The Effect of Perioperative Comprehensive Nursing on Patients Undergoing Ovary Endometriosis Laparoscopic Surgery.

Objective: To assess the effectiveness of perioperative nursing interventions in improving outcomes and satisfaction for patients undergoing laparoscopic surgery for ovarian endometriosis. Methods: From July 2021 to September 2022, 80 patients with endometriosis underwent laparoscopic surgery at Shijiazhuang Fourth Hospital and were randomly assigned to the conventional (n=40) and experimental (n=40) groups. During the perioperative period, patients in the conventional group received standard nursing interventions, while patients in the experimental group received comprehensive nursing interventions. The two groups were compared in terms of postoperative clinical indicators, self-rated anxiety scale (SAS) and self-rated depression scale (SDS) scores, nursing compliance, complications, and nursing satisfaction. Results: comprehensive nursing resulted in better postoperative clinical indices (time to get out of bed, hospital stay) versus routine nursing (all P < .001). The comprehensive nursing led to significantly lower SAS and SDS scores versus routine nursing. The nursing compliance of the patients in the experimental group was significantly higher than that of the patients in the conventional group (P < .001). Comprehensive nursing was associated with a significantly lower incidence of complications versus routine nursing (P < .001). Comprehensive nursing contributed to significantly higher nursing satisfaction versus routine nursing (P < .001). Conclusion: Comprehensive perioperative nursing interventions for patients with ovarian endometriosis undergoing laparoscopic surgery considerably accelerate patient recovery and enhance nursing compliance, as well as minimize patient negative emotions and improve patient satisfaction with nursing.  The comprehensive approach addresses the specific needs of patients during the recovery period, minimizing postoperative complications, accelerating patient recovery, and improving overall quality of life. By integrating psychological support, tailored strategies for pain management, early mobilization, and prompt intervention for complications, this intervention sets a benchmark for holistic care in gynecological surgery.

Admission Systolic Blood Pressure and In-hospital Mortality in Acute Type A Aortic Dissection: A Retrospective Observational Study.

Background: Evidence between admission systolic blood pressure (SBP) and in-hospital deaths in acute type A aortic dissection (AAD) patients is inadequate. Here, we examined the relationship between SBP and in-hospital deaths in AAD patients. Methods: 703 AAD patients were enrolled from January 2014 to December 2018. The independent and dependent variables targeted were admission SBP and in-hospital deaths, respectively. Gender, age, body mass index (BMI), chronic renal insufficiency, smoking, hypertension, diabetes, laboratory indicators, and management were used as covariates. Results: The 703 participants had a mean age of 50.48 ± 11.35. About 76.24% of the participants were male. After adjusting for confounders, there was a negative correlation between AAD patients' admission SBP and in-hospital deaths (OR = 0.88, 95%CI 0.80-0.96). Consequently, a non-linear relationship of point 120 (mmHg) was detected between admission SBP and in-hospital deaths for AAD patients. Confidence intervals and effect sizes of the right (SBP >120 mmHg) and left (SBP ≤ 120 mmHg) sides of the inflection point were 0.96 (0.85-1.09) and 0.67 (0.51-0.88), respectively. The change in the male population and non-diabetes people was more pronounced according to subgroup analysis. Conclusions: Correlation between admission SBP and in-hospital mortality of AAD patients is non-linear. SBP negatively correlated with in-hospital mortality when ≤120 mmHg.

A candidate PpRPH gene of the D locus controlling fruit acidity in peach.

KEY MESSAGE: A candidate gene, designate PpRPH, in the D locus was identified to control fruit acidity in peach. Fruit acidity has a strong impact on organoleptic quality of fruit. Peach fruit acidity is controlled by a large-effect D locus on chromosome 5. In this study, the D locus was mapped to a 509-kb interval, with two markers, 5dC720 and 5C1019, co-segregating with the non-acid/acid trait of peach fruit. Within this interval, a candidate gene encoding a putative small protein, designated PpRPH, showed a consistency between gene expression and fruit acidity, with up- and down-regulation in non-acidic and acidic fruits, respectively. Transient ectopic expression of PpRPH in tobacco leaves caused an increase of pH by approximately 40% compared to the control transformed with empty vector. Whereas, the concentrations of citrate and malate decreased significantly by 22% and 37%, respectively, with respect to the empty vector control. All these results suggest that PpRPH is a strong candidate gene of the D locus. These findings contribute to our overall understanding of the complex mechanism underlying fruit acidity in peach as well as that in other fruit crops.

Association of Lactate Dehydrogenase with In-Hospital Mortality in Patients with Acute Aortic Dissection: A Retrospective Observational Study.

