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Bleeding from the lower uterine segment (LUS) during caesarean section remains a life-threatening obstetric problem, particularly in women with placenta praevia or partial placenta accreta in the LUS. Various conservative measures for the surgical treatment of postpartum haemorrhage have been studied for decades. In this paper we describe a funnel compression suture to staunch intractable bleeding from LUS for placenta praevia accreta. The suture brings the anterior and posterior walls of the LUS together using absorbable thread and was successful in the overwhelming majority of women. It is an easy, safe and effective conservative surgical treatment to stop severe bleeding of the LUS. [ABSTRACT FROM AUTHOR]

Introduction: Genicular nerve radiofrequency ablation (GNRFA) is a minimally invasive intervention for patients with chronic knee pain (CKP) not responding to conservative treatments. Few investigations have compared treatment outcomes of cooled-RFA (c-RFA) and thermal-RFA (t-RFA), two common approaches of GNRFA. This study aims to investigate and compare outcomes, including probability of treatment success, between c-RFA and t-RFA in patients with CKP., Methods: This retrospective cohort study analyzed a total of 208 propensity score matched patients, including 104 patients who received c-RFA and 104 patients who received t-RFA. The primary outcome was probability of pain relief after the procedure, defined as reduction in Numeric Rating Scale (NRS) pain score of 2 or greater. The secondary outcomes were degree of NRS pain score reductions, duration of relief, and the probability of patients receiving TKA within 1 year of treatment., Results: T-RFA was associated with a higher probability of pain relief within 1, 3, and 6 months after procedure when compared with c-RFA. Probabilities of pain relief from t-RFA and c-RFA were 62% (95% CI 51% to 71%) and 43% (95% CI 34% to 53%; p=0.01) within 1 month, 78% (95% CI 68% to 85%) and 55% (95% CI 45% to 64%; p<0.001) within 3 months, and 79% (95% CI 70% to 86%) and 59% (95% CI 49% to 68%; p<0.01) within 6 months, respectively. t-RFA was also associated with greater mean NRS pain score reduction at 1 month after procedure: -4.71 (95% CI -5.3 to -4.1) when compared with -3.59 (95% CI -4.3 to -2.9; p=0.02) from c-RFA. T-RFA and c-RFA were comparable in pain score reduction at 3, 6, 9 and 12 months after procedure. Both groups demonstrated comparable duration of relief and probability of patients receiving TKA within 1 year., Discussion: Both t-RFA and c-RFA effectively reduced NRS pain scores in most patients with CKP within the 1 year follow-up period. Genicular nerve t-RFA was associated with a higher probability of treatment success and a greater degree of pain relief at 1 month after the procedure when compared with c-RFA in propensity score matched patients with CKP., Competing Interests: Competing interests: The authors have no conflict of interest related to this manuscript. JX is a consultant for Genentech. RBB is a consultant for Medtronic, Agnovos, and Pfizer., (© American Society of Regional Anesthesia & Pain Medicine 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

Mitochondrial stress triggers a response in the cell's mitochondria and nucleus, but how these stress responses are coordinated in vivo is poorly understood. Here, we characterize a family with myopathy caused by a dominant p.G58R mutation in the mitochondrial protein CHCHD10. To understand the disease etiology, we developed a knockin (KI) mouse model and found that mutant CHCHD10 aggregated in affected tissues, applying a toxic protein stress to the inner mitochondrial membrane. Unexpectedly, the survival of CHCHD10-KI mice depended on a protective stress response mediated by the mitochondrial metalloendopeptidase OMA1. The OMA1 stress response acted both locally within mitochondria, causing mitochondrial fragmentation, and signaled outside the mitochondria, activating the integrated stress response through cleavage of DAP3-binding cell death enhancer 1 (DELE1). We additionally identified an isoform switch in the terminal complex of the electron transport chain as a component of this response. Our results demonstrate that OMA1 was critical for neonatal survival conditionally in the setting of inner mitochondrial membrane stress, coordinating local and global stress responses to reshape the mitochondrial network and proteome.

PRKN mutations are the most common recessive cause of Parkinson's disease and are a promising target for gene and cell replacement therapies. Identification of biallelic PRKN patients at the population scale, however, remains a challenge, as roughly half are copy number variants and many single nucleotide polymorphisms are of unclear significance. Additionally, the true prevalence and disease risk associated with heterozygous PRKN mutations is unclear, as a comprehensive assessment of PRKN mutations has not been performed at a population scale. To address these challenges, we evaluated PRKN mutations in two cohorts with near complete genotyping of both single nucleotide polymorphisms and copy number variants: the NIH-PD + AMP-PD cohort, the largest Parkinson's disease case-control cohort with whole genome sequencing data from 4094 participants, and the UK Biobank, the largest cohort study with whole exome sequencing and genotyping array data from 200 606 participants. Using the NIH-PD participants, who were genotyped using whole genome sequencing, genotyping array, and multi-plex ligation-dependent probe amplification, we validated genotyping array for the detection of copy number variants. Additionally, in the NIH-PD cohort, functional assays of patient fibroblasts resolved variants of unclear significance in biallelic carriers and suggested that cryptic loss of function variants in monoallelic carriers are not a substantial confounder for association studies. In the UK Biobank, we identified 2692 PRKN copy number variants from genotyping array data from nearly half a million participants (the largest collection to date). Deletions or duplications involving exon 2 accounted for roughly half of all copy number variants and the vast majority (88%) involved exons 2, 3, or 4. In the UK Biobank, we found a pathogenic PRKN mutation in 1.8% of participants and two mutations in ∼1/7800 participants. Those with one PRKN pathogenic variant were as likely as non-carriers to have Parkinson's disease [odds ratio = 0.91 (0.58-1.38), P-value 0.76] or a parent with Parkinson's disease [odds ratio = 1.12 (0.94-1.31), P-value = 0.19]. Similarly, those in the NIH-PD + AMP + PD cohort with one PRKN pathogenic variant were as likely as non-carriers to have Parkinson's disease [odds ratio = 1.29 (0.74-2.38), P-value = 0.43]. Together our results demonstrate that heterozygous pathogenic PRKN mutations are common in the population but do not increase the risk of Parkinson's disease., (Published by Oxford University Press on behalf of the Guarantors of Brain 2022. This work is written by (a) US Government employee(s) and is in the public domain in the US.)

