The molecular mechanisms mediating mammalian fertilization.

Fertilization is a key biological process in which the egg and sperm must recognize one another and fuse to form a zygote. Although the process is a continuum, mammalian fertilization has been studied as a sequence of steps: sperm bind and penetrate through the zona pellucida of the egg, adhere to the egg plasma membrane and finally fuse with the egg. Following fusion, effective blocks to polyspermy ensure monospermic fertilization. Here, we review how recent advances obtained using genetically modified mouse lines bring new insights into the molecular mechanisms regulating mammalian fertilization. We discuss models for these processes and we include studies showing that these mechanisms may be conserved across different mammalian species.

An exploratory randomised controlled trial evaluating text prompts in Lebanon to encourage health-seeking behaviour for hypertension.

AIMS OF THE STUDY: The current study evaluates the effectiveness of an opportunistic mobile screening on the percentage of people who are aware of whether they may be hypertensive (in an observational study) and the effectiveness of reminder prompts on the percentage of people who seek further medical attention (in a randomised controlled trial). METHODS USED TO CONDUCT THE STUDY: The screening of 1227 participants (529 female) was conducted during the registration period of the 2018 Beirut International Marathon in Lebanon. Next, 266 participants whose screening indicated hypertension (64 Female) were randomly allocated to a treatment group or a control group in a 1:1 fashion. The treatment group received a reminder prompt to seek further medical attention for their potential hypertension and the control group did not. The overt nature of the text message meant that participants in the treatment group could not be blinded to their group allocation. The primary outcome is participants' self-reports of whether they sought further medical attention. RESULTS OF THE STUDY: For the opportunistic screening, a 25% prevalence rate and a 24% awareness rate of hypertension was indicated. A McNemar analysis suggested that the screening increased participant awareness (X2 (N = 1227) = 72.16, P < .001). For the randomised controlled trial, 219 participants provided follow-up data via a phone call (82% retention). A Chi-squared analysis suggested that the reminder prompt successfully encouraged more participants to seek further medical attention, 45.5% treatment group vs 28.0% control group (X2 (1, N = 219) = 7.19, P = .007, φ = 0.18). CONCLUSIONS DRAWN AND CLINICAL IMPLICATIONS: Extra support in the form of a brief reminder message can increase the percentage of people who seek further medical attention after attending an opportunistic screening at a marathon event. The discussion reviews how the results align with previous research, strengths and limitations of the current study, and implications for future research and practice.

Alarming high prevalence of metabolic syndrome among Jordanian adults.

OBJECTIVE: To evaluate the prevalence and the individual components of metabolic syndrome (MetS) in Jordanian adults. METHODS: In this cross sectional study, 630 adult subjects (308 men and 322 women) aged between 20-70 years were recruited from the clinics at the King Hussein Medical Center. The diagnosis of MetS was made according to the International Diabetes Federation (IDF) criteria-2005. Blood samples were collected after 10-12 hours overnight fasting and serum was obtained for biochemical analysis. RESULTS: The prevalence of metabolic syndrome according to IDF criteria was 51% (46.4% in men and 55.3% in women). Prevalence of increased waist circumference in the total sample was 71.6%, 46% for high blood pressure, 42.4% for elevated fasting blood glucose, 43.5% for low high density lipoprotein, and 50.2% for hypertriglyceridemia. CONCLUSION: The prevalence and individual components of MetS in Jordan were high. Screening of MetS is needed at national level to reduce the incidence of Type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD).

A new approach for evaluating the water resistance of sunscreens on consumers: tap water vs. salt water vs. chlorine water.

OBJECTIVE: An efficient sunscreen product needs to offer broad spectrum photostable UV protection during consumer use. Water resistance has become an additional criterion requested by consumers spending time near water or outdoors. Polymers generally provide water resistance to formulations and are critical to the formation and stability of a sunscreen film on skin when exposed to water. The present work introduces a new in vivo screening approach to measure water resistance using UVA-induced fluorescence imaging. METHODS: The approach has been applied to several formulations containing different polymers and compared to commercial products, for the three main water types: tap, salt and chlorinated water. All testing has been performed on the forearms of 10 subjects using UVA imaging. In addition, the skin whitening has been measured for all formulations on five subjects when exposed to water by visible light imaging. RESULTS: Our approach showed clear differences in water resistance values among the formulations tested, reflecting the importance of the formulation and the polymers used. The method proved capable of discriminating not only sunscreen performances with different water proofing ingredients but also water specific sunscreens such as a beach dedicated product showing a 20% higher resistance to salt water vs. tap and chlorine waters. CONCLUSION: The use of UVA-induced fluorescence imaging on skin proved a useful in vivo approach for measuring the water resistance performances for various sunscreen lotions with a wide range of skin whitening effects in water. Our method showed how high water resistance can be combined in a Wet skin(®) sunscreen with superior non whitening effect on the skin.