BACKGROUND: Evidence regarding the relationship between serum lactate dehydrogenase (LDH) levels and in-hospital mortality in acute aortic dissection (AAD) patients is extremely limited. We aimed to investigate the relationship between LDH and in-hospital mortality in AAD patients. METHODS: The present study was a retrospective observational study. A total of 1526 participants with acute aortic dissection were involved in a hospital in China from January 2014 to December 2018. The target-independent variable was LDH measured at baseline, and the dependent was all-cause mortality during hospitalization. Covariates involved in this study included age, gender, body mass index (BMI), hypertension, diabetes, smoking, stroke, atherosclerosis, systolic blood pressure (SBP), diastolic blood pressure (DBP), white blood cell (WBC), hemoglobin (Hb), alanine transaminase (ALT), aspartate aminotransferase (AST), albumin (ALB), creatinine (Cr), symptom, type of AAD (Stanford), and management. RESULTS: The average age of 1526 selected participants was 52.72 ± 11.94 years old, and about 80.41% of them were male. The result of the fully adjusted model showed LDH was positively associated with in-hospital mortality in AAD patients after adjusting confounders (OR = 1.09, 95% CI 1.05 to 1.13). A nonlinear relationship was detected between LDH and in-hospital mortality in AAD patients after adjusting for potential confounders (age, gender, BMI, hypertension, diabetes, stroke, atherosclerosis, smoking, symptom, SBP, DBP, WBC, Hb, ALT, AST, ALB, Cr, type of AAD (Stanford), and management), whose point was 557. The effect sizes and the confidence intervals of the left and right sides of the inflection point were 0.90 (0.74-1.10) and 1.12 (1.06-1.19), respectively. Subgroup analysis in participants showed that the relationship between LDH and in-hospital mortality was stable, and all of the P value for the interaction in different subgroup were more than 0.05. CONCLUSIONS: The relationship between LDH and in-hospital mortality in AAD patients is nonlinear. LDH was positively related with in-hospital mortality when LDH is more than 557.

Activator-type R2R3-MYB genes induce a repressor-type R2R3-MYB gene to balance anthocyanin and proanthocyanidin accumulation.

Anthocyanin and proanthocyanidin (PA) accumulation is regulated by both myeloblastosis (MYB) activators and repressors, but little information is available on hierarchical interactions between the positive and negative regulators. Here, we report on a R2R3-MYB repressor in peach, designated PpMYB18, which acts as a negative regulator of anthocyanin and PA accumulation. PpMYB18 can be activated by both anthocyanin- and PA-related MYB activators, and is expressed both at fruit ripening and juvenile stages when anthocyanins or PAs, respectively, are being synthesized. The PpMYB18 protein competes with MYB activators for binding to basic Helix Loop Helixes (bHLHs), which develops a fine-tuning regulatory loop to balance PA and anthocyanin accumulation. In addition, the bHLH binding motif in the R3 domain and the C1 and C2 repression motifs in the C-terminus of PpMYB18 both confer repressive activity of PpMYB18. Our study also demonstrates a modifying negative feedback loop, which prevents cells from excess accumulation of anthocyanin and PAs, and serves as a model for balancing secondary metabolite accumulation at the transcriptional level.

Modulation of UVB-induced Carcinogenesis by Activation of Alternative DNA Repair Pathways.

The molecular basis for ultraviolet (UV) light-induced nonmelanoma and melanoma skin cancers centers on cumulative genomic instability caused by inefficient DNA repair of dipyrimidine photoproducts. Inefficient DNA repair and subsequent translesion replication past these DNA lesions generate distinct molecular signatures of tandem CC to TT and C to T transitions at dipyrimidine sites. Since previous efforts to develop experimental strategies to enhance the repair capacity of basal keratinocytes have been limited, we have engineered the N-terminally truncated form (Δ228) UV endonuclease (UVDE) from Schizosaccharomyces pombe to include a TAT cell-penetrating peptide sequence with or without a nuclear localization signal (NLS): UVDE-TAT and UVDE-NLS-TAT. Further, a NLS was engineered onto a pyrimidine dimer glycosylase from Paramecium bursaria chlorella virus-1 (cv-pdg-NLS). Purified enzymes were encapsulated into liposomes and topically delivered to the dorsal surface of SKH1 hairless mice in a UVB-induced carcinogenesis study. Total tumor burden was significantly reduced in mice receiving either UVDE-TAT or UVDE-NLS-TAT versus control empty liposomes and time to death was significantly reduced with the UVDE-NLS-TAT. These data suggest that efficient delivery of exogenous enzymes for the initiation of repair of UVB-induced DNA damage may protect from UVB induction of squamous and basal cell carcinomas.

