Feasibility of implementing public-private mix approach for tuberculosis case management in Pokhara Metropolitan City of western Nepal: a qualitative study.

Background: The Public-Private Mix (PPM) approach is a strategic initiative that involves engaging all private and public health care providers in the fight against tuberculosis using international health care standards. For tuberculosis control in Nepal, the PPM approach could be a milestone. This study aimed to explore the barriers to a public-private mix approach in the management of tuberculosis cases in Nepal.

Clinical profile and biochemical abnormalities in Scrub Typhus: A cross-sectional study.

Introduction: Scrub Typhus (ST) is an acute febrile illness caused by obligate intracellular bacteria of the family Rickettsia. It is often unrecognized and neglected but prevalent in tropical regions of endemic areas. The tragedy behind this diagnostic dilemma is non-specific clinical signs and symptoms, limited awareness, unavailability of diagnostic facilities, and low index of suspicion among the physicians.

Clinical profile and biochemical abnormalities in brucellosis: A cross-sectional study.

Introduction: Brucellosis is the commonest zoonotic disease worldwide and a common public health problem in Nepal. Because of the highly variable clinical presentation and non-specific manifestations, it remains a big challenge for clinicians from developing countries. Brucellosis has a tropism for the reticuloendothelial system, the liver is frequently involved.

Dengue virus disrupts Daxx and NF-κB interaction to induce CD137-mediated apoptosis.

Dengue virus (DENV) is a positive-strand RNA virus of the Flavivirus family with 4 different serotypes. Clinical manifestations of DENV infection include dengue fever, dengue hemorrhagic fever, and dengue shock syndrome. Following DENV infection, apoptosis of hepatic cells is observed both in vitro and in vivo.

Inhibition of p38MAPK and CD137 signaling reduce dengue virus-induced TNF-α secretion and apoptosis.

Background: Hepatic injury in dengue virus (DENV) infection is authenticated by hepatomegaly and an upsurge in transaminase levels. DENV replicates in hepatocytes and causes hepatocyte apoptosis both in vitro and in vivo. Understanding the molecular mechanisms of DENV-induced hepatic injury could facilitate the development of alternate chemotherapeutic agents and improved therapies.

Role of CD137 signaling in dengue virus-mediated apoptosis.

Hepatic dysfunction is a well recognized feature of dengue virus (DENV) infection. However, molecular mechanisms of hepatic injury are still poorly understood. A complex interaction between DENV and the host immune response contributes to DENV-mediated tissue injury.

Decreased paraoxonase 1 activity and increased oxidative stress in low lead-exposed workers.

Paraoxonase 1 (PON1) has been proposed as an antioxidant enzyme. Although lead-inhibited PON1 activity has been demonstrated mostly based on in vitro experiments, it is uncertain whether this phenomenon is relevant in pathogenesis of lead-induced oxidative stress in the lead exposure. We examined associations of blood lead levels (BLL) and PON1 activity along with oxidative stress parameters in lead exposure workers.

Effect of atorvastatin on paraoxonase1 (PON1) and oxidative status.

It has been proposed that paraoxonase1 (PON1), a high density lipoprotein (HDL)-associated esterase/lactonase, has anti-atherosclerotic properties. The activity of PON1 is influenced by PON1 polymorphisms. However, the influence of PON1 polymorphisms on PON1 activity and oxidative stress in response to lipid-lowering drugs remains poorly understood.