Infection control management strategy for operating room during COVID-19 pandemic.

Coronavirus disease 2019 (COVID-19) outbreaks have occurred in many countries around the world. The numbers of confirmed cases and deaths continue to increase. It is increasingly likely that COVID-19 patients will require emergency surgeries in the operating room (OR). As COVID-19 can easily be transmitted to healthcare workers and other patients during surgery, it is important to establish a set of infection prevent and control management strategy to prevent COVID-19 from spreading in the OR. Based on our experience in COVID-19 prevention and control in the OR, we introduce this COVID-19 prevention and control management strategy for preventing COVID-19 from spreading in the OR. This management strategy includes a number of COVID-19 prevention and control procedures including (I) conduct COVID-19 knowledge training at the early stage of outbreak, (II) formulate the surgery arrangement procedures and suspend the elective surgery if the patient confirmed to COVID-19, (III) divide an isolated OR area for COVID-19 surgery, (IV) preoperative preparation procedures, (V) procedures for wearing and removing personal protective equipment, (VI) anesthesia management, intraoperative management, (VII) post-operative disposable waste management and disinfection. This management strategy has worked very effectively since the outbreak of COVID-19 in Wuhan at the end of 2019. We have performed emergency surgeries on several COVID-19 confirmed patient and dozens of COVID-19 suspected patients under this COVID-19 prevention and control management strategy, and have achieved an excellent result of zero COVID-19 infection in the OR.

RNA Helicase DDX24 Stabilizes LAMB1 to Promote Hepatocellular Carcinoma Progression.

Hepatocellular carcinoma (HCC) is one of the most aggressive malignancies. Elucidating the underlying mechanisms of this disease could provide new therapeutic strategies for treating HCC. Here, we identified a novel role of DEAD-box helicase 24 (DDX24), a member of the DEAD-box protein family, in promoting HCC progression. DDX24 levels were significantly elevated in HCC tissues and were associated with poor prognosis of HCC. Overexpression of DDX24 promoted HCC migration and proliferation in vitro and in vivo, whereas suppression of DDX24 inhibited both functions. Mechanistically, DDX24 bound the mRNA618-624nt of laminin subunit beta 1 (LAMB1) and increased its stability in a manner dependent upon the interaction between nucleolin and the C-terminal region of DDX24. Moreover, regulatory factor X8 (RFX8) was identified as a DDX24 promoter-binding protein that transcriptionally upregulated DDX24 expression. Collectively, these findings demonstrate that the RFX8/DDX24/LAMB1 axis promotes HCC progression, providing potential therapeutic targets for HCC. SIGNIFICANCE: The identification of a tumor-promoting role of DDX24 and the elucidation of the underlying regulatory mechanism provide potential prognostic indicators and therapeutic approaches to help improve the outcome of patients with hepatocellular carcinoma.

The NRF2-dependent transcriptional axis, XRCC5/hTERT drives tumor progression and 5-Fu insensitivity in hepatocellular carcinoma.

Human telomerase reverse transcriptase (hTERT) is highly expressed in many tumors and is essential for tumorigenesis and metastasis in multiple cancers. However, the molecular mechanisms underlying its high expression level in hepatocellular carcinoma (HCC) remain unclear. In this study, we identified X-ray repair cross-complementing 5 (XRCC5), a novel hTERT promoter-binding protein in HCC cells, using biotin-streptavidin-agarose pull-down assay. We found that XRCC5 was highly expressed in HCC cells, in which it transcriptionally upregulated hTERT. Functionally, the transgenic expression of XRCC5 promoted HCC progression and 5-fluorouracil resistance, whereas short hairpin RNA knockdown of XRCC5 had converse effects in vitro and in vivo. Moreover, hTERT overexpression reversed XRCC5 knockdown- or 5-fluorouracil (5-Fu)-mediated HCC inhibition. Mechanistically, nuclear-factor-erythroid-2-related factor 2 (NRF2) interacted with XRCC5, which in turn upregulated hTERT. However, the upregulation was insignificant when NRF2 was reduced, suggesting that the XRCC5-mediated hTERT expression was NRF2 dependent. The HCC patients with high expression levels of XRCC5 and hTERT had shorter overall survival times compared with those with low XRCC5 and hTERT levels in their tumor tissues. Collectively, our study demonstrates the molecular mechanisms of the XRCC5/NRF2/hTERT signaling in HCC metastasis, which will aid in the identification of novel strategies for the diagnosis and treatment of HCC.

