Does the proximal humeral bone quality influence alignment after reverse total shoulder arthroplasty with short humeral stems?

PURPOSE: When compared to standard-length humeral stem in reverse total shoulder arthroplasty (RTSA), short humeral stems in RTSA require good proximal humeral metaphyseal bone quality to gain proper and secure fixation during prosthetic implantation. Shorter humeral stems potentially carry more risk of misalignment than standard or long humeral stems. The hypothesis was that misalignment of the short humeral stems is influenced by regional bone quality. METHODS: RTSA with a short curved humeral stem with neck-shaft angle (NSA) default of 132.5° was reviewed. The study group included 35 cases at a mean age of 75.97 (± 6.23) years. Deltoid-tuberosity index (DTI) was measured to evaluate proximal humeral bone quality. The deltoid tuberosity index was measured at immediately above position of the upper end of the deltoid tuberosity. Stem alignment was given by the angle measured in degrees between the intramedullary humeral shaft axis and the axis of the humeral implant stem. RESULTS: The patient's mean DTI was 1.37 ± 0.16 (median, 1.32; range, 1.12-1.80). 22 patients had poor bone quality (DTI < 1.4), compared to 13 patients with acceptable bone quality (DTI > 1.4). After RTSA, ten humeral components (29%) were neutrally aligned, whereas 25 humeral components (71%) were misaligned. There was no correlation between misalignment and DTI (r = 0.117; p = 0.504). But there was a strong correlation between misalignment and the patient's own NSA (r = - 0.47; p = 0.004). The postoperative stem position and stem misalignment are not associated with functional outcomes (p > 0.05). CONCLUSION: The misalignment of the short curved humeral stem frequently occurs. Poor reginal humeral bone quality does not influence misalignment after RTSA with a short humeral stem. Postoperative stem alignment is associated with the patient's preoperative NSA and method of neck cut. The misalignment does not affect functional outcomes for midterm follow-up. Further long-term follow-up studies are needed to confirm its clinical relevance.

Programmed Death Ligand 1 Regulatory Crosstalk with Ubiquitination and Deubiquitination: Implications in Cancer Immunotherapy.

Programmed death ligand 1 (PD-L1) plays a pivotal role in cancer immune evasion and is a critical target for cancer immunotherapy. This review focuses on the regulation of PD-L1 through the dynamic processes of ubiquitination and deubiquitination, which are crucial for its stability and function. Here, we explored the intricate mechanisms involving various E3 ubiquitin ligases and deubiquitinating enzymes (DUBs) that modulate PD-L1 expression in cancer cells. Specific ligases are discussed in detail, highlighting their roles in tagging PD-L1 for degradation. Furthermore, we discuss the actions of DUBs that stabilize PD-L1 by removing ubiquitin chains. The interplay of these enzymes not only dictates PD-L1 levels but also influences cancer progression and patient response to immunotherapies. Furthermore, we discuss the therapeutic implications of targeting these regulatory pathways and propose novel strategies to enhance the efficacy of PD-L1/PD-1-based therapies. Our review underscores the complexity of PD-L1 regulation and its significant impact on the tumor microenvironment and immunotherapy outcomes.

Role of Carbohydrate response element-binding protein in mediating dexamethasone-induced glucose transporter 5 expression in Caco-2BBE cells and during the developmental phase in mice.

