Objective:To systematically evaluate the experience and needs of parental care for premature infants during the transition from hospital to home.Methods:Qualitative studies on the experience and needs of parental care for premature infants transitioning from hospital to home were electronically searched in Cochrane Library, PubMed, Embase, Web of Science, Scopus, PsycINFO, CINAHL, China National Knowledge Infrastructure, VIP, China Biomedical Medline Disc, and WanFang Data. The search period was from the establishment of the database to June 3, 2023. The retrieved studies were evaluated using the quality evaluation criteria for qualitative research of the Joanna Briggs Institute Evidence-Based Health Care Center. The qualitative research results were integrated using the method of aggregation integration.Results:A total of 14 articles were included, 39 research results were extracted, categorized into nine categories. These categories were integrated into three synthesized results, namely the dependency period (parents of premature infants coexisted with joy and concern, and relied on professional support from medical and nursing staff), shock period (parents of premature infants developed negative emotions, faced dual difficulties in home care and role switching, and needed internal and external professional support from the family), adaptation period (parents of premature infants actively responded to changes, sought peer support, and transitioned to the "new normal" of life) .Conclusions:The transition from hospital to home is a dynamic process. During the transition process, parents of premature infants undergo complex emotional experiences and role transitions, requiring support from healthcare professionals, family members, and peers. Medical and nursing workers should pay attention to the psychological changes and diverse needs of parents, provide professional support and guidance to help them adapt to the role of parents, and promote the healthy growth of premature infants.

Poria cocos is a classic Chinese medicine with homology of food and medicine,which is beneficial to water infiltration,spleen and stomach,calming the heart and calming the mind,etc.It is known as"nine Poria cocos in ten prescriptions".Poria cocos contains polysaccharide,triterpenoids and steroids,among them polysaccharide and triterpenoid are considered as the main active components.Modern studies have shown that Poria cocos polysaccharide triterpenes display pharmacological activities such as anti-tumor,immunomodulatory and anti-oxidation.The dissolution rate of poria cocos and triterpenes was low in the traditional decocting process,and the oral absorption rate of poria cocos was low,but the activity of poria cocos and triterpenes was still very good,indicating the high activity of poria cocos and triterpenes.Therefore,this paper systematically reviews the extraction and separation,structural identification,content determination,structural modification,biosynthesis,pharmacological activity and potential product development value of Poria cocos polysaccharide and triterpenoids,in order to provide literature reference for the development of Poria cocos grand health industry.

Alzheimer's disease (AD) is the most prevalent neurodegenerative disease featuring progressive cognitive impairment. Although the etiology of late-onset AD remains unclear, the close association of AD with apolipoprotein E (APOE), a gene that mainly regulates lipid metabolism, has been firmly established and may shed light on the exploration of AD pathogenesis and therapy. However, various confounding factors interfere with the APOE-related AD risk, raising questions about our comprehension of the clinical findings concerning APOE. In this review, we summarize the most debated factors interacting with the APOE genotype and AD pathogenesis, depict the extent to which these factors relate to APOE-dependent AD risk, and discuss the possible underlying mechanisms.
Alzheimer Disease/pathology* ; Apolipoprotein E4/genetics* ; Apolipoproteins E/genetics* ; Genotype ; Humans ; Lipid Metabolism ; Neurodegenerative Diseases ; Risk Factors

Colorectal cancer (CRC) and hepatocellular carcinoma (HCC) are the second and third most common causes of death by cancer, respectively. The etiologies of the two cancers are either infectious insult or due to chronic use of alcohol, smoking, diet, obesity and diabetes. Pathological changes in the composition of the gut microbiota that lead to intestinal inflammation are a common factor for both HCC and CRC. However, the gut microbiota of the cancer patient evolves with disease pathogenesis in unique ways that are affected by etiologies and environmental factors. In this review, we examine the changes that occur in the composition of the gut microbiota across the stages of the HCC and CRC. Based on the idea that the gut microbiota are an additional "lifeline" and contribute to the tumor microenvironment, we can observe from previously published literature how the microbiota can cause a shift in the balance from normal → inflammation → diminished inflammation from early to later disease stages. This pattern leads to the hypothesis that tumor survival depends on a less pro-inflammatory tumor microenvironment. The differences observed in the gut microbiota composition between different disease etiologies as well as between HCC and CRC suggest that the tumor microenvironment is unique for each case.

Objective:To investigate the expression level of TRPM7 in breast cancer tissues and adjacent carcinoma tissues and to analyze its clinicalpathological characteristics.Methods:The expressions of TRPM7 in 87 breast cancer and 47 adjacent tissues were detected by immunohistochemistry, and then the relationship between expression and clinicopathological characteristics was analyzed.Results:The positive rate of TRPM7 in breast cancer tissues was 66.7%, significantly higher than that in para-cancer tissues (10.6%) ( P<0.001) . Meanwhile, TRPM7 expression was much higher in those with tumor diameter≥2 cm ( P=0.023) , TNM stage III ( P=0.001) and lymph node metastasis ( P=0.015) . The expression of TRPM7 has nothing to do with patients’ age ( P=0.455) or histological grade ( P=0.577) . Conclusions:High expression of TRPM7 is associated with the development of breast cancer. TRPM7 may become a potential biological indicator to monitor the prognosis of breast cancer in the future.

