{"title":"Antibiofilm activities of lactoferricin-related Trp- and Arg-rich antimicrobial hexapeptides against pathogenic <i>Staphylococcus aureus</i> and <i>Pseudomonas aeruginosa</i> strains.","authors":"Gopal Ramamourthy, Hans J Vogel","doi":"10.1139/bcb-2024-0183","DOIUrl":"10.1139/bcb-2024-0183","url":null,"abstract":"<p><p>Recently, several antimicrobial peptides (AMPs), varying in length from 12 to 37 residues, have been shown to act as antibiofilm agents. Here, we report a study of 23 hexapeptides modeled after four different Trp- and Arg-rich AMPs, including the RRWQWR-NH<sub>2</sub> peptide, derived from bovine lactoferrin. They were tested against the pathogenic Gram-negative <i>Pseudomonas aeruginosa</i> PAO1 strain and a Gram-positive <i>Staphylococcus aureus</i> MRSA strain. Both strains were engineered to express the green fluorescent protein (GFP) protein, and fluorescence detection was used to measure the ability of the peptides to prevent biofilm formation (minimum biofilm inhibitory concentration (MBIC)) or to cause the breakdown of established biofilms (minimum biofilm eradication concentration (MBEC)). Similar antibiofilm activities were obtained with the standard crystal violet dye assay. Most Trp- and Arg-rich hexapeptides displayed a potent antibiofilm activity against the Gram-positive <i>S. aureus</i> MRSA strain. In particular, hexapeptides with 3 Arg and 3 Trp were very effective, especially when they contained the three Trp in sequence. Somewhat unexpectedly, the antimicrobial (MIC) values correlated with the MBIC and MBEC values, which has not been seen for several other AMP/antibiofilm peptides. Our results demonstrate that short Trp- and Arg-rich peptides merit further studies as antibiofilm agents that could be deployed to address part of the antimicrobial resistance problem.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xuanxuan Ma, Kun Zhang, Na Yang, Ya Hao, Ruoyu Mao, Da Teng, Jianhua Wang
{"title":"Treatment of lactoferrin and antimicrobial peptide N6 on bacterial enteritis caused by <i>Escherichia coli</i> in mice.","authors":"Xuanxuan Ma, Kun Zhang, Na Yang, Ya Hao, Ruoyu Mao, Da Teng, Jianhua Wang","doi":"10.1139/bcb-2024-0103","DOIUrl":"10.1139/bcb-2024-0103","url":null,"abstract":"<p><p>Enterotoxigenic <i>Escherichia coli</i> (ETEC) is a major cause of diarrhea in humans and animals. The study aimed to evaluate the efficacy of bovine lactoferrin (bLf) as an adjuvant combined with AMP (N6) in the treatment of <i>E. coli</i>-induced bacterial enteritis. Firstly, 40 female ICR mice were randomly divided into four groups. The ETEC-A, ETEC-B, and ETEC-C groups were gavaged with 0.2 mL of ETEC K88 at 5 × 10<sup>9</sup>, 5 × 10<sup>8</sup>, and 5 × 10<sup>7</sup> CFU/mL for three consecutive days, respectively, the CK control group was given PBS. Based on the clinical symptoms and intestinal changes, the optimal model dose of ETEC K88 was determined to be 5 × 10<sup>8</sup> CFU/mL. Sixty female ICR mice were randomly divided into six groups: CK group (uninfected), NC group (infected and untreated), N6 treatment group (20 mg/kg), bLf treatment group (100 mg/kg), bLf + N6-A treatment group (10 mg/kg N6+100 mg/kg bLf), and bLf + N6-B group (20 mg/kg N6+100 mg/kg bLf). The clinical symptoms, intestinal morphology, inflammatory response and serum metabolites were monitored. The results showed that compared with the NC group, the bLf-N6-A and bLf-N6-B treatment groups had significant reductions in TNF-α and IL-6, significant increases in IL-10, and significant reductions in endotoxin and DAO in plasma (<i>p</i> < 0.05). Meanwhile, the bLf-N6-A and bLf-N6-B treatment groups significantly increased the expression of ZO-1, claudin-1 and occludin, increased the height of small intestinal mucosal villi and VH/CD after ETEC K88-induced intestinal injury (<i>p</i> < 0.05). The combination of bLf and N6 relieved enteritis by balancing intestinal mucosal immunity, improving intestinal morphology and barrier function. BLf combined with N6 can be used as an effective therapeutic strategy for the treatment of bacterial enteritis.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142405978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inés Abad, Andrea Bellés, Ana Rodríguez-Largo, Lluís Luján, Ignacio de Blas, Dimitra Graikini, Laura Grasa, Lourdes Sánchez