Glucose transporter 5 (GLUT5), the main fructose transporter in mammals, is primarily responsible for absorbing dietary fructose in the small intestine. The expression of this intestinal gene significantly increases in response to developmental and dietary cues that reach the glucocorticoid receptor and carbohydrate response element-binding protein (ChREBP), respectively. Our study demonstrates that ChREBP is involved in the dexamethasone (Dex)-induced expression of GLUT5 in Caco-2BBE cells and the small intestine of both wild-type and ChREBP-knockout mice. Dex, a glucocorticoid, demonstrated an increase in GLUT5 mRNA levels in a dose- and time-dependent manner. While the overexpression of ChREBP moderately increased GLUT5 expression, its synergistic increase in the presence of Dex was noteworthy, whereas the suppression of ChREBP significantly reduced Dex-induced GLUT5 expression. Dex did not increase ChREBP protein levels but facilitated its nuclear translocation, thereby increasing the activity of the GLUT5 promoter. In vivo experiments conducted on 14-day-old mice pups treated with Dex for three days revealed that only wild-type mice (not ChREBP-knockout mice) exhibited Dex-mediated Glut5 gene induction, which further supports the role of ChREBP in regulating GLUT5 expression. Collectively, our results provide insights into the molecular mechanisms involved in the regulation of GLUT5 expression in response to developmental and dietary signals mediated by glucocorticoids and ChREBP. General significance: The transcription factor ChREBP is important for Dex-mediated Glut5 gene expression in the small intestine.

New Insights into the Role of KLF10 in Tissue Fibrosis.

Fibrosis, characterized by excessive extracellular matrix accumulation, disrupts normal tissue architecture, causes organ dysfunction, and contributes to numerous chronic diseases. This review focuses on Krüppel-like factor 10 (KLF10), a transcription factor significantly induced by transforming growth factor-ß (TGF-ß), and its role in fibrosis pathogenesis and progression across various tissues. KLF10, initially identified as TGF-ß-inducible early gene-1 (TIEG1), is involved in key biological processes including cell proliferation, differentiation, apoptosis, and immune responses. Our analysis investigated KLF10 gene and protein structures, interaction partners, and context-dependent functions in fibrotic diseases. This review highlights recent findings that underscore KLF10 interaction with pivotal signaling pathways, such as TGF-ß, and the modulation of gene expression in fibrotic tissues. We examined the dual role of KLF10 in promoting and inhibiting fibrosis depending on tissue type and fibrotic context. This review also discusses the therapeutic potential of targeting KLF10 in fibrotic diseases, based on its regulatory role in key pathogenic mechanisms. By consolidating current research, this review aims to enhance the understanding of the multifaceted role of KLF10 in fibrosis and stimulate further research into its potential as a therapeutic target in combating fibrotic diseases.

KLF10 Inhibits TGF-ß-Mediated Activation of Hepatic Stellate Cells via Suppression of ATF3 Expression.

Liver fibrosis is a progressive and debilitating condition characterized by the excessive deposition of extracellular matrix proteins. Stellate cell activation, a major contributor to fibrogenesis, is influenced by Transforming growth factor (TGF-ß)/SMAD signaling. Although Krüppel-like-factor (KLF) 10 is an early TGF-ß-inducible gene, its specific role in hepatic stellate cell activation remains unclear. Our previous study demonstrated that KLF10 knockout mice develop severe liver fibrosis when fed a high-sucrose diet. Based on these findings, we aimed to identify potential target molecules involved in liver fibrosis and investigate the mechanisms underlying the KLF10 modulation of hepatic stellate cell activation. By RNA sequencing analysis of liver tissues from KLF10 knockout mice with severe liver fibrosis induced by a high-sucrose diet, we identified ATF3 as a potential target gene regulated by KLF10. In LX-2 cells, an immortalized human hepatic stellate cell line, KLF10 expression was induced early after TGF-ß treatment, whereas ATF3 expression showed delayed induction. KLF10 knockdown in LX-2 cells enhanced TGF-ß-mediated activation, as evidenced by elevated fibrogenic protein levels. Further mechanistic studies revealed that KLF10 knockdown promoted TGF-ß signaling and upregulated ATF3 expression. Conversely, KLF10 overexpression suppressed TGF-ß-mediated activation and downregulated ATF3 expression. Furthermore, treatment with the chemical chaperone 4-PBA attenuated siKLF10-mediated upregulation of ATF3 and fibrogenic responses in TGF-ß-treated LX-2 cells. Collectively, our findings suggest that KLF10 acts as a negative regulator of the TGF-ß signaling pathway, exerting suppressive effects on hepatic stellate cell activation and fibrogenesis through modulation of ATF3 expression. These results highlight the potential therapeutic implications of targeting the KLF10-ATF3 axis in liver fibrosis treatment.

