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A study published in the journal Clinical & Translational Medicine suggests that analyzing microbial communities could be a useful tool for diagnosing and predicting the prognosis of pancreatic tumors. The researchers examined fecal and intratumor microbial samples from patients with pancreatic tumors and healthy volunteers. They discovered that specific bacteria in fecal samples could potentially serve as non-invasive biomarkers for early detection of pancreatic tumors. Furthermore, they observed differences in the microbial composition of pancreatic tissues between malignant and non-malignant tumors. These findings indicate that microbial profiling may offer a promising approach for improving the early detection and treatment of pancreatic tumors. [Extracted from the article]

Background: The status of the hypothalamic‐pituitary‐gonadal (HPG) axis is important for assessing the onset of physiological or pathological puberty. The reference standard gonadotropin‐releasing hormone (GnRH) stimulation test requires hospital admission and repeated blood samples. A simple noninvasive method would be beneficial. Objectives: To explore a noninvasive method for evaluating HPG axis activation in children using an MRI radiomics model. Study Type: Retrospective. Population: Two hundred thirty‐nine children (83 male; 3.6–14.6 years) with hypophysial MRI and GnRH stimulation tests, randomly divided a training set (168 children) and a test set (71 children). Field Strength/Sequence: 3.0 T, 3D isotropic fast spin echo (CUBE) T1‐weighted imaging (T1WI) sequences. Assessment: Radiomics features were extracted from sagittal 3D CUBE T1WI, and imaging signatures were generated using the least absolute shrinkage and selection operator (LASSO) with 10‐fold cross‐validation. Diagnostic performance for differential diagnosis of HPG status was compared between a radiomics model and MRI features (adenohypophyseal height [aPH] and volume [aPV]). Statistical Tests: Receiver operating characteristic (ROC) and decision curve analysis (DCA). A P value <0.05 was considered statistically significant. Results: Eight hundred fifty‐one radiomics features were extracted and reduced to 10 by the LASSO method in the training cohort. The radiomics model based on CUBE T1WI showed good performance in assessment of HPG axis activation with an area under the ROC curve (AUC) of 0.81 (95% CI: 0.71, 0.91) in the test set. The AUC of the radiomics model was significantly higher than that of aPH (0.81 vs. 0.65) but there was no significant difference compared to aPV (0.81 vs. 0.78, P = 0.58). In DCA analysis, the radiomics signature showed higher net benefit over the aPV and aPH models. Data Conclusions: The MRI radiomics model has potential to assess HPG axis activation status noninvasively, potentially providing valuable information in the diagnosis of patients with pathological puberty onset. Evidence Level: 4 Technical Efficacy: Stage 2 [ABSTRACT FROM AUTHOR]

Background and Aim: Several indicators are recognized in the development of clinically relevant postoperative pancreatic fistula (CR‐POPF) after pancreaticoduodenectomy (PD). However, drain fluid volume (DFV) remains poorly studied. We aimed to discover the predictive effects of DFV and guide clinical management. Methods: We retrospectively reviewed the clinical data of patients that received PD between January 2015 and December 2019 in a high‐volume center. DFV was analyzed as a potential risk factor and postoperative short‐term outcomes as well as drain removal time were compared stratified by different DFV levels. Receiver operating characteristic curves and area under curves (AUC) were compared for DFV alone and DFV combined with drain fluid amylase (DFA). Subgroup analysis of DFV stratified by DFA evaluated the predictability of CR‐POPF. Results: CR‐POPF occurred in 19.7% of 841 patients. Hypertension, postoperative day 3 (POD3) DFA ≥ 300 U/L, and POD3 DFV ≥ 30 mL were independent risk factors, while pancreatic main duct diameter ≥ 3 mm was a protective factor. POD3 DFV ≥ 30 mL increased the overall occurrences of CR‐POPF and major complications (P = 0.017; P = 0.029). POD3 DFV alone presented a low predictive value (AUC 0.602), while POD3 DFV combined with DFA had a high predictive value (AUC 0.759) for CR‐POPF. Subgroup analysis showed that the combination of POD3 DFV ≥ 30 mL and DFA ≥ 300 U/L led to higher incidences of CR‐POPF (P = 0.003). Conclusion: CR‐POPF is common after PD, and high DFV combined with DFA may predict its occurrence and facilitate appropriate management. [ABSTRACT FROM AUTHOR]

