Organoid-on-a-chip technology represents a promising interdisciplinary advancement that merges two cutting-edge biomedical platforms: stem cell-derived organoids and microfluidics-based organ-on-a-chip systems. Organoids are self-organizing three-dimensional (3D) cell cultures that mimic the key structural and functional features of in vivo organs. However, traditional organoid culture systems are often static, lacking dynamic environmental cues and suffering from limitations such as batch-to-batch variability, low stability, and low throughput. Organ-on-a-chip platforms, by contrast, utilize microfluidic technologies to simulate the dynamic physiological microenvironment of human tissues and organs, enabling more controlled cell growth and differentiation. By integrating the advantages of organoids and organ-on-a-chip technologies, organoid-on-a-chip systems transcend the limitations of conventional 3D culture models, offering a more physiologically relevant and controllable in vitro platform. In organoid-on-a-chip systems, stem cells or pre-formed organoids are cultured in micro-engineered environments that mimic in vivo conditions, enabling precise control over fluid flow, mechanical forces, and biochemical cues. Specifically, these platforms employ advanced strategies including bio-inspired 3D scaffolds for structural support, precise spatial cell patterning via 3D bioprinting, and integrated biosensors for real-time monitoring of metabolic activities. These synergistic elements recreate complex extracellular matrix signals and ensure high structural fidelity. Based on structural complexity, organoid-on-a-chip systems are classified into single-organoid and multi-organoid types, forming a trajectory from unit biomimicry to systemic simulation. Single-organoid chips focus on highly biomimetic units by integrating vascular, immune, or neural functions. Multi-organoid chips simulate inter-organ crosstalk and systemic homeostasis, advancing complex disease modeling and PK/PD evaluation. This emerging technology has demonstrated broad application potential in multiple fields of biomedicine. Organoid-on-a-chip systems can recapitulate organ developmentin vitro, facilitating research in developmental biology. They mimic organ-specific physiological activities and mechanisms, showing promising applications in regenerative medicine for tissue repair or replacement. In disease modeling, they support the reconstruction of models for neurodegenerative, inflammatory, infectious, metabolic diseases, and cancers. These platforms also enable in vitro drug testing and pharmacokinetic studies (ADME). Patient-derived chips preserve genetic and pathological features, offering potential for precision medicine. Additionally, they reduce species differences in toxicology, providing human-relevant data for environmental, food, cosmetic, and drug safety assessments. Despite progress, organoid-on-a-chip systems face challenges in dynamic simulation, extracellular matrix (ECM) variability, and limited real-time 3D imaging, requiring improved materials and the integration of developmental signals. Current bottlenecks also include the high technical threshold for automation and the lack of standardized validation frameworks for regulatory adoption. Meanwhile, the concept of a “human-on-a-chip” has been proposed to mimic whole-body physiology by integrating multiple organoid modules. This approach enables systemic modeling of drug responses and toxicity, with the potential to reduce animal testing and revolutionize drug development. Future advancements in bio-responsive hydrogels and flexible biosensors will further empower these platforms to bridge the gap between bench-side research and personalized clinical interventions. In conclusion, organoid-on-a-chip technology offers a transformative in vitro model that closely recapitulates the complexity of human tissues and organ systems. It provides an unprecedented platform for advancing biomedical research, clinical translation, and pharmaceutical innovation. Continued development in biomaterials, microengineering, and analytical technologies will be essential to unlocking the full potential of this powerful tool.

