Ventriculoperitoneal (VP) shunting in cryptococcal meningitis (CM) patients with high intracranial pressure (ICP) has been studied extensively. A total of 74 CM patients with ICP were identified, including 27 patients with or without ventriculomegaly receiving VP shunting. Through retrospective analysis, there was an obvious decline in ICP as well as Cryptococcus count after VP shunting. Damage to the cranial nerves was improved after the surgery. For those patients receiving VP shunting, there was an obvious decline in ICP as well as Cryptococcus count, with less usage of mannitol. Hydrocephalus or ventriculomegaly was improved, and both the clearance time of Cryptococcus and the hospitalization time were shortened (p<0.05). The complications of VP shunting were not common. For patients diagnosed with CM and with apparent ICP, VP shunting can be considered regardless of whether there is damage to the cranial nerves or hydrocephaly.

As the most common cancer of the genitourinary system, prostate cancer (PCa) is a global men′s health problem whose treatments are an urgent research issue. Treatment options for PCa include active surveillance (AS), surgery, endocrine therapy, chemotherapy, radiation therapy, immunotherapy, etc. However, as the cancer progresses, the effectiveness of treatment options gradually decreases, especially in metastatic castration-resistant prostate cancer (mCRPC), for which there are fewer therapeutic options and which have a shorter survival period and worse prognosis. For this reason, oncolytic viral therapy (PV), with its exceptional properties of selective tumor killing, relatively good safety in humans, and potential for transgenic delivery, has attracted increasing attention as a new form of anti-tumor strategy for PCa. There is growing evidence that OV not only kills tumor cells directly by lysis but can also activate anticancer immunity by acting on the tumor microenvironment (TME), thereby preventing tumor growth. In fact, evidence of the efficacy of this strategy has been observed since the late 19th century. However, subsequently, interest waned. The renewed interest in this therapy was due to advances in biotechnological methods and innovations at the end of the 20th century, which was also the beginning of PCa therapy with OV. Moreover, in combination with chemotherapy, radiotherapy, gene therapy or immunotherapy, OV viruses can have a wide range of applications and can provide an effective therapeutic result in the treatment of PCa.

Immune checkpoint inhibitor-induced immune-mediated hepatitis (ICI-IMH) in patients with hepatocellular carcinoma (HCC) has been established to increase the risk of liver failure (LF). Given the accumulating evidence supporting the efficacy of artificial liver support systems (ALSS) in mitigating both IMH and LF, a single-center, non-blinded, randomized controlled clinical trial is proposed to investigate the efficacy and safety of ALSS for HCC patients with ICI-LF. and analysis: Sixty eligible participants will be enrolled in this trial and randomly assigned to one of two groups in a 1:1 ratio. In addition to standard pharmacological management, patients in the trial group will receive treatment with a double plasma molecular adsorption system (DPMAS) and low-volume plasma exchange (LPE) on three occasions, while patients in the control group will undergo PE three times. Patient assessments, including symptoms and laboratory tests, will be conducted at baseline, before and after the three ALSS treatments, and at 2, 4, 8, and 12 weeks post-enrollment. The primary outcome is the mortality rate at 12-week follow-up. Secondary outcomes include changes in the Model for End-Stage Liver Disease (MELD) score following ALSS treatment and the incidence of adverse events (AEs). ICI-LF in HCC patients is associated with a high mortality rate and lacks effective treatment options. Our study aims to evaluate the efficacy and safety of ALSS for this patient population, comparing the effectiveness of two ALSS modalities (DPMAS + LPE vs. PE). This clinical trial has been registered on ClinicalTrials.gov with the identifier NCT05484908 (Release Date: July 30, 2022) (https://clinicaltrials.gov/study/NCT05484908).

Liver cancer is the fifth most common cancer in the world, with China bearing a disproportionate burden of cases. Typically diagnosed at advanced stages, liver cancer often utilizes surgical treatments such as resection, tran... | Find, read and cite all the research you need on Tech Science Press

Background: Oncolytic virus M1 (OVM), a naturally occurring alphavirus, has demonstrated potent antitumor activity in various solid tumor models by inducing immunogenic cell death and activating CD8 ⁺ T cells. However, its in vivo efficacy varies widely, and resistance mechanisms remain poorly understood. Tumor-associated macrophages (TAMs), key immunosuppressive cells within the tumor microenvironment, may limit OVM therapeutic potential. Methods: We investigated the role of TAMs in OVM resistance using multiple syngeneic mouse tumor models (MC38 colorectal cancer, KPC1199 pancreatic cancer, RM1 prostate cancer, and B16F10 melanoma). TAMs were depleted using clodronate liposomes or CSF1R (Colony Stimulating Factor 1 Receptor) antibodies. Flow cytometry, mass cytometry, quantitative reverse transcription-PCR, and transcriptomic sequencing were employed to assess TAMs infiltration, viral load, and immune responses. CD8 ⁺ T cells were selectively depleted to determine their functional relevance. Results: TAMs infiltration was positively correlated with resistance to OVM across tumor models. Depletion of TAMs increased intratumoral viral load and promoted accumulation of GZMB ⁺ CD8 ⁺ T cells. RNA sequencing analysis revealed upregulation of antiviral and T-cell immune pathways in TAMs-depleted tumors. Importantly, the therapeutic benefit of TAMs depletion was abrogated on CD8 ⁺ T-cell depletion, confirming their essential role in mediating OVM efficacy. In both OVM non-responsive and responsive tumors, TAMs depletion enhanced OVM-mediated tumor suppression and survival. Conclusions: TAMs, particularly M1-like subsets, play a critical role in mediating resistance to OVM therapy by reducing viral persistence and suppressing CD8 ⁺ T-cell responses. Targeting TAMs significantly improves the antitumor efficacy of OVM in solid tumors. These findings support the development of TAMs-targeted combination strategies to optimize oncolytic virotherapy.

Background: Histone deacetylase (HDAC) inhibitors have shown therapeutic promise in various cancers, including hepatocellular carcinoma (HCC), due to their ability to regulate cell proliferation, differentiation, and apoptosis. However, their role in metabolic reprogramming and differentiation therapy in HCC remains underexplored.Methods: This study investigated the effects of the HDAC inhibitor MS275 on HCC cells in vitro and in vivo. Cell viability, differentiation marker expression, cell cycle distribution, metabolic activity, and reactive oxygen species (ROS) production were evaluated using CCK-8 assays, qRT-PCR, flow cytometry, Seahorse metabolic analysis, and western blotting. A xenograft mouse model was used to validate in vivo efficacy.Results: MS275 significantly suppressed HCC cell proliferation by inducing G0/G1 phase arrest without triggering apoptosis. MS275 also upregulated hepatocyte-specific markers (GLUL, HNF1A, HNF3A), indicating that it promoted differentiation. Mechanistically, MS275 reprogrammed cellular metabolism by enhancing oxidative phosphorylation and reducing glycolysis, accompanied by increased expression of the metabolic enzyme PKM1. This metabolic shift led to elevated ROS production, which was essential for MS275-induced differentiation. Knockdown of PKM1 abolished both the differentiation and anti-proliferative effects. In vivo, MS275 significantly reduced tumor growth and promoted differentiation without systemic toxicity.Conclusion: MS275 suppresses HCC cell proliferation and induces hepatocyte-like differentiation through PKM1-mediated metabolic reprogramming and ROS signaling. These findings support the potential of MS275 as a differentiation-based therapeutic strategy for HCC.