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Background: To date, the gold-standard treatment for sternoclavicular septic arthritis has been surgery due to the high failure and complication rates of medical treatment. In particular, presentation of Fusobacterium sternoclavicular septic arthritis has been rarely reported and very sparsely investigated, and only one other case report of septic arthritis caused by this pathogen exists in literature. Case presentation: We report a case of an otherwise healthy 38-year-old Caucasian woman who presented with sternoclavicular septic arthritis as a complication of Fusobacterium necrophorum mediastinitis. Our patient underwent successful management through nonstandard, conservative treatment of 7 weeks of intravenous piperacillin + tazobactam followed by 6 weeks of oral amoxicillin + clavulanic acid. Conclusion: We highlight a case of the rare presentation of Fusobacterium necrophorum sternoclavicular septic arthritis that did not require surgical intervention for successful management. Though infection of the sternoclavicular joint is unusual, it continues to be seen in thoracic surgery, and there are increasing numbers of antibiotic-resistant organisms. This case broadens insight into the clinical course and treatment of such conditions. The success of conservative management in this case aligns with the similar nonsurgical course of the one previous report of Fusobacterium sternoclavicular septic arthritis occurrence. Thus, further discussion and thought for reevaluating the current standard practice of surgery for sternoclavicular joint infection is suggested. Our case supports assessing a patient's overall health, causative organism, and extent of infection in interventional course and taking the feasibility of conservative management into more weighted consideration. [ABSTRACT FROM AUTHOR]

Background: Intramedullary hip nails may be classified as blades or screws depending on the type of lag screw used. Recently, a combination of lag screw types with a U-clip insertion has also been used. The purpose of this study was to evaluate the clinical and radiological outcomes of these new screw types. Methods: A total of 185 patients with trochanteric femoral fractures (age ≥ 65 years) who underwent surgery with intramedullary nails were selected. Surgeries with InterTrochanteric/SubTrochanteric (ITST), Proximal Femoral Nail Antirotation (PFNA), and Gamma 3 U-Blade lag screws were performed between January 2011 and June 2016. The AO/OTA classification, presence of a basicervical fracture type on 3D-CT, BMI, BMD, reduction quality, position of the lag screw, TAD (tip apex distance) of the lag screw, sliding distance of the lag screw, varus change (neck shaft angle), radiological union period, fixation failure and functional outcome as determined by walking ability were analyzed. Results: There were 3/60 (5.0%) cases of fixation failure in the ITST group, all caused by cut-out; 4/57 (7.0%) in the PFNA II group: 3 caused by cut-through and 1 by metal fracture; 1/68 (1.5%) in the Gamma 3 U-Blade lag screw group (P = 0.301). In each group, the sliding distance of the lag screw showed a significant difference (P = 0.017), whereas significant sliding over 10 mm showed no statistically significant results. Conclusion: There was only one (1.5%) case of fixation failure in the Gamma 3 U-Blade lag screw group. The sliding distance of the U-Blade was found to be in the middle, between the PFNA II (shorter) and ITST (longer) implants. The new rotational control lag screw seems to be comparable to other screw types. [ABSTRACT FROM AUTHOR]

Background: Mutations in glucocerebrosidase (GBA) cause Gaucher disease (GD) and increase the risk of developing Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). Since both genetic and environmental factors contribute to the pathogenesis of sporadic PD, we investigated the susceptibility of nigrostriatal dopamine (DA) neurons in L444P GBA heterozygous knock-in (GBA+/L444P) mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a selective dopaminergic mitochondrial neurotoxin. Method: We used GBA+/L444P mice, α-synuclein knockout (SNCA-/-) mice at 8 months of age, and adeno-associated virus (AAV)-human GBA overexpression to investigate the rescue effect of DA neuronal loss and susceptibility by MPTP. Mitochondrial morphology and functional assay were used to identify mitochondrial defects in GBA+/L444P mice. Motor behavioral test, immunohistochemistry, and HPLC were performed to measure dopaminergic degeneration by MPTP and investigate the relationship between GBA mutation and α-synuclein. Mitochondrial immunostaining, qPCR, and Western blot were also used to study the effects of α-synuclein knockout or GBA overexpression on MPTP-induced mitochondrial defects and susceptibility. Results: L444P GBA heterozygous mutation reduced GBA protein levels, enzymatic activity and a concomitant accumulation of α-synuclein in the midbrain of GBA+/L444P mice. Furthermore, the deficiency resulted in defects in mitochondria of cortical neurons cultured from GBA+/L444P mice. Notably, treatment with MPTP resulted in a significant loss of dopaminergic neurons and striatal dopaminergic fibers in GBA+/L444P mice compared to wild mice. type (WT) mice. Levels of striatal DA and its metabolites were more depleted in the striatum of GBA+/L444P mice. Behavioral deficits, neuroinflammation, and mitochondrial defects were more exacerbated in GBA+/L444P mice after MPTP treatment. Importantly, MPTP induced PD-like symptoms were significantly improved by knockout of α-synuclein or augmentation of GBA via AAV5-hGBA injection in both WT and GBA+/L444P mice. Intriguingly, the degree of reduction in MPTP induced PD-like symptoms in GBA+/L444P α-synuclein (SNCA)-/- mice was nearly equal to that in SNCA-/- mice after MPTP treatment. Conclusion: Our results suggest that GBA deficiency due to L444P GBA heterozygous mutation and the accompanying accumulation of α-synuclein render DA neurons more susceptible to MPTP intoxication. Thus, GBA and α-synuclein play dual physiological roles in the survival of DA neurons in response to the mitochondrial dopaminergic neurotoxin, MPTP. [ABSTRACT FROM AUTHOR]

