Pediatric pulmonary actinomycosis: A misdiagnosed case report.

Background: Pulmonary actinomycosis is an uncommon kind of bacterial illness caused by actinomycetes, involving the chest wall in extraordinarily rare cases. Due to non-specific clinical signs and perplexing radiological characteristics, this kind of pulmonary actinomycosis is frequently misinterpreted as a malignant tumor or lung abscess. Case presentation: An 11-year-old child presented with a palpable lump on his left chest and periodic chest discomfort. An irregular soft-tissue mass in the left upper zone with bony destruction was first identified as a malignant small round cell tumor (MSRCT) known as an Askin tumor on post-contrast CT. However, pathological biopsy of the pulmonary lesion through the chest wall revealed actinomycosis. Conclusion: Pulmonary actinomycosis is an uncommon bacterial illness that has a variety of clinical manifestations, particularly in young patients. A chest lump with nearby "lace-like" rib bone destruction was the distinguishing characteristic of our case. For appropriate treatment and diagnosis, infection with actinomycosis should be considered when observing a similar chest lump. Pathological biopsy, as a valuable diagnostic tool, can help to distinguish between infectious diseases and thoracic tumors. The pathological manifestations of actinomycosis are characterized by inflammatory lesions that range from purulent to granuloma-like inflammatory processes, and second-generation sequencing of alveolar lavage fluid can help to confirm pathogens.

The favorable prognosis of cystic biliary atresia may be related to early surgery and mild liver pathological changes.

OBJECTIVE: The objectives of this study is to compare the prognostic differences between cystic biliary atresia (CBA) and non-CBA, analyze the clinical and liver pathological differences between the two groups, and explore the possible factors that affect the native liver survival of infants with CBA after Kasai portoenterostomy (KPE). METHODS: From 2013 to 2020, 131 infants with BA were admitted to Tianjin Children's Hospital. A total of 108 infants with BA were included after excluding those who did not undergo surgery after diagnosis (n = 23), including 12 cases of CBA and 96 cases of non-CBA. The clinical data, native liver survival and liver pathology, including liver fibrosis, bile ductular proliferation (BDP), bile plug, and portal area inflammation infiltration of the two study groups were compared. RESULTS: CBA accounts for 9.16% (12/131) and type I CBA accounts for 6.87% (9/131) of all types of BA. 16.7% (2/12) of CBA were detected prenatally with diagnosis of choledochal cyst (CC). The age at KPE, total bilirubin, direct bilirubin, and total bile acid levels of CBA were significantly lower than those of non-CBA (P = 0.047, P = 0.013, P = 0.009, P = 0.010, respectively). The long and wide diameters of the gallbladder were significantly larger than those of non-CBA (both P < 0.001). The 1-, 3-, and 5-year survival rates of CBA were 83.3%, 71.4%, and 71.4%, respectively, and 56.5%, 32.5%, and 29.8%, respectively, in non-CBA. The difference between the two groups was statistically significant (P = 0.031). The degree of liver fibrosis and bile plug in non-CBA was higher than that of CBA (P = 0.004, P < 0.001, respectively). There was no difference of BDP and inflammation infiltration between the two groups (P = 0.285, P = 0.243, respectively). CONCLUSION: CBA is a distinct type different from non-CBA, with different pathological processes, pathological manifestations, and clinical prognosis. The favorable prognosis of CBA may be derived from the early diagnosis, early operation, and mild pathological changes.

Celastrol inhibits colorectal cancer cell proliferation and migration through suppression of MMP3 and MMP7 by the PI3K/AKT signaling pathway.

Colorectal cancer (CRC) is one of the most frequent malignant tumors. Signaling by the PI3K/AKT pathway is crucial for CRC development and progression, including proliferation and migration. Celastrol has an anticancer effect, but its mechanism needs to be determined. Here, we showed that celastrol suppressed CRC cell proliferation and migration. Celastrol treatment also decreased the PI3K/AKT pathway components, and MMP3 and MMP7 expression levels. In addition, knockdown of AKT, not mTOR, inhibited MMP3 and MMP7 expression levels and AKT silencing promoted the celastrol-induced effects on CRC cell proliferation and migration. Taken together, these findings indicated that the celastrol-induced antitumor effects were mediated through MMP3 and MMP7 by the PI3K/AKT signaling pathway.

Role of angiotensin-converting enzyme (ACE) and ACE2 in a rat model of smoke inhalation induced acute respiratory distress syndrome.

Smoke inhalation induced acute respiratory distress syndrome (ARDS) has become more and more common throughout the world and it is hard to improve the outcome. The present research was to investigate possible roles of angiotensin-converting enzyme (ACE) and ACE2 in lung injury resulted from smoke exposure. Rats were exposed to dense smoke to induce ARDS. Histological changes, blood gases, bronchoalveolar lavage fluids (BALF) and wet-to-dry weight were analyzed to evaluate lung injury after smoke inhalation; beside, we also measured the expression of ACE and ACE2 at different time points to explore the possible mechanism of those changes. The results showed that pH of arterial blood, partial blood oxygen (PaO2) and blood oxygen saturation (SO2) decreased after smoke inhalation at different time points (P<0.01); while, partial blood carbon dioxide (PaCO2), wet-to-dry weight ratio, leukocytes count, protein concentration and inflammatory cytokines in BALF increased after smoke exposure (P<0.01). More importantly, both immunohistochemical staining and Western blot results showed that ACE and ACE2 expression in lungs from the experimental groups significantly increased compared with that of the control group (P<0.05). This study indicated that inflammation pulmonary edema and histological changes resulted from smoke inhalation induced lung injury were possibly attributed to abnormal expression of ACE and ACE2 related pathway.