Regulation of endocytosis by CUP-5, the Caenorhabditis elegans mucolipin-1 homolog.

Loss of the human mucolipin-1 gene underlies mucolipidosis type IV (MLIV), a lysosomal storage disease that results in severe developmental neuropathology. Unlike other lysosomal storage diseases, MLIV is not associated with a lack of lysosomal hydrolases; instead, MLIV cells display abnormal endocytosis of lipids and accumulate large vesicles, indicating that a defect in endocytosis may underlie the disease. Here we report the identification of a loss-of-function mutation in the Caenorhabditis elegans mucolipin-1 homolog, cup-5, and show that this mutation results in an enhanced rate of uptake of fluid-phase markers, decreased degradation of endocytosed protein and accumulation of large vacuoles. Overexpression of cup-5(+) causes the opposite phenotype, indicating that cup-5 activity controls aspects of endocytosis. Studies in model organisms such as C. elegans have helped illuminate fundamental mechanisms involved in normal cellular function and human disease; thus the C. elegans cup-5 mutant may be a useful model for studying conserved aspects of mucolipin-1 structure and function and for assessing the effects of potential therapeutic compounds.

Lepidium sativum Seed Extract-Mediated Synthesis of Zinc Oxide Nanoparticles: Structural, Morphological, Optical, Hemolysis, and Antibacterial Studies.

Nanomaterials have unique physicochemical properties compared to their bulk counterparts. Besides, biologically synthesized nanoparticles (NPs) have proven superior to other methods. This work aimed to biosynthesize zinc oxide (ZnO) NPs using an aqueous extract of Lepidium sativum seed. The obtained ZnO NPs were characterized by X-ray diffraction, scanning electron microscopy, Fourier transform infrared, and ultraviolet-visible spectroscopy. The in vitro antibacterial activity of ZnO NPs against Gram-positive (S. aureus) and Gram-negative (E. coli) bacteria was assessed using the disk diffusion technique. The hemolytic impact was quantified spectrophotometrically. The results indicated a 24.2 nm crystallite size, a hexagonal structure phase, and a 3.48 eV optical bandgap. Antibacterial studies revealed a dose-dependent response with comparable activity to the standard drug (gentamicin) and higher activity against S. aureus than E. coli, e.g., the zone of inhibition at 120 mg/mL was 23 ± 1.25 and 16 ± 1.00 mm, respectively. The hemolysis assay showed no potential harm due to ZnO NPs toward red blood cells if utilized in low doses. As a result, it could be concluded that the reported biogenic method for synthesizing ZnO NPs is promising, resulting in hemocompatible NPs and comparable bactericidal agents.

The efficacy of aerobic training on the pulmonary functions of hemophilic A patients: a randomized controlled trial.

OBJECTIVE: The present study investigated the efficacy of a program of aerobic exercise on pulmonary functions in adult males with hemophilia A (HA). PATIENTS AND METHODS: 40 patients with HA who met the eligibility criteria (40 HA; age range: 20-39 years) were invited to participate in the study. The patients were divided into two groups, 20 per each. Participants in the study group (A) underwent selected physical therapy program, along with aerobic training sessions on a cycle ergometer (50-60% heart rate reserve, moderate intensity), while the control group (B) underwent a selected physical therapy program only. The pulmonary functions (FVC, FEV1, FEV1/FVC, PEF, PIF, and MVV) were measured before and after treatment program. RESULTS: There were noteworthy statistical differences between pre- and post-measurements in the study group in all measured variables (p < 0.05). There were also significant statistical differences between the study and control groups in all measured variables post treatment (p < 0.05). CONCLUSIONS: This study has demonstrated that hemophilic A patients' pulmonary functions have improved significantly following aerobic exercise training. As a result, aerobic exercise can be used in addition to medical treatment for hemophilic A patients.

Current gaps in management and timely referral of cardiorenal complications among people with type 2 diabetes mellitus in the Middle East and African countries: Expert recommendations.

