Study of the Adsorption and Separation Behavior of Scandium and Zirconium by Trialkyl Phosphine Oxide-Modified Resins in Sulfuric and Hydrochloric Acid Media.

Zirconium is recognized as one of the main impurities of the rare earth element scandium during purification. It presents significant challenges due to its similar chemical properties, making separating it difficult. This study used trialkyl phosphine oxide (TRPO) as a functional ligand, and the effects of carrier type and acidity on adsorption performance were first investigated. Among these, the novel extraction resin SiO2-P as a carrier for TRPO demonstrated more prominent separation performance in 0.2 M H2SO4 and 5 M HCl solutions. The kinetic and isotherm data were consistent with the pseudo-secondary kinetics and Langmuir model, respectively, and the adsorption process could be regarded as homogeneous monolayer adsorption subject to the dual effects of chemisorption and internal diffusion. In addition, thermodynamic analysis showed that the adsorption process of zirconium under the experimental conditions was a spontaneous endothermic process. Combined with the results of SEM-EDS, FT-IR, and XPS analyses, scandium and zirconium were successfully adsorbed by the resin and uniformly distributed on its surface, and the greater affinity of the P=O groups on the resin for zirconium was the critical factor contributing to the separation of scandium and zirconium. Finally, scandium and zirconium in sulfuric acid and hydrochloric acid media were extracted and separated by column experiments, and the purity of scandium could reach 99.8% and 99.99%, respectively.

Acyltransferase zinc finger DHHC-type containing 2 aggravates gastric carcinoma growth by targeting Nrf2 signaling: A mechanism-based multicombination bionic nano-drug therapy.

The significant regulatory role of palmitoylation modification in cancer-related targets has been demonstrated previously. However, the biological functions of Nrf2 in stomach cancer and whether the presence of Nrf2 palmitoylation affects gastric cancer (GC) progression and its treatment have not been reported. Several public datasets were used to look into the possible link between the amount of palmitoylated Nrf2 and the progression and its outcome of GC in patients. The palmitoylated Nrf2 levels in tumoral and peritumoral tissues from GC patients were also evaluated. Both loss-of-function and gain-of-function via transgenic experiments were performed to study the effects of palmitoylated Nrf2 on carcinogenesis and the pharmacological function of 2-bromopalmitate (2-BP) on the suppression of GC progression in vitro and in vitro. We discovered that Nrf2 was palmitoylated in the cytoplasmic domain, and this lipid posttranslational modification causes Nrf2 stabilization by inhibiting ubiquitination, delaying Nrf2 destruction via the proteasome and boosting nuclear translocation. Importantly, we also identify palmitoyltransferase zinc finger DHHC-type palmitoyltransferase 2 (DHHC2) as the primary acetyltransferase required for the palmitoylated Nrf2 and indicate that the suppression of Nrf2 palmitoylation via 2-bromopalmitate (2-BP), or the knockdown of DHHC2, promotes anti-cancer immunity in vitro and in mice model-bearing xenografts. Of note, based on the antineoplastic mechanism of 2-BP, a novel anti-tumor drug delivery system ground 2-BP and oxaliplatin (OXA) dual-loading gold nanorods (GNRs) with tumor cell membrane coating biomimetic nanoparticles (CM@GNRs-BO) was established. In situ photothermal therapy is done using near-infrared (NIR) laser irradiation to help release high-temperature-triggered drugs from the CM@GNRs-BO reservoir when needed. This is done to achieve photothermal/chemical synergistic therapy. Our findings show the influence and linkage of palmitoylated Nrf2 with tumoral and peritumoral tissues in GC patients, the underlying mechanism of palmitoylated Nrf2 in GC progression, and novel possible techniques for addressing Nrf2-associated immune evasion in cancer growth. Furthermore, the bionic nanomedicine developed by us has the characteristics of dual drugs delivery, homologous tumor targeting, and photothermal and chemical synergistic therapy, and is expected to become a potential platform for cancer treatment.

KBTBD2 promotes proliferation and migration of gastric cancer via activating EGFR signaling pathway.

