Genome-Wide Identification and Expression Analyses of the FAR1/FHY3 Gene Family Provide Insight into Inflorescence Development in Maize.

As transcription factors derived from transposase, FAR-RED IMPAIRED RESPONSE1 (FAR1) and its homolog FHY3 play crucial roles in the regulation of light signaling and various stress responses by coordinating the expression of downstream target genes. Despite the extensive investigation of the FAR1/FHY3 family in Arabidopsis thaliana and other species, a comprehensive examination of these genes in maize has not been conducted thus far. In this study, we employed a genomic mining approach to identify 16 ZmFAR1 genes in the maize inbred line B73, which were further classified into five subgroups based on their phylogenetic relationships. The present study characterized the predicted polypeptide sequences, molecular weights, isoelectric points, chromosomal distribution, gene structure, conserved motifs, subcellular localizations, phylogenetic relationships, and cis-regulatory elements of all members belonging to the ZmFAR1 family. Furthermore, the tissue-specific expression of the 16 ZmFAR1 genes was analyzed using RNA-seq, and their expression patterns under far-red light conditions were validated in the ear and tassel through qRT-qPCR. The observed highly temporal and spatial expression patterns of these ZmFAR1 genes were likely associated with their specific functional capabilities under different light conditions. Further analysis revealed that six ZmFAR1 genes (ZmFAR1-1, ZmFAR1-10, ZmFAR1-11, ZmFAR1-12, ZmFAR1-14, and ZmFAR1-15) exhibited a response to simulated shading treatment and actively contributed to the development of maize ears. Through the integration of expression quantitative trait loci (eQTL) analyses and population genetics, we identified the presence of potential causal variations in ZmFAR1-14 and ZmFAR1-9, which play a crucial role in regulating the kernel row number and kernel volume weight, respectively. In summary, this study represents the initial identification and characterization of ZmFAR1 family members in maize, uncovering the functional variation in candidate regulatory genes associated with the improvement of significant agronomic traits during modern maize breeding.

A new glance at autophagolysosomal-dependent or -independent function of transcriptional factor EB in human cancer.

Autophagy-lysosome system plays a variety of roles in human cancers. In addition to being implicated in metabolism, it is also involved in tumor immunity, remodeling the tumor microenvironment, vascular proliferation, and promoting tumor progression and metastasis. Transcriptional factor EB (TFEB) is a major regulator of the autophagy-lysosomal system. With the in-depth studies on TFEB, researchers have found that it promotes various cancer phenotypes by regulating the autophagolysosomal system, and even in an autophagy-independent way. In this review, we summarize the recent findings about TFEB in various types of cancer (melanoma, pancreatic ductal adenocarcinoma, renal cell carcinoma, colorectal cancer, breast cancer, prostate cancer, ovarian cancer and lung cancer), and shed some light on the mechanisms by which it may serve as a potential target for cancer treatment.

Hernandezine induces autophagic cell death in human pancreatic cancer cells via activation of the ROS/AMPK signaling pathway.

Hernandezine (Her) is a bisbenzylisoquinoline alkaloid extracted from the traditional Chinese herbal medicine Thalictrum glandulosissimum. Evidence shows that Her is a natural agonist of adenosine monophosphate (AMP)-activated protein kinase (AMPK) and induces apoptosis and autophagy in tumor cells. In this study, we investigated the role of autophagy in Her-induced cell death in human pancreatic cancer cell lines. We showed that Her dose-dependently suppressed cell proliferation, promoted autophagy and induced autophagic death in pancreatic ductal adenocarcinoma (PDAC) cell lines Capan-1 and SW1990. The IC50 values of Her in inhibition of Capan-1 and SW1990 cells were 47.7 µM and 40.1 µM, respectively. Immunoblotting showed that Her (1-40 µM) promoted the conversion of LC3-I to LC3-II, and Her exerted concentration-dependent and time-dependent effects on autophagy activation in PDAC cells. In transmission electron microscopy and fluorescence image analysis, we found that autophagic vacuoles were significantly increased in Her-treated cells. Knockdown of ATG5, a key gene in the autophagy pathway, alleviated the activation of autophagy by Her. These results demonstrated that Her induced autophagy in PDAC cells. Intensely activated autophagy could promote cell death. The autophagy inhibitors, BafA1 and HCQ significantly inhibited Her-induced cell death, implying that Her induced autophagic cell death in PDAC cells. Moreover, we showed that Her activated autophagy by increasing the phosphorylation of AMPK and decreasing the phosphorylation of mTOR/p70S6K. Knockdown of AMPKα relieves the autophagic cell death induced by Her. Furthermore, Her concentration-dependently enhanced reactive oxygen species (ROS) generation in PDAC cells. Antioxidants could reduce the phosphorylation of AMPK and suppress autophagic cell death induced by Her. Our study provides evidence for the development of Her as a therapeutic agent for the treatment of pancreatic cancer.