Background: Major depressive disorder (MDD) and anxiety were recognized in treating pancreatic ductal adenocarcinoma (PDAC). This longitudinal study identified risk factors for MDD and anxiety and established associations with patients' quality of life (QoL) and survival outcomes. Materials and Methods: We used PHQ‐9 and GAD‐7 questionnaires to diagnose MDD and anxiety in PDAC patients between October 2021 and March 2022 at a Chinese center. Characteristics and clinical data were analyzed for risk factors and EORTC QLQ‐C30 questionnaire was administered for QoL before the first chemotherapy. Furthermore, chemotherapy compliance and 1‐year survival were compared during follow‐up. Results: MDD and anxiety occurred in 51.8% and 44.7% of 114 patients over the half‐year period. Employment at work (odds ratio [OR]: 5.514, p = 0.001; OR: 3.420, p = 0.011) was an independent risk factor, while radical surgery (OR: 0.342, p = 0.034; OR: 0.238, p = 0.004) was a protective factor. Several aspects of decreased QoL were discovered after their onsets. Higher incidences of physical disorders (p = 0.004; p < 0.001), mental disorders (p = 0.001; p < 0.001), anti‐therapy emotions (p = 0.002; 0.001), and chemotherapy suspensions (p = 0.001; p = 0.043) were observed. Furthermore, the 1‐year mortalities for all patients and those receiving radical surgeries were correlated with MDD (p = 0.007; 0.036) and anxiety (p = 0.010; 0.031). Conclusions: MDD and anxiety are common in PDAC patients and correlated with poor QoL and survivals. Therefore, appropriate mental management is required in future. [ABSTRACT FROM AUTHOR]

Background: While an association between postoperative acute kidney injury (AKI) and adverse events exists, the incidence and impact of postoperative AKI after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma remain unclear. This study aimed to diagnose AKI and investigate the risk factors for and prognostic value of postoperative AKI. Methods: Clinical characteristics of patients who underwent pancreaticoduodenectomy between 2013 and 2020 at a high‐volume centre were collected retrospectively. The Kidney Disease Improving Global Outcomes criteria were used to diagnose AKI. A 1:2 propensity score matching (PSM) was used to minimise bias between the AKI and non‐AKI groups. Short‐term surgical and long‐term survival outcomes were compared between groups. Multivariate logistic regression analysis assessed the independent risk factors for AKI development, major complications, and 30‐day mortality. Results: Postoperative AKI occurred in 10.7% of 1312 patients. Total bilirubin level > 250 μmol/L (odds ratio [OR]: 3.24; p < 0.001), estimated glomerular filtration rate < 60 ml/min/1.73 m2 (OR: 2.30; p = 0.048), and intraoperative estimated blood loss >1000 ml (OR: 2.96; p = 0.001) were independent risk factors for postoperative AKI. After PSM, higher incidences of major complications (p < 0.001) and 30‐day mortality (p < 0.001) were observed in the AKI group than in the non‐AKI group. There was no difference in long‐term overall survival outcomes between both groups (p = 0.535). AKI was an independent predictor of major complications (OR: 3.06; p < 0.001) and 30‐day mortality (OR: 2.87; p = 0.034). Conclusions: Postoperative AKI is common after pancreaticoduodenectomy for pancreatic ductal adenocarcinoma and has a predictive effect on major complications and 30‐day mortality. Therefore, prevention and proper management of postoperative AKI are required in clinical practice. [ABSTRACT FROM AUTHOR]

