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Combination therapy based on sonodynamic therapy (SDT) combined with immune checkpoint blockers anti-PD-L1 provides effective anti-tumor effects. We designed a combination therapy based on M1/PLGA@IR780/CAT NPs of SDT-enhanced immunity combined with immune checkpoint blockers against PD-L1, which was based on M1 macrophage membrane-encapsulated poly (lactic-co-glycolic acid) (PLGA) nanoparticles loaded with the acoustic sensitizer IR780 and catalase (CAT) to successfully realize it. SDT based on M1/PLGA@IR780/CAT NPs could induce tumor cell death by promoting dendritic cell (DC) maturation and modulating the tumor immune microenvironment. In particular, the systemic anti-tumor immune response and potent immune memory induced upon combination with anti-PD-L1 checkpoint blockade not only alleviated the progression of mammary cancer in 4T1 mice and effectively blocked distant metastasis, but also prevented tumor recurrence, providing a promising new therapeutic strategy for clinical tumor therapy.
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Inhibidores de Puntos de Control Inmunológico , Nanopartículas , Animales , Ratones , Biomimética , Recurrencia Local de Neoplasia , Inmunoterapia , Macrófagos , Línea Celular Tumoral , Microambiente TumoralRESUMEN
Background: Intelligent hydrogels continue to encounter formidable obstacles in the field of cancer treatment. A wide variety of hydrogel materials have been designed for diverse purposes, but materials with satisfactory therapeutic effects are still urgently needed. Methods: Here, we prepared an injectable hydrogel by means of physical crosslinking. Carbon nanoparticle suspension injection (CNSI), a sentinel lymph node imaging agent that has been widely used in the clinic, with sodium ß-glycerophosphate (ß-GP) were added to a temperature-sensitive chitosan (CS) hydrogel (CS/GP@CN) as an agent for photothermal therapy (PTT). After evaluating the rheological, morphological, and structural properties of the hydrogel, we used 4T1 mouse breast cancer cells and B16 melanoma cells to assess its in vitro properties. Then, we intratumorally injected the hydrogel into BALB/c tumor-bearing mice to assess the in vivo PTT effect, antitumor immune response and the number of lung metastases. Results: Surprisingly, this nanocarbon hydrogel called CS/GP@CN hydrogel not only had good biocompatibility and a great PTT effect under 808nm laser irradiation but also facilitated the maturation of dendritic cells to stimulate the antitumor immune response and had an extraordinary antimetastatic effect in the lungs. Discussion: Overall, this innovative temperature-sensitive nanocarbon hydrogel, which exists in a liquid state at room temperature and transforms to a gel at 37 °C, is an outstanding local delivery platform with tremendous PTT potential and broad clinical application prospects.
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Quitosano , Neoplasias Pulmonares , Ratones , Animales , Hidrogeles/química , Temperatura , Terapia Fototérmica , Quitosano/químicaRESUMEN
Diabetic kidney disease (DKD) is one of the most serious complications of diabetes mellitus (DM) and the main cause of end-stage renal failure. However, the pathogenesis of DKD is complicated. In this study, we found that miR-124-3p plays a key role in regulating renal mitochondrial function and explored its possible mechanism in DKD progression by performing a series of in vitro and in vivo experiments. Decreased expression of miR-124-3p was found in db/db mice compared to db/m mice. Moreover, miR-124-3p down-regulated FOXQ1 by targeting FOXQ1 mRNA 3'-UTR in NRK-52E cells. Also, an increase in FOXQ1 and down-regulation of Sirt4 were found in db/db mouse kidney and renal tubular epithelial cells cultured with high glucose and high lipid. Overexpression of FOXQ1 could further down-regulate the expression of Sirt4 and aggravate the damage of mitochondria. Conversely, the knockdown of the FOXQ1 gene induced Sirt4 expression and partially restored mitochondrial function. To verify the effects of miR-124-3p on Sirt4 and mitochondria, we found that miR-124-3p mimics could up-regulate Sirt4 and inhibit ROS production and MitoSOX, thus restoring the number and morphology of mitochondria. These results showed that under high-glucose and high-lipid conditions, the down-regulation of miR-124-3p induces FOXQ1 in renal tubular epithelial cells, which in turn suppresses Sirt4 and leads to mitochondrial dysfunction, promoting the development of DKD.
