Why we are not preventing Diabetes?

Diabetes mellitus is going to affect the health of millions if it is allowed to continue to raise in the present manner and we are aware of this noncommunicable disease epidemic. There are some measures to delay the onset or prevent the diabetes mellitus. It is going to be essential to findout why these measures are not adequately implemented in the countries. There studies to find out the reasons for the indequate preventive measure implementation.

The Diabetes Prevention Program (DPP) clinical trial and its 10-year outcomes study (DPPOS), both sponsored by the National Institutes of Health (NIH), showed that certain interventions could prevent or substantially delay the onset of type 2 diabetes both safely and cost-effectively. Yet diabetes prevention is not widely practiced in the United States, and the disease's staggering human and financial costs continue to grow. It is therefore essential to identify the factors impeding the full realization of the DPP interventions' potential for preventing diabetes.

In DPP trial (3234) overweight or obese adults with IGT (prediabetes) were assigned to receive one of three interventions: lifestyle intervention aimed at modest weight loss through diet and exercise, treatment with generic metformin, or a placebo control. DPP findings published in 2002 indicated that, relative to placebo, lifestyle intervention and metformin reduced the rate of conversion to diabetes by 58% and 31%, respectively, over 3 years.1

Metformin worked well in younger women with history of gestational diabetes. Exercise and life style modifications worked well in people ( both genders) above 60 years of age.

Most DPP participants (88%) enrolled in the DPPOS ( 10 year study) , in which continued follow-up demonstrated that the 10-year risk reduction for type 2 diabetes was 31% for lifestyle intervention and 18% for metformin.2

We need to wait and see in India for the effectiveness of life style modifications in the rural and urban populations in preventing IGT conversion to diabetes mellitus, this can avert major risks associated with the potential epidemic of diabetes in the coming years.

18F-Fludeoxyglucose PET/CT in the evaluation of large-vessel vasculitis

British Journal of Radiology (2012) 85, e188-e194 

¹⁸F-Fludeoxyglucose PET/CT in the evaluation of large-vessel vasculitis: diagnostic performance and correlation with clinical and laboratory parameters  N D Papathanasiou Correspondence: Dr Jamshed Bomanji, Institute of Nuclear Medicine, University College Hospital, 235 Euston Road, London NW1 2BU, UK. E-mail: jamshed.bomanji@uclh.nhs.uk

Abstract

Objective: To investigate the diagnostic performance of ¹⁸F-fludeoxyglucose (¹⁸F-FDG) positron emission tomography (PET)/CT in patients with suspected large-vessel vasculitis and its potential to evaluate the extent and activity of disease.

Methods: 78 consecutive patients (mean age 63 years; 53 females) with suspected large-vessel vasculitis were evaluated with ¹⁸F-FDG PET/CT. ¹⁸F-FDG uptake in the aorta and major branches was visually graded using a four-point scale and quantified with standardised uptake values (SUV_max). According to clinical diagnosis, patients were classified into three groups: (a) steroid-naïve, large-vessel vasculitis (16 patients), (b) vasculitis on steroid treatment (18 patients) and (c) no evidence of vasculitis (44 patients). Analysis of variance and linear regression were used to investigate the association of ¹⁸F-FDG uptake with clinical diagnosis and inflammatory markers.

Results: ¹⁸F-FDG PET/CT was positive (visual uptake ≥2; equal to or greater than liver) in all patients with steroid-naïve, large-vessel vasculitis. The thoracic aorta, the carotid and the subclavian arteries were most frequently involved. 

Conclusion: ¹⁸F-FDG PET/CT can detect the extent and activity of large-vessel vasculitis in untreated patients and is unreliable in diagnosing vasculitis in patients on steroids.

Metallo Beta lactamase producing pseudomonas aeruginosa and its association with diabetic foot.

Diabetic foot infections are common and there is increasing possibility that they are getting resistant to all antibiotics available due to inadequate or inappropriate use of them. Infection with multi drug resistance organisms (MDROs) is common in diabetic foot ulcers and is associated with inadequate glycemic control and increased requirement for surgical treatment.

Pseudomonas aeruginosa strains that produce metallo beta lactamases (MBLs) are becoming increasingly prevalent in wound infections

Indian J Surg. 2011 Aug;73(4):291-4. Epub 2011 May 3.