BACKGROUND: To explore the role of Kelch repeat and BTB (POZ) domain containing 2 (KBTBD2) in Gastric cancer(GC) via studying the level of KBTBD2 and its impact on GC cells and mice model. METHODS: Expression of KBTBD2 in GC was analyzed by analysis of TCGA data, Western blotting and Real-time quantitative polymerasechain reaction (RT-qPCR). The role of KBTBD2 on GC cells proliferation, viability, invasion, migration and apoptosis in vitro were assessed by using western blotting，RT-qPCR，CCK-8, EDU, Colony Formation Assay, Wound healing assay, Transwell, JC-1 mitochondrial membrane potential and flow cytometry assay, respectively. And levels of Bcl-2, BAX, PARP, E-cadherin, Vimentin, N-cadherin, EGFR, SOS1, NROS, BRAF,ERK1/2 and GAPDH were tested by western blotting. Relation of KBTBD2 and epidermal growth factor receptor (EGFR) was predicted by KEGG analysis. KBTBD2 gene GSEA enrichment was analyzed by using R language. Moreover, CCK-8, western blotting, and wound healing assays were used to verify the correlation of KBTBD2 and EGFR pathway. Finally, tumor growth in mice was also investigated. Cells proliferation, migration and apoptosis were detected by Ki67 staining, Tunnel staining and mouse lung metastasis model. RESULTS: KBTBD2 was highly expressed in GC, and was related to poor prognosis. Moreover, silencing KBTBD2 suppressed GC cell proliferation, migration and invasion, while also inhibited the EMT, but promoted apoptosis. At the same time, KBTBD2 overexpression showed opposite results. In addition, KBTBD2 regulated the EGFR pathway. Further, silencing KBTBD2 inhibited tumor growth, cell proliferation and migration but promoted apoptosis in vivo, and KBTBD2 overexpression showed opposite results. CONCLUSIONS: KBTBD2 was highly expressed in GC. KBTBD2 promotes the progress of GC by activating EGFR signal pathway. KBTBD2 may thus be a novel target for treating GC.

Synthesis and Application of a Novel Multi-Branched Block Polyether Low-Temperature Demulsifier.

In this paper, a low-temperature thick oil demulsifier with high polarity was prepared by introducing ethylene oxide, propylene oxide block, and butylene oxide using m-diphenol as a starting agent. The main reasons for the difficulty involved in the low-temperature emulsification of extractive fluids were explained by analyzing the synthetic influencing factors and infrared spectra of the star comb polymer (PR-D2) and by analyzing the four fractions, interfacial energies, and zeta potentials of crude oils from the Chun and Gao fields. The effects of PR-D2 surfactant on the emulsification performance of crude oil recovery fluids were investigated via indoor and field experiments. The experimental results indicate that the optimal synthesis conditions for this emulsion breaker are as follows: a quality ratio of ionic reaction intermediates and meso-diphenol of R = 10:1; 1 g of the initiator; a polymerization temperature of 80 °C; and a reaction time of 8 h. Colloidal asphaltenes in the crude oil were the main factor hindering the low-temperature demulsification of the Gao oilfield's extractive fluids, and the reason for the demulsification difficulty of the extractive fluids in the Chun oilfield is that the temperature of demulsification is lower than the wax precipitation point. The demulsification rate of the Chun oilfield's extractive fluids reached more than 98% when the PR-D2 concentration reached 150 mg/L at 43 °C. The demulsification rate of the Gao oilfield's extractive fluids reached more than 98% at a PR-D2 concentration of 150 mg/L at 65 °C. The field experiments show that the Chun oilfield's extractive fluids can still demulsify after the temperature is reduced to 43 °C in winter. The emulsification temperature of the Gao oilfield's extractive fluids was reduced from 73 °C to 68 °C, with an excellent demulsification effect.

Efficient Demulsification Performance of Emulsified Condensate Oil by Hyperbranched Low-Temperature Demulsifiers.

