Despite receiving blood thinners and other clot prevention treatment, some patients still develop potentially lethal blood clots in the first month after their operations anyway, especially if they developed a surgical-site infection while in the hospital, according to results of a study at Johns Hopkins.
The research found that patients who experience a surgical-site infection after their abdominal surgery are four times more likely than infection-free patients to develop a deep-vein thrombosis (DVT) in the legs, or its more deadly cousin, a pulmonary embolism (PE) in the lungs. While only 4 percent of patients developed a DVT, 92 percent of those who did had received prophylaxis that previous research has shown is the best practice for prevention.
‘We need heightened awareness about the potential for venous thromboembolism (VTE) in patients with surgical-site infections,’ says study leader Susan L. Gearhart, M.D., an associate professor of surgery at the Johns Hopkins University School of Medicine. ‘We need to think beyond the prophylaxis we are already giving these patients. We need to think smarter.’
Nearly all surgical patients at The Johns Hopkins Hospital are routinely given proven treatments to prevent VTEs, usually the regular administration of low-dose blood thinners and the use of compression devices to keep blood flowing in the legs. Typically the treatments cease when people are discharged from the hospital.
Gearhart notes that much work in hospitals has gone into ensuring compliance with prophylaxis measures, including automated checklists to remind health care workers of their importance. VTEs are considered a form of preventable harm, and the Centers for Medicare & Medicaid Services may penalise hospitals where patients develop clots after some orthopedic procedures. But this new study shows that even when hospitals comply with prevention guidelines, VTEs can still occur.
For their study, Gearhart and her colleagues reviewed the records of 615 adults who underwent colorectal surgery at The Johns Hopkins Hospital between July 2009 and July 2011. Twenty-five (4.1 percent) developed VTE. Among patients who experienced a VTE, 92 percent had been given risk-appropriate VTE prophylaxis.
What was even more interesting to Gearhart, she says, was that 14 of the 25 patients with VTE (56 percent) also developed postoperative infections compared with 168 patients (28.5 percent) without VTE. The infectious complications in nine of the 14 patients (64.3 percent) occurred prior to or on the same day as the VTE. She says she had never before seen a link between infections and VTE in surgical patients.
One theory for the apparent link is that an increase of inflammatory protein molecules that accompanies an infection affects the functioning of platelets in the blood, which could increase the risk of thrombosis. Platelets are the sticky cells that facilitate clot formation in the blood.
Gearhart says it may be time to conduct more intense monitoring of colorectal surgery patients who develop surgical-site infections, and consider frequent screening for clots in those with infections. Such screening can be done with ultrasound equipment. She also suggests such patients be kept on blood thinners for 30 days after surgery regardless of when they are discharged. Johns Hopkins Medicine

Nanodiamonds bound to the chemotherapy drug epirubicin are enclosed within a lipid membrane and coupled to antibodies specific to hard-to-treat tumors.
Recently, doctors have begun to categorise breast cancers into four main groups according to the genetic makeup of the cancer cells. Which category a cancer falls into generally determines the best method of treatment.

But cancers in one of the four groups

Blind mice can see again, after Oxford University researchers transplanted developing cells into their eyes and found they could re-form the entire light-sensitive layer of the retina.
The researchers say the approach has relevance for treating patients with retinitis pigmentosa, a condition in which the light-sensing cells in the retina gradually die leading to progressive blindness.
The study was led by Professor Robert MacLaren in the Nuffield Department of Clinical Neurosciences at the University of Oxford, together with Dr Mandeep Singh, an eye surgeon from the National University Hospital of Singapore who is currently undertaking PhD studies in Oxford
The researchers worked with mice that are blind due to complete loss of the light-sensing photoreceptor cells in their retinas. This is the most relevant mouse model for treating patients who are blind from retinitis pigmentosa.
After two weeks, the researchers showed the cells transplanted into the eye had re-formed a full light-detecting layer on the retina and the mice could see.
The cells used were mouse ‘precursor’ cells that are on an initial path towards developing into retinal cells.
A pupil constriction test showed that, of the 12 mice that received the cell transplant, 10 showed improved pupil constriction in response to light. This shows that the retinas of the mice were sensing the light once more, and this was being transmitted down the optic nerve to the brain.
Dr Singh says: ‘We found that if enough cells are transplanted together, they not only become light sensing but they also regenerate the connections required for meaningful vision.’
Dr Mandeep Singh Professor MacLaren explains: ‘Stem cells have been trialled in patients to replace the pigmented lining of the retina, but this new research shows that the light-sensing layer might also be replaced in a similar way. The light-sensing cells have a highly complex structure and we observed that they can resume function as a layer and restore connections after transplantation into the completely blind retina.’
In looking forward towards potential cell treatments for blindness in humans, Professor MacLaren explains that they would like to use induced pluripotent stem cells, or iPS cells. These are stem cells that have been generated from the patient

A scan that offers patients a less invasive test, sometimes called a

Researchers at Imperial College London have begun the first UK clinical trials of a gene therapy for heart failure.

Heart failure, when the heart is unable to pump blood adequately, affects more than 750,000 people in the UK, causing breathlessness and hindering day-to-day activities. The therapy is designed to increase the levels of SERCA2a protein in heart muscle cells by using a harmless virus to insert extra genes into the cells.

The two clinical trials announced mark the culmination of more than 20 years of research funded by the British Heart Foundation (BHF) at Imperial and the Royal Brompton Hospital, which have identified SERCA2a as an important factor affecting how well heart muscle cells can contract in people with heart failure.

The trials will be led in the UK by cardiologists and scientists at Brompton and Imperial, in collaboration with doctors at several UK hospitals including Harefield in London, Papworth in Cambridge and the Golden Jubilee National Hospital in Scotland. The announcement coincides with Fight For Every Heartbeat, a new hard-hitting campaign from the BHF that hails research as the weapon needed to win the battle against heart disease.

Dr Alexander Lyon, BHF Senior Lecturer at Imperial College London and Consultant Cardiologist at the Royal Brompton Hospital, who is the UK lead investigator for both studies, said: ‘Heart failure affects more than three quarters of a million people across the UK. Once heart failure starts, it progresses into a vicious cycle where the pumping becomes weaker and weaker, as each heart cell simply cannot respond to the increased demand.

‘Our goal is to fight back against heart failure by targeting and reversing some of the critical molecular changes arising in the heart when it fails.’

The trials are the next step in the research after laboratory studies found that the gene therapy can be used to effectively restore function to the failing heart, in collaboration with colleagues from the United States.

Doctors plan to study the gene therapy in two separate clinical trials. The first, called CUPID2, will begin treating people with heart failure in the next few weeks in the Cardiovascular Biomedical Research Unit at the Royal Brompton Hospital.

CUPID2 will assess whether cardiac gene therapy to increase SERCA2a is safe and can improve both quality and length of life, and reduce emergency hospital admissions, for heart failure patients. The trial will involve 200 patients with heart failure from the Royal Brompton Hospital and other centres across the world, and is funded by US biotech company Celladon.

The second trial, called SERCA-LVAD, is due to start recruitment in the summer of 2013. Co-funded by the BHF, this trial will test the SERCA2a gene therapy in 24 UK heart failure patients already fitted with mechanical heart pumps, known as left ventricular assist devices (LVADs). It will give vital information about the effectiveness of the therapy by measuring the amount of the SERCA2a gene and protein that has been introduced into heart muscle.

Professor Sian Harding, Professor of Cardiac Pharmacology and Head of the BHF Centre for Regenerative Medicine at Imperial College London, who developed the treatment, said: ‘It