Background: Postoperative hypotension and hypoxaemia are common and often unrecognised. With intermittent nursing vital signs, hypotensive or hypoxaemic episodes might be missed because they occur between scheduled measurements, or because the process of taking vital signs arouses patients and temporarily improves arterial blood pressure and ventilation. We therefore estimated the fraction of desaturation and hypotension episodes that did not overlap nursing assessments and would therefore usually be missed. We also evaluated the effect of taking vital signs on blood pressure and oxygen saturation., Methods: We estimated the fraction of desaturated episodes (arterial oxygen saturation <90% for at least 90% of the time within 30 continuous minutes) and hypotensive episodes (MAP <70 mm Hg for 15 continuous minutes) that did not overlap nursing assessments in patients recovering from noncardiac surgery. We also evaluated changes over time before and after nursing visits., Results: Among 782 patients, we identified 878 hypotensive episodes and 2893 desaturation episodes, of which 79% of the hypotensive episodes and 82% of the desaturation episodes did not occur within 10 min of a nursing assessment and would therefore usually be missed. Mean BP and oxygen saturation did not improve by clinically meaningful amounts during nursing vital sign assessments., Conclusions: Hypotensive and desaturation episodes are mostly missed because vital sign assessments on surgical wards are sparse, rather than being falsely negative because the assessment process itself increases blood pressure and oxygen saturation. Continuous vital sign monitoring will detect more disturbances, potentially giving clinicians time to intervene before critical events occur., (Copyright © 2021 British Journal of Anaesthesia. Published by Elsevier Ltd. All rights reserved.)

Aims: Clinical registry-derived data are widely used to represent patient populations. In New Zealand (NZ), a national registry-the All New Zealand Acute Coronary Syndrome Quality Improvement (ANZACS-QI) registry-aims to include all patients undergoing coronary angiography; other acute coronary syndrome (ACS) patients are also registered but without complete capture. This study compares national hospitalization data of all first-time ACS admissions in NZ with patients in the ANZACS-QI registry, to investigate the use of clinical registry-derived data in research and in assessing clinical care., Methods and Results: Patients admitted with first-time ACS in the NZ National Hospitalisation Dataset between 1 January 2015 and 31 December 2016 were included. Clinical characteristics and time to 12-month clinical outcomes were compared between patients captured and not-captured in the registry. A total of 16 569 patients were admitted with first-time ACS, median age 69 years, 61% male; 60% (n = 9918) were enrolled in ANZACS-QI. Registry-captured patients were younger, more often male, and with a lower comorbidity burden than non-captured patients. Overall, 16% patients died within 12 months, 15% experienced a non-fatal cardiovascular (CV) readmission, and 28% either died or were readmitted. Patients not captured in the registry were more than twice as likely to have experienced death or a non-fatal CV readmission within 12 months as captured patients., Conclusions: First-time ACS patients captured in the ANZACS-QI registry had very different clinical characteristics and outcomes than those not captured. Cardiovascular registry-derived data are dependent on registry design and may not be representative of the wider patient population; this must be considered when using registry-derived data., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com.)

Background: Until recently, most patients with diabetes worldwide have been diagnosed when symptomatic and have high cardiovascular risk, meaning most should be prescribed cardiovascular preventive medications. However, in New Zealand, a world-first national programme led to approximately 90% of eligible adults being screened for diabetes by 2016, up from 50% in 2012, identifying many asymptomatic patients with recent-onset diabetes. We hypothesised that cardiovascular risk prediction equations derived before widespread screening would now significantly overestimate risk in screen-detected patients., Methods: New Zealanders aged 30-74 years with type 2 diabetes and without known cardiovascular disease, heart failure, or substantial renal impairment were identified from the 400 000-person PREDICT primary care cohort study between Oct 27, 2004, and Dec 30, 2016, covering the period before and after widespread screening. Sex-specific equations estimating 5-year risk of cardiovascular disease were developed using Cox regression models, with 18 prespecified predictors, including diabetes-related and renal function measures. Equation performance was compared with an equivalent equation derived in the New Zealand Diabetes Cohort Study (NZDCS), which recruited between 2000 and 2006, before widespread screening., Findings: 46 652 participants were included in the PREDICT-1° Diabetes subcohort, of whom 4114 experienced first cardiovascular events during follow-up (median 5·2 years, IQR 3·3-7·4). 14 829 (31·8%) were not taking oral hypoglycaemic medications or insulin at baseline. Median 5-year cardiovascular risk estimated by the new equations was 4·0% (IQR 2·3-6·8) in women and 7·1% (4·5-11·2) in men. The older NZDCS equation overestimated median cardiovascular risk by three times in women (median 14·2% [9·7-20·0]) and two times in men (17·1% [4·5-20·0]). Model and discrimination performance measures for PREDICT-1° Diabetse equations were also significantly better than for the NZDCS equation (eg, for women: R 2 =32% [95% CI 29-34], Harrell's C=0·73 [0·72-0·74], Royston's D=1·410 [1·330-1·490] vs R 2 =24% [21-26], C=0·69 [0·67-0·70], and D=1·147 [1·107-1·187])., Interpretation: International treatment guidelines still consider most people with diabetes to be at high cardiovascular risk; however, we show that recent widespread diabetes screening has radically changed the cardiovascular risk profile of people with diabetes in New Zealand. Many of these patients have normal renal function, are not dispensed glucose-lowering medications, and have low cardiovascular risk. These findings have clear international implications as increased diabetes screening is inevitable due to increasing obesity, simpler screening tests, and the introduction of new-generation glucose-lowering medications that prevent cardiovascular events. Cardiovascular risk prediction equations derived from contemporary diabetes populations, with multiple diabetes-related and renal function predictors, will be required to better differentiate between low-risk and high-risk patients in this increasingly heterogeneous population and to inform appropriate non-pharmacological management and cost-effective targeting of expensive new medications., Funding: Health Research Council of New Zealand, Heart Foundation of New Zealand, and Healthier Lives National Science Challenge., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Objective: To minimize the adverse events of uterine compression suture in controlling postpartum hemorrhage (PPH) and to search for a prophylactic approach to potential PPH., Methods: A retrospective analysis was performed in 39 women with removable retropubic uterine compression suture (RRUCS) to stop PPH due to uterine atony during cesarean section (CS). The procedure was to suspend and compress the uterus to the retropubic abdominal wall using an absorbable suture., Results: The technique was sufficient to stanch bleeding immediately in 36 patients (92.31%, 36/39). No morbidity or abnormalities occurred in women who underwent RRUCS. Subsequent pregnancies occurred in 10 cases, but the others lacked the desire for future pregnancy., Conclusion: RRUCS is a simple, safe, and effective technique in controlling atonic PPH; it is also used as a prophylactic application in patients with potential PPH after CS., (© 2021 Japan Society of Obstetrics and Gynecology.)

