ObjectiveTo investigate the role of the Toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway in intestinal mucosal barrier damage in ulcerative colitis， as well as the intervention mechanism of Shaoyaotang. MethodsSixty SD rats were allocated into a blank group， a model group， a mesalazine （0.42 g·kg^-1） group， and low-， medium-， and high-dose （11.1， 22.2， 44.4 g·kg^-1， respectively） Shaoyaotang groups. A model of ulcerative colitis was induced by 2，4，6-trinitrobenzenesulfonic acid （TNBS）. After successful modeling， rats were administrated with corresponding agents via gavage for 7 days. Changes in colon length and colon weight were observed. Hematoxylin-eosin staining was performed to examine the pathological changes of the colon， and immunohistochemistry was employed to detect the expression of the inflammatory cytokine interleukin-8 （IL-8）， cyclooxygenase-2 （COX-2）， junction adhesion molecule-1 （JAM-1）， and claudin-1 in the colon. Western blot analysis was performed to determine the protein levels of TLR4， MyD88， and NF-κB in the colon. ResultsCompared with the blank group， the model group showed elevated DAI score （P<0.01）， reduced colon length and colon weight （P<0.01）， down-regulated protein levels of JAM-1 and claudin-1 （P<0.01）， and up-regulated protein levels of IL-8， COX-2， TLR4， MyD88， and NF-κB p65 （P<0.01） in the colon tissue. Compared with the model group， each treatment group showed decreased DAI score （P<0.05， P<0.01）， increased colon length and colon weight （P<0.05， P<0.01）， up-regulated protein levels of JAM-1 and claudin-1 （P<0.01）， and down-regulated protein levels of IL-8， COX-2， TLR4， MyD88， and NF-κB p65 （P<0.01） in the colon tissue. ConclusionShaoyaotang alleviates intestinal inflammation and intestinal mucosal damage to protect intestinal barrier integrity by regulating the TLR4/MyD88/NF-κB signaling pathway.

To analyze the disease burden, temporal trends, and attributable risk factors of early-onset female breast cancer (EOBC) in China and globally from 1990 to 2021.

Ulcerative colitis （UC）is a chronic inflammatory bowel disease caused by multiple factors ，and its etiology and pathogenesis remain unclear . Tofacitinib，a small molecule rapidly absorbed by oral administration ，treats UC primarily by inhibiting Janus kinase （JAK）. Tofacitinib has been approved by the FDA and the European Medicines Agency for the treatment of moderate to severe UC . Many clinical studies on tofacitinib in the treatment of UC have been carried out abroad ，but there is no relevant report on its use in UC in China . This paper summarizes the relevant research advances of tofacitinib in the treatment of UC from its mechanism ，clinical application and safety . The results show that tefatinib mainly treats UC by inhibiting the expression of JAK and proinflammatory factors , regulating the overexpressed signaling transducers and activators of transcription , and repairing the intestinal mucosal barrier . Tofacitinib has good clinical efficacy ，but safety studies have shown that the risks of herpes zoster and thrombosis should not be ignored ，and the drug should be used with caution in pregnant ，children，adolescents， and elderly patients . The efficacy and safety of tofacitinib in Chinese population should be further studied in the future ，since it has not been used in UC patients in China .

With the increasing number of immunocompromised hosts, the epidemiological characteristics of fungal infections have undergone enormous changes worldwide, including in China. In this paper, we reviewed the existing data on mycosis across China to summarize available epidemiological profiles. We found that the general incidence of superficial fungal infections in China has been stable, but the incidence of tinea capitis has decreased and the transmission route has changed. By contrast, the overall incidence of invasive fungal infections has continued to rise. The occurrence of candidemia caused by Candida species other than C. albicans and including some uncommon Candida species has increased recently in China. Infections caused by Aspergillus have also propagated in recent years, particularly with the emergence of azole-resistant Aspergillus fumigatus. An increasing trend of cryptococcosis has been noted in China, with Cryptococcus neoformans var. grubii ST 5 genotype isolates as the predominant pathogen. Retrospective studies have suggested that the epidemiological characteristics of Pneumocystis pneumonia in China may be similar to those in other developing countries. Endemic fungal infections, such as sporotrichosis in Northeastern China, must arouse research, diagnostic, and treatment vigilance. Currently, the epidemiological data on mycosis in China are variable and fragmentary. Thus, a nationwide epidemiological research on fungal infections in China is an important need for improving the country's health.
Animals ; China ; epidemiology ; Fungi ; genetics ; pathogenicity ; Genotype ; Humans ; Incidence ; Mycoses ; epidemiology ; transmission