The upsurge of type 2 diabetes mellitus is a major public health concern in the Middle East and North Africa (MENA) and Africa (AFR) region, with cardiorenal complications (CRCs) being the predominant cause of premature morbidity and mortality. High prevalence of cardiometabolic risk factors, lack of awareness among patients and physicians, deficient infrastructure, and economic constraints lead to a cascade of CRCs at a significantly earlier age in MENA and AFR. In this review, we present consensus recommendations by experts in MENA and AFR, highlighting region-specific challenges and potential solutions for management of CRCs. Health professionals who understand sociocultural barriers can significantly increase patient awareness and encourage health-seeking behavior through simple educational tools. Increasing physician knowledge on early identification of CRCs and personalized treatment based on risk stratification, alongside optimum glycemic control, can mitigate therapeutic inertia. Early diagnosis of high-risk people with regular and systematic monitoring of cardiorenal parameters, development of region-specific care pathways for timely referral to specialists, followed by guideline-recommended care with novel antidiabetics are imperative. Adherence to guideline-recommended care can catalyze utilization of sodium glucose cotransporter 2 inhibitors and glucagon-like peptide 1 receptor agonists with demonstrated cardiorenal benefits-thus paving the way for overcoming care gaps in a cost-effective manner. Leveraging digital technology like electronic medical records can help generate real-world data and provide insights on voids in adoption of newer antidiabetic medications. A patient-centric approach, collaborative care among physicians from different specialties, alongside involvement of policy makers are key for improving patient outcomes and quality of care in MENA and AFR.

WAO-ARIA consensus on chronic cough - Part III: Management strategies in primary and cough-specialty care. Updates in COVID-19.

Background: Chronic cough management necessitates a clear integrated care pathway approach. Primary care physicians initially encounter the majority of chronic cough patients, yet their role in proper management can prove challenging due to limited access to advanced diagnostic testing. A multidisciplinary approach involving otolaryngologists and chest physicians, allergists, and gastroenterologists, among others, is central to the optimal diagnosis and treatment of conditions which underly or worsen cough. These include infectious and inflammatory, upper and lower airway pathologies, or gastro-esophageal reflux. Despite the wide armamentarium of ancillary testing conducted in cough multidisciplinary care, such management can improve cough but seldom resolves it completely. This can be due partly to the limited data on the role of tests (eg, spirometry, exhaled nitric oxide), as well as classical pharmacotherapy conducted in multidisciplinary specialties for chronic cough. Other important factors include presence of multiple concomitant cough trigger mechanisms and the central neuronal complexity of chronic cough. Subsequent management conducted by cough specialists aims at control of cough refractory to prior interventions and includes cough-specific behavioral counseling and pharmacotherapy with neuromodulators, among others. Preliminary data on the role of neuromodulators in a proof-of-concept manner are encouraging but lack strong evidence on efficacy and safety. Objectives: The World Allergy Organization (WAO)/Allergic Rhinitis and its Impact on Asthma (ARIA) Joint Committee on Chronic Cough reviewed the recent literature on management of chronic cough in primary, multidisciplinary, and cough-specialty care. Knowledge gaps in diagnostic testing, classical and neuromodulator pharmacotherapy, in addition to behavioral therapy of chronic cough were also analyzed. Outcomes: This third part of the WAO/ARIA consensus on chronic cough suggests a management algorithm of chronic cough in an integrated care pathway approach. Insights into the inherent limitations of multidisciplinary cough diagnostic testing, efficacy and safety of currently available antitussive pharmacotherapy, or the recently recognized behavioral therapy, can significantly improve the standards of care in patients with chronic cough.

The septins: roles in cytokinesis and other processes.

The septins are a novel family of proteins that were first recognized in yeast as proteins associated with the neck filaments. Recent work has shown that septins are also present in other fungi, insects, and vertebrates. Despite the apparent differences in modes of cytokinesis amongst species, septins appear to be essential for this process in both fungal and animal cells. The septins also appear to be involved in various other aspects of the organization of the cell surface.

WAO-ARIA consensus on chronic cough - Part 1: Role of TRP channels in neurogenic inflammation of cough neuronal pathways.