Residents vs attending surgeons

Coronary Artery Bypass Graft Patency: Residents Versus Attending Surgeons

Faisal G. Bakaeen, MD, Gulshan Sethi, MD, Todd H. Wagner, PhD,
Rosemary Kelly, MD, Kelvin Lee, PhD, Anjali Upadhyay, MS, Hoang Thai, MD,
Elizabeth Juneman, MD, Steven Goldman, MD, and William L. Holman, MD
Michael E. DeBakey Veterans Affairs Medical Center and Division of Cardiothoracic Surgery, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas; Division of Cardiovascular Surgery, Texas Heart Institute at St. Luke’s Episcopal Hospital, Houston, Texas; Department of Cardiothoracic Surgery, University of Arizona Health Science Center, Tucson, Arizona; Veterans Affairs Palo Alto Health Care System, Palo Alto, California; Department of Cardiovascular Surgery, University
of Minnesota Hospital, Minneapolis, Minnesota; Southern Arizona Veterans Affairs Health Care System and University of Arizona, Tucson, Arizona; and Division of Cardiothoracic Surgery, University of Alabama, Birmingham, Alabama 

Background. Data are limited regarding the patency of coronary artery bypass grafts performed by residents versus attending surgeons.
 

Methods. We analyzed data from a multicenter, randomized Veterans Affairs Cooperative Study in which the left internal mammary artery was used preferentially to graft the left anterior descending coronary artery, and the best remaining coronary vessel received (per random assignment) either a radial artery or a saphenous vein graft. The study vessel’s 1-year graft patency was the primary outcome measure. Secondary outcomes included operative times, operative morbidity, mortality, repeat revascularization, cost, angina symptoms, and quality of life. Multivariate analyses were used to compare patient outcomes for residents versus attendings. 

Results. Residents were designated as primary surgeons in 23% of cases (167 of 725). Among the 531 patients who had a 1-year angiogram, study graft patency rates for resident cases (n 122) and attending cases (n 409) were not significantly different (86% versus 90%, p 0.22). Residents’ cases had longer perfusion time (119 versus 105 minutes, p < 0.0001) and cross-clamp time (84 versus 68 minutes, p < 0.0001). After risk adjustment, all outcome measures did not differ between the two groups, and there was no apparent interaction effect between resident/ attending designation and radial artery versus saphenous
vein use or on-pump versus off-pump approach.

Conclusions. Surgeons in training perform coronary artery bypass surgery without compromising graft patency or patient outcomes. Ongoing evaluation of residents’ performance and surgical outcomes is needed, given the major changes that are occurring in residency training.

(Ann Thorac Surg 2012;94:482– 8) © 2012 by The Society of Thoracic Surgeons

Low-density lipoprotein lowering does not improve calf muscle perfusion, energetics, or exercise performance in peripheral arterial disease.

J Am Coll Cardiol. 2011 Aug 30;58(10):1068-76.

West AM, Anderson JD, Epstein FH, Meyer CH, Wang H, Hagspiel KD, Berr SS, Harthun NL, Weltman AL, Dimaria JM, Hunter JR, Christopher JM, Kramer CM.

Source

Department of Medicine, University of Virginia Health System, University of Virginia, Charlottesville, Virginia.

Abstract

OBJECTIVES:

We hypothesized that low-density lipoprotein (LDL) reduction regardless of mechanism would improve calf muscle perfusion, energetics, or walking performance in peripheral arterial disease (PAD) as measured by magnetic resonance imaging and magnetic resonance spectroscopy.

BACKGROUND:

Statins improve cardiovascular outcome in PAD, and some studies suggest improved walking performance.

METHODS:

Sixty-eight patients with mild to moderate symptomatic PAD (age 65 ± 11 years; ankle-brachial index [ABI] 0.69 ± 0.14) were studied at baseline and annually for 2 years after beginning simvastatin 40 mg (n = 20) or simvastatin 40 mg/ezetimibe 10 mg (n = 18) if statin naïve, or ezetimibe 10 mg (n = 30) if taking a statin. Phosphocreatine recovery time was measured by (31)P magnetic resonance spectroscopy immediately after symptom-limited calf exercise on a 1.5-T scanner. Calf perfusion was measured using first-pass contrast-enhanced magnetic resonance imaging with 0.1 mM/kg gadolinium at peak exercise. Gadolinium-enhanced magnetic resonance angiography was graded. A 6-min walk and a standardized graded Skinner-Gardner exercise treadmill test with peak Vo(2) were performed. A repeated-measures model compared changes over time.

