Funderernst3222
To study reduction in pain score after treatment with intravenous regional anesthesia (IVRA) and Stellate ganglion block (SGB) combination on complex regional pain syndrome (CPRS) patients and to quantify patients' satisfaction with treatment and occurrence of complications.
This is a record-based retrospective review carried out in 2020, targeting patients treated in the University of Jordan Hospital, Amman, Jordan, over the years 2002-2020.
Among 99 patients, a significant drop in pain scores occurred in 88% of the patients' sample. Gender, age, type of CRPS, and duration of symptoms didn't affect statistical results. An average of 8.6 sessions needed to achieve 50% drop in pain score, and 2-3 sessions for first clinical improvement. Patients with previous application of plaster of Paris had increased success rates.
We find it practical, inexpensive, safe, and straightforward to combine SGB with IVRA for CRPS patients.
We find it practical, inexpensive, safe, and straightforward to combine SGB with IVRA for CRPS patients.Delayed and chronic wounds result from the dysregulation of molecular and cellular events associated with wound healing, including migration, inflammation, angiogenesis, extracellular matrix (ECM) remodeling, and re-epithelialization. Adipose tissue is an abundant, easily accessible, and rich source of mesenchymal stem cells (MSCs) with high therapeutic potential. In addition to their capability to differentiate into various lineages with specialized functions, adipose-derived MSCs (AMSCs) can mediate to the wound repair process through the secretion of different growth factors and mediators rather than making structural contribution alone. Adipose-derived MSCs mediate the formation of blood vessels, recruit progenitor cells, stimulate cell differentiation and ECM formation, and promote wound healing by releasing immune mediators and exosomes. Herein, we discuss and review the therapeutic potential of AMSCs for wound repair via acceleration of wound closure, re-epithelialization, enhancement of angiogenesis and immunomodulation of prolonged inflammatory responses, as well as the current challenges in clinical implementation.
Hypoxia facilitates an aggressive phenotype and immune evasion in solid tumors including bladder cancer (BC). PACAP 1-38 mw Sphingosine kinase 1 (SphK1) is aberrantly expressed and correlated with poor prognosis in BC patients. However, its roles in hypoxia-evoked malignancies and immune evasion in BC remain elusive.
The expression of SphK1 in BC tissues was analysed using a bioinformatics database. BC cells were transfected with si-SphK1 or recombinant HIF-1α plasmids under hypoxic conditions. The mRNA level, activity and protein expression of SphK1 were determined. Transwell assay was performed to evaluate cell invasion. After co-culture with natural killer (NK) cells, NK cell cytotoxicity to BC cells was assessed. The involvement of sphingosine-1-phosphate (S1P)/HIF-1α signaling was analysed by ELISA, qRT-PCR and western blot.
UALCAN and GEPIA database confirmed high expression of SphK1 in BC tissues. Moreover, hypoxia increased the expression and activity of SphK1. Loss of SphK1 inhibited hypoxia-induced cell invasion. IL-2 induced NK cell activation by secreting TNF-α and IFN-γ. Hypoxia antagonized NK cell activation-evoked cytotoxicity to BC cells. Intriguingly, SphK1 knockdown reversed hypoxia-induced cell resistance to NK cell killing. Mechanically, SphK1 loss inhibited hypoxia-activated the S1P/HIF-1α signaling. However, S1P addition reversed the inhibitory effects of SphK1 down-regulation on hypoxia-activated S1P/HIF-1α signaling. Notably, reactivating HIF-1α overturned the suppressive roles of SphK1 loss in decreasing hypoxia-induced cell invasion and resistance to NK cell cytotoxicity.
Targeting SphK1 may inhibit hypoxia-evoked invasion and immune evasion via the S1P/HIF-1α signaling, indicating a promising therapeutic target for BC.
Targeting SphK1 may inhibit hypoxia-evoked invasion and immune evasion via the S1P/HIF-1α signaling, indicating a promising therapeutic target for BC.
Limited data are available on the performance of SARS-CoV-2 antibody assays and data collected during pregnancy vary widely. The objective of this study was to estimate the seroprevalence of antibodies against SARS-CoV-2 in pregnant individuals in Rhode Island and to evaluate whether the prevalence differed by month of collection, age, county of residence, or economic status as estimated by zip code.
Pre-pandemic (2019) and early pandemic (2020) serum samples, collected for prenatal screening between 15 and 22 weeks of gestation, were analyzed utilizing two SARS-CoV-2 immunoglobulin G (IgG) automated assays that targeted the viral nucleocapsid (anti-N) or spike (anti-S) receptor binding domain proteins.
Among 756 pre-pandemic samples, one anti-S IgG and 13 anti-N IgG were identified. No samples were positive for both. Among 787 pandemic specimens, 16 (2.03%) were positive for both anti-N IgG and anti-S IgG. When stratified by month of collection, there was a significant increase in seropositivity rate (
=0.023). Seropositivity rates were associated with lower income levels (
=0.08) but this was not statistically significant. No trend by maternal age was found (
=0.70).
When a positive result was defined as both anti-N IgG and anti-S IgG, false positives were unlikely. Based on this methodology, serology could be utilized to monitor infection trends during pregnancy.
When a positive result was defined as both anti-N IgG and anti-S IgG, false positives were unlikely. Based on this methodology, serology could be utilized to monitor infection trends during pregnancy.