Evidence of SARS-CoV-2 infection in gallbladder and aggravating cholecystitis to septic shock: a case report.

Coronavirus disease 2019 (COVID-19) has threatened human health worldwide and could lead to multiple organs injury. However, the impact on the virus infecting the biliary system, especially the gallbladder, has remained unclear and no pathological evidence has been reported yet. A case of SARS-CoV-2 infection in a gallbladder with cholecystitis, which progressed rapidly to sepsis and required an emergency operation was investigated and reported. Clinical specimens of the COVID-19 patient including serum, oropharyngeal swabs, sputum, bile, abdominal drainage fluid, urine, stool, and gallbladder tissue were collected and tested for SARS-CoV-2 RNA using a quantitative polymerase chain reaction (qPCR) assay. Fresh normal gallbladder tissue and gangrenous gallbladder tissue were also collected for further research including hematoxylin and eosin (HE), immunohistochemistry (IHC), and immunofluorescent (IF) staining, and compared with the gallbladder from the COVID-19 patient. The bile, as well as the serum, oropharyngeal swabs, sputum, abdominal drainage fluid, urine, and rectal swabs were consecutively negative for SARS-CoV-2 RNA. The viral host receptor angiotensin-converting enzyme 2 (ACE2) was highly expressed in gallbladder epithelial cells, and viral nucleocapsid protein (NP) was visualized in the cytoplasm of gallbladder epithelial cells. Immune cells including CD2, CD3, CD4, CD8, CD20, CD38, CD68, and MPO were positive in gangrenous gallbladder tissues without SARS-CoV-2 infection, and were relatively downregulated in SARS-CoV-2 infective gallbladder tissue. This study provided evidence of SARS-CoV-2 infection in the gallbladder and verified that the gallbladder was one of the target organs that SARS-CoV-2 could attack and damage using ACE2 as a cell receptor. Due to the immune dysregulation involved, more vigilant management and early assessment is needed for COVID-19 patients with the comorbidity of cholecystitis.

Baicalin Magnesium Salt Attenuates Lipopolysaccharide-Induced Acute Lung Injury via Inhibiting of TLR4/NF-κB Signaling Pathway.

Baicalin (BA) magnesium salt (BA-Mg) is a good water-soluble ingredient extracted from Scutellaria baicalensis Georgi, a commonly used traditional Chinese medicine. This study is aimed at investigating whether BA-Mg could exert a better protective effect on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) in mice and illuminate the underlying mechanisms in vivo and in vitro. Mice were intraperitoneally administrated with equimolar BA-Mg, BA, and MgSO4 before LPS inducing ALI. Lung tissues and bronchoalveolar lavage fluid were collected for lung wet/dry ratio, histological examinations, cell counts, and biochemical analyses at 48 h post-LPS exposure. Meanwhile, the protein expressions of TLR4/NF-κB signaling pathway and proinflammatory cytokines in lung tissues and lung bronchial epithelial cells (BEAS-2B) were detected. The results showed BA-Mg pronouncedly ameliorated LPS-induced inflammatory response and histopathological damages, elevated antioxidant enzyme activity (SOD), and downregulated myeloperoxidase (MPO) and malonaldehyde (MDA) levels through the inhibition of TLR4/NF-κB signaling pathway activation. Moreover, the effect of BA-Mg was significantly better than that of BA and MgSO4 in ameliorating symptoms. Overall, BA-Mg can effectively relieve inflammatory response and oxidative stress triggered by LPS, indicating it may be a potential therapeutic candidate for treating ALI.