Value of postoperative computed tomography for the diagnosis of lateral hinge fracture in medial opening-wedge supramalleolar osteotomy.

INTRODUCTION: It remains unclear whether computed tomography (CT) is superior to plain radiography in detecting lateral hinge fractures after medial opening-wedge supramalleolar osteotomy (SMO) of the ankle joint. This study aimed to evaluate the disparity between postoperative plain radiography and CT in detecting lateral hinge fractures after medial opening-wedge SMO and to identify the predictive factors of lateral hinge fractures. MATERIALS AND METHODS: This retrospective study included 39 patients who underwent medial opening-wedge SMO. The immediate postoperative plain radiography and CT scan images were retrieved, and the presence of lateral hinge fractures was independently determined. Depending on the fracture gap, the lateral hinge fractures were subclassified as stable (gap < 2 mm) or unstable (gap ≥ 2 mm) fractures. To investigate the predictive factors, the cases were divided based on diagnostic tools such as plain radiography and CT. RESULTS: The incidence of lateral hinge fractures was 48.7% (19/39) on plain radiographs and 61.5% (24/39) on CT scans. Five cases of lateral hinge fractures additionally detected on CT scans were stable fractures, and all had been classified as no fracture on plain radiographs. The unstable fractures that had been subclassified based on plain radiographs did not change on CT scans. None of the variables were associated with the presence of lateral hinge fractures on plain radiographs and CT scans. CONCLUSIONS: Postoperative CT after medial opening-wedge SMO has no additional diagnostic value if the lateral hinge fracture has already been diagnosed on plain radiography. Therefore, postoperative CT is only recommended when lateral hinge fractures are not visible on plain radiographs.

Does stress shielding after radial head arthroplasty affect functional outcomes?

BACKGROUND: Various complications related to the prosthesis, such as implant loosening and stress shielding phenomenon, could develop after prosthetic replacement of the radial head. Stress shielding is known to occur around rigidly fixed implants. The purpose of this study was to evaluate the clinical influence and causative factors of the stress shielding phenomenon after radial head arthroplasty (RHA). METHODS: Clinical records and radiographs of 56 patients with unreconstructable radial head fractures who received radial head replacement between 2009 and 2019 were reviewed. Exclusion criteria were infection, loosening, and follow-up of less than 24 months. After exclusion, 35 patients were enrolled. Patients were divided into two groups: an anatomical press-fit group (Anatomical Radial Head System; Acumed, Hillsboro, OR, USA) and a round bipolar cemented group (RHS; Tornier, Montbonnot Saint-Martin, France). Stress shielding around the prosthesis was assessed in the serial radiological examination. Clinical results were assessed using Mayo elbow performance score (MEPS), Quick Disabilities of the Arm, Shoulder, and Hand (q-DASH) score, range of motion (flexion-extension arc and pronation-supination arc), and visual analog scale score (VAS). Correlations between stress shielding phenomenon and demographic data and functional results were analyzed. RESULTS: At an average follow-up of 43.06 (± 14.6) months, 14 (40%) out of 35 fixed stems demonstrated stress shielding. Our results showed that the rate of stress shielding was significantly higher in cases with a bilateral ligament injury and in the anatomical press-fit group (p = 0.028 and p = 0.0091, respectively). However, stress shielding around prostheses did not affect the clinical results (p > 0.05). CONCLUSION: The stress shielding phenomenon around radial head prosthesis may vary according to prosthetic design and severity of ligament injuries. Stress shielding does not affect the mid-term outcomes in the treatment of acute fractures of the radial head. LEVEL OF EVIDENCE III: Retrospective Cohort Comparison; Treatment Study.