PRéCIS:: Publications in glaucoma have seen an increase in the number of authors and disclosures per article, authors with dual degrees, and international authors, but contributions of women to articles published remains low., Purpose: Authorship trends have been studied across many medical specialties and in ophthalmology as a whole, but not specifically in glaucoma. The authors explored the authorship trends of original scientific articles in the Journal of Glaucoma., Materials and Methods: The authors recorded the number of authors and disclosures per article, degree type of first and last authors, geographical origin of the corresponding author, and sex of first and last authors of original content from the Journal of Glaucoma published in 1992, 1997, 2002, 2007, 2012, and 2017., Results: A total of 642 articles were analyzed. From 1992 to 2017, annual published articles increased from 38 to 242 (P=0.02), the mean number of authors per article increased from 3.2 to 5.2 (P<0.01), the mean number of disclosures per article increased from 0.3 to 1.0 (P=0.04), the proportion of first and last authors with dual degrees (medical plus advanced degrees) also increased (both P<0.03), whereas the proportion with a sole medical degree decreased (both P<0.05). There was a proportional decrease in articles from North America (P=0.03), and proportional increase from the "Far East" (P=0.04) and "Other" regions (P=0.04). No significant changes in proportions of female first and last authors were found (both P>0.28)., Conclusions: Consistent with authorship trends across various other medical specialties, glaucoma has seen an increase in the number of authors and disclosures per article, authors with dual degrees, and authors from the "Far East" and "Other" regions. However, contributions of women to articles published in Journal of Glaucoma remain low.

Dominant mutations in the mitochondrial paralogs coiled-helix-coiled-helix (CHCHD) domain 2 (C2) and CHCHD10 (C10) were recently identified as causing Parkinson's disease and amyotrophic lateral sclerosis/frontotemporal dementia/myopathy, respectively. The mechanism by which they disrupt mitochondrial cristae, however, has been uncertain. Using the first C2/C10 double knockout (DKO) mice, we report that C10 pathogenesis and the normal function of C2/C10 are intimately linked. Similar to patients with C10 mutations, we found that C2/C10 DKO mice have disrupted mitochondrial cristae, because of cleavage of the mitochondrial-shaping protein long form of OPA1 (L-OPA1) by the stress-induced peptidase OMA1. OMA1 was found to be activated similarly in affected tissues of mutant C10 knock-in (KI) mice, demonstrating that L-OPA1 cleavage is a novel mechanism for cristae abnormalities because of both C10 mutation and C2/C10 loss. Using OMA1 activation as a functional assay, we found that C2 and C10 are partially functionally redundant, and some but not all disease-causing mutations have retained activity. Finally, C2/C10 DKO mice partially phenocopied mutant C10 KI mice with the development of cardiomyopathy and activation of the integrated mitochondrial integrated stress response in affected tissues, tying mutant C10 pathogenesis to C2/C10 function., (Published by Oxford University Press 2020.)

Introduction: The Vascular Risk in Adult New Zealanders (VARIANZ) datasets contain a range of routinely-collected New Zealand health data relevant to cardiovascular disease (CVD) and related conditions. The datasets enable exploration of cardiovascular-related treatment, service utilisation, outcomes and prognosis., Processes: Each dataset is constructed by anonymised individual-level linkage of eight national administrative health databases to identify all New Zealand adults aged ≥20 years who have recorded contact with publicly-funded New Zealand health services during a given year from 2006 onwards, when data quality is considered sufficient., Data Contents: Individual-level data for each VARIANZ dataset can include variables covering demography, dispensing of cardiovascular disease (CVD) preventive medications and prior hospitalisations for atherosclerotic CVD, heart failure, atrial fibrillation and diabetes. If required, VARIANZ datasets can be individually linked to follow-up national routinely collected health data in subsequent years, including all-cause mortality events and fatal/non-fatal CVD events, to create VARIANZ longitudinal cohorts. Bespoke linkage can also be undertaken to include other national and regional administrative health data such as non-CVD related hospitalisations in order to explore CVD comorbidities or novel risk factors. Furthermore, a subset of the VARIANZ datasets based on specific health contacts (such as CVD hospitalisations only) can also be identified, and some data can be requested for years prior to 2006. The New Zealand routinely-collected health databases used to construct the VARIANZ datasets do not capture primary care diagnostic classifications or certain CVD risk factor data such as smoking status, blood pressure or lipid profiles., Conclusion: The Vascular Risk in Adult New Zealanders (VARIANZ) datasets capture the majority of the New Zealand population in a given year and are available from 2006 onwards, or earlier than 2006 for some datasets based on specific health contacts. VARIANZ data can be used to explore a range of research questions regarding management, outcomes and prognosis for CVD., Competing Interests: Statement on conflicts of Interest: Outside of this study, SW has received a research grant from Roche Diagnostics Limited. No other authors declare any conflict of interest.

Mutations in paralogous mitochondrial proteins CHCHD2 and CHCHD10 cause autosomal dominant Parkinson Disease (PD) and Amyotrophic Lateral Sclerosis/Frontotemporal Dementia (ALS/FTD), respectively. Using newly generated CHCHD2, CHCHD10 and CHCHD2/10 double knockout cell lines, we find that the proteins are partially functionally redundant, similarly distributed throughout the mitochondrial cristae, and form heterodimers. Unexpectedly, we also find that CHCHD2/CHCHD10 heterodimerization increases in response to mitochondrial stress. This increase is driven by differences in the proteins' stability and mutual affinity: CHCHD2 is preferentially stabilized by loss of mitochondrial membrane potential, and CHCHD10 oligomerization depends on CHCHD2 expression. Exploiting the dependence of CHCHD10 oligomerization on CHCHD2, we developed a heterodimer incorporation assay and demonstrate that CHCHD2 and CHCHD10 with disease-causing mutations readily form heterodimers. As we also find that both proteins are highly expressed in human Substantia nigra and cortical pyramidal neurons, mutant CHCHD2 and CHCHD10 may directly interact with their wild-type paralogs in the context of PD and ALS/FTD pathogenesis. Together, these findings demonstrate that differences in the stability and mutual affinity of CHCHD2 and CHCHD10 regulate their heterodimerization in response to mitochondrial distress, revealing an unanticipated link between PD and ALS/FTD pathogenesis.

