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Background: Cognitive impairment is a progressive disorder that affects the aging population. With the increase in the mean age of our population, it is becoming a public health problem. Homocysteinemia has been implicated in cognitive impairment. While it is modulated by vitamins B12 and folate, it acts through MMPs 2 and 9.Objectives: To assesses the relationship of cognitive impairment with homocysteine, B12, folate, and MMPs 2 and 9, with the intention of detecting cases of mild cognitive impairment which are potentially reversible.Materials and Methods: Blood samples were drawn from 73 enrolled subjects, with and without cognitive impairment on basis of Montreal cognitive assessment (MoCA) score >25, respectively. Homocysteine, B12, folate, and MMPs2 and 9 were estimated. Correlation between MoCA score and these parameters was elucidated.Results: After adjusting for age and sex, homocysteine was the only significant independent predictor of MoCA score. Cut off of homocysteine for prediction of MoCA Conclusions: Homocysteine >13.5mmol/L predicts low MoCA (13.5mmol/L should be carefully evaluated for the presence/progression of dementia and administered vitamins of the B group as a measure towards amelioration of the modifiable risk factor of cognitive decline, i.e. homocysteinemia.

Prevalence of anemia in India is almost 40% with no significant change since 1998–99, whereas globally this prevalence has been reduced to

Point-of-care testing (POCT), also referred to as bedside or near-patient testing, represents the future of diagnostics and is currently dominating innovations in the medical field. This technology has brought diagnostics out of the central laboratory to the patient bedside. POCT offers several advantages over the traditional testing carried out in the central laboratories. Small compact devices and faster reports leading to rapid diagnosis and consequent appropriate treatment/interventions form a major benefit of POCT. In addition, it has reduced the sample requirements in comparison with the volumes required by the main laboratories and has played an important role in testing of labile analytes. However, numerous challenges remain in the use of POCT. POCT reagents are costly and are performed by non–laboratory-trained operators who are focused neither on the internal quality control protocols nor on the guidelines of the regulatory and accreditation bodies. Thus, training and experience of the staff remains a major issue. Because POCT contributes to better patient management by facilitating early diagnosis, internal quality protocols must be defined and incorporated in the daily routine of testing. ISO 22870:2016 “Point-of-care testing – Requirements for Quality and Competence” was introduced by the ISO and is intended for use in conjunction with ISO 15189:2012 (Medical Laboratory Testing). Newer point-of-care (POC) trends are emerging which will further strengthen the impact of POCTs in medical testing. Hence, it is essential that quality is of the optimum consideration to ensure consistency in the POC test results.

HbA1c is used extensively for the diagnosis and management of diabetes mellitus. It constitutes 80% of glycated HbA1(Glycated haemoglobin(GHb)A), and depends upon blood glucose and RBC life span. RBC life span varies with anemia, leading to a consequent alteration in the HbA1c value irrespective of the circulating blood glucose concentration. But to the best of our knowledge no Hb cut offs have been derived for appropriate interpretation of HbA1c. The prevalence of anemia in Indian population is nearly 40% as per its definition by WHO—Hb

Though a topic of speculation since the early ages, the true nature, mechanisms and functions of the reproductive hormones have been understood only fairly recently. The earliest known description was in the Sushruta in 1400 BCE, but it was not till the 17th century that the physiological processes involved started becoming lucid. Another few decades passed before experiments revealed the mechanism of action of these hormones. The reproductive hormones are secreted by the anterior pituitary gland as well as the gonads, and include both steroid and peptide hormones. It was elucidated that these reproductive hormones act through receptors whereby they alter transcriptional activation of target genes. Prolactin and the gonadotropin hormones i.e. Follicle Stimulating Hormone and Luteinizing Hormone are released from the anterior lobe of the pituitary gland. The major gonadal hormones include Estrogen, Progesterone and Testerosterone and the placental hormone, Human Chorionic Gonadotropin. Recently, the Anti-Mullerian Hormone has been included as a unique marker of gonadal function. Testing of these hormones provides significant insight into the underlying pathology and can thus be highly useful in aiding clinical decisions; however, interpreting the results can be challenging. In view of the intricate mechanisms and complex interactions of the reproductive hormones, this review aims to highlight briefly, the physiology, metabolism and the most important clinical aspects of these hormones, to facilitate their optimal utilization in clinical practice.

