Recently, various attempts have been made to apply diverse types of nanoparticles in biotechnology. Silica nanoparticles (SNPs) have been highlighted and studied for their selective accumulation in diseased parts, strong physical and chemical stability, and low cytotoxicity. SNPs, in particular, are very suitable for use in drug delivery and bioimaging, and have been sought as a treatment for ischemic diseases. In addition, mesoporous silica nanoparticles have been confirmed to efficiently deliver various types of drugs owing to their porous structure. Moreover, there have been innovative attempts to treat ischemic diseases using SNPs, which utilize the effects of Si ions on cells to improve cell viability, migration enhancement, and phenotype modulation. Recently, external stimulus-responsive treatments that control the movement of magnetic SNPs using external magnetic fields have been studied. This review addresses several original attempts to treat ischemic diseases using SNPs, including particle synthesis methods, and presents perspectives on future research directions.

BACKGROUND: Various methods based on gold nanoparticles (AuNPs) have been applied to enhance the photothermal effect. Among these methods, combining gold nanoparticles and stem cells has been suggested as a new technique for elevating the efficiency of photothermal therapy (PT) in terms of enhancing tumor targeting effect. However, to elicit the efficiency of PT using gold nanoparticles and stem cells, delivering large amounts of AuNPs into stem cells without loss should be considered. METHODS: AuNPs, AuNPs-decorated silica nanoparticles, and silica-capped and AuNPs-decorated silica nanoparticles (SGSs) were synthesized and used to treat human mesenchymal stem cells (hMSCs). After evaluating physical properties of each nanoparticle, the concentration of each nanoparticle was estimated based on its cytotoxicity to hMSCs. The amount of AuNPs loss from each nanoparticle by exogenous physical stress was evaluated after exposing particles to a gentle shaking. After these experiments, in vitro and in vivo photothermal effects were then evaluated. RESULTS: SGS showed no cytotoxicity when it was used to treat hMSCs at concentration up to 20 lg/mL. After intravenous injection to tumor-bearing mice, SGS-laden hMSCs group showed significantly higher heat generation than other groups following laser irradiation. Furthermore, in vivo photothermal effect in the hMSC-SGS group was significantly enhanced than those in other groups in terms of tumor volume decrement and histological outcome. CONCLUSION Our results suggest that additional silica layer in SGSs could protect AuNPs from physical stress induced AuNPs loss. The strategy applied in SGS may offer a prospective method to improve PT.

Background: Transforming growth factor beta 1 (TGFβ1) plays an essential role in maintaining cartilage homeostasis. TGFβ1 is known to upregulate anabolic processes in articular cartilage, but the role of TGFβ1 in chondrocyte catabolism remains unclear. Thus, we examined whether TGFβ1 increases catabolic processes in the osteoarthritic joint via transglutaminase 2 (TG2). In this study, we investigated whether interplay between TGFβ1 and TG2 mediates chondrocyte catabolism and cartilage degeneration in osteoarthritis. Methods: To investigate the role of TGFβ1 and TG2 in osteoarthritis, we performed immunostaining to measure the levels of TGFβ1 and TG2 in 6 human non-osteoarthritic and 16 osteoarthritic joints. We conducted quantitative reverse transcription polymerase chain reaction and western blot analysis to investigate the relationship between TGFβ1 and TG2 in chondrocytes and determined whether TG2 regulates the expressions of matrix metalloproteinase (MMP)-13, type II, and type X collagen. We also examined the extent of cartilage degradation after performing anterior cruciate ligament transection (ACLT) and destabilization of the medial meniscus (DMM) surgery in TG2 knock-out mice. Results: We confirmed the overexpression of TGFβ1 and TG2 in human osteoarthritic cartilage compared with non-osteoarthritic cartilage. TGFβ1 treatment significantly increased the expression of TG2 via p38 and ERK activation. TGFβ1-induced TG2 also elevated the level of MMP-13 and type X collagen via NF-κB activation in chondrocytes. Cartilage damage after ACLT and DMM surgery was less severe in TG2 knock-out mice compared with wild-type mice. Conclusion TGFβ1 modulated catabolic processes in chondrocytes in a TG2-dependent manner. TGFβ1-induced TG2 might be the therapeutic target for treating cartilage degeneration and osteoarthritis.

