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Two kinds of chitosan of different molecular weight (50 kDa and 400 kDa) were employed to form nanoparticles with 32P-labeled plasmid DNA at different N/P ratios by complex coacervation method. The characteristics of chitosan gene nanoparticles (CGN) were measured. The cellular uptake of DNA nanoparticles was evaluated by A10 and K562 cells. The in vitro cytotoxicity of DNA nanoparticles was determined by the MTT assays. Cellular uptake of the DNA nanoparticles increased with increasing chitosan molecular weight and N/P ratio. It also correlated with the zeta potential of the DNA nanoparticles. Chitosan-DNA nanoparticles were much less cytotoxic when compared with Lipofectamine 2000-DNA nanoparticles.

The consequences of including amide bonds into the structure of short-chain nonionic surfactants have been studied. Of particular interest were the possible effects of the hydrogen bonding ability of the amide group on the micellar shape. The aggregate structure and hydration of two different amide-containing surfactants, C7H15CO-NH-(CH2CH2O)(4)H and C7H15CO-(NH-C3H6-CO)(2)N(CH3)(2), were investigated using NMR diffusometry (pulsed gradient spin echo NMR) as the main technique. Data from experiments on the surfactants, the hydrophobic probe molecule hexamethyldisilane (HMDS), and water were interpreted to gain information about the solution structures, and the results were compared to those on a previously studied alcohol ethoxylate surfactant of similar size, C8E4. Both of the amide-containing surfactants form small micelles within the whole investigated concentration range. At the critical micelle concentration, the aggregates are most probably spherical, and with increasing surfactant concentration there are indications of either a minor aggregate growth or agglomeration of the micelles. In addition, it was found that the presence of amide groups in the surfactant inhibits the intermicellar transport of HMDS, which occurs in the C8E4 system. From measurements on water diffusion in the three surfactant systems, it could be concluded that the surfactant hydration is higher when amide bonds are present.

Xia Dong, Lanxia Liu, Dunwan Zhu, Hailing Zhang, Xigang Leng Laboratory of Bioengineering, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin Key Laboratory of Biomedical Materials, Tianjin, People’s Republic of China Abstract: Carbon nanotube (CNT)-based drug delivery vehicles might find great potential in cancer therapy via the combination of chemotherapy with photothermal therapy due to the strong optical absorbance of CNTs in the near-infrared region. However, the application of CNTs in cancer therapy was considerably constrained by their lack of solubility in aqueous medium, as well as the cytotoxicity caused by their hydrophobic surface. Intracellular delivery efficiency is another factor determining the application potential of CNTs in cancer therapy. In the present study, low-molecular-weight chitosan conjugated with transactivator of transcription (TAT) peptide was used for noncovalent functionalization of multiwalled carbon nanotubes (MWCNTs), aiming at providing a more efficient drug delivery vehicle for cancer therapy. The TAT–chitosan-conjugated MWCNTs (MWCNTs-TC) were further investigated for their water solubility, cytotoxicity, cell-penetrating capability, and accumulation in tumor. It was found that MWCNTs-TC were essentially nontoxic with satisfying water solubility, and they were more efficient in terms of cancer-targeted intracellular transport both in vitro and in vivo as compared with chitosan-modified MWCNTs (MWCNTs-CS), suggesting the great application potential of MWCNTs-TC in cancer therapy. Keywords: carbon nanotube, TAT, chitosan, drug delivery

The preparation and cell transfection of chitosan-DNA nanoparticles were studied. The TFPI (tissue factor pathway inhibitor) or EGFP (enhanced green fluorescent protein) plasmid DNA was encapsulated with chitosan to form gene nanoparticles. The results with TEM showed that the nanoparticles were of sphere shape. The mean diameter of the nanoparticles was 149 nm and the diameter ranged from 80-250 nm, which were measured by the photo related spectrometry (PCS). The encapsulation efficiency of DNA was 96% +/- 1.38% and the DNA content in the nanoparticles was 37% +/- 3.0%. The encapsulated DNA could be protected from the degradation by DNase I. The transfection efficiency of chitosan nanoparticles were about equivalent to that of the LipofectAMINETM reagent. Our results also showed that chitosan nanoparticles were nontoxic to cultured cells.