T lymphocytes from malignant hyperthermia-susceptible mice display aberrations in intracellular calcium signaling and mitochondrial function.

Gain-of-function RyR1-p.R163C mutation in ryanodine receptors type 1 (RyR1) deregulates Ca2+ signaling and mitochondrial function in skeletal muscle and causes malignant hyperthermia in humans and mice under triggering conditions. We investigated whether T lymphocytes from heterozygous RyR1-p.R163C knock-in mutant mice (HET T cells) display measurable aberrations in resting cytosolic Ca2+ concentration ([Ca2+]i), Ca2+ release from the store, store-operated Ca2+ entry (SOCE), and mitochondrial inner membrane potential (ΔΨm) compared with T lymphocytes from wild-type mice (WT T cells). We explored whether these variables can be used to distinguish between T cells with normal and altered RyR1 genotype. HET and WT T cells were isolated from spleen and lymph nodes and activated in vitro using phytohemagglutinin P. [Ca2+]i and ΔΨm dynamics were examined using Fura 2 and tetramethylrhodamine methyl ester fluorescent dyes, respectively. Activated HET T cells displayed elevated resting [Ca2+]i, diminished responses to Ca2+ mobilization with thapsigargin, and decreased rate of [Ca2+]i elevation in response to SOCE compared with WT T cells. Pretreatment of HET T cells with ryanodine or dantrolene sodium reduced disparities in the resting [Ca2+]i and ability of thapsigargin to mobilize Ca2+ between HET and WT T cells. While SOCE elicited dissipation of the ΔΨm in WT T cells, it produced ΔΨm hyperpolarization in HET T cells. When used as the classification variable, the amplitude of thapsigargin-induced Ca2+ transient showed the best promise in predicting the presence of RyR1-p.R163C mutation. Other significant variables identified by machine learning analysis were the ratio of resting cytosolic Ca2+ level to the amplitude of thapsigargin-induced Ca2+ transient and an integral of changes in ΔΨm in response to SOCE. Our study demonstrated that gain-of-function mutation in RyR1 significantly affects Ca2+ signaling and mitochondrial fiction in T lymphocytes, which suggests that this mutation may cause altered immune responses in its carrier. Our data link the RyR1-p.R163C mutation, which causes inherited skeletal muscle diseases, to deregulation of Ca2+ signaling and mitochondrial function in immune T cells and establish proof-of-principle for in vitro T cell-based diagnostic assay for hereditary RyR1 hyperfunction.

Ca2+ influx and clearance at hyperpolarized membrane potentials modulate spontaneous and stimulated exocytosis in neuroendocrine cells.

Neuroendocrine adrenal chromaffin cells release neurohormones catecholamines in response to Ca2+ entry via voltage-gated Ca2+ channels (VGCCs). Adrenal chromaffin cells also express non-voltage-gated channels, which may conduct Ca2+ at negative membrane potentials, whose role in regulation of exocytosis is poorly understood. We explored how modulation of Ca2+ influx at negative membrane potentials affects basal cytosolic Ca2+ concentration ([Ca2+]i) and exocytosis in metabolically intact voltage-clamped bovine adrenal chromaffin cells. We found that in these cells, Ca2+ entry at negative membrane potentials is balanced by Ca2+ extrusion by the Na+/Ca2+ exchanger and that this balance can be altered by membrane hyperpolarization or stimulation with an inflammatory hormone bradykinin. Membrane hyperpolarization or application of bradykinin augmented Ca2+-carrying current at negative membrane potentials, elevated basal [Ca2+]i, and facilitated synchronous exocytosis evoked by the small amounts of Ca2+ injected into the cell via VGCCs (up to 20 pC). Exocytotic responses evoked by the injections of the larger amounts of Ca2+ via VGCCs (> 20 pC) were suppressed by preceding hyperpolarization. In the absence of Ca2+ entry via VGCCs and Ca2+ extrusion via the Na+/Ca2+ exchanger, membrane hyperpolarization induced a significant elevation in [Ca2+]i and asynchronous exocytosis. Our results indicate that physiological interferences, such as membrane hyperpolarization and/or activation of non-voltage-gated Ca2+ channels, modulate basal [Ca2+]i and, consequently, segregation of exocytotic vesicles and their readiness to be released spontaneously and in response to Ca2+ entry via VGCCs. These mechanisms may play role in homeostatic plasticity of neuronal and endocrine cells.