RESULTS:

LDL reduction from baseline to year 2 was greater in the simvastatin 40 mg/ezetimibe 10 mg group (116 ± 42 mg/dl to 56 ± 21 mg/dl) than in the simvastatin 40 mg group (129 ± 40 mg/dl to 90 ± 30 mg/dl, p < 0.01). LDL also decreased in the ezetimibe 10 mg group (102 ± 28 mg/dl to 79 ± 27 mg/dl, p < 0.01). Despite this, there was no difference in perfusion, metabolism, or exercise parameters between groups or over time. Resting ABI did improve over time in the ezetimibe 10 mg group and the entire study group of patients.

CONCLUSIONS:

Despite effective LDL reduction in PAD, neither tissue perfusion, metabolism, nor exercise parameters improved, although rest ABI did. Thus, LDL lowering does not improve calf muscle physiology or functional capacity in PAD. (Comprehensive Magnetic Resonance of Peripheral Arterial Disease; NCT00587678).

Statins and Peripheral Arterial Disease

Based on the Heart Protection Study, persons with PAD should be treated with statins regardless of age, gender, or initial serum lipids levels. 

In addition to that  - Three double-blind, randomized, placebo-controlled studies have also demonstrated that statins improve walking performance in persons with PAD.

In a study of 69 persons, mean age 75 years, with intermittent claudication, a mean ABI of 0.63, and a serum LDL cholesterol of 125 mg/dl or higher, 3 of 34 persons (9%) treated with simvastatin and 6 of 35 persons (17%) treated with placebo died before the 1-year study was completed . Compared with placebo, simvastatin significantly increased treadmill exercise time until the onset of intermittent claudication by 24% at 6 months and by 42% at 1 year after therapy. 

In a study of 354 persons, mean age 68 years, with intermittent claudication and hypercholesterolemia, at 1-year follow-up, compared with placebo, atorvastatin 80 mg daily significantly improved pain-free treadmill walking distance by 40% and significantly improved community-based physical activity. 

In a study of 86 persons, mean age 67 years, with intermittent claudication and hypercholesterolemia, at 6-month follow-up, compared with placebo, simvastatin 40 mg daily significantly improved pain-free walking distance and total walking distance on a treadmill, significantly improved the mean ABI at rest and after exercise, and significantly improved symptoms of claudication.

It is also interesting to note that Statin use is also associated with superior leg functioning independent of cholesterol levels and other potential confounders. The data suggest that non-cholesterol-lowering properties of statins may influence functioning in persons with and without PAD.

1. Aronow WS, Nayak D, Woodworth S, Ahn C. Effect of simvastatin versus placebo on treadmill exercise time until the onset of intermittent claudication in older patients with peripheral arterial disease at 6 months and at 1 year after treatment. Am J Cardiol. 2003;92:711–2. 

2. Mohler ER, III, Hiatt WR, Creager MA., the Study Investigators Cholesterol reduction with atorvastatin improves walking distance in patients with peripheral arterial disease. Circulation. 2003;108:1481–6.

3. Mondillo S, Ballo P, Barbati R, et al. Effects of simvastatin on walking performance and symptoms of intermittent claudication in hypercholesterolemic patients with peripheral vascular disease. Am J Med. 2003;114:359–64.

Lancet. 2002 Jul 6;360(9326):7-22. 

MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial.

Heart Protection Study Collaborative Group.

Abstract  : Throughout the usual LDL cholesterol range in Western populations, lower blood concentrations are associated with lower cardiovascular disease risk. In such populations, therefore, reducing LDL cholesterol may reduce the development of vascular disease, largely irrespective of initial cholesterol concentrations.

METHODS: 20,536 UK adults (aged 40-80 years) with coronary disease, other occlusive arterial disease, or diabetes were randomly allocated to receive 40 mg simvastatin daily (average compliance: 85%) or matching placebo (average non-study statin use: 17%). Analyses are of the first occurrence of particular events, and compare all simvastatin-allocated versus all placebo-allocated participants. These "intention-to-treat" comparisons assess the effects of about two-thirds (85% minus 17%) taking a statin during the scheduled 5-year treatment period, which yielded an average difference in LDL cholesterol of 1.0 mmol/L (about two-thirds of the effect of actual use of 40 mg simvastatin daily). Primary outcomes were mortality (for overall analyses) and fatal or non-fatal vascular events (for subcategory analyses), with subsidiary assessments of cancer and of other major morbidity.