Objective: This study aimed to explore the existing knowledge about midwives' views and experiences of providing care for women in the context of task shifting.Methods: We conducted a qualitative systematic review using meta-ethnography to describe the views and experiences of midwives on providing care in the context of task shifting. Comparative textual analysis of published qualitative studies involved translation of first-order key concepts and meanings from included studies to generate second-and third-order concepts. A grid was made to identify core findings and compare them reciprocally. Results: Thirty-six qualitative studies met the inclusion criteria. The literature comprised of 32 first key concepts. Eight second-order constructs emerged, and three third-order interpretations were generated. The three overarching themes were: (1) midwives perceived themselves as providing culturally competent and high quality women-centered care; (2) they valued their profession but saw it as complex and challenging; (3) as health professionals, they reported a variety of organizational, cultural, and professional barriers to providing women-centered care. Conclusions: While performing a specific task in the task shifting context, midwives perceived their crucial roles and responsibilities, along with achieved value and reward. However, due to a range of existing barriers, the caring task posed great challenges in completely implementing women-centered care. It is essential for systems to identify and eliminate these barriers early, to consider midwives' emotional well-being, and to develop overall strategies to better support the midwifery workforce. Policy makers and administrators should establish a supportive environment to facilitate midwives to perform women-centered caring tasks in more effective and efficient ways.

Objective: To investigate the role of lectin-like Ox-LDL receptor-1( LOX-1) in the activation and oxidative stress of cultured human umbilical vein endothelial cell(HUVEC) after human cytomegalovirus(HCMV) infection. Methods: HUVEC were divided into four groups: HCMV, Control, Carrageenan, and HCMV+ Carrageenan. After HCMV AD169 infection, the supernatant of the culture was extracted, and cells were lysed. The levels of LOX-1 mRNA, intercellular adhesion molecule-1(ICAM-1) mRNA and vascular cellular adhesion molecule-1(VCAM-1) in HUVEC were measured by real-time PCR. And the content of nitrogen monoxidum(NO) of the supernatant was detected by nitrate reductase method accordingly. Results: 24 h after infection, the mRNA expression of LOX-1, ICAM-1 and VCAM-1 in HUVEC of HCMV infected group increased obviously compared to control, and NO quantity increased accordingly. The mRNA expression of LOX-1, ICAM-1 and VCAM-1 and the quantity of NO decreased after adding the LOX-1 inhibitor carrageenan. There was significant difference between groups(P<0.05). Conclusions HCMV may increase the mRNA expression of ICAM-1 and VCAM-1 and quantity of NO by upregulating the mRNA expresion of LOX-1, which may contribute to the formation of a therosclerosis(AS).

Objective: To explore the clinical and genetic characteristics of infantile nephrotic syndrome caused by COQ2 variants. Methods: The clinical and genetic data of a patient with nephrotic syndrome caused by COQ2 variants diagnosed at pediatric department of Peking University First Hospital from February 2018 to March 2018 were retrospectively analyzed. Related literature retrieved from PubMed, CNKI and Wanfang databases were searched to date (up to July 2018) with "COQ2 gene" or "primary coenzyme Q10 deficiency" and "nephrotic syndrome" or "nephropathy" as key words. Results: A 14-month-old male, presented to local hospital at 11 months of age with edema and severe proteinuria, without hematuria, hypertension or renal dysfunction. He did not have infection or seizure in the course of the disease. He had no response to a more than four-week full-dose prednisone treatment. He had normal birth, mild motor development retardation and moderate language retardation. He was born to non-consanguineous healthy parents. He had two unaffected older sisters and one older sister died of "nephropathy" at one year of age. Genetic testing identified compound heterozygous variants in COQ2 gene: c.518G>A and c.973A>G, both could be predicted by in silico tools to be deleterious in protein function. These variants are not single nucleotide polymorphism and rare in normal populations. Both variants have previously been reported as pathogenic. These missense mutations were inherited from parents in autosomal recessive manner tested by Sanger sequencing. The patient was supplemented with high-dose of coenzyme Q10, at 30 mg/(kg·day) and glucocorticoid was withdrawn. Within three weeks of high dose coenzyme Q10 treatment, the edema disappeared. After seven weeks of high dose coenzyme Q10 treatment, the patient had decreased proteinuria and improved serum albumin levels. The urine protein to creatinine ratio decreased from 22.87 mg/mg to 1.98 mg/mg; Serum albumin increased from 14.2 g/L to 39.9 g/L, with normal kidney function and improved motor development. Primary CoQ10 deficiency is reported to be a rare autosomal recessive mitochondrial disorder with heterogeneous renal, neurologic, and muscular manifestations. To date, COQ2 variants have been reported in 14 children with glomerular involvement. Their age at onset ranged from neonatal period to 10-year-old (8 patients within the first year of life). Steroid resistant nephrotic syndrome (SRNS) is the most common phenotype. Some of these children also had progressing encephalopathy and myopathy, and seizures. Patients with COQ2 variants might show clinical improvement with early high-dose oral CoQ10 supplementation. Literature review revealed two Chinese articles, mainly about adults with neurologic symptoms. SRNS was previously not reported in Chinese pediatric patients. Conclusions It is necessary to carry out genetic testing for infant with SRNS. The coexistence of some degree of encephalomyopathy, such as development retardation, should raise suspicion of a mitochondrial defect caused by COQ2 variants. Timely diagnostic genetic testing and early high dose of coenzyme Q10 supplement could significantly improve their prognosis.

