BACKGROUND Hypospadias and cryptorchidism, two relatively common male genital anomalies, may be caused by altered maternal hormone levels, blood glucose levels, or nutritional deficiencies. Maternal obesity, which increases risk of diabetes and could influence hormone levels, may therefore be associated with risk of hypospadias and cryptorchidism. The purpose of this study was to assess the association between pre-pregnancy maternal obesity and hypospadias and cryptorchidism. METHODS We conducted a case-control study of hypospadias and cryptorchidism in male singleton newborns using Washington State birth records from 1992 to 2008 linked to birth-hospitalization discharge records. Maternal pre-pregnancy body mass index (BMI) was calculated from pre-pregnancy weight and height. Adjusted odds ratios (aORs) and 95% confidence intervals (95% CIs) for hypospadias or cryptorchidism were estimated by fitting multivariable logistic regression models adjusted for year of birth, and maternal age, education, parity, race, and cigarette smoking during pregnancy. RESULTS The complete-case analysis included 2,219 hypospadias cases, 2,563 cryptorchidism cases, and 32,734 controls. Maternal obesity (BMI ≥ 30 kg/m2) was not associated with risk of hypospadias or cryptorchidism in male offspring (aOR(95% CI), hypospadias: 1.07(0.95–1.21); cryptorchidism: 0.99(0.89–1.11)), and no trend in risk with increasing maternal BMI was found. There was little indication of risk associated with BMI among any sub-group of mothers examined, including women with pre-existing diabetes or hypertension, women who developed preeclampsia, non-Hispanic white women, first-time mothers, or mothers aged ≥30 years. CONCLUSIONS The results of this study do not support the hypothesis that pre-pregnancy maternal obesity is a cause of hypospadias or cryptorchidism in male infants.

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level III.

CXC chemokine receptor 4 (CXCR4) is involved in many human malignant tumors and plays an important role in tumor growth and metastasis. To explore the effects of CXCR4 expression on the malignant cells of oral squamous cell carcinoma (OSCC), Tca8113 and SCC-9 cell lines, as well as their xenograft models, of nude mice were used to detect cancer cell proliferation alteration. This study also examined the corresponding molecular mechanism after CXCR4 knockdown using a recombinant lentiviral vector expressing small interference RNA (siRNA) for CXCR4. RNA interference-mediated knockdown of CXCR4 in highly aggressive (Tca8113 and SCC-9) tumor cells significantly inhibited the proliferation of the two cell lines in vitro and in vivo. The expression levels of >1,500 genes involved in cell cycle, apoptosis, and multiple signaling pathways were also altered. These results provide new evidence of CXCR4 as a promising tumor gene therapeutic target.

Since 2016, the highly pathogenic avian influenza H5N8 virus has emerged in the Central Asian flyway and Europe, causing massive deaths in poultry and wild birds. In this study, we isolated and identified three H5N8 viruses from swan goose and black swans in Hubei province during the 2016/2017 winter season. Whole-genome sequencing and phylogenetic analysis revealed that the three viruses clustered into a group of H5N8 viruses from Qinghai Lake and Europe. A novel reassortment virus from swan goose was distinguished from that of black swans, in that its PA and NP genes were distinct from those of Qinghai Lake viruses. Molecular dating revealed that the ancestral strain of these H5N8 viruses emerged around July 2015. From sequence comparison, we discovered eight amino acid substitutions in HA and NA during the adaption process from poultry to wild birds. The three viruses were isolated from wild birds in the East Asian-Australasian flyway; however, the viral genomes were similar to H5N8 viruses circulating along the Central Asian flyway. From these data, we conclude that wetlands and lakes in Central China may play a key role in disseminating H5N8 viruses between the East Asian-Australasian and Central Asian flyways.

BackgroundEpidermal growth factor receptor (EGFR) is involved in the development of many human malignant tumors and plays an important role in tumor growth and metastasis. Antagonists of EGFR can suppress the growth of several malignancies; however, their therapeutic effect in adenoid cystic carcinoma (ACC) is controversial.ResultsThe increased proliferation of two ACC cell lines induced by EGF-treatment was reversed by nimotuzumab. Regardless of EGF stimulation, nimotuzumab-treated ACC cells were arrested in G1 phase and showed decreased expression of Ki67. In addition, EGF activated the MAPK-dependent pathway and up-regulated the expression of matrix metalloproteinase-9 and Snail, enhancing the invasive potential of an ACC cell line (ACC-M). The effects of EGF were down-regulated by nimotuzumab treatment.ConclusionsThese results suggest that nimotuzumab can inhibit the growth and invasion of ACC cells induced by EGF, probably through inactivation of ERK phosphorylation. Thus, nimotuzumab should be considered as a promising novel agent for the treatment of ACC.

Surgical treatment for metacarpal neck fractures may be indicated for malrotation, palmar angulation exceeding 30° or metacarpal shortening exceeding 3 mm, although these thresholds have not been firmly established. In a retrospective study, we compared the clinical and radiographic results of 54 patients with displaced fifth metacarpal neck fractures who were treated with either medial locking plates (14 patients) or retrograde intramedullary K-wires (40 patients). At a mean follow-up of 26 months (range 12 to 62), metacarpal shortening and angulation were 2 mm greater and 4° greater, respectively, in the K-wire group. The plate group had an earlier return to work and greater aesthetic satisfaction, but operative time and complication incidence were higher. Range of motion, time to union, grip strength and Quick Disability of the Arm, Shoulder and Hand scores were similar. We conclude that medial plating offers no clear advantage over K-wire fixation in treating metacarpal neck fractures. Level of evidence: III

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