Notes

[TRAUMATIC INTRAORGANIC HEPATIC And also SPLENIC HEMATOMAS].
000 and 0.006, respectively) were significant predictors of lnWMHV in the aICAS group. In sex-stratified analyses, there was a significant association between PI and lnWMHV in males with aICAS (P=0.038).

This study suggest there might be a likely association between increased intracranial pulsatility and WMH burden in males with aICAS.
This study suggest there might be a likely association between increased intracranial pulsatility and WMH burden in males with aICAS.The availability, effectiveness, and access to antenatal care are directly linked with good maternal and neonatal outcomes, making antenatal care an important determinant in health. But to be effective, care must always be appropriate, not excessive, not insufficient. Perinatal outcomes vary within and between countries, raising questions about practices, the use of best evidence in clinical decisions and the existence of clear and updated guidance. Through a scoping review methodology, this study aimed to map the available antenatal care policies for low-risk pregnant women in high-income countries with a universal health system, financed by the government through tax payments. Following searches on the main databases and grey literature, the authors identified and analysed ten antenatal care policies using a previously piloted datachart Australia, Denmark, Finland, Iceland, Italy, Norway, Portugal, Spain, Sweden and the United Kingdom. Some policies were over 10 years old, some recommendations did not present a rationale or context, others were outdated, or were simply different approaches in the absence of strong evidence. Whilst some recommendations were ubiquitous, others differed either in the recommendation provided, the timing, or the frequency. Similarly, we found wide variation in the methods/strategy used to support the recommendations provided. These results confirm that best evidence is not always assimilated into policies and clinical guidance. Further research crossing these differences with perinatal outcomes and evaluation of cost could be valuable to optimise guidance on antenatal care. Similarly, some aspects of care need further rigorous studies to obtain evidence of higher quality to inform recommendations.
The present case report describes the 5-year follow-up results of an atypical knee disarticulation of a man previously treated with an oncologic total knee arthroplasty due to an Ewing sarcoma.

The patient presented an aseptic loosened tibial component of a tumor prosthesis system and requested final amputation, as he had previously suffered from five revision surgeries. To encourage the most functional outcome regarding an exoskeletal prosthesis, we decided to disarticulate the knee joint while retaining the currently fixed femoral component to create a full end-bearing stump.

The patient could be mobilized as a functional knee disarticulated amputee. Seven months after amputation, he showed a slightly less symmetrical gait compared to the preoperative status (preoperative mean Symmetry Index 0.984 for kinematics and 0.940 for kinetics, 7-month postoperative Symmetry Index 0.858 and 0.915). At the 5-year follow-up, the femoral component is still stably fixated and shows no loosening signs. In addition, the Symmetry Index increased to 0.908 and 0.949.

Even after 5years, the presented amputation appears to be consistent with "conventional" knee disarticulation. The femoral component still withstands the altered loads and the patient shows a further improved gait pattern.
Even after 5 years, the presented amputation appears to be consistent with "conventional" knee disarticulation. The femoral component still withstands the altered loads and the patient shows a further improved gait pattern.B-type procyanidin dimers and (+)-catechin dimeric oxidation products were analyzed in grape seed extracts and red wines (UHPLC-Q-Orbitrap MS). The different dimers had different fragmentation patterns according to their interflavan linkage position. Oxidation dimeric compounds had a specific fragment ion at m/z 393, missing for B-Type dimers fragmentations. A fragment ion at m/z 291 occurred and was specific for oxidation dimeric compounds with a COC linkage. Higher level oxidation products had abundant specific fragments m/z 425, 397 and 245. These fragmentations were useful to identify them in complex samples such as grape seed extracts and wines. Three grape varieties and three ripening stages were selected and the corresponding seed extracts were obtained. The analyses revealed an increasing trend for the oxidation markers during grape ripening. The analysis of Syrah wines (2018, 2014, 2010) showed a decreasing trend of these molecules during wine ageing which might be due to further oxidation.A patient with Parkinson's disease (PD) who was examined as a candidate for DBS was initially rejected due to extensive brain calcifications. Upon second opinion and planning of trajectories she underwent successful surgery. Genetic analyses identified a mutation in SLC20A2, a gene known to cause brain calcifications, but no mutation known to cause PD was found.
Cognitive training (CT) has been proposed as a treatment option for cognitive impairment in Parkinson's disease (PD). We aimed to assess the efficacy of adaptive, computerized CT on cognitive function in PD.

In this double-blind, randomized controlled trial we enrolled PD patients that experienced substantial subjective cognitive complaints. Over a period of eight weeks, participants underwent 24 sessions of computerized multi-domain CT or an active control intervention for 45min each (randomized 11). The primary outcome was the accuracy on the Tower of London task; secondary outcomes included effects on other neuropsychological outcomes and subjective cognitive complaints. Outcomes were assessed before and after training and at six-months follow-up, and analyzed with multivariate mixed-model analyses.