Objective To establish the methodology of combining BOLD and 1H-MRS for investigating correlation between the deactivation in medial prefrontal cortex (MPFC) and gamma-aminobutyric acid (GABA) concentration by acupuncture at LI4 (Point Hegu),and to optimize the experimental technique and procedure.Methods Twenty healthy adult volunteers were enrolled.During fMRI-BOLD scanning,each subject received acupuncture at right LI4 (Point Hegu).MRS scanning was based on MEGA-PRESS sequence,and ROIs were located at bilateral MPFC.The task BOLD fMRI was block design,including 3 stimulations (30 s) with 2 intervals (2 min).Then MRS scanning was performed before and after BOLD.The quantitative values of the BOLD positive and negative activations (Pm) and GABA concentrations were calculated.Results All 20 subjects completed BOLD fMRI scanning,and met the postprocessing requirements.MRS images of 9 subjects with good image quality were included in analysis.Among all 20 subjects,positive activation (Pm=1.17± 0.16) was observed in 9,while negative activation (Pm =-1.31 ± 0.17) was observed in 11 subjects.The GABA average values before and after the acupuncture were (19.93 ±1.04) nmol/L and (20.04±0.81)nmol/L,respectively,and the average amplitude between post-and pre-acupuncture was (0.11 ± 1.60)nmol/L.Conclusion The success rate of this method for quantitative study of brain function established multimodal-functional (BOLD-fMRI and MRS) was acceptable,and the multimodal brain function changes as well as the quantitative values were observed in the brain region during acupuncture.Combined BOLD and MRS quantitative method is feasible for testing acupuncture response in the brain.

OBJECTIVETo explore the inhibitory effect of thalidomide combined with interferon (IFN) on the human acute myeloid leukemia cell line Kasumi- 1 and its mechanism.

METHODSThe inhibitiory effect of Kasumi- 1 cells by thalidomide, interferon or combination was detected by CCK- 8 method, the apoptosis by flow cytometry, the expression of apoptosis related proteins by Western blot, vascular endothelial growth factor (VEGF) concentration in culture supernatant by ELISA.

RESULTSThalidomide inhibited the proliferation of Kasumi- 1 in a dose- dependent manner from 50 μg/ml to 500 μg/ml with an IC₅₀ of (451.13 ± 6.92）μg/ml at 24 h and (362.50 ± 14.52）μg/ml at 48 h. IFN also demonstrated the inhibitory capacity in a dose-dependent manner from 500 U/ml to 5 000 U/ml, with an IC₅₀ of (2 209 ± 127) U/ml at 24 h and (1 393±63) U/ml at 48 h. The apoptosis rates of Kasumi-1 cells treated with thalidomide 350 μg/ml or IFN 1 400 U/ml for 48 h were (14.68 ± 2.61) % and (21.71 ± 0.71)%, respectively, significantly higher than control group (P<0.01). In combination group the inhibition and the apoptosis rate were (88.50 ± 2.40) % and (41.95 ± 3.41)%, significantly higher than control and each single agent group (P<0.01). The VEGF concentrations of combination group [(94.61 ± 5.46) ng/L decreased significantly, as compared to thalidomide group [(141.11 ± 3.70) ng/L and IFN group [(119.90 ± 2.00) ng/L (P < 0.05). Western blot analysis showed Bcl-2 expression of Kasumi-1 cells decreased, while p-P38, Bax, cytochrome C, cleaved-Caspase-3, 8, 9 increased after treated with thalidomide 350 μg/ml or IFN 1 400 U/ml for 48 h. When treated with the combination agents, the expression of Bcl-2 further decreased and p-P38, Bax, cytochrome C, cleaved-Caspase-3, 8, 9 further increased as compared with each single agent (P < 0.05).

CONCLUSIONThalidomide and IFN could synergistically inhibit the proliferation of Kasumi-1 cells probably through inducing apoptosis via the mitochondrial pathway, death receptor pathway and P38 MAPK pathway, as well as inhibiting VEGF secretion.

Apoptosis ; Caspases ; metabolism ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; Humans ; Interferons ; pharmacology ; Leukemia, Myeloid, Acute ; pathology ; MAP Kinase Signaling System ; Thalidomide ; pharmacology ; Vascular Endothelial Growth Factor A ; metabolism