Though the etiology of hemifacial atrophy is still unknown, the aim of its reconstruction is cosmetic amelioration of the defect. Among many techniques introduced, microsurgical reconstruction has become the gold standard to restore the symmetry of the face. Seven free anterolateral thigh adipofascial flaps were used to reconstruct hemifacial atrophy between September 1999 and May 2005. There were 1 male and 6 females in the series. All the patients had unilateral disease (6 right and 1 left). The average age of onset of disease was 11.9 years. The average duration of atrophy was 6.7 years. The patients' average age was 25 years (range, 21 to 32 years), and the average follow-up period was 12.6 months (range, 6 to 36). The size of the transferred flap ranged from 8 × 6 cm to 12 × 13 cm. All adipofascial flaps survived completely. No complications occurred. The result is stable, and no recurrence of facial atrophy was seen in the patients after follow-up. One patient received minor revision because of the bulky reconstructed face. The esthetic appearance of the reconstructed face was acceptable. Despite a variable vascular anatomy that can give rise to some surgical challenge in raising the anterolateral thigh adipofascial flap, the authors conclude that this is a safe and reliable adipofascial flap for hemifacial atrophy.

Eleven triamides bearing long alkyl chains have been synthesized to produce a new class of amphiphilic compounds (dubbed "peptoad"). The properties of these molecules have been investigated by X-ray analysis, solubility studies, light and electron microscopy, surface tensiometry, light scattering, drug dissolution, and molecular dynamics. In the solid state, the peptoads assemble in layers with both intra- and interlayer hydrogen bonding coupled to side-by-side proximity of the hydrocarbon chains. Peptoads with a terminal primary amide and a total of three amide NH sites are water-insoluble owing presumably to attractive forces in the solid state. However, peptoads with terminal -CONMe(2) groups and two internal amide NH sites are water-soluble at room temperature. This solubility is critically dependent upon the chain length. For example, a C(7)-chained peptoad is 1600 times more soluble than its C(9) analogue. High concentrations (6-8 M) of C(7) peptoads in water are clear and do not gel. Light microscopy shows long fibers floating in an isotropic liquid. Water-soluble peptoads are highly surface-active, lowering water's surface tension as effectively as a soap with a much longer chain. Surface tension plots show a "critical aggregation concentration", but it is believed from light scattering and molecular dynamics that the aggregates grow continuously as more peptoad is added to the water. In answer to the inevitable (but valid) question, "What possible good are they?", it can be pointed out that a peptoad solubilizes a water-insoluble drug, paclitaxel (Taxol), as efficiently as does Cremophor EL, a commercial excipient widely used with paclitaxel and other nonpolar drugs. Peptoads, being small molecules and consisting of hydrolyzable amide groups, are likely biodegradable and less prone to the hypersensitivity and neurotoxicity found with Cremophor EL.

The objectives of the present study were to determine the effect of nicotine on MAPK signaling and on the proliferation of AR42J cells as well as to assess the relationship between MAPK activation and exocrine secretion in these cells. AR42J cells were incubated with nicotine and analyzed for the activation of MAPK by Western blot analysis using their respective antibodies and confirmed by immunohistochemistry. The effect of nicotine on cell proliferation was determined by the spectrophotometric method, and cell function was assessed by cholecystokinin (CCK)-stimulated amylase release into the culture medium. Nicotine at a dose of 100 μM induced phospho-ERK1/2 activation maximally in 3 min compared with untreated cells. Furthermore, immunofluorescence study confirmed the nicotine-induced increase in translocation of phospho-ERK1/2 to the nucleus. Activation of phospho-ERK1/2 was inhibited by an ERK1/2 pathway inhibitor but not by a nicotine receptor antagonist. At the same dose, there was significantly enhanced proliferation of AR42J cells until 72 h without toxic effect, as the percentage of lactate dehydrogenase release remained unchanged. Other MAPKs, c-Jun NH2-terminal kinase 1/2 and p38 MAPK, were not affected by nicotine treatment. At a nicotine dose of 100 μM, the CCK-stimulated release of amylase was maximal at 6 min, and, although a nicotinic receptor antagonist inhibited this response, it was not inhibited by the ERK1/2 pathway inhibitor. We conclude that nicotine treatment induced activation of ERK1/2 and increased the proliferation of AR42J cells. The data further indicate that MAPK signaling by nicotine is independent of the secretory response.