A high circulating concentration of the non proteinogenic amino acid homocysteine has been implicated as a risk factor for Alzheimer's Disease and its prodromal stage, mild cognitive impairement. Furthermore, hyperhomocysteinaemia has been directly attributed to a deficiency in vitamins B12, folate, and B6. Several studies have demonstrated decrease in progression of mild cognitive impairement to Alzheimer's Disease, and some have even shown an improvement in cognition after vitamin supplements with B12 and folate. Plausible mechanisms linking hyperhomocysteinaemia to Alzheimer's and cognitive impairement have been hypothesized and demonstrated in hyperhomocysteinemic mice models. However, some studies have not elucidated any benefit of vitamin supplements in subjects with cognitive impairment. Hence, multicentric clinical studies need to be conducted to substantiate the mechanisms of neuronal degeneration due to hyperhomocysteinaemia and to demonstrate the beneficial effect of folate, B6 and B12 supplements on cognition.

In recent times, cell-therapies like T-activated cells, dendritic cells and natural killer cells have shown increasing promise in treating cancers as evidenced by both animal and human studies in the literature. In addition, stem cells are also being considered as potent anti-cancer agents since they act through multi-pronged approaches (chemokines, cytokines, paracrine action). In this review, we have attempted to discuss the inferences of studies that have used different sub-types of stem cells namely mesenchymal stem cells (MSCs), hematopoietic stem cells (HSCs) and neural stem cells (NSCs) in in-vitro/in-vivo mice and/or human studies as a treatment modality for pancreatic cancer. Pancreatic cancers are diagnosed in late/metastatic stages hence limiting its progress to partial/disease-free status. Recent literature supports evidences of stem cell therapy in pancreatic cancer with promising results; yet their impact remains inconclusive due to limited studies in human subjects. With reference to the treatment options for pancreatic cancer, the most studied sub-type of stem cells was HSCs as evident from the available clinical trials. The suggested mechanism of the HSC-transplantation is presumably via the graft-versus-tumor effect that elicits an anti-tumor immune response activated by the T-cell repertoires. On the other hand, the property of MSCs like tropism, migration to tumor site and activation of host immune cells by its secretome, appear to be able to regulate pancreatic tumor microenvironment. Further, drug delivery potential could be mediated via engineered MSCs to enhance the bioavailability of drug/prodrug at tumor site. Conclusively, stem cells have shown great potentials as next-generation therapeutic options.

Highly reactive molecules with an unpaired electron are known as free radicals. They collide with other molecules and set up a chain reaction by either passing on the unpaired electron to the neighbouring molecule or getting quenched by it. In biological systems, the most damaging free radicals are the oxygen radicals – also termed as the reactive oxygen species [ROS] – namely superoxide, hydroxyl, and perhydroxyl. Oxidation/peroxidation of lipids, DNA bases and structural membranes through these radicals results in different pathological events depending on the site of oxidation.

Preanalytical errors constitute about 40-65% of laboratory errors, of which 60% are due to hemolysis. This leads to imprecise reporting and misinterpretation of the actual concentration of analytes. Hence the aim of this study was to estimate the extent of different degrees of interference by visible hemolysis. 25 hemolysed samples along with their fresh unhemolysed sample were studied. Hemolyzed serum was mixed with unhemolyzed serum in predefined serial ratios from 100%, 70%, 50%, 30% and 10% to achieve different grades of hemolysis. Each dilution was analysed for BUN, creatinine, uric acid, phosphorus, Na, K, total protein, amylase, lipase, LDH, tacrolimus and methotrexate. Percentage difference of each dilution of the hemolyzed sample as compared to the unhemolyzed sample was calculated and considered acceptable only if less than TEa. It was observed that Percentage difference of BUN, creatinine, amylase and lipase in all dilutions of hemolyzed samples were within TEa while phosphorus, Na, K, total protein and LDH were beyond the acceptance criteria. Hence It was concluded that it may be safe to analyse a hemolysed sample for BUN, creatinine, amylase, lipase, tacrolimus and methotrexate while uric acid may be estimated in a moderately hemolysed sample. Phosphorus, sodium, potassium, total protein and LDH must never be analyzed in any hemolysed sample.

