A Cross-Sectional Study on Craniofacial Measurements and Their Relationships with the Stature in Adult Bangladeshi Manipuri Males

Introduction: Craniofacial anthropometry can be useful forforensic scientist, physical anthropologist, genetic counsellorsas well as reconstructive surgery for the purposes ofidentification of an individuals and understanding humanphysical variation, gender and ethnicity especially with facialrecognition as a tool in recent advances in biometrics. Statureis one of the important criteria for personal identification whichhave a proportional biological relationship with every parts ofthe human body like head, face, trunk, extremities andvertebral column.Objective: In this study our main goal is to measure theselected linear craniofacial measurements from head and faceregion and the stature using the direct physical procedure.Materials and Methods: This cross-sectional study wascarried out in 100 healthy adult males from March 2017 toFebruary 2018 in the Department of Anatomy, BangabandhuSheikh Mujib Medical University (BSMMU), Dhaka. Descriptivestatistics and testing of hypotheses were used for the analysisusing SPSS software (version 22.0).Results: Here positive correlations of the stature with themaximum cranial length, maximum cranial breadth,morphological face height, maximum facial breadth, butsignificant positive correlations of the stature with the maximumcranial breadth, maximum facial breadth, was found. The Mean(±SD) of Maximum cranial length (g-op) was 17.73 (±0.74),Maximum cranial breadth (eu-eu) was 14.27 (±0.75),Morphological face height (n-gn) was 11.15 (±0.86) andMaximum facial breadth (zy-zy) was 12.56 (±0.59).Conclusion: This study will be anticipated to provide baselinequantitative data on the linear craniofacial measurements andthe stature of adult Bangladeshi Manipuri males and usinglarger samples with non-contact measurement technique willhelp in defining craniofacial anthropometric profiling of the adultBangladeshi Manipuri males.

Gene Therapy: A Veracity or Myth.

Gene therapy is a novel approach to treat, cure, or ultimately prevent disease by changing the expression of a person’s gene. It involves the transfer of a therapeutic or working gene copy into specific cells of an individual in order to repair a faulty gene copy. Thus it may be used to replace a faulty gene, or to introduce a new gene whose function is to cure or to favorably modify the clinical course of a condition. The scope of this new approach to the treatment of a condition is broad, with potential in the treatment of many genetic conditions. Though single gene disorders are best treated than multifactorial disorder; the challenge of developing successful gene therapy for any specific condition is considerable. The problem of ‘gene delivery’ into the desired tissues is very complex and challenging. Some of the ‘vectors’ for delivering the working copy of the gene to the target cells include using harmless viruses and non viral vectors. Till date, in gene therapy, only somatic cells and not the germ cells are targeted for treatment. The possible genetic manipulation of the germ cells remains the subject of intense ethical and philosophical discussion. Though some devastation was recorded in gene therapy trial; the potential benefits of new treatments must always be balanced against such risks. In particular, safety will appropriately remain an important consideration as the field of gene therapy evolves. The purpose of this review is to focus on merit and demerit of gene therapy and to provide information about its future prospective.

Genetic and Clinical Aspects of Brugada Syndrome.

Death is always dreadful and the diseases those causes sudden death are universal threats in health concern. Brugada syndrom is a recently identified entity of arrhythmia and sudden cardiac death. This genetic and male dominant disorder is prevalent in Southeast Asian region. At least seven genes have been identified to associate with its occurrence though the detail pathophysiological mechanism is till to be resolved. The correlation of ion channel genes to Brugada syndrom is still dubious as the same genes also related to other cardiac diseases. Here we review the genetic aspects of Brugada syndrom with a breif overview of epidemiology, diagnosis and management system.

Brugada Syndrome: A Major Cause of Sudden Cardiac Death.

In 1992 a new syndrome was described consisting of syncopal episodes or sudden death in patients with a structurally normal heart and an electrocardiogram characteristic of right bundle branch block with ST segment elevation in leads V1 to V3. Brugada syndrome is an autosomal dominant disorder. It has been shown to be associated with mutations in the gene (SCN5A) that encodes for the sodium ion channel in cardiac myocyte. Over 160 mutations of gene SCN5A have been identifi ed. Th e incidence of the disease is diffi cult to estimate, but it causes sudden deaths of 5 per 10,000 inhabitants per year and involved much more frequently in people of Asian ancestry. Diagnosis can be easily made by means of genetic analysis and ECG. Recent data suggest that loss of the action potential dome in the right ventricular epicardium underlies ST segment elevation seen in this syndrome. Right ventricular epicardium is preferentially aff ected because of the predominance of transient outward current in this tissue. Antiarrhythmic drugs like amiodarone and beta-blockers do not prevent death in symptomatic or asymptomatic individuals. Th ough Implantation of an automatic cardioverter–defi brillator is the only recently proven eff ective therapy; Quinidine has been found to decrease Ventricular fi brillation and could prove to be a secured option of implantable cardioverter–defi brillator. However, researcher set focus on gene therapy that may off er an enduring cure in future years. Th e purpose of this brief review is to record the past highlights that have brought us to our present understanding of Brugada syndrome.