Dural arteriovenous fistulas in the falx cerebri: case series and literature review.

Dural arteriovenous fistulas (DAVFs) within the falx cerebri are infrequently documented and may be linked with the falcine sinus/venous plexus. The falcine sinus/venous plexus, often regarded as a normal venous structure, can exhibit pathological characteristics, differing from the persistent fetal falcine sinus. A retrospective analysis was conducted at a single center to identify all cases of DAVFs within the falx cerebri spanning from 2002 to 2022. Demographic data, fistula features, treatment modalities, clinical outcomes, and fistula closure were collected and analyzed. Additionally, relevant literature on DAVFs in this location was reviewed. Ten cases were identified at our center, supplemented by 13 cases reported in the literature. In our cohort, patients had an average age of 49.4 ± 8.1 years, with a male predominance of 90%. Trans-arterial embolization (TAE) alone achieved immediate complete occlusion in eight cases, while conservative treatment was pursued in two cases. No treatment-related complications or fistula recurrences were observed. In the literature, seven patients underwent direct surgery, three underwent TAE, and one underwent both direct surgery and radiosurgery for complete fistula closure. No instances of fistula recurrence or treatment complications were reported. Dural arteriovenous fistulas within the falx cerebri are rare, with limited literature available. They typically present as aggressive lesions. Treatment options include direct surgery or TAE. However, due to a lack of long-term DSA follow-up, the cure and recurrence rates are unknown for endovasdcular therapy. Further investigation is warranted to elucidate the involvement of the falcine sinus/venous plexus in falx cerebri DAVFs.

Efficacy and safety of combined anlotinib-oral etoposide treatment for patients with platinum-resistant ovarian cancer.

OBJECTIVE: Despite the availability of numerous treatment options, managing patients with platinum-resistant ovarian cancer (PROC) remains challenging, and the prognosis of PROC is notably unfavorable. This retrospective study aimed to assess the efficacy and safety of combined anlotinib-oral etoposide treatment for patients with PROC. METHODS: Data of 23 patients who were diagnosed with PROC from January 2020 to November 2022 and treated with anlotinib combined with oral etoposide for at least 2 cycles were retrospectively analyzed. RESULTS: Among per-protocol patients, 9 (45.0%; 95% confidence interval [CI]=21.1-68.9) of 20 patients achieved partial response and 17 (85.0%, 95% CI=67.9-100.0) of 20 patients achieved disease control. The median progression-free survival was 8.7 months (95% CI=5.3-11.6). The incidence of adverse events (any grade) was 100%, and the incidence of grade 3-4 adverse events was 54.5%. CONCLUSION: Anlotinib combined with etoposide emerged effective for the treatment of PROC.

Updated prevalence of latent prostate cancer in Chinese population and comparison of biopsy results: An autopsy-based study.

Prostate cancer detected by autopsy is named latent prostate cancer. As the repertoire of clinical prostate cancer, latent cancer may better reflect the disease burden. Unlike clinical prostate specimens, which are obtained exclusively from biopsy-positive cases, prostate specimens obtained through autopsy provide information on biopsy-negative cases, helping calculate the true sensitivity of prostate biopsy. From 2014 to 2021, we collected autopsy specimens of the prostate from body donors in China and performed transperineal and transrectal biopsies on specimens before step-sectioning and pathological measurements. We found that the crude prevalence of latent prostate cancer in middle-aged and elderly men was 35.1% (81/231), which was higher than previous estimates for Chinese populations. The overall per-patient sensitivities of transperineal and transrectal biopsies were not significantly different (33.3% vs. 32.1%, p = 0.82), but the two approaches differed in preferential sampling area along the proximal-distal axis of the prostate. Transperineal biopsy had a higher sensitivity for detecting clinically significant lesions in the distal third (34.7% vs. 16.3%, p = 0.02) and distal half (30.6% vs. 18.1%, p = 0.04), while transrectal biopsy had a higher sensitivity for lesions in the proximal half (25.0% vs. 13.9%, p = 0.046). Both transperineal and transrectal methods of biopsy missed most small lesions (<0.1 mL) and 35.3% (6/17) of large lesions (>0.5 mL). In conclusion, the prevalence of latent prostate cancer in China has increased over the past 2 decades. Systematic transperineal and transrectal methods of biopsy had comparable sensitivities but had different preferential sampling areas. Both approaches miss one-third of large lesions.

