Isolated bovine pancreatic islets as an alternate in vitro model for diabetes research.

Background & objectives Isolation of functional pancreatic islets for diabetes research and clinical islet transplantation stands as a big challenge despite the advancements in the field. In this context, the non-availability of human/animal tissues is one of the major impediments to islet-based research, which has tremendous scope for translation. The current study explores the feasibility of using the bovine pancreas as an alternative source to isolate pancreatic islets and assess its functionality for in vitro studies. Methods The bovine pancreas was collected from a registered slaughterhouse and transported in an ice-cold medium - Hank's Balanced Salt Solution (HBSS) to the laboratory. Islets were isolated by sequential collagenase digestion followed by a two-step filtration and purification by density gradient separation method. After isolation, islets were identified with dithizone staining and the islet function was assayed in vitro for assessing the dynamic insulin secretory function by monitoring the glucose-stimulated insulin secretion (GSIS), in response to low and high glucose. Staining techniques were also used to understand the cytoarchitecture of the bovine pancreas. Results The islet yield was 157±23 islets per gram of pancreas and was viable. The cold ischaemia time was reduced to 60-75 min. The islets released insulin with glucose stimulation. The insulin release was observed more with high glucose (28 mM) than with low glucose (2.8 mM). Dithizone staining confirmed the presence of islets after isolation and the size of islets ranged from 50 to 600 µm size. The mantled islets (islets with acinar tissue) were also noted with the pure islets in culture. Hematoxylin and eosin (H&E) and aldehyde- fuchsin showed islets interspersed in the acinar tissue of the bovine pancreas. Special stain defined the islets better than regular staining. Fluorescent and diaminobenzidine (DAB) staining with insulin, glucagon and somatostatin revealed the arrangement of the cells in each islet. The beta cells were majorly found in the islet core with alpha cells interspersed with the delta cells in the periphery. Interpretation & conclusions The isolation procedure described in this study yielded viable islets for in vitro studies which showed a differential response to glucose challenge, confirming their viability. We provide a simple and reproducible method for small-scale isolation of functional islets from the bovine pancreas. This model proffers the beginner a hands-on in islet experiments and helps to re-iterate the process that could be extrapolated to other pancreatic tissues as well as to expand on diabetes research.

Tankyrase inhibition promotes endocrine commitment of hPSC-derived pancreatic progenitors.

Human pluripotent stem cells (hPSCs) have the potential to differentiate into various cell types, including pancreatic insulin-producing ß cells, which are crucial for developing therapies for diabetes. However, current methods for directing hPSC differentiation towards pancreatic ß-like cells are often inefficient and produce cells that do not fully resemble the native counterparts. Here, we report that highly selective tankyrase inhibitors, such as WIKI4, significantly enhances pancreatic differentiation from hPSCs. Our results show that WIKI4 promotes the formation of pancreatic progenitors that give rise to islet-like cells with improved ß-like cell frequencies and glucose responsiveness compared to our standard cultures. These findings not only advance our understanding of pancreatic development, but also provide a promising new tool for generating pancreatic cells for research and potential therapeutic applications.

The safety and efficacy of stapler method for transection of the pancreatic parenchyma during pancreatoduodenectomy (STRAP-PD trial): study protocol for a randomized control trial.

