Effect of modified Blumgart pancreaticojejunostomy on nutritional status in elderly patients after pancreaticoduodenectomy.

OBJECTIVE: To evaluate the effect of modified Blumgart pancreaticojejunostomy on the nutritional status in elderly patients after pancreaticoduodenectomy. METHODS: Fifty-eight elderly patients who underwent pancreaticoduodenectomy in our hospital were evenly divided into the traditional group (receiving traditional Blumgart pancreaticojejunostomy) and the modified group (receiving modified Blumgart pancreaticojejunostomy). RESULTS: In the modified group, intraoperative blood loss and 24-h VAS score were lower and time to off-bed activity and postoperative hospital stay were shorter than those in the traditional group (P<0.05). The levels of d-lactic acid, diamine oxidase, and endotoxin were increased after surgery and were higher in the modified group than those in the traditional group, while the digestive symptoms and cancer pain scores at 6 months after surgery and postoperative complication rate were lower than those of the traditional group (all P<0.05). The nursing satisfaction was higher in the modified group than that in the traditional group (P<0.05). The nutritional status, pancreatic endocrine function and pancreatic exocrine function showed no significant differences between the two groups. CONCLUSION: The modified Blumgart pancreaticojejunostomy can reduce the pain level, expedite postoperative rehabilitation, and improve the intestinal mucosal barrier function and quality of life of patients while not significantly affecting postoperative nutritional status and pancreatic function.

Upregulation of miR­335 exerts protective effects against sepsis­induced myocardial injury.

Septicemia is associated with excessive inflammation, oxidative stress and apoptosis, causing myocardial injury that results in high mortality and disability rates worldwide. The abnormal expression of multiple microRNAs (miRNAs/miRs) is associated with more severe sepsis­induced myocardial injury (SIMI) and miR­335 has been shown to protect cardiomyocytes from oxidative stress. The present study aimed to investigate the role of miR­335 in SIMI. An SIMI model was established by cecal ligation and puncture (CLP) in mice. An miRNA­335 precursor (pre­miR­335) was transfected to accelerate miR­335 expression and an miR­335 inhibitor (anti­miR­335) was used to inhibit miR­335 expression. CLP or sham surgery was performed on pre­miR­335, anti­miR­335 and wild­type mice and miR­335 expression was determined by reverse transcription­quantitative PCR. Inflammatory factors (TNF­α, IL­6 and IL­10) and troponin (cTNI), brain natriuretic peptide (BNP), creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) were assessed using commercial kits. Apoptosis was detected by flow cytometry and cardiac function was assessed using a Langendorff isolated cardiac perfusion system. miR­335 expression was upregulated and an elevation in inflammatory factors and cTNI, BNP, CK, LDH and AST was observed. Compared with the wild­type control group, pre­miR­335 mice treated with CLP exhibited significantly reduced left ventricular development pressure, maximum pressure increased reduction rates, as well as decreased levels of TNF­α, IL­6 and IL­10, myocardial injury and apoptosis; by contrast, these features were amplified in CLP­treated anti­miR­335 mice. In conclusion, the upregulation of miR­335 exerted ameliorative effects on myocardial injury following sepsis and may indicate a novel therapeutic intervention for SIMI.

Salidroside inhibits endothelial­mesenchymal transition via the KLF4/eNOS signaling pathway.

Homocysteine (Hcy) was discovered to be an independent risk factor for the development of atherosclerosis (AS). Moreover, endothelial­mesenchymal transition (EndMT) was found to be one of main mechanisms contributing to the pathogenesis of AS. Salidroside (SAL) has diverse pharmacological activities, including anti­inflammatory, anti­cancer, anti­oxidative and anti­fibrosis properties. However, whether SAL serves a beneficial role in Hcy­induced EndMT remains unknown. The present study aimed to investigate whether SAL exerted its effects on Hcy­induced EndMT via the Kruppel­like factor 4 (KLF4)/endothelial nitric oxide (NO) synthase (eNOS) signaling pathway. HUVECs were pretreated with high and low doses (10 or 50 µmol/l) of SAL for 2 h, followed by 1 mmol/l Hcy for 48 h to induce EndMT. Western blotting was used to analyze the protein expression levels of the endothelial marker, VE­cadherin, the mesenchymal cell marker, α­smooth muscle actin (SMA), and the nuclear transcription factors, KLF4 and eNOS. Wound healing assays were used to determine the cell migratory ability, and the levels of NO in the cell culture supernatants were measured using a nitrate reductase assay. Cellular immunofluorescence was used to analyze the expression and localization of KLF4. Small interfering (si)RNA targeting KLF4 (siKLF4) was used to knock down KLF4 expression in HUVECs. The results of the present study revealed that treatment with SAL upregulated the expression levels of VE­cadherin, downregulated the expression levels of α­SMA, reduced cell migration and activated the eNOS/NO signaling axis, as well as downregulated KLF4 expression and translocation to the nucleus. Compared with the SAL + siKLF4 co­administration group, no significant differences were observed in the expression levels of the phenotypic markers in the SAL or siKLF4 groups. In conclusion, the findings of the present study revealed that SAL may inhibit Hcy­induced EndMT via regulation of the KLF4/eNOS signaling pathway.

