Clinical Associations of Bitter Taste Perception and Bitter Taste Receptor Variants and the Potential for Personalized Healthcare.

Bitter taste receptors (T2Rs) consist of 25 functional receptors that can be found in various types of cells throughout the human body with responses ranging from detecting bitter taste to suppressing pathogen-induced inflammation upon activation. Numerous studies have observed clinical associations with genetic or phenotypic variants in bitter taste receptors, most notably that of the receptor isoform T2R38. With genetic variants playing a role in the response of the body to bacterial quorum-sensing molecules, bacterial metabolites, medicinal agonists and nutrients, we examine how T2R polymorphisms, expression levels and bitter taste perception can lead to varying clinical associations. From these genetic and phenotypic differences, healthcare management can potentially be individualized through appropriately administering drugs with bitter masking to increase compliance; optimizing nutritional strategies and diets; avoiding the use of T2R agonists if this pathway is already activated from bacterial infections; adjusting drug regimens based on differing prognoses; or adjusting drug regimens based on T2R expression levels in the target cell type and bodily region.

Early versus delayed treatment of lateral condylar fracture of the humerus with > 2 mm displacement in children: a retrospective study.

BACKGROUND: The purpose of this study was to investigate the clinical and functional outcomes of early versus delayed treatment of pediatric lateral condylar fractures of the humerus with a displacement greater than 2 mm. METHODS: Sixty-seven children treated surgically at our hospital from March 2016 to September 2021 for lateral condylar fracture of the humerus with displacement > 2 mm were retrospectively analyzed. The children were divided into two groups where early surgery consisted of patients being operated on within 24-h post-injury (n = 36) and delayed surgery consisted of children operated after 24-h post-injury (n = 31). Clinical and functional results were compared between the two groups. RESULTS: There were no significant differences between the two groups in terms of operation time, blood loss and incidences of perioperative complications. However, mean length of incision was significantly greater (P < 0.0001) in the delayed treatment group (5.68 ± 1.08 cm) compared to the early treatment group (3.89 ± 0.82 cm). No differences were found in functional outcomes, consisting of the Baumann angle of the affected limb, the carrying angle, Mayo Elbow Performance Score, and Flynn's criteria at final follow-up. CONCLUSIONS: Delay in surgery for more than 24 h after injury does not influence the clinical and functional results for lateral condylar fracture of the humerus with displacement > 2 mm in children. However, delayed open reduction and pinning may increase the incision length possibly due to increased edema.

Progress in Photobiomodulation for Bone Fractures: A Narrative Review.

Objective: The aim of this article is to examine current concepts and the future direction of implementing photobiomodulation (PBM) for fracture treatment. Background data: The effectiveness of PBM for bone regeneration has been demonstrated throughout in vitro studies and animal models. Yet, insufficient clinical trials have been reported on treating fractures with PBM. Materials and methods: A narrative review was composed on the basis of a literary search. Inclusion criteria consisted of studies between 2000 and 2019 using animal or human fracture models. Exclusion criteria consisted of studies that did not pertain to complete fractures or used other forms of intervention. Results: Ten animal studies on rats and rabbits and four clinical trials were found on using PBM for complete fractures. Conclusions: Based on positive outcomes in animal trials, parameter optimization of PBM for human fractures still requires extensive research on factors such as dosage, wavelength, penetration depth, treatment frequency, and the use of pulsed waves.

Ossotide promotes cell differentiation of human osteoblasts from osteogenesis imperfecta patients by up-regulating miR-145.

Ossotide as an effective bone formation compound preparation has been proved to promote osteoblasts differentiation. MiR-145 is significantly decreased in osteogenesis imperfecta (OI) patients, but it is still unknown whether ossotide performed its effect by regulating miR-145. In this study, we investigated the effect of ossotide on regulating miR-145 expression and osteoblasts differentiation. The primary osteoblasts cells were isolated from OI patients and then cultured with different concentrations (0, 25, 50, 100, 200µg/l) of ossotide. The cell proliferation was detected with CCK-8 Elisa kit after ossotide treatment. The level of miR-145 expression was determined using qRT-PCR. In order to study whether ossotide up regulated miR-145, miR-145 mimic and miR-145 inhibitor were used to up regulate and down regulate the miR-145 levels in osteoblasts. The expressions of Runx2, Osx, ß-catenin, TCF-1 were detected using Western blot and qRT-PCR. We observed that miR-145 was up regulated by ossotide treatment in miR-145 mimic or miR-145 inhibitor treated osteoblasts. What's more, up regulated miR-145 increased the expression of osteoblasts differentiation regulated protein Runx2 and Osx. In addition, Wnt signaling related ß-catenin, TCF-1 were activated by up-regulated miR-145 which was induced by ossotide treatment. In summary, ossotide induced cell differentiation and Wnt signaling activation in osteoblasts by up regulating miR-145.

Heritability and sibling recurrent risk of developmental dysplasia of the hip in Chinese population.

BACKGROUND: Previous familial segregation studies supported that developmental dysplasia of the hip (DDH) is a multifactorial genetic disease. However, the exact extent of genetic effects has not been fully evaluated, especially in Asian population. The aim of this study is to estimate the sibling recurrent risk and heritability of DDH in a large Chinese cohort. MATERIALS AND METHODS: Four hundred and twenty-nine DDH probands and 534 matched normal controls were recruited from a screening programme for DDH, including 628 siblings in families of probands and 889 siblings in those of controls, respectively. The detailed information of family history was obtained, and the prevalence of DDH among siblings of probands, as well as controls, was determined. The sibling recurrent risk and heritability was estimated using classical liability threshold model. RESULTS: Eighty-seven siblings (13.85%) in families of proband and 14 siblings (1.57%) in normal control families were diagnosed as DDH. The recurrent risk in siblings of probands was at least tenfolds that in siblings of controls. Compared with the normal controls, the sibling recurrent risk was about 12-fold increase in male sib, and 9-fold increase in female sib. Overall, a high heritability of 83.59 ± 4.90% (h(2) ± SE) was observed. When stratified by genders, it was even higher for female siblings (91.02 ± 7.25%). CONCLUSION: This study for the first time exhibits a high sibling recurrent risk and heritability for DDH in Asian population. It also shows there is a high probability to identify the underlying predisposition genes in future genetic study.