BACKGROUND: Pancreaticoduodenectomy is a highly difficult and invasive type of gastrointestinal surgery. Prevention of postoperative pancreatic fistula is important, and this may be possible by the stapler method. METHODS: STRAP-PD is a single center randomized controlled trial. We compare a method of transecting the pancreatic parenchyma in pancreaticoduodenectomy using a surgical stapler device with a conventional transecting method using energy devices (e.g., scalpel, ultrasonic coagulator and incision devices). Patients with soft pancreas who are scheduled to undergo pancreaticoduodenectomy are randomized to arm A (conventional method) or arm B (stapler method). We aim to examine the safety and usefulness of dissection by the automatic suture device, with attention to the rate of pancreatic fistula ISGPF grade B or C and to postoperative complications. This is a single-center randomized study, which began in September 2023 at Wakayama Medical University Hospital. DISCUSSION: Pancreatic parenchymal transection is typically performed either by direct incision using a scalpel or by employing energy devices such as ultrasonic coagulating cutting devices during pancreaticoduodenectomy. In a prospective pilot study, we conducted pancreatic parenchymal transection in 20 consecutive normal pancreatic cases during pancreaticoduodenectomy, observing postoperative pancreatic fistula grade B in one case (5%). Traditional methods involving scalpel incision or the use of ultrasonic coagulating cutting devices have been historically favored but perceived as technically challenging, and they have been reliant upon the surgeon's skill. Notably, relatively high incidences of postoperative pancreatic fistula among patients with soft pancreas have also been observed. Our proposed stapler method may therefore be a useful method responsible for reducing the development of pancreatic fistula. This method would be as part of minimally-invasive surgery for pancreaticoduodenectomy. It uses an endoscopic linear stapler to cut the pancreatic parenchyma, so it is likely to be more convenient than conventional methods and can be used universally. TRIAL REGISTRATION: University Hospital Medical Information Network Clinical Trials Registry, UMIN000052089. the Registration Date on 1st September 2023.

Maternal diet during pregnancy and adaptive changes in the maternal and fetal pancreas have implications for future metabolic health.

Fetal and neonatal development is a critical period for the establishment of the future metabolic health and disease risk of an individual. Both maternal undernutrition and overnutrition can result in abnormal fetal organ development resulting in inappropriate birth size, child and adult obesity, and increased risk of Type 2 diabetes and cardiovascular diseases. Inappropriate adaptive changes to the maternal pancreas, placental function, and the development of the fetal pancreas in response to nutritional stress during pregnancy are major contributors to a risk trajectory in the offspring. This interconnected maternal-placental-fetal metabolic axis is driven by endocrine signals in response to the availability of nutritional metabolites and can result in cellular stress and premature aging in fetal tissues and the inappropriate expression of key genes involved in metabolic control as a result of long-lasting epigenetic changes. Such changes result is insufficient pancreatic beta-cell mass and function, reduced insulin sensitivity in target tissues such as liver and white adipose and altered development of hypothalamic satiety centres and in basal glucocorticoid levels. Whilst interventions in the obese mother such as dieting and increased exercise, or treatment with insulin or metformin in mothers who develop gestational diabetes, can improve metabolic control and reduce the risk of a large-for-gestational age infant, their effectiveness in changing the adverse metabolic trajectory in the child is as yet unclear.

Machine learning-assisted mid-infrared spectrochemical fibrillar collagen imaging in clinical tissues.

Significance: Label-free multimodal imaging methods that can provide complementary structural and chemical information from the same sample are critical for comprehensive tissue analyses. These methods are specifically needed to study the complex tumor-microenvironment where fibrillar collagen's architectural changes are associated with cancer progression. To address this need, we present a multimodal computational imaging method where mid-infrared spectral imaging (MIRSI) is employed with second harmonic generation (SHG) microscopy to identify fibrillar collagen in biological tissues. Aim: To demonstrate a multimodal approach where a morphology-specific contrast mechanism guides an MIRSI method to detect fibrillar collagen based on its chemical signatures. Approach: We trained a supervised machine learning (ML) model using SHG images as ground truth collagen labels to classify fibrillar collagen in biological tissues based on their mid-infrared hyperspectral images. Five human pancreatic tissue samples (sizes are in the order of millimeters) were imaged by both MIRSI and SHG microscopes. In total, 2.8 million MIRSI spectra were used to train a random forest (RF) model. The other 68 million spectra were used to validate the collagen images generated by the RF-MIRSI model in terms of collagen segmentation, orientation, and alignment. Results: Compared with the SHG ground truth, the generated RF-MIRSI collagen images achieved a high average boundary F -score (0.8 at 4-pixel thresholds) in the collagen distribution, high correlation (Pearson's R 0.82) in the collagen orientation, and similarly high correlation (Pearson's R 0.66) in the collagen alignment. Conclusions: We showed the potential of ML-aided label-free mid-infrared hyperspectral imaging for collagen fiber and tumor microenvironment analysis in tumor pathology samples.