FINDINGS: All-cause mortality was significantly reduced (1328 [12.9%] deaths among 10,269 allocated simvastatin versus 1507 [14.7%] among 10,267 allocated placebo; p=0.0003), due to a highly significant 18% (SE 5) proportional reduction in the coronary death rate (587 [5.7%] vs 707 [6.9%]; p=0.0005), a marginally significant reduction in other vascular deaths (194 [1.9%] vs 230 [2.2%]; p=0.07), and a non-significant reduction in non-vascular deaths (547 [5.3%] vs 570 [5.6%]; p=0.4).  

The proportional reduction in the event rate was similar (and significant) in each subcategory of participant studied, including: those without diagnosed coronary disease who had cerebrovascular disease, or had peripheral artery disease, or had diabetes; men and, separately, women; those aged either under or over 70 years at entry; and--most notably--even those who presented with LDL cholesterol below 3.0 mmol/L (116 mg/dL), or total cholesterol below 5.0 mmol/L (193 mg/dL). The benefits of simvastatin were additional to those of other cardioprotective treatments. The annual excess risk of myopathy with this regimen was about 0.01%. There were no significant adverse effects on cancer incidence or on hospitalisation for any other non-vascular cause.

 

INTERPRETATION: Adding simvastatin to existing treatments safely produces substantial additional benefits for a wide range of high-risk patients, irrespective of their initial cholesterol concentrations. Allocation to 40 mg simvastatin daily reduced the rates of myocardial infarction, of stroke, and of revascularisation by about one-quarter. After making allowance for non-compliance, actual use of this regimen would probably reduce these rates by about one-third. Hence, among the many types of high-risk individual studied, 5 years of simvastatin would prevent about 70-100 people per 1000 from suffering at least one of these major vascular events (and longer treatment should produce further benefit). The size of the 5-year benefit depends chiefly on such individuals' overall risk of major vascular events, rather than on their blood lipid concentrations alone.

Vascular malformations in the forearm subcutaneous tissues can be completely excised. This video shows the excision of the Lymphovenous malformation on the lateral aspect of the upper and middle 1/3rd of the forearm in the cephalic vein zone.

Age related differences in Endothelial response to smoke?

Buerger's disease in young men who started smoking in teen age!

In few countries Buerger's disease affecting the small blood vessels in the leg disappeared, but in the other countries it is still a problem. This disease is more often noted in the rural population or societies where childhood or teenage smoking is a problem. It gives us the suspicion that the endothelium may be responding in different ways depending on the age, but that fact was not tested and published till now. Here is one paper trying the test that hypothesis in rats.

Cigarette smoke causes oxidative stress in the lung resulting in injury and disease. The purpose of this study was to determine if there were age-related differences in cigarette smoke extract (CSE)-induced production of reactive species in single and co-cultures of alveolar epithelial type I (AT I) cells and microvascular endothelial cells harvested from the lungs (MVECLs) of neonatal, young and old male Fischer 344 rats.

Cultures of AT I cells and MVECLs grown separately (single culture) and together (co-culture) were exposed to CSE (1, 10, 50, 100%). Cultures were assayed for the production of intracellular reactive oxygen species (ROS), hydroxyl radical (OH), peroxynitrite (ONOO(-)), nitric oxide (NO) and extracellular hydrogen peroxide (H(2)O(2)). Single and co-cultures of AT I cells and MVECLs from all three ages produced minimal intracellular ROS in response to CSE. All ages of MVECLs produced H(2)O(2) in response to CSE, but young MVECLs produced significantly less H(2)O(2) compared to neonatal and old MVECLs. Interestingly, when grown as a co-culture with age-matched AT I cells, neonatal and old MVECLs demonstrated ~50% reduction in H(2)O(2) production in response to CSE. However, H(2)O(2) production in young MVECLs grown as a co-culture with young AT I cells did not change with CSE exposure. 