AVL9 promotes colorectal carcinoma cell migration via regulating EGFR expression.

BACKGROUND: Despite advanced treatments could inhibit progression of colorectal carcinoma (CRC), the recurrence and metastasis remain challenging issues. Accumulating evidences implicated that AVL9 played a vital role in human cancers, but it's biological function and mechanism in CRC remain unclear. AIM: To investigate the biological role and mechanism of AVL9 in colorectal carcinoma. RESULTS: AVL9 expression was significantly upregulated in tumor tissues than that in matched normal tissues both at mRNA and protein levels. High expression of AVL9 was closely correlated with M status, stages and poor prognosis of colorectal carcinoma (CRC) patients. Functionally, AVL9 overexpression promoted cell migration rather than cell proliferation in vitro, whereas AVL9 knockdown exhibited the contrary results. Mechanistically, AVL9 regulated EGFR expression, and knockdown of EGFR restrained AVL9-induced cell migration. CONCLUSION: These findings demonstrated that AVL9 contributed to CRC cell migration by regulating EGFR expression, suggesting a potential biomarker and treatment target for CRC.

Tubulin colchicine site binding agent LL01 displays potent antitumor efficiency both in vitro and in vivo with suitable drug-like properties.

Through rational drug design, we previously identified an indenoprazole derivative, 2-(6-ethoxy-3-(3-ethoxyphenylamino)-1-methyl-1,4-dihydroindeno[1,2-c]pyrazol-7-yloxy)acetamide (LL01), as a potent tubulin polymerization inhibitor targeting the tubulin colchicine binding site. In this study, we further demonstrated that LL01 was not a P-gp substrate. It potently inhibited the growth of a variety of tumor cells, including those with multidrug resistance, with GI50 values in the low nanomole ranges. In vitro liver microsome stability assay, LL01 was modest stable in the liver microsomes of human, mouse and rat, but was fast metabolized in dog. After single oral administration of LL01 at a dose of 10 mg/kg in SD male rats, LL01 showed acceptable PK properties with a mean bioavailability of 41%. In human HepG2 hepatoma xenograft, at the oral doses of 25 mg/kg/day and 12.5 mg/kg/day, LL01 inhibited the tumor growth by 61.27%, and 43.74%, respectively, which is much better than the positive drug sorafenib (29.45%; 30 mg/kg/day). Therefore, LL01 might be a potential drug candidate for further investigation for hepatocellular carcinoma therapy.

Transparent organic light-emitting diodes with balanced white emission by minimizing waveguide and surface plasmonic loss.

It is challenging in realizing high-performance transparent organic light-emitting diodes (OLEDs) with symmetrical light emission to both sides. Herein, an efficient transparent OLED with highly balanced white emission to both sides is demonstrated by integrating quasi-periodic nanostructures into the organic emitter and the metal-dielectric composite top electrode, which can simultaneously suppressing waveguide and surface plasmonic loss. The power efficiency and external quantum efficiency are raised to 83.5 lm W-1 and 38.8%, respectively, along with a bi-directional luminance ratio of 1.26. The proposed scheme provides a facile route for extending application scope of transparent OLEDs for future transparent displays and lightings.

Light outcoupling enhanced flexible organic light-emitting diodes.

Flexible organic light-emitting diodes (OLEDs) are emerging as a leading technology for rollable and foldable display applications. For the development of high-performance flexible OLEDs on plastic substrate, we report a transparent nanocomposite electrode with superior mechanical, electrical, and optical properties, which is realized by integrating the nanoimprinted quasi-random photonic structures into the ultrathin metal/dielectric stack to collectively optimize the electrical conduction and light outcoupling capabilities. The resulting flexible OLEDs with green emission yield the enhanced device efficiency, reaching the maximum external quantum efficiency of 43.7% and luminous efficiency of 154.9 cd/A, respectively.

[Expression of vasoactive intestinal peptide in peripheral blood of children with hand, foot and mouth disease].