Background: Most cardiovascular disease risk prediction equations in use today were derived from cohorts established last century and with participants at higher risk but less socioeconomically and ethnically diverse than patients they are now applied to. We recruited a nationally representative cohort in New Zealand to develop equations relevant to patients in contemporary primary care and compared the performance of these new equations to equations that are recommended in the USA., Methods: The PREDICT study automatically recruits participants in routine primary care when general practitioners in New Zealand use PREDICT software to assess their patients' risk profiles for cardiovascular disease, which are prospectively linked to national ICD-coded hospitalisation and mortality databases. The study population included male and female patients in primary care who had no prior cardiovascular disease, renal disease, or congestive heart failure. New equations predicting total cardiovascular disease risk were developed using Cox regression models, which included clinical predictors plus an area-based deprivation index and self-identified ethnicity. Calibration and discrimination performance of the equations were assessed and compared with 2013 American College of Cardiology/American Heart Association Pooled Cohort Equations (PCEs). The additional predictors included in new PREDICT equations were also appended to the PCEs to determine whether they were independent predictors in the equations from the USA., Findings: Outcome events were derived for 401 752 people aged 30-74 years at the time of their first PREDICT risk assessment between Aug 27, 2002, and Oct 12, 2015, representing about 90% of the eligible population. The mean follow-up was 4·2 years, and a third of participants were followed for 5 years or more. 15 386 (4%) people had cardiovascular disease events (1507 [10%] were fatal, and 8549 [56%] met the PCEs definition of hard atherosclerotic cardiovascular disease) during 1 685 521 person-years follow-up. The median 5-year risk of total cardiovascular disease events predicted by the new equations was 2·3% in women and 3·2% in men. Multivariable adjusted risk increased by about 10% per quintile of socioeconomic deprivation. Māori, Pacific, and Indian patients were at 13-48% higher risk of cardiovascular disease than Europeans, and Chinese or other Asians were at 25-33% lower risk of cardiovascular disease than Europeans. The PCEs overestimated of hard atherosclerotic cardiovascular disease by about 40% in men and by 60% in women, and the additional predictors in the new equations were also independent predictors in the PCEs. The new equations were significantly better than PCEs on all performance metrics., Interpretation: We constructed a large prospective cohort study representing typical patients in primary care in New Zealand who were recommended for cardiovascular disease risk assessment. Most patients are now at low risk of cardiovascular disease, which explains why the PCEs based mainly on old cohorts substantially overestimate risk. Although the PCEs and many other equations will need to be recalibrated to mitigate overtreatment of the healthy majority, they also need new predictors that include measures of socioeconomic deprivation and multiple ethnicities to identify vulnerable high-risk subpopulations that might otherwise be undertreated., Funding: Health Research Council of New Zealand, Heart Foundation of New Zealand, and Healthier Lives National Science Challenge., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Composition and changes in free volatiles have been extensively studied in citrus fruit such as mandarin. However, components of glycosidically bound volatiles and changes during fruit ripening have been rarely investigated. A total of 56 glycosidically-bound volatiles were identified in fruit peel at four ripening stages. The highest concentrations in glycosidically-bound volatiles were observed for methyl salicylate in ripening fruit. Concentration of total bound volatiles increased from color conversion stage at 150days after bloom (DAB), peaked at yellow stage (190DAB), followed by a decrease at orange stage (210DAB). Satsuma mandarin fruit at different ripening stages could be separated in a partial least squares-discriminant analysis (PLS-DA) plot using glycosidically bound volatiles as variables. In total 35 glycosidically bound volatiles were identified with variable importance in projection (VIP) score exceeding 1, which may be potential markers for separating fruit at different ripening stages., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Objective: To analyze the epidemiological characteristics and spatial distribution of human brucellosis in Fujian province during 2011-2016, and provide evidence for the prevention and control of the disease. Methods: The surveillance data of human brucellosis in Fujian during 2011-2016 was analyzed with software R 3.3.1, ArcGIS 10.3.1, GeoDa 1.8.8 and SaTScan 9.4.3. Results: During 2011-2016, a total of 319 human brucellosis cases were reported, the incidence increased year by year ( F =11.838, P =0.026) with the annual incidence of 0.14/100 000. The male to female rate ratio of the incidence was 2.50 ∶ 1. Farmers and herdsmen accounted for 57.37 % . The incidence was 0.40/100 000 in Zhangzhou and 0.32/100 000 in Nanping, which were higher than other areas. The number of affected counties (district) increased from 12 in 2011 to 28 in 2016, showing a significant increase ( F =13.447, P =0.021). The Moran's I of brucellosis in Fujian between January 2011 and December 2016 was 0.045, indicating the presence of a high value or low value clustering areas. Local spatial autocorrelation analysis showed that, high-high clustering area (hot spots) were distributed in Zhangpu, Longhai, Longwen, etc , while high-low clustering areas were distributed in Nan'an and Jiaocheng, etc . Temporal scanning showed that there were three clustering areas in areas with high incidence, the most possible clustering, occurring during January 1, 2013- December 31,2015, covered 6 counties, including Yunxiao, Pinghe, Longhai, etc , and Zhangpu was the center, ( RR =7.96, LLR =92.62, P <0.001). Conclusions: The epidemic of human brucellosis in Fujian is becoming serious, and has spread to general population and non-epidemic areas. It is necessary to strengthen the prevention and control of human brucellosis in areas at high risk.

Objective: To investigate the molecular mechanism by which LKB1 regulates epithelial-mesenchymal transition (EMT) in Peutz-Jeghers hamartoma and intestinal epithelial cells., Methods: Immunohistochemistry was used to detect gene expression of LKB1, E-cadherin, and vimentin in 20 hamartoma tissues and 10 normal intestinal tissues, and collagen fiber deposition was analyzed using Masson trichrome staining. Normal intestinal epithelial NCM460 cells were transfected with LKB1 shRNA plasmid or negative control via lentiviral vectors, and the role of LKB1 in cell polarization and migration were determined using CCK8 and Transwell assays. Western blotting, quantitative real-time PCR (qPCR) and immunofluorescence were used to assess the alterations of EMT markers in the cells with LKB1 knockdown., Results: Compared with normal intestinal tissues, hamartoma polyps showed significantly decreased LKB1 and E-cadherin expressions and increased vimentin expression with increased collagen fiber deposition. The cells with LKB1 knockdown exhibited enhanced cell proliferation and migration activities (P<0.01). Western blot analysis, qPCR and immunofluorescence all detected decreased E-cadherin and increased N-cadherin, vimentin, Snail, and Slug expressions in the cells with LKB1 knockdown., Conclusion: s LKB1 deficiency triggers EMT in intestinal epithelial cells and Peutz-Jeghers hamartoma, suggesting that EMT can serve as the therapeutic target for treatment of Peutz-Jeghers syndrome.

