Post-TB bronchiectasis: from pathogenesis to rehabilitation.

The destruction of lung parenchyma caused by TB can result in pulmonary sequelae that are classified as bronchiectasis due to traction (radiological sequelae), and bronchiectasis persisting with an inflammatory bronchial component and opportunistic bronchial infection. There is a lack of studies that comprehensively analyse whether post-TB bronchiectasis differs in clinical, prognostic or therapeutic aspects from bronchiectasis arising from other aetiologies. However, it has been noted that post-TB bronchiectasis tends to appear more frequently in the upper lung lobes. In many countries, TB is the most frequent known cause of bronchiectasis, but there is currently no targeted management of bronchiectasis due to TB as opposed to other aetiologies. It is imperative to first prevent TB, and when that fails to provide early diagnosis and adequate treatment for TB disease. In addition, efforts should be made to limit additional lung insults such as tobacco use and provide management of post TB bronchiectasis to minimise further pulmonary sequelae. The objective of this minireview was to provide an update on post-TB bronchiectasis, its definition, epidemiological data, pathophysiology, and clinical, diagnosis and therapeutic aspects.

LncRNA HAND2-AS1 inhibits proliferation and promotes apoptosis of chronic myeloid leukemia cells by sponging with micRNA-1275.

OBJECTIVE: The long noncoding RNA (lnc) HAND2-AS1 is down-regulated and microRNA-1275 (miR-1275) is up-regulated in many types of cancers. However, their expressions and the relationship between HAND2-AS1 and miR-1275 in chronic myeloid leukemia (CML) remain unknown and to be further investigated. PATIENTS AND METHODS: Bone marrow samples from 30 CML patients and 10 healthy donors were collected; HAND2-AS1 and miR-1275 were detected by RT-PCR. The correlation between HAND2-AS1 and miR-1275 was analyzed. After lentiviral (LV) HAND2-AS1 and miR-1275 inhibitors were respectively transfected into KCL22 and K562 cells, the expressions of HAND2-AS1 and miR-1275 were detected by RT-PCR. MTT assay was performed to evaluate cell viability and mRNA and proteins levels of Bcl-2, Caspase-3, MMP-2, MMP-9 were detected by RT-PCR and Western blot (WB). Luciferase reporter assay was performed to explore the binding site of HAND2-AS1 and miR-1275. RESULTS: Results showed that HAND2-AS1 was significantly downregulated than healthy control (p<0.05), and HAND2-AS1 expressions on stages of AP and BP were much lower than that of CP (p<0.05). The miR-1275 expression was significantly upregulated than healthy control (p<0.05), and the expressions in stages of accelerated phase (AP) and blast phase (BP) were much higher than that in the stage of chronic phase (CP) in CML (p<0.05). Furthermore, HAND2-AS1 was negatively correlated with miR-1275 in CML, but not in healthy control (p<0.05). After lentiviral HAND2-AS1 transfection, the HAND2-AS1 expression was significantly up-regulated while miR-1275 was significantly down-regulated (p<0.05). Then, the cell proliferation was inhibited after 72 h. Furthermore, the mRNA and protein levels of Bcl-2, MMP-2 and MMP-9 were significantly down-regulated (p<0.05), while the expression of Caspase-3 was significantly up-regulated (p<0.05). Luciferase reporter assay showed that HAND2-AS1 was a target gene of miR-1275. And after treating with miR-1275 inhibitor, HAND2-AS1 was significantly upregulated (p<0.01) and cell proliferation was inhibited (p<0.01). Furthermore, the expressions of Bcl-2, MMP-2, and MMP-9 were significantly decreased, while Caspase-3 was significantly increased (p<0.01). CONCLUSIONS: HAND2-AS1 was downregulated and miR-1275 was upregulated in CML, and HAND2-AS1 inhibited proliferation and promoted apoptosis of CML cells by sponging with microRNA-1275, which might be a novel therapeutic target for CML.