Organoid-on-a-chip technology represents a promising interdisciplinary advancement that merges two cutting-edge biomedical platforms: stem cell-derived organoids and microfluidics-based organ-on-a-chip systems. Organoids are self-organizing three-dimensional (3D) cell cultures that mimic the key structural and functional features of in vivo organs. However, traditional organoid culture systems are often static, lacking dynamic environmental cues and suffering from limitations such as batch-to-batch variability, low stability, and low throughput. Organ-on-a-chip platforms, by contrast, utilize microfluidic technologies to simulate the dynamic physiological microenvironment of human tissues and organs, enabling more controlled cell growth and differentiation. By integrating the advantages of organoids and organ-on-a-chip technologies, organoid-on-a-chip systems transcend the limitations of conventional 3D culture models, offering a more physiologically relevant and controllable in vitro platform. In organoid-on-a-chip systems, stem cells or pre-formed organoids are cultured in micro-engineered environments that mimic in vivo conditions, enabling precise control over fluid flow, mechanical forces, and biochemical cues. Specifically, these platforms employ advanced strategies including bio-inspired 3D scaffolds for structural support, precise spatial cell patterning via 3D bioprinting, and integrated biosensors for real-time monitoring of metabolic activities. These synergistic elements recreate complex extracellular matrix signals and ensure high structural fidelity. Based on structural complexity, organoid-on-a-chip systems are classified into single-organoid and multi-organoid types, forming a trajectory from unit biomimicry to systemic simulation. Single-organoid chips focus on highly biomimetic units by integrating vascular, immune, or neural functions. Multi-organoid chips simulate inter-organ crosstalk and systemic homeostasis, advancing complex disease modeling and PK/PD evaluation. This emerging technology has demonstrated broad application potential in multiple fields of biomedicine. Organoid-on-a-chip systems can recapitulate organ developmentin vitro, facilitating research in developmental biology. They mimic organ-specific physiological activities and mechanisms, showing promising applications in regenerative medicine for tissue repair or replacement. In disease modeling, they support the reconstruction of models for neurodegenerative, inflammatory, infectious, metabolic diseases, and cancers. These platforms also enable in vitro drug testing and pharmacokinetic studies (ADME). Patient-derived chips preserve genetic and pathological features, offering potential for precision medicine. Additionally, they reduce species differences in toxicology, providing human-relevant data for environmental, food, cosmetic, and drug safety assessments. Despite progress, organoid-on-a-chip systems face challenges in dynamic simulation, extracellular matrix (ECM) variability, and limited real-time 3D imaging, requiring improved materials and the integration of developmental signals. Current bottlenecks also include the high technical threshold for automation and the lack of standardized validation frameworks for regulatory adoption. Meanwhile, the concept of a “human-on-a-chip” has been proposed to mimic whole-body physiology by integrating multiple organoid modules. This approach enables systemic modeling of drug responses and toxicity, with the potential to reduce animal testing and revolutionize drug development. Future advancements in bio-responsive hydrogels and flexible biosensors will further empower these platforms to bridge the gap between bench-side research and personalized clinical interventions. In conclusion, organoid-on-a-chip technology offers a transformative in vitro model that closely recapitulates the complexity of human tissues and organ systems. It provides an unprecedented platform for advancing biomedical research, clinical translation, and pharmaceutical innovation. Continued development in biomaterials, microengineering, and analytical technologies will be essential to unlocking the full potential of this powerful tool.

PURPOSE: Lateral patellar compression syndrome (LPCS) is characterized by a persistent abnormally high stress exerted on the lateral articular surface of the patella due to lateral patellar tilt without dislocation and lateral retinaculum contracture, leading to anterior knee pain. The purpose of this study is to evaluate the efficacy and prognosis of lateral retinaculum release (LRR) combined with chondroplasty in the treatment of LPCS. METHODS: This retrospective study evaluated 40 patients who underwent LRR combined with chondroplasty for LPCS between 2020 and 2021. The assessment included improvement in postoperative tenderness and knee joint function. Patients were evaluated using the Lysholm, Tegner, and International Knee Documentation Committee 2000 scoring systems, as well as the visual analog scale, both preoperatively and postoperatively, with the paired comparisons analyzed using a t-test. Additionally, intraoperative observations were made regarding knee joint lesions, including cartilage damage and osteophyte formation, with analysis by the Chi-square test. RESULTS: The visual analog scale score for tenderness showed a significant decrease after surgery (p < 0.001). Evaluation of knee joint function also indicated significant improvements, as demonstrated by increased Lysholm, Tegner, and International Knee Documentation Committee 2000 scores postoperatively (p < 0.001, p = 0.011, p < 0.001, respectively). Furthermore, all LPCS patients included in the study presented with cartilage injuries and osteophyte formation. Significant differences were noted in the incidence of cartilage damage and osteophyte formation at different locations within the knee among patients with LPCS. CONCLUSION LRR combined with chondroplasty is an effective surgical approach for treating patients with LPCS, with satisfactory recovery observed at the 1-year follow-up. Additionally, the incidence of cartilage damage and osteophyte formation in LPCS patients varies significantly depending on the specific location within the knee joint.
