Sosacrawford3268
019], as preoperative SL (OR 0.82,
=0.037) or PL (OR 0.68,
=0.028) increased, and as the cage became more posterior (OR 1.10,
=0.032).
Changes in SL after MIS-TLIF appear to be associated with preoperative SL and PL, index level, and Yc. An index level at L4/5 instead of L3/4, smaller preoperative SL or PL, and an anterior position of the cage are likely to result in increased SL after MIS-TLIF.
Changes in SL after MIS-TLIF appear to be associated with preoperative SL and PL, index level, and Yc. An index level at L4/5 instead of L3/4, smaller preoperative SL or PL, and an anterior position of the cage are likely to result in increased SL after MIS-TLIF.
We aimed to analyze changes in suprascapular nerve (SSN) position within the suprascapular notch during in vivo shoulder abduction.
Three-dimensional models of the shoulder complex were constructed based on magnetic resonance imaging of the brachial plexus (BP-MR) in a patient diagnosed with SSN dysfunction but normal scapular movement. Using BP-MR in neutral position and computed tomography data on shoulder abduction, shoulder abduction was simulated as the transition between two positions of the shoulder complex with overlapping of a neutral and abducted scapula. SSN movement during abduction was evaluated using the finite element method. Contact stress on the SSN was measured in the presence and absence of the transverse scapular ligament (TSL).
In the neutral position, the SSN ran almost parallel to the front of the TSL until entering the suprascapular notch and slightly contacted the anterior-inferior border of the TSL. As shoulder abduction progressed, contact stress decreased due to gradual loss of contact with the TSL. In the TSL-free scapula, there was no contact stress on the SSN in the neutral position. Towards the end of shoulder abduction, contact stress increased again as the SSN began to contact the base of the suprascapular notch in both TSL conditions.
We identified changes in the position of the SSN path within the suprascapular notch during shoulder abduction. The SSN starts in contact with the TSL and moves toward the base of the suprascapular notch with secondary contact. These findings may provide rationale for TSL release in SSN entrapment.
We identified changes in the position of the SSN path within the suprascapular notch during shoulder abduction. The SSN starts in contact with the TSL and moves toward the base of the suprascapular notch with secondary contact. These findings may provide rationale for TSL release in SSN entrapment.
In women, menopause manifests with a variety of symptoms related to sex-hormone deficiency. Supplementing steroid hormones with pharmacological drugs has been widely practiced. However, considering the possible complications associated with artificial hormone therapy, studies have been conducted to find an alternative to pharmacological hormone replacement therapy. Accordingly, this study aimed to evaluate the efficacy of tissue-based hormone replacement therapy (tHRT) for treating post-menopausal signs and symptoms.
CD-1 mice were ovariectomized, and the ovaries were cryopreserved. Following artificial induction of post-menopausal osteoporosis, cryopreserved ovaries were subcutaneously autografted, and indexes related to bone health were monitored for 12 weeks. Bone mineral density (BMD), bone mineral contents (BMC), total bone volume (BV), and body fat mass were measured by dual energy X-ray absorptiometry. Uterine atrophy was assessed histologically, and bone microstructures were imaged by micro-computed tomography analysis.
Regardless of the number of grafted ovaries, the BMC, BMD, and BV values of mice that underwent ovary transplantation were better than those that did not undergo transplantation. The uteruses in these mice were thicker and heavier after auto-transplantation. Furthermore, the bone microstructure recovered after tHRT.
Recovery of menopause-related bone loss and uterine atrophy was achieved through tHRT. Ovarian tissue cryopreservation and transplantation may be applicable not only in patients wanting to preserve fertility but also in sex hormone-deficient post-menopausal women.
Recovery of menopause-related bone loss and uterine atrophy was achieved through tHRT. Ovarian tissue cryopreservation and transplantation may be applicable not only in patients wanting to preserve fertility but also in sex hormone-deficient post-menopausal women.
The aims of the study were to develop and evaluate a machine learning model with which to predict postnatal growth failure (PGF) among very low birth weight (VLBW) infants.
Of 10425 VLBW infants registered in the Korean Neonatal Network between 2013 and 2017, 7954 infants were included. PGF was defined as a decrease in Z score >1.28 at discharge, compared to that at birth. Six metrics [area under the receiver operating characteristic curve (AUROC), accuracy, precision, sensitivity, specificity, and F1 score] were obtained at five time points (at birth, 7 days, 14 days, 28 days after birth, and at discharge). Machine learning models were built using four different techniques [extreme gradient boosting (XGB), random forest, support vector machine, and convolutional neural network] to compare against the conventional multiple logistic regression (MLR) model.
The XGB algorithm showed the best performance with all six metrics across the board. When compared with MLR, XGB showed a significantly higher AUROC (
=0.03) for Day 7, which was the primary performance metric. Using optimal cut-off points, for Day 7, XGB still showed better performances in terms of AUROC (0.74), accuracy (0.68), and F1 score (0.67). AUROC values seemed to increase slightly from birth to 7 days after birth with significance, almost reaching a plateau after 7 days after birth.
We have shown the possibility of predicting PGF through machine learning algorithms, especially XGB. Such models may help neonatologists in the early diagnosis of high-risk infants for PGF for early intervention.
We have shown the possibility of predicting PGF through machine learning algorithms, especially XGB. Such models may help neonatologists in the early diagnosis of high-risk infants for PGF for early intervention.
Interleukin (IL)-17A has been suggested to play a role in the growth and organization of thrombi. We examined whether IL-17A plays a role in the early stages of thrombosis and whether there are sex differences in the effects of IL-17A.