Considerable data support adiponectin as an important adipose-derived insulin sensitizer that enhances fatty acid oxidation and alters hepatic gluconeogenesis. Adiponectin acts by way of two receptors, ADIPOR1 and ADIPOR2. ADIPOR1 is widely expressed in tissues, including muscle, liver, and pancreas, and binds the globular form of adiponectin with high affinity. To test the hypothesis that sequence variations in or near the ADIPOR1 gene contribute to the risk of developing type 2 diabetes and the metabolic syndrome, we screened the eight exons (including the untranslated exon 1) of the ADIPOR1 gene with flanking intronic sequences and the 5′ and 3′ flanking sequences. We identified 22 single nucleotide polymorphisms (SNPs) in Caucasian and African-American subjects, of which a single nonsynonymous SNP (N44K) in exon 2 was present only in African-American subjects. We typed 14 sequence variants that had minor allele frequencies >5%. No SNP was associated with type 2 diabetes in Caucasians or African Americans, and no SNP was a determinant of insulin sensitivity or insulin secretion among nondiabetic members of high-risk Caucasian families. However, the two alleles of a SNP in the 3′ untranslated region were expressed unequally, and ADIPOR1 mRNA levels were significantly lower among transformed lymphocytes from diabetic African-American individuals than among control cell lines. This altered gene expression might suggest a role for ADIPOR1 in the metabolic syndrome.

Increased flux of glucose through the hexosamine biosynthetic pathway has been implicated in insulin resistance, altered insulin secretion, and diabetic nephropathy. Glutamine:fructose-6-phosphate amidotransferase (GFPT), the rate limiting enzyme in hexosamine biosynthesis, is encoded by the unlinked but highly homologous genes GFPT1 and GFPT2. We tested the hypothesis that GFPT2 sequence variation contributed to the susceptibility to type 2 diabetes mellitus (T2DM) and diabetic nephropathy in Caucasian and African-American individuals. We identified 11 single nucleotide polymorphisms (SNPs), of which seven were common. A single variant in exon 14, I471V, altered the amino acid sequence, is conserved between human and mouse genes, and was associated with T2DM among Caucasians (P = 0.05). A trend to an association was noted with diabetic nephropathy among African-American individuals (P = 0.15). Several variants in the 3' untranslated region (UTR) and exon 18 were also associated with T2DM in Caucasian individuals (P0.05), and the SNP in the 3' UTR was associated with diabetic nephropathy in African-American subjects (P = 0.047). GFPT2 mRNA levels in transformed lymphocytes from study subjects were significantly increased among African-American subjects compared with Caucasian individuals, regardless of diagnosis. Furthermore, the associated allele of the 3' UTR SNP was approximately 2-fold overexpressed. We propose that the 3' UTR variant results in increased GFPT2 mRNA levels with resultant increased hexosamine flux. The I471V variant may contribute to altered protein function or may simply be in linkage disequilibrium with the 3' UTR.

We studied the changes of met-enkephalin (Met-Enk) content and preproenkephalin (PPE) mRNA in the striatum in a mouse model of nicotine abstinence. Nicotine, 2 mg/kg, s.c., was administered four times daily for 14 days and Met-Enk and PPE mRNA evaluated at various times (4-96 h) following drug discontinuation. Met-Enk, assayed by radioimmunoassay, was increased in the ventral (nucleus accumbens) but not dorsal (putamen/caudate) striatum, while PPE mRNA, assayed in whole striatum by Northern blotting was elevated. Both changes were seen early during withdrawal and lasted over 72 h. In situ hybridization revealed enhanced signal in the dorsal striatum, mostly laterally, and smaller increases in the rostral pole, core and shell of the nucleus accumbens. These observations indicate that during nicotine withdrawal, striatal enkephalinergic neurons undergo adaptative responses, which might contribute to the abstinence behavioral syndrome.

Lanxia Liu, Xia Dong, Dunwan Zhu, Liping Song, Hailing Zhang, Xigang G LengLaboratory of Bioengineering, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin Key Laboratory of Biomedical Materials, Tianjin, People’s Republic of ChinaAbstract: To develop a chitosan-based nonviral gene carrier capable of delivering genes specifically into hepatoma cells, a bifunctional peptide composed of the TAT (transactivator of transcription) peptide and luteinizing hormone-releasing hormone (LHRH) was conjugated with low molecular weight chitosan, resulting in a TAT-LHRH-chitosan conjugate (TLC). TLC/DNA nanoparticles (TLCDNPs) were characterized by agarose gel retardation, atomic force microscopy, and dynamic light scattering analysis. In vitro targeting specificity and transfection efficiency were analyzed with a GE IN Cell Analyzer2000High-Content Cellular Analysis System. The results demonstrated that TLC had stronger DNA condensing power than unmodified chitosan, and that TLCDNPs were of roughly round shape with average diameter of70–85nm and zeta potential of +30mV and were relatively stable in solution. The in vitro study demonstrated TLC was highly selective for hepatoma cells and essentially nontoxic.Keywords: nanoparticles, cancer treatment, gene therapy, hepatoma, targeted gene delivery

