Effect of individualized nutrition interventions on clinical outcomes of pregnant women with gestational diabetes mellitus

BACKGROUND Gestational diabetes mellitus(GDM)can lead to excessive pregnancy weight gain(PWG),abnormal glucolipid metabolism,and delayed lactation.Therefore,it is necessary to provide appropriate and effective interventions for pregnant women with GDM.AIM To clarify the effects of individualized nutrition interventions on PWG,glucolipid metabolism,and lactation in pregnant women with GDM.METHODS The study population consisted of 410 pregnant women with GDM who received treatment at the Northern Jiangsu People's Hospital of Jiangsu Provinceand Yangzhou Maternal and Child Health Hospital between December 2020 and December 2022,including 200 who received routine in-terventions[control(Con)group]and 210 who received individualized nutrition interventions[research(Res)group].Data on PWG,glucolipid metabolism[total cholesterol,(TC);triglycerides(TGs);fasting blood glucose(FPG);glycosylated hemoglobin(HbA1c)],lactation time,perinatal complications(cesarean section,premature rupture of membranes,postpartum hemorrhage,and pregnancy-induced hypertension),and neonatal adverse events(premature infants,fetal macrosomia,hypo-glycemia,and respiratory distress syndrome)were collected for comparative analysis.RESULTS The data revealed markedly lower PWG in the Res group vs the Con group,as well as markedly reduced TG,TC,FPG and HbA1c levels after the intervention that were lower than those in the Con group.In addition,obviously earlier lactation and statistically lower incidences of perinatal complications and neonatal adverse events were observed in the Res group.CONCLUSION Individualized nutrition interventions can reduce PWG in pregnant women with GDM,improve their glucolipid metabolism,and promote early lactation,which deserves clinical promotion.

Diaphragmatic hernia complicated with intestinal obstruction with colon perforation after surgery for esophageal cancer:a case report

We reported a case of diaphragmatic hernia complicated with intestinal obstruction with colon perforation after surgery for esophageal cancer. In this case, the conservative treatment took too long, which delayed the diagnosis and treatment and resulted in colon perforation. After computed tomography confirmed the diagnosis, an emergency operation was performed. During the operation, we found colon perforation. Because pollution of thoracic cavity was serious, we performed proximal end colon neostomy. The patient recovered and discharged with active treatment 35 days after operation. We consider surgical repair of the diaphragmatic hernia is recommended to avoid the potentially disastrous complications, such as strangulation or perforation of the herniated contents, which can threaten the life of the patient if diagnosis is delayed.

EGB761 on retinal light injury in rats

Background Retinal light injury can lead to degeneration of the photoreceptor cell layer. It has been hypothesized that the mechanism for this process is the photochemical damage. Ginkgo balboa extract （Ginkgo biloba extract EGB761） EGB761 is a free radical scavenger. The purpose of this study was to investigate the possible effect of orally administered EGB761 on retinal light damage of mouse photoreceptor cells. Methods Kunming mice were randomly chosen for the following groups containing 20 animals in each： control group, light damage group, saline control group, and drug treatment group. The drug treatment group and saline control group were given daily gavage of EGB761 （150 mg.kgl.d-1） one week before light exposure. At 7, 14, and 30 days after light exposure, animals were sacrificed and eyes were examined by light microscopy, electron microscopy, and retinal histopathology using in situ detection of apoptotic cells. Results In the light damage group after 7 days there was visible edema, and the outer nuclear layer appeared withered with deeply stained dead cells, leaving only a thin nuclear layer of 7-8 cells. After 14 days, the photoreceptor cell layer disappeared, leaving only the outer nuclear layer of 1-3 cells with an average thickness of （37.988＋1.207） pm. The average thickness of the retina was （126.32~2.31） pm. In the drug treatment group, the photoreceptor cell layer and outer nuclear layer damage were significantly lower than the saline group （t=-21.993, P 〈0.001）, demonstrating that EGB761, especially at 14 days after light exposure, can reduce retinal light damage in mice.Conclusion Oral administration of EGB761 can partially inhibit apoptosis of photoreceptor cells, resulting in increased photoreceptor cell survival.

Universal MOF nanozyme-induced catalytic amplification strategy for label-free electrochemical immunoassay

Label-free immunoassay is confronted with a great challenge that its insufficient sensitivity for low concentration analytes,which can be assigned to the low catalytic efficiency of modified materials towards electroactive molecules.Herein,a universal MOF nanozyme-induced catalytic amplification strategy was proposed for constructing highly sensitive label-free electrochemical immunoassay.Specifically,the synthesized Cu Fe-MOF nanozyme with superior peroxidase(POD)-like activity,regarding as a MOF nanozyme model,can catalyze hydrogen peroxide to produce hydroxyl radicals(·OH),which can efficiently oxidize electroactive probe(such as 1,2-phenylenediamine(o-PD))accompanying with intense electrochemical signals.Modification of MOF nanozyme on the electrode and capture of antibodies for binding target antigens hinder the catalytic process of MOF nanozyme toward o-PD,resulting in a gradual decrease in electrochemical signal with increasing target antigen concentration,enabling quantitative label-free immunoassay.Thus,a highly sensitive label-free immunosensor using MOF nanozyme-induced catalytic amplification achieved effective detection of Immunoglobulin G(Ig G)with a wide linear range of 0.001-50 ng/mL and low detection limit of 0.45 pg/mL.This work proposes a promising nanozyme-induced catalytic amplification strategy for the development of label-free electrochemical immunoassay.

Deletion of Luzp Does Not Cause Hearing Loss in Mice

Deafness is the prevailing sensory impairment among humans,impacting every aspect of one's existence.Half of congenital deafness cases are attributed to genetic factors.Studies have shown that Luzp2 is expressed in hair cells(HCs)and supporting cells of the inner ear,but its specific role in hearing remains unclear.To determine the importance of Luzp2 in auditory function,we generated mice deficient in Luzp2.Our results revealed that Luzp2 has predominant expression within the HCs and pillar cells.However,the loss of Luzp2 did not result in any changes in auditory threshold.HCs or synapse number and HC stereocilia morphology in Luzp2 knockout mice did not show any notable distinctions.This was the first study of the role of Luzp2 in hearing in mice,and our results provide important guidance for the screening of deafness genes.