BACKGROUND: Cough features a complex peripheral and central neuronal network. The function of the chemosensitive and stretch (afferent) cough receptors is well described but partly understood. It is speculated that chronic cough reflects a neurogenic inflammation of the cough reflex, which becomes hypersensitive. This is mediated by neuromediators, cytokines, inflammatory cells, and a differential expression of neuronal (chemo/stretch) receptors, such as transient receptor potential (TRP) and purinergic P2X ion channels; yet the overall interaction of these mediators in neurogenic inflammation of cough pathways remains unclear. OBJECTIVES: The World Allergy Organization/Allergic Rhinitis and its Impact on Asthma (WAO/ARIA) Joint Committee on Chronic Cough reviewed the current literature on neuroanatomy and pathophysiology of chronic cough. The role of TRP ion channels in pathogenic mechanisms of the hypersensitive cough reflex was also examined. OUTCOMES: Chemoreceptors are better studied in cough neuronal pathways compared to stretch receptors, likely due to their anatomical overabundance in the respiratory tract, but also their distinctive functional properties. Central pathways are important in suppressive mechanisms and behavioral/affective aspects of chronic cough. Current evidence strongly suggests neurogenic inflammation induces a hypersensitive cough reflex marked by increased expression of neuromediators, mast cells, and eosinophils, among others. TRP ion channels, mainly TRP V1/A1, are important in the pathogenesis of chronic cough due to their role in mediating chemosensitivity to various endogenous and exogenous triggers, as well as a crosstalk between neurogenic and inflammatory pathways in cough-associated airways diseases.

WAO-ARIA consensus on chronic cough - Part II: Phenotypes and mechanisms of abnormal cough presentation - Updates in COVID-19.

BACKGROUND: Chronic cough can be triggered by respiratory and non-respiratory tract illnesses originating mainly from the upper and lower airways, and the GI tract (ie, reflux). Recent findings suggest it can also be a prominent feature in obstructive sleep apnea (OSA), laryngeal hyperresponsiveness, and COVID-19. The classification of chronic cough is constantly updated but lacks clear definition. Epidemiological data on the prevalence of chronic cough are informative but highly variable. The underlying mechanism of chronic cough is a neurogenic inflammation of the cough reflex which becomes hypersensitive, thus the term hypersensitive cough reflex (HCR). A current challenge is to decipher how various infectious and inflammatory airway diseases and esophageal reflux, among others, modulate HCR. OBJECTIVES: The World Allergy Organization/Allergic Rhinitis and its Impact on Asthma (WAO/ARIA) Joint Committee on Chronic Cough reviewed the current literature on classification, epidemiology, presenting features, and mechanistic pathways of chronic cough in airway- and reflux-related cough phenotypes, OSA, and COVID-19. The interplay of cough reflex sensitivity with other pathogenic mechanisms inherent to airway and reflux-related inflammatory conditions was also analyzed. OUTCOMES: Currently, it is difficult to clearly ascertain true prevalence rates in epidemiological studies of chronic cough phenotypes. This is likely due to lack of standardized objective measures needed for cough classification and frequent coexistence of multi-organ cough origins. Notwithstanding, we emphasize the important role of HCR as a mechanistic trigger in airway- and reflux-related cough phenotypes. Other concomitant mechanisms can also modulate HCR, including type2/Th1/Th2 inflammation, presence or absence of deep inspiration-bronchoprotective reflex (lower airways), tissue remodeling, and likely cough plasticity, among others.

Berardinelli-Seip Syndrome and Essential Thrombocytosis: An Unusual Association.

Congenital generalized lipodystrophy (Berardinelli-Seip syndrome) is an autosomal recessive condition, presenting during infancy with generalized loss of fat. We report a 30-year-old female patient with diabetes who has acromegaloid features, prominent umbilicus, prominent muscles, prominent subcutaneous veins, and gross hepatomegaly. Near-total loss of subcutaneous fat was confirmed by whole-body magnetic resonance imaging and laboratory data revealed significant hypertriglyceridemia, uncontrolled diabetes mellitus, and heavy proteinuria with stage IIIa chronic kidney disease. Her blood film revealed thrombocytosis that on further evaluation by bone marrow biopsy was confirmed to be a myeloproliferative neoplasm (MPN); essential thrombocytosis (ET). She also had skin lesions that were proven to be reactive perforating collagenosis and necrobiosis lipoidica diabeticorum. She was managed conservatively and received interferon injections with fair general condition and control of her ET. However, her kidney function deteriorated furthermore to stage V chronic kidney disease requiring regular treatment with hemodialysis. We believe this is a unique case of Berardinelli-Seip syndrome with MPN that could be a coincidental association or part of a new syndrome.

