Notes

An uncommon physiological deviation of the submental artery.
Parechovirus type 3 (HPeV-3) infection is an important cause of illness in neonates. We present the first case of an infant with a HPeV-3 meningoencephalitis which presumably commenced in utero. Severe developmental delay was seen. In the case of inexplicable neonatal meningoencephalitis, an intrauterine onset of HPeV-3 infection might be the cause.
Chronic kidney disease (CKD) is a global health burden, and the current treatment options only slow down the disease progression. GLP-1 receptor agonists (GLP-1 RA) have shown a renal protective effect in models of CKD; however, the mechanism behind the beneficial effect is not understood. In this study, we investigate the effect of the GLP-1 RA liraglutide in the nephrotoxic serum nephritis (NTN) CKD model. Moreover, we compare the gene expression pattern of liraglutide-treated mice to the gene expression pattern of mice treated with the angiotensin converting enzyme inhibitor, enalapril.

The effect of liraglutide was tested in the NTN model by evaluating the glomerular filtration rate (GFR), albuminuria, mesangial expansion, renal fibrosis, and renal inflammation. Furthermore, the regulation of selected genes involved in CKD and in glomerular, cortical tubulointerstitial, and whole kidney structures was analyzed using a gene expression array on samples following laser capture microdissection.

Treatment with liraglutide improved CKD hallmarks including GFR, albuminuria, mesangial expansion, renal inflammation, and renal fibrosis. The gene expression revealed that both liraglutide and enalapril reversed the regulation of several fibrosis and inflammation associated genes, which are also regulated in human CKD patients. Furthermore, liraglutide and enalapril both regulated genes in the kidney involved in blood pressure control.

Treatment with liraglutide improved the kidney function and diminished renal lesions in NTN-induced mice. Both liraglutide and enalapril reversed the regulation of genes involved in CKD and regulated genes involved in blood pressure control.
Treatment with liraglutide improved the kidney function and diminished renal lesions in NTN-induced mice. Both liraglutide and enalapril reversed the regulation of genes involved in CKD and regulated genes involved in blood pressure control.
Lenvatinib is an oral anticancer drug for patients with unresectable advanced hepatocellular carcinoma (HCC). We evaluated whether a reduction in tumor stain at 2 weeks after lenvatinib treatment in patients with unresectable HCC is a predictor of early treatment efficacy at 12 weeks.

Of the 23 patients who initiated lenvatinib treatment between April 2018 and January 2019, treatment efficacy was measured in 15 patients for more than 12 weeks after treatment. Changes in tumor stain, tumor size on contrast-enhanced computed tomography (CT), and serum levels of tumor markers were evaluated 2 weeks after lenvatinib treatment. Therapeutic efficacy was assessed by tumor stain and tumor size by contrast-enhanced CT within the first 12 weeks, according to the modified Response Evaluation Criteria in Solid Tumors (mRECIST) guidelines.

At 12 weeks, efficacy evaluation of 15 patients revealed that 11 of them experienced partial responses, for a response rate of 73.3%. In the first 2 weeks, 13 patients (86.7%) expks after lenvatinib treatment may be an early biomarker of efficacy at 12 weeks in patients with unresectable HCC.
Smoking is a highly prevalent addictive behavior with severe and life-shortening health consequences. This is the first study to evaluate the efficacy of a newly developed imaginal variant of approach bias modification (ABM) (i.e., imaginal retraining) for the reduction of craving for tobacco and actual smoking behavior.

We randomized 345 smokers to imaginal retraining (self-help manual) or a control group (either active control or wait-list control). Assessments were carried out online. The treatment interval was 6 weeks. Craving for tobacco represented the primary outcome. The study was registered as DRKS00016860.

Retention was 79.7% with no difference between groups. The intention-to-treat (ITT) analyses were significant for the primary outcome (Visual Analogue Scale on craving for tobacco) as well as subjective reduction of smoking (45.5 vs. 26.4%) in favor of imaginal retraining. In the treatment group, 47.6% performed the exercises at least once. SB939 cell line This subgroup (per-protocol [PP] sample) showed a sal retraining may reduce craving for tobacco and actual smoking behavior in a subgroup of smokers. In view of the large subgroup that did not read the manual or did not perform the exercises, alternative ways of conveying the imaginal retraining technique should be sought (e.g., demonstration via video clips). To conclude, imaginal retraining may represent a simple low-threshold technique to reduce smoking and assist current evidence-based treatment programs targeted at abstinence. It needs to be tested whether its mechanism of action deviates from standard ABM.
A regimen of S-1 combined with oxaliplatin (SOX) has been widely used as the first-line regimen for advanced gastric cancer. To further improve the antitumor efficacy for gastric cancer patients with peritoneal metastasis, we added nab-paclitaxel to the established SOX regimen (NSOX). Nab-paclitaxel (nanoparticle albumin-bound paclitaxel) has effective transferability to tumor tissues and strong antitumor effects for peritoneal metastasis. We performed a phase 1 study of this regimen to determine the maximum tolerated dose (MTD) and the recommended dose (RD) in patients with gastric cancer with peritoneal metastasis.

The NSOX regimen involved 21-day cycles with escalated doses of nab-paclitaxel (50 [level 1] to 80 [level 4] mg/m2 on days 1 and 8) and fixed doses of oxaliplatin (100 mg/m2 on day 1) and S-1 (80 mg/m2/day for 2 weeks).