Isoflurane-induced expression of miR-140-5p aggravates neurotoxicity in diabetic rats by targeting SNX12.

MicroRNAs (miRNAs) are widely known as critical regulators in isoflurane-induced neurotoxicity during the development of brain. Moreover, isoflurane could aggravate cognitive impairment in diabetic rats. The present study was designed to investigate the role and mechanism of miR-140-5p on isoflurane-induced neurotoxicity in diabetic rats. Firstly, a diabetic rat model was established by injection of streptozotocin (STZ) and identified by Morris water maze test. The result indicated that isoflurane treatment exacerbated STZ-induced cognitive impairment, as demonstrated by increase of the latency to the platform and decrease of the proportion of time spent in the target quadrant. Secondly, miR-140-5p was up-regulated in diabetic rats treated with isoflurane. Functional assays revealed that knockdown of miR-140-5p attenuated neurotoxicity in diabetic rats, which was shown by a decrease of the latency to the platform and an increase of the proportion of time spent in the target quadrant. Mechanistically, we demonstrated that miR-140-5p directly bonded to SNX12 (sorting nexin 12). At last, the neuroprotective effect of miR-140-5p knockdown against isoflurane-aggravated neurotoxicity in diabetic rats was dependent on up-regulation of SNX12 and inhibition of cell apoptosis. In summary, these meaningful results demonstrated the mitigation of miR-140-5p knockdown against isoflurane-aggravated neurotoxicity in diabetic rats via SNX12, suggesting a novel target for neuroprotection in diabetes under isoflurane treatment.

Withdrawn: Isoflurane-induced miR-140-5p Aggravates Neurotoxicity in Diabetic Rats by Targeting SNX12

The article has been withdrawn on the request of the authors and the editor of the journal Current Neurovascular Research. Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused. Bentham Science Disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers, if and when the article is accepted for publication.

Ku80 promotes melanoma growth and regulates antitumor effect of melatonin by targeting HIF1-α dependent PDK-1 signaling pathway.

Melanoma is one of the most malignant and aggressive cancers with high cancer-related deaths. However, it is unclear whether Ku80 regulates tumor growth in human melanoma. In this study, we screened a siRNA library targeting 6024 human genes and identified Ku80 as a potential therapeutic target in melanoma cells. Knockdown of Ku80 significantly suppressed melanoma cell proliferation and induced apoptosis, as well as enhanced the antitumor effect of melatonin in melanoma in vitro and in vivo. Overexpression of Ku80, however, promoted melanoma growth and increased the insensitivity of melanoma cells to melatonin. Mechanistically, we found that Ku80 bound to the PDK1 promoter and activated the transcription of PDK1. Moreover, we showed that the binding of Ku80 at the PDK-1 promoter was HIF1-α dependent, and melatonin degraded HIF1-α in melanoma cells. Furthermore, clinical data revealed that the expression of Ku80 and PDK-1 proteins were positively correlated and elevated in the tumor tissues of melanoma patients, and high expression of Ku80 predicted a poor prognosis in melanoma. Collectively, our study demonstrated that Ku80 promoted melanoma growth and regulated antitumor activity of melatonin by targeting HIF1-α dependent PDK-1 signaling pathway, suggesting that Ku80 may be a potential molecular target for melanoma treatment.

The current status of malignant hyperthermia.