Laparoscopic specimen extraction in vitro: preliminary experience.

BACKGROUND: The last procedure performed by the surgeon in laparoscopic surgery is to extract the specimen through the smallest incision possible. This experiment aimed to explore the maximum diameter of specimens that can be extracted through auxiliary incisions of different lengths and shapes by in vitro physical experiments. MATERIALS AND METHODS: We used the abdominal wall with the muscle layer, fixed on a square wooden frame, to simulate the human abdominal wall. Then, specimen extraction ports were made with circular, inverted Y-shaped and straight-line incisions of different sizes and lengths, and specimens of different sizes were made from tissues of different species. These specimens were extracted from different incisions with a force gauge. The tension value (N) was measured, and records were made of the length or diameter of the smallest auxiliary incision through which a given specimen could pass, as well as the largest specimen diameter that could pass through an incision of a given size. This experiment provides us with preliminary experience-based knowledge of how to choose the appropriate auxiliary incision for surgical specimen extraction according to the diameter of the specimen. RESULTS: The maximum diameters of specimens that could be extracted with circular ostomy diameters of 2.4, 2.7 and 3.3 cm were 4.0, 4.5 and 6.0 cm, respectively. Specimens with diameters of 6.0, 8.0 and 10.0 cm could be extracted through inverted Y-shaped incisions with a length around the umbilicus of 1 cm and an extension length of 1.0, 3.0, and 4.0 cm, respectively. Moreover, these same specimens could be extracted through inverted Y-shaped incisions with a length around the umbilicus of 2 cm and extension lengths of 0.0, 1.0 and 2.0 cm. Tough tissue specimens (made from chicken gizzards) with diameters of 1.0, 2.0, 4.0 and 6.0 cm, respectively, could be removed through straight-line incisions measuring 1.0, 2.0, 3.0 and 4.0 cm in length. CONCLUSION: Along with preoperative imaging, surgical planning and trocar position, the shape and length of auxiliary incisions can be used to improve the extraction of specimens via laparoscopic surgery.

18F-FDG PET/CT features of ureteral metastases from breast cancer: a case report.

Breast cancer metastasis to the ureter is rare. Fluorine-18-fluorodeoxyglucose positron emission tomography (18F-FDG PET)/computed tomography (CT) is widely used to identify primary lesions of metastatic tumours, however, 18F-FDG PET/CT imaging features of ureteral metastasis from breast cancer are rarely reported. Herein, the case of a 46-year-old woman with recurrent left flank pain for 5 months, who was admitted to the Cancer Hospital of Guangxi Medical University and Guangxi Cancer Research Institute, is described. She had undergone right radical mastectomy 5 years previously and had received tamoxifen treatment for 5 years. Assessment by 18F-FDG PET/CT revealed tumours on the ureter presenting as a long segmental lesion, radioactive concentrations, and a low maximum standardized uptake value (SUVmax), with no radioactive concentrations in the urine and no significant change in the ureteral contour. The severity of the ureteral lesion was not consistent with the severity of hydronephrosis. A tumour biopsy was performed laparoscopically, and postoperative pathological examination confirmed a primary breast cancer tumour. The patient did not consent to treatment and was lost to follow-up.

Unilateral T-shaped incomplete duplex nephrectomy in an adolescent under laparoscopy: A case report.