MsrB1-regulated GAPDH oxidation plays programmatic roles in shaping metabolic and inflammatory signatures during macrophage activation.

Classically activated pro-inflammatory macrophages are generated from naive macrophages by pro-inflammatory cues that dynamically reprogram their fuel metabolism toward glycolysis. This increases their intracellular reactive oxygen species (ROS) levels, which then activate the transcription and release of pro-inflammatory mediators. Our study on mice that lack methionine sulfoxide reductase (Msr)-B1 shows that the resulting partial loss of protein methionine reduction in pro-inflammatory macrophages creates a unique metabolic signature characterized by altered fuel utilization, including glucose and pyruvate. This change also associates with hyper-inflammation that is at least partly due to sustained oxidation of an exposed methionine residue (M44) on glyceraldehyde 3-phosphate dehydrogenase (GAPDH), thereby inducing GAPDH aggregation, inflammasome activation, and subsequent increased interleukin (IL)-1ß secretion. Since MsrB1-knockout mice exhibit increased susceptibility to lipopolysaccharide (LPS)-induced sepsis, the MsrB1-GAPDH axis may be a key molecular mechanism by which protein redox homeostasis controls the metabolic profile of macrophages and thereby regulates their functions.

Flexion-extension-supination test compared to arthroscopic findings of biceps long head pathology: A physical examination that reflect anatomical evolution of human shoulder girdle.

The accuracy of physical examination for diagnosing lesions of the long head of the biceps tendon (LHBT) remains unsatisfactory. The purpose of this study was to describe a new diagnostic test, the Flexion-Extension-Supination (FES) test for diagnosing lesions of the long head of biceps tendon. A prospective study of 162 patients was performed to evaluate the diagnostic value of FES test. All the participants were evaluated on the basis of their clinical presentation, physical examination (FES test), radiologic findings and arthroscopic examination. Shoulder arthroscopy findings were used as the gold standard. To reduce the omission of the hidden lesion, LHBT was checked at the intra- and the extraarticular side via arthroscopic examination. Surgical findings related to biceps pathology were as follows: rotator cuff tears, 89.5% (145/162); subacromial impingement, 8.6% (14/162); and biceps tendinitis, 1.9% (3/162). The prevalence of biceps pathology was 77.2% (125/162) of all arthroscopic procedures. No significant differences for LHBT lesions were observed between the FES test and the arthroscopic findings (P = .850). The interrater reliability of the FES test was 0.747. After excluding inconclusive results between examiners, the sensitivity, specificity, positive predictive value, and negative predictive value of the FES test were 87.9%, 66.7%, 82.9%, and 63.2%, respectively. Positive and negative likelihood ratios were 2.67 and 0.18, respectively. The maneuvers of the FES test irritate intra- and extraarticular lesion of LHBT. The FES test is a reproducible and reliable test that can be used during physical examinations to evaluate patients with LHBT lesions.

Biosensor-Linked Immunosorbent Assay for the Quantification of Methionine Oxidation in Target Proteins.

Methionine oxidation is involved in regulating the protein activity and often leads to protein malfunction. However, tools for quantitative analyses of protein-specific methionine oxidation are currently unavailable. In this work, we developed a biological sensor that quantifies oxidized methionine in the form of methionine-R-sulfoxide in target proteins. The biosensor "tpMetROG" consists of methionine sulfoxide reductase B (MsrB), circularly permuted yellow fluorescent protein (cpYFP), thioredoxin, and protein G. Protein G binds to the constant region of antibodies against target proteins, specifically capturing them. Then, MsrB reduces the oxidized methionine in these proteins, leading to cpYFP fluorescence changes. We assessed this biosensor for quantitative analysis of methionine-R-sulfoxide in various proteins, such as calmodulin, IDLO, LegP, Sacde, and actin. We further developed an immunosorbent assay using the biosensor to quantify methionine oxidation in specific proteins such as calmodulin in animal tissues. The biosensor-linked immunosorbent assay proves to be an indispensable tool for detecting methionine oxidation in a protein-specific manner. This is a versatile tool for studying the redox biology of methionine oxidation in proteins.

