Observation of the Exotic 0_{2}

We report here the first observation of the 0_{2}^{+} state of ^{8}He, which has been predicted to feature the condensatelike α+^{2}n+^{2}n cluster structure. We show that this state is characterized by a spin parity of 0^{+}, a large isoscalar monopole transition strength, and the emission of a strongly correlated neutron pair, in line with theoretical predictions. Our finding is further supported by the state-of-the-art microscopic α+4n model calculations. The present results may lead to new insights into clustering in neutron-rich nuclear systems and the pair correlation and condensation in quantum many-body systems under strong interactions.

[Morphological and molecular identification of trematode isloates from laying ducks in Nanchang City].

OBJECTIVE: To identify the species of trematodes isolated from laying ducks in Nanchang City using morphological and molecular approaches. METHODS: Trematodes were isolated from the hepatobiliary duct, gallbladder and large intestine of market-sold laying ducks in Nanchang City. Following morphological characterization, total DNA was extracted from all trematode specimens, and internal transcribed spacer region (ITS) and cytochrome C oxidase subunit 1 (Cox1) genes were amplified using PCR assay and sequenced. Sequence alignment was performed using the Blast software, and homology and phylogenetic analyses were done in the trematode isolates based on ITS and Cox1 gene sequences. RESULTS: The morphological characteristics of two trematode isolates from the large intestine of laying ducks were similar to those of Echinostoma revolutum and E. miyagawai, and the morphological characteristics of eight trematode samples isolated from the hepatobiliary duct and gallbladder of laying ducks were similar to those of Amphimerus anatis. The ITS and Cox1 gene sequences of the two trematode isolates from the large intestine of laying ducks had 99.3% and 98.9%-99.4% homology with E. miyagawai, and the phylogenetic analysis showed that two trematode isolates had the closest genetic relationship with E. miyagawai based on ITS and Cox1 gene sequences. The ITS gene sequences of eight trematode isolates from the hepatobiliary duct and gallbladder of laying ducks shared 95.1%-95.5% with Opisthorchis sudarikovi and Clonorchis sinensis, while the Cox1 gene sequences of eight trematode isolates from the hepatobiliary duct and gallbladder of laying ducks shared 86.3%-86.4% and 85.5%-85.7% with O. viverrini and O. sudarikovi. ITS gene sequence-based phylogenetic analysis showed that the duck-derived trematode isolates had the closest genetic relationship with C. sinensis, and Cox1 gene sequence-based phylogenetic analysis showed that the duck-derived trematode isolates had the closest genetic relationship with Metorchis orientalis and O. viverrini. CONCLUSIONS: The trematode isolates from the large intestine of laying ducts in Nanchang City may be E. miyagawai, and the trematode isolates from the hepatobiliary duct and gallbladder may be an unidentified trematode species of the family Opisthorchiidae.

[Risk factors associated with acute kidney injury caused by pesticide poisoning].

Objective: To analyze the clinical characteristics of pesticide poisoning patients and explore the risk factors of acute kidney injury (AKI) . Methods: In September 2020, the clinical data of 155 patients with pesticide poisoning in the department of nephropathy, the Affiliated Hospital of Southwest Medical University from September 2018 to August 2020 were retrospectively analyzed. The patients were divided into AKI group (44 cases) and non AKI group (111 cases) according to the occurrence of AKI. The clinical characteristics, organ or system involvement and auxiliary examination results of the two groups were analyzed. Logistic regression was used to analyze the risk factors of AKI in patients with pesticide poisoning. Results: The types of pesticides causing poisoning mainly included herbicides, insecticides and biochemical pesticides. Compared with non AKI group, patients in AKI group had higher proportion of blood purification treatment and ICU monitoring treatment (P<0.05) , and were more likely to be complicated with acute respiratory failure, pulmonary fibrosis, myocardial injury, multiple organ dysfunction syndrome (MODS) , acute pancreatitis and coagulation abnormalities (P<0.05) . The mortality of AKI group (18.2%, 8/14) was significantly higher than that of non AKI group (0.9%, 1/111) (P<0.05) . Univariate analysis showed that the time from poisoning to treatment > 6 h, high WBC count, neutrophil count, alanine aminotransferase, aspartate aminotransferase, high sensitive troponin T, myoglobin and creatine kinase isoenzyme were the risk factors of AKI in patients with pesticide poisoning (P<0.05) . Multivariate logistic regression analysis showed that the time from poisoning to treatment >6 h was an independent risk factor for AKI in patients with pesticide poisoning (P<0.05) . Conclusion: The mortality of AKI secondary to pesticide poisoning is high. Attention should be paid to the time from poisoning to treatment, inflammatory state and changes of liver and myocardial function.