OBJECTIVE: To investigate the expression of vasoactive intestinal peptide (VIP) in peripheral blood of children with hand, foot and mouth disease and its significance. METHODS: According to the condition of the disease, 86 children with hand, foot and mouth disease were classified into phase 1 group (19 children) and phase 2 group (67 children). ELISA was used to measure the concentrations of plasma VIP, interferon-γ (IFN-γ), and interleukin-4 (IL-4) in peripheral blood. Flow cytometry was used to measure CD3+, CD4+, and CD8+ T lymphocyte subsets. RT-PCR was used for qualitative detection of enterovirus 71 (EV71) RNA in stool. RESULTS: Compared with the phase 1 group, the phase 2 group had a significantly higher positive rate of EV71-RNA (P<0.05) and significantly higher serum levels of IgG, IgA, IgM, and C3 (P<0.05). The phase 2 group had significantly lower proportions of peripheral CD3+, CD4+, and CD8+ T lymphocyte subsets than the phase 1 group (P<0.05), as well as significantly lower proportion of peripheral B cells and CD4+/CD8+ ratio than the phase 1 group (P<0.05). The phase 2 group also had a significantly lower concentration of VIP in peripheral blood than the phase 1 group (P<0.05). In the 86 children with hand, foot and mouth disease, the concentration of VIP in peripheral blood was positively correlated with the proportion of CD4+ T lymphocyte subset and CD4+/CD8+ ratio (r=0.533 and 0.532 respectively; P<0.05). CONCLUSIONS: VIP may be an important marker of the severity of hand, foot and mouth disease.

Highly regioselective synthesis of 3-alkenyl-oxindole ring-fused 3,3'-disubstituted oxindoles via direct gamma-substitution of Morita-Baylis-Hillman carbonates of isatins with 3-substituted oxindoles.

The first phase transfer-catalysed direct γ-substitution of Morita-Baylis-Hillman carbonates of isatins with 3-substituted oxindoles has been developed, which affords 3-alkenyl-oxindole ring-fused 3,3'-disubstituted oxindoles in up to 83% yield under mild reaction conditions. Furthermore, their biological activity has been preliminarily demonstrated by in vitro evaluation against human prostate cancer cells PC-3 and human leukemia cells K562, using MTT-based assays with the commercially available standard drug Cisplatin as a positive control. Gratifyingly, compounds 3aa, 3ba and 3ca exhibited comparable in vitro inhibitory activities against human prostate cancer cells (PC-3) to Cisplatin. What's more, 3ba also had a good inhibition ability against human leukemia cells K562. These results indicate that 3-alkenyl-oxindole ring-fused 3,3'-disubstituted oxindole analogs may be potential lead compounds for further biological screening.

Primary repair of broad bilateral complete cleft palate with hard palate rotation flap.

It was hard to achieve primary repair for infants with broad bilateral complete cleft palate, and usually multiple procedures are demanded, resulting in multiple injuries and scar hyperplasia, which could influence infants' long-term phonetic function. In this study, primary repair was carried out on 12 cases of 18- to 30-month-old infants who had complete cleft palate by using rotated hard palate flap with a pedicle on the edge of the fissure modified on the basis of traditional von Langenbeck palatoplasty. Eight infants were subjected to initial phonetic sound evaluation at 1 to 2 years after the operation. All the 12 cases of infant complete cheilopalatognathus had fine healing, and no complications such as dyspnea and fistulous opening in palate were observed. The effects of phonetic sound in 8 infants who had this disease were significantly improved as observed in the long-term follow-up. Thus, we consider it as a reliable and feasible procedure to perform hard palate mucosa rotation flap for the primary repair of broad bilateral complete cleft palate. The procedure is simple, while it produces satisfactory therapeutic effects, by which the patients with complete cleft palate could achieve good recovery in their phonetic functions.

Comparing the survival rates of patients with stage IIIC endometrial cancer undergoing sandwich therapy to those undergoing sequential chemotherapy and radiotherapy: a meta-analysis.