Background: Transforming growth factor beta 1 (TGFβ1) plays an essential role in maintaining cartilage homeostasis. TGFβ1 is known to upregulate anabolic processes in articular cartilage, but the role of TGFβ1 in chondrocyte catabolism remains unclear. Thus, we examined whether TGFβ1 increases catabolic processes in the osteoarthritic joint via transglutaminase 2 (TG2). In this study, we investigated whether interplay between TGFβ1 and TG2 mediates chondrocyte catabolism and cartilage degeneration in osteoarthritis. Methods: To investigate the role of TGFβ1 and TG2 in osteoarthritis, we performed immunostaining to measure the levels of TGFβ1 and TG2 in 6 human non-osteoarthritic and 16 osteoarthritic joints. We conducted quantitative reverse transcription polymerase chain reaction and western blot analysis to investigate the relationship between TGFβ1 and TG2 in chondrocytes and determined whether TG2 regulates the expressions of matrix metalloproteinase (MMP)-13, type II, and type X collagen. We also examined the extent of cartilage degradation after performing anterior cruciate ligament transection (ACLT) and destabilization of the medial meniscus (DMM) surgery in TG2 knock-out mice. Results: We confirmed the overexpression of TGFβ1 and TG2 in human osteoarthritic cartilage compared with non-osteoarthritic cartilage. TGFβ1 treatment significantly increased the expression of TG2 via p38 and ERK activation. TGFβ1-induced TG2 also elevated the level of MMP-13 and type X collagen via NF-κB activation in chondrocytes. Cartilage damage after ACLT and DMM surgery was less severe in TG2 knock-out mice compared with wild-type mice. Conclusion TGFβ1 modulated catabolic processes in chondrocytes in a TG2-dependent manner. TGFβ1-induced TG2 might be the therapeutic target for treating cartilage degeneration and osteoarthritis.

Purpose: Nutritional status and support in critically ill patients are important factors in determining patient recovery and prognosis.The aim of this study was to analyze the early nutritional status and the methods of nutritional support in critically ill patients with acute poisoning and to evaluate the effect of nutritional status on prognosis. Methods: A retrospective study was conducted in tertiary care teaching hospital from January 2018 to December 2020. in an emergency department of university hospital, 220 patients who were stayed more than 2 days of poisoning in intensive care unit were enrolled. Results: 155 (70.5%) of patients with acute poisoning had low-risk in nutritional risk screening (NRS). Patients with malignancy had higher NRS (low risk 5.2%, moderate risk 18.5%, high risk 13.2%, p=0.024). Patients of 91.4% supplied nutrition via oral route or enteral route. Parenteral route for starting method of nutritional support were higher in patients with acute poisoning of herbicide or pesticide (medicine 3.2%, herbicide 13.8%, pesticide 22.2%, p=0.000). In multivariate logistic regression analysis, herbicide or pesticide intoxication, higher risk in NRS and sequential organ failure assessment over 4.5 were affecting factor on poor recovery at discharge. Conclusion NRS in patients intoxicated with herbicide or pesticide were higher than that in patients intoxicated with medicine intoxication. Enteral nutrition in patients intoxicated with herbicide or pesticide was less common. Initial NRS was correlated with recovery at discharge in patient with intoxication. It is expected to be helpful in finding patients with high-risk nutritional status in acute poisoning patients and establishing a treatment plan that can actively implement nutritional support.

Background: Endoscope-assisted surgery is a surgical method that has been used in oral and maxillofacial surgical fields. It provides good illumination, clear, and magnified visualization of the operative field. The purpose of this article is to describe the early clinical experiences to conduct minimally invasive surgery with endoscope-assisted enucleation of cysts on the jaw. It appears that this approach may be a superior alternative to the conventional approach. Methods: In this study, 24 patients (9 females, 15 males, average age 41.5) underwent endoscope-assisted cyst enucleation under general anesthesia. All operations were done by one surgeon. The cases were classified depending on whether bone penetration occurred at the cyst site. The cystic lesions were enucleated using an endoscope with a 0°, 1.9 mm diameter, or a 30°, 2.7 mm diameter. Two bony windows were used for the insertion of a syringe for irrigation, curettes, suction tips, sinus blades, surgical drills, and an endoscope. An additional small channel was made for the insertion of endoscopic instruments. Results: The 24 patients who underwent cyst enucleation were regularly observed for 3 to 12 months to evaluate for complications. Although some patients experienced swelling and numbness, these symptoms did not persist, and the patients soon returned to normal and there was no sign of recurrence. Conclusions The results of this study have suggested the possibility of minimally invasive surgery with endoscopes when it comes to cyst removal in the oral and maxillofacial region. Nevertheless, this study has limitations designed as a preliminary report focusing on the feasibility of endoscope-assisted cyst enucleation in the oral and maxillofacial regions.