Association Between Overweight Sarcopenic Population and Acute Vertebral Osteoporotic Compression Fractures in Females: Retrospective, Cross-Sectional Study.

Background: This study aimed to determine whether the prevalence of acute vertebral osteoporotic compression fractures (VOCF) in the elderly population is related to the distribution of muscles and fat in the human body. Methods: Data of acute VOCF and non-VOCF patients presenting at our institution between January 2018 and May 2020 were analyzed. Patients aged 65 years and older, who underwent body composition test and dual-energy X-ray absorptiometry at the same time were enrolled. After applying exclusion criteria, patients were divided into four groups: normal, sarcopenia without obesity, obesity without sarcopenia, and sarcopenic obesity. Body mass index ≥25 kg/m2 was considered obesity, and sarcopenia was defined as skeletal muscle index lower than 7.0 kg/m2 in males and 5.4 kg/m2 in females. The VOCF rate was analyzed between the groups. Discussion: A total of 461 patients were included, of whom 103 were males. Among them, 163 (35.36%) had normal body composition, 151 (32.75%) had sarcopenia without obesity, 110 (23.86%) had obesity without sarcopenia, and 37 (8.03%) had sarcopenic obesity. The sarcopenic obesity group had the highest rate of acute VOCF (37.8%), which was statistically significant. Specifically, females with sarcopenic obesity and sarcopenia without obesity had significantly higher acute VOCF rates compared to those with normal body compositions. Multivariate analysis showed that sarcopenic obesity was significantly associated with acute VOCF rate overall, as well as in females. Conclusion: Sarcopenic obesity is strongly associated with acute VOCF, especially in females, and it could be an essential criterion for the prevention of acute VOCF.

X-ray CT Analysis of the Cross-Section of a 3D-Printed Deformed Layer.

In this study, we experimentally analyzed the deformation shape of stacked layers developed using three-dimensional (3D) printing technology. The nozzle traveling speed was changed to 80, 90, 100, and 110 mm/s when printing the layers to analyze its effect on layer deformation. Furthermore, the cross-sectional area and the number of layers were analyzed by printing five layers with overall dimensions of 1000 (w) × 2200 (l) × 50 (h) mm (each layer was 10 mm high) using Vernier calipers. Moreover, we analyzed the interface and cross-sectional area of layers that are difficult to confirm visually using X-ray computed tomography (X-ray CT) analysis. As a result of measuring the deformation at the center of the layer, it was confirmed that the deformation was greater for lower nozzle traveling speeds. Consequently, the X-ray CT analysis verified that the layer had the same cross-sectional area irrespective of the layer printing order at the same nozzle travel speed, even if the layer was deformed.

Comparison of the Probiotic Potential between Lactiplantibacillus plantarum Isolated from Kimchi and Standard Probiotic Strains Isolated from Different Sources.