To begin investigating for a potential mechanism to explain the reduction in H(2)O(2) production in the co-cultures, we evaluated single and co-cultures for extracellular total antioxidant capacity. We also performed gene expression profiling specific to oxidant and anti-oxidant pathways. The total antioxidant capacity of the AT I cell supernatant was ~5 times greater than that of the MVECLs, and when grown as a co-culture and exposed to CSE (≥ 10%), the total antioxidant capacity of the supernatant was reduced by ~50%. There were no age-related differences in total antioxidant capacity of the cell supernatants. Gene expression profiling found eight genes to be significantly up-regulated or down-regulated. This is the first study to describe age-related differences in MVECLs exposed to CSE.

Microvasc Res. 2011 Nov;82(3):311-7. Epub 2011 Oct 6.

Is there an urgent need to look for medicines (Drugs) to reduce the growth of aortic aneurysms and prevent their rupture?

The incidence of abdominal aortic aneurysm increases as the advances. As the life expectancy is increasing more number of people are going to face the cardiovascular problems towards the later part of their life. In Tromso study ¹ (Norway) an aneurysm (>29 mm) was present in 8.9% men and 2.2% women (p < 0.001) aged between 25-84 years of age. Aorta > 39 mm diameter was in 2.3% of men 0.4% of women aged between 25 to 84 years. The prevalence of abdominal aortic aneurysm increased with age. In India with one billion people, we can assume that at least 10 million people will be at risk of aortic aneurysm development. It is considered that operations for aortic aneurysms are major and they are associated with high risk even in the best hospitals. The recently introduced Endorepairs (very expensive) are less invasive and considered to be associated with less pain, shorter hospital stay. But one would still ask for some medicine which can avoid intervention or operation if the aneurysms are detected early enough. So, this question of medical therapies is more relevant to us in India. On theoretical grounds, multiple medications can suppress AAA formation and subsequent expansion, reducing the risk of rupture or the need for surgical correction. However, none have been conclusively shown to reverse the pathology in the aortic wall or to have a clinically beneficial effect on slowing AAA growth. Because of potential side effects, many of these drugs remain of experimental interest only.

        However, despite the paucity of good clinical information, it would appear that there is sufficient experimental and observational evidence to support using some of these medications. It would seem appropriate to control elevations in blood pressure with ACE inhibitors or ARBs. In patients who are normotensive, either ACE inhibitors or ARBs could still be used in low doses provided patients can tolerate these medications. Addition of vitamin E should not be harmful and can be beneficial. COX-2 inhibitors in patients with concomitant arthritis or pain syndromes can have an additive benefit by reducing aneurysm expansion. Doxycycline is an inexpensive medication with few side effects. Statins should be considered in all AAA patients irrespective of cholesterol levels because of their pleiotropic effects, which might not only reduce AAA expansion but also improve overall cardiovascular risk. They can also benefit operative outcomes in patients who ultimately come to elective or emergency surgery.

Probably we can also think in terms of some kind of vaccination to prevent the progressive changes in the aortic diameter. It should become a mandatory thing in all the people above 50 years of age without smoking, above 30 year of age in case of smokers just like the vaccinations in paediatrics. The understanding at the genetic and molecular level may help us to find out a way to revert the aneurysmal changes in the aorta or its branches. It is important to invest money in this direction while continuing to think and develop mechanical solutions for the biological problems such as smooth muscle cell apoptosis, elastin degradation, inflammatory cell infiltration, synthetic abnormalities of collagen in the wall of the aorta. The proposed cost of treating the cardiovascular disease and aneurysmal disease in our country with mechanical (repetitive) means (stents and devices) is beyond imagination of the common man. So, there should be adequate encouragement, planning and funding for the development of such programs in Hospitals, Medical universities and other Educational institutions which can prevent non communicable diseases (NCDs).

[1] Reference: K Singh, KH Bonna, BK Jacobsen  et al. Prevalence of and risk factors for abdominal aortic aneurysms in a population based study. Tromso study. Am J Epidemiol 2001; 154(3): 236-44

Post lumbar puncture headache after varicose veins surgery

Headache is a complication of lumbar puncture that has been known for more than a hundred years. Post-dural puncture headache (PDPH) is characterized by the occurrence of a headache with a significant orthostatic component within 5 days of a lumbar puncture.