Focusing on the problem of poor demulsification performance of light crude oil emulsions in low-permeability oilfields at low temperatures, the composition of the emulsion samples, clay particle size distribution, and the viscosity-temperature relationship curve of samples were analyzed. Based on the results of emulsion composition analysis and characteristics, the bottle test method was used to analyze the demulsifying effect of different commercial types of demulsifiers, revealing the demulsification mechanism. The field tests confirm the demulsification capabilities of Polyoxyethylene polyoxypropylene quaternized polyoxyolefins surfactants (PR demulsifiers). The results reveal that PR demulsifiers combine the features of decreasing the interfacial tension between oil and water and adsorbing SiO2, allowing for quick demulsification and flocculation at low temperatures. This research serves as a theoretical and practical foundation for the study and advancement of low-temperature demulsification technology in oilfields.

Single-cell analysis of gastric signet ring cell carcinoma reveals cytological and immune microenvironment features.

Gastric signet ring cell carcinoma (GSRC) is a special subtype of gastric cancer (GC) associated with poor prognosis, but an in-depth and systematic study of GSRC is lacking. Here, we perform single-cell RNA sequencing to assess GC samples. We identify signet ring cell carcinoma (SRCC) cells. Microseminoprotein-beta (MSMB) can be used as a marker gene to guide the identification of moderately/poorly differentiated adenocarcinoma and signet ring cell carcinoma (SRCC). The upregulated differentially expressed genes in SRCC cells are mainly enriched in abnormally activated cancer-related signalling pathways and immune response signalling pathways. SRCC cells are also significantly enriched in mitogen-activated protein kinase and oestrogen signalling pathways, which can interact and promote each other in a positive feedback loop. SRCC cells are shown to have lower cell adhesion and higher immune evasion capabilities as well as an immunosuppressive microenvironment, which may be closely associated with the relatively poor prognosis of GSRC. In summary, GSRC exhibits unique cytological characteristics and a unique immune microenvironment, which may be advantageous for accurate diagnosis and treatment.

OASL knockdown inhibits the progression of stomach adenocarcinoma by regulating the mTORC1 signaling pathway.

The present study investigated the effects of 2'-5' oligoadenylate synthetase-like (OASL) on the biological functions of stomach adenocarcinoma (STAD) cells and tumor formation in nude mice. The differential expression levels of OASL in the different cancer types from TCGA dataset were analyzed using gene expression profiling interactive analysis. Overall survival and the receiver operating characteristic were analyzed using the KM plotter and R, respectively. Furthermore, OASL expression and its effects on the biological functions of STAD cells were detected. The possible upstream transcription factors of OASL were predicted using JASPAR. The downstream signaling pathways of OASL were analyzed using GSEA. Tumor formation experiments were performed to evaluate the effect of OASL on tumor formation in nude mice. The results showed that OASL was highly expressed in STAD tissues and cell lines. OASL knockdown markedly inhibited cell viability, proliferation, migration, and invasion and accelerated STAD cell apoptosis. Conversely, OASL overexpression had the opposite effect on STAD cells. JASPAR analysis revealed that STAT1 is an upstream transcription factor of OASL. Furthermore, GSEA showed that OASL activated the mTORC1 signaling pathway in STAD. The protein expression levels of p-mTOR and p-RPS6KB1 were suppressed by OASL knockdown and promoted by OASL overexpression. The mTOR inhibitor, rapamycin, markedly reversed the effect of OASL overexpression on STAD cells. Additionally, OASL promoted tumor formation and increased tumor weight and volume in vivo. In conclusion, OASL knockdown suppressed the proliferation, migration, invasion, and tumor formation of STAD cells by inhibiting the mTOR signaling pathway.

Loss of cancer-associated fibroblast-derived exosomal DACT3-AS1 promotes malignant transformation and ferroptosis-mediated oxaliplatin resistance in gastric cancer.

