The first imported case of monkeypox in Taiwan.

he first imported case of monkeypox in Taiwan was diagnosed in an Asian man with HIV-1 infection and asymptomatic COVID-19, returning from Germany. Atypical presentations included asynchronous skin lesions, anogenital lesions and prominent inguinal lymphadenopathy. Whole genomic sequence alignment indicate that the Taiwan strain clustered together with human monkeypox virus West African clade B.1, currently circulating in Europe. Prompt diagnosis and infection control measures are crucial to mitigate the spread of monkeypox.

Perirectal epidermoid cyst in a patient with sacrococcygeal scoliosis and anal sinus: A case report.

BACKGROUND: Perirectal epidermoid cysts are rare masses arising from the ectodermal germ cell layer of the hindgut and are predominantly found in middle-aged women. It is often difficult to make an accurate diagnosis of these cysts and it is equally challenging to distinguish it from other developmental cysts. CASE SUMMARY: We report the case of an 18-year-old female patient with a perirectal mass who presented to the hospital with constipation. The patient experienced sacrococcygeal falls and burns on the left buttocks during growth. Three-dimensional computed tomography scans indicated abnormal sacral vertebrae with the sacral canal partially enlarged and opened. Pelvic magnetic resonance imaging showed a 55 mm × 40 mm × 35 mm unilocular cystic mass in the perirectal space and a solitary sinus in the left ischiorectal fossa. The cyst was completely resected posteriorly using the sacrococcygeal approach. The pathology was verified to be an epidermoid cyst. The patient remained recurrence-free after 6 mo of follow-up. CONCLUSION: Successful treatment of perirectal epidermoid cysts depends on comprehensive evaluation. This is significant for the surgical approach and prognosis.

MicroRNA-205-5p targets the HOXD9-Snail1 axis to inhibit triple negative breast cancer cell proliferation and chemoresistance.

MicroRNA-205 (miR-205) is believed to be related to the progress of tumors. HOXD9 has been proved to be expressed abnormally in several kinds of cancers. However, the role of miR-205 and HOXD9 in breast cancer remains unclear. The biological role of miR-205 in breast cancer cell proliferation and chemoresistance was investigated. The expression of miR-205 in clinical tissues and breast cancer cell lines were analyzed using quantitative real-time PCR test (qRT-PCR). Overexpression and knockdown models of miR-205 were established to study cell proliferation and chemotherapy-resistant. Moreover, the potential relationships between miR-205 and HOXD9/Snail1 were measured using qRT-PCR, western blot, and chemotherapy-resistant study. miR-205 was lowly expressed in breast cancer tissues and cell lines. Overexpression of miR-205 could inhibit cell proliferation and chemotherapy-resistance. Moreover, we proved that miR-205 could target the HOXD9-Snail1 axis to suppress triple negative breast cancer cell proliferation and chemoresistance. The activation of Snail1 gene by HOXD9 was also proved in this study. The present study may provide a novel insight for the therapeutic strategies of breast cancer through targeting miR-205/HOXD9/Snail1.

Construction of High-Nuclearity Manganese-Cluster-Organic Frameworks by Using a Tripodal Alcohol Ligand.

Two novel cluster-organic frameworks based on the 12-nuclearity manganese-cluster secondary building unit (SBU), [MnIII4MnII8(L)4(Ac)8(MeO)2(µ5-O)2(H2O)4](Ac)2·16H2O (1) and [MnIII4MnII8(L)4(Ac)8(MeO)2(µ5-O)2(H2O)4](Ac)2·12H2O (2), where Ac = CH3COO- and MeO = CH3O, have been constructed from solvothermal reactions of the 3-nuclearity manganese cluster [Mn3(µ3-O)(Ac)6(py)3](ClO4) (Mn3, where py = pyridine) with a tripodal alcohol ligand containing a 4-pyridyl group. 1 and 2 represent the first examples of metal-organic frameworks containing 12-nuclearity manganese-cluster SBUs. In addition, 1 exhibits an integration of the porosity and magnetic properties from both the framework and cluster in a porous material.

The up-regulation of heme oxygenase-1 expression in human gingival fibroblasts stimulated with nicotine.

BACKGROUND: Cigarette smoking is a major risk factor in the development and further progression of periodontal diseases. Heme oxygenase-1 (HO-1) is known as a stress-inducible protein and functions as an antioxidant enzyme. There is limited information on the expression of HO-1 in smoking-associated periodontal disease. OBJECTIVES: The aim of the present study was to investigate the effects of nicotine on the expression of HO-1 protein in cultured human gingival fibroblasts in vitro and further to compare HO-1 expression in gingival tissues obtained from cigarette smokers and non-smokers in vivo. METHODS: Western blot assay was used to investigate the effects on human gingival fibroblasts exposed to nicotine. In addition, antioxidants catalase, superoxide dismutase (SOD), and N-acetyl-l-cysteine (NAC) were added to test how they modulated the effects on nicotine-induced HO-1 expression. Gingival biopsies taken from the flap surgery of 20 male patients with periodontal disease (10 cigarette smokers and 10 non-smokers) were examined by immunohistochemistry. RESULTS: The exposure of quiescent human gingival fibroblasts to 10 mm nicotine resulted in the induction of HO-1 protein expression in a time-dependent manner (p < 0.05). The addition of glutathione (GSH) precursor NAC inhibited the nicotine-induced HO-1 protein expression (p < 0.05). However, SOD and catalase did not decrease the nicotine-induced HO-1 protein expression (p > 0.05). The results from immunohistochemistry demonstrated that HO-1 expression was significantly higher in cigarette smokers (p < 0.05). HO-1 was noted in the basal layers of epithelium, inflammatory cells, and fibroblasts in specimens from cigarette smoking. CONCLUSIONS: Taken together, these results suggest that HO-1 expression is significantly up-regulated in gingival tissues from cigarette smokers, and nicotine may, among other constituents, be responsible for the enhanced HO-1 expression in vivo. The regulation of HO-1 expression induced by nicotine is critically dependent on the intracellular GSH concentration.