Malignant hyperthermia (MH) is a rare and life-threatening pharmacogenetic disorder triggered by volatile anesthetics, the depolarizing muscle relaxant succinylcholine, and rarely by strenuous exercise or environmental heat. The exact prevalence of MH is unknown, and it varies from 1:16 000 in Denmark to 1:100 000 in New York State. The underlying mechanism of MH is excessive calcium release from the sarcoplasmic reticulum (SR), leading to uncontrolled skeletal muscle hyper-metabolism. Genetic mutations in ryanodine receptor type 1 ( RYR1) and CACNA1S have been identified in approximately 50% to 86% and 1% of MH-susceptible (MHS) individuals, respectively. Classic clinical symptoms of MH include hypercarbia, sinus tachycardia, masseter spasm, hyperthermia, acidosis, muscle rigidity, hyperkalemia, myoglobinuria, and etc. There are two types of testing for MH: a genetic test and a contracture test. Contracture testing is still being considered as the gold standard for MH diagnosis. Dantrolene is the only available drug approved for the treatment of MH through suppressing the calcium release from SR. Since clinical symptoms of MH are highly variable, it can be difficult to establish a diagnosis of MH. Nevertheless, prompt diagnosis and treatments are crucial to avoid a fatal outcome. Therefore, it is very important for anesthesiologists to raise awareness and understand the characteristics of MH. This review summarizes epidemiology, clinical symptoms, diagnosis and treatments of MH and any new developments.

[Transcription factors analysis of subchondral bone in early experimental osteoarthritis based on gene expression profiles].

OBJECTIVE: To identify the master transcription factors (TF) that might be responsible for the gene expression alteration of OA. METHODS: Raw expression data for rat OA model(GSE30322) was downloaded from NCBI GEO database. Microarray data analysis for rat and human was carried out separately using functions from limma packagein R, gene expression was considered as significantly changed between conditions if adjusted P-value<0.05 and the absolute value of fold change>=2. iRegulon was applied to differentially up-regulated and down-regulated genes in OA separately. RESULTS: (1)15 TFs, including FOXN4, NANOS1, E2F6, RAD21, MECOM, ETS1, MEF2A, POU2F3, BRCA1, GATA3, ZNF706, ZBTB33, SUZ12, DBP and SETDB1, were identified as the potential master TFs of up-regulated DEGs with statistical significance. (2)12 TFs, including ARID3A, YY1, RDBP, ATF1, CRX, TAF1, XBP1, SOX3, E2F4, PGR, TIMM8A and HOXA2, were identified as the potential master TFs of down-regulated DEGs with statistical significance. CONCLUSIONS: The newly identified TFs maybe play important roles in pathogenesis of early experimental osteoarthritis, and our study provides new diagnostic markers or therapeutic targets for OA.

Protective role of microRNA-126 in intracerebral hemorrhage.

Intracerebral hemorrhage (ICH) is a disease associated with high mortality and morbidity. MicroRNAs (miRNAs) are important regulators of translation and have been reported to be associated with the pathogenesis of numerous cerebrovascular diseases, including ICH. The present study explored the role of miRNA (miR)­126 in ICH. Adult male Wistar rats were randomly assigned to ICH model and sham groups. ICH was induced by intracerebral injection of collagenase. The mRNA expression levels of miR­126 in the two groups were determined. The miR­126 lentivirus expression vector pWPXL­miR­126 or negative control vector was then constructed and delivered via intraparenchymal injection. Following transduction, behavioral testing (rotarod and limb placement tests), relative hemorrhagic lesion size, apoptotic cells and protein levels of vascular endothelial growth factor (VEGF)­A and caspase­3 were determined. The relative expression levels of miR­126 were significantly decreased in the ICH group compared to the sham group (P=0.026). Overexpression of miR­126 significantly improved the relative duration of stay on the rotarod at day 2 (P=0.029) and 3 (P=0.033), and statistically reduced the deficit score (P=0.036), the relative size of hemorrhagic lesion (P=0.019) and the number of apoptotic cortical neurons (P=0.024) compared with the sham group. Additionally, the protein levels of VEGF­A were significantly elevated, however levels of caspase­3 were downregulated by overexpression of miR­126 compared with the negative control group. MiR­126 therefore exhibits a protective role in ICH. Overexpression of miR­126 protects against ICH, and may be involved in the process of angiogenesis and exhibit an anti-apoptotic effect.