Surgical treatment of chronic pancreatitis with an inflammatory pancreatic head mass: a retrospective study.

BACKGROUND: Conservative treatment of chronic pancreatitis has only a limited effect in most patients. Surgery offers very good long-term results, even in the early stages of the disease. Unfortunately, only a minority of patients undergo surgical treatment. The aim of this work was to summarise the current treatment options for patients with an inflammatory mass of the pancreatic head. Data from patients in our study demonstrates that the surgery is a safe method, and here we compare the perioperative and early postoperative outcomes of patients who underwent a pancreatoduodenectomy and duodenum-preserving pancreatic head resection for chronic pancreatitis. METHODS: All patients who underwent a pancreaticoduodenectomy or a duodenum-preserving pancreatic head resection in our department between 2014 and 2022 were included in this study. Perioperative and early postoperative results were statistically analysed and compared. RESULTS: Thirty-eight pancreaticoduodenectomies and 23 duodenum-preserving pancreatic head resections were performed. The overall mortality was 3%, whereas the in-hospital mortality after pancreaticoduodenectomy was 5%. The mortality after duodenum-preserving pancreatic head resection was 0%. No statistically significant differences in the hospital stay, blood loss, and serious morbidity were found in either surgery. Operative time was significantly shorter in the duodenum-preserving pancreatic head resection group. CONCLUSIONS: Both pancreatoduodenectomy and duodenum-preserving pancreatic head resection are safe treatment options. Duodenum-preserving pancreatic head resection showed a statistically significant superiority in the operative time compared to pancreaticoduodenectomy. Although other monitored parameters did not show a statistically significant difference, the high risk of complications after pancreaticoduodenectomy with a mortality of 5%; maintenance of the duodenum and upper loop of jejunum, and lower risk of metabolic dysfunctions after duodenum-preserving pancreatic head resection may favour duodenum-preserving pancreatic head resection in recommended diagnoses. Attending physicians should be more encouraged to use a multidisciplinary approach to assess the suitability of surgical treatment in patients with chronic pancreatitis.

DRG payment for major pancreatic surgery: analysis of resource consumption and suggestions from a tertiary hospital in China.

Aim: To investigate the cost homogeneity within the Diagnosis-Related Group (DRG) "major operation of pancreas and liver, with general complications or comorbidities" (HB13), its cost-influencing factors, and to propose suggestions for better grouping efficacy. Methods: Medical and insurance settlement data of inpatients covered by the DRG payment system at the author's institution were collected from March 15, 2022 to December 31, 2023. The cost homogeneity of group HB13 was assessed using the coefficient of variation (CV). Clinical factors that may have an impact on hospitalization cost for patients undergoing pancreatic surgery were identified through a semi-structured interview administered to the pancreatic surgeons in author's department, their significance was analyzed using multiple linear regression, along with their impact on the cost of different service categories. A proposal to subdivide HB13 was made and evaluated by CV and t-test. Results: The CV of the HB13 group was 0.4. Robotic-assisted surgery and pancreaticoduodenectomy were two independent factors that significantly affected the total cost. Patients undergoing robotic-assisted surgery have an average increase of 41,873 CNY in total cost, primarily derived from operation fee. Patients undergoing pancreaticoduodenectomy have an average increase of 37,487 CNY in total cost, with significant increases across all service categories. HB13 was subdivided based on whether pancreaticoduodenectomy was performed. The newly formed groups exhibited lower CVs than the original HB13. Conclusion: The cost homogeneity of HB13 was lower than that of other DRG groups in author's department. It is recommended to introduce a supplementary payment for patients requiring robotic-assisted surgery, to guarantee their access to this advanced technology. It is recommended to establish a new group with higher payment standard for patients undergoing pancreaticoduodenectomy. A tiered CV criterion for the evaluation of grouping efficacy is recommended to increase intra-group homogeneity, facilitating a better allocation of health insurance funds, and the prevention of unintended negative outcomes such as service cuts and cherry-picking.