Objective To explore the effect of PGE1 on the cognitive impairment and the expression of VEGF and BDNF in the hippocampus after bilateral common carotid artery occlusion in adult rats. Methods Forty-eight rats were randomly divided into PGE1 group (10μg·kg-1·d-1, iv), PGE1+VEGFR antagonist group (PGE1, 10μg·kg-1·d-1, iv;SU5416, 25 mg·kg-1·d-1, ip), saline group and sham group (n=12 each). Morris Water Maze test (MWM) was used to examine cognitive function in rats. Drugs and saline were given to VD rats at 24 d for 7 consecutive days following opera?tion. Half of the rats in each group were sacrificed for Western Blot at 6 days after MWM test. Western Blot was conduct?ed to examine the relative expression levels of VEGF and BDNF in the hippocampus. Results Compared to saline and PGE1+VEGFR antagonist groups, the escape latency in PGE1 group was shorter (P<0.05), and the times that rats swam across the platform location and time percentage in previous platform quadrant in PGE1 group was longer (5.77±0.83 vs.2.88 ± 0.47 vs. 2.63 ± 0.44, P<0.01;32.28%± 4.56%vs. 20.42%± 5.50%, 23.08%± 5.06%, P<0.05). Compared with saline group and sham group, PGE1 group had higher levels of VEGF (0.057±0.005 vs. 0.038±0.002 vs. 0.027±0.002, P<0.05) and BDNF (0.481±0.049 vs. 0.339±0.021 vs. 0.224±0.04, P<0.05). but the increase in VEGF expression in PGE1 group was no significant (0.057±0.005 vs. 0.053±0.003, P>0.05) compared with PGE1+VEGFR antagonist group, while the aug?ment of BDNF in PGE1 group was remarkable (0.481±0.049 vs. 0.373±0.034, P<0.05). Conclusions PGE1 can upregu?late VEGF and BDNF expression and modify cognitive impairment in VD rats, while the effects of PGE1 on cognitive function and BDNF expression can be partially blocked by VEGFR antagonist SU5416.

Objective To report a case of disseminated cryptococcosis with cutaneous manifestations and osteomyelitis. Methods and Results A 33 year old female was admitted due to multiple nodules and ulcers on the upper arms, shoulders, buttocks and thighs for one year. The patient was pregnant when admitted, and gave birth to a premature baby during her illness. The nodules increased half a month after delivery, which was suspected to be hematogenously disseminated pulmonary tuberculosis and was given anti tuberculous therapy for three months but failed. Physical examination showed there were 39 nodules or ulcers on the face, gum, trunk, buttocks and extre mities. The bone structure of the left tibia and fibula destroyed and a sinus developed on the left fibula. Microbiologic examination showed that lots of spores were seen in the smear of pus and necrotic tissues, which produced yeast like colonies in culture with positive urease and caffeic acid test. Cryptococcus neoformans, serotype A was identified by API yeast reaction band and serology. Inoculation with mice and rats showed that their brains, lungs and livers were involved easily. Further identification as C.neoformans var.neoformans was obtained based on sequence analysis of ribosomal internal transcribed spacer region 2. The anti tuberculous therapy was stopped and anti fungal therapy was initiated at once. Intravenous and topical amphotericin B in combination with fluconazole were chosen in the initial therapy and itraconazole for maintenance. The nodules disappeared after 30 days and the last ulcer in the left tibia healed completely after 200 days. The anti fungal therapy was discontinued after 277 days and the patient was completely cured.