Molecular genetics of blood-fleshed peach reveals activation of anthocyanin biosynthesis by NAC transcription factors.

Anthocyanin pigmentation is an important consumer trait in peach (Prunus persica). In this study, the genetic basis of the blood-flesh trait was investigated using the cultivar Dahongpao, which shows high levels of cyanidin-3-glucoside in the mesocarp. Elevation of anthocyanin levels in the flesh was correlated with the expression of an R2R3 MYB transcription factor, PpMYB10.1. However, PpMYB10.1 did not co-segregate with the blood-flesh trait. The blood-flesh trait was mapped to a 200-kb interval on peach linkage group (LG) 5. Within this interval, a gene encoding a NAC domain transcription factor (TF) was found to be highly up-regulated in blood-fleshed peaches when compared with non-red-fleshed peaches. This NAC TF, designated blood (BL), acts as a heterodimer with PpNAC1 which shows high levels of expression in fruit at late developmental stages. We show that the heterodimer of BL and PpNAC1 can activate the transcription of PpMYB10.1, resulting in anthocyanin pigmentation in tobacco. Furthermore, silencing the BL gene reduces anthocyanin pigmentation in blood-fleshed peaches. The transactivation activity of the BL-PpNAC1 heterodimer is repressed by a SQUAMOSA promoter-binding protein-like TF, PpSPL1. Low levels of PpMYB10.1 expression in fruit at early developmental stages is probably attributable to lower levels of expression of PpNAC1 plus the presence of high levels of repressors such as PpSPL1. We present a mechanism whereby BL is the key gene for the blood-flesh trait in peach via its activation of PpMYB10.1 in maturing fruit. Partner TFs such as basic helix-loop-helix proteins and NAC1 are required, as is the removal of transcriptional repressors.

Endothelin downregulates SERCA2 gene and protein expression in adult rat ventricular myocytes: regulation by pertussis toxin-sensitive Gi protein and cAMP.

Downregulation of the sarcoplasmic reticulum calcium ATPase (SERCA2) is associated with diastolic dysfunction in the failing heart. Elevated plasma endothelin-1 (ET) levels are correlated with congestive heart failure suggesting that ET may play a pathophysiological role. We have investigated the ability of ET to regulate SERCA2 gene expression in isolated adult rat ventricular myocytes. We find that ET enhances net protein synthesis by approximately 40% but significantly downregulates SERCA2 mRNA expression, time dependently, by approximately 30-50%, and the expression of SERCA2 protein by approximately 50%. In myoyctes, ET binds to ET(A) receptor that couples to G(q) and G(i) proteins. Inhibition of G(q)-PLC-induced phosphoinositide (PI) hydrolysis with U73122 (1 muM) or inhibition of G(i) protein with pertussis toxin (PTX) abolishes the ability of ET to downregulate SERCA2 mRNA gene expression. Further investigation suggests that ET coupling to PTX-sensitive G(i) with consequent lowering of cAMP is required for downregulation of SERCA2 mRNA levels. Increasing intracellular cAMP quantity using cAMP-specific PDE inhibitor Ro20-1724 or cAMP analog dibutyryl-cAMP reverses ET-induced downregulation of SERCA2 mRNA levels. The data indicate that, in adult myocytes, ET downregulates SERCA2 mRNA and protein levels, and the effect requires cross-talk between G(q) and PTX-sensitive G(i) pathways.

Mutation of COOH-terminal lysines in overexpressed alpha B-crystallin abrogates ischemic protection in cardiomyocytes.

High levels of alpha B-crystallin are present in the cardiomyocyte, yet little is understood about the function and importance of this protein. Like many other small heat shock proteins, alpha B-crystallin forms large oligomeric complexes whose size can be regulated by posttranslational modifications. The size of these complexes can modify the function of the protein. A naturally occurring COOH-terminal mutant has many detrimental effects in the lens of the eye and altered oligomerization. Therefore, we mutated the two COOH-terminal lysines of alpha B-crystallin to glycines (K174/175G) and adenovirally mounted them to transduce cardiomyocytes. We analyzed the effect of this mutation on oligomerization, microtubular stabilization, and ischemic outcome. A nearly 45% downward shift in complex size was observed with the mutant by native PAGE followed by immunoblotting. The overexpressed protein no longer protected the tubulin cytoskeleton against ischemic stress by confocal analysis. The mutant caused a 30% increase in cytosolic enzyme release with ischemia compared with control, whereas a 33% decrease was associated with wild-type alpha B-crystallin overexpression. We conclude that the COOH terminus of alpha B-crystallin is crucial to its proper function.