AIMS: Long non-coding RNAs (lncRNAs), as one of the components of exosomes derived from cancer-associated fibroblasts (CAFs), exhibit a crucial role in the pathogenesis and chemoresistance of gastric cancer (GC). Herein, we investigated the role and mechanism of a novel lncRNA disheveled binding antagonist of beta catenin3 antisense1 (DACT3-AS1) and its involvement in GC. METHODS: DACT3-AS1 was identified by RNA-sequencing and verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The functional role of DACT3-AS1 in GC was evaluated using in vitro and in vivo experiments including Transwell assay, 5-Ethynyl-2'-deoxyuridine (EdU) assay, immunoblotting, and xenograft tumor mouse model. Dual-luciferase reporter assay was performed to assess the association between genes. RESULTS: DACT3-AS1 was downregulated and involved in poor prognosis of patients with GC. The results from both in vitro and in vivo experiments showed that DACT3-AS1 suppressed cell proliferation, migration, and invasion through targeting miR-181a-5p/sirtuin 1 (SIRT1) axis. Additionally, DACT3-AS1 was transmitted from CAFs to GC cells mainly via exosomes. Exosomal DACT3-AS1 alleviated xenograft tumor growth. DACT3-AS1 conferred sensitivity of cancer cells to oxaliplatin through SIRT1-mediated ferroptosis both in vitro and in vivo. CONCLUSIONS: CAFs-derived exosomal DACT3-AS1 is a suppressive regulator in malignant transformation and oxaliplatin resistance. DACT3-AS1 could be used for diagnosis and treatment of GC.

AKAP8L enhances the stemness and chemoresistance of gastric cancer cells by stabilizing SCD1 mRNA.

Gastric cancer (GC) remains the third leading cause of cancer-related deaths. Chemoresistance is the major determinant of GC treatment failure. To explore the molecular mechanisms of GC chemoresistance, mass spectrometry was performed to detect the genes altered in expression between chemoresistant and chemosensitive GC. PRKA kinase anchor protein 8L (AKAP-8L) was identified as one of the top upregulated genes in chemoresistant GC tissues. Moreover, the higher AKAP-8L expression was associated with the lower survival rate in GC patients. Overexpression of AKAP-8L enhanced the GC cell stemness and chemoresistance of oxaliplatin in vivo and in vitro. AKAP-8L deficiency obtained the opposite results. Mechanistically, AKAP-8L interacted with Stearoyl-CoA desaturase 1 (SCD1) mRNA and IGF2BP1 protein, and regulated SCD1 mRNA stability via IGF2BP1-dependent manner. SCD1 played a critical role in mediating the function of AKAP-8L in GC cell stemness and chemoresistance. Clinically, AKAP-8L and SCD1 protein levels was positively associated with human GC chemoresistance. Taken together, our results demonstrated that AKAP-8L facilitates GC chemoresistance via regulating SCD1-mediated stemness of GC cells. AKAP8L may represent a novel therapeutic target to overcome GC chemoresistance.

The Inhibitory Effect of the Deregulation Short-Sale on Private Equity Placement.

In countries with a high degree of equity concentration, such as China, the second type of agency problem is serious in which major shareholders of listed companies encroach on the interests of small and medium shareholders through private placement. As a financial transaction system, the short-selling mechanism has the function of external corporate governance. Therefore, this paper examines the impact of relaxing short-selling controls on companies' private placements. Based on the quasi-natural experiment of China's gradual relaxation of short-selling controls since 2010, a double-difference model (DID) test is constructed to find that relaxing short-selling controls reduces companies' private placement tendency and amount, and this effect is mainly reflected in samples with a higher degree of equity checks and balances. Further analysis found that when the size of the company's financing constraints is different, the impact of relaxing short-selling control on the company's private placement tendency and amount is different; when the chairman and the general manager have two positions, relaxing short-selling control reduces the company's private placement options, but it has a negative impact on the company's private placement. There is no difference in the impact of the company's private placement amount. It can be excluded that the relaxation of short-selling control suppresses the company's placement through financing constraints and corporate governance mechanisms. Compared to a good information environment, when the company's information environment is poor, relaxing short-selling controls reduces the company's private placement tendency and amount. Significantly, it shows that the relaxation of short-selling control policy and supervision inhibits the company's private placement through the information environment mechanism, and promotes the sustainable development of enterprises. It not only improves the literature in the field of short-selling mechanism affecting corporate behavior, but it also enriches the research on the transfer of benefits of private placement of companies.

CircPTN promotes angiogenesis via the MiR-595/LYRM5 signaling pathway in non-small cell lung cancer.

