TEL AVIV, Israel, Dec. 11 (UPI) — Children whose mothers were depressed throughout their first year of life have a higher risk of mental disorders themselves by age 6, researchers in Israel say.

Ruth Feldman, a professor at Bar-Ilan University in Israel, found 60 percent of children born to mothers who were consistently depressed across the first year of the children’s lives exhibited mental disorders when they were older. The children, similar to their mothers, also showed disordered functioning of the Oxytocin system.

Oxytocin, a mammalian hormone, is involved with sexual reproduction, childbirth, breastfeeding and pair bonding.

Researchers studied the mental health status, Oxytocin levels, genetic variation in Oxytocin receptors and interactions in 155 mother-child pairs during at-home visits. The mothers were surveyed for mental health symptoms at the birth of their child, and at 6 and 9 months after the birth of their child.

Of the pairs participating when the child reached 6 years of age, 30 percent of mothers were diagnosed with depression and had demonstrated symptoms of depression throughout the child’s first year of life. On average, these mothers had disordered Oxytocin functioning and produced less peripheral Oxytocin in their saliva.

Most children born to depressed mothers exhibited mental disorders, but 40 percent demonstrated more normal functioning of the Oxytocin system, no signs of mental illness, better social engagements and empathic behaviors.

“We found Oxytocin system functioning helps safeguard some children against the effects of chronic maternal depression,” Feldman said.

The findings were presented at the American College of Neuropsychopharmacology annual meeting.

PARIS (AFP) – Swine flu can infect cells deeper in the lungs than seasonal flu, thus helping to boost the severity of the illness, a study released on Thursday said.

The paper provides the first laboratory corroboration of reports from front-line doctors that some patients with a (H1N1) virus suffer worse symptoms compared to those with run-of-the-mill seasonal flu.

Influenza viruses penetrate cells by attaching themselves to molecules called receptors, located on the outside of the cell wall.

The virus’ docking spike and the receptor are like a key and a lock. some viruses only open a few cells, while others have something rather closer to a pass key, making it possible to infect a larger cell variety.

Once inside, the virus uses the cell’s machinery to replicate, eventually bursting the cell and going on to attack others.

Seasonal strains attach themselves almost exclusively to cells found in the nose, throat and upper airway, producing a some of influenza’s signature symptoms: runny nose, scratchy throat, a dry cough.

But the new research, published in the journal Nature Biotechnology, shows that the new swine flu — by sticking to a greater range of receptors — can also breach cells deep in the lungs.

Lab-dish experiments were carried out by ten Feizi of Imperial College London and colleagues in which 86 different receptors were exposed to both seasonal and pandemic flu.

The seasonal strains only locked onto the kind of receptors found in the upper respiratory track.

But the swine flu virus was also able to latch onto receptors found deep inside the lungs, albeit more weakly. the adhesion results in a more severe lung infection.

Feizi spelt out the risk of what could happen if natural selection encourages viral strains that favour this deep-lung penetration.

"If the flu virus mutates in the future, it may attach to the receptors deep inside the lungs more strongly, and this could mean that more people would experience severe symptoms," said Feizi.

"we think scientists should be on the lookout for these kinds of changes in the virus so we can try to find ways to minimise the impact."

Using a statistical technique, epidemiologists sifting through data from other countries have found similarly disquieting patterns.

French epidemiologist Antoine Flahault has reported a 100-fold increase, compared to seasonal flu, in the number of swine flu deaths in Mauritius and new Caledonia attributed directly to the virus itself rather than secondary bacterial infections or underlying conditions.

Many of those deaths were caused by acute respiratory disease syndrome (ARDS), which requires intensive-care treatment for an average of three weeks. only 50 percent of ARDS patients survive.

© Copyright (c) AFP

was going through biology past papers and this question baffled me

'Cholera bacteria priduce a toxin which causes the epithelial cells of the intestine to secrete chloride ions into the lumen of the intestine. explain why diarrhoea is a symptom of choler?'

the question is a three marker, so i guess, it'll want three points, but i have no idea what it is going on about,

anyone have any clue?

Just to extend on the above answers (and to make sure you get all the points you possibly can), the cholera toxin binds to receptors that upregulate the action of adenylate cyclase in the cell, which therefore increases cAMP production. this acts on the chloride channels in the cell, increasing the Cl- efflux into the lumen. this is what causes the massive amount of water to enter the lumen. this diagram ebi.ac.uk/interpro/potm/2005_… explains it better than me.

bacteria secrete a toxin, chloeragen, which disrupts the funtion of the epithelium causing salts and water to leave the blood. THis lack of salt nd water causes Diarrhoea