Objective: To observe the efficacy and safety of a uterine folding hemostatic technique in controlling atonic postpartum hemorrhage (PPH) during cesarean delivery., Methods: Thirty-nine women with severe postpartum bleeding from uterine inertia, which did not react to conventional initial management protocols, underwent a uterine folding hemostasis. The procedure was to fold the uterine fundus onto the anterior wall of the corpus uterus using an absorbable suture that thread tautly through the inner myometrial layer of the uterus 1-3 cm below the fundus (not entered into uterine cavity) and 1-2 cm above and below the CS incision (entered into uterine cavity 2-4 cm medal to bilateral border of the uterus)., Results: The technique was sufficient to stanch bleeding immediately in 32 patients (82.1 %). Seven women underwent hypogastric arteries ligation (1 case) or uterine arterial embolization (6 cases) because of continuous bleeding after the procedure. There were no morbidities or abnormalities of the uterus in these 32 patients. Eight women had pregnancies after this hemostasis and the others lacked the desire for future pregnancy., Conclusion: Uterine folding hemostasis is a simple, safe and effective technique to control the atonic PPH.

Bleeding from the lower uterine segment (LUS) during caesarean section remains a life-threatening obstetric problem, particularly in women with placenta praevia or partial placenta accreta in the LUS. Various conservative measures for the surgical treatment of postpartum haemorrhage have been studied for decades. In this paper we describe a funnel compression suture to staunch intractable bleeding from LUS for placenta praevia accreta. The suture brings the anterior and posterior walls of the LUS together using absorbable thread and was successful in the overwhelming majority of women. It is an easy, safe and effective conservative surgical treatment to stop severe bleeding of the LUS., (© 2015 Royal College of Obstetricians and Gynaecologists.)

Cancer immunotherapy has primarily been focused on attacking tumor cells. However, given the close interaction between tumor cells and cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TME), CAF-targeted strategies could also contribute to an integrated cancer immunotherapy. Fibroblast activation protein α (FAP α) is not detectible in normal tissues, but is overexpressed by CAFs and is the predominant component of the stroma in most types of cancer. FAP α has both dipeptidyl peptidase and endopeptidase activities, cleaving substrates at a post-proline bond. When all FAP α-expressing cells (stromal and cancerous) are destroyed, tumors rapidly die. Furthermore, a FAP α antibody, FAP α vaccine, and modified vaccine all inhibit tumor growth and prolong survival in mouse models, suggesting FAP α is an adaptive tumor-associated antigen. This review highlights the role of FAP α in tumor development, explores the relationship between FAP α and immune suppression in the TME, and discusses FAP α as a potential immunotherapeutic target., Competing Interests: No potential conflicts of interest were disclosed.

Aim: There is a lack of consensus in the international literature pertaining to the prevalence of tinnitus for the overall population, as well as sex and age sub-groups, suggesting the need for country-specific prevalence estimates. We aim to find prevalence estimates of tinnitus that are representative of the New Zealand population., Method: We obtained data from random-digit dialled telephone surveys of households, conducted by Roy Morgan Research Limited between August, 2007, and July, 2013, for people aged ≥ 14 years in New Zealand (n=69,976). As part of the survey, participants were asked whether they have had tinnitus in the last 12 months. The response options were "yes" or "no". Estimates were standardised to the New Zealand population structure based on the 2013 national census. Sex, age and ethnic differences were explored., Results: The overall weighted prevalence for any tinnitus was 6.0% in the total New Zealand population age ≥ 14 years. Tinnitus was higher among males (6.5%) compared to females (5.5%). Males were 55% more likely to report tinnitus compared to females among young adults aged 14 to 24 years, while males were 32% more likely to report tinnitus compared to females among adults aged 50 to 64 years. Tinnitus prevalence increased with age, peaking at 13.5% for older adults aged ≥ 65 years. Adults aged ≥ 65 years are three times more likely to report tinnitus than people aged below 65 years. Tinnitus prevalence was highest among people identifying as European (7.05%) and lowest among people identifying as Asian (1.00%)., Conclusion: This is the first nationally representative study of tinnitus prevalence in New Zealand and largest study sample internationally for tinnitus prevalence to date. Tinnitus is a public health problem affecting approximately 207,000 people in the New Zealand population aged ≥ 14 years. This study has highlighted the importance of sex and age in defining a high-risk tinnitus population, but our knowledge falls short of profiling their ethnic and social-economic characteristics.

Fibroblast activation protein α (FAPα) is a potential target for cancer therapy. However, elimination of FAPα+ fibroblasts activates secretion of IFN-γ and TNF-α. IFN-γ can in turn induce expression indolamine-2,3-dioxygenase (IDO), thereby contributing to immunosuppression, while TNF-α can induce EMT. These two reactive effects would limit the efficacy of a tumor vaccine. We found that curcumin can inhibit IDO expression and TNF-α-induced EMT. Moreover, FAPαc vaccine and CpG combined with curcumin lavage inhibited tumor growth and prolonged the survival of mice implanted with melanoma cells. The combination of FAPαc vaccine, CpG and curcumin stimulated FAPα antibody production and CD8+ T cell-mediated killing of FAPα-expressing stromal cells without adverse reactive effects. We suggest a combination of curcumin and FAPαc vaccine for melanoma therapy.

