UNASSIGNED: The Knee Society Scoring System (KSS) is a frequently used outcome score which quantifies functional patients\' outcomes before and after total knee arthroplasty (TKA). Several problems arise when trying to implement KSS for obtaining postoperative outcomes after more personalised aligned TKAs. Scoring for valgus femorotibial angle (FTA) intervals outside moderate ranges is often poorly explained, the specific version of KSS used for outcome collection is frequently unclear and the exact measuring methods are typically not described in the literature. The aims of this systematic review were to investigate the latest user practice, the application of KSS and its limitations after kinematically aligned (KA) TKA.
UNASSIGNED: A systematic literature search following PRISMA guidelines was conducted on PubMed, Embase, Medline and Scopus to identify potentially relevant articles for this review, published from the beginning of January 2013 until the end of January 2023. Broad Mesh terms such as \'kinematic alignment\', \'total knee arthroplasty\' and \'knee society score\' were used for building search strategy in each database accordingly. Articles reporting postoperative values of the objective surgeon-assessed KSS after KA TKA or KA and mechanically aligned TKA were included. For assessing included randomised control trials (RCTs), an Agency for Healthcare Research and Quality\'s design-specific scale for assessing RCTs was used. The non-RCTs were assessed by using the Joanna Briggs Institute Critical Appraisal Tool. The Ottawa-Newcastle Score system was also used. Studies were additionally evaluated for their radiological methodology by using a five-question checklist (Radiological Assessment Qualit criteria).
UNASSIGNED: The initial search identified 167 studies, of which 129 were considered for screening. Ten studies reporting outcomes after KA TKA did not use the objective surgeon-assessed part of KSS for clinical outcome measurement, and 30 studies reporting outcomes after KA TKA did not use KSS at all for clinical and/or functional outcomes. From the 10 included studies, only six have used the latest KSS score (2011), the rest using its 1989 variant; and out of these six studies, only two presented values of the FTA, which is needed for calculating the KSS\'s \'alignment\' subcomponent, the rest presenting hip-knee-ankle angle (HKA) values. Additionally, when converting these HKA values to FTA intervals, the authors of this systematic review found that KA TKA FTA intervals display limits, which tend to be outside the \'well-scored\' KSS anatomical alignment interval.
UNASSIGNED: The inconsistent and nonstandardised use of the surgeon-assessed KSS across studies reviewed compromises assessment reliability and patient outcome scores. To enhance precision and comparability, it is crucial to standardise the KSS application, incorporating personalised alignment strategies for more accurate patient evaluations.
UNASSIGNED: Level III.

暂无摘要。

Keratoameloblastoma (KA) and solid variant of odontogenic keratocyst (SOKC) are rare odontogenic lesions, and their relationship and differences are unclear. The present study described a case that started as an odontogenic keratocyst (OKC) and transformed to SOKC/KA upon recurrence. Briefly, a 26‑year‑old man presented with swelling in the right cheek and was referred to the Department of Oral and Maxillofacial surgery, Hiroshima University Hospital (Hiroshima, Japan). At the initial visit, unicystic bone permeation was observed extending from the right canine to the molar, maxillary sinus and nasal cavity. After the biopsy, the patient underwent excisional surgery and was diagnosed with OKC. Thereafter, the lesion recurred six times over a period of 13 years and showed different histopathological features from those of the primary lesion, all consisting of numerous cysts with keratinization, which were diagnosed as SOKC/KA. The Ki‑67 positivity rate was ~10%, which was higher than that of the primary lesion, but there was no atypia. Genetic analysis of the recurrent lesion revealed mutations in adenomatous polyposis coli and Kirsten rat sarcoma viral oncogene homolog. This case originated from OKC, and the morphological features of OKC and KA were mixed upon recurrence, supporting the commonality and association between the two. However, multiple mutations different from those of OKC and ameloblastoma were detected, suggesting an association of SOKC/KA with increased proliferative activity and a high recurrence rate.