Background: Non-small cell lung carcinoma (NSCLC) is a highly malignant tumor with a poor prognosis worldwide. Some studies have demonstrated that circular pleiotrophin (circPTN) plays critical roles in tumorigenesis and tumor development. However, little is known about the role of circPTN in NSCLC. Methods: The circPTN expression in human NSCLC tissues was measured via quantitative real-time polymerase chain reaction (qRT-PCR). The function and potential mechanisms of circPTN in NSCLC angiogenesis were also investigated. We aimed to explore the function and potential mechanisms and clinical significance of circPTN in NSCLC. Results: We first found that circPTN was markedly upregulated in NSCLC tissues. A higher circPTN level was closely associated with angiogenesis and significantly shorter overall survival in patients with NSCLC. We then found that circPTN promoted angiogenesis in NSCLC. More importantly, we found that circPTN facilitated angiogenesis by regulating the expression of LYRM5 in NSCLC. Mechanistically, LYRM5 could be a direct target of microRNA-595 (miR-595). Additionally, we demonstrated that circPTN upregulated LYRM5 expression by sponging miR-595, which promoted NSCLC angiogenesis in NSCLC. Conclusions: We found that circPTN serves as a competing endogenous ribonucleic acid that promotes angiogenesis via the miR-595/LYRM5 signaling pathway in NSCLC. Targeting circPTN might be a promising new therapeutic strategy for NSCLC.

Circular RNA circTADA2A promotes the proliferation, invasion, and migration of non-small cell lung cancer cells via the miR-450b-3p/HMGN5 signaling pathway.

Background: Circular RNAs (circRNAs) have been confirmed to exert important roles in promoting tumor initiation and progression. However, the expression, effect, and underlying mechanism of circTADA2A in non-small cell lung cancer (NSCLC) remain unclear. Methods: A total of 60 paired clinical samples of NSCLC tissues and corresponding normal adjacent tissues were obtained. Quantitative real-time PCR was used to verify circTADA2A, miR-450b-3p, and HMGN5 mRNA expression. The NSCLC cell Lines A549 and H1299 were individually transfected with circTADA2A and HMGN5. The regulatory interaction between circTADA2A and miR-450b-3p was investigated by dual-luciferase reporter assay. HMGN5 protein expression was detected by Western blotting. Results: CircTADA2A expression was significantly upregulated and correlated with poor overall survival of NSCLC patients. Functionally, circTADA2A inhibition successfully suppressed the proliferation, invasion, and migration of A549 and H1299 cells. circTADA2A functioned as a competing endogenous RNA to sponge miR-450b-3p to promote the expression of HMGN5 mRNA and protein. Furthermore, a positive relationship between circTADA2A and HMGN5 existed in NSCLC tissues. There were negative relationships between circTADA2A and miR-450b-3p as well as miR-450b-3p and HMGN5 in NSCLC tissues. Conclusions: These findings suggest that circTADA2A might act as an oncogenic circRNA that promotes NSCLC progression by sponging miR-450b-3p and promoting HMGN5 expression, indicating that the suppression of circTADA2A could become a potential therapeutic target for restraining NSCLC.

Ginsenoside Rh2 activates α-catenin phosphorylation to inhibit lung cancer cell proliferation and invasion.

The efficacy of ginsenoside Rh2 (Rh2) in cancer therapy has been reported; however, its function in lung cancer remains unknown. To analyze the role of Rh2 in the inhibition of lung cancer cell proliferation in the present study, protein expression levels of E-cadherin, vimentin, ß-catenin, Smo, Gli1, and α-catenin were assessed by western blotting, whilst mRNA expression levels of TCF7 FZD8, Smo, Gli1, Gli2, and Gli3 were determined by reverse transcription-quantitative PCR in the A549 cell line. Phosphorylation sites were detected by proteomic methods and cell proliferation was analyzed by MTT assay. The present study revealed that Rh2 treatment significantly inhibited cell proliferation. Western blotting indicated that the expression levels of E-cadherin were increased and vimentin was downregulated in Rh2-treated cells compared with control cells. Treatment of A549 cells with Rh2 suppressed phosphorylation of five distinct proteins and increased phosphorylation of nine proteins. Among them, the phosphorylation of α-catenin at S641 was significantly induced. Rh2 treatment suppressed the expression levels of key genes involved in Wnt (Wnt3, transcription factor 7 and frizzled class receptor 8) and hedgehog [smoothened, frizzled class receptor (Smo), GLI family zinc finger (Gli)1, Gli2, and Gli3] signaling. Immunoblotting results indicated that ß-catenin, Smo and Gli1 protein expression levels were also suppressed by treatment with Rh2 compared with control treatment. Expression of α-catenin S641D, a phosphomimetic form of α-catenin, inhibited the accumulation of ß-catenin and Gli1 and inhibited cell proliferation and invasion. Furthermore, knockdown of ß-catenin (CTNNB1) or Gli1 with specific small interfering RNAs inhibited cell proliferation, whereas overexpression of these genes had an opposite effect. Additionally, overexpression of ß-catenin or Gli1 activated cell proliferation, even in the presence of Rh2, suggesting that Rh2 affects A549 cell proliferation through inhibition of Wnt and hedgehog signaling by phosphorylation of α-catenin at S641. Together, these data suggested that Rh2 treatment may inhibit the proliferation of A549 lung cancer cells. Further exploration of the underlying mechanism by which Rh2 inhibits cell proliferation is warranted.

