The percentage of U.S. parents and caregivers refusing a standard vitamin K shot for infants at birth has accelerated sharply this year, putting more newborns at risk of life-threatening bleeding episodes.

Researchers have identified 36 genes that substantially raise the risk for obsessive-compulsive disorder and chronic tic disorders, a discovery that could lead to new treatments.

OCD is characterized by persistent intrusive thoughts and repetitive behaviors, while chronic tic disorders, including Tourette syndrome, involve sudden, repeated movements or vocalizations that are difficult to control.

“In the past we knew about a couple of strong genes, so there were few opportunities for the pharmaceutical industry to develop drugs,” coauthor Jay Tischfield, an emeritus distinguished professor in New Jersey’s Rutgers School of Arts and Sciences, said in a statement.

“Now you’ve got over 30 targets, and that opens up new possibilities for treatment development.”

The study published on Tuesday in Nature Neuroscience analyzed DNA from nearly 4,000 people diagnosed with these conditions.

Many of the newly identified genes are shared between OCD and chronic tic disorders. At the biological level, the disorders appear to involve many of the same brain pathways, the researchers found.

“These genes don’t act individually,” said Tischfield. “They act in networks. And now you can target whole networks, which will make it easier to design new therapies.”

The researchers also found several of the identified genes were previously linked to autism and schizophrenia, reinforcing increasing evidence that multiple psychiatric conditions may stem from related disruptions in brain development and communication.

Brain cells communicate using chemical signals called neurotransmitters that carry messages from one nerve cell to another. The genes identified in the study appear to influence how those signals move through the brain's circuitry.

By revealing the biological systems behind the disorders, the findings could aid the design of drugs that target the underlying mechanisms rather than simply managing symptoms, the researchers said.

A protein inside the “energy factories” of liver cells appears to trigger the damage seen in some patients with fatty liver disease, researchers have discovered.

Obesity-related liver disease affects hundreds of millions of people worldwide, but only a fraction of those livers develop scarring, become inflamed, and eventually fail, the researchers noted in a report published on Tuesday in the Journal of Clinical Investigation.

EFHD1, a calcium-binding protein in the membrane of the mitochondria, drives that process, they found. Blocking it protects against liver injury in human cells and in mice consuming a high-fat diet.

Using biochemical and imaging tests, the team found that EFHD1 tethers mitochondria to a nearby organelle called the endoplasmic reticulum and helps trigger mitochondrial division.

When mice are fed a fatty, sugary diet, excess lipids drive up EFHD1 levels, which makes the mitochondria divide so much that they start leaking their contents into the rest of the cell. Those contents include double-stranded RNA, which can also appear in the presence of certain viruses, like hepatitis C. Upon detecting the double-stranded RNA, the cell activates an antiviral defense pathway.

That response, meant to prevent viral replication in infected cells, instead shuts down healthy liver cells, worsening injury, according to the researchers.

When the researchers blocked or reduced the levels of EFHD1, measures of inflammation and liver scarring dropped by roughly 30% to 60% in mice with liver injuries resulting from diet or drug treatments and in miniature models of human livers in test tubes.

The researchers also found that mice engineered to lack EFHD1 have normal activity levels, weight gain, and other measures of metabolism, which suggests that treatments that block EFHD1 may have few side effects. They said they are currently working to develop such a drug.

“This research may help people by identifying new biological pathways which can be targeted with drugs to help stave off liver disease by limiting how fat buildup damages the liver,” study leader David Eberhardt of University of Utah Health said in a statement.