Immunoglobulin G galactosylation levels are decreased in systemic sclerosis patients and differ according to disease subclassification.

Objectives: Scleroderma is a connective tissue immune disease that features collagen overproduction and can be categorized into two subtypes, localized scleroderma (LSc) and systemic sclerosis (SSc). SSc is clinically classified into two subsets: limited cutaneous (lcSSc) and diffuse cutaneous (dcSSc) SSc. The immunoglobulin G-galactosylation (IgG-Gal) ratio is abnormal in a number of immune diseases and has not been evaluated in SSc.Method: The study recruited 93 LSc patients, 298 SSc patients, and 436 healthy controls. N-glycans of purified IgG were obtained from plasma and detected by tandem mass spectrometry. The IgG-Gal ratio was measured by calculating the relative intensities of agalactosylated (G0), monogalactosyl (G1), and digalactosyl (G2) N-glycans according to the formula G0/(G1 + G2 × 2). Furthermore, we examined whether the IgG-Gal ratio differed between different subtypes of SSc.Results: The IgG-Gal ratio was significantly higher in SSc patients (1.139 ± 0.870) than in LSc patients (0.485 ± 0.280) and controls (0.395 ± 0.190). The IgG-Gal ratio successfully distinguished SSc patients from LSc and controls (area under the curve = 0.88 and 0.81, respectively). The IgG-Gal ratio was significantly higher in dcSSc patients than in lcSSc patients and increased along with increases in modified Rodnan skin score (p = 6.03 × 10-5, Pearson's coefficient = 0.26) and erythrocyte sedimentation rate (p = 2.95 × 10-10, Pearson's coefficient = 0.38).Conclusion: IgG-Gal ratios were abnormal in SSc patients and were associated with disease severity. The IgG-Gal ratio therefore shows potential as a biomarker for the diagnosis of SSc.

Investigation of Streptococcus agalactiae using pcsB-based LAMP in milk, tilapia and vaginal swabs in Haikou, China.

AIMS: To develop a pcsB-based Loop-mediated isothermal amplification (LAMP) method for the detection of Streptococcus agalactiae (GBS) in milk, tilapia and vaginal swabs. METHODS AND RESULTS: The sensitivity of the LAMP method using real-time turbidity monitoring was 1 pg of template within 1 h at 64°C, 100-fold higher than conventional PCR. The sensitivity of visual detection dropped an order of magnitude using SYBR Green I or hydroxynaphthol blue. The validity of the visual LAMP assay was assessed by the detection of GBS in 180 vaginal swabs from one hospital, 14 brain tissues samples of diseased tilapias from two fishponds and fresh milk of 67 dairy cattle from one farm. In total, 17 samples (4 vaginal swabs, 13 tilapia brain tissues but no milk sample) tested positive for GBS. Subsequent bacterial identification confirmed the specificity and reliability of the LAMP method. Molecular serotyping and multilocus sequence typing demonstrated that all 13 tilapia GBS isolates were identical (serotype Ia, ST7), whereas the four human GBS isolates were more diverse and could be classified into two serotypes (Ia, III) and four sequence types (ST19, ST23, ST24, ST862). Virulence gene testing showed that only the bac, rib and lmb genes were not present in all isolates. Antimicrobial susceptibility profiles of the isolates were basically consistent with their genotypes, except for sulphonamide and fluoroquinolone. CONCLUSIONS: We developed a reliable pcsB-based LAMP assay for GBS detection. Our results demonstrated that the prevalence of GBS was 92·9% among diseased tilapia, 2·2% among female patients and 0% on a dairy farm in Hainan. SIGNIFICANCE AND IMPACT OF THE STUDY: The pcsB-based LAMP method is suitable for GBS detection and contains great potential of application in dairy industry, aquiculture and clinical.

Three species of Aeromonas (A. dhakensis, A. hydrophila and A. jandaei) isolated from freshwater crocodiles (Crocodylus siamensis) with pneumonia and septicemia.