Expression and functional analysis of Krüppel-like factor 2 in chicken adipose tissue.

Studies in mammalian species showed that Krüppel-like factor 2 (KLF2) regulates adipogenesis. However, its role in birds is unclear. The objective of the current study was to explore the expression and function of KLF2 in chicken adipogenesis. Results showed that chicken KLF2 (Gallus gallus KLF2 [gKLF2]) was greatly expressed in abdominal adipose tissue, and its transcripts fluctuated during adipose tissue development. In addition, gKLF2 transcripts in abdominal adipose tissue of lean broilers were greater at 1 wk of age but lower at 3, 5, and 8 wk of age than those in fat broilers (P < 0.05). The gKLF2 was more greatly expressed in preadipocytes than in mature adipocytes (P < 0.05), and its expression level decreased during the preadipocyte differentiation in vitro (P < 0.05). The functional analysis showed that gKLF2 overexpression inhibited chicken preadipocyte differentiation (P < 0.05), accompanied by the reduced expression of CCAAT/enhancer binding protein α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) and the elevated expression of GATA binding protein 2 (GATA2). Additionally, the luciferase reporter assays showed that gKLF2 overexpression suppressed the promoter activities of chicken C/EBPα and PPARγ (P < 0.05). In conclusion, our results indicated that gKLF2 inhibits chicken adipogenesis, at least in part, through inhibition of PPARγ and C/EBPα expression.

A nonlocal shell model for mode transformation in single-walled carbon nanotubes.

A second-order strain gradient nonlocal shell model is established to study the mode transformation in single-walled carbon nanotubes (SWCNTs). Nonlocal length is calibrated carefully for SWCNTs in reference to molecular dynamics (MD) simulations through analysis of nonlocal length effects on the frequencies of the radial breathing mode (RBM) and circumferential flexural modes (CFMs) and its effects on mode transformation. All analyses show that only a negative second-order nonlocal shell model is appropriate to SWCNTs. Nonlocal length is evidently related to vibration modes and the radius-to-thickness ratio. It is found that a nonlocal length is approximately 0.1 nm in an average sense when RBM frequency is concerned. A nonlocal length of 0.122-0.259 nm is indicated for the mode transformation in a selected group of armchair SWCNTs. 2:1 and 1:1 internal resonances are found for the same SWCNT based on different models, which implies that the internal resonance mechanism depends on the model employed. Furthermore, it is shown that an effective thickness of approximately 0.1 nm is more appropriate to SWCNTs than 0.066 nm.

Changes in rat adipocyte and liver glucose metabolism following repeated restraint stress.

Rats exposed to repeated restraint weigh less than controls even 8 weeks after stress. Stress-induced weight loss is lean tissue, but the post-stress difference in weight between control and restrained rats is lean and fat mass. Whole-body glucose clearance is enhanced 1 day after stress, but adipocyte glucose utilization is inhibited and muscle glucose transport is unchanged. The studies described here demonstrated that glucose transport was increased in both restrained and pair-fed rats, but that glycogen synthesis was increased only in restrained rats, which may account for the improved whole-body glucose clearance. Adipocyte glucose transport was inhibited and adipose plasma membrane beta-adrenergic receptor number was increased 1 day post-stress in restrained rats when weight loss was lean tissue, but were not different from control rats 5 days post-stress, when both fat and lean tissue were reduced. Thus, repeated restraint induces reversible changes in adipocyte metabolism that may represent a transition from the catabolic state of stress to a new energetic equilibrium in rats that maintain a reduced body weight for an extended period of time.

The dynamic change of plasma endothelin-1 during the perioperative period in patients with rheumatic valvular disease and secondary pulmonary hypertension.