{"title":"Lactoferrin modulates oxidative stress and inflammatory cytokines in a murine model of dysbiosis induced by clindamycin.","authors":"Inés Abad, Andrea Bellés, Ana Rodríguez-Largo, Lluís Luján, Ignacio de Blas, Dimitra Graikini, Laura Grasa, Lourdes Sánchez","doi":"10.1139/bcb-2024-0087","DOIUrl":"10.1139/bcb-2024-0087","url":null,"abstract":"<p><p>Antibiotics, specifically clindamycin (Clin), cause intestinal dysbiosis, reducing the microbiota with anti-inflammatory properties. Furthermore, Clin can induce alterations in the immune responses and oxidative stress. Lactoferrin, among other activities, participates in the maintenance of intestinal homeostasis and reduces dysbiosis induced by antibiotic treatment. The aim of this study was to analyze the effect of native and iron-saturated bovine LF in a murine model of dysbiosis induced by Clin. Six groups of male C57BL/6 mice were treated with saline (control), Clin, native lactoferrin (nLF), iron-saturated lactoferrin (sLF), nLF/Clin, or sLF/Clin. Oxidation caused in the intestinal cells of the ileum of animals subjected to different treatments was analyzed, focusing on lipid peroxidation and protein carbonyl content. The expression of inflammatory mediators was determined by qRT-PCR. Treatment with Clin did not modify lipid peroxidation, but significantly increased protein carbonyl levels up to almost 5-fold respect to the control, an effect that was reversed by orally administering sLF to mice. Furthermore, Clin increased the expression of interleukin-6 and TNF-α by 1- and 2-fold change, respectively. This effect was reversed by treatment with nLF and sLF, decreasing the expression to basal levels. In conclusion, this study indicates that lactoferrin can prevent some of the effects of Clin on intestinal cells and their associated immune system.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Interconnected roles of fungal nuclear- and intron-encoded maturases: at the crossroads of mitochondrial intron splicing.","authors":"Jigeesha Mukhopadhyay, Georg Hausner","doi":"10.1139/bcb-2024-0046","DOIUrl":"10.1139/bcb-2024-0046","url":null,"abstract":"<p><p>Group I and II introns are large catalytic RNAs (ribozymes) that are frequently encountered in fungal mitochondrial genomes. The discovery of respiratory mutants linked to intron splicing defects demonstrated that for the efficient removal of organellar introns there appears to be a requirement of protein splicing factors. These splicing factors can be intron-encoded proteins with maturase activities that usually promote the splicing of the introns that encode them (<i>cis</i>-acting) and/or nuclear-encoded factors that can promote the splicing of a range of different introns (<i>trans</i>-acting). Compared to plants organellar introns, fungal mitochondrial intron splicing is still poorly explored, especially in terms of the synergy of nuclear factors with intron-encoded maturases that has direct impact on splicing through their association with intron RNA. In addition, nuclear-encoded accessory factors might drive the splicing impetus through translational activation, mitoribosome assembly, and phosphorylation-mediated RNA turnover. This review explores protein-assisted splicing of introns by nuclear and mitochondrial-encoded maturases as a means of mitonuclear interplay that could respond to environmental and developmental factors promoting phenotypic adaptation and potentially speciation. It also highlights key evolutionary events that have led to changes in structure and ATP-dependence to accommodate the dual functionality of nuclear and organellar splicing factors.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"351-372"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141247167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mimi Mu, Gao Liu, Xiaoyu Ding, Lijun Xue, Dandan Li, Yunhua Zhu, Nan Zhang, Jia Wu, Junjun Wang
{"title":"miR-520e and its promoter region DNA methylation as potential biomarkers in atherosclerosis.","authors":"Mimi Mu, Gao Liu, Xiaoyu Ding, Lijun Xue, Dandan Li, Yunhua Zhu, Nan Zhang, Jia Wu, Junjun Wang","doi":"10.1139/bcb-2023-0326","DOIUrl":"10.1139/bcb-2023-0326","url":null,"abstract":"<p><p>In atherosclerosis, DNA methylation plays a key regulatory role in the expression of related genes. However, the molecular mechanisms of these processes in human umbilical vein endothelial cells (HUVECs) are unclear. Here, using high-throughput sequencing from the Infinium HumanMethylation450 assay, we manifested that the cg19564375 methylation of miR-520e promoter region in the peripheral blood of acute coronary syndrome (ACS) patients was higher than that of healthy controls. As shown by RQ-MSP, the upstream DNA methylation level of the miR-520e promoter region was considerably increased in ACS patients. miR-520e was markedly downregulated in ACS patients compared with healthy controls. In the oxidized low-density lipoprotein (ox-LDL)-induced HUVECs injury model, DNA methylation of the upstream region of miR-520e was significantly increased. With increasing concentrations of the methylase inhibitor 5-Aza, miR-520e expression was upregulated. The silence of methyltransferase DNMT1, rather than DNMT3a or DNMT3b, abolished the influence of miR-520e expression by ox-LDL treatment in HUVECs. A dual luciferase reporter assay revealed that miR-520e regulated the TGFBR2 3'-untranslated region region. After silencing TGFBR2, the promoting effect of miR-520e inhibitor on cell proliferation and migration may be attenuated. In conclusion, the expression of miR-520e is modified by its promoter region DNA methylation, and miR-520e and its promoter region DNA methylation may be potential biomarkers in atherosclerosis.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"385-393"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141449559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sampurna Ghosh, Sk Eashayan Tanbir, Tulika Mitra, Sib Sankar Roy
