Objective To analyze the rates of drug resistance of carbapenem-resistant Klebsiella pneumoniae (CRKP) and extended-spectrum β-lactamase-producing Escherichia coli (ESBL-E.coli) in bronchoalveolar lavage fluid (BALF) of critically ill patients with severe pneumonia and artificial airway and risk factors of CRKP. Methods Patients with severe pneumonia and artificial airway treated in the Center of Emergency and Intensive Care Unit, Jinshan Hospital, Fudan University from May 2022 to May 2025 were selected. Klebsiella pneumoniae (K. pneumoniae) and Escherichia coli (E.coli) isolated and cultured from BALF of these patients were analyzed. The drug resistance rates of the two bacteria were compared. The multivariate logistic regression was used to analyze related risk factors for CRKP infection. Results A total of 384 patients were included, and 384 strains were cultured, including 330 strains (85.9%) of K. pneumoniae and 54 strains (14.1%) of E.coli. The infection rate of K. pneumoniae was higher. Compared with E.coli, the drug-resistant gene expression rate of K. pneumoniae was lower (37.3% vs 57.4%, P＜0.01). The resistance rates of CRKP to cefotaxime, cefepime, aztreonam, and imipenem were higher than those of ESBL-E.coli (P＜0.003). Both CRKP and ESBL-E.coli had high sensitivity to polymyxin and tigecycline. Multivariate logistic regression showed duration of mechanical ventilation ≥ 7 days, and combination of ≥ 2 antibiotics for over 7 days were independent risk factors for CRKP infection (P＜0.01). Conclusions For patients with severe pneumonia and artificial airway in ICU, K. pneumoniae is the main bacterial infection. CRKP and ESBL-E.coli in BALF exhibit different degrees of drug resistance to various antibacterial agents, both have the characteristic of multidrug resistance, and are sensitive to polymyxin and tigecycline. Prevention and control of risk factors related to CRKP should be formulated particularly.

Objective To quantitatively analyze the volumetric characteristics of each subregion of the basal ganglia in patients with hepatolenticular degeneration （also known as Wilson disease ，WD） using brain magnetic resonance imaging （MRI） and brain segmentation technology， to explore the specific imaging findings of choreiform symptoms， and to assess the clinical value of caudate nucleus atrophy as an imaging indicator for this symptom. Methods A retrospective analysis was performed for 40 WD patients with choreiform symptoms and 40 patients without choreiform symptoms from June 2023 to June 2025， and clinical indicators were compared between the two groups. In addition， the two groups were compared in terms of the volume of the basal ganglia after estimated total intracranial volume （eTIV） correction， and the correlation between the volume of differential brain regions and the chorea subscale score of Unified Wilson's Disease Rating Scale （UWDRS） was explored. Results There were no significant differences in baseline data between the two groups. UWDRS scores showed that the choreiform group had a higher neurological function score （P=0.005）， a significantly higher chorea subscale score （P<0.01）， and a lower hepatic function score （P<0.01）. The choreiform group had a significantly smaller caudate nucleus volume than the non-choreiform group （P<0.001）， suggesting severe subregional atrophy， and in contrast， the choreiform group had a significant increase in thalamus volume （P=0.002）. Caudate nucleus volume ratio was significantly negatively correlated with chorea subscale score in the choreiform group （P<0.001）. Conclusion Caudate nucleus atrophy is a specific imaging finding of choreiform symptoms in WD patients， and a quantitative analysis of caudate nucleus volume is expected to become an objective imaging indicator for assessing the severity of choreiform symptoms and monitoring disease progression in WD.

