ObjectiveTo study the effect of Bufei Tongbi decoction on pulmonary fibrosis in diabetic rats via the transforming growth factor-β₁ （TGF-β₁）/phosphorylated Smad family member 3 （p-Smad3） signaling pathway. MethodsStreptozotocin （60 mg·kg^-1） and bleomycin （24.80 U·kg^-1） were used to prepare the rat model of diabetes with pulmonary fibrosis by intratracheal injection. Sixty rats were randomly assigned into blank， model， low-， medium-， and high-dose （3.98， 7.95， and 15.90 g·kg^-1， respectively） Bufei Tongbi decoction， and pirfenidone （0.36 mg·kg^-1） groups （n=10）. The successfully modeled rats in each group were administrated with corresponding agents once per day for four consecutive weeks. After drug administration， fasting blood glucose and lung function indicators were measured. Chemical immunoassay was employed to determine the serum levels of hydroxyproline （Hyp）， hyaluronic acid （HA）， and laminin （LN）. The lung index was determined by the wet and dry methods. The pathological changes in the lung tissue were observed by hematoxylin-eosin （HE） staining， and the degree of fibrosis was detected by Masson staining. The mRNA and protein levels of TGF-β₁， p-Smad3， Smad3， α-smooth muscle actin （α-SMA）， collagen type Ⅰ alpha 1 （Col1A1）， and fibronectin were determined by PCR and Western blotting， respectively. ResultsCompared with the blank group， the model group showed alveolar septa thickening， obvious thickening of the basement membrane of pulmonary blood vessels， severe destruction of the alveolar structure， structural disarrangement of the lung parenchyma， and an increase in the proportion of inflammatory cell infiltration in the lung tissue， together with a large amount of blue collagen deposition and a large amount of collagen fibroplasia in the bronchial wall， vessel wall， interstitium， and alveolar wall， which indicated severe fibrosis. Bufei Tongbi decoction groups and the pirfenidone group showed lower fasting blood glucose level （P<0.05） and higher forced vital capacity （FVC）， cytoplasmic dynein （Cydn）， FEV_0.3/FEV ratio， and lung index （P<0.05） than the model group. Moreover， these groups demonstrated alleviated lung fibrosis， elevated Hyp， HA， and LN levels， down-regulated mRNA levels of α-SMA， Col1A1， and fibronectin， and down-regulated protein levels of TGF-β₁， Smad3， p-Smad3， α-SMA， Col1A1， and fibronectin （P<0.05）. ConclusionBufei Tongbi decoction can inhibit pulmonary fibrosis in diabetic rats by inhibiting the TGF-β₁/p-Smad3 signaling pathway.

Objective: To explore the distribution of traditional Chinese medicine (TCM) syndromes in children with hepatolenticular degeneration (Wilson disease, WD) based on factor analysis and cluster analysis. Methods: From November 2018 to November 2023, general information (gender, age of admission, age of onset, course of disease, clinical staging, Western medicine clinical symptoms, and family history) and TCM four-examination informations (symptoms and signs) were retrospectively collected from 757 cases of children with WD at the First Affiliated Hospital of Anhui University of Chinese Medicine, and factor analysis and cluster analysis were used to investigate TCM syndromes in children with WD. Results: A total of 757 children with WD were included, of which 483 were male and 274 were female; the median age at admission was 12.58 years, the median age at onset was 8.33 years, and the median course of disease was 24.37 months; clinical typing result indicated 506 cases of hepatic type, 133 cases of brain type, 99 cases of mixed-type, and 19 cases of other type; 36.46% of the children had no clinical symptoms (elevated aminotransferases or abnormalities in copper biochemistry); a total of 177 cases had a definite family history, and 10 cases had a suspected family history. Forty-three TCM four-examination information were obtained, with the top 10 in descending order being feeling listless and weak, brown urine, slow action, inappetence, dim complexion, slurred speech, angular salivation, body weight loss, hand and foot tremors, and abdominal fullness. In children with WD, the syndrome element of disease location was primarily characterized by the liver, involving the spleen and kidney, and the syndrome elements of disease nature were characterized by dampness, heat, and yin deficiency. Based on factor analysis and cluster analysis, five TCM syndromes were derived, which were, in order, syndrome of dampness-heat accumulation (265 cases, 35.01%), syndrome of yin deficiency of the liver and kidney (202 cases, 26.68%), syndrome of liver hyperactivity with spleen deficiency (185 cases, 24.44%), syndrome of qi and blood deficiency (79 cases, 10.44%), and syndrome of yang deficiency of the spleen and kidney (26 cases, 3.43%). Conclusion The TCM syndromes of children with WD were primarily syndromes of dampness-heat accumulation, yin deficiency of the liver and kidney, and liver hyperactivity with spleen deficiency. The liver was the main disease location, and the disease nature was characterized by deficiency in origin and excess in superficiality, excess and deficiency mixed. These findings suggest that treating children with WD should be based on the liver while also considering the spleen and kidney.

