A Case of Severe Pneumonia with Rhabdomyolysis Caused by Mycoplasma Pneumonia

Biotech and App Biochem

Mozafari

Bandehpour

et al. 2015

Electrospun silk fibroin nanofibrous scaffolds (ESFNSs) were successfully prepared by electrospinning of various Bombyx mori silk fibroin concentrations (10, 12, and 14% in formic acid). After characterizing the purified silk fibroin, the morphology, porosity, fibers' diameter, and uniformity of the prepared scaffolds were examined in detail. In addition, biological responses such as effects on bone marrow cell viability, cytotoxicity, and cell adhesion were evaluated in vitro. Biocompatibility and bioactivity properties of the ESFNSs were evaluated in vitro and in vivo by cell culturing and subcutaneous implantation in rat models for 7 and 28 days, respectively. According to the obtained results, no beaded fibers were seen in any of the prepared scaffolds, whereas ESFNS-10% provided more uniformity and porosity with nanoscaled fibers (90 ± 0.021 nm). Furthermore, the scaffolds also showed good cell adhesion and spreading (68.7 ± 11.8 and 7.6 ± 3.3 total length and width, respectively) with no detectable effect on cell viability and cytotoxicity. The in vivo biocompatibility evaluation indicated that the scaffolds did not stimulate detectable cellular inflammatory response (lymphocytes) and increased the total cell number (cellularity) in the implantation area. Furthermore, the results suggest the potential use of the prepared ESFNS-10% bone marrow cell constructs in direct implantation for tissue engineering applications.

Section: Resultsmentioning

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Optimization of nanofibrous silk fibroin scaffold as a delivery system for bone marrow adherent cells: in vitro and in vivo studies

Biotech and App Biochem

Mozafari

Bandehpour

et al. 2015

“…Damaged or dead cells release lactate dehydrogenase (LDH) enzyme into the medium . To evaluate the cytotoxicity effect of the HAp/SF, the culture medium in which the cells were cultured for 24, 48, and 72 H was collected, and LDH activity in the medium was measured with a LDH kit (Zist Shimi kits, Co., Nos.…”

Section: Methodsmentioning

confidence: 99%

In vitro and in vivo evaluations of three‐dimensional hydroxyapatite/silk fibroin nanocomposite scaffolds

Mozafari

Biotech and App Biochem

et al. 2015

In this study, three-dimensional hydroxyapatite/silk fibroin (HAp/SF) nanocomposite scaffolds were successfully prepared through layer solvent casting combined with the freeze-drying technique for tissue engineering applications. Various SF aqueous concentrations, ranging from 2.5% to 10%, were used to control the physicochemical properties of the prepared scaffolds. Biologic responses of the rat bone marrow stromal cells (rBMSCs) to the HAp/SF scaffolds were examined by culturing the cells within them. In addition, biodegradation and biocompatibility of the scaffolds were evaluated in vitro and in vivo, respectively. Among the prepared scaffolds, HAp/SF-2.5% was the most brittle sample and showed porous structure with lowest mechanical properties. The average pore diameters were 350 ± 67 and 112 ± 89 µm and decreased with the increase in the SF concentration from 5% to 10%, respectively. The pores formed in the scaffolds, made up of the 5% SF, were more uniform and regular than those of the scaffolds made up of 5% and 10% SF. The HAp/SF scaffolds did not change the rBMSCs viability and were not cytotoxic compared with the control sample. The scanning electron microscopy micrographs showed that the cells migrated into the pores and well attached to the scaffolds and their cytoplasm was extended in all directions, indicating a promising cell adhesion, high biocompatibility, and no cytotoxicity of the HAp/SF-5% nanocomposite scaffolds. Subcutaneous implantation of the HAp/SF-5% scaffolds in rat models suggested an excellent biocompatibility. All data obtained from this study suggest the potential use of the HAp/SF-5% for hard tissue engineering.

J Biochem & Molecular Tox

“…For evaluation of MeHg‐induced cell membrane impairment, LDH release was measured according to the 2,4‐dinitrobenzene hydrazine methods as previously described. [ 35 ] In brief, cells were incubated with 0, 0.25, 0.5, or 1 μM MeHgCl for 1–6 h. The LDH leakage was then measured with an analysis kit according to the manufacturer's instructions. The absorbance was measured at 440 nm by a microplate reader, following the LDH activity quantification.…”

Section: Methodsmentioning

confidence: 99%

Unbalanced ER‐mitochondrial calcium homeostasis promotes mitochondrial dysfunction and associated apoptotic pathways activation in methylmercury exposed rat cortical neurons

Pan

Wei

et al. 2022

Methylmercury (MeHg) is a cumulative environmental pollutant that can easily cross the blood–brain barrier and cause damage to the brain, mainly targeting the central nervous system. The purpose of this study is to investigate the role of calcium ion (Ca2+) homeostasis between the endoplasmic reticulum (ER) and mitochondria in MeHg‐induced neurotoxicity. Rat primary cortical neurons exposed to MeHg (0.25–1 μm) underwent dose‐dependent cell damage, accompanied by increased Ca2+ release from the ER and elevated levels of free Ca2+ in cytoplasm and mitochondria. MeHg also increased the protein and messenger RNA expressions of the inositol 1,4,5‐triphosphate receptor, ryanodine receptor 2, and mitochondrial calcium uniporter. Ca2+ channel inhibitors 2‐aminoethyl diphenylborinate and procaine reduced the release of Ca2+ from ER, while RR and 4,4′‐diisothiocyanatostilbene‐2,2′‐disulfonate inhibited Ca2+ uptake from mitochondria. In addition, pretreatment with Ca2+ chelator BAPTA‐AM effectively restored mitochondrial membrane potential levels, inhibited over opening of mitochondrial permeability transition pore, and maintained mitochondrial function stability. Meanwhile, the expression of mitochondrial apoptosis‐related proteins recovered to some extent, along with the reduction of the early apoptosis ratio. These results suggest that Ca2+ homeostasis plays an essential role in mitochondrial damage and apoptosis induced by MeHg, which may be one of the important mechanisms of MeHg‐induced neurotoxicity.