UNASSIGNED: This study aimed to evaluate the changes in posterior corneal astigmatism after cataract surgery and provide a theoretical basis to accurately evaluate the total corneal astigmatism (TA) to be corrected before toric intraocular lens (IOL) implantation.
UNASSIGNED: Sixty-two patients (89 eyes) who underwent phacoemulsification combined with toric IOL implantation (AcrySof IQ Toric SN6AT2-T9) at Shanxi Eye Hospital between January 2017 and September 2018 were enrolled. Surgically induced astigmatism of the posterior cornea (SIAPA) was analysed using vector analysis during pentacam examination.
UNASSIGNED: The vector variances of keratometric astigmatism (KA), TA, and posterior corneal astigmatism (PA) preoperatively and postoperatively in the \"with-the-rule (WTR) astigmatism\" group and \"overall patient\" group were statistically significant (P < 0.05). A statistically significant difference was observed between surgically induced KA (SIAKA) and surgically induced astigmatism of the total cornea (SIATA) for all patients, including those with WTR astigmatism. For all patients, SIAKA was less than SIATA by 0.05 ± 0.21 D, and for patients with WTR astigmatism, SIAKA was less than SIATA by 0.09 ± 0.22 D. For patients in the \"against-the-rule (ATR) astigmatism\" group, there were no statistically significant differences between SIAKA and SIATA, although SIAKA was greater than SIATA by 0.03 ± 0.18 D. When PA ≤0.4 D or KA ≤2.0 D, SIAPA can be ignored. However, when PA >0.4 D or KA >2.0 D, ignoring SIAPA caused by cataract surgery incision will cause SIAKA in patients with WTR astigmatism to underestimate SIATA, while SIAKA in patients with ATR astigmatism will cause an overestimation of SIATA.
UNASSIGNED: SIA on the posterior corneal astigmatism may have a significant role on more precise planning of toric IOL implantation, especially in cases with higher preoperative anterior or posterior corneal astigmatism.

Exposure to environmental pollutants and endogenous metabolites that induce aryl hydrocarbon receptor (AhR) expression has been suggested to affect cognitive development and, particularly in boys, also motor function. As current knowledge is based on epidemiological and animal studies, in vitro models are needed to better understand the effects of these compounds in the human nervous system at the molecular level. Here, we investigated expression of AhR pathway components and how they are regulated by AhR ligands in human motor neurons. Motor neurons generated from human induced pluripotent stem cells (hiPSCs) were characterized at the molecular level and by electrophysiology. mRNA levels of AhR target genes, CYP1A1 and CYP1B1 (cytochromes P450 1A1/1B1), and AhR signaling components were monitored in hiPSCs and in differentiated neurons following treatment with AhR ligands, 2,3,7,8,-tetrachlodibenzo-p-dioxin (TCDD), L-kynurenine (L-Kyn), and kynurenic acid (KA), by RT-qPCR. Changes in AhR cellular localization and CYP1A1 activity in neurons treated with AhR ligands were also assessed. The neurons we generated express motor neuron-specific markers and are functional. Transcript levels of CYP1B1, AhR nuclear translocators (ARNT1 and ARNT2) and the AhR repressor (AhRR) change with neuronal differentiation, being significantly higher in neurons than hiPSCs. In contrast, CYP1A1 and AhR transcript levels are slightly lower in neurons than in hiPSCs. The response to TCDD treatment differs in hiPSCs and neurons, with only the latter showing significant CYP1A1 up-regulation. In contrast, TCDD slightly up-regulates CYP1B1 mRNA in hiPSCs, but downregulates it in neurons. Comparison of the effects of different AhR ligands on AhR and some of its target genes in neurons shows that L-Kyn and KA, but not TCDD, regulate AhR expression and differently affect CYP1A1 and CYP1B1 expression. Finally, although TCDD does not significantly affect AhR transcript levels, it induces AhR protein translocation to the nucleus and increases CYP1A1 activity. This is in contrast to L-Kyn and KA, which either do not affect or reduce, respectively, CYP1A1 activity. Expression of components of the AhR signaling pathway are regulated with neuronal differentiation and are differently affected by TCDD, suggesting that pluripotent stem cells might be less sensitive to this toxin than neurons. Crucially, AhR signaling is affected differently by TCDD and other AhR ligands in human motor neurons, suggesting that they can provide a valuable tool for assessing the impact of environmental pollutants.