The intention-to-treat population consisted of 136 participants (n=68 vs. n=68, age M 62.9y, female 39.7%). Multivariate mixed-model analyses showed no group difference on the Tower of London accuracy corclinically meaningful and lasting effects.mTOR activation is a hallmark of T-cell acute lymphoblastic leukemia (T-ALL) and is associated with resistance to glucocorticoid (GC)-based chemotherapy. We previously showed that altering redox homeostasis primes T-ALL cells to GC-induced apoptosis. Here we investigated the connection between the mTOR pathway and redox homeostasis using pharmacological inhibitors and gene silencing. In vitro studies performed on T-ALL cell lines and CG-resistant patient-derived T-ALL xenograft (PDX) cells showed that the mTOR inhibitor everolimus increased reactive oxygen species (ROS) levels, augmented lipid peroxidation, and activated the ROS-controlled transcription factor NRF2. These effects were accompanied by a decrease in the levels of NADPH and of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway (PPP), which is a major source of cytosolic NADPH needed for maintaining the cellular ROS-scavenging capacity. The mTOR inhibitor everolimus induced mitochondrial inner membrane depolarization and dose-dependent apoptosis of T-ALL cells, but did not kill normal T-cells. Importantly, the combination of everolimus and the GC dexamethasone had a synergistic effect on killing T-ALL cells. The effects of mTOR inhibition were blunted by ROS scavengers and phenocopied by siRNA-mediated G6PD silencing. In vivo studies of NOD/SCID mice inoculated with refractory T-ALL PDX demonstrated that everolimus overcame dexamethasone resistance in conditions of high tumor burden that mimicked the clinical setting of acute leukemia. These findings provide insight into the crosstalk between mTOR and ROS homeostasis in T-ALL cells and furnish mechanistic evidence to support the combination of glucocorticoids with mTOR inhibitors as a therapeutic avenue for treating refractory T-ALL.Mitochondrial quality control (MQC) consists of multiple processes the prevention of mitochondrial oxidative damage, the elimination of damaged mitochondria via mitophagy and mitochondrial fusion and fission. Several studies proved that MQC impairment causes a plethora of pathological conditions including cardiovascular diseases. However, the precise molecular mechanism by which MQC reverses mitochondrial dysfunction, especially in the heart, is unclear. The mitochondria-specific peroxidase Peroxiredoxin 3 (Prdx3) plays a protective role against mitochondrial dysfunction by removing mitochondrial reactive oxygen species. Therefore, we investigated whether Prdx3-deficiency directly leads to heart failure via mitochondrial dysfunction. Fifty-two-week-old Prdx3-deficient mice exhibited cardiac hypertrophy and dysfunction with giant and damaged mitochondria. Mitophagy was markedly suppressed in the hearts of Prdx3-deficient mice compared to the findings in wild-type and Pink1-deficient mice despite the increased mitochondrial damage induced by Prdx3 deficiency. Under conditions inducing mitophagy, we identified that the damaged mitochondrial accumulation of PINK1 was completely inhibited by the ablation of Prdx3. We propose that Prdx3 interacts with the N-terminus of PINK1, thereby protecting PINK1 from proteolytic cleavage in damaged mitochondria undergoing mitophagy. Our results provide evidence of a direct association between MQC dysfunction and cardiac function. The dual function of Prdx3 in mitophagy regulation and mitochondrial oxidative stress elimination further clarifies the mechanism of MQC in vivo and thereby provides new insights into developing a therapeutic strategy for mitochondria-related cardiovascular diseases such as heart failure.Facioscapulohumeral muscular dystrophy (FSHD) is characterised by descending skeletal muscle weakness and wasting. FSHD is caused by mis-expression of the transcription factor DUX4, which is linked to oxidative stress, a condition especially detrimental to skeletal muscle with its high metabolic activity and energy demands. Oxidative damage characterises FSHD and recent work suggests metabolic dysfunction and perturbed hypoxia signalling as novel pathomechanisms. However, redox biology of FSHD remains poorly understood, and integrating the complex dynamics of DUX4-induced metabolic changes is lacking. Here we pinpoint the kinetic involvement of altered mitochondrial ROS metabolism and impaired mitochondrial function in aetiology of oxidative stress in FSHD. Transcriptomic analysis in FSHD muscle biopsies reveals strong enrichment for pathways involved in mitochondrial complex I assembly, nitrogen metabolism, oxidative stress response and hypoxia signalling. We found elevated mitochondrial ROS (mitoROS) levelsrequired.
Cholangiocarcinoma (CCA) is the second most common liver malignancy with poor prognosis after hepatocellular carcinoma (HCC). Emerging evidences have proved that circular RNAs (circRNAs) are involved in the progression of multiple cancers, while their roles in tumorigenesis of CCA remains largely unclear. In the present study, we found circ_0000591 was upregulated in CCA cells and tissues. The highly expressed circ_0000591 could promote the proliferation, migration, invasion and carcinogenesis of CCA cells invitro and invivo. Functionally, circ_0000591 induced the proliferation, migration and invasion of CCA cells through sponging miR-326. Moreover, silencing of circ_0000591 attenuated LPS-induced anti-apoptosis of CCA cells through the TLR4/MyD88/IL6 pathway. In conclusion, this study revealed a novel regulatory mechanism that circ_0000591 contributed to the progression of CCA via miR-326/TLR4/MyD88/IL6 axis. These findings enhanced our knowledge of potential molecular mechanism involved in the malignant progression of CCA.
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