BACKGROUND: Mannitol increases blood–brain barrier permeability and can improve the efficiency of systemically administered stem cells by facilitating stem cell entry from the periphery into the injured brain. The aim of this study was to elucidate the neuroprotective effects of a combination of mannitol pretreatment and stem cell transplantation on strokeinduced neural injury. METHODS: The experimental rats were randomly assigned to three groups 24 h after middle cerebral artery occlusion and reperfusion. One group received intravenous (IV) injections of phosphate-buffered saline (vehicle), another group received IV injections of human adipose-derived stem cells (hADSCs), and the last group received IV injections of hADSCs 10 min after IV mannitol injections. Neurobehavioral functions and infarct volume were compared. Immunohistochemistry (IHC) analyses were performed using antibodies against ionized calcium binding adapter-1 (IBA-1), rat endothelial antigen-1 (RECA-1), and bromodeoxyuridine/doublecortin (BrdU/DCX). RESULTS: PKH-26 labeling revealed no difference in the number of stem cells that had migrated into the injured brain, and hADSC transplantation did not improve the infarct volume. However, neurobehavioral functions improved in the mannitol group. IHC showed higher numbers of RECA-1-positive cells in the peri-infarcted brain and BrdU-/DCXcolocalized cells in the subventricular zone in the mannitol group. IBA-1-positive cell number decreased in the hADSConly and mannitol-pretreatment groups compared with the vehicle group even though there was no difference between the former two groups. CONCLUSION Combinatorial treatment with mannitol and hADSC transplantation may have better therapeutic potential than hADSC monotherapy for ischemic stroke.

BACKGROUND: Mannitol increases blood–brain barrier permeability and can improve the efficiency of systemically administered stem cells by facilitating stem cell entry from the periphery into the injured brain. The aim of this study was to elucidate the neuroprotective effects of a combination of mannitol pretreatment and stem cell transplantation on strokeinduced neural injury. METHODS: The experimental rats were randomly assigned to three groups 24 h after middle cerebral artery occlusion and reperfusion. One group received intravenous (IV) injections of phosphate-buffered saline (vehicle), another group received IV injections of human adipose-derived stem cells (hADSCs), and the last group received IV injections of hADSCs 10 min after IV mannitol injections. Neurobehavioral functions and infarct volume were compared. Immunohistochemistry (IHC) analyses were performed using antibodies against ionized calcium binding adapter-1 (IBA-1), rat endothelial antigen-1 (RECA-1), and bromodeoxyuridine/doublecortin (BrdU/DCX). RESULTS: PKH-26 labeling revealed no difference in the number of stem cells that had migrated into the injured brain, and hADSC transplantation did not improve the infarct volume. However, neurobehavioral functions improved in the mannitol group. IHC showed higher numbers of RECA-1-positive cells in the peri-infarcted brain and BrdU-/DCXcolocalized cells in the subventricular zone in the mannitol group. IBA-1-positive cell number decreased in the hADSConly and mannitol-pretreatment groups compared with the vehicle group even though there was no difference between the former two groups. CONCLUSION Combinatorial treatment with mannitol and hADSC transplantation may have better therapeutic potential than hADSC monotherapy for ischemic stroke.

BACKGROUND: Although microfracture is widely accepted as an effective treatment option for knee chondral lesions, little is known about the deterioration of clinical outcomes and radiological progression in middle-aged patients. Therefore, this study was conducted to evaluate the clinical and radiological changes after microfracture of knee chondral lesions in middle-aged Asian patients. METHODS: A total of 71 patients were included in the study. They were between the ages of 40 and 60 years and underwent arthroscopic microfracture for localized full-thickness cartilage defects of the knee from January 2000 to September 2015. The recovery status of chondral lesions was assessed by using the magnetic resonance observation of cartilage repair tissue (MOCART) score in postoperative magnetic resonance imaging (MRI). Clinical and radiological results were reviewed, and survival rate with conversion to arthroplasty or osteotomy as an end point was evaluated. RESULTS: The mean age of the patients at surgery was 51.3 ± 4.7 years (range, 40 to 60 years), and the mean follow-up period was 7.2 ± 2.6 years (range, 1.0 to 17.4 years). The MOCART scores of 32 patients at mean postoperative 2.1 years showed three cases (9%) of full recovery, two cases (7%) of hyperplastic recovery, 23 cases (70%) with more than 50% filling, and four cases (14%) with less than 50% filling. Clinical scores improved significantly at 1 year after surgery (p < 0.05); however, the scores deteriorated over time after postoperative 1 year, and the mean values reached preoperative levels at postoperative 10 years. Significant radiological progression of arthritis (Kellgren-Lawrence grade) was observed at 5 years after surgery. Four patients underwent total knee arthroplasty during follow-up. CONCLUSIONS: Most patients showed more than 50% of defect filling at 2 years after surgery on MRI. Clinical results of microfracture of knee chondral lesion showed the best improvement at postoperative 1 year but gradually worsened thereafter until postoperative 10 years. Radiological progression of arthritis was observed from 5 years after surgery.
Arthritis ; Arthroplasty ; Arthroplasty, Replacement, Knee ; Asian Continental Ancestry Group ; Cartilage ; Follow-Up Studies ; Humans ; Knee ; Magnetic Resonance Imaging ; Osteotomy ; Survival Rate ; Treatment Outcome