Background: Previous studies showed that genetic polymorphisms of glutathione S-transferase P1 (GSTP1) were involved in glutathione metabolism and genetic polymorphisms of ribonucleotide reductase (RRM1) were correlated with DNA synthesis. Here we explored the effects of these polymorphisms on the chemosensitivity and clinical outcome in Chinese non-small cell lung cancer (NSCLC) patients treated with gemcitabine-cisplatin regimens., Materials and Methods: DNA sequencing was used to evaluate genetic polymorphisms of GSTP1 Ile105Val and RRM1 C37A-T524C in 47 NSCLC patients treated with gemcitabine-cisplatin regimens. Clinical response was evaluated according to RECIST criteria after 2 cycles of chemotherapy and toxicity was assessed by 1979 WHO criteria (acute and subacute toxicity graduation criteria in chemotherapeutic agents)., Results: There was no statistical significance between sensitive and non-sensitive groups regarding the genotype frequency distribution of GSTP1 Ile105Val polymorphism (p>0.05). But for RRM1 C37A-T524C genotype, sensitive group had higher proportion of high effective genotype than non-sensitive group (p=0.009). And according to the joint detection of GSTP1 Ile105Val and RRM1 C37A-T524C polymorphisms, the proportion of type A (A/A+high effective genotype) was significantly higher in sensitive group than in non-sensitive group (p=0.009). Toxicity showed no correlation with the genotypes between two groups (p>0.05)., Conclusions: Compared with single detection of genetic polymorphisms of GSTP1 Ile105Val or RRM1 C37A-T524C, joint detection of both may be more helpful for patients with NSCLC to receive gemcitabine-cisplatin regimens as the first-line chemotherapy. Especially, genetic polymorphism of RRM1 is more likely to be used as an important biomarker to predict the response and toxicity of gemcitabine-cisplatin combination chemotherapy in NSCLC.

Three novel triphenylamine (TPA) derivatives having perfluorinated cyclopentenyl and benzo[b]thiophene unit are obtained from 4-bromo-N,N-diphenyl-2-methylbenzo[b]thiophen-5-amine. The new compounds are expected to find their use in thin film devices as charge transport materials and host organic light-emitting materials. It is found that the new compounds show relatively strong fluorescence either in solution or in solid state, and are amorphous due to a special conformation which is elucidated by the fine structure of (19)F NMR. Molecular structure and properties of these compounds is characterized by (1)H NMR, (13)C NMR (broadband decoupled), ESI-HRMS, elemental analysis and thermal analysis (DSC). Fluorescent quantum yield in solution is measured using 9,10-diphenylanthrancene (DPA) as standard fluorescent substance., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Within the same pathogen-stress framework as proposed by Fincher & Thornhill (F&T), we argue further that pathogen stress promotes matrilocal rather than patrilocal family ties which, in turn, slow down the process of modernity; and that pathogen stress promotes social learning or copying, including the adoption of foreign religions.

Objective: To detect the expression of important proteins associated with transforming growth factor-beta (TGF-beta)/Smad signaling pathway in Peutz-Jeghers syndrome (PJS) and investigate the correlation of these proteins to LKB1 gene expression., Methods: The expression and localization of LKB1, TGFbeta1 and pSmad2 proteins in 20 PJS polyp samples and normal intestinal mucosal tissues were detected with immunohistochemical staining., Results: The expressions of LKB1, TGFbeta1 and pSmad2 were lower in PJS polyps than in normal mucosa, and the differences in LKB1 and TGFbeta1 proteins were significantly different between them (P<0.05). In PJS polyps, positive correlations were found between LKB1 and TGFbeta1 and between TGFbeta1 and pSmad2 expressions., Conclusion: TGFbeta/Smad pathway is probably subjected to the regulation by LKB1 and may play a role in the occurrence of PJS.

Little is known about what enzyme complexes or mechanisms control global lysine acetylation in the amino-terminal tails of the histones. Here, we show that glucose induces overall acetylation of H3 K9, 18, 27 and H4 K5, 8, 12 in quiescent yeast cells mainly by stimulating two KATs, Gcn5 and Esa1. Genetic and pharmacological perturbation of carbon metabolism, combined with (1)H-NMR metabolic profiling, revealed that glucose induction of KAT activity directly depends on increased glucose catabolism. Glucose-inducible Esa1 and Gcn5 activities predominantly reside in the picNuA4 and SAGA complexes, respectively, and act on chromatin by an untargeted mechanism. We conclude that direct metabolic regulation of globally acting KATs can be a potent driving force for reconfiguration of overall histone acetylation in response to a physiological cue.

Objective: To detect the mRNA and protein expression of interferon-inducible transmembrane protein-1 (IFITM1) in Peutz-Jeghers syndrome (PJS) and investigate the role of IFITM1 in the occurrence, development and carcinogenesis of PJS polyps., Methods: Reverse transcription-PCR was employed to detect the mRNA expression of IFITM1 in 16 PJS polyp samples, adenomatous polyp tissues, colon adenocarcinoma samples, and normal intestinal mucosal tissues. The protein expression and localization of IFITM1 in these tissues (32 cases for each) were detected with immunohistochemical (IHC) staining., Results: The IFITM1 mRNA expression was detected in all these tissues, and the expression intensity increased in the order of normal intestinal mucosa, PJS polyp, adenomatous polyp, and colon adenocarcinoma (F=92.704, P=0.000). IHC revealed that IFITM1 protein was localized mainly on the cell membrane and in the cytoplasm, with increased expression intensity in the same order as its mRNA and showing significant differences between the tissues by several rank-sum test (Kruskal-Wallis H, chi(2)=37.036, p=0.000)., Conclusion: The expression level of IFITM1 is associated with the progression of the carcinogenetic process in PJS polyp, and can be used as a sensitive biomarker for diagnosis and prognostic evaluation of PJS.

In this work, InAs quantum dots (QDs) grown on a linear graded InGaAs metamorphic buffer layer by molecular beam epitaxy have been investigated. The growth of the metamorphic buffer layers was carefully optimized, yielding a smooth surface with a minimum root mean square of roughness of less than 0.98 nm as measured by atomic force microscopy (AFM). InAs QDs were then grown on the buffer layers, and their emission wavelength at room-temperature is 1.49 microm as measured by photoluminescence (PL). The effects of post-growth rapid thermal annealing (RTA) on the optical properties of the InAs QDs were investigated. After the RTA, the PL peak of the QDs was blue-shifted and the full width at half maximum decreased.

We report a case of 30-year-old woman with Peutz-Jeghers syndrome (PJS). Because of small intestinal obstruction, she received the small intestinal polypectomy in 2001, and the pathological diagnosis was Peutz-Jeghers polyp canceration (mucinous adenocarcinoma, infiltrating full-thickness of the intestine). The patient did not feel uncomfortable after 6 mo of chemotherapy and other management. We kept a follow-up study on her and found that she suffered from cervical cancer in 2007, with a pathological diagnosis of cervical adenosquamous carcinoma.The patient presented with typical features of PJS, but without a family history. The PJS accompanied with both small intestinal and cervical malignancies has not been reported so far in the world.