Discovery of natural anthraquinones as potent inhibitors against pancreatic lipase: structure-activity relationships and inhibitory mechanism.

Obesity is acknowledged as a significant risk factor for various metabolic diseases, and the inhibition of human pancreatic lipase (hPL) can impede lipid digestion and absorption, thereby offering potential benefits for obesity treatment. Anthraquinones is a kind of natural and synthetic compounds with wide application. In this study, the inhibitory effects of 31 anthraquinones on hPL were evaluated. The data shows that AQ7, AQ26, and AQ27 demonstrated significant inhibitory activity against hPL, and exhibited selectivity towards other known serine hydrolases. Then the structure-activity relationship between anthraquinones and hPL was further analysed. AQ7 was found to be a mixed inhibition of hPL through inhibition kinetics, while AQ26 and AQ27 were effective non-competitive inhibition of hPL. Molecular docking data revealed that AQ7, AQ26, and AQ27 all could associate with the site of hPL. Developing hPL inhibitors for obesity prevention and treatment could be simplified with this novel and promising lead compound.

The effects of Cannabis sativa and cannabinoids on the inhibition of pancreatic lipase - An enzyme involved in obesity.

INTRODUCTION: Obesity is a chronic noncommunicable disease characterized by excessive body fat that can have negative health consequences. Obesity is a complex disease caused by a combination of genetic, environmental, and lifestyle factors. It is characterized by a discrepancy between caloric intake and expenditure. Obesity increases the risk of acquiring major chronic diseases, including heart disease, stroke, cancer, and Type 2 diabetes mellitus (T2DM). Currently, the inhibition of pancreatic lipases (PL) is a promising pharmacological therapy for obesity and weight management. In this study, the inhibition of pancreatic lipase by Cannabis sativa (C. sativa) plant extract and cannabinoids was investigated. METHODS: The inhibitory effect was assessed using p-nitrophenyl butyrate (pNPB), and the results were obtained by calculating the percentage relative activity and assessed using one-way analysis of variance (ANOVA). Kinetic studies and spectroscopy techniques were used to evaluate the mode of inhibition. Diet-induced; and diabetic rat models were studied to evaluate the direct effects of C. sativa extract on PL activity. RESULTS: Kinetic analyses showed that the plant extracts inhibited pancreatic lipase, with tetrahydrocannabinol (THC) and cannabinol (CBN) being the potential cause of the inhibition noted for the C. sativa plant extract. CBN and THC inhibited the pancreatic lipase activity in a competitive manner, with the lowest residual enzyme activity of 52 % observed at a 10 µg/mL concentration of CBN and 39 % inhibition at a 25 µg/mL concentration of THC. Circular dichroism (CD) spectroscopy revealed that the inhibitors caused a change in the enzyme's secondary structure. At low concentrations, THC showed potential for synergistic inhibition with orlistat. C.sativa treatment in an in vivo rat model confirmed its inhibitory effects on pancreatic lipase activity. CONCLUSION: The findings in this study provided insight into the use of cannabinoids as pancreatic lipase inhibitors and the possibility of using these compounds to develop new pharmacological treatments for obesity.

Epigenetic Regulation of Pancreas Development and Function.