Surface observations are the main conventional observations for weather forecasts. However, in modern numerical weather prediction, the use of surface observations, especially those data over complex terrain, remains a unique challenge. There are fundamental difficulties in assimilating surface observations with three-dimensional variational data assimilation (3DVAR). In this study, a series of observing system simulation experiments is performed with the ensemble Kalman filter (EnKF), an advanced data assimilation method to compare its ability to assimilate surface observations with 3DVAR. Using the advanced research version of the Weather Research and Forecasting (WRF) model, results from the assimilation of observations at a single observation station demonstrate that the EnKF can overcome some fundamental limitations that 3DVAR has in assimilating surface observations over complex terrain. Specifically, through its flow-dependent background error term, the EnKF produces more realistic analysis increments over complex terrain in general. More comprehensive comparisons are conducted in a short-range weather forecast using a synoptic case with two severe weather systems: a frontal system over complex terrain in the western US and a low-level jet system over the Great Plains. The EnKF is better than 3DVAR for the analysis and forecast of the low-level jet system over flat terrain. However, over complex terrain, the EnKF clearly performs better than 3DVAR, because it is more capable of handling surface data in the presence of terrain misrepresentation. In addition, results also suggest that caution is needed when dealing with errors due to model terrain representation. Data rejection may cause degraded forecasts because data are sparse over complex terrain. Owing to the use of limited ensemble sizes, the EnKF analysis is sensitive to the choice of horizontal and vertical localisation scales. Keywords: data assimilation, ensemble Kalman filter, 3DVAR, complex terrain, short-range weather forecasting, surface observations (Published: 15 March 2013) Citation: Tellus A 2013, 65 , 19620, http://dx.doi.org/10.3402/tellusa.v65i0.19620

Introduction Chronic lymphocytic leukemia (CLL) is a lymphoproliferative disorder (LPD) derived from mature B-cells with heterogeneous outcomes. High-grade lymphoma can arise from CLL in 3-10% of cases, a process known as Richter’s transformation (RT). The majority of RT results in high grade B-cell lymphomas, though rarely transformation to Hodgkin lymphoma (HL) has been reported. Epstein Barr virus (EBV) viremia can arise in patients with CLL secondary to immunosuppression and can lead to an EBV driven LPD. In patients with CLL, this has been seen with fludarabine based treatments but has been reported with alemtuzumab. HL is also been associated with EBV virus in tumor cells but cases of HL and EBV viremia have not been reported. We report the first two cases in the English literature of CLL with EBV viremia and HL. Cases Case 1 A 66 year old male was diagnosed with a RAI stage I, del13q14, Zap-70 (-), IgvH mutated, CD38 (+) CLL in 2004. Worsening thrombocytopenia resulted in the initiation of treatment in April 2012 using Ofatumumab and high dose methylprednisolone followed by lenalidomide maintenance therapy (HiLOG clinical trial). The patient responded to induction therapy and was continued on lenalidomide maintenance for 12 cycles. In May of 2013 the patient developed progressive fevers, chills, cough, weakness, weight loss, and hypercalcemia. Evaluation revealed an EBV viremia with whole blood PCR titers of 484,550 copies/mL. Bone marrow biopsy was consistent with CLL and full body PET CT scan showed diffuse lymphadenopathy with max SUV of 30.7 and splenomegaly. Biopsy of a left external iliac node showed large atypical lymphoid cells that were surrounded by small lymphocytes. The large atypical lymphoid cells were CD30 (+), EBV (+), Pax-5 (+), CD 20 (-), CD15 (-), CD5 (-), and CD3 (-) confirming HL. The patient has currently received 4 weekly treatments with rituximab for EBV driven LPD and one cycle of Adriamycin, bleomycin, vinblastine, and dexamethasone (ABVD) for HL with resolution of symptoms and a whole blood EBV PCR to Case 2 A 68 year old male was diagnosed in England with an unknown stage del13q and IgVH unmutated CLL in 2002. He was started on treatment with 5 cycles of fludarabine, cyclophosphamide, rituximab in 2011 and achieved a complete response. His post therapy course was complicated with infection resulting in septic shock with renal failure resulting in dialysis. He stabilized but continued to have hypogammaglobulenemia and required intravenous immunoglobulin (IVIG) replacement. In April of 2013 he developed fevers to 104F, night sweats, weight loss and, fatigue. PET CT scan showed diffuse adenopathy with max SUV of 22.5, and bone marrow biopsy showed 60% CLL and a component of large cells that were CD 30 (+), CD15 (+), Mum1 (+), and EBER-ISH (+). The patient’s whole blood EBV PCR was 276,600 copies/mL. Based on the clinical picture the patient was diagnosed with an EBV positive HL, EBV viremia, and chronic CLL. He has completed 4 weekly treatments with rituximab for EBV driven LPD and cycle 1 of ABVD for HL with resolution of symptoms and a whole blood EBV PCR of Discussion Although EBV viremia has been reported in CLL and EBV staining can be positive in HL, these two cases are the first to report CLL with EBV viremia and EBV positive HL. The high EBV viral load likely provided a base for an EBV driven LPD, in these cases HL. In patients with constitutional symptoms who have stable CLL disease burden, the clinician should screen for RT and EBV viremia. When a concurrent process is found, as in our cases, treatment against both the EBV driven LPD and HL should be initiated. Further research is needed to establish a biological relationship between EBV viremia and HL in patients with CLL. Disclosures: No relevant conflicts of interest to declare.