Background: Corticospinal tract (CST) injury has been shown to exert a major influence on functional recovery after ischemic stroke. Purpose To evaluate the prognostic value of CST injury estimated using a recent developed tractometry‐based method. Study Type: Prospective. Population: Forty‐eight patients with CST damage induced by stroke lesion who underwent brain magnetic resonance imaging within 7 days from onset. Sequence Diffusion‐weighted imaging (b = 1000 seconds/mm2) and diffusion kurtosis imaging (DKI) spin‐echo echo‐planar sequence with three b‐values (0, 1250, and 2500 seconds/mm2) at 3.0 T. Assessment A recently developed approach that combines tract segmentation and orientation mapping was used for CST‐specific tractography and tractometry. CST injury was estimated using the proposed method with diffusion metrics extracted from DKI sequence and with the first principal component (PC1) of the metrics. We also calculated the weighted lesion load (wLL) for comparison. Clinical evaluation included the National Institutes of Health Stroke Score in the acute phase and the modified Rankin scale at 3 months post‐stroke. The correlations between CST injury and initial motor impairment, as well as the prognostic values of CST injury for functional outcomes were evaluated. Statistical Tests: Pearson correlation and logistic regression. Area under the receiver operating characteristic curve. P < 0.05 was considered statistically significant. Results: CST injury calculated with diffusion metrics except fractional anisotropy all showed significant correlations with initial motor impairment. PC1 achieved the largest correlation coefficient (R = 0.65) compared with wLL and other diffusion metrics. In addition to wLL, DKI_AK, AFD_total, and PC1 maximum all showed predictive values for functional outcomes. Data Conclusion: Structural injury to CST is important for the assessment of the extent of injury and the prediction of functional outcome. The method proposed in our study could provide an imaging indicator to quantify the CST injury after ischemic stroke. Level of Evidence: 2 Technical Efficacy: Stage 1 [ABSTRACT FROM AUTHOR]

Haematopoietic stem/progenitor cell (HSPC) integrates intracellular signal network from growth factors (GFs) and utilizes its proliferation feature to generate high yields of transplantable cells upon ex vivo culture. However, the molecular basis for HSPC activation and proliferation is not completely understood. The goal of this study was to investigate proliferation regulator in the downstream of GFs and develop HSPC expansion strategy. Microarray and Ingenuity Pathway Analysis were performed to evaluate differentially expressed genes in cytokine‐induced CD34+ cells after ex vivo culture. We identified that MEK1 was a potential HSPC proliferation regulator, which represented indispensable roles and MEK1 silence attenuated the proliferation of HSPC. Notably, 500 nM MEK1 agonist, PAF C‐16, increased the numbers of phenotypic HSPC and induced cell cycling of HSPC. The PAF C‐16 expanded HSPC demonstrated comparative clonal formation ability and secondary expansion capacity compared to the vehicle control. Our results provide insights into regulating the balance between proliferation and commitment of HSPC by targeting the HSPC proliferation‐controlling network. This study demonstrates that MEK1 critically regulates HSPC proliferation and cell production in the ex vivo condition for transplantation. [ABSTRACT FROM AUTHOR]

Recently, the first‐line anti‐diabetic drug metformin shows versatile protective effects against several diseases and is potentially prescribed to healthy individual for prophylactic use against ageing or other pathophysiological processes. However, for healthy individuals, it remains unclear what effects metformin treatment will induce on their bodies. A systematic profiling of the molecular landscape of metformin treatment is expected to provide crucial implications for this issue. Here, we delineated the first transcriptomic landscape induced by metformin in 10 tissues (aorta, brown adipose, brain, eye, heart, liver, kidney, skeletal muscle, stomach and testis) of healthy mice by using RNA‐sequencing technique. A comprehensive computational analysis was performed. The overrepresentation of cardiovascular disease‐related gene sets, positive correlation with hypertension‐related transcriptomic signatures and the associations of drugs with hypertensive side effect together indicate that although metformin does exert various beneficial effects, it would also increase the risk of hypertension in healthy mice. This prediction was experimentally validated by an independent animal experiments. Together, this study provided important resource necessary for investigating metformin's beneficial/deleterious effects on various healthy tissues, when it is potentially prescribed to healthy individual for prophylactic use. [ABSTRACT FROM AUTHOR]