The field of epigenetics broadly seeks to define heritable phenotypic modifications that occur within cells without changes to the underlying DNA sequence. These modifications allow for precise control and specificity of function between cell types-ultimately creating complex organ systems that all contain the same DNA but only have access to the genes and sequences necessary for their cell-type-specific functions. The pancreas is an organ that contains varied cellular compartments with functions ranging from highly regulated glucose-stimulated insulin secretion in the ß-cell to the pancreatic ductal cells that form a tight epithelial lining for the delivery of digestive enzymes. With diabetes cases on the rise worldwide, understanding the epigenetic mechanisms driving ß-cell identity, function, and even disease is particularly valuable. In this chapter, we will discuss the known epigenetic modifications in pancreatic islet cells, how they are deposited, and the environmental and metabolic contributions to epigenetic mechanisms. We will also explore how a deeper understanding of epigenetic effectors can be used as a tool for diabetes therapeutic strategies.

Metabolic landscape of the healthy pancreas and pancreatic tumor microenvironment.

Pancreatic cancer, one of the deadliest human malignancies, is characterized by a fibro-inflammatory tumor microenvironment and wide array of metabolic alterations. To comprehensively map metabolism in a cell type-specific manner, we harnessed a unique single-cell RNA-sequencing dataset of normal human pancreata. This was compared with human pancreatic cancer samples using a computational pipeline optimized for this study. In the cancer cells we observed enhanced biosynthetic programs. We identified downregulation of mitochondrial programs in several immune populations, relative to their normal counterparts in healthy pancreas. Although granulocytes, B cells, and CD8+ T cells all downregulated oxidative phosphorylation, the mechanisms by which this occurred were cell type specific. In fact, the expression pattern of the electron transport chain complexes was sufficient to identify immune cell types without the use of lineage markers. We also observed changes in tumor-associated macrophage (TAM) lipid metabolism, with increased expression of enzymes mediating unsaturated fatty acid synthesis and upregulation in cholesterol export. Concurrently, cancer cells exhibited upregulation of lipid/cholesterol receptor import. We thus identified a potential crosstalk whereby TAMs provide cholesterol to cancer cells. We suggest that this may be a new mechanism boosting cancer cell growth and a therapeutic target in the future.

The BRD4 Inhibitor I-BET-762 Reduces HO-1 Expression in Macrophages and the Pancreas of Mice.

In pancreatic cancer, the tumor microenvironment (TME) accounts for up to 90% of the tumor mass. Pancreatitis, characterized by the increased infiltration of macrophages into the pancreas, is a known risk factor for pancreatic cancer. The NRF2 (nuclear factor erythroid 2-related factor 2) transcription factor regulates responses to oxidative stress and can promote cancer and chemoresistance. NRF2 also attenuates inflammation through the regulation of macrophage-specific genes. Heme oxygenase 1 (HO-1) is expressed by anti-inflammatory macrophages to degrade heme, and its expression is dependent on NRF2 translocation to the nucleus. In macrophages stimulated with conditioned media from pancreatic cancer cells, HO-1 protein levels increased, which correlated with higher NRF2 expression in the nuclear fraction. Significant differences in macrophage infiltration and HO-1 expression were detected in LSL-KrasG12D/+; Pdx-1-Cre (KC) mice, Nrf2 whole-body knockout (KO) mice and wildtype mice with pancreatitis. Since epigenetic modulation is a mechanism used by tumors to regulate the TME, using small molecules as epigenetic modulators to activate immune recognition is therapeutically desirable. When the bromodomain inhibitor I-BET-762 was used to treat macrophages or mice with pancreatitis, high levels of HO-1 were reduced. This study shows that bromodomain inhibitors can be used to prevent physiological responses to inflammation that promote tumorigenesis.

Oleuropein Relieves Pancreatic Ischemia Reperfusion Injury in Rats by Suppressing Inflammation and Oxidative Stress through HMGB1/NF-κB Pathway.