In the present study, the properties of the Lactiplantibacillus (Lpb.) plantarum WiKim0112 isolated from kimchi were evaluated by comparing its probiotic properties to those of Lpb. plantarum WCFS1 and KACC 11451 isolated from different sources. In both pH 2 and 3, media containing pepsin, Wikim0112, and WCFS1 showed higher cell viability than KACC11451. Viability of all Lpb. plantarum strains in a medium containing pancreatin and bile salt oxgall was significantly decreased compared to the control. WCFS1 showed the highest thermotolerance, followed by Wikim0112 and KACC11451. Wikim0112 showed a similar level of antibacterial activity to WCFS1 and exhibited an overall higher antibacterial activity than KACC11451 against six pathogens. All Lpb. plantatum strains showed high antioxidant activities in SOD, DPPH, and ABTS assays, especially Wikim0112 and WCFS1 exhibited a higher antioxidant activity than KACC11451. All Lpb. plantarum strains showed approximately 60-62% adhesion rates to Caco-2 cells. Moreover, in LPS-stimulated Caco-2 cells, all Lpb. plantarum strains significantly decreased the mRNA expression of pro-inflammatory cytokines (i.e., IL-1ß, IL-6, and TNF-α); Wikim0112 significantly increased the mRNA expression of IL-4 and IFN-γ. Wikim0112 was resistant to streptomycin and vancomycin, whereas WCFS1 and KACC11451 were resistant to four (clindamycin, ciprofloxacin, tetracycline, and vancomycin) and three (ciprofloxacin, tetracycline, and vancomycin) antibiotics, respectively. These results, taken together, indicated that compared to Lpb. plantarum strains isolated from different sources, Wikim0112 showed desirable probiotic properties, suggesting its potential applications in the food and pharmaceutical industries.

Nicotinamide Riboside Vitamin B3 Mitigated C26 Adenocarcinoma-Induced Cancer Cachexia.

Nicotinamide riboside (NR), vitamin B3, is a substrate for nicotinamide adenine dinucleotide (NAD+)-consuming enzymes and is a coenzyme for hydride-transfer enzymes, including adenosine diphosphate (ADP)-ribose transferases, poly (ADP-ribose) polymerases, cADP-ribose synthases, and sirtuins, which play a central role in the aging process, neurodegenerative processes, and myopathy. Since cancer cachexia is a disease condition presenting with weight loss, skeletal muscle atrophy, and loss of adipose tissue in patients with advanced cancer, we hypothesized that NR intake could ameliorate sarcopenia. In this study, we investigated whether preemptive administration of NR ameliorated C26 adenocarcinoma-induced cancer cachexia and explored anti-cachexic mechanisms focused on the changes in muscle atrophy, cachexic inflammation, and catabolic catastrophe. Dietary intake of the NR-containing pellet diet significantly attenuated cancer cachexia in a mouse model. Starting with significant inhibition of cachexic factors, tumor necrosis factor alpha, and interleukin-6, NR significantly inhibited muscle-specific ubiquitin-proteasome ligases, such as atrogin-1, muscle RING-finger protein-1 (MuRF-1), mitofusin-2, and peroxisome proliferator-activated receptor gamma coactivator-1-alpha (PCG-1α). Significant inhibition of epididymal fat lipolysis was noted with significant inhibition of adipose triglyceride lipase (ATGL) gene. Furthermore, NR administration significantly increased the levels of crucial enzymes involved in the biosynthesis of NAD+ and nicotinamide phosphoribosyl transferase and significantly inhibited the NAD+-sensitive deacetylase sirtuin 1 (SIRT1). Preemptive intake of NR in patients vulnerable to cachexia can be a preemptive option to ameliorate cancer cachexia.

Transcriptome profiling analysis of the response to walnut polyphenol extract in Helicobacter pylori-infected cells.