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Nefropatías Diabéticas , MicroARNs , Ratones , Animales , MicroARNs/metabolismo , Células Epiteliales/metabolismo , Nefropatías Diabéticas/metabolismo , Ratones Endogámicos , Glucosa/metabolismo , Mitocondrias/metabolismo , Lípidos/farmacologíaRESUMEN
Previous studies have shown mitochondrial dysfunction in various acute kidney injuries and chronic kidney diseases. Lipoic acid exerts potent effects on oxidant stress and modulation of mitochondrial function in damaged organ. In this study we investigated whether alpha lipoamide (ALM), a derivative of lipoic acid, exerted a renal protective effect in a type 2 diabetes mellitus mouse model. 9-week-old db/db mice were treated with ALM (50 mg·kg-1·d-1, i.g) for 8 weeks. We showed that ALM administration did not affect blood glucose levels in db/db mice, but restored renal function and significantly improved fibrosis of kidneys. We demonstrated that ALM administration significantly ameliorated mitochondrial dysfunction and tubulointerstitial fibrotic lesions, along with increased expression of CDX2 and CFTR and decreased expression of ß-catenin and Snail in kidneys of db/db mice. Similar protective effects were observed in rat renal tubular epithelial cell line NRK-52E cultured in high-glucose medium following treatment with ALM (200 µM). The protective mechanisms of ALM in diabetic kidney disease (DKD) were further explored: Autodock Vina software predicted that ALM could activate RXRα protein by forming stable hydrogen bonds. PROMO Database predicted that RXRα could bind the promoter sequences of CDX2 gene. Knockdown of RXRα expression in NRK-52E cells under normal glucose condition suppressed CDX2 expression and promoted phenotypic changes in renal tubular epithelial cells. However, RXRα overexpression increased CDX2 expression which in turn inhibited high glucose-mediated renal tubular epithelial cell injury. Therefore, we reveal the protective effect of ALM on DKD and its possible potential targets: ALM ameliorates mitochondrial dysfunction and regulates the CDX2/CFTR/ß-catenin signaling axis through upregulation and activation of RXRα. Schematic figure illustrating that ALM alleviates diabetic kidney disease by improving mitochondrial function and upregulation and activation of RXRα, which in turn upregulated CDX2 to exert an inhibitory effect on ß-catenin activation and nuclear translocation. RTEC renal tubular epithelial cell. ROS Reactive oxygen species. RXRα Retinoid X receptor-α. Mfn1 Mitofusin 1. Drp1 dynamic-related protein 1. MDA malondialdehyde. 4-HNE 4-hydroxynonenal. T-SOD Total-superoxide dismutase. CDX2 Caudal-type homeobox transcription factor 2. CFTR Cystic fibrosis transmembrane conductance regulator. EMT epithelial mesenchymal transition. α-SMA Alpha-smooth muscle actin. ECM extracellular matrix. DKD diabetic kidney disease. Schematic figure was drawn by Figdraw ( www.figdraw.com ).
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Diabetes Mellitus Tipo 2 , Nefropatías Diabéticas , Ácido Tióctico , Animales , Ratones , Ratas , beta Catenina/metabolismo , Regulador de Conductancia de Transmembrana de Fibrosis Quística/metabolismo , Diabetes Mellitus Tipo 2/complicaciones , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Diabetes Mellitus Tipo 2/metabolismo , Nefropatías Diabéticas/tratamiento farmacológico , Nefropatías Diabéticas/patología , Transición Epitelial-Mesenquimal , Fibrosis/tratamiento farmacológico , Fibrosis/metabolismo , Glucosa/metabolismo , Riñón/patología , Mitocondrias/efectos de los fármacos , Mitocondrias/metabolismo , Ácido Tióctico/farmacología , Ácido Tióctico/uso terapéutico , Receptor alfa X Retinoide/efectos de los fármacos , Receptor alfa X Retinoide/metabolismoRESUMEN
Sonodynamic therapy (SDT) is a promising new anti-tumor therapy that inhibits tumor growth by ultrasound activation of sonosensitizers to produce reactive oxygen species (ROS). However, the problems of hypoxia in the microenvironment within solid tumors and the effectiveness of SDT will decrease due to the little accumulation of sonosensitizers at the tumor site, as well as tumor cell tolerance, have limited the development of SDT. To overcome these problems, a core-shell structured nanoparticle (IR780/PLGA@MnO2 NPs) loaded with IR780 and manganese dioxide (MnO2) was developed as a nanocarrier to transport the sonosensitizer IR780 and the generated oxygen into the tumor tissue. The MnO2 shell layer of IR780/PLGA@MnO2 NPs can prevent the premature release of IR780 in the blood and also it can react with acidic and high H2O2, the generated oxygen can relieve tumor tissue hypoxia, and the generated Mn can enhance magnetic resonance imaging (MRI) signal intensity by acting as a contrast agent for MRI. More importantly, the released IR780 can produce ROS to kill tumor cells under ultrasound excitation. This PH-responsive and H2O2-triggered SDT based on the IR780/PLGA@MnO2NPs is an effective platform to inhibit tumor growth with negligible systemic toxicity. This work develops a multifunctional therapeutic integrated nanoplatform for breast cancer treatment, which is expected to be used in the clinic.
