[Clinical Status and Research Progress of Tuberculous Peritonitis].

Tuberculous peritonitis(TBP)is currently one of the common manifestations of extrapulmonary tuberculosis.Due to the atypical clinical features,diverse types of diseases to be distinguished,and limited detection methods,TBP is difficult to be diagnosed and the fatality caused by delayed diagnosis increases significantly.We studied the current research status of TBP and found that T cells spot test,abdominal CT,and laparoscopic biopsy were of high diagnostic value for TBP.However,the application of ascites Xpert-MTB/RIF-ultra assay,ascites ADA,and whole-body positron emission tomography/computed tomography remained to be studied.Serum CA125 helps to judge the efficacy of anti-tuberculosis treatment.

BNIP3 interacting with LC3 triggers excessive mitophagy in delayed neuronal death in stroke.

INTRODUCTION: A basal level of mitophagy is essential in mitochondrial quality control in physiological conditions, while excessive mitophagy contributes to cell death in a number of diseases including ischemic stroke. Signals regulating this process remain unknown. BNIP3, a pro-apoptotic BH3-only protein, has been implicated as a regulator of mitophagy. AIMS: Both in vivo and in vitro models of stroke, as well as BNIP3 wild-type and knock out mice were used in this study. RESULTS: We show that BNIP3 and its homologue BNIP3L (NIX) are highly expressed in a "delayed" manner and contribute to delayed neuronal loss following stroke. Deficiency in BNIP3 significantly decreases both neuronal mitophagy and apoptosis but increases nonselective autophagy following ischemic/hypoxic insults. The mitochondria-localized BNIP3 interacts with the autophagosome-localized LC3, suggesting that BNIP3, similar to NIX, functions as a LC3-binding receptor on mitochondria. Although NIX expression is upregulated when BNIP3 is silenced, up-regulation of NIX cannot functionally compensate for the loss of BNIP3 in activating excessive mitophagy. CONCLUSIONS: NIX primarily regulates basal level of mitophagy in physiological conditions, whereas BNIP3 exclusively activates excessive mitophagy leading to cell death.

3,5,3'-Trihy-droxy-4'-meth-oxy-7-(3-methyl-but-2-en-yloxy)flavone.

The title compound pteleifolosin C, C(21)H(20)O(7), was isolated from the petroleum ether-soluble fraction of an indigenous Chinese tree Melicope pteleifolia (Rutaceae). The dihedral angle between the benzene rings is 2.7 (2)°. Intra-molecular O-H⋯O hydrogen bonds occur. In the crystal, mol-ecules are linked by inter-molecular O-H-O hydrogen bonds.

[Causes and revision endoscopic sinus surgery for recurrent sinusitis].

OBJECTIVE: To investigate the causes of revision endoscopic sinus surgery (RESS), and to evaluate the clinical effect and experience of RESS in the patients with recurrent sinusitis. METHODS: Before the revision surgery, 168 patients (225 sides) with recurrent sinusitis were examed by CT scans and nasal endoscopy. All patients were operated by revision endoscopic sinus surgery. RESULTS: Among the 168 patients, 95 cases (121 sides) had incomplete middle turbinate, 51 cases (75 sides) had maxillary sinus ostium stenosis, 85 cases (117 sides) had nasal cavity adhesion, 48 cases (57 sides) had uncinate process residual, 38 cases (65 sides) had ethmoid hyperostosis, and 25 cases had nasal septum deviation. One hundred and six patients (134 sides) were cured, 40 patients (56 sides) were improved, useful 22 patients (35 sides) were ineffective. CONCLUSION: The most common surgical causes of failures in endoscopic sinus surgery are the disease area remnant, nasal cavity adhesion, maxillary sinus ostium stenosis, uncinate process residual, ethmoid hyperostosis, and nasal septum deviation. Revision endoscopic sinus surgery is a useful way to treat recurrent sinusitis. Preoperative CT scan, correct choice of the anatomic marks of orientation and direction function are the key to operation successful.