PVT1 Promotes Angiogenesis by Regulating miR-29c/Vascular Endothelial Growth Factor (VEGF) Signaling Pathway in Non-Small-Cell Lung Cancer (NSCLC).

BACKGROUND Lung cancer is a common tumor. Non-small-cell lung cancer (NSCLC) accounts for over 85% of lung cancer and has a high degree of malignancy. Angiogenesis plays an important role in NSCLC progression. Some studies have found that PVT1 can promote angiogenesis in tumor tissues, but the role of PVT1 in angiogenesis in NSCLC, as well as the underlying mechanism, is unclear. MATERIAL AND METHODS To explore the role of PVT1 in NSCLC, qRT-PCR, Western blot, luciferase reporter assay, and ELISA were carried out for detecting the relationship among PVT1, miR-29c, and VEGF. Tube formation assay was used to assess the role of PVT1 in angiogenesis in NSCLC. RESULTS Our results showed that higher PVT1 was expressed in NSCLC and the elevated PVT1 was closely related to angiogenesis and poor prognosis in NSCLC. Further functional analysis showed that higher PVT1 expression could promote angiogenesis by regulating VEGF in NSCLC. Mechanistically, the luciferase reporter assay confirmed that VEGF was the targeted gene of miR-29c. In addition, we found that miR-29c is an inhibitory target of PVT1. CONCLUSIONS We found that PVT1 promotes angiogenesis through targeting the miR-29c/VEGF signaling pathway in NSCLC.

Primary pulmonary leiomyosarcoma: A case report.

Primary pulmonary leiomyosarcoma (PPL) is an extremely rare malignant tumor. It has been revealed that PPL may originate from the smooth muscle of the pulmonary parenchyma, pulmonary arteries and bronchi. Patients with PPL may be asymptomatic or present with symptoms similar to those observed in other primary lung tumors. The present study reports the case of a 48-year-old man who presented with a lung mass and underwent a right upper-middle lobe bronchoscope tumor resection. The patient was subsequently diagnosed with PPL. Following the bronchoscopic tumor resection, chemotherapy was administered to the patient; however, the patient succumbed to the disease after the second cycle of chemotherapy.

Clinical analysis of pulmonary cryptococcosis in non-HIV patients in south China.