Unlabelled: Overexpression of HER-2/Neu occurs in about 25-30% of breast cancer patients and is indicative of poor prognosis. While Her2/Neu overexpression is primarily a result of erbB2 amplification, it has recently been recognized that erbB2 levels are also regulated on the protein level. However, factors that regulate Her2/Neu protein stability are less well understood. The prolyl isomerase Pin1 catalyzes the isomerization of specific pSer/Thr-Pro motifs that have been phosphorylated in response to mitogenic signaling. We have previously reported that Pin1-catalyzed post-phosphorylational modification of signal transduction modulates the oncogenic pathways downstream from c-neu. The goal of this study was to examine the expression of prolyl isomerase Pin1 in human Her2+ breast cancer, and to study if Pin1 affects the expression of Her2/Neu itself., Methods: Immunohistochemistry for Her2 and Pin1 were performed on two hundred twenty-three human breast cancers, with 59% of the specimen from primary cancers and 41% from metastatic sites. Pin1 inhibition was achieved using siRNA in Her2+ breast cancer cell lines, and its effects were studied using cell viability assays, immunoblotting and immunofluorescence., Results: Sixty-four samples (28.7%) stained positive for Her2 (IHC 3+), and 54% (122/223) of all breast cancers stained positive for Pin1. Of the Her2-positive cancers 40 (62.5%) were also Pin1-positive, based on strong nuclear or nuclear and cytoplasmic staining. Inhibition of Pin1 via RNAi resulted in significant suppression of Her2-positive tumor cell growth in BT474, SKBR3 and AU565 cells. Pin1 inhibition greatly increased the sensitivity of Her2-positive breast cancer cells to the mTOR inhibitor Rapamycin, while it did not increase their sensitivity to Trastuzumab, suggesting that Pin1 might act on Her2 signaling. We found that Pin1 interacted with the protein complex that contains ubiquitinated erbB2 and that Pin1 inhibition accelerated erbB2 degradation, which could be prevented by treatments with the proteasome inhibitor ALLnL., Conclusion: Pin1 is a novel regulator of erbB2 that modulates the ubiquitin-mediated degradation of erbB2. The overexpression of Pin1 in a majority of Her2-overexpressing breast cancer may contribute to maintain erbB2 levels. Pin1 inhibition alone and in conjunction with mTOR inhibition suppresses the growth of Her2+ breast cancer cells.

The potential role of stem cells in neoplasia is a subject of recent interest. Three markers of melanocytic stem cells have been described recently. CD166 is expressed on the surface of mesenchymal stem cells and has been found on human melanoma cell lines. CD133 is expressed on the surface of dermal-derived stem cells that are capable of differentiating into neural cells. Nestin is an intermediate filament expressed in the cytoplasm of neuroepithelial stem cells. In this study, we evaluate the expression of these markers and possible differences among banal nevi, primary melanoma, and metastastic melanoma. Tissue microarrays containing normal tissue and 226 melanocytic lesions (71 banal nevi, 71 in situ and invasive melanomas, and 84 metastatic melanomas) were studied by immunohistochemistry using monoclonal antibodies CD166, CD133, and nestin. A significantly greater percentage of melanomas (combined primary and metastatic) contained cells that expressed CD166 (P=0.005), CD133 (P=0.003), and nestin (P=0.03) than banal nevi. Only nestin showed a statistical difference when comparing primary and metastatic melanoma (P=0.05). A stepwise increase in the proportion of lesions expressing all three markers was observed from banal nevi (2/19) to primary melanomas (8/17) to metastatic melanoma (19/28), P=0.0005. All cases of metastatic melanoma expressed at least one stem cell marker. The increased expression of CD166, CD133, and nestin in melanoma suggests that progression to malignant melanoma likely involves genetic pathways instrumental to stem cell biology and normal tissue development. Further studies and characterization of these pathways may also reveal new prognostic markers for a disease whose prognosis in advanced stages is dismal.

Porcine teschovirus 1 (PTV-1) (Swine/CH/IMH/03) was isolated from piglets in a farm in Inner Mongolia Province, P.R. China. It was confirmed by electron microscopy, RT-PCR, and sequencing. Comparison of the sequences of the amino acid and nucleotides and phylogenetic analysis of the polyprotein showed that PTV Swine/CH/IMH/03 strain is PTV-1. The isolated virus has closest relationship with Talfan strain, they shared 98.9% and 99.5% homology of amino acids and nucleotides, respectively, in the ORF of polyprotein. To our knowledge, this is the first report about isolation and identification of a PTV in China.

Objective: To investigate the relation of peripheral blood estradiol, progesterone and testosterone levels with irritable bowel syndrome (IBS)., Methods: Forty-eight patients with IBS identified according to Rome II diagnostic criteria and 30 healthy subjects as controls were analyzed for peripheral blood sex hormone levels by radioimmunoassay and corresponding software., Results: In male patients with IBS, blood testosterone level was significantly lower than that of the control group (P<0.05), but blood estradiol and progesterone showed no significant differences between the two groups (P>0.05). In the female patients, blood estradiol level was significantly lower than that of the control group (P<0.05), whereas blood progesterone and testosterone levels had no significant differences between the two groups (P>0.05)., Conclusion: Peripheral blood testosterone level in male IBS patients and estradiol level in female patients are lower than those of healthy subjects, suggesting that IBS might be associated with blood sex hormone disorder.

Background and Aim: Non-alcoholic steatohepatitis (NASH) is increasingly recognized as an important cause of chronic liver disease. However, data on Asians with NASH is lacking in the literature. The aim of the present study was to describe the clinical, biochemical and histological characteristics of NASH in Asians and to determine the predictors for septal fibrosis., Method: Sixty consecutive patients aged over 18 years with elevated serum alanine transferase, sonographic evidence of steatosis, and consent for liver biopsy were included. Patients with chronic hepatitis B or C, alcoholic, autoimmune, genetic, or drug-induced liver disease were excluded. Clinical, biochemical and histological variables were tested for association with septal liver fibrosis (F2/3)., Results: Median age of the cohort was 45.5 years (range 21-75 years) and 63% were male. Ninety percent of patients were obese (body mass index [BMI]>or= 25), 70% had hypertriglyceridemia, 68% had hypercholesterolemia, 58% had metabolic syndrome, 53% had hypertension, 47% had diabetes mellitus (DM), and 18% had obstructive sleep apnea. Sixty-eight percent had gamma-glutamyl transferase (GGT) >or= 2 x upper limit of normal (ULN), 55% had alanine aminotransferase (ALT) >or= 2 x ULN, and 23% had aspartate aminotransferase (AST) >or= 2 x ULN. Of the 40 non-diabetic patients undergoing oral glucose tolerance testing, 45% had normal tests, 30% had impaired glucose tolerance, 23% DM, and 2% impaired fasting glucose. Eighteen patients (30%) had septal fibrosis (F2/3), but none had cirrhosis. Necroinflammatory grade >or= 2 (odds ratio [OR] 13), AST >or= 2 x ULN (OR 5.3) and DM (OR 5) were significantly and independently correlated with septal fibrosis., Conclusion: Septal fibrosis is common in Asians with NASH. Necroinflammatory grade >or= 2, AST >or= 2 x ULN and DM are independent predictors for septal fibrosis.