Background: To investigate directional deviations between pilot holes and final pedicle screw trajectories in freehand placement and analyze risk factors for misplacement. While pedicle screws are widely used in thoracolumbosacral surgery, directional deviations between pilot holes and final screw trajectories remain understudied as potential risk factors for misplacement. Methods: Thirty-three patients undergoing posterior fixation were prospectively enrolled. Inertial measurement units (IMUs) tracked the spatial positions of pedicle finders and screwdrivers via custom software. Surgeons (n = 6) were stratified into senior, middle, and junior groups. Analyzed variables included the use of tapping, surgeon experience, spinal deformity status, screw tip morphology, and surgical parameters. Results: Among 198 implanted screws (6.00 ± 2.88/patient), all exhibited trajectory deviations (8.12° ± 3.47°). Tapping significantly reduced deviations (7.23° ± 3.23° vs. 8.87° ± 3.31°, p < 0.01). Senior surgeons achieved smaller deviations (7.34° ± 3.33°) than the middle group (8.60° ± 3.51°, p = 0.039) and junior group (8.68° ± 3.49°, p = 0.022). Multivariate analysis confirmed tapping (p = 0.001) and senior experience (p = 0.023) as protective factors. No significant associations emerged for spinal deformity (8.43° ± 3.73° vs. 7.97° ± 3.35°, p = 0.377), screw tip type (cylindrical, 8.43° ± 3.26° vs. tapered, 8.07 ± 3.51°; p = 0.637), obesity, or surgical position parameters. Conclusions Freehand pedicle screw placement consistently produces trajectory deviations from pilot holes, and surgeon experience and tapping are modifiable protective factors. The IMU-based tracking system enables quantitative surgical motion analysis, suggesting its utility for training optimization and technique standardization.

ObjectiveTo explore the effects of mechanical pressure regulation on the migration and bone-promoting ability of suture dural cells （S-DCs） and non-suture dural cells （NS-DCs）. MethodsDural cells （S-DCs）， non-cranial suture dural cells （NS-DCs） and cranial suture mesenchymal stem cells （CS-MSCs） of 5-day-old SD rats were isolated and cultured. Four experimental conditions， namely S-DCs-Normal， S-DCs-Stress， NS-DCs-Normal and NS-DCs-Stress， were set according to the source of the cells and whether mechanical pressure （1.07 kPa， 24 hours） was applied. The migration ability of dural cells was detected by cell scratch test. Four experimental condition culture media were collected and co-cultured with CS-MSCs for osteogenic induction. Calcium salt deposition was detected by alizarin red staining， and the expression of osteogenesis-related proteins was detected by Western blot. ResultsCompared with the Normal group， the migration abilities of both S-DCs and NS-DCs decreased after Stress treatment （P<0.05）. Compared with S-DCs， NS-DCs has a weaker migration ability under the same processing conditions （P<0.05）. The conditioned medium experiment showed that Stress treatment reduced the osteogenic ability of CS-MSCs （P<0.05）， and the osteogenic effect of the conditioned medium derived from NS-DCs was weaker than that of S-DCs （P<0.05）. The Western blot results were consistent with the trend of alizarin red staining. Both Stress treatment and NS-DCs sources could down-regulate the expression of osteogenesis-related proteins （P<0.05）. ConclusionMechanical stress can significantly inhibit the migration of dural cells and the osteogenic differentiation process of CS-MSCs mediated by it. The mechanical tolerance and osteogenic regulation ability of S-DCs are significantly better than those of NS-DCs.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