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Introduction: Follicular thyroid carcinoma (FTC) rarely metastasizes to regional lymph nodes, as they mainly metastasize through hematogenous route; in particular, a large FTC with only lateral lymph node metastasis and without distant metastasis has rarely been reported. Case report: We present a 66-year-old male patient with a progressively growing thyroid for more than 20 years, causing tracheal compression and narrowing. Neck ultrasonography, computed tomography (CT), magnetic resonance (MR) imaging and positron emission tomography-computed tomography (PET/CT) were carried out to obtain images of the thyroid and surrounding tissues. Total thyroidectomy and cervical lateral and central lymph node dissection were undertaken, and histopathological, and immunohistochemical evaluations and molecular pathology confirmed the diagnosis of FTC with multiple cervical lymph node metastases. Conclusion: We have reported a rare case of large FTC with diffuse nodal involvement but no distant metastases. We present the thyroid ultrasound, neck CT, MR and whole body PET/CT.
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Introduction: Papillary thyroid microcarcinoma (PTMC) that metastasizes to bone, especially metastasizes to contralateral humerus with so large mass, is rarely reported before. Case report: We presented a 50-year-old female patient with a large painful mass in the right humerus for 5 years, presenting with swelling of the right shoulder with limited mobility. Positron emission tomography-computed tomography (PET/CT) showed a large mass in the right humerus, bilateral lung lesions, and enlarged lymph nodes in the right supraclavicular fossa. Right humerus lesion biopsy and immunohistochemical evaluations confirmed that the lesion originated from the thyroid tissue. Then, the thyroid ultrasonography showed a hypo-echoic solid nodule with an irregular taller-than-wide shape in the upper of left thyroid lobe and enlarged lymph nodes with the absence of fatty hilum in the contralateral right IV compartment. The total thyroidectomy and cervical lymph node dissection were undertaken; the histopathology confirmed the diagnosis of PTMC with contralateral cervical lymph node metastasis. Conclusion: We reported a case of PTMC with contralateral large humerus and cervical lymph node metastasis and demonstrated the PET/CT images of the metastatic large humerus and thyroid ultrasonographic appearances of the PTMC and enlarged cervical lymph node.
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OBJECTIVE: Through retrospective analysis of the admission and treatment of patients in the department of critical care medicine of the Affiliated Hospital of Guizhou Medical University over the past 5 years, it provides a basis for the construction of the subspecialty of intensive care medicine. METHODS: Collect clinical data of patients admitted to the department of critical care medicine of the Affiliated Hospital of Guizhou Medical University from January 1, 2016 to December 31, 2020, including gender, age, first consultation department, intensive care unit (ICU) hospitalization time, ventilator use time, main diagnosis, acute physiology and chronic health evaluation II (APACHE II) when transferred into and out of ICU, treatment results, whether to give mechanical ventilation, whether to use a non-invasive ventilator to assist breathing, whether to die in 24 hours, rescue times and success rate, etc. Changes in the above indicators during the 5 years were analyzed. RESULTS: In the past 5 years, our hospital has treated 2 668 patients in the comprehensive ICU with severe neurological, severe circulation, and severe trauma as the main treatment area, including 1 648 males and 1 020 females; aged 6 months to 94 years old, the average age (53.49±19.03) years old. Neurosurgery (907 cases) was the most frequently diagnosed department, the top 3 diseases were cerebral hemorrhage (539 cases), septic shock (214 cases), and hypovolemic shock (200 cases); ICU hospitalization time was 126 (52, 253) hours, ventilator time was 65 (17, 145) hours, APACHE II scores were 23.29±8.12 and 12.99±6.37 when transferred into and out of ICU. The proportion of receiving mechanical ventilation was 92.94% (2 147/2 310), and 314 cases used non-invasive ventilators. 84 cases died within 24 hours (mortality was 3.15%). A total of 2 585 rescues were performed, and the rescue success rate was 92.84% (2 400/2 585). From 2016 to 2020, the 5-year cure rates were 65.92%, 65.83%, 61.53%, 65.64%, 69.06%, respectively, and the 5-year mortality were 13.13%, 14.29%, 18.89%, 16.69%, 13.38%, respectively. CONCLUSIONS: With the continuous expansion of critical care medicine, the establishment of classified subspecialties can focus on the admission of patients, so that treatment can be professionalized and standardized, improve the cure rate, and reduce mortality. At the same time, medical staff can focus on management and learning related expertise to master the disease, it is also more in-depth, which is helpful for doctors to improve themselves, and is conducive to the proficiency of related sub-specialties, and lays a good foundation for the development of the department.
