Cassaine diterpenoids as erythrofordins A-C (1-3), pseudo-erythrosuamin (4), and erythrofordin U (5) isolated from the leaves of Vietnamese Erythrophleum fordii Oliver were tested cytotoxic activity against human leukemia cancer cells. The results showed that these metabolites exhibited dose-dependent cytotoxicity against human leukemia HL-60 and KG cells with IC50 values ranging from 15.2 ± 1.5 to 42.2 ± 3.6 µM. Treatment with erythrofordin B led to the apoptosis of HL-60 and KG cells due to the activation of caspase 3, caspase 9, and poly (ADP-ribose) polymerase (PARP). Erythrofordin B significantly increased Bak protein expression, but downregulated the anti-apoptotic protein Bcl-2, in HL-60 cells.  https://www.selleckchem.com/products/forskolin.html  In silico results demonstrated that erythrofordin B can bind to both the procaspase-3 allosteric site and the PARP-1 active site, with binding energies of -7.36 and -10.76 kcal/mol, respectively. These results indicated that the leaves of Vietnamese E. fordii, which contain cassaine diterpenoids, can induce the apoptosis of human leukemia cancer cells.In the present study, we newly synthesized three types of novel fullerene derivatives pyridinium-type derivatives trans-3a and 4a-5b, piperidinium-type derivative 9, and proline-type derivatives 10a-12. Among the assessed compounds, 5a, 10e, 10f, 10i, 11a-d, and 12 were found to inhibit both HIV reverse transcriptase and HIV protease (HIV-PR), with IC50 values in the low micromolar range being observed. Regarding HIV-PR inhibition activity, proline-type derivatives 11a-11d and 12, bearing an alkyl chain between the hydroxylmethylcarbonyl (HMC) moiety and pyrrolidine ring, were more potent than other derivatives. This result might indicate that connecting HMC moieties with proline-type fullerene derivatives through properly sized alkyl chain leads to improved HIV-PR inhibitory activity.
  Recently, surface EMG of parasternal intercostal muscle has been incorporated in the "ERS Statement of Respiratory Muscle Testing" as a clinical technique to monitor the neural respiratory drive (NRD). However, the anatomy of the parasternal muscle risks confounding EMG "crosstalk" activity from neighboring muscles.
 
  To determine if surface "parasternal" EMG 1) reliably estimates parasternal intercostal EMG activity, 2) is a valid surrogate expressing neural respiratory drive (NRD).
 
  Fine wire electrodes were implanted into parasternal intercostal muscle in 20 severe COPD patients along with a pair of surface EMG electrodes at the same intercostal level. We recorded both direct fine wire parasternal EMG (EMGPARA) and surface estimated "parasternal" EMG (SurfEMGpara) simultaneously during resting breathing, volitional inspiratory maneuvers, apnoea with extraneous movement of upper extremity, and hypercapnic ventilation.
 
  Surface estimated "parasternal" EMG showed spurious "pseudobreathing" activity withouimate of parasternal intercostal EMG may not faithfully express NRD and is of limited utility as a biomarker in clinical applications.Nasal saline irrigation is frequently utilised in rhinosinusitis management, and after nasal and sinus surgery. Nasal saline irrigation improves mucociliary transport and assists inflammatory mediator and post-surgical debris removal. The aim of this study was to assess the influence different head positions, irrigation inflow nostril, and the nasal cycle have on Neti pot nasal saline volume filling within the nasal passages and maxillary sinuses. Computational fluid dynamics modelling using anatomically correct nasal geometry found only minor difference in nasal cavity volume filling with inflow from either side of the nose however both head position and inflow direction were both found to have a major influence on maxillary sinus volume filling. Computational modelling flow velocity results at the nasopharynx were validated using particle image velocimetry. It was also found that directing irrigation inflow into the patent side of the nose while in the head-back position achieved the highest volume filling of both maxillary sinuses.
  The purpose of this study was to determine if altered central chemoreceptor characteristics contributed to the elevated ventilation relative to carbon dioxide production (V̇
  /V̇CO
  ) response during exercise in mild chronic obstructive pulmonary disease (COPD).
 
  Twenty-nine mild COPD and 19 healthy age-matched control participants undertook lung function testing followed by symptom-limited incremental cardiopulmonary exercise testing . On a separate day, basal (non-chemoreflex) ventilation (V̇
  ), the central chemoreflex ventilatory recruitment threshold for CO
  (VRTCO
  ), and central chemoreflex sensitivity (V̇
  ) were assessed using the modified Duffin's CO
  rebreathing method. Resting arterialized blood gas data were also obtained.
 
  At standardized exercise intensities, absolute V̇
  and V̇
  /V̇CO
  were consistently elevated and the end-tidal partial pressure of CO
  was relatively decreased in mild COPD versus controls (all p < 0.05). There were no between-group differences in resting arterialized blood gas parameters, basal V̇
  , VRTCO
  , or V̇
  (all p > 0.05).
 
  These data have established that excessive exercise ventilation in mild COPD is not explained by altered central chemosensitivity.
 These data have established that excessive exercise ventilation in mild COPD is not explained by altered central chemosensitivity.TNF-α is the key inflammatory cytokine. TNF-α receptors are expressed in brain stem regions involved in respiratory control and also in the carotid bodies, which are the sensory organs monitoring arterial blood O2. We hypothesised that the circulating tumour necrosis factor (TNF)-α may affect the lung ventilation and modulate the hypoxic ventilatory response via activation of cyclooxygenase (COX) and nitric oxide synthase (NOS) pathways. The aim of the current study was to compare the respiratory effects of TNF-α before and after pretreatment with diclofenac or L-NG-nitro arginine methyl ester (L-NAME) nonspecific inhibitors of COX and NOS, respectively. The hypoxic ventilatory response was measured in anaesthetised rats using rebreathing techniques. We found that TNF-α increased the lung ventilation in normoxia but decreased the ventilatory response to hypoxia. Pretreatment with each of these inhibitors reduced respiratory effects of TNF-α. We believe that activation of COX and NOS-related pathways and also "cross-talk" between them mediates the TNF-α respiratory effects and underlies the impact of inflammation on the respiratory function.