Background information. STAT3 (signal transducer and activator of transcription 3) is an important transcription factor involved in many biological events, including apoptosis, tumorigenesis, angiogenesis and epithelial‐to‐mesenchymal transition. However, no direct evidence for a role of STAT3 in 3T3‐L1 adipocyte differentiation has been reported. Results. In the present study, we found that rapid activation of STAT3, lasting for more than 48 h, was elicited upon induction of adipogenesis. Both the STAT3‐selective inhibitor stattic and the JAK2 (Janus kinase 2)/STAT3‐selective inhibitors AG490 and Gö6976 inhibited STAT3 activation, leading to the suppression of adipocyte differentiation. Adipocyte differentiation was also suppressed by STAT3 siRNA (small interfering RNA) or dominant‐negative STAT3. Interestingly, the PPARγ (peroxisome‐proliferator‐activated receptor γ) agonist TAZ (troglitazone) abolished the STAT3‐inhibitor‐ and RNAi (RNA interference)‐mediated suppression of adipogenesis. However, TAZ treatment had no effect on the stattic‐ and AG490‐mediated down‐regulation of STAT3 activation, suggesting that STAT3 regulates adipocyte differentiation through signalling that occurs upstream of PPARγ. Conclusion. These data indicate that STAT3 functions as a critical factor for adipogenesis via a mechanism involving the PPARγ activation pathway. [ABSTRACT FROM AUTHOR]

Background and Aim Methods Results Conclusion Early predictors of morbidity after pancreaticoduodenectomy (PD) can guide tailored postoperative management. Preoperative inflammatory data in patients who underwent PD remained poorly studied in investigating the clinical significance of predicting postpancreatectomy acute pancreatitis (PPAP) and PPAP‐associated postoperative pancreatic fistula (POPF).The clinical data of 467 patients receiving PD between January 2020 and December 2022 were retrospectively reviewed. Preoperative inflammatory data were stratified according to PPAP, and independent risk factors were analyzed. Multivariate logistic regression and subgroup analyses were conducted to compare risk factors of PPAP‐associated POPF and non‐PPAP‐associated POPF.PPAP occurred in 17.6% of patients. The incidence of other complications increased following PPAP. Among the preoperative inflammatory factors, only interleukin‐6 (IL‐6) increased (P < 0.001), leading to a higher incidence of PPAP and POPF (P < 0.001; P = 0.002). The area under the curve of IL‐6 in predicting PPAP was 0.71 (0.65–0.77; P < 0.001). Abnormal preoperative IL‐6 levels (odds ratio [OR]: 5.01; P < 0.001), soft pancreatic texture (OR: 2.15; P = 0.007), and pathology (OR: 2.03; P = 0.012) were independent risk factors for PPAP. The subgroup analysis showed that increased IL‐6 (OR: 1.01; P = 0.006) and soft pancreatic texture (OR: 2.05; P = 0.033) resulted in a higher risk of PPAP‐associated POPF, while increased IL‐8 (OR: 1.01; P = 0.007), older age (OR: 1.05; P = 0.008), and higher body mass index (OR: 1.12; P = 0.021) correlated with non‐PPAP‐associated POPF.PPAP is common after PD; a high preoperative IL‐6 level can predict its occurrence, in addition to associated POPF, which could be due to a preoperative proinflammatory status. [ABSTRACT FROM AUTHOR]

Background Information: STAT3 (signal transducer and activator of transcription 3) is an important transcription factor involved in many biological events, including apoptosis, tumorigenesis, angiogenesis and epithelial-to-mesenchymal transition. However, no direct evidence for a role of STAT3 in 3T3-L1 adipocyte differentiation has been reported., Results: In the present study, we found that rapid activation of STAT3, lasting for more than 48 h, was elicited upon induction of adipogenesis. Both the STAT3-selective inhibitor stattic and the JAK2 (Janus kinase 2)/STAT3-selective inhibitors AG490 and Gö6976 inhibited STAT3 activation, leading to the suppression of adipocyte differentiation. Adipocyte differentiation was also suppressed by STAT3 siRNA (small interfering RNA) or dominant-negative STAT3. Interestingly, the PPARgamma (peroxisome-proliferator-activated receptor gamma) agonist TAZ (troglitazone) abolished the STAT3-inhibitor- and RNAi (RNA interference)-mediated suppression of adipogenesis. However, TAZ treatment had no effect on the stattic- and AG490-mediated down-regulation of STAT3 activation, suggesting that STAT3 regulates adipocyte differentiation through signalling that occurs upstream of PPARgamma., Conclusion: These data indicate that STAT3 functions as a critical factor for adipogenesis via a mechanism involving the PPARgamma activation pathway.