Assessment of Angiogenesis and Cell Survivability of an Inkjet Bioprinted Biological Implant in an Animal Model

The rapidly growing field of tissue engineering hopes to soon address the shortage of transplantable tissues, allowing for precise control and fabrication that could be made for each specific patient. The protocols currently in place to print large-scale tissues have yet to address the main challenge of nutritional deficiencies in the central areas of the engineered tissue, causing necrosis deep within and rendering it ineffective. Bioprinted microvasculature has been proposed to encourage angiogenesis and facilitate the mobility of oxygen and nutrients throughout the engineered tissue. An implant made via an inkjet printing process containing human microvascular endothelial cells was placed in both B17-SCID and NSG-SGM3 animal models to determine the rate of angiogenesis and degree of cell survival. The implantable tissues were made using a combination of alginate and gelatin type B; all implants were printed via previously published procedures using a modified HP inkjet printer. Histopathological results show a dramatic increase in the average microvasculature formation for mice that received the printed constructs within the implant area when compared to the manual and control implants, indicating inkjet bioprinting technology can be effectively used for vascularization of engineered tissues.     

Anti-ischaemic effect of ivabradine.

Ivabradine, the first representative of a new class of exclusive heart rate-reducing agents, selectively inhibits the I(f) current in the sinoatrial node. The direct electrophysiological consequence of this inhibition is a reduction in the slope of the diastolic depolarisation curve and a decrease in heart rate. Pharmacological inhibition of the I(f) current with ivabradine has been shown to preserve coronary vasodilatation upon exercise, i.e., myocardial perfusion, with no negative inotropic effects and maintenance of cardiac contractility. Ivabradine protects the myocardium during ischaemia, improves left ventricular function in congestive heart failure, and reduces remodelling subsequent to myocardial infarction. Pure heart rate reduction by specific and selective I(f) inhibition decreases oxygen demand, improves myocardial energetics and improves perfusion of the ischaemic myocardium. We can expect distinct clinical benefits from long-term heart rate reduction in patients with chronic ischaemic disease.     

Assessment of the value of detecting specific IgA antibodies for the diagnosis of a recently acquired primary Toxoplasma infection

OBJECTIVE: To assess the value of detecting IgA antibodies for the diagnosis of a recently acquired primary Toxoplasma infection. METHODS: IgA antibodies were screened in sera from 87 women with different serological profiles of Toxoplasma gondii IgM and IgG antibodies and Toxoplasma-specific IgG avidity. The IgM and IgG antibodies and the IgG avidity were measured with an automated Vitek Immuno Diagnostic Assay System (VIDAS). Anti-T.gondii IgA was measured with Platelia Toxo IgA TMB kits. RESULTS: All 12 sera obtained from women with clinical and/or serological evidence of a recently acquired Toxoplasma infection were positive for IgA. In 42 serum samples obtained more than 6 months after T. gondii infection from women with no clinical evidence of infection, but who had a positive IgM test and a high IgG avidity index, the IgA-enzyme linked immunosorbent assay (ELISA) test results were positive, negative, and doubtful in 16 (38.1%), 23 (54.8%), and 3 (7.1%) sera, respectively. In eight women, IgA was detected in sera collected more than 9 months after the onset of infection. The IgA test result was also positive in 11 of 12 sera (91.7%) obtained from women with no clinical evidence of toxoplasmosis, but who had a positive IgM test and a borderline IgG avidity index. The IgA-ELISA was negative in 21 sera obtained more than 2 years after the onset of T. gondii infection from women with no clinical evidence of toxoplasmosis, but who had a negative IgM test and a positive IgG test. CONCLUSION: These results show that IgA is not a dependable marker for a recently acquired primary Toxoplasma infection.     

Fetal facial profile in Pallister-Killian syndrome

Pallister-Killian syndrome (PKS) is a sporadic chromosomal anomaly, caused by a tissue-specific mosaic distribution of an additional isochromosome 12p. About 60 cases of prenatal diagnosis of PKS have been reported. Only 1 case of PKS is described on the basis of prenatal screening, presenting increased nuchal translucency. An abnormal fetal facial profile is described prenatally as sonographic evidence of PKS. We report a case of prenatal diagnosis in a fetus undergoing second-level scan due to positive triple screen with ultrasound features of PKS.