Background: Although the association between maternal exposure to antibiotics and the risk of atopic dermatitis (AD) in childhood has been studied extensively, there still is a lack of clarity on the topic. The aim of this study was to summarize the published data and to examine if maternal exposure to antibiotics increases the risk of AD in childhood.Methods: Systematic search was performed in PubMed, Scopus, Web of Science, and Embase for all types of studies on the review subject independent of any language restrictions and published up to 28th December 2022. Data was analyzed using random-effects model and presented as pooled odds ratio (OR) with 95% confidence intervals (CI).Results: A total of 18 studies (5,354,282 mother-child pairs) were included. Maternal exposure to antibiotics was associated with an increased risk of AD in childhood (OR: 1.14, 95% CI: 1.06, 1.22, I²= 85%, p = 0.0003). The significance of the results was not affected by the location of the study (Asia or Europe). While subgroup analysis based on exposure assessment or diagnosis of AD demonstrated a tendency of increased risk of AD, the association was not statistically significant in multiple subgroups. Segregating data based on the timing of exposure did not affect the significance of the results for studies on all trimesters. However, there was no association between antibiotic exposure in the third trimester or just before delivery and the risk of childhood AD.Conclusion: The results of this meta-analysis suggest that maternal exposure to antibiotics may lead to a modestly increased risk of AD in offspring. The evidence is limited by high interstudy heterogeneity and bias in exposure and outcome assessment. Future studies are needed to explore if the timing of exposure, the dose, the number of prescriptions, and the type of antibiotic affect this association.Systematic Review Registration: https://www.crd.york.ac.uk/prospero/, identifier CRD42023387233.

Plerixafor in combination granulocyte‑colony stimulating factor (G‑CSF) has been used for the mobilization of hematopoietic stem cells (HSCs) to the peripheral blood for collection and subsequent autologous transplantation in patients with non‑Hodgkin lymphoma (NHL) and multiple myeloma (MM). The aim of this study was to systematically search the published literature and analyze evidence on the efficacy of additional plerixafor for successful HSC mobilization in patients with NHL and MM, and to evaluate the safety of the drug. The PubMed, Scopus, Cochrane Central Register of Controlled Trials (CENTRAL) and Google scholar databases were searched electronically for studies published in the English language up to March, 2019. Five studies (3 on NHL and 2 on MM) were included in this review article. The meta‑analysis of data of 364 patients in the treatment group and 368 patients in the control group, indicated that the mobilization of ≥5/6x106 CD34+ cells/kg in 4 or less apheresis days was superior with plerixafor + G‑CSF than with G‑CSF alone (RR=2.59, 95% CI: 1.40 to 4.81; P<0.0001). Similarly, a greater proportion of patients in the treatment group exhibited the mobilization of ≥2x106 CD34+ cells/kg in 4 or less apheresis days (RR=1.46, 95% CI: 1.01 to 2.12; P=0.04). The addition of plerixafor significantly increased the total collection of CD34+ cells (random: MD=4.21; 95% CI: 2.85 to 5.57; P<0.00001). Meta‑analysis indicated no significant increase in adverse events with the addition of plerixafor for HSC mobilization (RR=1.03, 95% CI: 0.99 to 1.06; P=0.16). On the whole, the findings of this study indicate that the addition of plerixafor to G‑CSF leads to an increased HSC collection in a shorter period of time with no concomitant increase in adverse events. Further randomized controlled trials with a larger sample size evaluating short term efficacy, as well as long term survival would help to further strengthen the evidence on this subject.