The coronaviruses are single-stranded RNA viruses, one of which is responsible for the current outbreak of coronavirus disease-19. COVID-19 has affected health-care workers including laboratory personnel worldwide in an alarming and unprecedented manner. In India too, the huge number of infected health-care staff has further weighed down our already over-burdened health-care system. While their protection is of paramount importance, it is also essential that these personnel adhere to the specific bio-safety practices to minimize their exposure to this disease. In this article, our objective is to provide guidelines for laboratories while working with COVID-19 samples to reduce the human and economic burden in the current pandemic. A risk assessment of all policies must be done and standard operating procedures on all 'Safe Laboratory Practices and Procedures' must be readily available for the staff. Dividing the laboratory functions into three broad phases, namely pre-examination, examination and post-examination, the precautions outlined for each stage must be followed stringently with the frequency defined as per the workload of the laboratory. The safety measures must cover all the laboratory processes including sample disposal. Decontamination too plays a major role and must be performed as per the standard national and international guidelines. Hence, following special precautions in the laboratory while working through the COVID-19 pandemic will not only minimize the risk of infection to the laboratory staff and but also help reduce the mortality and morbidity associated with this disease.

The history of research on the natriuretic peptides can be traced back to 1956 when early studies using the electron microscope showed that granules similar to those in endocrine glands were found in the cells of the atria. Along with its role in maintaining blood volume homeostasis, its association with inflammatory process and markers during cardiovascular diseases has been recently under observation. In clinical settings, B type natriuretic peptides (BNP or NT-ProBNP) characteristics need to be better understood as diagnostic and prognostic biomarkers. Hence role of BNP/NT-ProBNP as inflammatory biomarker has been evaluated in this review article.

Aim of the Study: Initial differentiation of sepsis from systemic inflammatory response syndrome (SIRS) is of prime importance for early institution of appropriate treatment. This study aimed to compare the differential diagnostic efficacy of absolute eosinophil count (AEC - a routinely available economic marker) with total leukocyte count (TLC) and procalcitonin (PCT - a costly marker available only in specialized settings). Materials and Methods: In this prospective observational study, 170 patients of sepsis (severe sepsis = 125; SIRS = 45) were enrolled. AEC, TLC, and PCT were measured in the blood of all patients at the time of admission and data analyzed statistically. Results: Median AEC was 0 cells/mm3 in both SIRS and sepsis. TLC and PCT levels were significantly higher (P < 0.001) in culture negative, culture positive, and overall sepsis groups in comparison to SIRS group. At a cutoff of < 50 cells/mm3, AEC demonstrated a sensitivity and specificity of 23% and 68%, respectively. The sensitivity, specificity, positive predictive value, and negative predictive value of TLC were 57%, 71%, 85%, 37% and of PCT were 82.4%, 82.2%, 93%, and 63%, respectively with area under curve of 0.455 for AEC, 0.640 for TLC, 0.908 for PCT. Conclusions: This study suggests that eosinopenia is not a reliable diagnostic tool to differentiate sepsis from SIRS. PCT and TLC are better differential diagnostic biomarkers.

Homocysteine has been seen to be directly related to the GFR. This is due to the fact that when renal function is compromised, the intra-renal homocysteine is downregulated, resulting in an increased level of circulating homocysteine. This is a contributory factor to the 30 times higher incidence of cardiovascular disease related deaths in the presence of end stage renal disease. In addition, there are reports of homocysteinemia-induced damage to the glomerular basement membrane through the modulation of MMP/TIMP axis which results in excessive oxidation of collagen IV in the membrane. Hence, it is important to address homocysteinemia in renal failure patients to prevent further co-morbidities.