Oleuropein (OLP) is a naturally occurring phenolic compound in olive plant with antioxidant and anti-inflammatory potential and can possibly be used in treating pancreatic injuries. This investigation aimed to follow the molecular mechanism behind the potential therapeutic effect of OLP against pancreatic injury persuaded by ischemia-reperfusion (I/R). Pancreatic I/R injury was induced by splenic artery occlusion for 60 min followed by reperfusion. Oral administration of OLP (10 and 20 mg/kg) for 2 days significantly alleviated I/R-persuaded oxidative damage and inflammatory responses in pancreatic tissue as indicated by the decreased malondialdehyde (MDA) content and increased glutathione peroxidase (GPx) activity, accompanied by the suppression of myeloperoxidase (MPO) activity and reduced levels of interleukin-1beta (IL-1ß), nuclear factor kappa B (NF-κB), and tumor necrosis factor alpha (TNF-α) in pancreatic tissues. Furthermore, OLP treatment markedly restored the serum levels of amylase, trypsinogen-activated peptide (TAP), and lipase, with concurrent improvement in pancreatic histopathological alterations. Moreover, treatment with OLP regulated the pancreatic expression of inducible nitric oxide synthase (iNOS) and high-mobility group box 1 (HMGB1) relative to rats of the pancreatic IR group. Thus, OLP treatment significantly alleviates the I/R-induced pancreatic injury by inhibiting oxidative stress and inflammation in rats through downregulation of HMGB1 and its downstream NF-κB signaling pathway.

Tangningtongluo Tablet ameliorates pancreatic damage in diabetic mice by inducing autophagy and inhibiting the PI3K/Akt/mTOR signaling pathway.

BACKGROUND: Diabetes is a metabolic disease characterized by hyperglycaemia. Tangningtongluo Tablet (TNTL) is an inpatient formula extensively utilized to treat diabetes mellitus (DM), but the protective mechanism is not clear. This study aimed to investigate the relevant mechanisms by which TNTL affects pancreatic damage in diabetic mice and autophagy. METHODS: The impact of TNTL on pancreatic damage in diabetic mice in vitro and in vivo was investigated via glucose and lipid metabolism analyses, HE staining, CCK-8, TUNEL staining, Annexin V/PI, and Western blotting. Molecular docking and Western blotting were used to verify the results of network pharmacological analysis, which was carried out to explore the mechanism by which TNTL affects DM. The autophagosome levels were visualized via RFP-GFP-LC3 and transmission electron microscopy, and lysosomal function was evaluated via Lysotracker red staining. Western blot, immunohistochemistry and immunofluorescence staining were used to detect the expression of the autophagy proteins LC3, p62 and LAMP2. RESULTS: Compared with the model group, TNTL protected pancreas from oxidative stress, decreased the level of MDA, increased the levels of SOD and GSH-px, induced the occurrence of autophagy and decreased the levels of apoptotic factors. Moreover, TNTL inhibited the protein expression of p-PI3K, p-Akt and p-mTOR, increased the levels of LC3 and LAMP2 and decreased the level of p62, and the autophagy inhibitor CQ blocked the protective effect of TNTL on pancreatic damage in diabetic mice. CONCLUSION: These results demonstrated that TNTL ameliorated pancreatic damage in diabetic mice by inhibiting the PI3K/Akt/mTOR signaling and regulating autophagy.

Bufalin alleviates inflammatory response and oxidative stress in experimental severe acute pancreatitis through activating Keap1-Nrf2/HO-1 and inhibiting NF-κB pathways.

