Observation on the Curative Effect of Different Anti-infective Treatment Regimens for Children with Acute Appendicitis.

Objective: To observe the efficacy of different anti-infective treatment regimens on acute appendicitis in children, a retrospective study was conducted by collecting previous cases. Methods: Ninety children with acute appendicitis who received laparoscopic appendectomy from May 2020 to September 2022 were included in this retrospective study. According to the different anti-infective treatment regimens, they were divided into Piperacillin-Tazobactam group, Piperacillin-Tazobactam+Metronidazole group, and Cefminox+Metronidazole group (n=30). Three groups of children received medication treatment before surgery. The postoperative recovery, treatment effect, bacterial clearance, complication rate, pharmacoeconomic evaluation, and adverse reactions were compared. Results: The effective rates in the three groups were 83.33%, 90.00%, and 90.00%, respectively (P > .05). There were no differences in the bacterial clearance, complication incidence, and incidence of pharmaceutical side effects among the three groups (P > .05). The total hospitalization cost, total drug cost, and antimicrobial drug cost in Cefminox + Metronidazole group were lower than those in Piperacillin-Tazobactam group and Piperacillin-Tazobactam + Metronidazole group, respectively (P < .05). The intensity of antibacterial drug use in Piperacillin-Tazobactam group was the lowest, followed by Piperacillin-Tazobactam + Metronidazole group and Cefminox + Metronidazole group (P < .05). Conclusion: The three anti-infective regimens have the same therapeutic effect on acute appendicitis in children. However, the regimen of Cefminox + Metronidazole is the most economical option and can be used as the preferred treatment for acute appendicitis in children. As the preferred treatment for acute appendicitis in children. The Piperacillin-Tazobactam group has the lowest intensity of antibiotic use and can reduce bacterial resistance.

The Effects of General Listening Anxiety and Listening Test Anxiety on Self-Perceived Listening Performance Among Chinese English Learners.

Purpose: This research seeks to conceptualize foreign language listening anxiety (FLLA) and provide its measurement, and further explore the influences of FLLA on self-perceived listening performance. Methods: In Study 1, semi-structured interviews explored FLLA-arousal situations. Follow-up reliability and validity tests for the newly-developed scale were testified. In Study 2, structural equation modeling explored the relationship between FLLA and self-perceived performance, which was followed by the comparison of the effects of different types of FLLA on self-perceived performance between English and non-English major students. Results: The componential factors of FLLA included two factors, namely general listening anxiety and listening test anxiety, and general listening anxiety was represented by FLLA in classroom, daily usage, and media learning. The results also showed that listening test anxiety negatively affected self-perceived performance; general listening anxiety positively affected listening test anxiety but did not affect self-perceived performance, and listening test anxiety played a full mediation role. Moreover, findings revealed that non-English major students' general listening anxiety was higher than that of English major students. However, the multi-group analysis showed that these two groups did not differ in the effect of general listening anxiety on listening test anxiety, and in the effects of listening anxieties on self-perceived performance. For the two groups, the mechanism of anxiety-and-performance relationship was consistent. Conclusion: The results of this research have expanded the knowledge of listening anxiety by distinguishing general listening anxiety from listening test anxiety. Moreover, by testifying the mediator of listening test anxiety, this research deepened the understanding of the effects of different types of FLLA on self-perceived listening performance and the intensity differences of listening anxieties in English and non-English majors. Furthermore, the research has contributed to the literature on FLLA research based on Complex Dynamic Systems Theory, and has practical pedagogical implications for future studies.

Compensatory movement detection by using near-infrared spectroscopy technology based on signal improvement method.

Introduction: Compensatory movements usually occur in stroke survivors with hemiplegia, which is detrimental to recovery. This paper proposes a compensatory movement detection method based on near-infrared spectroscopy (NIRS) technology and verifies its feasibility using a machine learning algorithm. We present a differential-based signal improvement (DBSI) method to enhance NIRS signal quality and discuss its effect on improving detection performance. Method: Ten healthy subjects and six stroke survivors performed three common rehabilitation training tasks while the activation of six trunk muscles was recorded using NIRS sensors. After data preprocessing, DBSI was applied to the NIRS signals, and two time-domain features (mean and variance) were extracted. An SVM algorithm was used to test the effect of the NIRS signal on compensatory behavior detection. Results: Classification results show that NIRS signals have good performance in compensatory detection, with accuracy rates of 97.76% in healthy subjects and 97.95% in stroke survivors. After using the DBSI method, the accuracy improved to 98.52% and 99.47%, respectively. Discussion: Compared with other compensatory motion detection methods, our proposed method based on NIRS technology has better classification performance. The study highlights the potential of NIRS technology for improving stroke rehabilitation and warrants further investigation.

Liquiritigenin reverses skin aging by inhibiting UV-induced mitochondrial uncoupling and excessive energy consumption.