Hundreds of farmed Siamese crocodiles (Crocodylus siamensis) died during July 2016 at a farm in Wenchang, Hainan, China. In two necropsied crocodiles, we observed symptoms of dermatorrhagia, hepatomegaly and hepatic congestion. Pulmonitis was diagnosed by pulmonary congestion and pulmonary fibrinous exudate. Septicaemia was diagnosed by isolation of three Aeromonas species from blood and visceral tissues; A. dhakensis, A. hydrophila and A. jandaei were identified by biochemical and molecular tests. We used a zebrafish model to determine the half-maximal lethal dose (LD50 ), and A. dhakensis was found to be the most virulent species, with an LD50 of 8·91 × 105 CFU per ml. The results of a drug sensitivity test indicated that these species were sensitive to 11 antibiotics. This is the first report of A. dhakensis, A. hydrophila and A. jandaei being isolated from a mixed infection in Siamese crocodiles. SIGNIFICANCE AND IMPACT OF THE STUDY: In this study, we isolated three species of Aeromonas (A. dhakensis, A. hydrophila and A. jandae) from farmed Siamese crocodiles with fatal fibrinous pneumonia and septicaemia. This is the first description of a mixed infection with three Aeromonas species among captive crocodilians.

[Long-term outcomes after cataract surgery in infants with congenital cataract].

Objective: To observe the long-term outcomes after congenital cataract surgery performed prior to 36 months of age. Methods: A retrospective case study was conducted. Thirty-two cases (57 eyes) of congenital cataract were included from January 2004 to January 2012. All patients received intraocular lens (IOL) implantation with posterior continuous curvilinear capsulorhexies and anterior vitrectomy after cataract extraction and were followed up. At the last visit, the best corrected visual acuity (BCVA) was determined and postoperative complications were evaluated during follow-up with a longest time of 13 years. Non-normal distribution showed in median M (minimum and maximum). Data were analyzed by Kruskal Wallis single factor variance analysis and multiple comparison. The independent Mann-Witney U test was used to analyze non-normal distribution data. Results: There were thirty-two cases (57 eyes) of congenital cataract including 7 unilateral cases and 25 bilateral cases. The median age at cataract extraction was 6.0months; the median IOL implantation age was 28.0 months and the median duration of follow-up after cataract extraction was 67.0 months. The median postoperative BCVA was (LogMAR) 0.52. Unilateral and bilateral cataract postoperative BCVA difference had no statistical significance (U=107, P>0.05). Patients received cataract surgery in 2 to 4 months, the postoperative BCVA was better than in 5 to 8 months. The difference was statistical significance (H=-15.33, P<0.05). BCVA after IOL implantation before 24 months were significantly better than after 30 months. The difference had statistical significance(H=-20.61,-20.78, P<0.05). Postoperative complications were posterior capsular opacity (5 eyes; 8.77%), glaucoma (2 eyes; 3.51%), strabismus (17 eyes; 29.82%) and nystagmus (30 eyes; 52.63%). Conclusions: Most infantile cataract surgeries performed prior to 36 mouths of life together with the implantation of IOL can achieve good visual acuity. No serious complications occurred. (Chin J Ophthalmol, 2017, 53: 266-273).

Molecular identification of hemoplasma and piroplasma species from Rattus edwardsi based on sequences analysis of ribosomal DNA, China.

The present study provides the first report on the molecular epidemiological data regarding infection by hemoplasma and piroplasma species in wild Rattus edwardsi, from China. In the current study, blood samples were investigated from 32 wild Rattus edwardsi from Hunan (23) and Guangxi (9) provinces, China. The prevalence of hemoplasma and piroplasma was 65.63% (21/32) and 6.25% (2/32), respectively. Phylogenetic analyses indicated that hemoplasmas (HQ183731, HQ183732) derived from wild Rattus edwardsi in China, can be grouped into a solitary clade closely related to H. muris (HMU82963) and M. haemomuris (AB758435). In addition, it was shown that piroplasmas from this study have very close genetic distance to other unidentified piroplasma species isolated from China (AB242140) and Japan (AB188086). The results suggested that hemoplasmas isolated in this study should be represented as a new genotype. Piroplasmas on the other hand needs more sequenced samples in its life-cycle and evidence to check its taxonomic status. These data may have important implications for researching on the epidemiology and population biology as well as for studying the taxonomy status of hemoplasmas and piroplasmids of wild rodents.

Failed cooperative, but not competitive, interaction between large-scale brain networks impairs working memory in schizophrenia.