The arterial plasma endothelin-1 concentration was substantially more elevated in 15 patients with rheumatic valvular disease and secondary pulmonary hypertension than in healthy volunteers (3.66 +/- 2.20 versus 1.17 +/- 0.38 pg/ml, mean +/- standard deviation; p < 0.01). The preoperative plasma endothelin-1 level was highly correlated with the pulmonary hemodynamics: pulmonary artery systolic pressure (r = 0.94, p < 0.001), pulmonary artery mean pressure (r = 0.86, p < 0.001), pulmonary capillary wedge pressure (r = 0.82, p < 0.001), and pulmonary vascular resistance (r = 0.63, p < 0.02). After valve replacement, the plasma endothelin-1 concentration declined substantially and the pulmonary hemodynamics improved markedly. Two weeks after the operation, the plasma endothelin-1 level in patients (1.26 +/- 0.45 pg/ml, mean +/- standard deviation) was not statistically different from that in the healthy volunteers. The plasma endothelin-1 concentration continuously increased during the course of cardiopulmonary bypass and peaked after cessation of bypass. The peak plasma endothelin-1 level (13.49 +/- 4.60 pg/ml, mean +/- standard deviation) positively correlated with the bypass time (r = 0.64, p < 0.02) and negatively correlated with the urine volume during bypass (r = -0.69, p < 0.01). We conclude that (1) increased plasma endothelin-1 might be implicated in the pathogenesis of secondary pulmonary hypertension caused by rheumatic valvular disease and (2) markedly elevated plasma endothelin-1 concentrations might be associated with the mechanism of cardiac or renal dysfunction after prolonged cardiopulmonary bypass.

[Hamartoma of the lung: an analysis of 24 cases].

Hamartoma is one of the most common benign tumors in the lung, and most of the lung hamartomas are located in the parenchyma. This report reviews 24 cases with this kind of tumor. The male-female ratio was 1.4:1 and the mean age 46.4 years. Sixteen patients of the 24 were asymptomatic, while in the remainder cases chest pain or distress, cough, short breath or hemoptysis were presented. Lung hamartoma is usually composed of cartilage, fat, smooth muscle and respiratory epithelium. X-ray findings of the parenchymal type in these cases were characterized by a round or oval sharply outlined mass, but only one with a mass in the shape of a dumbbell. 33% cases showed calcification. In 19 cases the mass was < 3.0 cm diameter (79%) and in 17 it was located in the superficial edge of the lung. The diagnosis was confirmed in only 6 cases preoperatively. The other cases were misdiagnosed as lung cancer, tuberculoma, metastatic tumors of the lung, etc. Enucleation or wedge resection is desirable for this kind of tumor.

The role of tachykinins in air ventilation-induced bronchoconstriction in postmortem guinea pigs.

To investigate the relationship between tachykinins and air ventilation-induced airway constriction after heart ligation, 26 guinea pigs were divided into three groups: Group 1, control (n = 15); Group 2, tachykinin depletion via pretreatment with capsaicin (n = 7); and Group 3, isocapnic ventilation (n = 4). To examine the age effect, the first two groups were further separated into two subgroups: young (n = 12) and mature (n = 10). Animals were anesthetized with pentobarbital, sternotomized and artificially ventilated with room air or with 5% CO2 gas mixture. Before (baseline) and after heart ligation, tidal volume and transpulmonary pressure (Ptp) were recorded during ventilation, and the maximal expiratory flow-volume curve was periodically obtained. Minimal volume (lung volume at Ptp = 0) was determined by neon dilution. Within 30 min after heart ligation in the control group, air ventilation significantly decreased dynamic compliance, vital capacity, peak maximal expiratory flow, maximal expiratory flow at 50% total lung capacity, and forced expiratory volume in 0.2 sec. Tachykinin depletion significantly prevented, whereas isocapnic (5% CO2) ventilation failed to alter, the above changes. Young and mature subgroups showed similar results. Our data indicate that air ventilation after heart ligation induced severe airway constriction and that this bronchoconstriction can be prevented by tachykinin depletion.