Humans ; Male ; Female ; Retrospective Studies ; Adult ; Middle Aged ; Patella/surgery* ; Knee Joint/physiopathology* ; Recovery of Function ; Young Adult ; Treatment Outcome ; Cartilage, Articular/surgery* ; Adolescent

Mycophenolic acid (MPA), the active moiety of both mycophenolate mofetil (MMF) and enteric-coated mycophenolate sodium (EC-MPS), serves as a primary immunosuppressant for maintaining solid organ transplants. Therapeutic drug monitoring (TDM) enhances treatment outcomes through tailored approaches. This study aimed to develop an evidence-based guideline for MPA TDM, facilitating its rational application in clinical settings. The guideline plan was drawn from the Institute of Medicine and World Health Organization (WHO) guidelines. Using the Delphi method, clinical questions and outcome indicators were generated. Systematic reviews, Grading of Recommendations Assessment, Development, and Evaluation (GRADE) evidence quality evaluations, expert opinions, and patient values guided evidence-based suggestions for the guideline. External reviews further refined the recommendations. The guideline for the TDM of MPA (IPGRP-2020CN099) consists of four sections and 16 recommendations encompassing target populations, monitoring strategies, dosage regimens, and influencing factors. High-risk populations, timing of TDM, area under the curve (AUC) versus trough concentration (C₀), target concentration ranges, monitoring frequency, and analytical methods are addressed. Formulation-specific recommendations, initial dosage regimens, populations with unique considerations, pharmacokinetic-informed dosing, body weight factors, pharmacogenetics, and drug‍-‍drug interactions are covered. The evidence-based guideline offers a comprehensive recommendation for solid organ transplant recipients undergoing MPA therapy, promoting standardization of MPA TDM, and enhancing treatment efficacy and safety.
Mycophenolic Acid/administration & dosage* ; Drug Monitoring/methods* ; Humans ; Organ Transplantation ; Immunosuppressive Agents/administration & dosage* ; Delphi Technique

Objective To explore the role of indole-3-propionic acid(IPA)in the pathogenesis of metabolic associated fatty liver disease(MAFLD)induced by high-fat diet(HFD)in order to reveal the role and related mechanism of adipose tissue metabolism in the process.Methods A mouse model of MAFLD was induced by HFD.Male C57BL/6J mice(6～7 weeks old)were randomly divided into control group(CON),HFD group,and HFD+IPA intervention group(HFD+IPA).The CON group was fed with control diet,and the HFD group and HFD+IPA group were fed with 60％of high-fat diet.The experiment period was 12 weeks,and IPA was administered at 20 mg/(kg·d)for 6 weeks starting from the 7th week.The body weight and food intake of each group were monitored weekly.After the intervention,the body composition of mice was detected by animal body composition analyzer.After the mice were euthanized,the morphological and structural changes in the liver and adipose tissues were observed by HE staining,the indicators relevant to lipid metabolism in the serum,l iver and adipose tissues were detected by automatic blood biochemical analyzer and biochemical kits,and the mRNA expression changes of lipid metabolism and inflammation related genes were detected by qRT-PCR.Results Compared with the CON group,the HFD group had significantly increased body weight and body fat percentage,obvious lipid deposition in the liver,obviously elevated serum alanine aminotransferase,aspartate aminotransferase,liver triglyceride and total cholesterol levels(P＜0.05),and raised mRNA levels of liver fatty acid transporter CD36(P＜0.05),while IPA intervention significantly reversed the above changes(P＜0.05).IPA intervention significantly inhibited the HFD-induced enlargement of visceral and brown fat cells,reduced the content of visceral adipose tissue(VAT)and serum level of free fatty acids(P＜0.05),and increased the mRNA expression levels of VAT lipolysis(HSL,CGI58),browning genes(Cidea,ND5,UCP1,Prdm16)(P＜0.05),as well as those of brown adipose tissue(BAT)lipolysis(HSL,ATGL)and fatty acid beta oxidation(Cpt1a,PPARα)genes(P＜0.05).Meanwhile,the mRNA levels of TNF-α,IL-1β,CXCL1 and CCL2 in VAT and BAT were decreased after IPA intervention(P＜0.05).Conclusion IPA can improve the occurrence of MAFLD induced by HFD,and its mechanism may be closely associated with its regulation of BAT and VAT morphology,and the mRNA expression of metabolic function and inflammation related genes.