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Cuidados Críticos , Unidades de Cuidados Intensivos , APACHE , Adulto , Anciano , Femenino , Hospitales , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , UniversidadesRESUMEN
Atorvastatin is a classical lipid-lowering drug. It has been reported to have renoprotective effects, such as reducing urinary protein excretion and extracellular matrix aggregation. The present study aimed to investigate the specific mechanism of action of Atorvastatin in type 1 diabetic mice (T1DM) in inhibiting renal tubular epithelial cell injury following treatment with high glucose and high fat. The anti-injury mechanism of Atorvastatin involved the inhibition of miR-21 expression and the upregulation of the transcription and expression of its downstream gene Peroxisome proliferator-activated receptors-α(PPARα). An increase in blood glucose and lipid levels was noted in the T1DM model, which was associated with renal fibrosis and inflammation. These changes were accompanied by increased miR-21 levels, downregulation of PPARα and Mfn1 expressions, and upregulation of Drp1 and IL6 expressions in renal tissues. These phenomena were reversed following the administration of Atorvastatin. miR-21 targeted PPARα by inhibiting its mRNA translation. Inhibition of miR-21 expression or Fenofibrate (PPARα agonist) administration prevented the decrease of PPARα in renal tubular epithelial cells under high glucose (HG) and high fat (Palmitic acid, PA) conditions, alleviating lipid metabolism disorders and reducing mitochondrial dynamics and inflammation. Consistent with the in vivo results, the in vitro findings also demonstrated that mRTECs administered with Atorvastatin in HG + PA increased PPARα expression and restored the normal expression of Mfn1 and Drp1, and effectively increasing the number of biologically active mitochondria and ATP content, reducing ROS production, and restoring mitochondrial membrane potential following Atorvastatin intervention. In addition, these effects were noted to the inhibition of FN expression and tubular cell inflammatory response; however, in the presence of miR-21mimics, the aforementioned effects of Atorvastatin were significantly diminished. Based on these observations, we conclude that Atorvastatin inhibits tubular epithelial cell injury in T1DM with concomitant induction of lipid metabolism disorders by a mechanism involving inhibition of miR-21 expression and consequent upregulation of PPARα expression. Moreover, Atorvastatin regulated lipid metabolism homeostasis and PPARα to restore mitochondrial function. The results emphasize the potential of Atorvastatin to exhibit lipid-regulating functions and non-lipid effects that balance mitochondrial dynamics.