The autophagy inhibitor 3-methyladenine restores sevoflurane anesthesiainduced cognitive dysfunction and neurons apoptosis.

This study was designed to explore the effect of 3-methyladenine (3-MA) on sevoflurane anesthesia-induced cognitive dysfunction. A total of 60 C57BL/6 (5-8 months old) mice were randomly arranged into 3 groups: Control, sevoflurane (Sev) and Sev+3-MA group with 3-MA administration was performed during Sev administration. Morris water maze and Y-maze test were performed to examine the behavioral disorders. Moreover, hippocampal neuronal cell apoptosis and expression of autophagy related genes were detected. Sevoflurane induced cognitive dysfunction in mice showing significant longer escape latency, lower number of correct response, higher apoptotic neurons, and higher expression of autophagy related genes. However, additional 3-MA administration inhibited the effect of sevoflurane on cognitive dysfunction by shorting escape latency, reducing correct response number, inhibiting neurons apoptosis and autophagy genes expression. 3-MA additional administration inhibited sevoflurane anesthesia-induced cognitive dysfunction on mice. 3-MA might be usefull as an inhibitor for sevoflurane anesthesia-induced cognitive dysfunction in clinical trials.

Multiple ectopic calcifications in subcutaneous tissues with chronic renal failure: A case report.

BACKGROUND: Multiple tumor-like ectopic calcifications is a rare syndrome characterized by subcutaneous mass deposits of calcium phosphate in periarticular tissues. Although several cases of the surgical treatment of tumoral calcinosis have been reported, the present case is unique in that multiple ectopic calcifications in subcutaneous tissues were found in a hemodialysis patient who had been operated on a total of five times within a period of 1.5 years. METHODS: A hemodialysis 60-year-old male presented with multiple tumor-like ectopic calcifications bilateral in the shoulders, right buttock and right thigh. He had been operated on a total of five times within a period of 1.5 years; the operations included a subtotal parathyroidectomy with parathyroid autotransplantation in the right forearm. RESULTS: Complete excisions of the ectopic calcifications were performed in the left shoulder, right buttock and right thigh, without signs of recurrence in the same sites at follow-up. Incomplete excision of the ectopic calcification in the right shoulder resulted in recurrence in the same site, and the patient was operated on two more times 1.5 years following the initial surgery. Subtotal parathyroidectomy with parathyroid autotransplantation decreased serum levels of PTH, but the levels of serum calcium and phosphorus remained unchanged post-surgery, which appeared not to inhibit the recurrence of ectopic calcification in patients with CRF. CONCLUSIONS: If conservative therapy failed, then early and complete surgical excision may be a good therapeutic option.

Comparison of recovery parameters for xenon versus other inhalation anesthetics: systematic review and meta-analysis.

STUDY OBJECTIVE: To summarize and evaluate the available data describing the recovery parameters of xenon anesthesia. DESIGN: Systematic review and meta-analysis. SETTING: Anesthesia for elective surgeries. PATIENTS: Systematic review of randomized controlled trials (RCTs) from databases including Medline (1964-2013), the Cochrane Central Register of Controlled Trials (CENTRAL, 1990-2012), and Google Scholar (1966-2013). INTERVENTIONS: Inhalation of xenon or other anesthetics was administered in elective surgery. MEASUREMENTS: Recovery parameters (time to recovery, alertness/sedation scale scores at "eye opening," bispectral index at "reaction on demand," time to extubation, and time to orientation). MAIN RESULTS: Eleven RCTs (N = 661 patients) met the inclusion criteria. Recovery from xenon anesthesia was significantly faster in terms of the time to eye opening (mean difference [MD], -4.18 minutes; 95% confidence interval [CI], -5.03 to -3.32 minutes; P < .00001), the time to reaction on demand (MD, -5.35 minutes; 95% CI, -6.59 to -4.11 minutes; P < .00001), the time to extubation (MD, -4.49 minutes; 95% CI, -5.40 to -3.58 minutes; P < .00001), and the time to orientation (MD, -4.99 minutes; 95% CI, -6.45 to -3.52 minutes; P < .00001). CONCLUSIONS: This meta-analysis confirmed that recovery from xenon anesthesia is faster than other inhalation anesthesia.