Objective To explore the effect of chenodeoxycholic acid(CDCA)on the expression of glucagon-like peptide-1(GLP-1)in the intestine of mice induced by high-fat diet(HFD)through farnesoid X receptor(FXR),and investigate the related mechanism.Methods Forty C57BL/6 mice were divided into control group,HFD group,HFD+CDCA group,HFD+Z-Gug(FXR antagonist)group,and HFD+CDCA+Z-Gug group,with 8 animals in each group.During intervention for 8 weeks,body weight and 24-hour food intake were measured every week.At the 8th week,oral glucose tolerance test(OGTT)and intraperitoneal glucose tolerance test(IPGTT)were conducted.After the mice were sacrificed,the serum levels of GLu,TG,CHO,LDL-C and HDL-C were detected;the expression levels of GLP-1 and FXR in intestinal tissues were detected by immunofluorescence assay;and the mRNA levels of TNF-α,IL-6,IL-1β,Gcg and FXR were detected by RT-qPCR;the serum level of GLP-1 was detected by ELISA,and the proportion of intraepithelial lymphocytes(IELs)subsets and the expression of CD26/DPP4 were detected by flow cytometry.Results Compared with the control group,the HFD group had increased body weight,abnormal serum glucose and lipid metabolism,impaired oral glucose tolerance,and weakened secretion of gastrointestinal hormones(P＜0.05),enhanced FXR expression at mRNA and protein levels,declined Gcg mRNA level and GLP-1 secretion level(P＜0.05),increased mRNA levels of intestinal inflammatory factors TNF-α,IL-6 and IL-1β(P＜0.05),raised proportions of TCRαβ+IELs,TCRαβ+CD8αα+IELs,and TCRαβ+CD8αβ+IELs but reduced proportion of TCRγδ+IELs,and increased total CD26/DPP4 expression in IELs(P＜0.05).Compared with the HFD group,HFD+CDCA treatment resulted in significantly increased body weight,impaired oral glucose tolerance,decreased secretion of gastrointestinal hormones,increased FXR mRNA and protein expression,and decreased Gcg mRNA expression and GLP-1 secretion(P＜0.05);decreased proportions of TCRαβ+IELs,TCRαβ+CD8αα+IELs and TCRααβ+CD8αβ+IELs but increased proportion of TCRγδ+ cells in IELs,and increased expression of total CD26/DPP4 in IELs(P＜0.05),which were significantly improved after Z-Gug intervention(P＜0.05).Conclusion CDCA may inhibit the expression and secretion of GLP-1 in intestinal tissue by activating FXR,and reduce the secretion of GLP-1.At the same time,CDCA may inhibit the expression of related inflammatory factors,regulate the proportions of IELs subsets,up-regulate the expression level of CD26/DPP4,promote the degradation of GLP-1 and aggravate insulin resistance.

Objective:To systematically evaluate the effectiveness of Kunxian capsule related regimens for patients with lupus nephritis(LN)in order to provide a reference basis for treatment strategies for LN patients.Methods:The computer searched the rele-vant studies of Kunxian capsule in PubMed,Web of Science,Cochrane Library,CBM,CNKI,Wanfang and VIP databases on the treatment of LN,the limited time for the establishment of the database is April 6,2022,and used R 4.0.2 software and Revman 5.3 software for Meta-analysis.Results:Four RCTs with 1 cohort study including 310 patients were finally included.The results of the Me-ta-analysis showed that:In terms of 24 h urinary protein and SLEDAI score,Glucocorticoid+Cyclophosphamide+Kunxian capsule achieved the best result after treatment;in terms of Scr,IgE,and IgG,the levels of each index were significantly lower in Glucocorti-coid+Cyclophosphamide+Kunxian capsules than in Glucocorticoid+Cyclophosphamide(P<0.05).Conclusion:The 5 regimens may work best as Glucocorticoids+Cyclophosphamide+Kunxian capsules in terms of clinical efficacy in treating LN patients.Because of the quality and quantity limitations of the included studies,more high-quality studies are needed for validation.

