Antibiotic effects on bacterial profile in osteonecrosis of the jaw

Oral Diseases (2011) 18 , 85–95 Objective: Oral infection is considered to play a critical role in the pathogenesis of bisphosphonate‐related osteonecrosis of the jaw (BRONJ), and antibiotic therapy has become a mainstay of BRONJ therapy. This study was aimed to investigate the effect of antibiotics on bacterial diversity in BRONJ tissues. Materials and methods: The bacterial profile from soft tissues associated with the BRONJ lesion was determined using 16S rRNA‐based denaturing gradient gel electrophoresis (DGGE) and sequencing. Twenty BRONJ subjects classified as stage 0–2 were enrolled in this study, and patient groups were divided into an antibiotic cohort (n = 10) treated with systemic antibiotic and a non‐antibiotic cohort (n = 10) with no prior antibiotic therapy. Results: The DGGE fingerprints indicated no significant differences in bacterial diversity of BRONJ tissue samples. Patients on antibiotics had higher relative abundance of phylum Firmicutes with bacterial species, Streptococcus intermedius, Lactobacillus gasseri, Mogibacterium timidum, and Solobacterium moorei, whereas patients without antibiotics had greater amounts of Parvimonas micra and Streptococcus anginosus. Thirty percent of bacterial populations were uncultured (yet‐to be cultured) phylotypes. Conclusion: This study using limited sample size indicated that oral antibiotic therapy may have a limited efficacy on the bacterial population associated with BRONJ lesions.     

Thygeson‘s superficial punctate keratopathy: A review and case series

Thygeson‘s superficial punctate keratitis (TSPK) is a chronic disorder with episodes of exacerbations and remissions which span over years to decades. Typical features of the disease include multiple, grayish white, intraepithelial corneal lesions with minimal or no conjunctival involvement. The exact etiopathogenesis of this entity is unknown. However, it may have a genetic association with HLA-DR3, an antigen proved to be associated with immunogenic responses. Treatment of the disease consists of artificial tears, topical corticosteroids, topical cyclosporine, topical tacrolimus, or usage of soft contact lenses. TSPK should be considered as a diagnosis of exclusion in cases of bilateral superficial punctate keratopathy of long duration. Thirteen patients of TSPK were examined during the last 6 years (2014–2019) at our Institute. Visual acuity was 20/20 to 20/30 in majority cases. All patients required lubricants.     

Correction: Non-thermal plasma assisted surface nano-textured carboxymethyl guar gum/chitosan hydrogels for biomedical applications

Correction for ‘Non-thermal plasma assisted surface nano-textured carboxymethyl guar gum/chitosan hydrogels for biomedical applications’ by Ganeswar Dalei et al., RSC Adv., 2019, 9, 1705–1716.

The authors regret that incorrect images were mistakenly included in Fig. 7 of the original article, and in the graphical abstract. The correct versions of Fig. 7 and the graphical abstract are presented below. These changes do not affect the overall conclusions of the paper.Open in a separate windowFig. 1SEM images of (a) HG@UT, (b) HG@Ar, (c) HG@O₂ and (d) HG@ Ar + O₂. The corrected graphical abstract is presented below.The Royal Society of Chemistry apologises for these errors and any consequent inconvenience to authors and readers.     

Cross-species genetic screens identify transglutaminase 5 as a regulator of polyglutamine-expanded ataxin-1

Many neurodegenerative disorders are caused by abnormal accumulation of misfolded proteins. In spinocerebellar ataxia type 1 (SCA1), accumulation of polyglutamine-expanded (polyQ-expanded) ataxin-1 (ATXN1) causes neuronal toxicity. Lowering total ATXN1, especially the polyQ-expanded form, alleviates disease phenotypes in mice, but the molecular mechanism by which the mutant ATXN1 is specifically modulated is not understood. Here, we identified 22 mutant ATXN1 regulators by performing a cross-species screen of 7787 and 2144 genes in human cells and Drosophila eyes, respectively. Among them, transglutaminase 5 (TG5) preferentially regulated mutant ATXN1 over the WT protein. TG enzymes catalyzed cross-linking of ATXN1 in a polyQ-length–dependent manner, thereby preferentially modulating mutant ATXN1 stability and oligomerization. Perturbing Tg in Drosophila SCA1 models modulated mutant ATXN1 toxicity. Moreover, TG5 was enriched in the nuclei of SCA1-affected neurons and colocalized with nuclear ATXN1 inclusions in brain tissue from patients with SCA1. Our work provides a molecular insight into SCA1 pathogenesis and an opportunity for allele-specific targeting for neurodegenerative disorders.     