Portal vein arterialization promotes liver regeneration after extended partial hepatectomy in a rat model.

In the current study, we sought to establish a novel rat model of portal vein arterialization (PVA) and evaluate its impact on liver regeneration after extended partial hepatectomy (PH). A total of 105 Sprague-Dawley rats were randomly assigned to three groups: 68% hepatectomy (the PH group), portal arterialization after 68% hepatectomy (the PVA group), and right nephrectomy only (the control group). Liver regeneration rate (LRR), 5-bromo-2-deoxyuridine (BrdU) labeling index, and liver functions were assessed on postoperative day 2, 7, 14 and 28. The 28-day survival rates were compared among the three groups. The 28-day survival rates were similar in all groups (P  =  0.331), and the anastomotic patency was 100%. The LRR in the PVA group was significantly higher than that of the PH group within postoperative 14 days (P < 0.05). The PVA and PH group had increased serum alanine aminotransferase levels (232 ± 61 U/L and 212 ± 53 U/L, respectively) compared with the control group (101 ± 13 U/L) on postoperative day 2, whereas from postoperative day 7 to day 28 there were no differences among the three groups. Serum albumin values were higher after the PVA procedure within postoperative day 14, which gradually became comparable on postoperative day 28 among the three groups. The peaks of BrdU labeling index appeared on postoperative day 2 in all rats, and the PVA procedure was associated with increased BrdU labeling index from postoperative day 7 to 28. The 28-day survival of the PVA rats was comparable. Our findings demonstrate that the PVA procedure utilizing portal vein trunk-renal artery microvascular reconstruction promotes remnant liver regeneration and confers beneficial effects on maintaining and even optimizing liver function after extended partial hepatectomy in rats.

The impact of laparoscopic converted to open colectomy on short-term and oncologic outcomes for colon cancer.

PURPOSE: This study was designed to evaluate the impact of laparoscopic converted to open colectomy on short-term and oncologic outcomes and to identify risk factors for long-term survival in patients undergoing colectomy for non-metastatic colon cancer. METHODS: A prospective database of consecutive operations for non-metastatic colon cancer was reviewed. Patients were grouped as conversion (CONV) group, completed laparoscopic resection (LAP) group, or open resection (OPEN) group. The clinical and perioperative parameters, pathologic features, and oncologic outcomes were collected. Univariate analysis was performed for comparing these data. Patients without evidence of recurrence at last follow-up or still alive at the end of study period were censored. Kaplan-Meier curves were utilized to analyze survival. A multivariate analysis was performed to identify predictors of poor disease-free survival (DFS) and overall survival (OS). RESULTS: The conversion rate was 15.2 %. The most common reason for conversion was locally advanced cancer (45.5 %). Converted patients were associated with a longer operative time (188 ± 29.1 min, P < 0.001), greater blood loss (147 ± 14 mL, P < 0.001), and a higher rate of intra-operative complications (15.2 %, P = 0.042) compared to the completely laparoscopic or open patients. Days to flatus, early ambulation, and length of hospitalization were significantly shorter in completed laparoscopic resection (LAP) group (P < 0.001); however, the outcomes were comparable between conversion (CONV) and open resection (OPEN) groups. The incidence of wound infection was significantly higher in the OPEN group than in the LAP group (P = 0.005), whereas there were no significant differences observed between the CONV group and the OPEN group (P = 1.000) or between the LAP group and the CONV group (P = 0.073). The 5-year DFS in CONV patients (46.5 %) was comparable to LAP patients (55.5 %, P = 0.138) and OPEN patients (59.1 %, P = 0.113). Moreover, there were no significant differences noted in terms of the 5-year OS in the CONV group (56.7 %) compared to the LAP group (67.3 %, P = 0.317) or the OPEN group (66.3 %, P = 0.420). The multivariate analysis showed that pT3-4 cancer (P < 0.001) and poor differentiation (P < 0.001) were independent predictors of both lower OS and lower DFS, whereas leakage (P = 0.008) and lack of adjuvant chemotherapy (P = 0.023) were independent risk factors only of lower DFS. CONCLUSION: Conversion to open colectomy from an initial laparoscopic approach does not worsen the long-term survival in patients with non-metastatic colon cancer.