The body’s defence mechanisms are specific for each aberration in its metabolism. These function to compensate the aberration in the initial stages till the body metabolism corrects itself. When the metabolic changes cannot be compensated, pathophysiology results.

As per Fig. 1.1, metabolism of homocysteine can be through oxidation to homocysteic acid by the action of vitamin C. This homocysteic acid is required for the synthesis of sulphated proteoglycans which are an integral part of the connective tissue in the walls of the blood vessels as well as in the bones.

Genes are the determinants of all our body’s anatomy, physiology and biochemistry – the normal functioning. They can also determine our responses to some variations to our environment. Epigenetics includes the processes involved in this phenotypic variation of our genotype.

In the preceding chapters, it has been suggested that the use of folate and B12 supplements for all these homocysteinemia-induced disease states minimizes the pathophysiological effects, even when the cause is genetic. In view of this, it would seem pertinent to fortify foods with folate as well as B12 to protect all systems from the deleterious effects of homocysteinemia. The western countries have implemented this in the early 1980s, but it has not been introduced in our country. Considering the evidence of widespread folate and vitamin B12 deficiency in our population, it would be pertinent to fortify our staple grains with these vitamins.

Though homocysteine was first implicated in atherothrombosis, high circulating levels of it have a myriad pathologic effects including oxidative as well as molecular mechanisms in almost all organ systems. However, this section details how homocysteinemia causes and promotes atherothrombosis, starting with the initial event of disruption of the endothelium and going on to its varied effects on the circulating lipids, platelets, the endothelial functions (proteins and factors influencing dilatation and lipid deposition), smooth muscle layer and the adventitial layer of the vessel walls.

Homocysteinemia causes vascular wall remodelling by altering the elastin/collagen ratio and by changing the molecular characteristics of the proteoglycans, both of which are brought about by various mechanisms. Consequently, vascular compliance is altered and blood pressure increases.

Homocysteinemia causes neurological damage through a variety of molecular mechanisms. The sequelae are, therefore, varied, ranging from neural tube defects to epilepsy to apoptosis and dementia.

Small dense (sd) LDL is a significant independent risk factor for premature coronary artery disease (CAD). Unfortunately, its estimation is not popular, due to the limited availability of specialized equipment, high cost and time-consuming technique. Non-HDL is a calculated, single index measure of all atherogenic apolipoprotein-B containing lipoproteins. This study aimed at identifying non-HDL as a superior surrogate marker of sdLDL cholesterol in a young Indian population. 161 healthy subjects

Homocysteine is an intermediate product in the metabolism of the essential amino acid methionine. Homocysteine is either remethylated to yield methionine or is further metabolized to cysteine and α-ketoglutarate which are both diverted to protein synthesis. These two metabolic processes – remethylation and transsulfuration pathways – are dependent on several enzymes and co-factors. The remethylation cycle is dependent on the rate-limiting enzyme methylene tetrahydrofolate reductase (MTHFR) and the B group vitamins folate and B12. The transsulfuration pathway is likewise dependent on cystathionine-β -synthase and pyridoxine. Thus, any alterations in the functions of these enzymes (due to polymorphisms of their genes) or a deficiency of any of these three vitamins of the B group (folate, B12 and pyridoxine) will result in reduced metabolism of homocysteine and its consequent accumulation. Homocysteine causes altered redox potential as well as modification of proteins.

Hyperhomocysteinemia (HHCY) has been demonstrated to affect cochlear microvasculature as well as cochlear epithelial cells directly, with a resultant alteration of the expression of matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs). Hence, ascertaining the optimum concentration of MMPs and TIMPs in the cochlea could help to inhibit hearing loss due to HHCY by the administration of appropriate MMP inhibitors, Since infections/inflammations as well as ototoxic antibiotics have a similar mechanism of otic pathology, the cochlear damage they cause could also be similarly prevented.