UNASSIGNED: Kinematic alignment (KA) has increased in popularity in recent years, becoming a viable alternative to MA with encouraging short- and mid-term follow-up results. Recently, the concept of restricted kinematic alignment (rKA) has been developed to restore native knee kinematics better, avoiding failure of coronal alignment. This systematic review aims to examine whether rKA improves outcome scores (PROMs) compared with MA and to evaluate the radiographic analysis of the lower limb alignment and the causes of complications and reoperations with the rKA approach.
UNASSIGNED: A systematic literature search was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines on the Pubmed/Medline, Scopus, Cochrane Library, and Embase databases. The following key terms were used: \"restricted kinematic alignment, rKA, kinematic alignment, primary total knee arthroplasty, primary total knee replacement, TKA rKA, and TKR rKA.\" The initial screening identified 328 studies. Each eligible article was evaluated according to the inclusion criteria: studies with levels of evidence (LoE) 1 to 4, written in English, published through May 2022, and involving human subjects. Criteria from the Methodological Index for Non-Randomized Studies (MINORS) were used to assess the methodological quality of the articles.
UNASSIGNED: Six clinical studies were included in this systematic review. The study was registered in the International Prospective Registry of Systematic Reviews (PROSPERO). A total of 574 knees were included. After excluding patients due to loss of follow-up or missing data, 475 knees were analyzed. The following rKA-related data were evaluated: patient-reported outcome scores (PROMs), radiographic analysis of the lower limb alignment, and causes of complications and reoperations.
UNASSIGNED: The rKA is an improved concept for restoring native knee kinematics, avoiding excessive coronal varus/valgus alignment. It provides equivalent or slightly better PROMs than MA without increasing the risk of short-middle-term implant failure. Clinical studies with extended follow-up are needed to confirm this trend.

Temporal lobe epilepsy (TLE) is the most common type of intractable epilepsy and is refractory to medications. However, the role and mechanism of H19 in regulating TLE remains largely undefined. Expression of H19 and miR-206 was detected using real-time quantitative PCR (RT-qPCR). Cell apoptosis, autophagy and inflammatory response were determined by flow cytometry, western blotting and enzyme-linked immunosorbent assay (ELISA). The interaction between H19 and miR-206 was predicted on the miRcode database and confirmed by luciferase reporter assay, RNA immunoprecipitation (RIP) and RNA pull-down. H19 was upregulated and miR-206 was downregulated in the rat hippocampus neurons after kainic acid (KA) treatment. Functionally, both H19 knockdown and miR-206 overexpression weakened KA-induced apoptosis, autophagy, inflammatory response, and oxidative stress in hippocampus neurons. Mechanically, the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway was activated by H19 knockdown and miR-206 was confirmed to be targeted and negatively regulated by H19. Moreover, downregulation of miR-206 could counteract the effects of H19 knockdown in KA-induced hippocampus neurons. Knockdown of H19 suppressed hippocampus neuronal apoptosis, autophagy and inflammatory response presumably through directly upregulating miR-206 and activating the PI3K/AKT signaling pathway.