LncRNAs PSMG3-AS1 and MEG3 negatively regulate each other to participate in endometrial carcinoma cell proliferation.

Endometrial carcinoma (EC), also known as corpus cancer or corpus uterine cancer, is the most frequently diagnosed genital cancer among women in developed countries. Our preliminary RNA-seq analysis revealed the inverse correlation between the expression of PSMG3-AS1 and MEG3 across EC tissues, indicating the possible interaction between them. This study aimed to explore the interaction between two long non-coding RNAs (lncRNAs) PSMG3-AS1 and MEG3 in EC. Investigation of the interaction between two lncRNAs in cancer biology is a novel topic. The expression of PSMG3-AS1 and MEG3 in EC and paired non-tumor tissues from 60 EC patients were determined by RT-qPCR. Correlations between them were analyzed by Pearson's correlation coefficient. PSMG3-AS1 and MEG3 were overexpressed in EC cells to study the relationship between them. The roles of PSMG3-AS1 and MEG3 in regulating the proliferation of EC cells were assessed by CCK-8 assay. PSMG3-AS1 was upregulated, while MEG3 was downregulated in EC. Across EC tissues, the expression of PSMG3-AS1 and MEG3 were inversely correlated. In EC cells, overexpression of PSMG3-AS1 and MEG3 resulted in the downregulation of each other. In cell proliferation assay, PSMG3-AS1 promoted cell proliferation, and MEG3 inhibited cell proliferation. Moreover, the proliferation rate of cells co-transfected with PSMG3-AS1 and MEG3 expression vectors was not different from that in cells without transfections. In conclusion, PSMG3-AS1 and MEG3 may negatively regulate each other to regulate EC cell proliferation.

Clostridium butyricum Helps to Alleviate Inflammation in Weaned Piglets Challenged With Enterotoxigenic Escherichia coli K88.

Background: Whether the probiotic Clostridium butyricum (CB) alleviates enterotoxigenic Escherichia coli (ETEC) K88-induced inflammation by regulating the activation of the toll-like receptor (TLR) signaling pathway is not clear, thus, we carried out this study. A total of 72 piglets (average body weight 7.09 ± 0.2 kg) were randomly divided into three groups of 24 piglets per group. Pigs were either fed a daily diet (NC, negative control), a diet tested every day by 1 × 109 CFU/mL ETEC K88 (PC, positive control), or a basal diet supplemented with 5 × 105 CFU/g CB and challenged with ETEC K88 (PC + CB group). Results: Our results showed that CB pretreatment attenuated the effect of ETEC K88 by decreasing C-reactive protein (CRP), which resulted in tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) production. Histological examination revealed that CB pretreatment alleviated intestinal villi injury caused by ETEC K88 challenge. Furthermore, CB pretreatment promoted mRNA expression of the negative regulators of TLR signaling, including myeloid differentiation factor (MyD88), toll-interacting protein (Tollip), and B cell CLL/lymphoma 3 (Bcl-3), in the intestines of ETEC K88-challenged piglets. ETEC K88-induced activation of nuclear factor kappa B (NF-κB) and nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha (IκBα) was attenuated by CB pretreatment. Conclusion: These findings indicate that CB helps to maintain and strengthen the shape of intestinal villi and limits detrimental inflammatory responses, partly by inhibiting toll-like receptor 2 (TLR-2), toll-like receptor 4 (TLR-4), and toll-like receptor 5 (TLR-5) expression and inhibiting NF-κB p65, and promoting IκBα activation and synergism among its negative regulators.

Sirtuin 1 promotes autophagy and proliferation of endometrial cancer cells by reducing acetylation level of LC3.

Endometrial cancer (EC) constitutes a common female genital tract tumor with a rising incidence rate. Sirtuin 1 (SIRT1) is a member of histone deacetylase, which extensively participates in the progression of aging, cell death, and tumorigenesis. This study explored the effect of SIRT1-mediated LC3 acetylation on autophagy and proliferation of EC cells. SIRT1 expression in EC tissues and adjacent tissues, EC cell lines and normal human epithelial cells was detected. SIRT1 expression was elevated in EC cell lines and tissues. Knockdown of SIRT1 inhibited proliferation, migration, and invasion of EC cells. Then, EC cells were starved in serum-free medium, and levels of autophagy-related proteins were detected. Starvation induced autophagy of EC cells. The starvation-treated EC cells showed an increased SIRT1 expression, a decreased LC3 acetylation level and an increased autophagy level. The proliferation and autophagy of EC cells under different treatments were evaluated. In EC cells transfected with overexpressing SIRT1, LC3 acetylation was inhibited and cell proliferation was promoted. Moreover, overexpressing SIRT1 facilitated growth and autophagy of transplanted tumors in nude mice. In conclusion, SIRT1 promoted autophagy and proliferation of EC cells by reducing acetylation level of LC3.

