Palmoplantar keratosis in oculodentodigital dysplasia with a GJA1 point mutation out of the C‐terminal region of connexin 43

Gap junction proteins are composed of 21 genes of the connexin (Cx) family. They play important roles in cell–cell contact by exchange of small molecules through hemichannels. Hence, mutations of Cx family genes affect various tissues of a body. The mutation of the GJA1 gene, which codes Cx43, causes oculodentodigital dysplasia (ODDD), commonly in an autosomal dominant manner with phenotypic variability. It has been believed that gene mutations causing truncation of the Cx43 C‐terminus is necessary and sufficient for palmoplantar keratosis (PPK) development in ODDD patients. Here, we report a case of an ODDD patient developing PPK with a GJA1 gene mutation (c.412G>A/p.Gly138Ser), which was previously reported in a case of ODDD without PPK and expected not to result in C‐terminal truncation of Cx43. This case suggests not only C‐terminal truncation, but also that a point mutation in the cytoplasmic region of Cx43 can cause PPK in ODDD patients.     

Factors affecting susceptibility of Staphylococcus aureus to antibacterial agents

Staphylococcus aureus is a major human pathogen that causes suppurative diseases, toxic shock syndrome, pneumonia, food poisoning, and staphylococcal scalded skin syndrome (SSSS). S. aureus can also cause osteomyelitis and radicular cysts that impact dental health. β-lactam antibiotics are frequently used for the treatment of S. aureus infections, but the emergence of methicillin-resistant S. aureus (MRSA) has caused serious problems for the antibiotic treatment of S. aureus infections. PBP2′ has a low affinity for methicillin antibiotics and is one of the factors responsible for resistance to these antibiotics. However, clinical MRSA isolates show various levels of resistance to methicillin that are not determined by the amount of PBP2′, indicating that other factors are also involved. Furthermore, while vancomycin is very effective against MRSA, vancomycin-resistant and vancomycin-intermediate S. aureus have recently been reported. Many studies have been undertaken to better understand methicillin and vancomycin resistance mechanisms through identification of the factors affecting susceptibility to β-lactams. We recently demonstrated that MRSA showed resistance to antimicrobial peptides produced by humans that are a component of the innate immune system, in addition to various antibiotics.     

Immunomodulation of dendritic cells differentiated in the presence of nicotine with lipopolysaccharide from Porphyromonas gingivalis

Tobacco smoking is a significant risk factor for periodontal diseases. Nicotine, one of the most studied constituents in cigarette smoke, is thought to modify immune responses. Dendritic cells (DCs), which are key mediators between innate and adaptive immunity, stimulate naive T cells to differentiate to effector T‐cell subsets that may be actively involved in the immunopathogenesis of periodontal diseases. In this study, we evaluated the effects of nicotine and lipopolysaccharide (LPS) from Porphyromonas gingivalis, alone and in combination, on the functions of human monocyte‐derived DCs to elucidate the mechanism of tissue destruction of smoking‐associated periodontal diseases. P. gingivalis LPS‐stimulated DCs differentiated with nicotine (NiDCs) induced lower T‐cell proliferation and human leukocyte antigen (HLA)‐DR expression, but elevated expression of programmed cell death ligand 1. Additionally, NiDCs impaired interferon‐γ production but maintained interleukin (IL)‐5 and IL‐10 production in co‐cultured T cells. Furthermore, NiDCs produced lower levels of proinflammatory cytokines compared with DCs differentiated in the absence of nicotine. Interestingly, NiDCs preferentially produced the T helper 2 (Th2)‐type chemokines macrophage chemotactic protein‐1 and macrophage‐derived chemokine. These results suggest that the presence of nicotine during differentiation of DCs modulates the immunoregulatory functions of P. gingivalis LPS‐stimulated DCs.     

Hematospermia—the added value of transrectal ultrasound to clinical evaluation: Is transrectal ultrasound necessary for evaluation of hematospermia?

Hematospermia is usually caused by nonspecific inflammation of the prostate and seminal vesicles. Transrectal ultrasound (TRUS) is a safe and inexpensive modality for evaluating patients with hematospermia. The aim of this study is to describe the findings of TRUS and its contribution to patients' management.A total of 115 consecutive patients presented with hematospermia and evaluated with TRUS between 2006 and 2012.All patients exhibited an abnormality in the TRUS examination. A 12-core TRUS-guided biopsy of the prostate was taken from 10 patients, but none of these samples were positive for tumor.In the vast majority of cases, a benign cause can be identified using TRUS. These causes usually do not require treatment.