Extrahepatic manifestations of hepatitis C

Hepatitis C affects approximately 170 million people worldwide. Extrahepatic manifestations of chronic hepatitis C infection are clinically evident in nearly 40% of patients. Much research has been done over the last decade to better understand their incidence, clinical presentation, mechanism of disease, and the role of antiviral therapy in their treatment. Of the commonly reported manifestations, cryoglobulinemia, membranoproliferative glomerulonephritis, and porphyria cutanea tarda remain the best understood manifestations. More recently, the association of insulin resistance and diabetes mellitus with chronic hepatitis C has been demonstrated. This paper serves to review the growing body of literature detailing the extrahepatic manifestations of chronic hepatitis C.     

Pancreatic INI1-deficient undifferentiated rhabdoid carcinoma achieves complete clinical response on gemcitabine and nab-paclitaxel following immediate progression on FOLFIRINOX: a case report

Introduction: INI1-deficient undifferentiated rhabdoid carcinoma is a rare pancreatic carcinoma for which the optimal treatment is unknown. Pancreatic ductal adenocarcinoma, the most common histology of pancreas cancer, is treated with combination chemotherapy in the advanced setting, a strategy supported by strong evidence in well powered studies. In patients with excellent performance status, first-line treatment usually consists of the three-drug regimen FOLFIRINOX, with the combination of gemcitabine with nab-paclitaxel, typically less toxic than the three-drug regimen, reserved for second-line therapy. Given the lack of published reports describing treatment outcomes for patients with rare forms of pancreatic cancer, the same treatment approach used for pancreatic ductal adenocarcinoma is typically employed. Observation: This case describes a patient with metastatic pancreatic INI1-deficient undifferentiated rhabdoid carcinoma who was primarily resistant to FOLFIRINOX therapy but who then achieved an immediate, marked and sustained response to gemcitabine with nab-paclitaxel. Conclusion: Given the lack of data informing on optimal management of INI1-deficient pancreatic undifferentiated rhabdoid carcinoma, and the exceptional response achieved by gemcitabine with nab-paclitaxel, this case report highlights a surprising and potentially informative anecdote. Additional studies are needed to confirm responses observed in this report which when taken together may strongly influence first-line therapy choice for this rare malignancy. Given the difficult in acquiring sufficient numbers of these rare histologies in any one institution, multi-institution collaboration in studying outcomes of rare pancreatic malignancies is likely essential.     

Use of immune function test in monitoring immunosuppression in liver transplant recipients

Immune function test (Immuknow^?) is a measure of cell‐mediated immunity based on peripheral CD4⁺ T cell adenosine triphosphate activity (desired range, 225–525 ng/mL). We evaluated the role of immune function test (IFT) in monitoring and adjustment of immunosuppression in orthotopic liver transplant (OLT) recipients. A total of 289 IFTs were obtained from 171 patients from March 2007 to June 2008. Graft/patient status was classified as stable, serious infection, or malignancy. IFT levels were analyzed with duration of follow‐up after OLT, graft/patient status, and the presence of hepatitis C (HCV) infection. The mean age was 54 ± 14 yr, with 62% men. The median follow‐up was 65 (2–249) months. Mean IFT levels were significantly lower in patients who were <24 months than in those ≥24 months post‐OLT (220 ± 19.5 vs. 257 ± 11.3 ng/mL, p = 0.03). Clinically stable patients had higher IFT levels than those with serious infection or malignancy (254 ± 11.1 vs. 162.5 ± 23.9, p < 0.001). HCV‐infected patients had lower IFT levels than uninfected patients (206.7 ± 15.7 vs. 273 ± 12.0 ng/mL, p < 0.001). Immunosuppression was reduced in 58 patients with IFT levels <225 ng/mL, and 90% maintained stable graft function after a median follow‐up of 22 (1–39) months. IFT may be a useful tool in monitoring and lowering of immunosuppression in long‐term OLT recipients.