Objective:To compare the clinical efficacy of the H-Loop knotless double-row technique and the suture bridge technique in repairing L-shaped rotator cuff tears under arthroscopy.Methods:A retrospective analysis was performed on 58 patients with L-shaped rotator cuff injuries who underwent arthroscopic repair at Sun Yat-sen Memorial Hospital, Sun Yat-sen University, between January 2019 and December 2021. The H-Loop knotless double-row technique was used in 16 cases (8 males and 8 females, mean age 63.69±8.78 years), while the suture bridge technique was used in 42 cases (24 males and 18 females, mean age 61.02±7.02 years). The American Shoulder and Elbow Surgeons (ASES) score, University of California Los Angeles Shoulder Score (UCLA), Simple Shoulder Test (SST), shoulder range of motion, and muscle strength were evaluated and compared between the two groups one year after surgery.Results:The follow-up period was 12.81±0.98 months for the H-Loop group and 13.29±0.94 months for the suture bridge group. No significant differences were found between the groups in terms of age, sex, dominant hand, preoperative symptom duration, tear shape, tear size, or long head tendon amputation (P>0.05). The operative time was significantly shorter in the H-Loop group 67.50±16.02 minutes compared to the suture bridge group 76.67±13.19 minutes ( t=2.234, P=0.031). Additionally, the number of anchors used was significantly lower in the H-Loop group 2.00±0 compared to the suture bridge group 4.14±0.35 ( t=16.573, P<0.001). The ASES scores increased significantly in both groups: from 57.44±15.91 to 92.00±4.41 in the H-Loop group and from 58.21±16.58 to 87.71±6.19 in the suture bridge group ( F=53.439, P<0.001; F=72.511, P<0.001). Similarly, the UCLA scores improved from 20.63±3.79 to 31.56±3.65 in the H-Loop group and from 20.83±5.78 to 30.36±4.71 in the suture bridge group ( F=57.788, P<0.001; F=50.043, P<0.001). The Constant-Murley scores also showed significant improvement: from 68.50±15.31 to 87.5±8.70 in the H-Loop group and from 66.21±16.51 to 86.33±9.14 in the suture bridge group ( F=6.733, P<0.001; F=30.173, P<0.001). SST scores increased from 6.38±3.76 to 9.06±2.59 in the H-Loop group and from 6.55±3.31 to 9.17±2.45 in the suture bridge group ( F=2.847, P<0.001; F=11.096, P<0.001). The shoulder flexion range of motion increased from 158.75°±21.25° to 178.75°±47.07° in the H-Loop group and from 139.29°±45.12° to 179.76°±3.42° in the suture bridge group ( t=3.814, P=0.002; t=5.877, P<0.001). Shoulder abduction motion increased from 145°±45.46° to 178.75°±3.42° in the H-Loop group and from 135.24°±47.07° to 179.76°±1.54° in the suture bridge group ( t=2.952, P=0.001; t=6.185, P<0.001). Muscle strength improved from 53.36±25.21 N to 73.69±24.09 N in the H-Loop group and from 43.31±24.49 N to 61.8±30.07 N in the suture bridge group ( t=4.916, P<0.001; t=5.623, P<0.001). The ASES score at one year post-surgery was significantly higher in the H-Loop group 92.00±4.41 compared to the suture bridge group 87.71±6.19 ( t=2.529, P=0.014). There were no significant differences in UCLA scores, Constant-Murley scores, SST scores, shoulder motion, or muscle strength between the groups ( P>0.05). Conclusion:The H-Loop technique provides a good early curative effect. Compared to the traditional suture bridge technique, the H-Loop technique offers a higher early postoperative ASES score, shorter operative time, and fewer anchors required.