Dietary intervention to prevent Helicobacter pylori (H. pylori)-associated gastric diseases seems to be ideal with no risk of bacterial resistance, safe long-term intervention, and correcting pathogenic mechanisms including rejuvenation of precancerous atrophic gastritis and anti-mutagenesis. A transcriptome as set of all RNAs transcribed by certain tissues or cells demonstrates gene functions and reveals the molecular mechanism of specific biological processes against diseases. Here, we have performed RNAseq and bioinformatic analysis to explain proof of concept that walnut intake can rescue from H. pylori infection and explore unidentified mode of actions of walnut polyphenol extract (WPE). As results, BIRC3, SLC25A4, f3 transcription, VEGFA, AZU1, HMOX1, RAB3A, RELBTNIP1, ETFB, INPP5J, PPME1, RHOB, TPI1, FOSL1, JUND.RELB, KLF2, MUC1, NDRG1, ALDOA, ENO1, PFKP, GPI, GDF15, and NRTN genes were newly discovered to be enriched with WPE, whereas CCR4, BLNK, CCR7, CXCR4, CDO1, KLSG1, SELE, RASGRP2, PIK3R3, TSPAN32, HOXC-AS3, HCG8, BTNL8, and CXCL3 genes as inhibitory targets by WPE in H. pylori infection. We identified additional genes what WPE afforded actions of avoiding H. pylori-driven onco-inflammation and rejuvenating precancerous atrophic gastritis. Conclusively, after applying RNAseq analysis in order to document walnut intake for precision medicine against H. pylori infection, significant transcriptomic profiling applicable for validation were drawn.

The Selenoprotein MsrB1 Instructs Dendritic Cells to Induce T-Helper 1 Immune Responses.

Immune activation associates with the intracellular generation of reactive oxygen species(ROS). To elicit effective immune responses, ROS levels must be balanced. Emerging evidenceshows that ROS-mediated signal transduction can be regulated by selenoproteins such asmethionine sulfoxide reductase B1 (MsrB1). However, how the selenoprotein shapes immunityremains poorly understood. Here, we demonstrated that MsrB1 plays a crucial role in the ability ofdendritic cells (DCs) to provide the antigen presentation and costimulation that are needed forcluster of differentiation antigen four (CD4) T-cell priming in mice. We found that MsrB1 regulatedsignal transducer and activator of transcription-6 (STAT6) phosphorylation in DCs. Moreover, bothin vitro and in vivo, MsrB1 potentiated the lipopolysaccharide (LPS)-induced Interleukin-12 (IL-12)production by DCs and drove T-helper 1 (Th1) differentiation after immunization. We propose thatMsrB1 activates the STAT6 pathway in DCs, thereby inducing the DC maturation and IL-12production that promotes Th1 differentiation. Additionally, we showed that MsrB1 promotedfollicular helper T-cell (Tfh) differentiation when mice were immunized with sheep red blood cells.This study unveils as yet unappreciated roles of the MsrB1 selenoprotein in the innate control ofadaptive immunity. Targeting MsrB1 may have therapeutic potential in terms of controllingimmune reactions.

Vertical Interfragmentary Doubled Suture for Displaced Patella Fractures: Sequential Compressive Tightening with Nice Knot.

In the treatment of displaced patella fractures, open reduction and internal fixation is essential for patellofemoral congruency and restoration of the knee extension mechanism. Various surgical techniques and materials can be used, and their clinical outcomes are favorable. However, soft-tissue and skin irritation, pain, and limited range of motion due to metallic hardware can occur, and removal of hardware such as screws and K-wire may be required after bony union. We present a vertical interfragmentary suture technique for patella fractures using sequential compressive tightening with the Nice knot. This knot-tying technique is low profile, provides stable fixation enough to hold displaced fractures, and does not require a secondary procedure for hardware removal.

Selection and Characterization of Staphylococcus hominis subsp. hominis WiKim0113 Isolated from Kimchi as a Starter Culture for the Production of Natural Pre-converted Nitrite.

