Neutrophil-to-lymphocyte ratio may predict renal function decline in diabetes

Researchers have found that Neutrophil-to-lymphocyte ratio is a predictor of renal dysfunction in diabetes patients.The study has been published in Diabetes Metabolic Syndrome: Clinical Research & Reviews. 

Inflammation play an important role in the pathogenesis of diabetic kidney disease.Neutrophil-to-lymphocyte ratio has been evaluated as a biomarker of inflammation and has been widely evaluated as a biomarker in various medical and surgical prognoses.However its usefulness in diabetic kidney disease is not yet known.

The researchers conducted a prospective observational study that included outpatients, comprising of 184 men aged 73 ± 11 (mean ± standard deviation) years and 174 women aged 76 ± 10 years at baseline, from a rural hospital. They examined the relationship between baseline NLR calculated by analyzing the differential leukocyte counts in the complete blood count and the 2-year estimated glomerular filtration rate (eGFR) decline rate (i.e. 2-year eGFR-baseline eGFR) ∗100/baseline eGFR. Rapid eGFR decline rate was defined as a value < -25%.

The researchers found that NLR (β = 0.138, p = 0.007) as well as presence of antidyslipidemic medication, hemoglobinA1c, and urinary albumin excretion stage were significantly and independently associated with a rapid eGFR decline rate.The multiple linear regression analysis using rapid eGFR decline rates as objective variables were adjusted for confounding factors as explanatory variables. 

The multivariate-adjusted odds ratios (95% confidence interval) of the 2nd and 3rd tertiles of baseline NLR for rapid eGFR decline rate were 3.62 (0.70-18.7) and 8.03 (1.54-41.9), respectively. 

Multivariate-adjusted mean eGFR (95% confidence interval) values after 2 years categorized by tertile of baseline NLR were: 1st, 63.9 (61.8-66.1); 2nd, 60.8 (58.7-62.9); and 3rd, 58.9 (56.8-61.0).
The researchers concluded that these results suggest that baseline Neutrophil-to-lymphocyte ratio might be a useful biomarker for renal function decline in outpatients with type 2 diabetes. This biomarker may help evaluate renal function in diabetics.

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Bacterial DNA promotes tau protein misfolding and aggregation, study shows

Researchers from Human Microbiology Institute (HMI) and Mitchell Center for Alzheimer’s disease at the University of Texas McGovern Medical School in Houston have discovered that bacterial extracellular DNA can trigger Tau protein misfolding into neurotoxic aggregates, a key process in Alzheimer’s disease pathogenesis.  The discovery sets bacterial DNA as a new potential therapeutic target for treatment of neurogenerative illnesses. The breakthrough study is published in Nature’s Scientific Reports.

This is the first report showing that DNA from some bacterial species can promote Tau misfolding and aggregation - a hallmark feature of Alzheimer’s.  In previous studies, George Tetz and colleagues demonstrated that the brain contains bacteria, as well as bacterial cell-free DNA, which get to the cerebrospinal fluid from systemic circulation due to an impaired blood brain barrier. In the current article, they show that bacterial DNA is capable to promote misfolding and aggregation of the Tau protein into aggregates that are similar to those found in the brains of patients with Alzheimer’s. Thus, bacterial DNA may act as a seeding and a promotional factor for Tau protein misfolding.

Recent data suggest that various bacteria are present in cerebrospinal fluid and postmortem brains of people with Alzheimer’s, but the role of brain-localized microorganisms has been elusive, until now.

This is the first report showing bacterial DNA playing a role in protein misfolding and aggregation, which may become a new target for the treatment not only of Alzheimer’s, but other neurogenerative diseases involving tau aggregation. The findings could have huge implications in how we fight a whole host of disorders. For decades, scientists have been frustrated with clinical trials failures in the Alzheimer’s space.  So, this is a whole new hypothesis - we may have found a principally new lead not only for treating Alzheimer’s, but also for its prevention.”George Tetz, Head of Research and Development at HMI

“The misfolding, aggregation and accumulation of Tau protein in the brain is implicated in Alzheimer’s disease and various other disorders collectively known as tauopathies. This study shows that bacterial DNA can promote tau aggregation in vitro. Many more studies need to be done to confirm and extend these observations in order to fully understand the potential role of bacterial DNA in the pathogenesis of Alzheimer’s disease,” said Claudio Soto, Director of George and Cynthia Mitchell Center for Alzheimer’s Disease and Related Brain Disorders at The University of Texas McGovern Medical School.

The number of deaths from Alzheimer's disease has more than doubled in recent years, according to the Alzheimer’s Association. 1 in 10 Americans over the age of 65 has Alzheimer’s, which cannot be cured or slowed down at the present time. 

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Bottle feeding linked to stomach obstruction in infants

New research says that bottle feeding appears to increase the risk of babies developing hypertrophic pyloric stenosis, a form of stomach obstruction characterized by severe and frequent projectile vomiting and most common among infants in their first 2 months of life.

Surgery, called pyloromyotomy, may be needed to clear the hypertrophic pyloric stenosis (HPS), which occurs when the smooth muscle layer of the pylorus (the "gateway" between the stomach and small intestines) thickens.

Doctors say in the study that although this is a fairly common condition - it occurs in approximately 2 in 1,000 births - the cause remains unknown.

This study,  sets out to establish if bottle feeding during early infancy increases the risk of developing HPS, and if so, how the risk is modified by other factors.

Largest study to date

The study reports that breastfeeding became a target of interest in the 1980s, as researchers noted that an upsurge in the breastfeeding rates coincided with a decrease in the number of cases of HPS.

The doctors claim that this study analyses the largest group of HPS patients with data on infant feeding practices yet studied.

Participants in the study had to be singleton babies under 6 months old who had been both diagnosed with HPS and undergone corrective surgery.

During the time period selected, researchers identified 714 such infants and matched them to "control" babies - ones without HPS.

The researchers do note that as the study is observational, all associations should be interpreted "with caution." They also point out the data of how a baby was fed is based on information provided when the mother and baby were discharged from the hospital.

Some babies who were breastfed initially could have switched to bottle feeding (or vice versa) prior to developing HPS, the researchers say.

There are many reasons why mothers stop breastfeeding their babies, including cracked and sore nipples or mastitis. A report, published by UNICEF, reports that 60% of women did not manage to breastfeed for as long as they would have wanted.

Another potential pitfall in this research is that babies bottle-fed expressed milk are coded as bottle-fed in the data, so interpretations regarding formula milk versus breast milk may also be skewed.

Bottle feeding 'may play a role in HPS'

The researchers found that the incidence of HPS decreased from 14 per 10,000 births in 2003 to 9 per 10,000 births in 2009. They note that the popularity of breastfeeding also increased during that time from 80% in 2003 to 94% in 2009.

The study revealed that bottle-fed infants were more likely to develop HPS, compared with controls (19.5% vs. 9.1%). The odds of an infant developing HPS also increased if they were male, and when mothers were 35 years and older and multiparous (having given birth more than once before.).

The study concludes:

"These data suggest that bottle feeding may play a role in HPS etiology, and further investigations may help to elucidate the mechanisms underlying the observed effect modification by age and parity."

In an accompanying editorial, Dr. writes:

"While the data seem convincing that bottle feeding increases the risk, the reason is not clear."  

"Further understanding of the pathogenesis of hypertrophic pyloric stenosis will come from both basic research and more detailed epidemiologic studies," Dr. concludes.

Dr. and his colleagues agree, adding:

"Further studies are warranted to validate these findings and to look more closely at the speculative mechanisms, including possible hormonal effects, underlying the bottle feeding-HPS association."

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