OBJECTIVE: Embryo implantation is directly affected by genes related to uterine receptivity. Studies have demonstrated the important roles of miRNAs in the regulation of gene expression. Our early miRNA chip analyses revealed that the mmu-miR-141 expression in endometrial tissue is lower after embryo implantation than before it. However, the possible roles of miR-141 in embryo implantation have not yet been elucidated. Here, mmu-miR-141 was designed to detect the expression and role of miR-141 in the endometria of mice in early pregnancy following embryo implantation. METHODS: Real-time PCR and in-situ hybridization were used to study mmu-miR-141 expression in mouse uterus. Cell proliferation was detected by tetrazolium dye (MTT) assay and flow cytometry. Real-time PCR and Western blot analysis were used to confirm the mRNA and protein levels of phosphatase and tensin homolog (PTEN) to determine whether it was the target gene of mmu-miR-141. Enhanced green fluorescent protein (EGFP) fluorescence reporter vector analysis was also performed. A functional study was performed by injecting mice uteri with mmu-miR-141 inhibitor or mimic vectors. RESULTS: mmu-miR-141 expression was lower on day 6 (D6) than day 4 (D4) and could be increased by progesterone. Reduced mmu-miR-141 could decrease the proliferation activity of stromal cells and promote apoptosis. Upregulation of mmu-miR-141 inhibited PTEN protein expression but downregulation of mmu-miR-141 increased it, while the mRNA level remained unchanged. EGFP fluorescence reporter vector analysis showed that miR-141 targets the 3'-untranslated region of the PTEN mRNA. In addition, when the physiological mmu-miR-141 level was altered on D2 by injecting with inhibitor or mimic, the embryo implantation sites were significantly decreased on D7. CONCLUSIONS: This study demonstrated that mmu-miR-141 might influence cell proliferation and apoptosis in the endometrium by negatively regulating PTEN expression, and could also influence the number of embryo implantation sites. mmu-miR-141 plays an essential role in embryo implantation.

The mesocorticolimbic dopamine (DA) system is thought to comprise part of a neural substrate participating in behavioral reinforcement. While much emphasis has been placed on mesolimbic terminal field activity, the existence of somatodendritic DA release has also been established. In the present study, the release of endogenous DA from the ventral tegmental DA cell body region of freely moving rats was measured, using in vivo chronoamperometry after presentation of several environmental stimuli. While presentation of a 9-s moderately intense light stimulus did not significantly modify DA release, palatable food presentation (FD), 3 min of social interaction (SI) with another male rat and a 3-min tail-pinch (TP) produced an increase in electrochemical signal, suggesting an increase in somatodendritic DA release. Mean peak signal increases (calibrated in nM DA concentration) were 104, 135 and 161 nM after FD, SI and TP stimulus, respectively. After daily presentation of all four stimuli, one of four DA active drugs was given s.c. When compared with preinjection baseline, apomorphine (APO) caused a decrease while nomifensine (NOMI), cocaine (COC) and haloperidol (HALO) caused an increase in electrochemical signal. When TP was given 30 min after drug injection, APO, NOMI and COC suppressed the TP-induced signal increase compared with the predrug response. HALO, on the other hand, did not alter TP-induced DA release. These data support the hypothesis that the cells of origin of the mesocorticolimbic system release dendritic DA after physiologically relevant stimuli.