INTRODUCTION: Duplicate kidneys are the most common congenital abnormality of the urinary system. The location of duplicate kidneys varies. We report a case of an adolescent with upper and lower kidneys that are arranged vertically and approximately T-shaped. PATIENT CONCERNS: A 16-year-old male teenager was examined for pain in the left side of the waist. The Computed Tomography scan revealed that the left kidney was incompletely duplicated and fused; the left upper urinary tract was incompletely obstructed. DIAGNOSIS: The abdominal tomography confirmed the diagnosis of incomplete duplicate kidney. INTERVENTIONS: The patient underwent laparoscopic surgery. The failure to ligate the renal pedicle resulted in increased bleeding during the operation and an open ureteral stump. OUTCOMES: No urine leakage occurred after the operation. Doppler ultrasound of the urinary system showed no hydronephrosis, and the patient was asymptomatic. CONCLUSION: Through this case report, we found that the duplicate kidneys could be arranged in a T-shape under laparoscopy. Although only the supply of the duplicate renal arteries can be ligated during surgical resection, the renal pedicle must also be ligated during the operation if there is a lot of bleeding.

Sarcomatoid carcinoma of the prostate with bladder invasion shortly after androgen deprivation: Two case reports.

BACKGROUND: To summarize the imaging, morphological and biological characteristics of sarcomatoid carcinoma (SC) of the prostate with bladder invasion not long after castration. CASE SUMMARY: Our two cases were initially diagnosed with adenocarcinoma of the prostate due to dysuria. However, prostate SC was diagnosed after transurethral resection of the prostate (TURP) and castration after only 5 and 10 mo, respectively. Distinctive liver-like tissues appeared in the second TURP procedure in case 1, while a white, fish flesh-like, narrow pedicled soft globe protruded from the prostate to the bladder in case 2. CONCLUSION: The sarcomatoid component of SC may arise from one of the specific groups of cancer cells that are resistant to hormonal therapy. Morphological characteristics of SCs can present as "red hepatization" and "fish flesh". SCs grow rapidly and have a poor prognosis, and thus, extensive TURP plus radiation may be the treatment of choice.

The Role of Oxymatrine in Amelioration of Acute Lung Injury Subjected to Myocardial I/R by Inhibiting Endoplasmic Reticulum Stress in Diabetic Rats.

BACKGROUND: Oxymatrine (OMT) is the primary pharmacological component of Sophora flavescens Aiton., which has been shown to possess potent antifibrotic, antioxidant, and anti-inflammatory activities. The aim of the present study was to clarify the protective mechanism of OMT on acute lung injury (ALI) subjected to myocardial ischemia/reperfusion (I/R). METHODS: A myocardial I/R-induced ALI model was achieved in diabetic rats by occluding the left anterior descending coronary artery for 1 h, followed by reperfusion for 1 h. The levels of inflammatory factors (tumor necrosis factor-α, interleukin- (IL-) 6, and IL-17) in bronchoalveolar lavage fluid were assessed using commercially available kits. The index of myocardial injury, including the detection of cardiac troponin I (cTnI), cardiac troponin T (cTnT), lactate dehydrogenase (LDH), and creatine kinase-MB (CK-MB), was also determined using commercially available kits. Hematoxylin and eosin staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling were used to identify histological changes. The expression levels of endoplasmic reticulum chaperone BiP (GRP78), DNA damage-inducible transcript 3 protein (CHOP), eukaryotic translation initiation factor 2-alpha kinase 3 (PERK), inositol dependent enzyme 1α (IRE1α), ATF6, caspase-3, -9, and-12, Bcl-2, and Bax were determined by Western blotting. The mRNA expression levels of GRP78 and CHOP were detected by reverse transcription-quantitative PCR. RESULTS: Myocardial I/R increased the levels of cTnI, cTnT, LDH, and CK-MB in diabetic rats. Damaged and irregularly arranged myocardial cells were also observed, as well as more serious ALI with higher lung injury scores and WET/DRY ratios and lower PaO2. Moreover, the expression of key proteins of endoplasmic reticulum stress (ERS) was increased by I/R injury, including phosphorylated- (p-) PERK, p-IRE1ɑ, and ATF6, as well as decreased levels of apoptosis. These effects were all significantly reversed by OMT treatment. CONCLUSIONS: OMT protects against ALI subjected to myocardial I/R by inhibiting ERS in diabetic rats.

New strain of Pediococcus pentosaceus alleviates ethanol-induced liver injury by modulating the gut microbiota and short-chain fatty acid metabolism.