[Expression of lipoprotein related genes in subchondral bone of early experimental osteoarthritis].

OBJECTIVE: To study the expression of lipoprotein related genes in subchondral bone of early experimental os-teoarthritis, which may play an important role in the pathogenesis of osteoarthritis. METHODS: Animals are equally divided into two groups: experimental group and control group, both of which contain fifteen rats of similar weight. The right knee joints of experimental group underwent surgery,which involved in both medial collateral ligament(MCL) transaction and medial meniscectomy, while the control group was only carried out with a sham operation. Rats were killed at 1, 2 and 4 weeks postsurgery to obtain the right knee joints. Total RNA of the subchondral bone was extracted,and then hybridized to Agilent Whole Rat Genome Microarray. Differentially expressed genes analysis was used to study the chemokine signaling pathway. RESULTS: Apoa5 expression was down-regulated at 1, 2 weeks post-surgery, Apoc2 expression was up-regulated at 1 week after surgery, Apol3 expression was up-regulated at 1 and down-regulated at 4 weeks post-surgery, Lrp1 expression was down-regulated at 1, 2 weeks after surgery. Lrp5 was down-regulated at 2 weeks after surgery. Gpihbp1, Lpl, Tfpi and Vldlr were up-regulated at 1 weeks after surgery. Lrpap1 and RGD1309808 were down-regulated at 4 weeks after surgery. CONCLUSION: Dysregulation of lipoprotein related genes plays an important role in pathogenesis of early experimental osteoarthritis.

Effects of sevoflurane pretreatment on renal Src and FAK expression in diabetic rats after renal ischemia/reperfusion injury.

The diabetic kidney is sensitive to ischemia-reperfusion (I/R) injury due to microvascular complications, such as cellular apoptosis and necrosis. The aim of this study was to determine if sevoflurane pretreatment could help preserve renal function in rats with diabetes mellitus (DM) by altering non-receptor tyrosine kinases steroid receptor coactivator (Src) and focal adhesion kinase (FAK) expression (Src and FAK are mediators of cellular apoptosis and necrosis). Male rats (N = 40) were randomly assigned to one of five groups: Group A, sham operation; Group B, renal I/R injury; Group C, DM + sham operation; Group D, DM + renal I/R injury; and Group E, DM + sevoflurane pretreatment + renal I/R injury. Sevoflurane pretreatment comprised exposure to 2.5 % sevoflurane for 30 min, followed by exposure to air for 10 min. After 24 h, serum creatinine (Cr) and blood urea nitrogen (BUN) levels, and renal Src and FAK expression (immunohistochemistry) were assessed. Compared with rats in C, rats in D had significantly higher Cr and BUN levels, but significantly lower renal Src and FAK expression. Rats in E had significantly lower serum Cr and BUN levels and significantly higher renal Src and FAK expression levels than rats in D. Our findings suggest that sevoflurane pretreatment in rats with DM protects the kidneys from ischemia/reperfusion injury in part due to increased renal Src and FAK expression.