{"title":"Unveiling stem-like traits and chemoresistance mechanisms in ovarian cancer cells through the TGFβ1-PITX2A/B signaling axis.","authors":"Sampurna Ghosh, Sk Eashayan Tanbir, Tulika Mitra, Sib Sankar Roy","doi":"10.1139/bcb-2024-0010","DOIUrl":"10.1139/bcb-2024-0010","url":null,"abstract":"<p><p>Ovarian cancer (OC) is the deadliest gynecological malignancy, having a high mortality rate due to its asymptomatic nature, chemoresistance, and recurrence. However, the proper mechanistic knowledge behind these phenomena is still inadequate. Cancer recurrence is commonly observed due to cancer stem cells which also show chemoresistance. We aimed to decipher the molecular mechanism behind chemoresistance and stemness in OC. Earlier studies suggested that PITX2, a homeobox transcription factor and, its different isoforms are associated with OC progression upon regulating different signaling pathways. Moreover, they regulate the expression of drug efflux transporters in kidney and colon cancer, rendering chemoresistance properties in the tumor cell. Considering these backgrounds, we decided to look for the role of PITX2 isoforms in promoting stemness and chemoresistance in OC cells. In this study, PITX2A/B has been shown to promote stemness and to enhance the transcription of ABCB1. PITX2 has been discovered to augment ABCB1 gene expression by directly binding to its promoter. To further investigate the regulatory mechanism of PITX2 gene expression, we found that TGFβ signaling could augment the PITX2A/B expression through both SMAD and non-SMAD signaling pathways. Collectively, we conclude that TGFβ1-activated PITX2A/B induces stem-like features and chemoresistance properties in the OC cells.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"394-409"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141557899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Berta Buey, Eva Latorre, Marta Castro, Marta Sofía Valero, Miguel Ángel Plaza, María Pilar Arruebo, Inés Abad, Ana Rodríguez-Largo, Lourdes Sánchez, José Emilio Mesonero
{"title":"Neuroprotective effects of whey and buttermilk-based formulas on a DSS-induced colitis murine model.","authors":"Berta Buey, Eva Latorre, Marta Castro, Marta Sofía Valero, Miguel Ángel Plaza, María Pilar Arruebo, Inés Abad, Ana Rodríguez-Largo, Lourdes Sánchez, José Emilio Mesonero","doi":"10.1139/bcb-2024-0153","DOIUrl":"10.1139/bcb-2024-0153","url":null,"abstract":"<p><p>Inflammatory bowel disease is a gut-brain axis disorder that comprises chronic inflammatory conditions affecting the gastrointestinal tract, where alterations in the mood of patients are common. Gut-brain axis is a bidirectional communication that link gut and brain. The close association between inflammatory bowel disease and neuroinflammation has far-reaching implications, as is increasingly recognized as a contributing factor to neuropsychiatric and neurodegenerative diseases. The increasing prevalence and high economic cost, together with the loss of life quality of people suffering from these diseases, point to the need to find alternatives to alleviate them. Exploring new therapeutic avenues prompts us to consider the potential benefits of milk fractions, taking advantage of the use of dairy by-products, such as whey and buttermilk. This study examines the impact of cow's whey- and buttermilk-based formulas supplemented with bovine lactoferrin and milk fat globule membrane on the expression of cytokines, as well as on the components of immune and serotonergic system of the brain in a murine model of dextran sodium sulfate-induced colitis. Our results show the potential of these dairy by-products, especially whey, as functional foods in ameliorating neuroinflammation and safeguarding the central nervous system function amid the neurological complications induced or concomitant with intestinal inflammatory processes.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Grace Martin, Dhuha Al-Sajee, Molly Gingrich, Rimsha Chattha, Michael Akcan, Cynthia M F Monaco, Megan C Hughes, Christopher G R Perry, Irena A Rebalka, Mark A Tarnopolsky, Thomas J Hawke