BACKGROUND: Intestinal dysbiosis has been shown to be associated with the pathogenesis of alcoholic liver disease (ALD), which includes changes in the microbiota composition and bacterial overgrowth, but an effective microbe-based therapy is lacking. Pediococcus pentosaceus (P. pentosaceus) CGMCC 7049 is a newly isolated strain of probiotic that has been shown to be resistant to ethanol and bile salts. However, further studies are needed to determine whether P. pentosaceus exerts a protective effect on ALD and to elucidate the potential mechanism. AIM: To evaluate the protective effect of the probiotic P. pentosaceus on ethanol-induced liver injury in mice. METHODS: A new ethanol-resistant strain of P. pentosaceus CGMCC 7049 was isolated from healthy adults in our laboratory. The chronic plus binge model of experimental ALD was established to evaluate the protective effects. Twenty-eight C57BL/6 mice were randomly divided into three groups: The control group received a pair-fed control diet and oral gavage with sterile phosphate buffered saline, the EtOH group received a ten-day Lieber-DeCarli diet containing 5% ethanol and oral gavage with phosphate buffered saline, and the P. pentosaceus group received a 5% ethanol Lieber-DeCarli diet but was treated with P. pentosaceus. One dose of isocaloric maltose dextrin or ethanol was administered by oral gavage on day 11, and the mice were sacrificed nine hours later. Blood and tissue samples (liver and gut) were harvested to evaluate gut barrier function and liver injury-related parameters. Fresh cecal contents were collected, gas chromatography-mass spectrometry was used to measure short-chain fatty acid (SCFA) concentrations, and the microbiota composition was analyzed using 16S rRNA gene sequencing. RESULTS: The P. pentosaceus treatment improved ethanol-induced liver injury, with lower alanine aminotransferase, aspartate transaminase and triglyceride levels and decreased neutrophil infiltration. These changes were accompanied by decreased levels of endotoxin and inflammatory cytokines, including interleukin-5, tumor necrosis factor-α, granulocyte colony-stimulating factor, keratinocyte-derived protein chemokine, macrophage inflammatory protein-1α and monocyte chemoattractant protein-1. Ethanol feeding resulted in intestinal dysbiosis and gut barrier disruption, increased relative abundance of potentially pathogenic Escherichia and Staphylococcus, and the depletion of SCFA-producing bacteria, such as Prevotella, Faecalibacterium, and Clostridium. In contrast, P. pentosaceus administration increased the microbial diversity, restored the relative abundance of Lactobacillus, Pediococcus, Prevotella, Clostridium and Akkermansia and increased propionic acid and butyric acid production by modifying SCFA-producing bacteria. Furthermore, the levels of the tight junction protein ZO-1, mucin proteins (mucin [MUC]-1, MUC-2 and MUC-4) and the antimicrobial peptide Reg3ß were increased after probiotic supplementation. CONCLUSION: Based on these results, the new strain of P. pentosaceus alleviated ethanol-induced liver injury by reversing gut microbiota dysbiosis, regulating intestinal SCFA metabolism, improving intestinal barrier function, and reducing circulating levels of endotoxin and proinflammatory cytokines and chemokines. Thus, this strain is a potential probiotic treatment for ALD.

The Attenuation of Traumatic Brain Injury via Inhibition of Oxidative Stress and Apoptosis by Tanshinone IIA.

Traumatic brain injury (TBI) is a major source of mortality and long-term disability worldwide. The mechanisms associated with TBI development are poorly understood, and little progress has been made in the treatment of TBI. Tanshinone IIA is an effective agent to treat a variety of disorders; however, the mechanisms of Tanshinone IIA on TBI remain unclear. The aim of the present study was to investigate the therapeutic potential of Tanshinone IIA on TBI and its underlying molecular mechanisms. Changes in microvascular permeability were examined to determine the extent of TBI with Evans blue dye. Brain edema was assessed by measuring the wet weight to dry weight ratio. The expression levels of CD11, interleukin- (IL-) 1ß, and tumor necrosis factor- (TNF-) α mRNA were determined by reverse transcription-quantitative PCR. Aquaporin-4 (AQP4), glial fibrillary acidic protein (GFAP), and p47phox protein expression levels were detected by western blotting. Superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-PX) activities, and malondialdehyde (MDA) content were determined using commercial kits. Cell apoptosis was detected by western blotting and TUNEL staining. Tanshinone IIA (10 mg/kg/day, intraperitoneal administration) significantly reduced brain water content and vascular permeability at 12, 24, 48, and 72 h after TBI. Tanshinone IIA downregulated the mRNA expression levels of various factors induced by TBI, including CD11, IL-1ß, and TNF-α. Notably, CD11 mRNA downregulation suggested that Tanshinone IIA inhibited microglia activation. Further results showed that Tanshinone IIA treatment significantly downregulated AQP4 and GFAP expression. TBI-induced oxidative stress and apoptosis were markedly reversed by Tanshinone IIA, with an increase in SOD and GSH-PX activities and a decrease in the MDA content. Moreover, Tanshinone IIA decreased TBI-induced NADPH oxidase activation via the inhibition of p47phox. Tanshinone IIA attenuated TBI, and its mechanism of action may involve the inhibition of oxidative stress and apoptosis.