BACKGROUND: A large-scale network named the default mode network (DMN) dynamically cooperates and competes with an external attention system (EAS) to facilitate various cognitive functioning that is prominently impaired in schizophrenia. However, it is unclear whether the cognitive deficit in schizophrenia is related to the disrupted competition and/or cooperation between these two networks. METHOD: A total of 35 schizophrenia patients and 30 healthy controls were scanned using gradient-echo echo-planar imaging during n-back working memory (WM) processing. Brain activities of the DMN and EAS were measured using general linear modelling of the functional magnetic resonance imaging data. Dynamic interaction between the DMN and EAS was decomposed into two directions using Granger causality analysis. RESULTS: We observed a significant failure of DMN suppression in patients with schizophrenia, which was significantly related to WM/attentional deficit. Granger causality modelling showed that in healthy controls, while the EAS inhibitorily influenced the DMN, the DMN exerted an 'excitatory' or cooperative influence back on the EAS, especially in those with lower WM accuracy. In schizophrenia, this 'excitatory' DMN→EAS influence within the reciprocal EAS-DMN loop was significantly reduced, especially in patients with WM/attentional deficit. CONCLUSIONS: The dynamic interaction between the DMN and EAS is likely to be comprised of both competitive and cooperative influences. In healthy controls, both the 'inhibitory' EAS→DMN interaction and 'excitatory' DMN→EAS interaction are correlated with WM performance. In schizophrenia, reduced 'cooperative' influence from the DMN to dorsal nodes of the EAS occurs in the context of non-suppression of the DMN and may form a possible pathophysiological substrate of WM deficit and attention disorder.

GATA4 represses an ileal program of gene expression in the proximal small intestine by inhibiting the acetylation of histone H3, lysine 27.

GATA4 is expressed in the proximal 85% of small intestine where it promotes a proximal intestinal ('jejunal') identity while repressing a distal intestinal ('ileal') identity, but its molecular mechanisms are unclear. Here, we tested the hypothesis that GATA4 promotes a jejunal versus ileal identity in mouse intestine by directly activating and repressing specific subsets of absorptive enterocyte genes by modulating the acetylation of histone H3, lysine 27 (H3K27), a mark of active chromatin, at sites of GATA4 occupancy. Global analysis of mouse jejunal epithelium showed a statistically significant association of GATA4 occupancy with GATA4-regulated genes. Occupancy was equally distributed between down- and up-regulated targets, and occupancy sites showed a dichotomy of unique motif over-representation at down- versus up-regulated genes. H3K27ac enrichment at GATA4-binding loci that mapped to down-regulated genes (activation targets) was elevated, changed little upon conditional Gata4 deletion, and was similar to control ileum, whereas H3K27ac enrichment at GATA4-binding loci that mapped to up-regulated genes (repression targets) was depleted, increased upon conditional Gata4 deletion, and approached H3K27ac enrichment in wild-type control ileum. These data support the hypothesis that GATA4 both activates and represses intestinal genes, and show that GATA4 represses an ileal program of gene expression in the proximal small intestine by inhibiting the acetylation of H3K27.

Conditional ablation of Gata4 and Fog2 genes in mice reveals their distinct roles in mammalian sexual differentiation.

Assembly of functioning testis and ovary requires a GATA4-FOG2 transcriptional complex. To define the separate roles for GATA4 and FOG2 proteins in sexual development of the testis we have ablated the corresponding genes in somatic gonadal cells. We have established that GATA4 is required for testis differentiation, for the expression of Dmrt1 gene, and for testis cord morphogenesis. While Sf1Cre-mediated excision of Gata4 permitted normal expression of most genes associated with embryonic testis development, gonadal loss of Fog2 resulted in an early partial block in male pathway and sex reversal. We have also determined that testis sexual differentiation is sensitive to the timing of GATA4 loss during embryogenesis. Our results now demonstrate that these two genes also have non-overlapping essential functions in testis development.

The occurrence of the feline "Candidatus Mycoplasma haemominutum" in dog in China confirmed by sequence-based analysis of ribosomal DNA.

In the present study, polymerase chain reaction (PCR) assay was used to detect haemoplasmas (haemotropic bacteria) in 40 clinically healthy pet dogs in Foshan city, Guangdong Province, China, and one dog was found positive. Comparison of its 16S ribosomal DNA (rDNA) sequence with relevant sequences showed that the isolated haemoplasma had greater sequence identity to feline species "Candidatus Mycoplasma haemominutum" (99%) than to "Candidatus Mycoplasma haematoparvum" (95%). This result, for the first time, indicates the presence of the feline "Candidatus Mycoplasma haemominutum" in Chinese dogs and it represents the first survey of its kind in China by using PCR assay. The results indicated that dog may represent one of the hosts for the feline "Candidatus Mycoplasma haemominutum".