Severe acute pancreatitis (SAP) is a prevalent acute inflammatory disease that is clinically manifested by systemic inflammation dysregulation, resulting in a significantly elevated mortality rate. Bufalin has been verified to have potent pharmacological properties, including analgesic, anti-tumor and anti-inflammatory effects. However, it remains unclear whether bufalin inhibits SAP. Thus, we aim to explore the impact of bufalin in SAP rats and to evaluate the potential mechanisms of action. In addition to analyzing serum biochemistry and pancreatic tissue pathology, we elucidated its mechanisms of action through enzyme-linked immunosorbent assay (ELISA), immunohistochemical analysis, Western blot, and quantitative real-time PCR. The results demonstrated that bufalin dose-dependently reversed the elevation of serum Amylase (Amy) and Lipase (LPS) levels in SAP rats, alleviating pancreatic tissue pathological damage. Bufalin exhibited potent antioxidant effects by reducing malondialdehyde (MDA) levels, decreasing Superoxide dismutase (SOD) and glutathione(GSH) consumption, inhibiting the interaction of Keap1-Nrf2, and increasing HO-1 expression. Furthermore, bufalin inhibited TNF-α, IL-6, IL-1ß, p-NF-κB-p65, p-IκBα, and NF-κB-p65 expression, while enhancing IκBα expression, ultimately confirming its anti-inflammatory effects on SAP. In summary, our findings suggest that bufalin exerts anti-inflammatory and antioxidant actions in NaT-SAP rats by inhibiting NF-κB and activating the Keap1-Nrf2/HO-1 pathway. This study represents the inaugural application of bufalin in NaT-induced SAP rats, indicating its potential as an effective therapeutic agent for SAP patients.

Accuracy of Clinical Staging in Early-Stage Pancreatic Ductal Adenocarcinoma.

This study evaluates the accuracy of clinical staging in early-stage pancreatic ductal adenocarcinoma.

Application of the pancreatic body suspension technique in laparoscopic splenectomy combined with selective pericardial varicosity dissection: An observational study.

To investigate the safety of pancreatic body suspension (PBS) technique in laparoscopic splenectomy combined with pericardial devascularization for patients. A retrospective study inclusive of 16 patients who underwent laparoscopic splenectomy combined with pericardial devascularization from 2017 to 2022 was performed. A total of 5 patients underwent PBS technique and 11 underwent the traditional technique. There was no significant difference in age, sex, body mass index (BMI), preoperative serum white cell count (WBC), platelets (PLT), hemoglobin (HB), albumin (ALB), prothrombin time (PT), total bilirubin (TBIL), or spleen size between the 2 groups (P > .05). In the PBS group, the operation time was 280 minutes. The estimated intraoperative blood loss (EBL) was 250 mL. The mean postoperative hospitalization length was 11.2 days. There was no conversion to an open procedure or postoperative bleeding. In the traditional method group, the mean operation time was 240.91 minutes. The EBL was 290.91 mL. There were 2 cases of conversion to open, 3 cases of postoperative bleeding, and 1 reoperation. The incidence of postoperative short-term complications (postoperative bleeding, reoperation) was significantly higher in the traditional method group than in the PBS group (36.36% vs 0%, P = .034). PBS technique improved the safety of laparoscopic splenectomy combined with pericardial dissection and is worthy of clinical promotion.

Acute toxicity and antidiabetic effect of the ethyl acetate fraction of Commelina diffusa Burm.f. on the high-fat diet and streptozotocin-induced type 2 diabetic mice.

Pharmacological studies proved that Commelina diffusa Burm.f. performs various biological activities. Nevertheless, the scientific evidence supporting the hypoglycemic activities of this medicinal plant is insufficient. Thus, this study aims to assess the acute toxicity and the antidiabetic activity of the ethyl acetate fraction of Commelina diffusa (CD.EAF) in type 2 diabetic mice model induced by a high-fat diet and streptozotocin injection. The oral acute toxicity assessment was conducted following Lorke's method. The in vivo study was conducted by feeding Swiss male mice with a high-fat diet for 8 weeks and giving them a single intraperitoneal injection of streptozotocin at 100mg/kg. When the experimental mice model was successfully induced, the CD.EAF at 100mg/kg/day and 300mg/kg/day doses were orally administered to animals for 14 days. After the treatment period, the repeated daily administration of the CD.EAF at both tested doses exposed significant antihyperglycemic activities in comparison with the untreated diabetic group (p<0.05). However, it did not affect the serum lipid levels of mice. Besides, there were significant ameliorations in the histopathological images of the liver and pancreas in mice treated with the CD.EAF. Our findings suggested that the CD.EAF might be a potential agent for drug development to prevent and treat type 2 diabetes.