ObjectiveTo explore the sequential effects of hypoxic exercising on miR-27/PPARγ and lipid metabolism target gene and protein expression levels in the obesity rats’ liver. Methods13-week-old male diet-induced obesity rats were randomly divided into three groups (n＝10): normal oxygen concentration quiet group (N), hypoxia quiet group (H), hypoxic exercise group (HE). Exercise training on the horizontal animal treadmill for 1 h/d, 5 d/week for a total of 4 week, and the intensity of horizontal treadmill training was 20 m/min (hypoxic concentration was 13.6%). Comparison of the weights of perirenal fat and epididymal fat in rats across different groups and calculation of Lee’s index based on body weight and body length of rats in each group were done. And the serum concentrations of total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) levels were detected. RT-PCR and Western Blot were used to detect the levels of miR-27, PPARγ, CYP7A1 and CD36. ResultsHypoxic exercise decreased the expression levels of miR-27 in the obese rats’ liver, however, the expression level of PPARγ was gradually increased. The expression levels of miR-27 in HE group were significantly lower than N group (P<0.05). The expression levels of PPARγ mRNA in N group were significantly lower than H group (P<0.05), especially lower than HE group (P<0.01). The protein expression of PPARγ protein in N group was significantly lower than that other groups (P<0.01). The expression of lipid metabolism-related genes and proteins increased in the obese rats’ liver. The expression of CYP7A1 mRNA in N group was significantly lower than H group (P<0.05), especially lower than HE group (P<0.01). The expression of CYP7A1 protein in the obese rats’ liver in N group was extremely lower than H group and HE group (P<0.01). The protein expression of CD36 in N group was significantly lower than that in HE group (P<0.05). Hypoxia exercise improved the related physiological and biochemical indexes of lipid metabolism disorder. The perirenal fat weight of obese rats in HE group was extremely lower than N group and H group (P<0.01), and the perirenal fat weight in N group was significantly higher than H group (P<0.05). The epididymal fat weight in N group was significantly higher than H group (P<0.05), and extremely higher than HE group (P<0.01). The Lee’s index in HE group was extremely lower than N group and H group (P<0.01). The serum concentration of TC in obese rats in HE group was extremely lower than N group and H group (P<0.01). The serum concentration of TG in HE group was extremely lower than N group and H group (P<0.01). The serum concentration of LDL-C in N group was extremely higher than HE group (P<0.01). The serum concentration of HDL-C in N group was extremely lower than H group (P<0.01). ConclusionHypoxia and hypoxia exercise may negatively regulate the levels of PPARγ by inhibiting miR-27 in the obese rats’ liver, thereby affecting the expression of downstream target genes CYP7A1 and CD36, and promoting cholesterol, fatty acid oxidation and HDL-C transport in the liver, and ultimately the lipid levels in obese rats were improved. The effect of hypoxia exercise on improving blood lipid is better than simple hypoxia intervention.

OBJECTIVE: Psoriasis, a common chronic inflammatory skin condition with genetic underpinnings, is traditionally managed with cupping therapy. Although used historically, the precise mechanical effects and therapeutic mechanisms of cupping in psoriasis remain largely unexamined. This study aimed to evaluate cupping therapy's efficacy for psoriasis and investigate its role in modulating inflammatory responses and cellular metabolism. METHODS: Psoriasis was induced in mice using topical imiquimod (IMQ). The effects of cupping on psoriatic lesions were assessed using the Psoriasis Area and Severity Index score, histology, immunohistochemistry, and immunofluorescence staining. polymerase chain reaction sequencing (RNA-seq) and Western blotting were conducted to examine changes in mRNA expression and the AMP-activated protein kinase (AMPK) signaling pathway. RESULTS: Cupping therapy significantly reduced inflammation, epidermal thickness, and inflammatory cell infiltration in mice with IMQ-induced psoriasis. Immunohistochemistry and immunofluorescence showed lower expression of inflammatory markers and a shift in T-cell populations. RNA-seq and Western blotting indicated that cupping upregulated Piezo1 and activated the AMPK pathway, improving energy metabolism in psoriatic skin. CONCLUSION Cupping therapy reduces epidermal hyperproliferation and inflammation in psoriasis, rebalancing the local immune microenvironment. Mechanistically, cupping promotes calcium influx via Piezo1, activates AMPK signaling, and supports metabolic homeostasis, suggesting therapeutic potential for psoriasis. Please cite this article as: Xi RF, Liu X, Wang Y, Lu HZ, Yuan SJ, Guo DJ, Zhu JY, Li FL, Duan YJ. Mechanosensory activation of Piezo1 via cupping therapy: Harnessing neural networks to modulate AMPK pathway for metabolic restoration in a mouse model of psoriasis. J Integr Med. 2025; 23(6):721-732.
Animals ; Psoriasis/chemically induced* ; Mice ; AMP-Activated Protein Kinases/metabolism* ; Disease Models, Animal ; Cupping Therapy/methods* ; Signal Transduction ; Imiquimod ; Ion Channels/genetics* ; Male ; Mechanotransduction, Cellular