Propofol inhibits proliferation and cisplatin resistance in ovarian cancer cells through regulating the microRNA­374a/forkhead box O1 signaling axis.

Ovarian cancer is a prominent disease that demonstrates high incidence rates in women and often presents multidrug resistance. Propofol has been demonstrated to suppress the malignancy of various types of human cancer; however, the underlying molecular mechanisms of propofol in ovarian cancer remain largely unknown. The present study aimed to investigate whether and how propofol inhibits proliferation and cisplatin (DDP) resistance in ovarian cancer cells. Ovarian cancer cell viability was assessed by the Cell Counting kit­8 assay; apoptosis and cell cycle progression were determined by flow cytometry; the relative expression levels of microRNA (miR)­374a and forkhead box O1 (FOXO1) were analyzed using reverse transcription­quantitative PCR; the binding ability of miR­374a to FOXO1 was assessed by the dual­luciferase reporter assay; cellular sensitivity to DDP was detected using the MTT assay; and finally, the protein expression levels of FOXO1, p27, and Bcl­2­like­protein 11 (Bim) were analyzed by western blotting. Propofol reduced viability, promoted apoptosis and decreased miR­374a expression levels in A2780 cells. In addition, the viability of A2780/DDP cells in the propofol + DDP treatment group was significantly inhibited, and the apoptotic rate was increased. In addition, miR­374a overexpression increased cell viability and the proportion of cells in the S phase, and decreased the proportion of cells in the G0/G1 phase. Conversely, genetic knockdown of miR­374a exerted the opposite effects on cell viability and cell cycle progression. Moreover, miR­374a was demonstrated to bind to FOXO1. Propofol promoted the expression of FOXO1, p27 and Bim, induced cell cycle arrest and decreased ovarian cancer cell viability. In addition, treatment with propofol and DDP regulated FOXO1 and increased apoptosis of ovarian cancer cells. In conclusion, propofol downregulated miR­374a and modulated the FOXO1 pathway to reduce proliferation and DDP resistance in ovarian cancer cells.

NIR absorbing reduced graphene oxide for photothermal radiotherapy for treatment of esophageal cancer.

Theranostic agents were drawing a huge attention in the personalized medication. In this study, we established a facile technique, plant extract-based technique for the synthesis of reduced nano-graphene oxide (RNGO) with low cytotoxicity. We formed platforms of photothermal (PT) therapy and further explained that the synthesized RNGO can be utilized as ready to use PT therapy without any additional surface adjustment. In the meantime, with the help of a constant-wave NIR laser (near-infrared), in vitro esophageal adenocarcinoma cell line (OE-19) cancer cells were effectively ablated, because of the PT impact of RNGO. The outcomes propose that the RNGO was appropriate for PT therapy and photoacoustic imaging of the tumor, which is assuring for theranostic nanomedicine.

The conditioned medium of human mesenchymal stromal cells reduces irradiation-induced damage in cardiac fibroblast cells.

Recently, multipotent mesenchymal stromal cell (MSC) treatment has attracted special attention as a new alternative strategy for stimulating regeneration. Irradiation myocardial fibrosis (IMF) is a major complication associated with total body irradiation for hematopoietic stem cell transplantation, nuclear accidents, and thoracic radiotherapy for lung cancer, esophageal cancer, proximal gastric cancer, breast cancer, thymoma, and lymphoma. The aim of the present study was to assess the therapeutic paracrine effects of human umbilical cord-derived mesenchymal stromal cells (UC-MSCs) in the cell model of IMF. For this purpose, primary human cardiac fibroblasts (HCF) cells were irradiated and cultured with the conditioned medium of UC-MSCs (MSCCM). MSCCM promoted cell viability, reduced collagen deposition as measured by Sircol assay and qPCR (Col1A1 and Col1A2), prevented oxidative stress and increased antioxidant status (as measured by malondialdehyde content and the activities and mRNA levels of antioxidant enzymes), and reduced pro-fibrotic TGF-ß1, IL-6 and IL-8 levels (as examined by ELISA kit and qPCR). Pretreatment with inhibitor of NF-κB led to a decrease in the levels of TGF-ß1 in cell lysate of HCF cells by ELISA kit. Furthermore, we also found that MSCCM prevented NF-κB signaling pathway activation for its proinflammatory actions induced by irradiation. Taken together, our data suggest that MSCCM could reduce irradiation-induced TGF-ß1 production through inhibition of the NF-κB signaling pathway. These data provide new insights into the functional actions of MSCCM on irradiation myocardial fibrosis.