Six patients with gastric cancer with peritoneal metastasis were enrolled. The MTD was determined to be dose level 2, as 2 of 3 patients experienced dose-limiting toxicities (DLTs), grade 4 non-hematological toxicities. One patient experienced acute myocardial infarction, and the other patient developed jejunal perforation. There were no treatment-related deaths. No patients experienced DLTs, so the RD was determined to be dose level 1.

The NSOX regimen was shown to be a tolerable regimen and may be a promising triplet therapy for patients with gastric cancer with peritoneal metastasis.
The NSOX regimen was shown to be a tolerable regimen and may be a promising triplet therapy for patients with gastric cancer with peritoneal metastasis.
Janus kinases (JAKs) are a family of non-receptor protein tyrosine kinases that are expressed in a variety of tissues. Several JAK-controlled cytokine receptor pathways are incriminated in the initiation and progression of psoriasis. Genetic polymorphisms influencing JAK expression would be anticipated to have a great impact on disease activity.

The aim of the study was to evaluate the association between JAK1 rs310241 and JAK3 rs3008 polymorphisms and the risk of developing psoriasis.

Blood samples of 150 patients and 120 controls were screened for nucleotide polymorphisms in JAK1 rs310241 and JAK3 rs3008 genes by using polymerase chain reaction (PCR)-restriction fragment length polymorphism technique.

The GG genotype of the JAK1 rs310241 and JAK3 rs3008 genes was significantly associated with an increase in psoriasis risk (p = 0.000, OR = 7.7, 95% CI = 2.8-21.5; p = 0.003, OR = 3.3, 95% CI = 1.5-6.9, respectively). The G allele of both genes was also associated with psoriasis susceptibility (p = 0.000, OR = 2.0, 95% CI = 1.4-2.8; p = 0.002, OR = 1.7, 95% CI = 1.2-2.4, respectively).

The results indicate a possible association between JAK1 rs310241 and JAK3 rs3008 gene polymorphisms and susceptibility to psoriasis. These findings validate the importance of these molecules in psoriasis and may enable the identification of the individuals most susceptible to the disease.
The results indicate a possible association between JAK1 rs310241 and JAK3 rs3008 gene polymorphisms and susceptibility to psoriasis. These findings validate the importance of these molecules in psoriasis and may enable the identification of the individuals most susceptible to the disease.
Transamniotic stem cell therapy (TRASCET) with mesenchymal stem cells (MSCs) can induce spina bifida coverage with neoskin. We initiated a mechanistic analysis of this host response.

Pregnant dams (n = 28) exposed to retinoic acid to induce fetal spina bifida were divided into an untreated group and 2 groups receiving intra-amniotic injections on gestational day 17 (E17; term = E21-22) of either amniotic fluid-derived MSCs (afMSCs; n = 105) or saline (n = 107). Gene expressions of multiple paracrine and cell clonality markers were quantified at term by RT-qPCR at the defect and fetal bone marrow. Defects were examined histologically for neoskin coverage. Comparisons were by Mann-Whitney U tests and logistic regression.

Defect coverage was associated with significant downregulation of both epidermal growth factor (Egf; p = 0.031) and fibroblast growth factor-2 (Fgf-2; p = 0.042) expressions at the defect and with significant downregulation of transforming growth factor-beta-1 (Tgfb-1; p = 0.021) and CD45 (p = 0.028) expressions at the fetal bone marrow.

Coverage of experimental spina bifida is associated with local and bone marrow negative feedback of select paracrine factors, as well as increased relative mesenchymal stem cell activity in the bone marrow. Further analyses informed by these findings may lead to strategies of nonsurgical induction of prenatal coverage of spina bifida.
Coverage of experimental spina bifida is associated with local and bone marrow negative feedback of select paracrine factors, as well as increased relative mesenchymal stem cell activity in the bone marrow. Further analyses informed by these findings may lead to strategies of nonsurgical induction of prenatal coverage of spina bifida.Cardiac autonomic neuropathy (CAN) is a least diagnosed complication of diabetes. Inflammation and oxidative stress play a crucial role in the pathophysiology of cardiomyopathy and neuropathy. Escin has anti-inflammatory activity and antioxidant activity. Hence, the present study was designed to evaluate the effect of escin in the management of CAN. Diabetes was induced in Sprague Dawley rats with streptozotocin (STZ). Diabetic animals were randomized in different groups after 6 weeks. Animals in the diabetic control group received no treatment, while animals in other groups received escin at dose 5, 10, and 20 mg/kg for 4 weeks. One group was kept as normal control. Various parameters like basic hemodynamic parameters, heart rate variability (HRV), oxidative stress parameters, and matrix metalloproteinase 9 (MMP-9) were assessed at the end of study. Escin significantly normalized hemodynamic parameters and HRV as compared to diabetic animals. Escin significantly reduced the malondialdehyde level and significantly increased reduced glutathione, catalase and superoxide dismutase levels in diabetic animals. Escin treatment significantly reduced plasma MMP-9 level in diabetic rats. The improvement in the studied parameters was found mainly with administration of higher doses of escin (10 and 20 mg/kg). The escin treatment mitigates CAN in diabetic rats. The results of study indicate that escin can be useful option for management of CAN.
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