Therapeutic neovascularization for peripheral arterial diseases: advances and perspectives.

Recently, with the better understanding of the mechanisms of neovascularization, many new therapeutic approaches to enhance neovascularization have emerged. Of these diverse emerging methods, use of growth factors and cells are the two major ones. This review will provide an update on the present understanding of the basic mechanisms of angiogenesis, vasculogenesis, and arteriogenesis, as a basis for designing future pro-neovascularization treatments. Several angiogenic factors including vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) have been implicated in augmenting the neovascularization process. However, single growth factors are not sufficient to generate functional vessels. In synergistic or complementary manner, these factors may be used in harmony to form long-term functional vessels. Cell therapy has the potential to supply stem/progenitor cells and multiple angiogenic factors to the region of ischemia. However, the efficacy of stem cells transplantation may be impaired by low survival rate, insufficient cell number and impaired function in aging and diseases. Combination of cells or cells primed with growth factor(s) or genetic modification may augment the therapeutic efficacy. This paper reviews critical literature in depth to elucidate the mechanism of therapeutic neovascularization, angiogenic factor therapy and cell transplantation. Based on past experience and actual knowledge, we propose future strategies for clinical application and discuss the problems and controversies that need to be addressed in order to fully exploit the potential of growth factors and/or cell transplantation with clinical relevance.

Chaperoning of estrogen receptor and induction of mammary gland proliferation by neuronal protein synuclein gamma.

Synucleins are emerging as central players in the formation of pathologically insoluble deposits characteristic of neurodegenerative diseases. However, synuclein gamma (SNCG), previously identified as a breast cancer specific gene (BCSG1), is also highly associated with breast cancer progression. Using transgenic mouse model, we demonstrated a role of SNCG in induction of highly proliferative pregnancy-like phenotype of mammary epithelial cells and branching morphology. SNCG participated in the heat shock protein-based multiprotein chaperone complex for steroid receptor signaling. Expression of SNCG in mammary epithelium resulted in a significant stimulation of ERalpha transcriptional activity. SNCG-induced mammary gland proliferation can be effectively blocked by antiestrogen and ovariectomy, indicating that the induced proliferation is mediated by ERalpha signaling and requires estrogen stimulation. These data indicate the chaperone activity of SNCG on stimulation of steroid receptor signaling in mammary gland and, thus induces extensive mammary gland proliferation and contributes to the hormonal impact on mammary tumorigenesis.

Evaluation of the role of I(KACh) in atrial fibrillation using a mouse knockout model.

OBJECTIVES: We sought to study the role of I(KACh) in atrial fibrillation (AF) and the potential electrophysiologic effects of a specific I(KACh) antagonist. BACKGROUND: I(KACh) mediates much of the cardiac responses to vagal stimulation. Vagal stimulation predisposes to AF, but the specific role of I(KACh) in the generation of AF and the electrophysiologic effects of specific I(KACh) blockade have not been studied. METHODS: Adult wild-type (WT) and I(KACh)-deficient knockout (KO) mice were studied in the absence and presence of the muscarinic receptor agonist carbachol. The electrophysiologic features of KO mice were compared with those of WT mice to assess the potential effects of a specific I(KACh) antagonist. RESULTS: Atrial fibrillation lasting for a mean of 5.7+/-11 min was initiated in 10 of 14 WT mice in the presence of carbachol, but not in the absence of carbachol. Atrial arrhythmia could not be induced in KO mice. Ventricular tachyarrhythmia could not be induced in either type of mouse. Sinus node recovery times after carbachol and sinus cycle lengths were shorter and ventricular effective refractory periods were greater in KO mice than in WT mice. There was no significant difference between KO and WT mice in AV node function. CONCLUSIONS: Activation of I(KACh) predisposed to AF and lack of I(KACh) prevented AF. It is likely that I(KACh) plays a crucial role in the generation of AF in mice. Specific I(KACh) blockers might be useful for the treatment of AF without significant adverse effects on the atrioventricular node or the ventricles.

[Diagnostic and differential diagnostic potential of mitochondrial DNA assessment in patients with Leber's hereditary optic neuropathy].