Patients after varicose vein surgery would like to go home on the same day or next day after surgery. But Varicose veins are generally operated under spinal anesthesia and if they develop head ache after surgery, their hospital stay gets prolonged . The incidence of head ache depends on a number of factors. Younger women with a previous history of headaches appear to be at highest risk. The incidence can be significantly reduced by using a thin lumbar puncture needle with an atraumatic tip. The condition is self-limiting and harmless, but leads to significant morbidity. Caffeine alleviates the symptoms and reduces the course of the illness. When bed rest and caffeine prove ineffective, an epidural blood patch works well for the majority, but there is no consensus on when such treatment should be offered. Headache frequently occurs after lumbar puncture for anesthesia in our hospitals. It is better to inform the patients about the same before surgery, so that their apprehensions can be relieved.  There is substantial evidence for recommending the use of a thin, atraumatic needle to reduce the incidence.

Corona Phlebectatica

Small veins ( venules ) are seen in the dermal and subdermal planes on the medial side. These fan-shaped intradermal telangiectases on the medial or lateral aspects of the foot can become troublesome in some patients. 

They can become tender, bleed or painful with small ulcerations. The significance of these veins is controversial and requires some thought. Sometimes it could be an early sign of advanced venous disease. Alternatively, it may occur in limbs with simple telangiectases elsewhere. Synonyms include malleolar flare and ankle flare.

CEAP Classification for venous disease

The field of chronic venous disorders (CVD) previously suffered from lack of precision in diagnosis. This deficiency led to conflicting reports in studies of management of specific venous problems, at a time when new methods were being offered to improve treatment for both simple and more complicated venous diseases. It was believed that these conflicts could be resolved with precise diagnosis and classification of the underlying venous problem.

TNM classification is popular for understanding the extent of cancers, their prognosis and to communicate outcomes of treatments with different people. In a similar way there has been a search for a classification to help us for better understanding chronic venous disease and communicate the results of the treatments for chronic venous disorders. The discussions of various committees on this issues resulted in CEAP classification which is also validated later on.  
The CEAP classification (Clinical-Etiology-Anatomy-Pathophysiology) was adopted worldwide to facilitate meaningful communication about CVD and serve as a basis for more scientific analysis of management alternatives. This classification, based on correct diagnosis, was also expected to serve as a systematic guide in the daily clinical investigation of patients as an orderly documentation system and basis for decisions regarding appropriate treatment.


Reference: 

• H.G. Beebe, J.J. Bergan, D. Bergqvist, B. Eklöf, I. Eriksson, M.P. Goldman et al. Classification and grading of chronic venous disease in the lower limbs: a consensus statement Vasc Surg, 30 (1996), pp. 5–11

First World Sepsis Day on Sept 13 this year.

An estimated 18 million cases of sepsis occur each year worldwide. We need to concentrate and aim to reduce the sepsis in our society and hospitals.Early goal directed therapy seems to be helpful in improving the results of treatment. 

Most important for outcome is early diagnosis, appropriate anti-infective treatment, and early goal-directed therapy that includes adequate oxygenation, correction of acidosis, fluid replacement, and use of inotropes and vasopressors.

Fighting Bacteria By Preventing Them From Talking To Each Other

Disruption of biological clocks can lead to neurodegeneration, early death, study suggests

Can we prevent the developement of antibacterial resistance?

Antibiotic resistance - Can we trace it from animal farms to the medical clinics?

The increasing incidence of hospital acquired infections with antibiotic resistant bacteria has become a major issue in the recent past. These infections due to the resistant bacteria not only increased morbidity and mortality but also increase cost of management in the hospitals. In one study from a premier medical institute in New Delhi, it was found that methicillin resistant staphylococcus bacterial infections were present in the 7.5% - 41% of cultures from these wounds from 3 different hospitals.(1).  About one quarter of healthy people carry one or more strains staphylococci asymptomatically at any given time, and infections are commonly endogenous being caused by the patient’s colonizing strain.(2). It was observed that use of antibiotics in the farm houses results in the development of resistance bacteria and it was felt this reaches the humans. Farmers regularly treat cattle, pigs, and chickens with antibiotics to dampen low-level infections that slow the growth of these animals. But wily bacteria quickly evolve resistance. Livestock farms often brim with resistant bugs that can pass to humans and potentially spread resistance to other microbes. Most farm screens have traced resistance only in pathogenic bugs—those that cause disease. But such organisms make up just a small percentage of gut microbes in pigs, The new data, he says, suggest that the common practice of using swine waste as a fertilizer is like spreading truckloads of antibiotic resistance on farmland. Those bacteria can share their resistance with other bacteria that happen to be on crops and in downstream aquatic ecosystems—bacteria that could cause illness, Chénier says. "This is a time bomb." Employees at slaughterhouses and meat-processing facilities say that they follow guidelines to keep the pigs' gut bacteria from contaminating the rest of the meat and the facility. "Risk assessment shows that by the time food gets to the consumer, there's very little resistant bacteria left in the meat".