Objective: To determine whether the eukaryotic initiation factor-4E (eIF-4E) is involved in the cap-dependent translational regulation of heparanase and study the correlation between heparanase expression and metastatic potential of LS-174T cells., Methods: The protein and mRNA levels of inhibited eIF-4E were tested by Western blot and RT-PCR. Heparanase activity was defined as the ability to degrade high molecular weight (40-100 000) radiolabeled ((35)S) heparan sulfate (HS) substrate into low molecular weight (5-15 000) HS fragments. The invasive potential of tumor cells in vitro was observed by Matrigel invasion assay system., Results: The 20-mer antisense oligonucleotide (asODN) against eIF-4E specifically and significantly inhibited eIF-4E expression at both transcriptional and translational levels. The expression and the activity of heparanase were effectively lowered, which further decreased the invasive potential of LS-174T., Conclusion: eIF-4E, probably being involved in translational regulation of heparanase in colon adenocarcinoma cell line LS-174T, can be a particularly interesting target for heparanase regulation, based on of its critical function.

Objective: To express the original human Fab antibody phage display library with positive recombined bacterium XL1-blue-Pcomb3 and identify its specific binding activity with colorectal cancer cells in vitro after screening with human colorectal cancer-related antigens., Method: The recombination rate of Fd fragment of the heavy chain and insertion of kappa chain of the antibodies was determined with PCR, and the original Fab library was expressed. The antigens were extracted from 3 sensitized colorectal cancer tissues previously used for construction of the original Fab library and from 13 non-sensitized colorectal cancer tissues, along with the antigens from LoVo, HT-29 and LS-174T cells cultured in vitro. The original Fab antibody library was screened with the 3 groups of mixed antigens derived in preceding procedure and 3 tertiary Fab antibody libraries were obtained, which were then mixed in equal volume for subsequent tests of binding activity with human colorectal cancer tissues and cells in vitro using enzyme-linked immunosorbent assay (ELISA) and immunohistochemical staining. Specimens of gastric and esophageal carcinomas and normal intestinal mucosa, together with liver cancer cells and gastric cancer cells were utilized as control., Result: The recombination rate of Fd and kappa chain were 40 % and 70 % respectively, and the rate of their simultaneous insertion into Pcomb3 vector was 28%. The capacity of library for Fab fragment genes was 2.1x10(6), and the original antibody libraries screened with the 3 groups of mixed antigens were enriched to varied degrees, which all displayed relatively specific binding activity with human colorectal cancer tissue and cells in vitro., Conclusion: Colorectal cancer-related antibody Fab fragments are obtained through screening phage display library, which show relatively specific binding activity with human colorectal cancer tissues and cells.

Aim: To review the present studies on early diagnosis of colorectal cancer., Methods: The detective rate for early cancer is 1.7%-26.1% based on various statistical data, with much higher detective rate in endoscopy. Since early cancer means invasion involved in the mucosa or submucosa, the diagnosis can only be made when the invasive depth is identified. Pathological tissue materials from both surgical operation or endoscopic resection are suitable for early cancer evaluation., Results: Incidence of polyp malignancy is 1.4%-20.4%. The various constitutive proportion of polyps may explain the different rates. Malignant incidence is higher in adenomatous polyps, that for villous polyps can reach 21.3%-58.3%. Type II early stage of colorectal carcinoma is rarely reported in China. It is shown that majority of them were not malignant, most of type IIa being adenoma or hyperplasia, and IIb being inflammatory and IIc might be the isolated ulcers. The occurrence of malignancy of type II is far lower than that of polypoid lesion. In China, the qualitative diagnosis and classification of neoplasm generally adopted the WHO standard, including surgical excision or biopsies. There is impersonal evaluation between colorectal pre-malignancy and cancer. The former emphasizes the dysplasia of nuclei and gland, while the latter is marked with cancer invasion. Diagnosis of early stage colorectal cancer in endoscopy is made with too much caution which made the detective rate much lower. Mass screening for asymptomatic subjects and follow-up for high risk population are mainly used to find the early stage colorectal cancer in China. Fecal occult blood test is also widely made as primary screening test, galactose oxygenase test of rectal mucus (T antigen), fecal occult albumin test are also used. The detective rate of colorectal cancer is 24-36.5 per 105 mass population., Conclusion: Although carcinoma associated antigen in blood or stool, microsatellite DNA instability for high risk familial history, molecular biology technology for stool oncogene or antioncogene, telomerase activity and exfoliative cytological examination for tumor marker, are utilized, none of them is used in mass screening by now.

Aim: To construct the natural immune Fab antibody phage display libraries of colorectal cancer and to select antibodies related with colorectal cancer., Methods: Extract total RNA from tissue of local cancer metastasis lymph nodes of patients with colorectal cancer. RT-PCR was used to amplify the heavy chain Fd and light chain kappa and the amplification products were inserted successively into the vector pComb3 to construct the human libraries of Fab antibodies. They were then panned by phage display technology. By means of Dot immunoblotting and ELISA, the libraries were identified and the Fab phage antibodies binding with antigens of colorectal cancer were selected., Results: The amplified fragments of Fd and kappa gained by RT-PCR were about 650 bp. Fd and kappa PCR products were subsequently inserted into the vector pComb3, resulting in a recombination rate of 40% and the volume of Fab phage display library reached 1.48 x 10(6). The libraries were enriched about 120-fold by 3 cycles of adsorption-elution-multiplication (panning). Dot immunoblotting showed Fab expressions on the phage libraries and ELISA showed 5 clones of Fab phage antibodies which had binding activities with antigens of colorectal cancer., Conclusion: The natural immune Fab antibody phage display libraries of colorectal cancer were constructed. They could be used to select the relative antibodies of colorectal cancer.