application-laparoscopic-partial-splenectomy-with-total-blood-flow

Application of Laparoscopic Partial Splenectomy with Total Blood Flow Occlusion in Benign Splenic Lesions

Laparoscopic partial splenectomy (LPS) is gradually becoming the preferred method for treating benign splenic lesions. However, due to the abundant blood ...

First People's Hospital of Shunde

To discuss the clinical value of percutaneous transhepatic cholangial drainage (PTCD) combined with nasojejunal tube for bile reinfusion and enteral nutrition for patients with malignant obstructive jaundice.

[Effect of percutaneous transhepatic cholangial drainage with bile reinfusion and enteral nutrition via the nasojejunal tube on visceral protein and hepatic function].

We report a 51-year-old female patient with a solitary lymphangioma located in the upper splenic pole which was managed successfully with laparoscopic partial splenectomy. Surgery lasted 170 min and did not require blood transfusions. The patient recovered well post-operatively and was asymptomatic at the 3-mo follow-up. She had a normal platelet count and no recurrence on ultrasonography or computed tomography. Laparoscopic partial splenectomy is a safe, minimally invasive technique for the treatment of solitary splenic lymphangiomas in the splenic pole. We performed the procedure using the Habib(TM) 4X device. This laparoscopic bipolar radiofrequency device ensured a "bloodless" splenic parenchymal resection.

Partial splenectomy using a laparoscopic bipolar radiofrequency device: a case report.

The role of laparoscopic selective esophagogastric devascularization and splenectomy (LSEGDS) in the treatment of esophagogastric variceal bleeding and hypersplenism in patients with cirrhotic portal hypertension has not been well studied.

Laparoscopic selective esophagogastric devascularization and splenectomy for patients with cirrhotic portal hypertension.

Pseudogenes are defined as key regulators in cancer initiation and progression. But their biological function and clinical significance in hepatocellular carcinoma (HCC) remain to be elucidated. In the current study, we identified a novel pseudogene, Annexin A2 pseudogene 1 (ANXA2P1), in HCC and explored its underlining molecular mechanism.

Pseudogene Annexin A2 Pseudogene 1 Contributes to Hepatocellular Carcinoma Progression by Modulating Its Parental Gene ANXA2 via miRNA-376a-3p.

NOTCH signaling has been shown to play a role in the production of interleukin-22 (IL-22) by CD4 T cells. Multiple T-helper (Th) cell populations secrete IL-22. Th22 (CD4IL22IFNγIL17A) cells are a subgroup of CD4 effector T cells that primarily generate IL-22. The regulatory mechanisms of the NOTCH signaling pathway involved in differentiation of the Th22 cell subset have not been completely elucidated. This study aimed to further explore the involvement of NOTCH signaling in Th22 differentiation.

The NOTCH-HES-1 axis is involved in promoting Th22 cell differentiation.

Ras homologue enriched in brain 1 (Rheb1), an upstream activator of the mechanistic target of rapamycin complex 1 (mTORC1), is known to modulate various cellular processes. However, its impact on bone metabolism  remains unknown. The study aimed at understanding the role of Rheb1 on bone homeostasis. We measured the serum parameters and performed histomorphometry, quantitative real-time polymerase chain reaction, and Western blotting, along with the generation of mouse gene knockout (KO) model, and conducted a microcomputed tomography analysis and tartrate-resistant acid phosphatase staining, to delineate the impacts of Rheb1 on bone homeostasis. In the Rheb1 KO mice, the results showed that Rheb1 KO caused significant damage to the bone microarchitecture, indicating that mTORC1 activity was essential for the regulation of bone homeostasis. Specifically, suppressed mineralization activity in primary osteoblasts and a decreased osteoblast number were observed in the Rheb1 KO mice, demonstrating that loss of Rheb1 led to impaired osteoblastic differentiation. Furthermore, the higher apoptotic ratio in Rheb1-null osteocytes could promote Tnfsf11 expression and lead to an increase in osteoclasts, indicating increased bone resorption activity in the KO mice. The findings confirmed that Rheb1 deletion in osteoblasts/osteocytes led to osteopenia due to impaired bone formation and enhanced bone resorption.

Deletion of  in Osteocytes Leads to Osteopenia Characterized by Reduced Bone Formation and Enhanced Bone Resorption.