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Background: Stemness acquirement is one of the hallmarks of cancer and the major reason for the chemoresistance and poor prognosis of colorectal cancer (CRC). Previous research has revealed the stimulatory role of paired related homeobox 1 (PRRX1) on CRC metastasis. However, the role of PRRX1 in stemness acquirement and chemoresistance of CRC is still not clear. Methods: A retrospective cohort study was performed to investigate the relationship between PRRX1 expression and multiple clinicopathological characteristics of CRC patients. The functional effects of PRRX1 on stemness and chemoresistance of CRC cells were validated by in vitro and in vivo assays. Gene set enrichment analysis (GSEA) and JASPAR software were performed to predict the underlying mechanisms. Enzyme-linked immunosorbent assay (ELISA), Western blot, immunofluorescence, and dual-luciferase reporter assays were used to confirm the PRRX1-mediated signaling and its downstream factors. Results: The expression of PRRX1 was up-regulated in CRC tissues and cell lines compared to normal epithelial tissues and cell lines. High expression of PRRX1 was tightly associated with the metastasis, chemoresistance, and poor prognosis of CRC patients. Additionally, PRRX1 significantly promoted the proliferation, viability, stemness, and chemoresistance of CRC cells, as well as the activation of the interleukin-6 (IL-6)/JAK2/STAT3 axis. Inhibiting the expression of IL-6 dramatically eliminated the effects of PRRX1 on CRC cell stemness and chemoresistance. Conclusions: PRRX1 plays a vital role in the stemness and chemoresistance of CRC cells via JAK2/STAT3 signaling by targeting IL-6. Further, PRRX1 may be a valid biomarker for predicting the effect of chemotherapy and prognosis of CRC patients.
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Introduction: Diabetic kidney disease (DKD) is one of the complications of diabetes; however, the pathogenesis is not yet clear. A recent study has shown that senescence is associated with the course of DKD. In the present study, we explored whether senescent renal tubular cells promote renal tubulointerstitial fibrosis by secreting Sonic hedgehog (Shh) which mediates fibroblast activation and proliferation in DKD. Methods: A 36-week-old db/db mice model and the renal tubular epithelial cells were cultured in high glucose (HG, 60 mmol/L) medium for in vivo and in vitro experiments. Results: Compared to db/m mice, blood glucose, microalbuminuria, serum creatinine, urea nitrogen, and UACR (microalbuminuria/urine creatinine) were markedly increased in db/db mice. Collagen III, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF-α) were also increased in db/db mice kidneys, suggesting fibrosis and inflammation in the organ. Moreover, the detection of SA-ß-galactosidase (SA-ß-Gal) showed that the activity of SA-ß-Gal in the cytoplasm of renal tubular epithelial cells increased, and the cell cycle inhibition of the expression of senescence-related gene cell cycle inhibitor p16 INK4A protein and p21 protein increased, indicating that renal fibrosis in db/db mice was accompanied by cell senescence. Furthermore, Shh is highly expressed in the injured renal tubules and in the kidney tissue of db/db mice, as detected by enzyme-linked immunosorbent assay (ELISA). The results of immunofluorescence staining showed increased positive staining for Shh in renal tubular epithelial cells of db/db mice and decreased positive staining for Lamin B1, but increased positive staining for γH2A.X in cells with high Shh expression; similar results were obtained in vitro. In addition, HG stimulated renal tubular epithelial cells to secrete Shh in the supernatant of the medium. D-gal treatment of renal tubular epithelial cells increased the protein levels of Shh and p21. We also found enhanced activation and proliferation of fibroblasts cultured with the supernatant of renal tubular epithelial cells stimulated by HG medium but the proliferative effect was significantly diminished when co-cultured with cyclopamine (CPN), an inhibitor of the Shh pathway. Discussion: In conclusion, HG induces renal tubular epithelial cell senescence, and the secretion of senescence-associated proteins and Shh mediates inflammatory responses and fibroblast activation and proliferation, ultimately leading to renal fibrosis.
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AIMS: Metaplastic breast cancer (MBC) comprises a heterogeneous group of tumors, of which MBC with osseous differentiation (MBC-OD) is extremely rare that only few cases have been reported. This study aimed to present the clinicopathologic and molecular features of MBC-OD. METHODS: We collected 6 cases of MBC-OD from five different centers and described its clinicopathologic and molecular characteristics based on the next-generation sequencing. Another 11 cases from the literature were also reviewed to better characterize the tumor. RESULTS: The tumor primarily showed an osteosarcoma-like appearance, which composed of high cellularity with spindle cells and osteoblast-like cells producing coarse lace-like neoplastic bone (4/6) or osteoid matrix (6/6). 55 somatic mutations including 39 missenses (70.9%), 9 frameshifts (16.4%), 3 splice sites (5.5%), 3 in-frame InDels (5.5%) and 1 nonsense (1.8%) were identified. TP53 was the most frequently mutated genes (5/6, 83.3%), followed by RB1 (3/6, 50.0%), BCOR (2/6, 33.3%), MED12 (2/6, 33.3%), PIK3CA (2/6, 33.3%), and TET2 (2/6, 33.3%). Genetic alterations suggesting therapies with clinical benefit, including mTOR inhibitors, tyrosine kinase inhibitors (TKI), and poly-ADP ribose polymerase inhibitor (PARPi), were observed in five cases. The median follow-up was 21 months (range, 3-80 months). Local recurrence was observed in two cases and three patients displayed distant metastasis. Two patients died of the disease at 3 months and 7 months, respectively. CONCLUSIONS: Based on this series, MBC-OD is a highly aggressive breast tumor with osteosarcoma-like morphology and a high incidence of recurrent disease showing specific genetic profiles.