Abstract 4305 Post-transplant lymphoproliferative disorder (PTLD) is one of the major complications of organ transplantation. Most PTLDs are associated with Epstein-Barr virus (EBV) infection of B-lineage lymphocytes. Central nervous system (CNS) involvement is rare. Although most PTLDs following solid organ transplants is of recipient origin, PTLDs following bone marrow or stem cell transplant are mostly of donor cell origin. Origin of the tumor cells are of crucial importance in deciding treatment and predicting prognosis. Here we report a case of PTLD of diffuse large B cell Lymphoma of donor tissue origin determined by chimerism analysis. The patient was a 52-year-old woman with myelofibrosis (Myeloproliferative disorder) who received unrelated donor peripheral blood stem cell transplantation. The donor was an ABO compatible, HLA matched unrelated donor. Post transplant immunosuppression therapy was administered. The post transplant history was complicated by multiple viral infections, including BK, CMV and EB virus. Four months after transplantation, the patient developed fever and mental status changes, MRI of brain showed multiple enhancing lesions. Brain biopsy revealed brain tissue with dense infiltration of large atypical lymphoid cells predominantly perivascular in location. Immunohistochemical stains reveal that the large atypical lymphoid cells are of B-cell origin and these cells are 100% positive for Ebstein Barr virus by EBV encoded RNA by in-situ hybridization. The flowcytometry study revealed a monoclonal population of B cells with Kappa light chain restriction. These findings support the diagnosis of post transplant lymphoproliferative disorder (PTLD) of diffuse large B-cell lymphoma type. To determine the origin of tumor cells, chimerism analysis of the host DNA (buccal) and tumor DNA were performed. Short tandem repeat (STR) multiplex PCR assay were performed using the AmpFlSTR Identifiler PCR amplification kit (Applied Biosystems, Foster City, CA). After amplification, samples were analyzed on an ABI 310 DNA Sequencer (Applied Biosystems). The allele distribution was significantly different between the recipient DNA (from buccal swab) compared to tumor DNA indicating donor origin of the tumor (PTLD). The patient was then placed on high dose methotrexate and dexamethasome, however her condition deteriorated dramatically and the patient expired shortly following the diagnosis. It is known that the major pathogenetic defect of PTLD is the insufficient EBV-specific cytotoxic T-cell control of EBV-driven B-cell proliferations. Despite this understanding, determining the right therapy for any given patient with PTLD remains a major clinical issue. It is important to identify patients who will benefit from reduction of immunosuppression, who will benefit from Rituximab. It is also important to develop more effective, less toxic chemotherapies for resistant or aggressive disease. The chimerism analysis performed on our patient to identify tumor cell origin is an unique and reliable method to help directing clinical management of PTLD. Disclosures: No relevant conflicts of interest to declare.

Background As a key link between innate and adaptive immune responses, the interferon (IFN) system is the first line of defense against viral infection. IFN, and in particular, IFN-α, has been used clinically as an effective therapeutic agent for viral infections. However, different subtypes of IFN-α demonstrate distinct antiviral activity. Therefore, it is important to identify IFN-α subtypes with high antiviral activity for the development of genetically engineered antiviral drugs. Results In this study, we cloned the genes for 13 IFN-α subtypes from peripheral blood lymphocytes of the mink. The homologies of the 13 mink IFN-α genes were 93.6–99.3% and 88.8–98.4% at the nucleotide and amino acid sequence levels, respectively. In contrast to human and canine IFN-α subtypes, most mink IFN-α subtypes contained two N-glycosylation sites. We expressed and purified 13 mink IFN-α subtypes in Escherichia coli. The cytopathic effect inhibition assay showed that all the 13 recombinant mink IFN-α subtypes inhibited the propagation of vesicular stomatitis virus in WISH cells, with IFN-α2 and IFN-α12 demonstrating the highest activities. Furthermore, recombinant mink IFN-α2 and IFN-α12 significantly suppressed the propagation of canine distemper virus in Vero cells, with IFN-α2 demonstrating the highest activity. Conclusions We identified the mink IFN-α2 subtype as a promising candidate for the development of effective antiviral drugs.