AIMS: The aim of this study was to investigate the clinical characteristics of pulmonary cryptococcosis occurring in non-HIV patients, and to develop early diagnosis of pulmonary cryptococcosis in immunocompetent cases as well. METHODS: We retrospectively reviewed the clinical data of 41 non-HIV infected patients with pulmonary cryptococcosis who were admitted to the First Affiliated Hospital of Wenzhou Medical University from January 2006 to April 2014. RESULTS: The study included a total of 41 patients (23 males and 18 females) with mean age of 47 years. 12.19% of patients had a history of direct exposure to pigeon droppings; 31.70% of the patients' working or living environments were potentially contaminated by fungal spores. Almost one-third of the patients involved into the study were asymptomatic. The most common clinical manifestations were cough, expectoration and hemoptysis. The most common radiological manifestation was single node or mass in lung, which was described as untypical. Of all cases, 11 patients were diagnosed by CT-guided percutaneous cutting needle biopsy (PCNB), 5 patients were diagnosed by operation, and Crytococcus spore was found in 7 patients' cerebrospinal fluid. 8 patients' blood Cryptococcus Neoformans capsular polysaccharide antigens latex agglutination tests were positive. 36 patients received antifungal therapy. 5 patients underwent surgical resection. During 6 to 24 months follow-up, 40 cases showed total recovery and 1 cases showed improvement. CONCLUSIONS: Pulmonary cryptococcosis in non-HIV subjects might be related to fungus-contaminated environmental exposure. The great variations and protean manifestations of its clinical features often lead to misdiagnosis. Recognition and invasive examination of non-HIV infected patients' pulmonary cryptococcosis in the early stage may help with improvement of its diagnosis and prognosis.

Spontaneous rupture of primary splenic angiosarcoma: A case report.

Primary angiosarcoma of the spleen is an extremely rare malignant neoplasm of vascular origin that often has a poor prognosis. The majority of cases presents with splenic rupture and hemorrhage. The present study retrospectively analyzed the case of 77-year-old female who presented with diffuse abdominal pain and distension. During laparotomy, a huge actively bleeding spleen was identified and a splenectomy was performed. Since an accurate diagnosis could not be achieved by abdominal computed tomography, a pathological examination was performed. The patient and the family refused post-operative adjuvant chemotherapy and radiation therapy. The patient succumbed to uncontrolled hemorrhagic shock and lung metastases at 2 weeks post-surgery.

Stereotactic neurosurgical technique and electrophysiological study in ablating the ventromedial shell of the nucleus accumbens.

OBJECTIVE: To describe in as much detail as possible the method for ablating the ventromedial shell of the nucleus accumbens (NAc) and investigate the efficacy and safety of the ablation treatment. METHODS: Sixty-five patients with drug addictions received operations within the time frame from 2004 to 2009. The ablation targets were located in the bilateral medial posterior inferior shell of the NAc. Intraoperative electrophysiological monitoring was performed. RESULTS: Tissue impedance in the shell of the NAc varied from 185 to 355 Ω. When stimulated with a low frequency (2 Hz) and a voltage above 3 V, 57 out of 65 (87.7%) patients experienced slight throbbing sensations. During the lesion procedure, fever was detected on the head and face of 59 patients (90.8%), the heart rate decreased in 19 cases (29.2%), and restlessness, irritability and hyperalgia were noted for all patients. Among the 65 patients, 52 (80%) no longer experienced a psychological craving for the drug. CONCLUSIONS: The shell of the NAc may be a promising surgical target for psychosurgery. Electrophysiological recordings revealed that the shell is indeed an appropriate structure.

Endovascular intervention for repositioning the distal catheter of ventriculo-atrial shunt.

Displacement of distal ventriculo-atrial (VA) shunt is not uncommon. However, misplacement of the distal catheter of VA shunt in the internal jugular vein is a possibility, especially when conducted without intraoperative monitoring. We describe a patient in whom a VA shunt was performed due to failure of ventriculo-peritoneal shunt and the distal catheter of the shunt was found to be misplaced in the left internal jugular vein. Endovascular intervention via femoral vein was used to retrieve the distal catheter.

Total phenolic contents and antioxidant capacities of herbal and tea infusions.

In order to supply new information on the antioxidant function of selected beverages for nutritionists and the general public, total phenolic contents of 51 kinds of herbal and tea infusions made in China were measured by the Folin-Ciocalteu method, and their antioxidant capacities were evaluated using ferric reducing antioxidant power (FRAP) and Trolox equivalent antioxidant capacity (TEAC) assays. A significant correlation between FRAP and TEAC values suggested that antioxidant components in these beverages were capable of reducing oxidants and scavenging free radicals. The high correlation between antioxidant capacities and total phenolic contents indicated that phenolic compounds could be one of the main components responsible for antioxidant activities of these beverages. Generally, these beverages had high antioxidant capacities and total phenolic contents, and could be important dietary sources of antioxidant phenolics for prevention of diseases caused by oxidative stress.