Objectives: Endothelial glycocalyx shedding has been recognized as a contributor in sepsis pathophysiology. Hence, we attempted to analyse hyaluronan and syndecan (glycocalyx components) as markers of morbidity and prognosis of sepsis by performing serial measurements in these patients. Design and methods: Subjects were community acquired sepsis, severe sepsis and septic shock patients (150) admitted to ICU of our tertiary care hospital and controls were 50 healthy volunteers. Serum concentrations of markers were measured on days 1,3,5,7 of ICU admission. Survival was assessed after 90 days. Statistical analysis was performed by SPSS version 17. Results: Hyaluronan and syndecan levels were significantly elevated in all categories of sepsis patients as compared to controls (p

Data from studies examining lipid peroxidation as a mechanism involved with hyperhomocysteinemia (HHcy)-induced vascular remodeling in patients with occlusive vascular disease have been contradictory. It has not yet been studied in Indians within the context of atherogenesis. Therefore, we measured the levels of homocysteine (Hcy), malondialdehyde (MDA) as a measure of lipid peroxides (LPOs), and total antioxidant status (TAS) in the serum of 167 patients with occlusive vascular disease [coronary artery disease (CAD) = 43; cerebrovascular disease (CVD) = 82; peripheral vascular disease (PVD) = 42]. Each of these groups was further divided into groups of individuals with or without HHcy. In the case of CAD and CVD, patients with HHcy had significantly higher LPOs than those without HHcy (p = 0.009, 0.001, respectively). TAS was significantly lower in CVD patients with HHcy than in those without (p = 0.014). In patients with CAD or CVD, Hcy directly correlated with LPOs (p = 0.002, 0.001, respectively). Lipid peroxidation is a significant mechanism in HHcy-induced vascular remodeling in CAD and CVD, but not in PVD, probably because it is not relevant in thrombosis (38 of 42 patients of PVD had deep-vein thrombosis). To explain the significantly lower TAS in CVD, we hypothesized that CVD patients present very early with grave symptoms, whereas CAD and PVD occur over a longer period of time. Therefore, when CVD presents, TAS is still overwhelmed by HHcy-induced oxidative stress. Hence, adjuvant therapy with antioxidants would benefit patients with CVD.

Hyperhomocysteinemia (HHcy) is associated with cognitive decline and hearing loss due to vascular dysfunction. Although we have shown that HHcy-induced increased expression of matrix metalloproteinase-9 (MMP-9) is associated with cochlear pathology in cystathionine-β-synthase heterozygous (CBS(+/-)) mice, it is still unclear whether MMP-9 contributes to functional deficit in cognition and hearing. Therefore, we hypothesize that HHcy-induced MMP-9 activation causes vascular, cerebral and cochlear remodeling resulting in diminished cognition and hearing. Wildtype (WT), CBS(+/-), MMP-9(-/-) and CBS(+/-)/MMP-9(-/-) double knock-out (DKO) mice were genotyped and used. Doppler flowmetry of internal carotid artery (ICA) was performed for peak systolic velocity [PSV], pulsatility index [PI] and resistive index [RI]. Cognitive functions were assessed by Novel Object Recognition Test (NORT) and for cochlear function Auditory brainstem response (ABR) was elicited. Peak systolic velocity, pulsatility and resistive indices of ICA were decreased in CBS(+/-) mice, indicating reduced perfusion. ABR threshold was increased and maximum ABR amplitude and NORT indices (recognition, discrimination) were decreased in CBS(+/-) mice compared to WT and MMP-9(-/-). All these parameters were attenuated in DKO mice suggesting a significant role of MMP-9 in HHcy-induced vascular, neural and cochlear pathophysiology. Regression analysis of PSV with ABR and cognitive parameters revealed significant correlation (0.44-0.58). For the first time, MMP-9 has been correlated directly to functional deficits of brain and cochlea, and found to have a significant role. Our data suggests a dual pathology of HHcy occurring due to a decrease in blood supply (vasculo-neural and vasculo-cochlear) and direct tissue remodeling.

