

Over time, the parasites evolved to resist the best of these drugs, chloroquine, and the global health community scrambled to find new ones.

Today’s most essential anti-malarial therapies include a compound called artemisinin that is found in sweet wormwood, which is used in traditional Chinese medicine. As with quinine, artemisinin gave chemists inspiration to make more effective drugs.

Artemisinin was combined with other effective drugs into a cocktail, known as artemisinin-based combination therapy (ACT), that became the standard malaria treatment. But resistance appeared once again.

“We’ve tracked artemisinin resistance for years in Southeast Asia, but we’re now seeing it spread to Africa, where 95% of cases and 95% of deaths occur,” said Phil Rosenthal, MD, professor of medicine at UCSF and co-author of the paper. “Given how long it takes to develop new drugs, there is widespread consensus that we need better drugs to circumvent this resistance ASAP.”

Saved by a quirk of drug chemistry

Artefenomel, a newer artemisinin-inspired variant, was intended to replace ACTs in time to stanch the spread of artemisinin resistance. It was potent enough that scientists hoped it could cure malaria in a single dose. This would have been an improvement over ACTs, which must be taken for three days in a row to be effective.

“For a disease like malaria, you would ideally like to cure the patient with one pill or a handful of pills and be done with it,” Renslo said. “A multi-day regimen risks missing a dose.”

But artefenomel proved difficult to study in clinical trials. Because it resisted dissolving, it needed to be shaken up with a liquid and swallowed quickly. This finicky nature also made it hard to combine with other drugs in a pill.

Children also had trouble keeping the liquid form down after drinking it, making it hard to know whether they had received the intended dose. In January of 2025, artefenomel was pulled from clinical trials.

Renslo and his team realized that the symmetry of the artefenomel molecule might be the problem. Highly symmetrical molecules tend to clump into crystals that are slow to dissolve.

The scientists thought that a less-symmetric version of artefenomel might avoid this clumping and dissolve more readily, making it easier to put into pill form. Their first successful attempt at making this molecule proved them right when it disappeared immediately into a water-like solution.

The team continued tweaking the new molecules, testing how they worked against malaria parasites in cells, and then animals, and finally against artemisinin-resistant parasites sourced from blood samples from malaria patients in Uganda.

The optimized compound passed with flying colors: it was just as potent as artefenomel, and much more effective than artemisinin, against artemisinin-resistant parasites.

“We’re optimistic that a simple chemical change like this can pave the way for an effective successor to artemisinin,” Renslo said, “one that’s cheap to make and easy to combine with other anti-malarial drugs.”

Authors: Other UCSF authors are Matthew T. Klope, PhD, Poulami Talukder, PhD, Brian R. Blank, PhD, Jun Chen, PhD, Ryan L. Gonciarz, PhD, Priyadarshini Jaishankar, MS, Jenny Legac, Vineet Mathur, Avani Narayan, Juan A.Tapia, MS, and Aswathy Vinod. For all authors see the paper.

Funding: This work was supported by the National Institutes of Health (AI075045, AI139179, AI105106, and CA260860).

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