BACKGROUND: The use of additional treatment after surgery for stage IIIC endometrial cancer (EC) according to the Federation of Gynecology and Obstetrics (FIGO) is still a topic of discussion. This meta-analysis examined the effects of sandwich treatment and sequential treatment on the survival of individuals diagnosed with stage IIIC EC. METHODS: We examined the literature from various databases regarding the overall survival (OS) and adverse effects of the two additional therapies following surgery in individuals diagnosed with stage IIIC EC. Revman 5.4.1 was utilized to combine hazard ratios (HR) and their corresponding 95% confidence intervals (95% CI) for OS and toxicities. RESULTS: The findings comprised of five retrospective investigations involving a combined total of 800 individuals. The patients who underwent sandwich treatment did not demonstrate a notable improvement in survival rates over a period of 3 years. Upon eliminating the impact of extensive samples, it was discovered that sandwich therapy exhibited a superior 5-year overall survival compared to patients receiving sequential therapy. The effectiveness of sandwich therapy was superior to sequential therapy in terms of a 3-year OS for non-endometrioid histology, although the outcome did not reach statistical significance. The toxicities of both treatments were similar. CONCLUSIONS: In terms of long-term survival, sandwich therapy was found to be more advantageous than sequential therapy for patients with stage IIIC EC, with no significant disparity observed in the 3-year OS and toxicities between the two treatments. Sandwich therapy exhibited a tendency towards improved effectiveness in patients with histology other than endometrioid.

Lactate-induced protein lactylation: A bridge between epigenetics and metabolic reprogramming in cancer.

Lactate is not only an endpoint of glycolysis but is gradually being discovered to play the role of a universal metabolic fuel for energy via the 'lactate shuttle' moving between cells and transmitting signals. The glycolytic-dependent metabolism found in tumours and fast-growing cells has made lactate a pivotal player in energy metabolism reprogramming, which enables cells to obtain abundant energy in a short time. Moreover, lactate can provide favourable conditions for tumorigenesis by shaping the acidic tumour microenvironment, recruiting immune cells, etc. and the recently discovered lactate-induced lactylation moves even further on pro-tumorigenesis mechanisms of lactate production, circulation and utilization. As with other epigenetic modifications, lactylation can modify histone proteins to alter the spatial configuration of chromatin, affect DNA accessibility and regulate the expression of corresponding genes. What's more, the degree of lactylation is inseparable from the spatialized lactate concentration, which builds a bridge between epigenetics and metabolic reprogramming. Here, we review the important role of lactate in energy reprogramming, summarize the latest finding of lactylation in tumorigenesis and try to explore therapeutic strategies in oncotherapy that can kill two birds with one stone.

Regulating Charge Carrier Recombination in the Interconnecting Layer to Boost the Efficiency and Stability of Monolithic Perovskite/Organic Tandem Solar Cells.

The charge carriers of single-junction solar cells can be fluently extracted and then collected by electrodes, leading to weak charge carrier accumulation and low energy loss (Eloss ). However, in tandem solar cells (TSCs), it is a considerable challenge to obtain a balance between the densities of the holes and electrons extracted from the two respective subcells to facilitate an efficient recombination in the interconnecting layer (ICL). Herein, a charge-carrier-dynamic management strategy for inorganic perovskite/organic TSCs is proposed, centered on the simultaneous regulation of the defect states of CsPbI1.9 Br1.1 perovskite in the front subcell and hole transport ability from the perovskite to ICL. The target hole density on the perovskite surface and the hole loss before reaching the ICL are significantly improved. As a result, the hole/electron density offset in the ICL can be effectively narrowed, leading to a balanced charge carrier recombination, which reduces the Eloss in TSCs. The resulting inorganic perovskite/organic 0.062-cm2 TSC exhibits a remarkable power conversion efficiency (PCE) of 23.17% with an ultrahigh open-circuit voltage (Voc ) of 2.15 V, and the PCE of the 1.004-cm2 device (21.69%) exhibited a weak size-dependence. This charge-carrier-dynamic management strategy can also effectively enhance the operational and ultraviolet-light stabilities of the TSCs.

CTHRC1 is upregulated by promoter demethylation and transforming growth factor-ß1 and may be associated with metastasis in human gastric cancer.