Avirulence and lysozyme secretion in Paneth cells after infection of BALB/c mice with oocysts of Toxoplasma gondii strains TgCatCHn2 (ToxoDB#17) and TgCatCHn4 (ToxoDB#9).

Toxoplasma gondii has a complex life cycle and pathogenic mechanisms. Acute T. gondii infections in mice often result in death, whereas in chronic infections, the parasites may persist in the host tissues as intraneuronal or intramuscular cysts. However, the virulence of T. gondii strains in mice varies with its genetic background. The present study investigated the pathogenicity and pathological lesions of two T. gondii isolates from China: namely, TgCatCHn2 (ToxoDB#17) and TgCatCHn4 (ToxoDB#9). The virulent (ToxoDB#216) and avirulent (VEG) strains were employed as controls. Toxoplasmosis was induced by inoculating BALB/c mice with oocysts of the strains of T. gondii VEG, ToxoDB#216, TgCatCHn2 (ToxoDB#17), and TgCatCHn4 (ToxoDB#9), respectively. As a result, one oocyst of ToxoDB#216 could kill a mouse within 10 days post inoculation (DPI). The survival time of the mice for T. gondii TgCatCHn2 and TgCatCHn4 was >60 DPI for 106/mL oocysts, but this concentration (106/mL oocysts) of VEG strain could kill mice within 11 DPI. Compared with the strains of T. gondii ToxoDB#216 and VEG, the lesions in the small intestines of the strains of TgCatCHn2- and TgCatCHn4-infected mice were significantly smaller (P < 0.01). The positive area of T. gondii antigen in the ileum of mice infected with the strains of T. gondii VEG, TgCatCHn2 and TgCatCHn4 were significantly lower than that T. gondii ToxoDB#216 at 8 DPI (P < 0.01). Paneth cells (PCs) in the small intestines was eliminated by ToxoDB#216 (5-6 DPI) (P < 0.05). The strains of T. gondii TgCatCHn2-, TgCatCHn4- and VEG-infected mice, the number of PCs and granules decreased in the intestines, compared to T. gondii free mice, but the difference was not significant (8 DPI, P > 0.05). However, the granules in the PCs showed negative lysozyme expression in the intestines of mice infected with T. gondii TgCatCHn2 and TgCatCHn4. Thus, T. gondii strains of TgCatCHn2 (ToxoDB#17) and TgCatCHn4 (ToxoDB#9) were avirulent strains, they triggered an inhibition of lysozyme expression in the granules of PCs of the mouse intestine. These effects may in turn lead to intestinal dysbiosis, which may be related to further parasitic invasion of the intestines. The findings of the present study further expand the spectrum of the pathogenic features of various Chinese isolates of T. gondii.

Evaluation of acute normovolemic hemodilution in patients undergoing intracranial meningioma resection: A quasi-experimental trial.

The aim of this study was to evaluate the safety of acute normovolemic hemodilution (ANH) for patients undergoing intracranial meningioma resection.Eighty patients (aged 48-65 years) with American Society of Anesthesiologists physical status I-II undergoing intracranial meningioma resection were included in this prospective observational study. The patients were randomly divided into group A (ANH group), which underwent a combination of ANH and intraoperative cell salvage (ICS), and group B (control group), which underwent ICS alone. The study parameters were recorded as baseline values before blood drainage (T0), after blood drainage (T1), and before (T2) and after (T3) retransfusion in group A. Whereas in group B, the same parameters were measured 10 minutes after anesthesia induction (T0), before surgery (T1), and before (T2) and after (T3) transfusion of autologous blood.When intraoperative blood loss was <2000 mL, the mean volume of homologous blood transfused in group A patients was 100.8 ±â€Š82.3 mL, compared with the 190.0 ±â€Š91.8 mL in group B. Reduction in homologous blood used in group A was statistically significant (P < .05). In group B, 15.1% patients received homologous blood, whereas only 5.9% patients received homologous blood in group A. The difference in heart rate between both groups at different time points was statistically nonsignificant (P > .05). The mean hemoglobin and hematocrit levels at T1 and T2 in group A were lower than in group B (P < .05). The prothrombin time and activated partial thromboplastin time in both groups were prolonged significantly after T2 (all P < .05), but were all within normal range. There were no significant differences in postoperative hospital stay, mortality, and postoperative infection between the 2 groups.For patients undergoing excision of intracranial meningioma, ANH is an effective procedure to reduce the need for allogeneic transfusions.