Background: The biological effects of CD24 (FL-80) cross-linking on breast cancer cells have not yet been established. We examined the impact of CD24 cross-linking on human breast cancer cell line MCF-7. Methods: MCF-7 and MDA-MB-231 cells were treated with anti-rabbit polyclonal IgG or antihuman CD24 rabbit polyclonal antibodies to induce cross-linking, and then growth was studied. Changes in cell characteristics such as cell cycle modulation, cell death, survival in threedimensional cultures, adhesion, and migration ability were assayed after CD24 cross-linking in MCF-7. Results: Expression of CD24 was analyzed by flow cytometry in MDA-MB-231 and MCF-7 cells where 2% and 66% expression frequencies were observed, respectively. CD24 cross-linking resulted in time-dependent proliferation reduction in MCF-7 cells, but no reduction in MDA-MB- 231 cells. MCF-7 cell survival was reduced by 15% in three-dimensional culture after CD24 crosslinking. Increased MCF-7 cell apoptosis was observed after CD24 cross-linking, but no cell cycle arrest was observed in that condition. The migration capacity of MCF-7 cells was diminished by 30% after CD24 cross-linking. Conclusion: Our results showed that CD24 cross-linking induced apoptosis and inhibited migration in MCF-7 breast cancer cells. We conclude that CD24 may be considered as a novel therapeutic target for breast cancer. [ABSTRACT FROM AUTHOR]

Heterozygous mutations in glucocerebrosidase 1 (GBA1) are a major genetic risk factor for Parkinson's disease and Dementia with Lewy bodies. Mutations in GBA1 leads to GBA1 enzyme deficiency, and GBA1-associated parkinsonism has an earlier age of onset and more progressive parkinsonism. To investigate a potential influence of GBA1 deficiency caused by mutations in GBA1 on the disease progression of PD, GBA1 mice carrying D409H knock-in mutation were crossbred with the human A53T (hA53T) α-synuclein transgenic mice. Here, we show that GBA1 enzyme activity plays a significant role in the hA53T α-synuclein induced α-synucleinopathy. The expression of D409H GBA1 markedly shortens the lifespan of hA53T α-synuclein transgenic mice. Moreover, D409H GBA1 expression exacerbates the formation of insoluble aggregates of α-synuclein, glial activation, neuronal degeneration, and motor abnormalities in the hA53T α-synuclein transgenic mice. Interestingly, the expression of D409H GBA1 results in the loss of dopaminergic neurons in the substantia nigra pars compacta of hA53T transgenic mice. Taken together, these results indicate that GBA1 deficiency due to D409H mutation affects the disease onset and course in hA53T α-synuclein transgenic mice. Therefore, strategies aimed to maintain GBA1 enzyme activity could be employed to develop an effective novel therapy for GBA1 linked-PD and related α-synucleinopathies. [ABSTRACT FROM AUTHOR]

Background: The biological effects of CD24 (FL-80) cross-linking on breast cancer cells have not yet been established. We examined the impact of CD24 cross-linking on human breast cancer cell line MCF-7.Methods: MCF-7 and MDA-MB-231 cells were treated with anti-rabbit polyclonal IgG or anti-human CD24 rabbit polyclonal antibodies to induce cross-linking, and then growth was studied. Changes in cell characteristics such as cell cycle modulation, cell death, survival in three-dimensional cultures, adhesion, and migration ability were assayed after CD24 cross-linking in MCF-7.Results: Expression of CD24 was analyzed by flow cytometry in MDA-MB-231 and MCF-7 cells where 2% and 66% expression frequencies were observed, respectively. CD24 cross-linking resulted in time-dependent proliferation reduction in MCF-7 cells, but no reduction in MDA-MB-231 cells. MCF-7 cell survival was reduced by 15% in three-dimensional culture after CD24 cross-linking. Increased MCF-7 cell apoptosis was observed after CD24 cross-linking, but no cell cycle arrest was observed in that condition. The migration capacity of MCF-7 cells was diminished by 30% after CD24 cross-linking.Conclusion: Our results showed that CD24 cross-linking induced apoptosis and inhibited migration in MCF-7 breast cancer cells. We conclude that CD24 may be considered as a novel therapeutic target for breast cancer. [ABSTRACT FROM AUTHOR]