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Neoplasias Óseas/patología , Neoplasias Óseas/secundario , Neoplasias de la Mama/patología , Adulto , Anciano , Biomarcadores de Tumor , Neoplasias de la Mama/genética , Femenino , Humanos , Mastectomía , Persona de Mediana Edad , MutaciónRESUMEN
PD-1/PD-L1 blockade therapies provide notable clinical benefits for patients with advanced cancers, but the factors influencing the effectiveness of the treatment remain incompletely cataloged. Here, the up-regulation of laminin γ2 (Ln-γ2) predicted the attenuated efficacy of anti-PD-1 drugs and was associated with unfavorable outcomes in patients with lung cancer or esophageal cancer. Furthermore, Ln-γ2 was transcriptionally activated by transforming growth factor-ß1 (TGF-ß1) secreted from cancer-associated fibroblasts via JNK/AP1 signaling, which blocked T cell infiltration into the tumor nests by altering the expression of T cell receptors. Coadministration of the TGF-ß receptor inhibitor galunisertib and chemotherapy drugs provoked vigorous antitumor activity of anti-PD-1 therapy in mouse tumor models. Therefore, Ln-γ2 may represent a useful biomarker to optimize clinical decisions and predict the response of cancer patients to treatment with anti-PD-1 drugs.
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OBJECTIVE: To analyze the pathogenic factors, clinical features and treatment measures of critically ill pregnant women so as to provide experience for improving the success rate of treatment. METHODS: The clinical data of 167 cases of critically ill pregnant women who admitted to intensive care unit (ICU) of the Affiliated Hospital of Guizhou Medical University from January 2013 to December 2017 were collected, and the disease distribution of patients, the causes of postpartum hemorrhage, the treatment situation and the results. Patients were divided into obstetrical complications group, pregnancy complicated with basic diseases group and other complicated diseases group according to disease types, and the treatment status of each group was analyzed. RESULTS: Among 167 critically ill pregnant women, 118 cases (70.6%) were in the obstetric complications group, 26 cases (15.6%) were in the pregnancy complicated with basic diseases group, and 23 cases (13.8%) were in the other complicated diseases group. Nine cases died in 167 critically ill pregnant women, with a mortality rate of 5.4%. Postpartum hemorrhage was the major obstetric complication (35.3%), and the coagulation function of 59 patients with postpartum hemorrhage was significantly improved 48 hours after active hemostasis and reasonable blood transfusion [compared to entering the ICU, prothrombin time (PT, s): 14.49±4.66 vs. 23.39±8.11, activated partial thromboplastin time (APTT, s): 52.94±36.36 vs. 87.35±74.69, fibrinogen (Fib, g/L): 2.91±1.03 vs. 1.03±0.65, platelet count (PLT, ×109/L): 94.85±30.09 vs. 43.15±24.07, all P < 0.01]. Compared with pregnancy complicated basic diseases group and other complicated diseases group, the acute physiology and chronic health evaluation II (APACHE II) scores was reduced significantly in obstetrical complications group (10.41±4.85 vs. 16.46±13.87, 16.90±8.82, both P < 0.05), the length of ICU stay was significantly reduced (hours: 57.83±34.67 vs. 79.64±36.01, 278.30±83.72, both P < 0.05). Compared with other complicated diseases group, the mechanical ventilation time [hours :14 (6, 38) vs. 43 (12, 396)] and mortality (0.8% vs. 13.0%) were significantly decreased in obstetrical complications group (both P < 0.05). CONCLUSIONS: Observe the changes of the condition closely, necessary hemodynamic treatment, respiratory support, and organ function support with critically ill pregnant women can improve the rescue success rate and prognosis.