The gene, collagen triple helix repeat containing 1 (CTHRC1), has been reported to increase in several kinds of human solid cancers and is associated with tumor invasion and metastasis. To date, the expression and function of CTHRC1 in gastric cancer (GC) have not been reported. The aim of this study was to investigate the expression levels and regulatory transcription mechanisms of CTHRC1 in GC. Immunohistochemical analysis revealed that CTHRC1 expression was markedly increased in carcinoma compared with normal gastric mucosa, chronic atrophic gastritis, and intestinal metaplasia (P < 0.05 for all), and this overexpression in tumor was related to depth of tumor invasion. Moreover, RNA interference-mediated knockdown and ectopic expression of CTHRC1 showed that CTHRC1 promoted tumor cell invasion in vitro. We then investigated the mechanisms underlying the aberrant expression of CTHRC1 in GC and found that CTHRC1 expression was restored after GC cell lines were treated with the demethylating agent, 5-aza-2'-deoxycytidine. Transforming growth factor-ß1 led to an increase in levels of CTHRC1 mRNA and protein. Overall, our data revealed that the upregulated expression of CTHRC1 in gastric carcinogenesis contributes to tumor cell invasion and metastasis, and promoter demethylation and transforming growth factor-ß1 may co-regulate the expression of CTHRC1.

A branched small molecule-drug conjugate nanomedicine strategy for the targeted HCC chemotherapy.

Off-target toxicity is one of the main challenges faced by anticancer chemotherapeutics. For tumor targeted and precision chemotherapy, we take the advantages of the ligand directed tumor active targeting of small molecule drug conjugates (SMDCs) and the passive tumor targeting of nanoparticles via the enhanced penetration and retention (EPR) effects, put forward a branched small molecule drug conjugate (BSMDC) nanomedicine design concept. In a proof of concept, we used pentaerythritol as the branched moiety, galactosamine (GalN) as the hepatocellular carcinoma (HCC) directing ligands, PTX as a payload, and a stearoyl moiety as the amphiphilic property adjusting group, designed and synthesized BSMDC 1 and prepared its NPs. In cellular level, the BSMDC 1 NPs targeted asialoglycoprotein receptor (ASGPR)-overexpressing HepG2 cells, were effectively taken up in the cells and released in tumor microenvironments, inhibited the HepG2 cell proliferation, arrested HepG2 cell in G2/M phase and induced tumor cell apoptosis. In HepG2 xenograft nude mice, the BSMDC 1 NPs were high specific to target the tumor and demonstrated a higher antitumor efficiency than BSMDC 1, having no apparent influences on mice body weights and major organs, supporting our BSMDC nanomedicine design concept. Therefore, this new strategy may find applications for cancer targeted and precision chemotherapy.

Repeated bacteremia and hepatic cyst infection lasting 3 years following pancreatoduodenectomy: A case report.

BACKGROUND: Simple hepatic cysts are commonly occurring lesions that are usually asymptomatic and require no treatment. Hepatic cyst infection, however, is considered a severe complication. We report a case of hepatic cyst infection following pancreatoduodenectomy with repeated fever lasting for almost 3 years, and two cysts were infected successively. CASE SUMMARY: A 72-year-old woman diagnosed with adenocarcinoma of duodenal papilla underwent pancreatoduodenectomy with Child reconstruction. She then suffered repeated occurrences of bacteremia and hepatic cyst infection for 3 years. Blood cultures were positive for Klebsiella pneumoniae and Escherichia coli a total of 7 times and 4 times, respectively. During the early stage, we suspected that postoperative reflux cholangitis was the cause of fever and bacteremia. Multiple cysts were observed, so it was difficult to determine which cyst was infected. Through repeat examination, we found the focus of infection, and we treated the patient with antimicrobials and performed percutaneous cyst drainage. The patient did not experience another cyst infection for more than 4 years. CONCLUSION: Biliary reconstruction inducing hepatic cyst infection is easily misdiagnosed as biliary reflux infection, Repeated imaging examination is a method for identifying the infected focus.

Synthesis and biological evaluation of selective histone deacetylase 6 inhibitors as multifunctional agents against Alzheimer's disease.

Histone deacetylase 6 (HDAC6) is a potential target for Alzheimer's disease (AD). In this study, a series of novel phenothiazine-, memantine-, and 1,2,3,4-tetrahydro-γ-carboline-based HDAC6 inhibitors with a variety of linker moieties were designed and synthesized. As a hydrochloride salt, the phenothiazine-based hydroxamic acid W5 with a pyridyl-containing linker motif was identified as a high potent and selective HDAC6 inhibitor. It inhibited HDAC6 with an IC50 of 2.54 nM and was more than 290- to 3300-fold selective over other HDAC isoforms. In SH-SY5Y cells, W5 dose-dependently increased the acetylated α-tubulin levels and reduced the hyperphosphorylated tau proteins at Ser396. As an effective metal chelator, W5 inhibited Cu2+-induced Aß1-42 aggregation and disaggregated Cu2+-Aß1-42 oligomers, and showed protective effects on the SH-SY5Y cells against Aß1-42- as well as Cu2+-Aß1-42 induced cell damages, serving as a potential ligand to target AD metal dyshomeostasis. Moreover, W5 promoted the differentiated neuronal neurite outgrowth, increased the mRNA expression of the recognized neurogenesis markers, GAP43, N-myc, and MAP-2. Therefore, W5 might be a good lead for the development of novel HDAC6 inhibitors targeting multi-facets of AD.