OBJECTIVE: To investigate the synergistic interaction between the deltoid muscle and the rotator cuff muscle group in patients with rotator cuff tears (RCT), as well as the impact of the critical shoulder angle (CSA) on deltoid muscle strength. METHODS: A retrospective analysis was conducted on clinical data from 42 RCT patients who met the selection criteria and were treated between March 2022 and March 2023. There were 13 males and 29 females, with an age range of 42-77 years (mean, 60.5 years). Preoperative visual analogue scale (VAS) score was 6.0±1.6. CSA measurements were obtained from standard anteroposterior X-ray films before operation, and patients were divided into two groups based on CSA measurements: CSA>35° group (group A) and CSA≤35° group (group B). Handheld dynamometry was used to measure the muscle strength of various muscle group in the shoulder (including the supraspinatus, infraspinatus, subscapularis, and anterior, middle, and posterior bundles of the deltoid). The muscle strength of the unaffected side was compared to the affected side, and muscle imbalance indices were calculated. Muscle imbalance indices between male and female patients, dominant and non-dominant sides, and groups A and B were compared. Pearson correlation analysis was used to examine the relationship between muscle imbalance indices and CSA as well as VAS scores. RESULTS: Muscle strength in all muscle groups on the affected side was significantly lower than on the unaffected side ( P<0.05). The muscle imbalance indices for the supraspinatus, subscapularis, infraspinatus, and anterior, middle, and posterior bundles of the deltoid were 14.8%±24.4%, 5.9%±9.7%, 7.2% (0, 9.1%), 17.2% (5.9%, 26.9%), 8.3%±21.3%, and 10.2% (2.8%, 15.4%), respectively. The muscle imbalance indices of the anterior bundle of the deltoid, supraspinatus, and infraspinatus were significantly lower in male patients compared to female patients ( P<0.05); however, there was no significant difference in muscle imbalance indices among other muscle groups between male and female patients or between the dominant and non-dominant sides ( P>0.05). There was a positive correlation between the muscle imbalance indices of infraspinatus and VAS score ( P<0.05), and a positive correlation between CSA and the muscle imbalance indices of middle bundle of deltoid ( P<0.05). There was no correlation between the muscle imbalance indices of other muscle groups and VAS score or CSA ( P>0.05). Preoperative CSA ranged from 17.6° to 39.4°, with a mean of 31.1°. There were 9 cases in group A and 33 cases in group B. The muscle imbalance indices of the anterior bundle of the deltoid was significantly lower in group A compared to group B ( P<0.05), while there was no significant difference in muscle imbalance indices among other muscle groups between group A and group B ( P>0.05). CONCLUSION Patients with RCT have a phenomenon of deltoid muscle strength reduction, which is more pronounced in the population with a larger CSA.
Male ; Female ; Humans ; Adult ; Middle Aged ; Aged ; Shoulder ; Rotator Cuff Injuries/surgery* ; Shoulder Joint/diagnostic imaging* ; Rotator Cuff/surgery* ; Muscle Strength ; Deltoid Muscle

OBJECTIVE: To explore the clinical characteristics of hospitalized patients with hematologic diseases complicated with carbapenem-resistant organisms (CRO) infection and analyze the risk factors of 30-day all-cause mortality. METHODS: The clinical data and laboratory test data of 77 hospitalized patients with hematologic diseases complicated with CRO infection in department of hematology of the Third Hospital of Shanxi Medical University from January 2015 to December 2020 were retrospectively analysed, the risk factors of 30-day all-cause mortality after CRO infection were analyzed by multivariate logistic regression. RESULTS: Among the total of 77 patients with hematologic diseases complicated with CRO infection, 29 died and 48 survived within 30 days of infection, with a case fatality rate of 37.66%. A total of 93 strains of CRO were isolated from these patients, of which Acinetobacter baumannii had the highest detection rate (25.81%, 24/93), followed by Pseudomonas aeruginosa (18.28%, 17/93). The lung was the most common site of CRO infection. The detected pathogens were highly resistant to carbapenems, and 64.52% (60/93) of the pathogens were resistant to imipenem with minimum inhibitory concentration (MIC)≥16 μg/ml. The results of the univariate analysis showed that albumin concentration <25 g/L (P =0.048), serum creatinine concentration≥120 μmol/L (P =0.023), age-adjusted Charlson comorbidity index (ACCI) (P =0.037) and primary treatments (supportive treatment, immunosuppressive therapy, chemotherapy, HSCT) (P =0.048) were significantly associated with 30-day all-cause mortality after infection. The results of multivariate logistic regression analysis showed that when CRO infection confirmed, albumin concentration <25 g/L (P =0.014, OR=6.171), serum creatinine concentration≥120 μmol/L (P =0.009, OR=10.867) were independent risk factors for 30-day mortality of patients with hematologic diseases complicated with CRO infection. CONCLUSION The mortality rate of CRO-infected patients with hematologic diseases is high. The detected pathogenic bacteria are highly resistant to imipenem. The albumin concentration <25 g/L and the serum creatinine concentration≥ 120 μmol/L at diagnosis of CRO infection were independent risk factors for 30-day mortality of the patients with hematologic diseases.
Humans ; Carbapenems/pharmacology* ; Retrospective Studies ; Creatinine ; Hematologic Diseases ; Risk Factors ; Imipenem ; Albumins