Lead exposure is increasingly becoming an important risk factor for osteoporosis. In adults, approximately 80–90 % of absorbed lead is stored in the bones. These bone lead deposits are released into the blood during periods of enhanced bone resorption like menopause, forming a potential endogenous source of lead exposure. Postmenopausal women are at a higher risk for bone lead release because of hormonal and age related changes in bone metabolism. Estrogen deficiency is associated with increase in osteoclasts number and activity leading to both the early and late form of osteoporosis. Hence, high blood lead level coupled with concomitant environmental exposure exposes women in this age group to lead related adverse outcomes like hypertension, reduced kidney and neurocognitive functions as well as increased risk of atherosclerosis and cardiovascular mortality. A few studies have also identified coexisting variates like ethnicity, occupation, residence, education, smoking, alcohol medications, water etc. as significant determinants of bone and blood lead in women, thus increasing the magnitude of postmenopausal bone changes. Hence, interventions focused on reducing the intensity of bone resorption during menopause will help decrease exposure to endogenous lead. This would play a significant role in decreasing the morbidity and mortality associated with menopause. Also, identification of modifiable factors that prevent bone lead release will reduce the risk of chronic lead exposure and improve the health outcomes of post-menopausal women.

Table of contentsP1 D-Dimer in adult patients with presumed sepsis and their clinical outcomesSurinder Kumar Sharma, Anurag Rohatgi, Mansi BajajP2 Diagnosis of infection utilizing Acellix CD64Charles L. Sprung, Ricardo Calderon Morales, Harvey Kasdan, Allon Reiter, Tobias Volker, Julien MeissonnierP3 High levels of phenylcarboxylic acids reflect the severity in ICU patients and affect phagocytic activity of neutrophilsNatalia Beloborodova, Viktor Moroz, Aleksandra Bedova, Yulia Sarshor, Artem Osipov, Katerina ChernevskayaP4 The role of bacterial phenolic metabolites in mitochondrial dysfunctionNadezhda Fedotcheva, Ekaterina Chernevskaya, Natalia BeloborodovaP5 The early diagnosis of severe sepsis and judgment of rapid transport to critical care center: better prognostic factorHisashi Imahase, Kosuke C Yamada, Yuichiro Sakamoto, Miho Ohta, Ryota Sakurai, Mayuko Yahata, Mitsuru Umeka, Toru Miike, Hiroyuki Koami, Futoshi Nagashima, Takashi Iwamura, Satoshi InoueP6 Translational neuromodulation of the immune systemZhifeng Li, Dennis Grech, Patrick Morcillo, Alex Bekker, Luis UlloaP7 Pathway-level meta-analysis reveals transcriptional signature of septic shockSamanwoy Mukhopadhyay, Abhay D Pandey, Samsiddhi Bhattacharjee, Saroj K MohapatraP8 Antibiotic dosing in septic patients on the critical care unit - a literature reviewJulie K WilsonP9 Pandemic of Escherichia coli clone O25: H4-ST131 producing CTX-M-15 extended spectrum- β- lactamase- as serious cause of multidrug resistance extraintestinal pathogenic E. coli infections in IndiaSavita Jadhav, Rabindra Nath Misra, Nageswari Gandham, Kalpana Angadi, Chanda Vywahare, Neetu Gupta, Deepali DesaiP10 Detection and characterization of meningitis using a DDA-based mass spectrometry approachAnahita Bakochi, Tirthankar Mohanty, Adam Linder, Johan MalmströmP11 Diagnostic usefulness of lipid profile and procalcitonin in sepsis and trauma patientsDimple Anand, Seema Bhargava, Lalit Mohan Srivastava, Sumit RayP12 Heparin – a novel therapeutic in sepsis?Jane Fisher, Peter Bentzer, Adam LinderP13 Hypothalamic impairment is associated with vasopressin deficiency during sepsisLuis Henrique Angenendt da Costa, Nilton Nascimentos dos Santos Júnior Carlos Henrique Rocha Catalão, Maria José Alves da RochaP14 Presepsin (soluble CD14 subtype) is a dependable prognostic marker in critical septic patientsAlfredo Focà, Cinzia Peronace, Giovanni Matera, Aida Giancotti, Giorgio Settimo Barreca, Angela Quirino, Maria Teresa Loria, Pio Settembre, Maria Carla Liberto, Bruno AmanteaP15 Safety and efficacy of gelatin-containing solutions versus crystalloids and albumin - a systematic review with quantitative and qualitative summariesChristiane Hartog, Christiane Hartog, Claudia Moeller, Carolin Fleischmann, Daniel Thomas-Rueddel, Vlasislav Vlasakov, Bram Rochwerg, Philip Theurer, Konrad ReinhartP16 Immunomodulatory properties of peripheral blood mesenchymal stem cells following endotoxin stimulation in an equine modelAnna E. Smith, Sandra D. TaylorP17 Frequency and outcome of early sepsis-associated coagulopathyChristopher Da Costa, Amanda Radford, Terry Lee, Joel Singer, John Boyd, David Fineberg, Mark Williams, James A Russell

