Publications by authors named "L L Lam"

Background: Conflicting results have been reported on the impact of tenofovir versus entecavir on liver-related outcomes.

Aims: To explore trends in clinical outcomes in chronic hepatitis B virus (HBV)-infected patients and compare the impact of tenofovir versus entecavir on the risk of hepatocellular carcinoma (HCC), liver transplantation (LT) and mortality.

Methods: We used the French National Health Insurance Databases (SNDS) to identify HBV-infected patients.

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Purpose: Children with complex communication needs face particular challenges during hospitalization. This study aimed to understand the situation for hospitalized Hong Kong Chinese children with complex communication needs.

Methods: Six group interviews were conducted with 23 participants, including nurses, doctors, adolescents with acquired brain injury, parents of children with acquired brain injury or cerebral palsy, and community-based therapists.

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Background: Alarmins mediate type 2 T helper cell (Th2) inflammation and serve as upstream signaling elements in allergic inflammation and autoimmune responses. The alarmin interleukin (IL)-25 binds to a multi-domain receptor consisting of IL-17RA and IL-17RB subunits, resulting in the release of Th2 cytokines IL-4, IL-5, IL-9 and IL-13 to drive an inflammatory response. Therefore, the blockage of IL-17RB via SM17, a novel humanized monoclonal antibody, offers an attractive therapeutic target for Th2-mediated diseases, such as asthma.

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Objective: To identify and synthesize the primary evidence on the effectiveness of Protection Motivation Theory on and cardiovascular disease and diseases that are risk factors for cardiovascular disease.

Method: An integrative review was conducted using the Whittemore and Knafl method (2005).

Results: Eleven articles met the inclusion and quality assessment criteria.

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Red blood cells (RBCs), traditionally recognized for their role in transporting oxygen, play a pivotal role in the body's immune response by expressing TLR9 and scavenging excess host cell-free DNA. DNA capture by RBCs leads to accelerated RBC clearance and triggers inflammation. Whether RBCs can also acquire microbial DNA during infections is unknown.

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