Ecologist Martin Chénier of McGill University in Montreal, Canada, and his colleagues examined bacteria on a university farm. This farm  in January 2007 banned all antibiotics, including two commonly used varieties: tylosin and chlortetracycline. They monitored gut bacterial populations in 10 pigs by searching for bacteria resistant to common drugs in their waste.

To the team's surprise, the entire bug community kept most of its armor against the antibiotics, even after 2 ½ years. When the researchers grew the bacteria in the lab, for example, 70% to 100% of them were still resistant to chlortetracycline when the pigs were slaughtered. "I didn't expect such high levels of resistance would remain," says Chénier, whose team will publish the results in the January issue of Microbial Ecology.

References:

1) Gadepalli R et al  Clinical and molecular characteristics of nosocomial methicillin-resistant Staphylococcus aureus skin and soft tissue isolates from three Indian hospitals J Hosp Infect. 2009 Nov;73(3):253-63. Epub 2009 Sep 25.

2)  Von Eiff C, Becker K, Machka K, Stammer H, Peters G. Nasal carriage as a source of Staphylococcus aureus bacteremia. Study Group. N Engl J Med. 2001; 344:11–26.

World Diabetes Day 2011

World diabetes day 14th Nov 2011

This is going to be challenge for India and Indian women to keep diabetes under control or prevent it altogether. The epidemiological surveys are saying the Indian diet, working habits, exercise patterns, better economic conditions and their genetic constitution are favoring the early onset of diabetes. So, Indian woman has to work very hard to keep herself and her family safe from the ill effects of diabetes. - Let us see the next decade and let us prove that epidemiologists are wrong once again!!! 

Endothelial progenitor cells - Vasculogenesis

Endothelial Progenitor Cells (EPCs) are immature cells. They have the capacity to proliferate, migrate and differentiate in to endothelial lineage cells.  Hematopoietic stem cells and EPCs are derived from the common precursor (hemangioblast). These two stem cells share similar surface marker antigens. They are Flk-1, Tie-2, c-Kit, Sca-1, AC133 (CD133) and CD34+.

It was interesting to note that in 1997 Asahara et al found the importance of CD34+ cells in the neovasculogenesis.  The antigens expressed on the surface differentiate the HSCs and EPCs from the leukocyte fraction of peripheral blood. CD34+ is expressed by all the HSCs but lost by the differentiated hematopoietic cells.

It was believed that the post natal neovascularisation (angiogenesis) is possible by the proliferation, migration, remodelling of the fully differentiated endothelial cells. Vasculogenesis was considered to be formation of embryonic blood vessels from the EPCs or angioblasts. Vasculogenesis begins as a cluster formation or blood island comprising angioblasts at the periphery and HSCs at the center. So, demonstration of HSCs and EPCs in the peripheral blood based on the surface antigens on them proves the fact that there are stem cells circulating in peripheral blood and they are involved in the neovasculogenesis. A potentially limiting factor in strategies designed to promote neovascularisation of ischemic tissues is the resident population of ECs, that is competent to respond to administered angiogenic cytokines.

Asahara et al felt that this issue may be successfully addressed with autologous EC transplants. The fact that progenitor ECs home to foci of angiogenesis suggests potential utility as autologous vectors for gene therapy. For antineoplastic therapies, MBCD34+ cells could be transfected with or coupled to antitumor drugs or angiogenesis inhibitors. For treatment of regional ischemia, angiogenesis could be amplified by transfection of MBCD34+ cells to achieve constitutive expression of angiogenic cytokines or provisional matrix proteins or both. In a recent study by Turan et al have shown that the circulating EPCs were reduced in patients with extensive coronary artery disease (3 vessel disease / SYNTAX score >33). We may need to understand more about this fact and bring to this point from bench to the routine bed side management of patients.

References

Asahara T, Murohara T, Sullivan  A  et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science. 1997; 275:964-967

Turan RG, Turan Ch, Bozdag-Turam I et al. Impaired mobilization of CD 133+bone derived circulating progenitor cells with an increased number of diseased coronary arteries in ischemic heart disease patients with diabetes. Circ J 2011; 75:2635-2641