The characteristics and spatial distributions of prostate cancer in autopsy specimens.

BACKGROUND: The characteristics of prostate cancer on autopsy and early-stage prostate cancer are identical. Using autopsy specimens, we analysed prostate cancer characteristics and clarified the spatial distributions of lesions. METHOD: We obtained prostate specimens from Chinese donors without a prostate cancer diagnosis and analyzed prostate cancer pathological characteristics on autopsy by whole-mount sampling. We determined the distributions of lesions in horizontal and vertical dimensions. The horizontal dimension included four horizontal quadrants (left-anterior, left-posterior, right-anterior, and right-posterior quadrants), the peripheral zone, and the transition zone. RESULT: The overall positive rate of prostate cancer among 113 specimens was 35.4%. There were 73 lesions in 40 prostates with prostate cancer. The positive rates of lesions in the left-anterior, left-posterior, right-anterior, and right-posterior quadrants were 24.7% (18/73), 27.4% (20/73), 26.0% (19/73), and 21.9% (16/73), respectively. The positive rate of prostate cancer was 74% in the areas between the apex above 0.5-0.8 cm and the middle slice. There were 22 (30.1%) and 51 (69.9%) lesions in the superior and inferior half of the prostate. There were no significant differences in the median volume and Gleason grade group between the superior and inferior half (p = .876 and p = .228). CONCLUSION: In the horizontal dimension, the positive rate of prostate cancer was consistent in the four quadrants. Prostate cancer mainly originated from the areas between the apex above 0.5-0.8 cm and the middle slice. Compared with the superior half, the inferior half of the prostate had a higher positive rate but the same lesion characteristics.

An Unusual Right-sided Suprarenal Accessory Spleen Misdiagnosed as an Atypical Pheochromocytoma.

Compared with left suprarenal splenosis, a right suprarenal accessory spleen is more likely to be misdiagnosed as an adrenal tumor because of its extreme rarity. Especially when splenosis mimics an atypical pheochromocytoma, preoperative diagnosis may become more difficult and elusive. Herein we report the case of a female patient with a right suprarenal mass, which was suspected to be an atypical pheochromocytoma based on a history of the classic triad and positive somatostatin receptor scintigraphy, but histopathology suggested a final diagnosis of right suprarenal splenosis.

Experimental study on killing tumor cells by activation of hematoporphyrin derivatives by bi-frequency focal ultrasound in vitro.

Tumor cells K562 were killed by the hematoporphyrin derivatives (HpD) activated by bi-frequency focal ultrasound in which a choice of irradiating parameter of ultrasound was tested by experiment. The effect of killing tumor cells was investigated by MTT method and compared with the contrast group. The results showed that the bi-frequency ultrasound exhibited an improved effect of killing tumor cells than single frequency ultrasound. It was 2-3 times higher than the single frequency ultrasound for the killing effect of tumor cells. After the irradiation of ultrasound, the cell-killing effect of hatching 16 h is better than that of hatching 4 h in the hatching tank. This might be due to delay of cell apoptosis.

Study of cell killing and morphology on S180 by ultrasound activating hematoporphyrin derivatives.

The inhibition of ascitic S180 and induced sarcoma 180 in vivo was studied with the combination of hematoporphyrin derivatives (HpD) and ultrasound (US) at the frequency of 1.1 MHz and different intensities by light microscopy observation, electronic microscopy observation, cytochemical analysis and fluorescence labeling. The present study indicated that the injury ofascitic S180 increased as time passed and the inhibitory effect was stronger in US plus HpD group than that in other groups. Our results also indicated that the changes in cell structure, cytochrome C oxidase activity, the degradation and missing of DNA were the important factors that inhibited the tumor cell growth and even induced cell death. The phenomenon of apoptosis of tumor cells indicated that cell death and induced apoptosis exist in the treatment of sonodynamic therapy (SDT). Our study investigated the mechanism underlying the killing effect of S180 induced by US activating HpD by the observation ofcell morphology and dynamic changes from seminal injury to succeeded injury even to death. It would provide rich reference for the study of SDT.