Hyperhomocysteinemia is more commonly associated with vascular disease in Indians than in the western populations. It is caused by genetic polymorphisms or dietary deficiencies of the B vitamins. We attempted to identify the association of hyperhomocysteinemia with vitamin B(12) and folate in Indian patients of vascular disease. Homocysteine, vitamin B(12) and folate levels were estimated in 100 controls and 100 patients of vascular disease. Homocysteine estimation was repeated in 73 patients on different vitamin supplements for 6 months. Homocysteine exhibited a significant negative correlation with B(12) only in cerebrovascular disease and peripheral vascular diseasepatients, and with folate in coronary artery disease and cerebrovascular disease patients as well as controls. Single daily dose of folate was as effective as a combination of folate and cobalamin in reducing plasma homocysteine concentrations. Low levels of B(12) contribute to the higher incidence of cerebrovascular disease and peripheral vascular disease, and low folate levels account for higher prevalence of hyperhomocysteinemia in coronary artery disease and cerebrovascular disease. Moreover, irrespective of the cause of hyperhomocysteinemia, folate is known to ameliorate it. Hence, large-scale corrective measures like food fortification or dietary supplementation with folate might benefit the Indian population and reduce the incidence and morbidity of vascular disease.

Background and objectives: Studies in different populations have shown that ischemic stroke can trigger an acute phase response resulting in a rise of plasma concentration of C-reactive protein (CRP) and high level of high-sensitivity CRP (hsCRP) is a risk factor for ischemic stroke. The objective of this study was to investigate the association of high hsCRP levels (≥ 1 mg/L) with ischemic stroke and its subtypes in Indian patients. Methods: This prospective observational case-control study included 150 patients (96 males, 54 females; aged 24–81 years) with first acute ischemic stroke who were admitted within 72 hours after onset, and 150 age- and sex-matched healthy controls. The study was conducted from July 2016 to July 2017. The patients were classified according to Trial of ORG 10172 in Acute Stroke Treatment classification. hsCRP levels were assessed in all included stroke patients. Results: The mean serum level of hsCRP was significantly higher in patients with first acute ischemic stroke than in healthy controls (P < 0.001). The mean serum level of hsCRP was higher in patients who had more severe stroke on admission. The prevalence of high serum level of hsCRP was highest in large-artery atherosclerosis (35.2%), followed by in cardioembolic (28.2%) stroke. The mean serum level of hsCRP was highest in large-artery atherosclerosis, followed by in stroke of undetermined etiology and cardioembolic subtype. High serum level of hsCRP was significantly associated with hypertension and age (P < 0.001 or P < 0.05). Multiple Logistic regression analysis revealed that high level of hsCRP was independently associated with acute ischemic stroke [odds ratio (OR) = 3.87, 95% confidence interval (CI): 2.39–6.27]. High hsCRP level was strongly associated with cardioembolic stroke (OR = 4.97, 95% CI: 2.5–9.65), large-artery atherosclerosis (OR = 4.75, 95% CI: 2.57–8.81), and stroke of undetermined etiology (OR = 3.36, 95% CI: 1.72–6.54). Conclusion: High hsCRP level is strongly associated with acute ischemic stroke and its subtypes, and it is an independent predictor of acute ischemic stroke. Ethics: The study was approved by the Sir Ganga Ram Hospital Ethics Committee (EC/07/14/701) on July 5, 2014.