Antibody Detection, Isolation, Genotyping, and Virulence of Toxoplasma gondii in Captive Felids from China.

The felids are the only definitive hosts of Toxoplasma gondii, which could excrete oocysts into the environment and provide an infection source for toxoplasmosis in various warm-blooded animal species, particularly the captive felids that live close to human communities. The infection rate of the captive felids is a perfect standard in detecting the presence of Toxoplasma gondii oocysts in the environment. In this study, sera or tissue samples from zoo (1 young tiger, 2 adult tigers, 6 young lions), farm (10 masked palm civets), and pet hospital (28 cats) from Henan Province (China) were collected. The sera (n = 47) were tested for immunoglobulin G (IgG) antibodies against T. gondii by using modified agglutination test (MAT), whereas the hearts tissue (n = 40) were bioassayed in mice to isolate T. gondii strains. The genotype was distinguished by using PCR-RFLP of 10 loci (SAG1, SAG2, SAG3, GRA6, BTUB, L358, c22-8, PK1, c29-2, and Apico). The detection rate for the T. gondii antibody in captive felids was 21.3% (10/47). One viable T. gondii strain (TgCatCHn4) was obtained from a cat heart tissue, and its genotype was ToxoDB#9. The oocysts of ToxoDB#9 were collected from a T. gondii-free cat. The virulence of TgCatCHn4 was low and no cysts were detected in the brain of mice at 60 days post-inoculation. The finding of the present study suggested a widespread exposure of T. gondii for felids in Henan Province of central China, particularly those from the zoological gardens and homes. ToxoDB#9 was the predominant strain in China. Preventive measures against T. gondii oocyst contamination of various components of the environment should thus be implemented, including providing pre-frozen meat, well-cooked cat food, cleaned fruits and vegetables, monitoring birds and rodents, inactive T. gondii oocysts in felids feces, and proper hygiene.

Hispidin induces autophagic and necrotic death in SGC-7901 gastric cancer cells through lysosomal membrane permeabilization by inhibiting tubulin polymerization.

Hispidin and its derivatives are widely distributed in edible mushrooms. Hispidin is more cytotoxic to A549, SCL-1, Bel7402 and Capan-1 cancer cells than to MRC5 normal cells; by contrast, hispidin protects H9c2 cardiomyoblast cells from hydrogen peroxide-induced or doxorubicin-induced apoptosis. Consequently, further research on how hispidin affects normal and cancer cells may help treat cancer and reduce chemotherapy-induced side effects. This study showed that hispidin caused caspase-independent death in SGC-7901 cancer cells but not in GES-1 normal cells. Hispidin-induced increases in LC3-II occurred in SGC-7901 cells in a time independent manner. Cell death can be partially inhibited by treatment with ATG5 siRNA but not by autophagy or necroptosis inhibitors. Ultrastructural evidence indicated that hispidin-induced necrotic cell death involved autophagy. Hispidin-induced lysosomal membrane permeabilization (LMP) related to complex cell death occurred more drastically in SGC-7901 cells than in GES-1 cells. Ca2+ rather than cathepsins from LMP contributed more to cell death. Hispidin induced microtubule depolymerization, which can cause LMP, more drastically in SGC-7901 cells than in GES-1 cells. At 4.1 µM, hispidin promoted cell-free tubulin polymerization but at concentrations higher than 41 µM, hispidin inhibited polymerization. Hispidin did not bind to tubulin. Alterations in microtubule regulatory proteins, such as stathmin phosphorylation at Ser16, contributed to hispidin-induced SGC-7901 cell death. In conclusion, hispidin at concentrations higher than 41 µM may inhibit tubulin polymerization by modulating microtubule regulatory proteins, such as stathmin, causing LMP and complex SGC-7901 cell death. This mechanism suggests a promising novel treatment for human cancer.

Cardioprotective Effects of Malvidin Against Isoproterenol-Induced Myocardial Infarction in Rats: A Mechanistic Study.