Immunopathological features of air pollution and its impact on inflammatory airway diseases (IAD).

Air pollution causes significant morbidity and mortality in patients with inflammatory airway diseases (IAD) such as allergic rhinitis (AR), chronic rhinosinusitis (CRS), asthma, and chronic obstructive pulmonary disease (COPD). Oxidative stress in patients with IAD can induce eosinophilic inflammation in the airways, augment atopic allergic sensitization, and increase susceptibility to infection. We reviewed emerging data depicting the involvement of oxidative stress in IAD patients. We evaluated biomarkers, outcome measures and immunopathological alterations across the airway mucosal barrier following exposure, particularly when accentuated by an infectious insult.

Role of the yeast Gin4p protein kinase in septin assembly and the relationship between septin assembly and septin function.

To identify septin-interacting proteins in Saccharomyces cerevisiae, we screened for mutations that are synthetically lethal with a cdc12 septin mutation. One of the genes identified was GIN4, which encodes a protein kinase related to Hsl1p/Nik1p and Ycl024Wp in S. cerevisiae and to Nim1p/Cdr1p and Cdr2p in Schizosaccharomyces pombe. The Gin4p kinase domain displayed a two-hybrid interaction with the COOH-terminal portion of the Cdc3p septin, and Gin4p colocalized with the septins at the mother-bud neck. This localization depended on the septins and on the COOH-terminal (nonkinase) region of Gin4p, and overproduction of this COOH-terminal region led to a loss of septin organization and associated morphogenetic defects. We detected no effect of deleting YCL024W, either alone or in combination with deletion of GIN4. Deletion of GIN4 was not lethal but led to a striking reorganization of the septins accompanied by morphogenetic abnormalities and a defect in cell separation; however, remarkably, cytokinesis appeared to occur efficiently. Two other proteins that localize to the neck in a septin-dependent manner showed similar reorganizations and also appeared to remain largely functional. The septin organization observed in gin4Delta vegetative cells resembles that seen normally in cells responding to mating pheromone, and no Gin4p was detected in association with the septins in such cells. The organization of the septins observed in gin4Delta cells and in cells responding to pheromone appears to support some aspects of the model for septin organization suggested previously by Field et al. (Field, C.M., O. Al-Awar, J. Rosenblatt, M.L. Wong, B. Alberts, and T.J. Mitchison. 1996. J. Cell Biol. 133:605-616).

Identification of a developmentally regulated septin and involvement of the septins in spore formation in Saccharomyces cerevisiae.

The Saccharomyces cerevisiae CDC3, CDC10, CDC11, and CDC12 genes encode a family of related proteins, the septins, which are involved in cell division and the organization of the cell surface during vegetative growth. A search for additional S. cerevisiae septin genes using the polymerase chain reaction identified SPR3, a gene that had been identified previously on the basis of its sporulation-specific expression. The predicted SPR3 product shows 25-40% identity in amino acid sequence to the previously known septins from S. cerevisiae and other organisms. Immunoblots confirmed the sporulation-specific expression of Spr3p and showed that other septins are also present at substantial levels in sporulating cells. Consistent with the expression data, deletion of SPR3 in either of two genetic backgrounds had no detectable effect on exponentially growing cells. In one genetic background, deletion of SPR3 produced a threefold reduction in sporulation efficiency, although meiosis appeared to be completed normally. In this background, deletion of CDC10 had no detectable effect on sporulation. In the other genetic background tested, the consequences of the two deletions were reversed. Immunofluorescence observations suggest that Spr3p, Cdc3p, and Cdc11p are localized to the leading edges of the membrane sacs that form near the spindle-pole bodies and gradually extend to engulf the nuclear lobes that contain the haploid chromosome sets, thus forming the spores. Deletion of SPR3 does not prevent the localization of Cdc3p and Cdc11p, but these proteins appear to be less well organized, and the intensity of their staining is reduced. Taken together, the results suggest that the septins play important but partially redundant roles during the process of spore formation.

A septin-based hierarchy of proteins required for localized deposition of chitin in the Saccharomyces cerevisiae cell wall.