Objective To investigate the changes in the prevalence of Babesia microti infections, spleen morphology and proportions of splenic immune cells in BALB/c mice following intravenous and intraperitoneal injections, so as to provide insights into unraveling the immune regulatory mechanisms of Babesia infections. Methods Laboratory - maintained B. microti strains were prepared into whole blood samples with 10% prevalence of B. microti infection. A total of 75 BALB/c mice were randomly divided into three groups, including the normal control group, intravenous injection group, and intraperitoneal injection group, of 25 mice in each group. Mice in the intravenous and intraperitoneal injection groups were administered 100 μL of whole blood samples with 10% prevalence of B. microti infection, with the day of injection recorded as d0, and animals in the normal control group were given no treatments. Blood was sampled from mice in each group via the tail tip on d7, d14, d21, d28 and d35, and prepared into thin-film blood smears, and B. microti infection was observed in red blood cells. Five mice were randomly sampled from each group and sacrificed on d7, d14, d21, d28 and d35, and spleen was collected for measurement of spleen size and weight. In addition, splenic cells were isolated, and the proportions of CD3e⁺ T cells, CD45R⁺ B cells, CD49b⁺ nature killer (NK) cells, and F4/80⁺ macrophages were detected in CD45⁺ lymphocytes using flow cytometry. Results The prevalence of B. microti infection in the intravenous (22.80%) and intraperitoneal injection groups (44.82%) peaked on d7 (χ² = 8.141, P < 0.01) and then rapidly decreased, and no parasites were observed on d35. The longest mouse spleen length [(32.91 ± 2.20) mm] and width [(9.82 ± 0.43) mm], and the greatest weight [(0.78 ± 0.10) g] were found on d14 in the intravenous injection group, and the longest spleen length [(32.42 ± 3.21) mm] and width [(10.25 ± 0.73) mm], and the greatest weight [(0.73 ± 0.09) g] were seen in the intra-peritoneal injection group on d21, d7 and d14, respectively. There were significant differences among the intravenous injection group, intraperitoneal injection group and the normal control group in terms of spleen length (F = 10.310, P < 0.05), width (F = 9.824, P < 0.05), and weight (F = 10.672, P < 0.05) on d21, and the mouse spleen length, width and weight were all significantly greater in the intraperitoneal injection group than in the intravenous injection group (allP values < 0.05). The proportions of splenic CD3e⁺ T cells [(60.60 ± 6.20)% and (39.68 ± 7.62)%], CD45R⁺ B cells [(43.32 ± 2.08)% and (49.53 ± 4.90)%], CD49b⁺ NK cells [(6.88 ± 1.34)% and (7.71 ± 1.59)%], and F4/80⁺ macrophages [(2.21 ± 0.29)% and (3.80 ± 0.35)%] peaked on d14, d21, d21 and d14 in the intravenous and intraperitoneal injection groups, respectively. There were significant differences in the proportions of CD3e⁺ T cells (F = 16.730, P < 0.05) and F4/80⁺ macrophages (F = 15.941, P < 0.05) among the intravenous injection group, intraperitoneal injection group and normal control group on d14, and a higher proportion of CD3e⁺ T cells and a lower proportion of F4/80⁺ macrophages were detected in the intravenous injection group than in the intraperitoneal injection group (both P values < 0.01). There were significant differences among the intravenous injection group, intraperitoneal injection group and normal control group on d21 in terms of proportions of splenic CD3e⁺ T cells (F = 9.252, P < 0.05), CD45R⁺ B cells (F = 14.349, P < 0.05), CD49b⁺ NK cells (F = 13.436,P < 0.05), and F4/80⁺ macrophages (F = 8.180, P < 0.05), and a higher proportion of CD3e⁺ T cells and lower proportions of CD45R⁺ B cells and F4/80⁺ macrophages were detected in the intravenous injection group than in the intraperitoneal injection group (all P values < 0.01). In addition, there was a significant difference in the proportion of CD3e⁺ T cells among the intravenous injection group, intraperitoneal injection group and normal control group on d28 (F = 9.772,P < 0.05), and a lower proportion of CD3e⁺ T cells was found in the intravenous injection group than in the intraperitoneal injection group (P < 0.01). Conclusions Both intraperitoneal and intravenous routes are effective to induce B. microti infections in BALB/c mice, and the prevalence of B. microti infections is higher in BALB/c mice through the intraperitoneal route than through the intravenous route. Intraperitoneal and intravenous injections with B. microti cause diverse spleen morphologies and proportions of splenic immune cells in mice, indicating routes of B. microti infections cause different impacts on immune response mechanisms in mice.

