Role of C3a in Regulating Thymocyte Infection by HIV-1

The primary physiological role of complement proteins lies in augmenting host defense to microorganisms. Among several cascade products, complement components C3 and C5 are cleaved and activated through proteolytic processing during immune activation following exposure to HIV-1. This reaction generates the small peptide anaphylatoxins C3a and C5a, which bind to G-protein coupled membrane receptors that sensitize the response of human T-lymphocytic cells to multiple cytokines including CXCL12/SDF-1. 

CXCL12 is an alpha chemokine that binds to the CXCR4 membrane receptor, which also functions as a co-receptor for X4-tropic HIV-1. Given the importance of complement activation in immune function and the bio active nature of complement cleavage products we investigated here the role of C3a in HIV-1 infection of human thymocytes. Our data illustrate a potential new link between HIV-1 infection and complement activation in which C3a anaphylatoxin may modulate infectivity by reducing the susceptibility of thymocytes to HIV-1 infection.

Tomorrow starts today…?

It’s really great pleasure to have possibility to create something new. New it means new idea to have dedicated combined experimental and clinical practice trauma journal. We know how important is clinical practice, but sometimes we miss new ideas or what’s happening in the trauma experimental field. Despite better diagnostic and treatment possibilities trauma especially in younger patients is one of the leading cause of disability. 

But in nowadays with longer life expectancy we have more and more elderly patients with low energy trauma demanding fast and effective treatment to return those patients to former social life. There is always need to improve prevention, diagnostic and treatment in trauma. Sometimes decision about the treatment in trauma case must be done in minutes. We need evidence based knowledge’s to choose best decision. It’s not enough to have just prospectively collected and analyzed data in trauma.

Fever induced Brugada syndrome masquerading as STEMI

Brugada Syndrome (BrS) is an autosomal dominant genetic disease determined by abnormal electrocardiographic (ECG) pattern and causes increased risk of sudden cardiac death. It is characterised by coved-type ST segment elevation in precordial leads V1-V3. There had been many proposed mechanisms explaining the link of sodium channel mutations and its electrophysiology. 

There are various triggering factors like fever, hypokalemia, ischemia, cocaine abuse and medications which unmask the ECG changes and these changes are usually transient. There is increased possibility of this cardiac rhythm to deteriorate into life threatening arrhythmias. Thus it is essential for the clinician to be aware of the conditions. We present such a scenario in which hyperthermia unmasked our patient’s Brugada syndrome.

Possible role for HIF-1β/ARNT in the regulation of vascular function in diabetes and cardiovascular disease

Cardiovascular disease is one of the major causes of morbidity and mortality in diabetic patients. In fact, almost 80% of deaths in diabetics are caused by cardiac complications. Because of the high rate of obesity and sedentary lifestyles inthe United States, the prevalence of diabetes has doubled over the past 30 years. Diabetes is one of the major risk factors that lead to cardiovascular disease (CVD). In fact, from the perspective of cardiovascular medicine, it may be appropriate to say, “Diabetes is a cardiovascular disease.” However, it is still not clear how diabetes promotes cardiac dysfunction