The somatic cells of a multicellular organism contain an identical complement of genes that need to be expressed specifically and appropriately to allow the normal development and functions associated with an organism. In the eukaryotic cell nucleus, genes are packaged with nucleoprotein histones into chromatin. The human growth hormone (GH)/chorionic somatomammotropin (CS) gene family offers an excellent model to study the relationship between chromatin structure and transcription factor binding in terms of tissue-specific gene expression. The GH/CS gene family consists of five genes (GH-N, GH-V, CS-A, CS-B and CS-L), contained in a single locus on chromosome 17. Although they share approximately 94% sequence similarity, GH-N expression is restricted to pituitary somatotropes while the four placental GH/CS genes are expressed in the villus syncytiotrophoblast. Appropriate expression in vivo is dependent on remote sequences found 14–32 kb upstream of GH-N in the loci of adjacent genes, and these sequences are characterized by five (I–V) nuclease-hypersensitive sites (HS). Pituitary-specific factor Pit-1 binds at HS I/II and plays an essential role in chromatin remodeling and GH-N expression; however, the processes that lead to HS I/II accessibility are unknown. We discuss the possibility that Pit-1-driven remodeling at HS III may precede that at HS I/II in the pituitary. Also, in pituitary chromatin, all five GH/CS genes share similar nuclease sensitivity, suggesting that the conformation of the placental genes is not inhibitory to transcription. Given that the promoters of both GH-N and the placental GH/CS genes contain Pit-1-binding sites, possible mechanisms to restrict placenta GH/CS promoter activity in the pituitary are discussed, including active repression via P sequences located upstream of each of the placental GH/CS genes. Positively or negatively influencing those components known to be important for pituitary transcription may link epigenetic events to key transcription factors in the overall picture of tissue-specific control of gene expression.

Platelet-derived polyphosphate has previously been indicated to induce coagulation. However, industrially synthesized polyphosphate has been found to have different effects from those of the platelet-derived form. The present study investigated whether synthetic sodium polyphosphate inhibits coagulation using routine coagulation tests and thromboelastography. Synthetic polyphosphate was found to inhibit adenosine diphosphate-, epinephrine-, arachidonic acid-, ristocetin-, thrombin-, oxytocin- and pituitrin-induced platelet aggregation. The effects of synthetic polyphosphate in clotting inhibition were revealed by the analysis of clotting factor activity and platelet aggregation tests. Synthetic polyphosphate may inhibit platelet aggregation by reducing platelet calcium levels, as indicated by the results of flow cytometric analysis and high-throughput fluorescent screening. Furthermore, analysis of thromboxane (TX)B2 by ELISA indicated that synthetic polyphosphate reduces platelet aggregation by inhibiting the TXA2 signaling pathway. In conclusion, synthetic polyphosphate inhibits clotting factor activity and endogenous coagulation by reducing the levels of calcium ions and TXA2 to curb platelet aggregation.

Pregnancy can lead to the recurrence or exacerbation of immune thrombocytopenia (ITP). Currently, first-line treatments of low-dose corticosteroids or intravenous immunoglobulin are considered safe and effective for both pregnant women and fetuses. However, there is no well-established treatment option for patients who are refractory to these medications. Herein, we report a case of a 31-year-old pregnant woman with recurrent and refractory ITP who was safely and effectively treated with hetrombopag, with no influence on the infant's platelet count. This case explores a new treatment option for the management of recurrent and refractory ITP in pregnancy.

Hemophagocytic lymphohistiocytosis (HLH) is an aggressive and life-threatening syndrome of excessive immune activation. Mesenchymal stem cells (MSCs) generate an immunosuppressive microenvironment by secreting cytokines and have been used to treat autoimmune diseases. We report the first case of refractory secondary HLH treated with umbilical cord MSCs. A 52-year-old Chinese female patient with a history of type 2 diabetes was diagnosed with refractory secondary HLH based upon the HLH-2004 protocol and was treated by infusion of third-party umbilical cord MSCs (1.4 × 10⁶ cells/kg of body weight, 70 × 10⁶ cells in total) from the stem cell bank of Hainan Province. Body temperature recovered to normal on the sixth day after infusion with umbilical cord MSCs, and the levels of inflammatory factors macrophage inflammatory protein (MIP)-1α, interleukin (IL)-12p70, stromal cell-derived factor (SDF)-1α, and IL-7 decreased significantly. Blood glucose levels were significantly lower than before treatment, and the amount of insulin needed was significantly reduced. Umbilical cord MSCs can relieve the symptoms of refractory secondary HLH and have a therapeutic effect on insulin resistance in type 2 diabetes mellitus.