The European Computer Driving Licence (ECDL) has been adopted as the reference standard for all NHS staff for basic IT skills. The objective of the study was to determine awareness of the ECDL amongst members of the Royal College of Obstetricians and Gynaecologists. An anonymous postal survey was conducted with members and fellows of the College in three UK regions. A total of 720 questionnaires were posted, and the response rate was 47.9 per cent. A fifth of all respondents were not aware of the ECDL at all, and only 10 per cent were trained in the ECDL. However, more than third had some other formal training in IT skills. Half the respondents suggested that the questionnaire had prompted them to train for the ECDL. Much needs to be done to increase awareness of the ECDL and offer incentives for its takeup.

OBJECTIVE. The aim of our population-based study was to compare the mortality and morbidity of late-preterm infants to those born at term. Advancement in the care of extremely preterm infants has led to a shift of focus away from the more mature preterms, who are being managed as “near terms” and treated as “near normal.” Some recent studies have suggested an increased risk of mortality and morbidity in this group compared with infants born at term. However, there are few population-based mortality and morbidity statistics for this cohort, particularly reflecting current practice. METHODS. Using data from the British Columbia Perinatal Database Registry we analyzed all singleton births between 33 and 40 weeks’ gestation from April 1999 to March 2002 in the province of British Columbia, Canada. We divided this birth cohort into late preterm (33–36 weeks, n = 6381) and term (37–40 weeks, n = 88 867) groups. We compared mortality and morbidity data and associated maternal factors between the 2 groups. RESULTS. Stillbirth rate and perinatal, neonatal, and infant mortality rates were significantly higher in the late-preterm group. Infants in this group needed resuscitation at birth more frequently than those in the term group. Late-preterm infants had a significantly higher incidence of respiratory morbidity and infection and had a significantly longer duration of hospital stay. Maternal factors that were more common in the late-preterm group included chorioamnionitis, hypertension, diabetes, thrombophilia, prelabor rupture of membranes, primigravida, and teenage pregnancy. CONCLUSIONS. Our data support recent literature regarding neonatal mortality and morbidity in late-preterm infants and warrants a review of care for this group at the local, national, and global levels. Reorganization of services and increased resource allocation may be needed in most hospitals and community settings to achieve optimization of care for this group of infants.

Studies on hyperhomocysteinemia in vascular occlusive disease have included mostly patients with arterial occlusion. However, more recent studies have included cases of venous occlusive disease as well. Our present study is aimed at comparing the prevalence of hyperhomocysteinemia in venous occlusive disease vis-a-vis arterial occlusive disease in the North Indian urban population. Homocysteine was estimated by chemiluminescent immunoassay in 205 normal controls and 536 patients, 244 presenting with arterial occlusion and 292 with venous thrombotic disease. The mean homocysteine in patients with arterial occlusion was 21.79 +/- 0.09 micromol/L (mean +/- standard error of measurement), in patients with venous thrombosis was 25.53 +/- 0.1 micromol/L, and in controls was 11.33 +/- 0.18 micromol/L. The prevalence of hyperhomocysteinemia (> 15 micromol/L) was 56.38% in arterial occlusive disease and 54.64% in venous thrombosis. In patients with peripheral vascular occlusive disease, patients with deep venous thrombosis (DVT) had the highest mean homocysteine level (25.51 micromol/L), which was even higher (32.14 micromol/L) when associated with pulmonary embolism (PE). There is a high prevalence of hyperhomocysteinemia in arterial and venous occlusive disease. Hence, in all patients with vascular occlusive disease, hyperhomocysteinemia should be elucidated and treated. In addition, long-term follow-up is required to ascertain whether the reduction in homocysteine decreases the thrombotic events and whether homocysteine levels can actually be of prognostic or predictive value in cases of DVT with PE.