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Bek Rocha posted an update 6 months, 3 weeks ago
criminatory practice in job recruitment procedures may be beneficial.
Black, Asian and Minority Ethnic nurses and midwives experience career progression inequalities. Interventions should improve transparency in recruitment procedures and enhance training opportunities.
Black, Asian and Minority Ethnic nurses and midwives experience career progression inequalities. Interventions should improve transparency in recruitment procedures and enhance training opportunities.
Intraspinal synovial cysts occurrence causing spinal canal occlusion are mostly seen in mobile segments of the spine (lumbar and cervical). Cysteine Protease inhibitor An appearance of the cyst in thoracic spine is a relatively rare occurrence. We present an interesting case of ‘double crush’ caused by Lumbar canal stenosis with a mid-dorsal Facet cyst.
A 67-year-old woman presented with complaints of back pain with neurogenic claudication with significant loss of touch sensation and motor power of MRC grade 3/5 in lower extremities bilaterally. However, patient was hyperreflexic with Babinski sign positive. She was unable to perform tandem walking test and complained of instability. MRI of lumbar spine revealed lumbar canal stenosis. However, in view of the UMN signs, an MRI of the dorsal spine was done. It revealed an extradural, well-delineated lesion along the dorsal aspect of spine at T6-7 level. Thus the patient had a ‘double crush’ due to the FC along with lumbar canal stenosis.
Two teams simultaneously operated the 2 pathologies and T6-7 laminectomy along with left sided TLIF at L4-5 level was performed. Presently she is asymptomatic for back pain, claudication distance has improved to 800 m.
Our case reiterates the importance of thorough clinical examination to avoid missing a diagnosis. Our case is the first in literature to report a ‘double crush’ due to a proximal dorsal FC and distal LCS. Both the pathologies were tackled in a single setting by two operating teams with a good functional outcome.
Our case reiterates the importance of thorough clinical examination to avoid missing a diagnosis. Our case is the first in literature to report a ‘double crush’ due to a proximal dorsal FC and distal LCS. Both the pathologies were tackled in a single setting by two operating teams with a good functional outcome.The current understanding of thyroid-related adverse outcome pathways (AOPs) with adverse neurodevelopmental outcomes in mammals has been reviewed. This served to establish if standard rodent toxicity test methods and in vitro assays allow identifying thyroid-related modes-of-action potentially leading to adverse neurodevelopmental outcomes, and the human relevance of effects – in line with the European Commission’s Endocrine Disruptor Criteria. The underlying hypothesis is that an understanding of the key events of relevant AOPs provides insight into differences in incidence, magnitude, or species sensitivity of adverse outcomes. The rodent studies include measurements of serum thyroid hormones, thyroid gland pathology and neurodevelopmental assessments, but do not directly inform on specific modes-of-action. Opportunities to address additional non-routine parameters reflecting critical events of AOPs in toxicological assessments are presented. These parameters appear relevant to support the identification of specific thyroid-related modes-of-action, provided that prevailing technical limitations are overcome. Current understanding of quantitative key event relationships is often weak, but would be needed to determine if the triggering of a molecular initiating event will ultimately result in an adverse outcome. Also, significant species differences in all processes related to thyroid hormone signalling are evident, but the biological implications thereof (including human relevance) are often unknown. In conclusion, careful consideration of the measurement (e.g. timing, method) and interpretation of additional non-routine parameters is warranted. These findings will be used in a subsequent paper to propose a testing strategy to identify if a substance may elicit maternal thyroid hormone imbalance and potentially also neurodevelopmental effects in the progeny.Background and purpose – Since the introduction of intramedullary bone transport nails only very few cases have been reported in the literature. Thus we evaluated the results and complications in a single institution retrospective cohort.Patients and methods – 15 (median age 40 years (18-70), 8 males) consecutive patients, were included and the electronic patient records and radiographs were reviewed. Complications were severity graded and categorized as device or non-device related.Results – The segmental bone loss was due to non-union site in 8 femurs and 4 tibias, or traumatic bone loss in 2 femurs and 1 tibia. The segmental bone defect was a median of 3 cm (0.5-10). 9 of 10 femoral cases and 4 of 5 tibial cases healed with the bone transport nail. All 15 patients had a healed docking site and regenerate at the end of treatment after a median of 13 months (6-38). 24 complications (15 device related and 9 non-device related) occurred in 11/15 patients with a minimum follow-up of 6 months after nail removal. The number of unplanned surgeries due to device related complications was 0 in 9 patients, 1 in 3 patients, 2 in 1 patient, 3 in 2 patients.Interpretation – Segmental bone defects can heal with a bone transport nail. However, the number of complications was high and 15 out of 24 complications were devicerelated. Optimizing nail design is therefore needed to reduce complications in intramedullary bone transport.Promoting the macroautophagy/autophagy-mediated degradation of specific proteins and organelles can potentially be utilized to induce apoptosis in cancer cells or sensitize tumor cells to therapy. To examine this concept, we enriched for autophagosomes from histone deacetylase inhibitor (HDACi)-sensitive U937 lymphoma cells and isogenic HDACi-resistant cells. Mass spectrometry on autophagosome-enriched fractions revealed that HDACi-resistant cells undergo elevated pexophagy, or autophagy of the peroxisome, an organelle that supports tumor growth. To disturb peroxisome homeostasis, we enhanced pexophagy in HDACi-resistant cells via genetic silencing of peroxisome exportomer complex components (PEX1, PEX6, or PEX26). This consequently sensitized resistant cells to HDACi-mediated apoptosis, which was rescued by inhibiting ATM/ataxia-telangiectasia mutated (ATM serine/threonine kinase), a mediator of pexophagy. We subsequently engineered melanoma cells to stably repress PEX26 using CRISPR interference (CRISPRi). Melanoma cells with repressed PEX26 expression showed evidence of both increased pexophagy and peroxisomal matrix protein import defects versus single guide scrambled (sgSCR) controls.
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