We performed a blinded, randomized, placebo-controlled study to compare time to thrombotic occlusion and sex differences therein between mice treated with IL-17A and those treated with saline using a ferric chloride-induced model. We also assessed thrombus histology, blood coagulation, and plasma levels of coagulation factors.
Time to occlusion values did not differ between the IL-17A group and the control group (94.6±86.9 sec vs. 121.0±84.4 sec,
=0.238). However, it was significantly shorter in the IL-17A group of female mice (74.6±57.2 sec vs. 130.0±76.2 sec,
=0.032). In rotational thromboelastometry, the IL-17A group exhibited increased maximum clot firmness (71.3±4.5 mm vs. 66.7±4.7 mm,
=0.038) and greater amplitude at 30 min (69.7±5.2 mm vs. 64.5±5.3 mm,
=0.040) than the control group. In Western blotting, the IL-17A group showed higher levels of coagulation factor XIII (2.2±1.5 vs. 1.0±0.9,
=0.008), monocyte chemoattractant protein-1 (1.6±0.6 vs. 1.0±0.4,
=0.023), and tissue factor (1.5±0.6 vs. 1.0±0.5,
=0.003).
IL-17A plays a role in the initial st ages of arterial thrombosis in mice. Coagulation factors and monocyte chemoattractant protein-1 may be associated with IL-17A-mediated thrombosis.
IL-17A plays a role in the initial st ages of arterial thrombosis in mice. Coagulation factors and monocyte chemoattractant protein-1 may be associated with IL-17A-mediated thrombosis.
Nonalcoholic fatty liver disease (NAFLD) is closely associated with metabolic diseases, including obesity and diabetes, and has gradually become the most common cause of chronic liver disease. We investigated the effects of sodium glucose cotransporter 2 (SGLT2) inhibitor canagliflozin on NAFLD in high-fat diet (HFD)-induced obese mice and possible underlying mechanisms.
Male C57BL/6 mice were fed a normal-diet, HFD, or HFD with canagliflozin for 14 weeks. AML-12 hepatocytes were treated with canagliflozin. Expression of related pathways was assessed.
Canagliflozin administration reduced body weight and fat mass, compared with HFD alone. Canagliflozin improved glucose and lipid metabolic disorders. Compared with HFD-fed mice, liver weight, serum alanine transaminase (ALT) levels, and hepatic lipid accumulation were decreased after canagliflozin administration. Additionally, canagliflozin upregulated lipolysis markers (CPT1a, ACOX1, and ACADM), downregulated lipogenesis markers (SREBP-1c and FASN), and suppressed the production of inflammatory cytokines (TNFα, MCP1, IL-1β, and IL-6), consistent with significantly increased LC3 II/I and Atg7 levels in the liver following canagliflozin treatment. In vitro, canagliflozin increased CPT1a, ACOX1, and ACADM expression, decreased SREBP-1c and FASN protein expression, and reduced TNFα, MCP1, IL-1β, and IL-6 mRNA levels in lipid mixture (LM)-induced hepatocytes in a dose-dependent manner. These changes were reversed by 3-MA, an autophagy inhibitor.
Our findings suggest that canagliflozin ameliorates the pathogenesis of NAFLD by regulating lipid metabolism and inhibiting inflammation, which may be associated with its promotion of autophagy.
Our findings suggest that canagliflozin ameliorates the pathogenesis of NAFLD by regulating lipid metabolism and inhibiting inflammation, which may be associated with its promotion of autophagy.
This study aimed to provide compelling evidence of anti-staphylococcal beta-lactam use for methicillin-susceptible
bloodstream infection (MSSA BSI).
We retrospectively collected data on patients with MSSA BSI who were admitted to two academic tertiary-care hospitals from 2010 to 2018. Only patients who received nafcillin, cefazolin, vancomycin, or teicoplanin as definitive therapy were included. The primary outcome was 28-day mortality. To perform unbiased comparisons between both treatments, we used inverse probability of treatment weighting (IPTW) analysis.
A total of 359 patients were divided into two groups based on the definitive therapy used beta-lactams (n=203), including nafcillin or cefazolin; and glycopeptides (n=156), including vancomycin or teicoplanin. LY2584702 In the IPTW analysis, glycopeptides were associated with significantly increased odds of 28-day mortality (adjusted odds ratio, 3.37; 95% confidence interval, 1.71-6.61;
<0.001). The rate of primary outcome in prespecified subgroups was largely consistent with the main analysis.
Definitive therapy with beta-lactams in patients with MSSA BSI was associated with lower 28-day mortality compared to definitive therapy with glycopeptides.
Definitive therapy with beta-lactams in patients with MSSA BSI was associated with lower 28-day mortality compared to definitive therapy with glycopeptides.
Currently, there are multiple options for the pharmacological treatment of asthma. This study aimed to compare the effects of different asthma medications on exacerbation in a real-world setting.
We retrospectively reviewed electronic medical records of asthma patients who visited the hospital from November 1, 2016 to October 31, 2019. The number of asthma exacerbations requiring administration of systemic steroids was the primary outcome. A time-varying Cox regression analysis was used to reflect the real-world setting variable usage times, discontinuation, and switching of medication.
Among 937 patients with asthma, 228 (24.3%) experienced asthma exacerbation during the study period. Asthma exacerbation was observed in patients using short-acting β
-agonists (SABA) alone (50.4% vs. 28.6%,
<0.001) as well as in patients not using inhaled corticosteroids (ICS) (58.8% vs. 40.3%,
<0.001), long-acting β
-agonists (LABA) (54.8% vs. 36.1%,
<0.001), and leukotriene receptor antagonists (71.5% vs.
