Haemangioma of the maxillary antrum

Haemangioma of the maxillary sinus is rare. Clinical diagnosis is of utmost importance for its operative treatment and prevention of hazards. A case is reported for its rarity and some unusual features.     

Effect of lycoriside,an acylglucosyloxy alkaloid,on mast cells

The effect of lycoriside, an acylglucosyloxy alkaloid from Crinum asiaticum Linn, (family Amaryllidaceae), with or without sitosterol-3-O--D-glucoside, was studied on the rate of degranulation of peritoneal mast cells of albino rats. Lycoriside, at lower concentrations (1–20 µg/ml), in vitro, produced statistically significant protection against Tween 80-induced degranulation, as also to sensitized mast cells challenged with an antigen (horse serum). It also provided protection against compound 48/80-induced degranulation of mast cells when administered in vivo (1–5 mg/kg, po). At higher concentrations (100 µg/ml and above), in vitro, however, it had a mast-cell degranulation effect per se. The addition of sitosterol-3-O--D-glucoside to lycoriside did not modify the effect of the latter compound. The mechanism of the dual response elicited by lycoriside is appraised in view of a concentration-dependent anti- or prerelease effect on mast-cell mediators.     

HEPATOPROTECTIVE EFFECT OF AMOORA ROHITUKA

Abstract

Antihepatotoxic activity of a resuspended residue of the alcohol extract of Amoora rohituka W & A. (Meliaceae) was studied in rats with hepatic injury induced by carbon tetrachloride. Carbon tetrachloride (1 ml/kg, i.p.) was administered twice a week for 3 weeks and an extract of A. rohituka (50 mg/kg/day) was given orally for the same period. The rats were sacrificed 24 h after the last CC1₄ challenge. Carbon tetrachloride induced elevations of alkaline phosphatase (ALP), glutamate pyruvate transaminase (CPT), alanine aminotransferase (ALAT), glutamate oxaloacetate transaminase (GOT), aspartate aminotransferase (ASAT) and lactate dehydrogenase (LDH) and total plasma bilirubin concentration as well as depression of total plasma cholesterol concentration were reduced significantly by the concurrent treatment of rats with A. rohituka suspension. Changes in the histological architecture of the liver produced by CC1₄ where also protected by the administration of A. rohituka suspension. These results indicate that A. rohituka suspension possesses hepatoprotective action.     

Posttraumatic Stress Disorder and Incident Heart Failure Among a Community-Based Sample of US Veterans

Objectives. We investigated the association between posttraumatic stress disorder (PTSD) and incident heart failure in a community-based sample of veterans.Methods. We examined Veterans Affairs Pacific Islands Health Care System outpatient medical records for 8248 veterans between 2005 and 2012. We used multivariable Cox regression to estimate hazard ratios and 95% confidence intervals for the development of heart failure by PTSD status.Results. Over a mean follow-up of 7.2 years, veterans with PTSD were at increased risk for developing heart failure (hazard ratio [HR] = 1.47; 95% confidence interval [CI] = 1.13, 1.92) compared with veterans without PTSD after adjustment for age, gender, diabetes, hyperlipidemia, hypertension, body mass index, combat service, and military service period. Additional predictors for heart failure included age (HR = 1.05; 95% CI = 1.03, 1.07), diabetes (HR = 2.54; 95% CI = 2.02, 3.20), hypertension (HR = 1.87; 95% CI = 1.42, 2.46), overweight (HR = 1.72; 95% CI = 1.25, 2.36), obesity (HR = 3.43; 95% CI = 2.50, 4.70), and combat service (HR = 4.99; 95% CI = 1.29, 19.38).Conclusions. Ours is the first large-scale longitudinal study to report an association between PTSD and incident heart failure in an outpatient sample of US veterans. Prevention and treatment efforts for heart failure and its associated risk factors should be expanded among US veterans with PTSD.Posttraumatic stress disorder (PTSD) is a psychiatric illness that affects approximately 7.7 million Americans aged older than 18 years.1 PTSD typically results after the experience of severe trauma, and veterans are at elevated risk for the disorder. The National Vietnam Veterans Readjustment Study reported the prevalence of PTSD among veterans who served in Vietnam as 15.2% among men and 8.1% among women.2 In fiscal year 2009, nearly 446 045 Veterans Administration (VA) patients had a primary diagnosis of PTSD, a threefold increase since 1999.3 PTSD is of growing clinical concern as evidence continues to link psychiatric illnesses to conditions such as arthritis,4 liver disease,5 digestive disease,6 and cancer.6 When the postwar health status of Vietnam veterans was examined, those with PTSD had higher rates of diseases of the circulatory, nervous, digestive, musculoskeletal, and respiratory systems.7The evidence linking PTSD to coronary heart disease (CHD) is substantial.8–10 Veterans with PTSD are significantly more likely to have abnormal electrocardiograph results, myocardial infarctions, and atrioventricular conduction deficits than are veterans without PTSD.11 In a study of 605 male veterans of World War II and the Korean War, CHD was more common among veterans with PTSD than among those without PTSD.12 Worldwide, adults exposed to the disaster at Chernobyl experienced increased rates of CHD up to 10 years after the event,13 and studies of stressors resulting from the civil war in Lebanon found elevated CHD mortality.14,15Although the exact biological mechanism by which PTSD contributes to CHD remains unclear, several hypotheses have been suggested, including autonomic nervous system dysfunction,16 inflammation,17 hypercoagulability,18 cardiac hyperreactivity,19 altered neurochemistry,20 and co-occurring metabolic syndrome.16 One of the hallmark symptoms of PTSD is hyperarousal,21 and the neurobiological changes brought on from sustained sympathetic nervous system activation affect the release of neurotransmitters and endocrine function.22 These changes have negative effects on the cardiovascular system, including increased blood pressure, heart rate, and cardiac output.22,23Most extant literature to date examining cardiovascular sequelae has shown a positive association between PTSD and coronary artery disease.8–10 Coronary artery disease is well documented as one of the most significant risk factors for future development of heart failure.24 Despite burgeoning evidence for the role of PTSD in the development of coronary artery disease, there are few studies specifically exploring the relationship between PTSD and heart failure. Limited data suggest that PTSD imparts roughly a threefold increase in the odds of developing heart failure in both the general population5 and in a sample of the elderly.25 These investigations, however, have been limited by cross-sectional study design, a small proportion of participants with PTSD, and reliance on self-reported measures for both PTSD and heart failure.5,25 Heart failure is a uniquely large public health issue, as nearly 5 million patients in the United States are affected and there are approximately 500 000 new cases each year.26 Identifying predictors of heart failure can aid in early detection efforts while simultaneously increasing understanding of the mechanism behind development of heart failure.To mitigate the limitations of previous investigations, we undertook a large-scale prospective study to further elucidate the role of prevalent PTSD and development of incident heart failure among veterans, while controlling for service-related and clinical covariates. Many studies investigating heart failure have relied on inpatient records; we leveraged outpatient records to more accurately reflect the community burden of disease.     

