Incidence and Causes of Cellulitis Among Patients at Tupua Tamasese Meaole Hospital in Upolu, Samoa in 2019.

OBJECTIVE: To study the incidence and causes of cellulitis in patients who visited the only tertiary hospital in Samoa, i.e., Tupua Tamasese Meaole (TTM) Hospital, in 2019. METHOD: Of the total of 14,198 patients who presented to TTM Hospital in 2019, a chart review of all 258 patients who presented with cellulitis was conducted. All charts with the final primary admitting diagnosis of cellulitis were extracted. No exclusion criteria were employed, and raw data were analyzed manually. RESULTS: Of the 14,198 patients who sought care at TTM Hospital in 2019, 258 patients received care for cellulitis. This represents an incidence rate of 1.8%. Most patients were male (62.4%). Those in the age group of 41 to 80 years old accounted for 79.5% of the total. The leg (94.6%) was the major site of infection. Of those who had blood cultures drawn, 76.4% had negative results. Of the 56 patients with positive microbial growth, Staphylococcus and Streptococcus species accounted for a combined total of 71.4% of the cases. The mainstay of antibiotic treatment was flucloxacillin alone or in conjunction with other antibiotics (92.2%). Of the many comorbidities affecting patients, diabetes (44.2%) was the most prevalent. Hospital admission, ranging from three to 10 days was needed in 63.5% of patients. CONCLUSION: The incidence rate of cellulitis at TTM in 2019 was 1.8%, which was marginally higher than noted in other parts of the world. Male patients and people over the age of 40 years are affected the most. The leg is affected the most mainly by Staphylococcus and Streptococcus species. Flucloxacillin is the main antibiotic used to treat cellulitis at the TTM Hospital. From the data analyses, it is inferred that a large proportion of patients who presented had moderate to severe cellulitis.

Fresh Noncultured Endothelial Progenitor Cells Improve Neonatal Lung Hyperoxia-Induced Alveolar Injury.

Treatment of preterm human infants with high oxygen can result in disrupted lung alveolar and vascular development. Local or systemic administration of endothelial progenitor cells (EPCs) is reported to remedy such disruption in animal models. In this study, the effects of both fresh (enriched for KDR) and cultured bone marrow (BM)-derived cell populations with EPC characteristics were examined following hyperoxia in neonatal mouse lungs. Intraperitoneal injection of fresh EPCs into five-day-old mice treated with 90% oxygen resulted in full recovery of hyperoxia-induced alveolar disruption by 56 days of age. Partial recovery in septal number following hyperoxia was observed following injection of short-term cultured EPCs, yet aberrant tissue growths appeared following injection of long-term cultured cells. Fresh and long-term cultured cells had no impact on blood vessel development. Short-term cultured cells increased blood vessel number in normoxic and hyperoxic mice by 28 days but had no impact on day 56. Injection of fresh EPCs into normoxic mice significantly reduced alveolarization compared with phosphate buffered saline-injected normoxic controls. These results indicate that fresh BM EPCs have a higher and safer corrective profile in a hyperoxia-induced lung injury model compared with cultured BM EPCs but may be detrimental to the normoxic lung. The appearance of aberrant tissue growths and other side effects following injection of cultured EPCs warrants further investigation. Stem Cells Translational Medicine 2017;6:2094-2105.

Targeting EphA3 inhibits cancer growth by disrupting the tumor stromal microenvironment.

Eph receptor tyrosine kinases are critical for cell-cell communication during normal and oncogenic tissue patterning and tumor growth. Somatic mutation profiles of several cancer genomes suggest EphA3 as a tumor suppressor, but its oncogenic expression pattern and role in tumorigenesis remain largely undefined. Here, we report unexpected EphA3 overexpression within the microenvironment of a range of human cancers and mouse tumor xenografts where its activation inhibits tumor growth. EphA3 is found on mouse bone marrow-derived cells with mesenchymal and myeloid phenotypes, and activation of EphA3(+)/CD90(+)/Sca1(+) mesenchymal/stromal cells with an EphA3 agonist leads to cell contraction, cell-cell segregation, and apoptosis. Treatment of mice with an agonistic α-EphA3 antibody inhibits tumor growth by severely disrupting the integrity and function of newly formed tumor stroma and microvasculature. Our data define EphA3 as a novel target for selective ablation of the tumor microenvironment and demonstrate the potential of EphA3 agonists for anticancer therapy.