Just before bud emergence, a Saccharomyces cerevisiae cell forms a ring of chitin in its cell wall; this ring remains at the base of the bud as the bud grows and ultimately forms part of the bud scar marking the division site on the mother cell. The chitin ring seems to be formed largely or entirely by chitin synthase III, one of the three known chitin synthases in S. cerevisiae. The chitin ring does not form normally in temperature-sensitive mutants defective in any of four septins, a family of proteins that are constituents of the "neck filaments" that lie immediately subjacent to the plasma membrane in the mother-bud neck. In addition, a synthetic-lethal interaction was found between cdc12-5, a temperature-sensitive septin mutation, and a mutant allele of CHS4, which encodes an activator of chitin synthase III. Two-hybrid analysis revealed no direct interaction between the septins and Chs4p but identified a novel gene, BNI4, whose product interacts both with Chs4p and Cdc10p and with one of the septins, Cdc10p; this analysis also revealed an interaction between Chs4p and Chs3p, the catalytic subunit of chitin synthase III. Bni4p has no known homologues; it contains a predicted coiled-coil domain, but no other recognizable motifs. Deletion of BNI4 is not lethal, but causes delocalization of chitin deposition and aberrant cellular morphology. Overexpression of Bni4p also causes delocalization of chitin deposition and produces a cellular morphology similar to that of septin mutants. Immunolocalization experiments show that Bni4p localizes to a ring at the mother-bud neck that lies predominantly on the mother-cell side (corresponding to the predominant site of chitin deposition). This localization depends on the septins but not on Chs4p or Chs3p. A GFP-Chs4p fusion protein also localizes to a ring at the mother-bud neck on the mother-cell side. This localization is dependent on the septins, Bni4p, and Chs3p. Chs3p, whose normal localization is similar to that of Chs4p, does not localize properly in bni4, chs4, or septin mutant strains or in strains that accumulate excess Bni4p. In contrast, localization of the septins is essentially normal in bni4, chs4, and chs3 mutant strains and in strains that accumulate excess Bni4p. Taken together, these results suggest that the normal localization of chitin synthase III activity is achieved by assembly of a complex in which Chs3p is linked to the septins via Chs4p and Bni4p.

Amplification of Trichloroisocyanuric Acid (TCCA) Reactivity for Chlorination of Arenes and Heteroarenes via Catalytic Organic Dye Activation.

Heteroarenes and arenes that contain electron-withdrawing groups are chlorinated in good to excellent yields (scalable to gram scale) using trichloroisocyanuric acid (TCCA) and catalytic Brilliant Green (BG). Visible-light activation of BG serves to amplify the electrophilic nature of TCCA, providing a mild alternative approach to acid-promoted chlorination of deactivated (hetero)aromatic substrates. The utility of the TCCA/BG system is demonstrated through comparison to other chlorinating reagents and by the chlorination of pharmaceuticals including caffeine, lidocaine, and phenazone.

Impact of metabolic syndrome's components on the development of cardiovascular disease in a Jordanian cohort with metabolic syndrome.

OBJECTIVE: To assess the gender differences in the prevalence of diabetes, composite cardiovascular disease, and the components of metabolic syndrome (MS) in a Jordanian cohort with MS. Secondly, to evaluate the impact of number of MS components on prevalence of diabetes, ischemic heart disease (IHD), and stroke. METHODS: We carried out a cohort study among participants who fulfilled the National Cholesterol Education Program (Adult Treatment Panel III) criteria for MS recruited from December 2006-2007 from Endocrine Outpatient Clinics of the King Hussein Medical Centre, Amman, and Prince Rashid Military Hospital, Irbid, Jordan. Patients were divided into groups according to gender, presence, or absence of diabetes, and were evaluated for MS components, presence of IHD, and stroke. RESULTS: Three hundred and fifty-seven patients 207 males and 150 females were included, type 2 diabetes was present in 226 (132 males) patients. No intergroup differences were found on waist circumference, systolic blood pressure, diastolic blood pressure, or fasting blood sugar. Female group was having a worst lipid profile, higher triglyceride levels and low high density lipoprotein. Metabolic syndrome components were more in males. Diabetic males have more composite cardiovascular disease (CCVD) [relative risk (RR)=1.88, 95% confidence interval: 1.01-3.59]. No difference in prevalence of CCVD between female subgroups neither between the 2 genders with MS. The prevalence of diabetes mellitus, IHD, and stroke increased with increasing number of MS components. Diabetes was the strongest predictor for development of CCVD (RR=1.8) and IHD (RR=2.18). CONCLUSION: Females with MS have the worst lipid profile compared to the males, diabetic males have the worst CCVD end point. The prevalence of diabetes and IHD correlates with the number of MS components.