SHARPIN is a tumor-associated gene involved in the growth and proliferation of many tumor types. A function of SHARPIN in cholangiocarcinoma (CCA) is so far unclear. Here, we studied the role and function of SHARPIN in CCA and revealed its relevant molecular mechanism. The expression of SHARPIN was analyzed in cholangiocarcinoma tissues from patients using immunohistochemistry, quantitative PCR, and western blot analysis. Expression of SHARPIN was suppressed/overexpressed by siRNA silencing or lentiviral overexpression vector, and the effect on cell proliferation was determined by the CCK-8 assay and flow cytometry. Accumulation of reactive oxygen species was measured with MitoTracker, and JC-1 staining showed mitochondrial fission/fusion and mitochondrial membrane potential changes as a result of the silencing or overexpression. The ferroptosis marker solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), and the antioxidant enzymes superoxide dismutase 1 (SOD-1) and SOD-2 were analyzed by western blot. The results showed that SHARPIN expression was increased in CCA tissue, and this was involved in cell proliferation. SHARPIN silencing resulted in accumulated reactive oxygen species, reduced mitochondrial fission, and a reduced mitochondrial membrane potential. Silencing of SHARPIN inhibited the ubiquitination and degradation of p53, and downregulated levels of SLC7A11, GPX4, SOD-1, and SOD-2, all of which contributed to excessive oxidative stress that leads to ferroptosis. Overexpression of SHARPIN would reverse the above process. The collected data suggest that in CCA, SHARPIN-mediated cell ferroptosis via the p53/SLC7A11/GPX4 signaling pathway is inhibited. Targeting SHARPIN might be a promising approach for the treatment of CCA.

SHARPIN promotes cell proliferation of cholangiocarcinoma and inhibits ferroptosis via p53/SLC7A11/GPX4 signaling.

Ferroptosis is a new form of programmed cell death, which achieved great breakthroughs in cell biology during past decade. However, the regulation of ferroptosis is yet to be identified thoroughly. The latest study published on Nature cell biology by Nguyen and colleagues found a new NADPH sensor, MARCHF6 an E3 ubiquitin ligase, mediates ferroptosis in tumor growth and animal development. This finding provides a novel insight into ubiquitin system and energy metabolism in regulation of ferroptosis, which may open up new avenues for tumor treatment.

An NADPH sensor that regulates cell ferroptosis.

Immunotherapy with immune checkpoint inhibitors had achieved great success. However, only a subset of patients responds positively to these therapies. The latest study published on  by Chou and colleagues found a new T cell subset from tumor-infiltrating T cells which lack PD-1 on the cell surface and potent cytotoxic activities against tumor cells. This finding provides a novel insight into the development of new therapies for tumors that do not respond to immune checkpoint blockade in the future.

The New T Cell Subset Opens a New Realm for Tumor Immunotherapy.

Disulfidptosis, a new form of cell death triggered by disulfide stress, is characterized by the collapse of cytoskeleton proteins and F-actin due to the intracellular accumulation of disulfides. This discovery will eventually aid in the development of therapeutic strategies against cancer.

Disulfidptosis: a new form of programmed cell death.

The increasing comprehension of spleen function has led to the gradual endorsement of laparoscopic partial splenectomy (LPS) as a treatment option for benign spleen lesions. However, it is important to note that the LPS technique remains challenging. This study explores the standardized process and surgical techniques in LPS, aiming to promote the application of this technique.

Weidong Wang

Department of Hepatobiliary and Pancreatic-Spleen Surgery,
Shunde Hospital of Southern Medical University,
Department of Hepatobiliary and Pancreatic-Spleen Surgery, Shunde Hospital of Southern Medical University

First People's Hospital of Shunde

Application of Laparoscopic Partial Splenectomy with Total Blood Flow Occlusion in Benign Splenic Lesions

Weidong Wang

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Hepatobiliary and Pancreatic-Spleen Surgery,Shunde Hospital of Southern Medical University,Department of Hepatobiliary and Pancreatic-Spleen Surgery, Shunde Hospital of Southern Medical University

First People's Hospital of Shunde

Application of Laparoscopic Partial Splenectomy with Total Blood Flow Occlusion in Benign Splenic Lesions

Department of Hepatobiliary and Pancreatic-Spleen Surgery,
Shunde Hospital of Southern Medical University,
Department of Hepatobiliary and Pancreatic-Spleen Surgery, Shunde Hospital of Southern Medical University