OBJECTIVE: To study the primary mutations of mitochondrial DNA (mtDNA) associated with Leber's hereditary optic neuropathy (LHON) in patients with optic neuropathy. METHODS: Seventy-nine patients with a variety of bilateral optic neuropathy were examined. Mutations at np 3,460, np 11,778 and np 14,484 of mtDNA were tested by PCR-restriction fragment length polymorphism technique to detect DNA in peripheral blood. The samples were taken from 16 cases of clinically diagnosed LHON, 44 cases of suspected LHON, two cases of alcohol amblyopia, four cases of multiple sclerosis, five cases of autosomal dominant hereditary optic atrophy, 4 cases with primary open-angle glaucoma, three cases of spinocerebellar degeneration, and one case of ethambutol-induced optic neuropathy. RESULTS: The mutation at np 11,778 was identified in 31 cases (39.2%), consisting of all the 16 clinically diagnosed LHON cases, thirteen cases (29.5%) of the suspected LHON, and the two cases of alcohol amblyopia. The remaining 48 cases were negative for mtDNA mutations at np 3,460, np 11,778, or np 14,484. CONCLUSION: Assessment of mtDNA provides a useful diagnostic aid in confirming and excluding the diagnosis of LHON, particularly useful in cases without a family hereditary history and cases with cause unknown bilateral optic neuritis.

ICln is essential for cellular and early embryonic viability.

pICln is a 26-kDa protein that is ubiquitously expressed and highly conserved from Xenopus laevis to Homo sapiens. The physiological functions of pICln remain to be established. To address this question, we disrupted the ICln gene in embryonic stem cells. We found that murine embryos lacking ICln die early in gestation (between stages E3.5 and E7.5). Furthermore, we found that ICln is essential for embryonic stem cell viability. Previously, we showed that pICln interacts directly with a homolog of a yeast protein that binds a PAK-like kinase and participates in the regulation of cell morphology and cell cycling. pICln also forms a complex with several core spliceosomal proteins, and this interaction may play a role in the regulation of spliceosomal biogenesis. Collectively, these data strongly suggest that pICln participates in critical cellular pathways, including regulation of the cell cycle and RNA processing.

Diagnostic potential of mitochondrial DNA assessment in patients with optic neuropathy.

OBJECTIVE: To study the primary mutations of mitochondrial DNA (mtDNA) associated with Leber's hereditary optic neuropathy (LHON) in patients with optic neuropathy. METHODS: Seventy-nine patients with a variety of bilateral optic neuropathies were examined. Mutations at np3460, np11,778 and np14,484 of mtDNA were tested by PCR-restriction detection in peripheral blood DNA from 16 cases of clinically probable LHON, 44 cases of possible LHON, 2 cases of alcohol amblyopia, 4 cases of multiple sclerosis, 5 cases of autosomal dominant optic atrophy, 4 cases of primary open-angle glaucoma, 3 cases of spinocerebellar degeneration, and 1 case of ethambutol-induced optic neuropathy. RESULTS: The mutation at np11778 was identified in 31 cases (39.2%) to establish LHON, which consisted of: all 16 of clinically probable LHON cases, 13 cases (29.5%) of possible LHON, and 2 cases of alcohol amblyopia. The remaining 48 cases were negative for mtDNA mutations at np3460, np11 778, and np14,484. CONCLUSION: Assessment of mtDNA provides a useful diagnostic aid in the definition and exclusion of LHON, in particular family history-negative, otherwise undefined bilateral optic nerve inflammatory disease.

pICln inhibits snRNP biogenesis by binding core spliceosomal proteins.

The U1, U2, U4, U5, and U6 small nuclear ribonucleoproteins (snRNPs) form essential components of spliceosomes, the machinery that removes introns from pre-mRNAs in eukaryotic cells. A critical initial step in the complex process of snRNP biogenesis is the assembly of a group of common core proteins (Sm proteins) on spliceosomal snRNA. In this study we show by multiple independent methods that the protein pICln associates with Sm proteins in vivo and in vitro. The binding of pICln to Sm proteins interferes with Sm protein assembly on spliceosomal snRNAs and inhibits import of snRNAs into the nucleus. Furthermore, pICln prevents the interaction of Sm proteins with the survival of motor neurons (SMN) protein, an interaction that has been shown to be critical for snRNP biogenesis. These findings lead us to propose a model in which pICln participates in the regulation of snRNP biogenesis, at least in part by interfering with Sm protein interaction with SMN protein.