FUT6 deficiency compromises basophil function by selectively abrogating their sialyl-Lewis x expression.

Sialyl-Lewis x (sLex, CD15s) is a tetra-saccharide on the surface of leukocytes required for E-selectin-mediated rolling, a prerequisite for leukocytes to migrate out of the blood vessels. Here we show using flow cytometry that sLex expression on basophils and mast cell progenitors depends on fucosyltransferase 6 (FUT6). Using genetic association data analysis and qPCR, the cell type-specific defect was associated with single nucleotide polymorphisms (SNPs) in the FUT6 gene region (tagged by rs17855739 and rs778798), affecting coding sequence and/or expression level of the mRNA. Heterozygous individuals with one functional FUT6 gene harbor a mixed population of sLex+ and sLex- basophils, a phenomenon caused by random monoallelic expression (RME). Microfluidic assay demonstrated FUT6-deficient basophils rolling on E-selectin is severely impaired. FUT6 null alleles carriers exhibit elevated blood basophil counts and a reduced itch sensitivity against insect bites. FUT6-deficiency thus dampens the basophil-mediated allergic response in the periphery, evident also in lower IgE titers and reduced eosinophil counts.

[Correlation of the methylation status of CpG islands in the promoter region of 10 genes with the 5-Fu chemosensitivity in 3 breast cancer cell lines].

OBJECTIVE: To explore the relationship between the methylation status of CpG islands in the promoter region of 10 genes in breast cancer cells and their sensitivity to 5-fluouracil (5-Fu), and to identify the genes responsible for the 5-Fu resistance in breast cancer. METHODS: Three cell lines (differently resistant to chemotherapy) were used in this study: Bcap-37 (IC(50): 289.77 microg/ml), T47D (IC(50): 134.16 microg/ml) and ZR-75-30 (IC(50): 4.20 microg/ml). The methylation profile of 10 genes (BAG1, C11ORF31, CBR1, CBR4, GJA1, FOXL2, IGFBP6, P4HA1, SRI and TYMS) in the 3 breast cancer cell lines was determined by methylation specific PCR. The steady-state mRNAs of ABCC8, CHFR and IGFBP6 genes were quantified by real-time RT PCR analysis. RESULTS: Among the 10 genes, only genes IGFBP6 and FOXL2 displayed differential DNA methylation pattern between the 5-Fu-resistant and 5-Fu-sensitive cell lines. The mRNA expression level of genes PRSS21, LOX, IGFBP6, ABCC8 and CHFR was quantified by real-time RT-PCR analysis. Except for CHFR, the expression level of the other 4 genes was correlated with the methylation status of CpG islands, namely, a lower expression level with methylation status and a higher level with demethylation status. CONCLUSION: The results of the present study have demonstrated that there are 8 genes with differential methylation status in chemosensitive and chemoresistant breast cancer cell lines, i.e. two genes more than the six genes we reported previously. Our findings provide both mechanistic insights for the drug resistance of breast cancer and the basis for further studies on potential application of the DNA methylation in this set of genes for prediction of chemosensitivity of breast cancer.

[Value of spiral CT in diagnosing infantile intestinal malrotation].

OBJECTIVE: To discuss the value of spiral CT in diagnosing infantile intestinal malrotation. METHODS: The spiral CT findings and clinical data of 23 cases of operatively-confirmed infantile intestinal malrotation were retrospectively analyzed. RESULTS: Twenty-three cases of infantile intestinal malrotation were all diagnosed by SCT and confirmed by surgery. The main findings were as follows: whirlpool or concentric circle sign in mesenteric root with midgut volvulus (n = 16); duodenum assumed as "Z" or olecranon spur sign (n = 18); inverted transposition or vertical arrangement of superior mesenteric artery and vein (n = 13); abnormal sign of ileocecal junction and colon in right lower quadrant (n = 23). CONCLUSION: Spiral CT scanning has an important value in the early diagnosis of infantile intestinal malrotation.