BACKGROUND: The accumulation of reactive oxygen species (ROS) generated by UV radiation can lead to lipid, protein, nucleic acid, and organelle damage, one of the core mechanisms mediating skin aging. In the photoaging process, how ROS drives the imbalance of the body's complex repair system to induce senescence-like features is not fully understood. METHODS: We irradiated human epidermal keratinocytes with 12 J/cm2 of UVA to establish an in vitro photoaging model. Then we employed whole-transcriptome sequencing and O2K mitochondrial function assay to reveal the photoprotective mechanisms of liquiritigenin (LQ). DISCUSSION: We found that skin reduces endogenous ROS by promoting mitochondrial oxidative phosphorylation uncoupling in response to UVA-induced damage. However, this also causes excessive consumption and idling of nutrients, leading to the inhibition of cell proliferation, and ultimately accelerating the skin aging process. Here, we demonstrated that LQ can reduce stress in keratinocytes, increase oxidative phosphorylation and ATP production efficiency, and block the massive loss of skin nutrients and net energy stress. Furthermore, LQ can promote collagen synthesis and keratinocyte proliferation through the PI3K-AKT pathway, thereby reversing photoaging. CONCLUSION: This work provides a new skin aging mechanism and solution strategy with high clinical translation value.

Hypomagnesemia in intestinal lymphangiectasia: a case report and review of the literature.

BACKGROUND: Intestinal lymphangiectasia (IL) is a rare disease characterized by dilation of lymphatic vessels and leakage of lymphatic fluids into the intestinal lumen, causing depletion of lymphocytes, protein, lipids, fat-soluble vitamins, and electrolytes. Hypomagnesemia can occur in IL patients but is seldom discussed. CASE PRESENTATION: A 30-year-old Tibetan woman who had chronic diarrhea, edema, tetany, and tingling was diagnosed with IL. Prominent hypomagnesemia was noticed. She was treated with a medium-chain triglyceride (MCT) diet and nutrient supplementation with satisfactory results. We also present a systematic review of hypomagnesemia in IL cases from the published literature. CONCLUSIONS: Hypomagnesemia may be an overlooked complication of IL, thus monitoring serum magnesium concentrations in IL patients is crucial.

Nicotinic Acid Riboside Regulates Nrf-2/P62-Related Oxidative Stress and Autophagy to Attenuate Doxorubicin-Induced Cardiomyocyte Injury.

Doxorubicin (Dox) is an effective chemotherapeutic drug for the treatment of various cancers. Due to its potential fatal cardiotoxic side effects, the clinical application is often limited. Dexrazoxane (Dex) is the only drug approved by the Food and Drug Administration (FDA) for the prevention of Dox-induced cardiotoxicity but has side effects. Thus, more protective strategies should be explored. If NAD+ plays a role in maintaining heart function, its precursor prospectively alleviates Dox-induced cellular injury. Here, we studied the protective effects of nicotinic acid riboside (NAR) on Dox-induced cardiotoxicity in vivo and in vitro. We found that NAR significantly improved the cardiac function of Dox-treated mice by restoring ejection fraction (EF), fractional shortening (FS), and serum level of cardiac troponin (cTnI). NAR not only reduced malondialdehyde (MDA), lactate dehydrogenase (LDH), and reactive oxygen species (ROS) levels in Dox-treated cardiomyocytes but also further promoted the activities of cardiac superoxide dismutase (SOD) and glutathione (GSH). Following exposure to 5 µM Dox, cotreatment with NAR exhibited increased cell viability with a decrease in the apoptosis cell population. Moreover, the levels of apoptosis-related proteins, as well as proteins involved in oxidative stress and autophagy, were altered after NAR treatment. Collectively, these findings underline the protective potential of NAR against Dox-induced cardiomyocyte injury by regulating Nrf-2/P62-related oxidative stress and autophagy, which could potentially promote survival.

Adenosine A1 Receptor Deficiency Aggravates Extracellular Matrix Accumulation in Diabetic Nephropathy through Disturbance of Peritubular Microenvironment.

