Periostin modulates extracellular matrix behavior in tendons.

Periostin, originally named osteoblast-specific factor 2 (OSF-2) has been identified primarily in collagen rich, biomechanically active tissues where its role has been implicated in mechanisms to maintain the extracellular matrix (ECM), including collagen fibrillogenesis and crosslinking. It is well documented that periostin plays a role in wound healing and scar formation after injury, in part, by promoting cell proliferation, myofibroblast differentiation, and/or collagen fibrillogenesis. Given the significance of periostin in other scar forming models, we hypothesized that periostin will influence Achilles tendon healing by modulating ECM production. Therefore, the objective of this study was to elucidate the effects of periostin during Achilles tendon healing using periostin homozygous (Postn -/-) and heterozygous (Postn +/-) mouse models. A second experiment was included to further examine the influence of periostin on collagen composition and function using intact dorsal tail tendons. Overall, Postn -/- and Postn +/- Achilles tendons exhibited impaired healing as demonstrated by delayed wound closure, increased type III collagen production, decreased cell proliferation, and reduced tensile strength. Periostin ablation also reduced tensile strength and stiffness, and altered collagen fibril distribution in the intact dorsal tail tendons. Achilles tendon outcomes support our hypothesis that periostin influences healing, while tail tendon results indicate that periostin also affects ECM morphology and behavior in mouse tendons.

Occipital alopecia in a young man.

Lipedematous alopecia is a rare, non-androgenic form of alopecia that is challenging to diagnose, often requiring clinical-pathological correlation. The condition has been reported predominantly in African-American females, but more recently has been described in a broader demographic [1,2]. We describe a rare case of a young Caucasian man with isolated lipedematous alopecia who presented with a boggy, erythematous plaque with alopecia of the occipital scalp and subcutaneous thickening with lymphocytic dermal infiltrate and decreased anagen hairs on histology.

Bioluminescence for in vivo detection of cell-type-specific inflammation in a mouse model of uveitis.

This study reports the use of cell-type-specific in vivo bioluminescence to measure intraocular immune cell population dynamics during the course of inflammation in a mouse model of uveitis. Transgenic lines expressing luciferase in inflammatory cell subsets (myeloid cells, T cells, and B cells) were generated and ocular bioluminescence was measured serially for 35 days following uveitis induction. Ocular leukocyte populations were identified using flow cytometry and compared to the ocular bioluminescence profile. Acute inflammation is neutrophilic (75% of ocular CD45 + cells) which is reflected by a significant increase in ocular bioluminescence in one myeloid reporter line on day 2. By day 7, the ocular T cell population increases to 50% of CD45 + cells, leading to a significant increase in ocular bioluminescence in the T cell reporter line. While initially negligible (< 1% of CD45 + cells), the ocular B cell population increases to > 4% by day 35. This change is reflected by a significant increase in the ocular bioluminescence of the B cell reporter line starting on day 28. Our data demonstrates that cell-type-specific in vivo bioluminescence accurately detects changes in multiple intraocular immune cell populations over time in experimental uveitis. This assay could also be useful in other inflammatory disease models.

Longer Breastfeeding Associated with Childhood Anemia in Rural South-Eastern Nigeria.

INTRODUCTION: Child mortality rate in sub-Saharan Africa is 29 times higher than that in industrialized countries. Anemia is one of the preventable causes of child morbidity. During a humanitarian medical mission in rural South-Eastern Nigeria, the prevalence and risk factors of anemia were determined in the region in order to identify strategies for reduction. METHODS: A cross-sectional study was done on 96 children aged 1-7 years from 50 randomly selected families. A study questionnaire was used to collect information regarding socioeconomic status, family health practices, and nutrition. Anemia was diagnosed clinically or by point of care testing of hemoglobin (Hb) levels. RESULTS: 96 children were selected for the study; 90 completed surveys were analyzed (43% male and 57% females). Anemia was the most prevalent clinical morbidity (69%), followed by intestinal worm infection (53%) and malnutrition (29%). Mean age (months) at which breastfeeding was stopped was 11.8 (±2.2) in children with Hb <11mg/dl (severe anemia), 10.5±2.8 in those with Hb = 11-11.9mg/dl (mild-moderate anemia), and 9.4±3.9 in children with Hb >12mg/dl (no anemia) (P=0.0445). CONCLUSIONS: The longer the infant was breastfed, the worse the severity of childhood anemia was. Childhood anemia was likely influenced by the low iron content of breast milk in addition to maternal anemia and poor nutrition. A family-centered preventive intervention for both maternal and infant nutrition may be more effective in reducing childhood anemia and child mortality rate in the community.

Gene profiling of the rat medial collateral ligament during early healing using microarray analysis.

Ligament heals in a synchronized and complex series of events. The remodeling process may last months or years. Experimental evidence suggests the damaged ligament does not recover its normal functional properties. Specific mechanisms to prevent scar formation and to regenerate the original mechanical function remain elusive but likely involve regulation of creeping substitution. Creeping substitution creates a larger hypercellular, hypervascular, and disorganized granulation tissue mass that results in an inefficient and nonregenerative wound healing process for the ligament. Control of creeping substitution may limit the extent of this tissue compromise and reduce the time necessary for healing. The objective of this study is to better understand the mechanism behind scar formation by identifying the extracellular matrix factors and other unique genes of interest differentially expressed during rat ligament healing via microarray. For this study, rat medial collateral ligaments were either surgically transected or left intact. Ligaments were collected at day 3 or 7 postinjury and used for microarray, quantitative PCR, and/or immunohistochemistry. Results were compared with the normal intact ligament. We demonstrate that early ligament healing is characterized by the modulation of several inflammatory and extracellular matrix factors during the first week of injury. Specifically, a number of matrix metalloproteinases and collagens are differentially and significantly expressed during early ligament healing. Additionally, we demonstrate the modulation of three novel genes, periostin, collagen-triple helix repeat containing-1, and serine protease 35 in our ligament healing model. Together, control of granulation tissue creeping substitution and subsequent downstream scar formation is likely to involve these factors.