BACKGROUND Malvidin (alvidin-3-glucoside) is a polyphenol that belongs to the class of natural anthocyanin, which is abundantly found in red wines, colored fruits, and the skin of red grapes. Therefore, the current investigation was intended to evaluate the effect of malvidin against myocardial infarction induced by isoproterenol in the rats. MATERIAL AND METHODS The cardioprotective effects was assessed by determining the effect of malvidin on the activities of endogenous antioxidants - catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) - and on the levels of lipid peroxidation and serum marker enzymes. The serum levels of IL-6 and TNF-α were also determined using an enzyme-linked immunosorbent assay (ELISA) kit. RESULTS The present study demonstrated a significant cardioprotective effect of malvidin by restoring the defensive activities of endogenous antioxidants - catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH) - and by reducing the levels of lipid peroxidation and serum marker enzymes lactate dehydrogenase (LD) and creatine kinase (CK). Malvidin significantly ameliorated the histopathological changes and impaired mitochondria in the cardiac necrosis stimulated with isoproterenol. Additionally, the results also demonstrated that nuclear translocation of Nrf-2 and subsequent HO-1 expression might be associated with nuclear factor kappa B (NF-κB) pathway activation. CONCLUSIONS Our findings suggest that malvidin exerts cardioprotective effects that might be due to possible strong antioxidant and anti-inflammatory activities. Therefore, this study provides the basis for the development of malvidin as a safe and effective treatment of myocardial infarction.

Hispolon inhibits breast cancer cell migration by reversal of epithelial-to-mesenchymal transition via suppressing the ROS/ERK/Slug/E-cadherin pathway.

Hispolon has been shown to have anticancer effects on various tumors. However, whether hispolon exerts anti-migration activity in breast cancer cells and the underlying mechanisms, have not been elucidated yet. In the present study, our data demonstrated that hispolon inhibited TPA-induced breast cancer MCF-7 cell migration at sub-toxic concentrations in vitro. Hispolon decreased the level of cellular ROS significantly and repressed TPA-induced phosphorylation of extracellular signal-regulated kinase (ERK), accompanied by upregulation of E-cadherin and downregulation of the transcriptional repressor Slug. Furthermore, N-acetyl-cysteine, an antioxidant agent, markedly suppressed TPA-induced epithelial-to-mesenchymal transition, cell migration and activation of ERK. Taken together, our results indicated that hispolon suppressed the migration of breast cancer cells via suppressing the ROS/ERK/Slug/E­cadherin pathway. Hispolon may be developed as a potential antimetastasis agent to breast cancer.

[Effect of Electroacupuncture at Distal and Proximal Acupoints on Expression of Spinal p 38 Mitogen-activated Protein Kinase and Cyclic Adenosine 3',5'-monophosphate in Rats with Lumbago].

OBJECTIVE: To observe the influence of Electroacupuncture (EA) stimulation of different distal-proximal acupoints combination groups on pain reaction, spinal p 38 mitogen-activated protein kinase (p 38 MAPK) expression and cyclic adenosine 3', 5'-monophosphate (cAMP) content in experimental lumbago rats. METHODS: Seventy-eight male SD rats were randomized into normal, model, sham operation, EX-B 2-BL 25 (proximal acupoints, PA), BL 40-BL 60 (distal acupoints, DA) and DA+PA groups. The lumbago model was established by implanting the autologous nucleus pulposus to the site close to the left L 5 dorsal root ganglion and the surface of dura mate of spinal cord. EA (2 Hz/100 HZ,1-3 mA) was applied at bilateral EX-B 2-BL 25 or BL 40-BL 60 or both for 20 minutes, once daily for 7 days. The mechanical pain threshold was measured, and the expression of p 38 MAPK in the lumbar spinal cord was detected by immunohistochemistry and Western blot, separately. The content of cAMP in spinal cord (L 4-L 6) was measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: After mode-ling, the mechanical pain threshold percentages were significantly decreased on day 3, 5 and 7 (P<0.01), and after EA stimulation of DA,PA and DA+PA, the decreased pain threshold was significantly increased at the 3 time-points (P<0.01), and the effects of both PA and DA+PA were markedly superior to that of DA (P<0.05, P<0.01). Following modeling, lumbar spinal p 38 MAPK immunoactivity and protein expression, and cAMP content were obviously up-regulated (P<0.01). Compared with the model group, the levels of p 38 MAPK immunoactivity and protein expression in the 3 EA groups and the sham group, and cAMP contents in both PA and DA+PA groups (not in the DA and sham groups) were considerably down-regulated (P<0.01, P<0.05). CONCLUSIONS: EA stimulation of distal+proximal acupoints and proximal acupoints near the focus can raise pain threshold in lumbago rats, which may be associated with their effects in suppressing lumbago-induced increase of expression of spinal p 38 MAPK protein and cAMP content. The effects of EA of distal+proximal acupoints and proximal acupoints are better than those of EA of simple distal acupoints.