{"title":"Skeletal muscle mitochondrial morphology negatively affected in mice lacking Xin.","authors":"Grace Martin, Dhuha Al-Sajee, Molly Gingrich, Rimsha Chattha, Michael Akcan, Cynthia M F Monaco, Megan C Hughes, Christopher G R Perry, Irena A Rebalka, Mark A Tarnopolsky, Thomas J Hawke","doi":"10.1139/bcb-2024-0034","DOIUrl":"10.1139/bcb-2024-0034","url":null,"abstract":"<p><p>Altered mitochondrial structure and function are implicated in the functional decline of skeletal muscle. Numerous cytoskeletal proteins are known to affect mitochondrial homeostasis, but this complex network is still being unraveled. Here, we investigated mitochondrial alterations in mice lacking the cytoskeletal adapter protein, XIN (XIN-/-). XIN-/- and wild-type littermate male and female mice were fed a chow or high-fat diet (HFD; 60% kcal fat) for 8 weeks before analyses of their skeletal muscles were conducted. Immuno-electron microscopy (EM) and immunofluorescence staining revealed XIN in the mitochondria and peri-mitochondrial areas, as well as the myoplasm. Intermyofibrillar mitochondria in chow-fed XIN-/- mice were notably different from wild-type (large, and/or swollen in appearance). Succinate dehydrogenase and Cytochrome Oxidase IV staining indicated greater evidence of mitochondrial enzyme activity in XIN-/- mice. No difference in body mass gains or glucose handling was observed between cohorts with HFD. However, EM revealed significantly greater mitochondrial density with evident structural abnormalities (swelling, reduced cristae density) in XIN-/- mice. Absolute Complex I and II-supported respiration was not different between groups, but relative to mitochondrial density, was significantly lower in XIN-/-. These results provide the first evidence for a role of XIN in maintaining mitochondrial morphology and function.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"373-384"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141282912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Giuditta Pollio, Luigi Rosa, Anna Maria Costanzo, Rosalba Paesano, Giovanni Tripepi, Piera Valenti
{"title":"Lactoferrin efficacy in treating hyperferritinemia in patients suffering from pathologies unrelated to hereditary hemochromatosis.","authors":"Giuditta Pollio, Luigi Rosa, Anna Maria Costanzo, Rosalba Paesano, Giovanni Tripepi, Piera Valenti","doi":"10.1139/bcb-2024-0061","DOIUrl":"10.1139/bcb-2024-0061","url":null,"abstract":"<p><p>Ferritin (Ftn), a globular protein, sequesters 4500 atoms of iron per molecule. Elevated serum Ftn levels (hyperferritinemia) is an indicator of iron homeostasis disorders. We present the results of an observational study involving 17 patients with hyperferritinemia unrelated to hereditary hemochromatosis (HH). All participants received treatment with 200 mg of bovine lactoferrin (bLf) once (<i>n</i> = 14) or twice (<i>n</i> = 3) a day before meals. The patients, treated with 200 mg/day of bLf, exhibited a significant increase in red blood cells (+10%, <i>p</i> < 0.001), hemoglobin (+4%, <i>p</i> < 0.001), and hematocrit (+15%, <i>p</i> = 0.004), accompanied by a significant reduction in serum Ftn levels (-52%, <i>p</i> < 0.001), C-reactive protein (CRP) (-85.0%, <i>p</i> < 0.001), and D-dimers (-19%, <i>p</i> < 0.001). Among the three patients treated with 400 mg/day of bLf, two had effects similar to those of patients bLf-treated with 200 mg/day and one experienced a strong reduction of Ftn, CRP, and erythrocyte sedimentation rate (from -97% to -75%). The decrease in serum Ftn levels due to bLf treatment was largely independent of gender (<i>p</i> = 0.78), age (<i>p</i> = 0.66), baseline symptoms (<i>p</i> = 0.20), and concomitant acute (<i>p</i> = 0.34) and chronic (<i>p</i> = 0.53) infections. Although this observational pilot study yields positive effects in patients with hyperferritinemia unrelated to HH treated with bLf, a larger sample size is needed for conclusive results.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"410-417"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141562566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"20 years of choices: a fight for increased funding for graduate students.","authors":"Fabian Rohden, Thomas Bailey, Sarah Laframboise","doi":"10.1139/bcb-2024-0029","DOIUrl":"10.1139/bcb-2024-0029","url":null,"abstract":"<p><p>After 20 years of stagnation, federal scholarships have finally been increased within the new budget of the Canadian government. Tuition fees, inflation, and costs of living kept rising, which has resulted a rising number of graduate students in the life sciences living below poverty line, despite working far more than 40 h a week on science research in Canada. This does not only negatively affect the students research projects and thus science and innovation in Canada, but also their downstream decisions on whether to continue a research career in Canada and what jobs and economic endeavors to pursue. Graduate students are not just a line item in the budgets of universities, but integral for science and innovation, as well as the future high-quality personnel of the country. This importance should be reflected in all stipends and salaries of graduate students, not just the ones with a government scholarship.</p>","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"346-350"},"PeriodicalIF":2.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142071857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}