Age and prior caffeine use alter the cardiovascular and adrenomedullary responses to oral caffeine

The effects of age and chronic caffeine use (approximately 300 mg/day) on the cardiovascular and humoral responses to 250 mg of oral caffeine (the equivalent of 2 to 3 cups of coffee) were examined. Older subjects had greater increases in blood pressure than younger subjects (p less than 0.03), and caffeine nonusers had greater blood pressure increases than caffeine users, regardless of age (p less than 0.05). Caffeine increased the product of systolic blood pressure and heart rate (an estimate of myocardial oxygen demand) in older caffeine nonusers, but this effect was absent in older caffeine users (p less than 0.01). Cardiovascular effects of caffeine could not be related temporally to changes in plasma epinephrine, which were greater in caffeine nonusers and younger subjects, or to plasma norepinephrine, renin activity or vasopressin, which did not change. Thus, age accentuates and moderate prior caffeine use attenuates the cardiovascular effects of oral caffeine; these effects are not mediated solely through the sympathoadrenal system.     

HLA class II allele polymorphism in an outbreak of chikungunya fever in Middle Andaman,India

A sudden upsurge of fever cases with joint pain was observed in the outpatient department, Community Health Centre, Rangat during July–August 2010 in Rangat Middle Andaman, India. The aetiological agent responsible for the outbreak was identified as chikungunya virus (CHIKV), by using RT‐PCR and IgM ELISA. The study investigated the association of polymorphisms in the human leucocyte antigen class II genes with susceptibility or protection against CHIKV. One hundred and one patients with clinical features suggestive of CHIKV infection and 104 healthy subjects were included in the study. DNA was extracted and typed for HLA‐DRB1 and DQB1 alleles. Based on the amino acid sequences of HLA‐DQB1 retrieved from the IMGT/HLA database, critical amino acid differences in the specific peptide‐binding pockets of HLA‐DQB1 molecules were investigated. The frequencies of HLA‐DRB1 alleles were not significantly different, whereas lower frequency of HLA‐DQB1*03:03 was observed in CHIKV patients compared with the control population [P = 0·001, corrected P = 0·024; odds ratio (OR)  = 0, 95% confidence interval (95% CI) 0·0–0·331; Peto's OR = 0·1317, 95% CI 0·0428–0·405). Significantly lower frequency of glutamic acid at position 86 of peptide‐binding pocket 1 coding HLA‐DQB1 genotypes was observed in CHIKV patients compared with healthy controls (P = 0·004, OR = 0·307, 95% CI 0·125–0·707). Computational binding predictions of CD4 epitopes of CHIKV by NetMHCII revealed that HLA‐DQ molecules are known to bind more CHIKV peptides than HLA‐DRB1 molecules. The results suggest that HLA‐DQB1 alleles and critical amino acid differences in the peptide‐binding pockets of HLA‐DQB1 alleles might have role in influencing infection and pathogenesis of CHIKV.     

Clinical effectiveness and safety of escitalopram and desvenlafaxine in patients of depression with anxiety: A randomized,open-label controlled trial

Aim:

Selective serotonin reuptake inhibitors (SSRI) and serotonin-norepinephrine reuptake inhibitors (SNRI) are effective in treating anxiety disorders associated with major depressive disorder (MDD). This randomized, controlled, parallel-group, open-label, phase 4 trial (CTRI/2012/08/002895) was undertaken to compare the effectiveness and safety of desvenlafaxine versus escitalopram, a standard antidepressant.

Materials and Methods:

Effectiveness was assessed using the Hamilton Depression Rating Scale (HAM-D₁₇) and Hamilton Anxiety Rating Scale (HAM-A). Response to treatment was assessed by ≥50% decrease of baseline scores (responder rate). Safety and tolerability was evaluated by changes in routine laboratory parameters, vital signs, and adverse events reported by the subject and/or observed by the clinician.

Results:

Responder rates for both HAM-A and HAM-D scores at 8 weeks were better in the escitalopram group compared to the desvenlafaxine group (HAM-A 76.92% vs. 71.05%; HAM-D 79.48% vs 73.68%) but the differences were not statistically significant (P = 0.59 and P = 0.61). Within group changes of both scores, from baseline to subsequent visits in both treatment arms were statistically significant (P < 0.01).

Conclusion:

The effectiveness of desvenlafaxine was comparable to escitalopram, but escitalopram was better tolerated.KEY WORDS: Anxiety, clinical trial, desvenlafaxine, escitalopram, major depressive disorder