Gastric cancer is one of the most common and deadly cancers worldwide. Basic leucine zipper transcription factor ATF-like 3 (BATF3) plays a key role in tumor immunity. However, the function of BATF3 in gastric cancer remains unclear. Here, we demonstrated BATF3 positively regulated proliferation and radioresistance of gastric cancer cells by regulating S1PR1/STAT3 pathway.
The RNA-seq analyzed the gene expression by UALCAN web portal and Tumor Immune Estimation Resource. RT-qPCR and western blot was performed to verify BATF3 expression in gastric cancer cells. The assays of CCK-8, EdU incorporation and colony formation were used to analyze cell proliferation, and radioresistance in AGS and MKN45 cells. Flow cytometry was used to detect the cell apoptosis of AGS and MKN45 in treatment with si-BATF3 or radiation. Finally, western blot was performed to measure the expression of cell apoptosis-related modules including Bax, cleaved-caspase3, cleaved-PARP and assess the regulation of S1PR1/STAT3 pathway.
BATF3 expression was upregulated in gastric cancer cells. Knockdown of BATF3 suppressed proliferation, radioresistance but promoted the radiation-induced apoptosis of gastric cancer cells through positively regulating S1PR1 expression and STAT3 phosphorylation.
Knockdown of BATF3 inhibits gastric cancer cell growth and radioresistance via S1PR1/STAT3 pathway. BATF3 would become a potential diagnostic indicator for gastric cancer and target of therapeutic treatment.
Knockdown of BATF3 inhibits gastric cancer cell growth and radioresistance via S1PR1/STAT3 pathway. BATF3 would become a potential diagnostic indicator for gastric cancer and target of therapeutic treatment.
To monitor fentanyl polydrug use over past six years.
Calculate percent of fentanyl and other drugs positive in urine drug tests.
Percent of fentanyl positive drug tests remained unchanged, but increases in fentanyl/methamphetamine and fentanyl/marijuana were observed.
Fentanyl laced illicit drugs remain a major substance abuse problem.
Fentanyl laced illicit drugs remain a major substance abuse problem.Granular acute lymphoblastic leukemia (ALL) is defined by the presence of intracytoplasmic granules in lymphoblastic blasts, mimicking acute myeloblastic leukemia. The disease is extremely rare in adults, and hence, the characteristics thereof are poorly understood. We report a case of a 70-year-old man diagnosed with granular ALL. Bone marrow examination showed blasts with azurophilic granules in the cytoplasm, but immunophenotyping showed B-ALL with aberrant expression of myeloid antigens CD13 and CD33. Karyotyping revealed monosomy 7, and targeted NGS showed DNMT3A mutation, which suggested poor prognosis. Despite conventional chemotherapy treatment, the patient did not achieve complete remission. He declined further chemotherapy treatment and was maintained on only supportive care. This is the first report of adult granular ALL with DNMT3A mutation and monosomy 7.
Solute carrier (SLC) genes are known to be involved in the development of human tumors. Here, we identified a group of non-small cell lung cancer (NSCLC) - associated SLC genes and explored the role and potential mechanism of action for
in NSCLC.
We used public NSCLC gene expression databases to select NSCLC-associated SLC genes. A Cox proportional risk model was used to estimate the hazard rate of selected NSCLC-associated SLC genes.
was selected as a candidate for further study. The expression and effect on survival of
in multiple NSCLC datasets were investigated. The expression of
was modulated in Calu-6 and A549 cells by transfection and a series of proliferation and migration assays were performed. Parameters related to glycolysis and HK2 expression were detected after transfection.
Fourteen SLC genes were identified as NSCLC-related SLC genes. Among them,
was downregulated in tumor tissues in multiple datasets. Low expression of
was indicative of poor prognosis in NSCLC. Knockdown of
promoted proliferation and migration in Calu-6 cells. Overexpression of SLC14A1 showed the opposite effect in A549 cells. Additionally,
changes were associated with glycolysis. This was demonstrated by HK2 mRNA and protein levels being regulated by SLC14A1.
In our study
suppressed the proliferation and migration of NSCLC cell lines Calu-6 and A549 and was associated with glycolysis. Therefore,
may be a diagnostic marker or therapeutic target for NSCLC patients.
In our study SLC14A1 suppressed the proliferation and migration of NSCLC cell lines Calu-6 and A549 and was associated with glycolysis. Therefore, SLC14A1 may be a diagnostic marker or therapeutic target for NSCLC patients.
The FDA approved adalimumab, an anti-tumor necrosis factor alpha agent, for the treatment of moderate to severe pediatric ulcerative colitis (UC) in February 2021. There are no real-world publications, however, on adalimumab as the first-line biologic in pediatric UC, a form of chronic inflammatory bowel disease (IBD).
A retrospective review was conducted to characterize the clinical courses of nine patients with moderate to severe pediatric UC who received adalimumab as their first biologic and had documented drug monitoring trough levels.
Seven of the nine patients, or 78%, were switched from adalimumab to another therapy due to continued symptoms or steroid-dependence at an average of 5 months from initiation. Six of these seven patients, or 86%, had adalimumab drug trough levels in the consensus therapeutic range. Three patients were successfully switched to infliximab.
Both the Crohn's disease-based dosing and the new FDA-approved pediatric UC dosing of adalimumab were ineffective in inducing remission in the majority of patients in our case series.