BACKGROUND: We previously observed that adenosine A1 receptor (A1AR) had a protective role in proximal tubular megalin loss associated with albuminuria in diabetic nephropathy (DN). In this study, we aimed to explore the role of A1AR in the fibrosis progression of DN. METHODS: We collected DN patients' samples and established a streptozotocin-induced diabetes model in wild-type (WT) and A1AR-deficient (A1AR-/-) mice. The location and expression of CD34, PDGFRß, and A1AR were detected in kidney tissue samples from DN patients by immunofluorescent and immunohistochemical staining. We also analyzed the expression of TGFß, collagen (I, III, and IV), α-SMA, and PDGFRß using immunohistochemistry in WT and A1AR-/- mice. CD34 and podoplanin expression were analyzed by Western blotting and immunohistochemical staining in mice, respectively. Human renal proximal tubular epithelial cells (HK2) were cultured in medium containing high glucose and A1AR agonist as well as antagonist. RESULTS: In DN patients, the expression of PDGFRß was higher with the loss of CD34. The location of PDGFRß and TGFß was near to each other. The A1AR, which was colocalized with CD34 partly, was also upregulated in DN patients. In WT-DN mice, obvious albuminuria and renal pathological leisure were observed. In A1AR-/- DN mice, more severe renal tubular interstitial fibrosis and more extracellular matrix deposition were observed, with lower CD34 expression and pronounced increase of PDGFRß. In HK2 cells, high glucose stimulated the epithelial-mesenchymal transition (EMT) process, which was inhibited by A1AR agonist. CONCLUSION: A1AR played a critical role in protecting the tubulointerstitial fibrosis process in DN by regulation of the peritubular microenvironment.

Rutin inhibited the advanced glycation end products-stimulated inflammatory response and extra-cellular matrix degeneration via targeting TRAF-6 and BCL-2 proteins in mouse model of osteoarthritis.

BACKGROUND: Osteoarthritis (OA) is degenerative joint disorder mainly characterized by long-term pain with limited activity of joints, the disease has no effective preventative therapy. Rutin (RUT) is a flavonoid compound, present naturally. The flavonoid shows range of biological activities such as anti-inflammatory and anti-cancer effect. We screened RUT for its activity against osteoarthritis with in vivo and in vitro models of osteoarthritis. METHODS: Animal model of OA was developed using C57BL/6 mice by surgical destabilization of medial meniscus. For in vitro studies the human articular cartilage tissues were used which were collected from osteoarthritis patients and were processed to isolate chondrocytes. The chondrocytes were submitted to advanced glycation end products (AGEs) for inducing osteoarthritis in vitro. Cell viability was done by CCK-8 assay, ELISA analysis for MMP13, collage II, PGE2, IL-6, TNF-α, ADAMTS-5 and MMP-13. Western blot analysis was done for expression of proteins and in silico analysis was done by docking studies. RESULTS: Pretreatment of RT showed no cytotoxic effect and also ameliorated the AGE mediated inflammatory reaction on human chondrocytes in vitro. Treatment of RT inhibited the levels of COX-2 and iNOS in AGE exposed chondrocytes. RT decreased the AGE mediated up-regulation of IL-6, NO, TNF-α and PGE-2 in a dose dependent manner. Pretreatment of RT decreased the extracellular matrix degradation, inhibited expression of TRAF-6 and BCL-2 the NF-κB/MAPK pathway proteins. The treatment of RT in mice prevented the calcification of cartilage tissues, loss of proteoglycans and also halted the narrowing of joint space is mice subjected to osteoarthritis. The in-silico analysis suggested potential binding affinity of RT with TRAF-6 and BCL-2. CONCLUSION: In brief RT inhibited AGE-induced inflammatory reaction and also degradation of ECM via targeting the NF-κB/MAPK pathway proteins BCL-2 and TRAF-6. RT can be a potential molecule in treating OA.

Continuous hypergammaglobulinemia and proteinuria after the recovery of the visceral Leishmaniasis: a case report.

BACKGROUND: Kidney involvement of visceral Leishmaniasis is previously reported, but knowledge is limited. Hypergammaglobulinemia is common in visceral leishmaniasis patients. Whether hypergammaglobulinemia after leishmaniasis depletion can cause kidney injury is not well reported yet. CASE PRESENTATION: We reported a patient who recovered from visceral Leishmaniasis but showed persistent hypergammaglobulinemia and elevated urinary protein. Kidney biopsy showed glomerular hypertrophy with mild segmental mesangial proliferation without tubulointerstitial involvement in light microscopy. No immune complex deposit was found in the mesangial area by neither immunofluorescent staining nor electronic microscope. Increased lysosomes were observed in proximal tubules by electronic microscope. Valsartan was administered to decrease urinary protein, and no immune-suppressive therapy was added. The urinary protein and serum IgG level gradually dropped, and serum creatinine level remained stable during three- month follow up. CONCLUSIONS: Hypergammaglobulinemia is unlikely to cause renal structural or functional damage in the short term. Angiotensin blockade significantly reduced urine protein, with a minor effect on IgG elimination.

Simulation and prediction of geologic hazards and the impacts on homestay buildings in scenery spots through BIM.

