Akhtar Saeed Medical and Dental College

Scaffold samples were fabricated using a commercial extrusion bioprinter equipped with a pneumatic printhead fitted with a 21G conical nozzle. The Pore Printability Index, and the area and perimeter of the pore within the grid patterns were quantified using ImageJ software (NIH, USA). Mechanical properties of scaffolds were assessed using atomic force microscopy. The phase composition and crystal structures were analyzed using X-ray diffraction and Raman mapping. Morphologies of human gingival fibroblastic cells were examined using scanning electron microscopy. Lactobacillus biofilms were generated for cytolysin peptide cleavage. A rabbit bone defect model with scaffold implantations was used to provide histologic specimens for measuring percentages of bone trabeculae, collagen fibers and inflammatory cells along with granulation tissue. The Primeway Total RNA Extraction Kit was used for RNA extraction.

All bioink formulations demonstrated successful printing of 3D grid and solid square patterned scaffolds achieving Pr values exceeding 0.9. _0.1 % K21 group showed the highest elastic modulus. XRD revealed a pattern producing around 90 % β-tricalcium phosphate displaying two peaks at 2θ angles. 0.1 % K21 and _0.1 % CHX did not alter scaffold's pore size and porosity. _0.1 % K21 group exhibited highest ratio (62.5 ± 6.1 θ), significantly surpassing control. Surface morphologies of cells were also well retained. TEM image shows a sequence of structural changes in fibroblastic cell structure when exposed to K21. 0.1 % K21 proved to be critical in completely eradicating the biofilm. _0.K21 group closed the openings of wound areas completely. Correlation coefficient of gene expression levels demonstrates sample variations and recurring instances among groupings.

3D-printing technologies with _0.1 % K21 represent a significant advancement over conventional regenerative medicine techniques for bone-related treatments.

Congenital heart disease (CHD) is an umbrella term describing a variety of structural cardiac malformations at birth. CHD affects approximately 1 % of live births, generating a large adult population with these abnormalities. Pulmonary hypertension (PH) in patients with adult CHD is heterogeneous, based on the type of defect and associated conditions, but is a known cause of adverse outcome.

We retrieved death certificate data from the CDC-WONDER database using ICD codes (I27.0, I27.2, I27.8, and I27.9., and Q20-26). Crude mortality rates (CMRs) and age-adjusted mortality rates (AAMRs) per 100,000 persons were calculated. Temporal trends were examined using the annual percent change (APC) and average annual percent change (AAPC) determined by Joinpoint regression.

From 1999 to 2020, an overall declining pattern was observed in the mortality rate. Men and women with congenital heart disease and pulmonary hypertension in the U.S. experienced a statistically significant decline in mortality rates. In terms of races, among White individuals, the decline was the most pronounced. All four U.S. census regions experienced statistically significant declines in mortality due to pulmonary hypertension among individuals with congenital heart disease. The rate of decline was steeper in rural areas compared to urban ones.

This study highlights that previously implemented targeted interventions significantly contributed to the reduction of mortality amongst patiemnts with congenital heart disease and pulmonary hypertension in the U.S. Still improvements are required in certain areas, including female gender, Hispanic or Latino, and the Northeast and West regions.