The FoxA genes belong to a conserved family of transcription factors, that play a crucial role in regulating embryonic development, cellular differentiation, and disease pathogenesis. Initially identified as hepatocyte nuclear factor 3α (Hnf3α), FoxA is pivotal in activating liver-specific genes and contributing to liver morphogenesis. Studies have shown that FoxA proteins interact with specific DNA sequences and nucleosome-bound DNA, altering the local chromatin structure to regulate gene expression. The unique ability has earned them the designation of “pioneer factors”. The FoxA family comprises three members: FoxA1, FoxA2, and FoxA3. FoxA1 is predominantly expressed in endoderm-derived organs such as the lungs, liver, pancreas, and prostate, where it regulates hormone metabolism, cell cycle, and cell proliferation. FoxA2 is primarily expressed in the floor plate of the vertebrate spinal cord, where it plays a key role in establishing the dorsal-ventral patterning of the neural tube. FoxA3 is mainly expressed in the testes, where it regulates germ cell formation. FoxA genes exhibit functional diversity in embryonic development across different species, offering insights into their evolutionary roles. For instance, zebrafish embryos with mutations in the foxa2^-/- gene can survive, providing an opportunity to study embryonic development mechanisms. Currently, a growing body of research suggests that FoxA genes are involved in early embryonic development, cancer, and metabolism-related diseases. This paper summarizes the discovery, expression patterns, and biological functions of the FoxA genes while identifying key scientific questions that remain unresolved. It aims to provide readers a solid scientific basis for understanding the molecular mechanisms through which FoxA genes regulate embryonic development and contribute to cancer pathogenesis.

ObjectiveTo investigate the influence of histone deacetylase 3 (HDAC3) on the occurrence, development of psoriasis-like inflammation in mice, and the relative immune mechanisms. MethodsHealthy C57BL/6 mice aged 6-8 weeks were selected and randomly divided into 3 groups: control group (Control), psoriasis model group (IMQ), and HDAC3 inhibitor RGFP966-treated psoriasis model group (IMQ+RGFP966). One day prior to the experiment, the back hair of the mice was shaved. After a one-day stabilization period, the mice in Control group was treated with an equal amount of vaseline, while the mice in IMQ group was treated with imiquimod (62.5 mg/d) applied topically on the back to establish a psoriasis-like inflammation model. The mice in IMQ+RGFP966 group received intervention with a high dose of the HDAC3-selective inhibitor RGFP966 (30 mg/kg) based on the psoriasis-like model. All groups were treated continuously for 5 d, during which psoriasis-like inflammation symptoms (scaling, erythema, skin thickness), body weight, and mental status were observed and recorded, with photographs taken for documentation. After euthanasia, hematoxylin-eosin (HE) staining was used to assess the effect of RGFP966 on the skin tissue structure of the mice, and skin thickness was measured. The mRNA and protein expression levels of HDAC3 in skin tissues were detected using reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot (WB), respectively. Flow cytometry was employed to analyze neutrophils in peripheral blood and lymph nodes, CD4⁺ T lymphocytes, CD8⁺ T lymphocytes in peripheral blood, and IL-17A secretion by peripheral blood CD4⁺ T lymphocytes. Additionally, spleen CD4⁺ T lymphocyte expression of HDAC3, CCR6, CCR8, and IL-17A secretion levels were analyzed. Immunohistochemistry was used to detect the localization and expression levels of HDAC3, IL-17A, and IL-10 in skin tissues. ResultsCompared with the Control group, the IMQ group exhibited significant psoriasis-like inflammation, characterized by erythema, scaling, and skin wrinkling. Compared with the IMQ group, RGFP966 exacerbated psoriasis-like inflammatory symptoms, leading to increased hyperkeratosis. The psoriasis area and severity index (PASI) skin symptom scores were higher in the IMQ group than those in the Control group, and the scores were further elevated in the IMQ+RGFP966 group compared to the IMQ group. Skin thickness measurements showed a trend of IMQ+RGFP966>IMQ>Control. The numbers of neutrophils in the blood and lymph nodes increased sequentially in the Control, IMQ, and IMQ+RGFP966 groups, with a similar trend observed for CD4⁺ and CD8⁺ T lymphocytes in the blood. In skin tissues, compared with the Control group, the mRNA and protein levels of HDAC3 decreased in the IMQ group, but RGFP966 did not further reduce these expressions. HDAC3 was primarily located in the nucleus. Compared with the Control group, the nuclear HDAC3 content decreased in the skin tissues of the IMQ group, and RGFP966 further reduced nuclear HDAC3. Compared with the Control and IMQ groups, RGFP966 treatment decreased HDAC3 expression in splenic CD4⁺ and CD8⁺ T cells. RGFP966 treatment increased the expression of CCR6 and CCR8 in splenic CD4⁺ T cells and enhanced IL-17A secretion by peripheral blood and splenic CD4⁺ T lymphocytes. Additionally, compared with the IMQ group, RGFP966 reduced IL-10 protein levels and upregulated IL-17A expression in skin tissues. ConclusionRGFP966 exacerbates psoriatic-like inflammatory responses by inhibiting HDAC3, increasing the secretion of the cytokine IL-17A, and upregulating the expression of chemokines CCR8 and CCR6.

[Objective] To compare the efficacy and safety of deglycerolized red blood cells (DRBC) and suspended red blood cells (SRBC) based on the propensity score matching (PSM) method, so as to provide evidence for the rational use of DRBC resources in clinical practice. [Methods] A total of 89 patients who received DRBC transfusion and 2 916 patients who received SRBC transfusion in our hospital from January 2023 to September 2024 were included. A 1∶1 nearest neighbor PSM was used to balance covariates such as gender, age, and body mass index (BMI). The changes of hemoglobin (Hb), red blood cell (RBC) count, hematocrit (HCT), and inflammatory markers such as white blood cell (WBC) count, neutrophil (NE) count, C-reactive protein (CRP), and Interleukin-6(IL-6) in the last 72 hours after transfusion were analyzed by SPSS 26.0 and R software to evaluate clinical efficacy and transfusion safety. [Results] The baseline of the two groups was balanced after PSM (P>0.05). There was no significant difference in the total effective rate between the DRBC group (80.9%) and the SRBC group (86.5%) (P>0.05). In the SRBC group, WBC (×10 /L) increased from 9.634±6.742 to 10.147±6.835, CRP (mg/dL) increased from 5.468±4.647 to 6.174±6.114, and IL-6(pg/mL) decreased from 213.733±587.191 to 157.255±552.626. In the DRBC group, WBC (×10 /L) decreased from 11.123±7.880 to 11.011±8.549, CRP (mg/dL) decreased from 5.729±4.761 to 5.326±4.466, and IL-6(pg/mL) decreased from 238.806±639.060 to 152.255±266.558. Compared with the before treatment, the differences between the SRBC group and DRBC group were not statistically significant (P>0.05). Among all patients included in the statistics, the overall incidence of transfusion adverse reactions was 0.205% (6/2 916) in the SRBC group, and no adverse reactions occurred in the DRBC group. The incidence in the SRBC group was higher than that in the DRBC group. [Conclusion] Based on PSM analysis, there was no significant difference in the efficacy and safety of DRBC transfusion compared with SRBC transfusion, which can provide evidence-based support for routine application.

