PubMed Health⌕ Search

Biomedical subjects

Nannan Chen

Publications and source records attributed to Nannan Chen.

6 recordsLinked to original sources
PubMed2006

Distant touch hydrodynamic imaging with an artificial lateral line.

Nearly all underwater vehicles and surface ships today use sonar and vision for imaging and navigation. However, sonar and vision systems face various limitations, e.g., sonar blind zones, dark or murky environments, etc. Evolved over millions of years, fish use the lateral line, a distributed linear array of flow sensing organs, for underwater hydrodynamic imaging and information extraction. We demonstrate here a proof-of-concept artificial lateral line system. It enables a distant touch hydrodynamic imaging capability to critically augment sonar and vision systems. We show that the artificial lateral line can successfully perform dipole source localization and hydrodynamic wake detection. The development of the artificial lateral line is aimed at fundamentally enhancing human ability to detect, navigate, and survive in the underwater environment.

Animals↗
PubMed2004

The expression and activation of protease-activated receptor-2 correlate with skin color.

Skin color results from the production and distribution of melanin in the epidermis. The protease-activated receptor-2 (PAR-2), expressed on keratinocytes but not on melanocytes, is involved in melanosome uptake via phagocytosis, and modulation of PAR-2 activation affects skin color. The pattern of melanosome distribution within the epidermis is skin color-dependent. In vitro, this distribution pattern is regulated by the ethnic origin of the keratinocytes, not the melanocytes. Therefore, we hypothesized that PAR-2 may play a role in the modulation of pigmentation in a skin type-dependent manner. We examined the expression of PAR-2 and its activator, trypsin, in human skins with different pigmentary levels. Here we show that PAR-2 and trypsin are expressed in higher levels, and are differentially localized in highly pigmented, relative to lightly pigmented skins. Moreover, highly pigmented skins exhibit an increase in PAR-2-specific protease cleavage ability. Microsphere phagocytosis was more efficient in keratinocytes from highly pigmented skins, and PAR-2 induced phagocytosis resulted in more efficient microsphere ingestion and more compacted microsphere organization in dark skin-derived keratinocytes. These results demonstrate that PAR-2 expression and activity correlate with skin color, suggesting the involvement of PAR-2 in ethnic skin color phenotypes.

Humans↗
PubMed2002

Selective inhibition of COX-2 is beneficial to mice infected intranasally with VSV.

Cyclooxygenase (COX) is the key enzyme for prostaglandin (PG) synthesis. PGs are mediators of many critical physiological and inflammatory responses. There are two isoforms, COX-1 and COX-2, both of which are constitutively expressed in the central nervous system (CNS). Studies have shown that COX-1 and COX-2 are involved in physiological and pathological conditions of the brain. However, little is known about the role(s) of COX in the host defense system against a viral infection in the CNS. In this report, we used Vesicular Stomatitis Virus (VSV) induced acute encephalitis to distinguish between the contribution(s) of the two isoforms. COX-2 activity was inhibited with a COX-2 selective drug, celecoxib (Celebrex), and COX-1 was antagonized with SC560. We found that inhibition of COX-2 led to decreased viral titers, while COX-1 antagonism did not have the same effect at day 1 post infection. 5-lipooxygenase (5-LO) expression and neutrophil recruitment in the CNS were increased in celecoxib-inhibited mice. Furthermore, mice treated with celecoxib expressed more Nitric Oxide Synthase-1 (NOS-1), a crucial component of the innate immune system in the restriction of VSV propagation. The expression of type 1 cytokines, IFN-gamma and IL-12, were also increased in celecoxib-treated mice.

Animals↗
PubMed2002

Distinct roles of eicosanoids in the immune response to viral encephalitis: or why you should take NSAIDS.

Prostaglandins (PGs) and leukotrienes (LTs) are important proinflammatory mediators. They are both derived from arachidonic acid (AA). Cyclooxygenase (COX), the key enzyme in transforming AA into PGs, has two isoforms: COX-1 is constitutively expressed, and COX-2, is inducible. Lipoxygenase (5-LO) is the key enzyme for LT production. PGs and LTs have been intensively studied. Release of these molecules is associated with mucus secretion, redness, pain, fever and other inflammatory manifestations. Both PGs and LTs are involved in host defense against various pathogens. In addition to mediating inflammatory symptoms, PGs might suppress some innate immune factors, including nitric oxide (NO) production. PGs also suppress a TH1 response. LTs have pathologic potential, especially in asthma. LTs also have been found to have positive roles in host defense, either against virus or bacteria. Finally, PGs and LTs might regulate the production of each other, possibly at the level of substrate competition by their enzymes. Because they are clinically important molecules, a further understanding of the roles that PGs and LTs played in host defense will have great impact on therapeutic research.

Animals↗
PubMed2002

Innate immunity in viral encephalitis: role of C5.

The complement system is a critical component of both the innate and acquired immune systems. It is important in host defense against viruses, bacteria, and fungi for opsonization and for lysis of pathogens. However, activated complement can also cause tissue damage. There is compelling evidence that complement factors are presented in the central nervous system (CNS). Complement activation (by any of the three pathways: classical, alternate, and lectin) can lead to inflammation and tissue damage, while at the same time may also restrict certain pathogens in the CNS. C5a is formed by proteolytic cleavage C5. C5a is considered the most potent proinflammatory mediator, often called an anaphylotoxin. In this communication, we examine the roles of C5 (C5a) in vesicular stomatitis virus (VSV)-induced encephalitis. We found that C5a is produced during VSV infection, but C5-deficient mice had similar pathology as their controls. We concluded that C5 is not a critical factor in mediating the host response during VSV encephalitis.

Animals↗