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These results imply oocyte sources modify the expression of development and adhesion related genes in blastocysts, which may elucidate a possible reasoning for the low development competence of buffalo SLH embryos.

Negative experiences contribute to provider dissatisfaction and burnout. Prior research suggests that negative experiences have greater impact on individuals than positive experiences.

Interviews were conducted with surgical and oncology care providers (107 MDs, 253 non-MDs) working in 10 geographically diverse, academic and community hospitals across the U.S. Using a thematic network approach, we identified core themes describing drivers of memorably negative experiences. We applied logistic regression with adjustments for multiple comparisons to evaluate the relationship between demographic characteristics and types of experiences.

We identified 13 themes from 360 experiences and from these, developed a framework describing how work culture, environment, individual factors, and patient experiences lead to memorably, negative provider experiences. Providers most frequently described negative work environment experiences (158/360) and poor communication experiences with patients and other care professionals (151/360). Across themes, one third of respondents attributed memorably negative experiences to patient experiences (119/360). Midwest providers described patient centeredness more than other providers (OR=3.9, p<0.001). Providers from the Northeast, MDs compared to non-MDs, and providers with 15+ years of work experience identified negative insurance-related experiences more frequently (OR=0.2, P=0.007; OR=2.9, P=0.002 OR=4.2, P<0.001).

We offer a framework for understanding negative experiences among providers. Our study suggests that across a broad set of causes, improving patient experiences could substantially improve the negative, memorable experiences of providers.

Addressing negative patient experiences may have the double benefit of improving patient care and reducing provider burnout.

Level III.

Level III.

Laparoscopic repeat hepatectomy is a technically challenging procedure owing to adhesions around the liver, causing difficulties in performing hepatic inflow control by conventional tourniquet method [1], and failure in hepatic mobilization [2].

Thus, we introduce our technique using double intercostal ports to manipulate the fixed liver under the rib cage and using the laparoscopic Satinsky vascular clamp to perform hepatic inflow control to overcome the aforementioned concerns in ipsilateral laparoscopic repeat hepatectomy after previous open hepatectomy.

The patient, with histories of abdominal aortic aneurysm repair and open Segment 7 subsegmentectomy, had recurrent hepatocellular carcinoma in the dorsal region of Segment 8. After establishing pneumoperitoneum with five abdominal ports, adhesiolysis around the liver was then performed, followed by identification of the caudal part of Spiegel’s lobe as the landmark for the space between the left-side of the hepatoduodenal ligament and the vena cava. opic Satinsky vascular clamp could be significant aids for performing safe ipsilateral laparoscopic repeat hepatectomy, even after previous open hepatectomy.

To assess the developmental progression and compare the developmental attainments of children treated with two hormonal therapies for infantile spasms (IS) over two years (seizure and EEG outcomes of this RCT published previously).

Newly diagnosed infants with IS were randomised to receive adrenocorticotrophin (ACTH) or prednisolone for 14 days. All underwent Bayley III Infant and Toddler Assessments in cognitive (Cog), receptive (RC) and expressive (EC) communication, fine (FM) and gross (GM) motor developmental subsets at baseline (T0), one-year (T1) and two-years (T2).

95 infants randomised to prednisolone (n=48) and ACTH (n=47) groups were eligible for developmental assessments. Mean age at initial assessment was 8.75 months (SD=6.37, range 1.46-34.4 months). N-Ethylmaleimide concentration 48 children presented for all three assessments. Mean composite scores of each developmental domain improved across the three time points; but the progression was significant only in relation to motor development (p=0.04). When comparing the trental outcomes at two years, but further comparative studies over longer periods are required for more definitive conclusions.Porcine deltacoronavirus (PDCoV) is a swine enteropathogenic coronavirus (CoV) that continues to spread globally, placing strain on economic and public health. Currently, the pathogenic mechanism of PDCoV remains largely unclear, and effective strategies to prevent or treat PDCoV infection are still limited. In this study, the interaction between autophagy and PDCoV replication in LLC-PK1 cells was investigated. We demonstrated that PDCoV infection induced a complete autophagy process. Pharmacologically induced autophagy with rapamycin increased the expression of PDCoV N, while pharmacologically inhibited autophagy with wortmannin decreased the expression of PDCoV N, suggesting that PDCoV-induced autophagy facilitates virus replication. Further experiments showed that PDCoV infection activated p38 signaling pathway to trigger autophagy. Besides, ergosterol peroxide (EP) alleviated PDCoV-induced activation of p38 to suppress autophagy, thus exerting its antiviral effects. Finally, we employed a piglet model of PDCoV infection to demonstrate that EP prevented PDCoV infection by suppressing PDCoV-induced autophagy via p38 signaling pathway in vivo. Collectively, these findings accelerate the understanding of the pathogenesis of PDCoV infection and provide new insights for the development of EP as an effective therapeutic strategy for PDCoV.MicroRNAs (miRNAs) are known to play important regulatory roles in host-virus interactions. Avian-origin H3N2 canine influenza virus (CIV) has emerged as the most prevalent subtype among dogs in Asia since 2007. To evaluate the roles of host miRNAs in H3N2 CIV infection, here, miRNA profiles obtained from primary canine bronchiolar epithelial cells (CBECs) and canine alveolar macrophages (CAMCs) were compared between infected and mock-infected cells with the H3N2 CIV JS/10. It was found that the expressions of cfa-miR-125b and cfa-miR-151, which have been reported to be associated with innate immunity and inflammatory response, were significantly decreased in CIV-infected canine primary cells. Bioinformatics prediction indicated that 5′ seed regions of the two miRNAs are partially complementary to the mRNAs of nucleoprotein (NP) and non-structural protein 1 (NS1) of JS/10. As determined by virus titration, quantitative real-time PCR (qRT-PCR) and western blotting, overexpression of the two miRNAs inhibited CIV replication in cell culture, while their inhibition facilitated this replication, suggesting that the two miRNAs could act as negative regulators of CIV replication.