[Objective] To retrospectively analyse the serological characteristics of hemolytic transfusion reactions caused by Rh and Kidd antibodies, and to provide reference for safe, timely, and effective blood transfusion. [Methods] Two cases of patients with RhCcEe and Kidd blood type who experienced allogeneic transfusion at Dazhou Central Hospital were selected. A series of immunohematological tests were performed, including ABO, RhDCcEe and Kidd blood typing, unexpected antibody screening and identification, crossmatching, direct antiglobulin test, acid elution test, and capillary centrifugation to separate the patient's own red blood cells from donated red blood cells. [Results] Unexpected antibody screening, antibody identification, and direct antiglobulin test were positive in both patients. Case 1 had anti-Jk in the plasma, but no specific antibodies were found in the eluate. Case 2 had anti-c and E in the plasma, and anti-E was detected in the eluate. High-speed capillary centrifugation revealed corresponding antigen-positive erythrocytes at the distal end of the blood samples of both patients. [Conclusion] Case 1 received Kidd allogeneic red blood cells, and case 2 received RhCcEe allogeneic red blood cells, and both patients developed the corresponding unexpected antibodies, which led to the occurrence of immune haemolytic blood transfusion reaction.

Objective: To explore the prospective association between multidimensional sleep indicators and the risk of newlyonset dental caries, providing a reference for childrens oral healthrelated sleep intervention. Methods: In October 2021, 1 417 students in grades 1 to 4 (aged 6 to 11) from two elementary schools in Bengbu, Anhui Province, were selected by cluster sampling method. Surveys and followup visits were conducted at baseline (T1), November 2022 (T2), May 2023 (T3), and November 2023 (T4), respectively, including parental questionnaires, oral health and physical examination. Bedtime, sleep duration, sleep midpoint, social jet lag, weekend catchup sleep, and sleep habits were collected and calculated. A multifactorial Cox proportional risk regression model was used to analyze the association between multidimensional sleep indicators and newlyonset caries in schoolaged children after 2 years. Results: The prevalence of dental caries in children was 65.1% at baseline, and the prevalence was 59.0% at the end of the 2year followup. Cox proportional risk regression model showed that for every 1point increase in the childrens bedtime resistance, nocturnal awakenings, parasomnias, and daytime sleepiness scores, the risk of newlyonset caries increased by 12% (HR=1.12, 95%CI=1.08-1.15), 22% (HR=1.22, 95%CI=1.15-1.29), 12% (HR=1.12, 95%CI=1.08-1.17), and 15% (HR=1.15, 95%CI=1.12-1.19), respectively; the risk of newlyonset caries increased by 23% for each 1 h increase in the length of weekend catchup sleep (HR=1.23, 95%CI=1.14 -1.33); compared with children who went to bed before 21:00 on school days, those who went to bed later than 22:00 had a 57% higher risk of newlyonset caries (HR=1.57, 95%CI=1.22-2.03). Compared to children who slept adequately (≥9 h/d), those with insufficient sleep had a 67% higher risk of new caries (HR=1.67, 95%CI=1.43-1.95) (P<0.01). Conclusions These findings suggest a significant association between sleep patterns/sleep disorders and the development of childhood dental caries. Incorporating sleep behavior optimization and sleep quality improvement into comprehensive caries prevention and oral health management protocols may represent a promising intervention strategy to enhance childrens oral health outcomes.