Synthetic nitrite is considered an undesirable preservative for meat products; thus, controlling synthetic nitrite concentrations is important from the standpoint of food safety. We investigated 1,000 species of microorganisms from various kimchi preparations for their potential use as a starter culture for the production of nitrites. We used 16S rRNA gene sequence analysis to select a starter culture with excellent nitrite and nitric oxide productivity, which we subsequently identified as Staphylococcus hominis subspecies hominis WiKim0113. That starter culture was grown in NaCl (up to 9%; w/v) at 10°C-40°C; its optimum growth was observed at 30°C at pH 4.0-10.0. It exhibited nonproteolytic activity and antibacterial activity against Clostridium perfringens, a bacterium that causes food poisoning symptoms. Analysis of Staphylococcus hominis subspecies hominis WiKim0113 with an API ZYM system did not reveal the presence of ß-glucuronidase, and tests of the starter culture on 5% (v/v) sheep blood agar showed no hemolytic activity. Our results demonstrated the remarkable stability of coagulase-negative Staphylococcus hominis subspecies hominis WiKim0113, especially in strain negative for staphylococcal enterotoxins and sensitive to clinically relevant antibiotics. Moreover, Staphylococcus hominis subspecies hominis WiKim0113 exhibited a 45.5% conversion rate of nitrate to nitrite, with nitrate levels reduced to 25% after 36 h of culturing in the minimal medium supplemented with nitrate (200 ppm). The results clearly demonstrated the safety and utility of Staphylococcus hominis subspecies hominis WiKim0113, and therefore its suitability as a starter culture.

Dolichos lablab L. extracts as pharmanutrient for stress-related mucosal disease in rat stomach.

Gastric stress-related mucosal disease (SRMD) presented from superficial gastritis to deep ulceration consequent to insufficient perfusion, ischemia, and oxidative stress. Though pharmacologic interventions to optimize tissue perfusion or to enhance defensive mechanism are essential, limited clinical outcome necessitates strong acid suppressors or natural agents. Under the hypothesis that Dolichos lablab L. (NKM 23-1) can enhance defense against SRMD, water immersion restraint stress (WIRS) were imposed to rats and additional groups pretreated with differing doses of NKM 23-1 were monitored. On gross and microscopic evaluation, they significantly rescued SRMD (p<0.01). The levels of inflammatory mediators such as IL-18, IL-1ß, IL-8, iNOS, TNF-α, caspase-1, NOXs as well as MMPs accompanied with NF-κB p50 activation were all significantly increased in WIRS, but their levels were significantly decreased in Groups pretreated with NKM 23-1. WIRS significantly increased apoptosis, but significantly decreased with NKM 23-1 accompanied with significantly increased levels of cyclin D/E and HSP70/HSP27. Gastric mucin was significantly preserved in Groups pretreated with NKM 23-1, while depleted in WIRS, accompanied with increased expressions of Muc5A. Gastric levels of HO-1 and NQO1 were significantly increased in Group treated with NKM 23-1 with transcriptional activation of Nrf2. Conclusively, preemptive intake of NKM 23-1 significantly rescued SRMD.

Dietary walnut as food factor to rescue from NSAID-induced gastrointestinal mucosal damages.

Nuclear factor erythroid-derived 2-like 2 (Nrf-2) is transcription factor implicated in the antioxidant response element-mediated induction of endogenous antioxidant enzyme such as heme oxygenase-1 (HO-1), glutamate-cysteine ligase, and NAD(P)H quinone dehydrogenase 1, among which HO-1 is an enzyme catalyzing the degradation of heme.producing biliverdin, ferrous iron, and carbon monoxide. In the stomach, as much as regulating gastric acid secretions, well-coordinated establishment of defense system stands for maintaining gastric integrity. In previous study, author et al. for the first time discovered HO-1 induction was critical in affording faithful gastric defense against various irritants including Helicobacter pylori infection, stress, alcohol, non-steroidal anti-inflammatory drugs (NSAIDs), aspirin, and toxic bile acids. In this review article, we can add the novel evidence that dietary walnut intake can be reliable way to rescue from NSAIDs-induced gastrointestinal damages via the induction of HO-1 transcribed with Nrf-2 through specific inactivation of Keap-1. From molecular exploration to translational animal model of indomethacin-induced gastrointestinal damages, significant induction of HO-1 contributed to rescuing from damages. In addition to HO-1 induction action relevant to walnut, we added the description the general actions of walnut extracts or dietary intake of walnut regarding cytoprotection and why we have focused on to NSAID damages.