The objectives are exploring the impacts of geologic hazards on the construction of homestays, improving the safety of homestay buildings, guaranteeing the safety of tourists, and enhancing the disaster-resistance of homestays in scenery spots. The computer simulation system and Building Information Modeling (BIM) technology are employed to construct a geologic hazard prediction model for homestays. The model utilizes a time history method to establish a complete early-warning and monitoring system by learning the geologic disaster data. The detection of various geologic hazards has verified the effectiveness of the proposed model. The results show that the model can reduce the losses in the case of water accumulation and landslides during storms, and the BIM technology-based homestay buildings will suffer fewer losses. In the case of earthquakes, BIM technology-based homestay buildings have no noticeable shaking and displacement. Compared to traditional construction methods, the displacement is reduced by 49.15%. In the case of a spontaneous fire, the burning area of the BIM technology-based homestay building is only 270m2. The most severe factors affecting the construction of homestay buildings are earthquakes and landslide risks. The BIM technology generates 3D building planning; therefore, planners can fully understand the problems in the building. In the meantime, the multi-source monitoring data of multiple geologic hazards can be monitored and fed back, thereby improving the timeliness of early-warning of geologic hazards. The results are of considerable significance to the prevention of losses caused by geologic hazards, which can significantly improve the understanding of geologic hazards.

Primary SjÓ§gren's syndrome with renal Fanconi syndrome: Good responses to treatment with glucocorticoids.

BACKGROUND: Renal Fanconi syndrome (FS) is rare in primary SjÓ§gren's syndrome (pSS). We aimed to describe the clinicopathological characteristics of pSS associated FS (pSS-FS) and its responses to treatment. METHODS: We reported 25 cases of pSS-FS patients and retrospectively reviewed their clinical records, kidney pathology and follow-up data. RESULTS: The 25 pSS-FS patients were mainly female (92.0%) and the mean age at diagnosis was 43.6±11.3 years. They showed different degrees of proximal tubular dysfunctions and eGFR decline (60.9±32.3 ml/min/1.73m2). Kidney pathology of pSS-FS patients showed tubulo-interstitial nephritis with defective brush border and lymphoplasmacytic infiltrates. After glucocorticoid treatment, the eGFR levels were significantly improved from 48.3±20.6 ml/min/1.73m2 to 55.0±19.9 ml/min/1.73m2 (P = 0.012) at the third month of follow-up. They also acquired good tubular (88.2%) and immunological (90.0%) responses. pSS-FS patients with young-onset pSS presented with a higher prevalence of positive anti-SSB antibody and hypocomplementemia, more severe hypokalemia, and better eGFR levels. CONCLUSIONS: In pSS-FS patients, use of glucocorticoids could improve eGFR and tubular functions. The young-onset pSS group presented with a particular pattern in immunological features and kidney involvement.

The effect of A1 adenosine receptor in diabetic megalin loss with caspase-1/IL18 signaling.

PURPOSE: In our previous study, exacerbation of albuminuria was observed in A1 adenosine receptor knockout (A1AR-/-) mice with diabetic nephropathy (DN), but the mechanism was unclear. Here, we investigated the relationship of megalin loss and albuminuria, to identify the protective effect of A1AR in megalin loss associated albuminuria by inhibiting pyroptosis-related caspase-1/IL-18 signaling of DN. METHODS: We successfully collected DN patients' samples and built diabetes mice models induced by streptozotocin. Megalin, cubilin, and A1AR expression were detected in kidney tissue samples from DN patients and mice through immunohistochemical and immunofluorescent staining. A1AR, caspase-1, interleukin-18 (IL-18) expression were analyzed using Western blotting in wild-type and A1AR -/- mice. Human renal proximal tubular epithelial cells (PTC) were cultured with high glucose to observe the effect of A1AR agonist and antagonist on caspase-1/IL-18 and megalin injury. RESULTS: The loss of megalin, co-localized with A1AR at PTC, was associated with the level of albuminuria in diabetic patients and mice. The injury of megalin-cubilin was accompanied with the A1AR upregulation (1.30±0.1 vs 0.98±0.2, P=0.042), the caspase-1 (1.33±0.1 vs 1.0±0.2, P=0.036), and IL-18 (1.26±0.2 vs 0.96±0.2, P=0.026) signaling activation in mice with DN. More severe pathological injury, 24 hrs urine albumin excretion (170.8±4.1 µg/d vs 132.0±2.9 µg/d vs 17.9±2.8 µg/d, P<0.001) and megalin-cubilin loss were observed in A1AR -/- DN mice with more pronounced caspase-1 (1.52±0.03 vs 1.20±0.01, P=0.017) and IL-18 (1.42±0.02 vs 1.21±0.02, P=0.018) secretion. High glucose could stimulate the secretion of caspase-1 (1.72 times, P≤0.01) and IL-18 (1.64 times, P≤0.01), which was abolished by A1AR agonist and aggravated by A1AR antagonist. CONCLUSION: A1AR played a protective role in proximal tubular megalin loss associated albuminuria by inhibiting the pyroptosis-related caspase-1/IL-18 signaling in DN.