Objective: To analyze the incidence of statutory and keymonitored infectious diseases among school students in Beijing from 2016 to 2020, so as to provide a reference for developing the prevention and control of infectious diseases in schools. Methods: A descriptive statistical analysis was conducted on student cases aged 6-22 years in Beijing from 2016 to 2020 selected from the China Disease Surveillance Information Reporting Management System. Rate comparisons were performed using the 2 test and trend 2 test. Results: From 2016 to 2020, the overall incidence of statutory and keymonitored infectious diseases among students in Beijing showed an upward trend (χ2trend=582.42), the incidence rates of Category B and other infectious diseases exhibited a downward trend (χ2trend=82.71, 18.34), while Category C infectious diseases demonstrated a significant upward trend (χ2trend=911.75) (P<0.01). Among Category B infectious diseases, scarlet fever, bacillary dysentery, tuberculosis, and HIV/AIDS were predominant, with annual average incidence rates of 61.33/100 000, 35.38/100 000, 13.88/100 000, and 3.78/100 000, respectively. Except for HIV/AIDS, the reported incidence rates of other infectious diseases showed a declining trend. Among Category C infectious diseases, influenza, other infectious diarrhea, hand-foot-mouth disease, and mumps were predominant, with annual average incidence rates of 956.13/100 000, 114.39/100 000, 111.37/100 000, and 28.24/100 000, respectively. Influenza showed a significant upward trend (χ2trend=1 508.30), while the other infectious diarrhea, hand-foot-mouth disease, and mumps exhibited a downward trend (χ2trend=13.84, 25.78, 6.13) (P<0.05). Among other infectious diseases, varicella was predominant (χ2trend=17.47, P<0.05). Scarlet fever, influenza, hand-foot-mouth disease, and mumps had higher incidence rates among primary and middle school students; other infectious diarrhea and varicella were more prevalent among high school students; tuberculosis and bacillary dysentery were more common among high school and college students; and HIV/AIDS had higher incidence rates among college and high school students. Conclusion From 2016 to 2020, the incidence of Category B infectious diseases among students in Beijing showed a declining trend, while influenza, a Category C infectious disease, exhibited a significant upward trend.

Fibrosis, the pathological scarring of vital organs, is a severe and often irreversible condition that leads to progressive organ dysfunction. It is particularly pronounced in organs like the liver, kidneys, lungs, and heart. Despite its clinical significance, the full understanding of its etiology and complex pathogenesis remains incomplete, posing substantial challenges to diagnosing, treating, and preventing the progression of fibrosis. Among the various molecular players involved, platelet-derived growth factor-C (PDGF-C) has emerged as a crucial factor in fibrotic diseases, contributing to the pathological transformation of tissues in several key organs. PDGF-C is a member of the PDGFs family of growth factors and is synthesized and secreted by various cell types, including fibroblasts, smooth muscle cells, and endothelial cells. It acts through both autocrine and paracrine mechanisms, exerting its biological effects by binding to and activating the PDGF receptors (PDGFRs), specifically PDGFRα and PDGFRβ. This binding triggers multiple intracellular signaling pathways, such as JAK/STAT, PI3K/AKT and Ras-MAPK pathways. which are integral to the regulation of cell proliferation, survival, migration, and fibrosis. Notably, PDGF-C has been shown to promote the proliferation and migration of fibroblasts, key effector cells in the fibrotic process, thus accelerating the accumulation of extracellular matrix components and the formation of fibrotic tissue. Numerous studies have documented an upregulation of PDGF-C expression in various fibrotic diseases, suggesting its significant role in the initiation and progression of fibrosis. For instance, in liver fibrosis, PDGF-C stimulates hepatic stellate cell activation, contributing to the excessive deposition of collagen and other extracellular matrix proteins. Similarly, in pulmonary fibrosis, PDGF-C enhances the migration of fibroblasts into the damaged areas of lungs, thereby worsening the pathological process. Such findings highlight the pivotal role of PDGF-C in fibrotic diseases and underscore its potential as a therapeutic target for these conditions. Given its central role in the pathogenesis of fibrosis, PDGF-C has become an attractive target for therapeutic intervention. Several studies have focused on developing inhibitors that block the PDGF-C/PDGFR signaling pathway. These inhibitors aim to reduce fibroblast activation, prevent the excessive accumulation of extracellular matrix components, and halt the progression of fibrosis. Preclinical studies have demonstrated the efficacy of such inhibitors in animal models of liver, kidney, and lung fibrosis, with promising results in reducing fibrotic lesions and improving organ function. Furthermore, several clinical inhibitors, such as Olaratumab and Seralutinib, are ongoing to assess the safety and efficacy of these inhibitors in human patients, offering hope for novel therapeutic options in the treatment of fibrotic diseases. In conclusion, PDGF-C plays a critical role in the development and progression of fibrosis in vital organs. Its ability to regulate fibroblast activity and influence key signaling pathways makes it a promising target for therapeutic strategies aiming at combating fibrosis. Ongoing research into the regulation of PDGF-C expression and the development of PDGF-C/PDGFR inhibitors holds the potential to offer new insights and approaches for the diagnosis, treatment, and prevention of fibrotic diseases. Ultimately, these efforts may lead to the development of more effective and targeted therapies that can mitigate the impact of fibrosis and improve patient outcomes.