In general, the evolutionary rate of proteins is not primarily related to protein and amino acid functions, and factors such as protein abundance, codon usage, and the protein\'s TM are more important. To better understand the factors that affect protein evolution, E. coli MG1655 orthologs were compared to those in closely related bacteria and to more distantly related prokaryotes, eukaryotes, and archaea. Also, the evolution of different types of proteins was studied. The analyses indicate that the amino acid conservation of enzymes that do not use macromolecules (e.g. DNA, RNA, and proteins) as substrates and that carry out metabolic processes involving small molecules (i.e. small molecule enzymes) is different than other enzymes. For example, the small molecule enzymes have a lower percent identity than other enzymes when sequences from closely related bacteria are compared. Analyses indicate the lower percent identity is not a result of the amino acid or codon usage of the small molecule enzymes. The small molecule enzymes also don\'t have a significantly lower protein abundance indicating that is also not likely an important factor driving differences in amino acid conservation. Analyses indicate different methods to measure the TM of proteins have different relationships between amino acid conservation over different evolutionary distances. In totality, the results demonstrate that the relationship between the factors thought to affect protein evolution (protein abundance, codon usage, and proteins TMs) and protein evolution are complex and depend on the factor, the organisms, and the type of proteins being analyzed.

Combined administration of N-Methyl-D-Aspartate (NMDA) and kainic acid (KA) on the inner retina was studied as a model of excitotoxicity. The right eye of C57BL6J mice was injected with 1 µL of PBS containing NMDA 30 mM and KA 10 mM. Only PBS was injected in the left eye. One week after intraocular injection, electroretinogram recordings and immunohistochemistry were performed on both eyes. Retinal ganglion cell (RGC) projections were studied by fluorescent-cholerotoxin anterograde labeling. A clear decrease of the retinal \"b\" wave amplitude, both in scotopic and photopic conditions, was observed in the eyes injected with NMDA/KA. No significant effect on the \"a\" wave amplitude was observed, indicating the preservation of photoreceptors. Immunocytochemical labeling showed no effects on the outer nuclear layer, but a significant thinning on the inner retinal layers, thus indicating that NMDA and KA induce a deleterious effect on bipolar, amacrine and ganglion cells. Anterograde tracing of the visual pathway after NMDA and KA injection showed the absence of RGC projections to the contralateral superior colliculus and lateral geniculate nucleus. We conclude that glutamate receptor agonists, NMDA and KA, induce a deleterious effect of the inner retina when injected together into the vitreous chamber.

To investigate the effects and mechanisms of NADPH on Kainic acid (KA)-induced excitotoxicity.
KA, a non-N-methyl-d-aspartate glutamate receptor agonist, was exposed to adult SD rats via intrastriatal injection and rat primary cortical neurons to establish excitotoxic models in vivo and in vitro, respectively. To determine the effects of NADPH on KA-induced excitotoxicity, neuronal survival, neurologically behavioral score and oxidative stress were evaluated. To explore the mechanisms of neuroprotective effects of NADPH, the autophagy-lysosome pathway related proteins were detected.
In vivo, NADPH (1 mg/kg or 2 mg/kg) diminished KA (2.5 nmol)-induced enlargement of lesion size in striatum, improved KA-induced dyskinesia and reversed KA-induced activation of glial cells. Nevertheless, the neuroprotective effect of NADPH was not significant under the condition of autophagy activation. NADPH (2 mg/kg) inhibited KA (2.5 nmol)-induced down-regulation of TP-53 induced glycolysis and apoptosis regulator (TIGAR) and p62, and up-regulation of the protein levels of LC3-II/LC3-I, Beclin-1 and Atg5. In vitro, the excitotoxic neuronal injury was induced after KA (50 μM, 100 μM or 200 μM) treatment as demonstrated by decreased cell viability. Moreover, KA (100 μM) increased the intracellular levels of calcium and reactive oxygen species (ROS) and declined the levels of the reduced form of glutathione (GSH). Pretreatment of NADPH (10 μM) effectively reversed these changes. Meanwhile NADPH (10 μM) inhibited KA (100 μM)-induced down-regulation of TIGAR and p62, and up-regulation of the ratio of LC3-II/LC3-I, Beclin-1, Atg5, active-cathepsin B and active-cathepsin D.
Our data provide a possible mechanism that NADPH ameliorates KA-induced excitotoxicity by blocking the autophagy-lysosome pathway and up-regulating TIGAR along with its antioxidant properties.