Diagnosis: Chronic kidney disease, now what!

The occupational health nurse can play an important role in supporting employees with CKD and ESRD by recognizing risk factors such as diabetes and hypertension associated with CKD. The occupational health nurse should encourage compliance with treatment regimens that retard or delay progression of kidney disease into the next stage, especially blood pressure and glucose control. When employees are in need of diagnostic testing, the occupational health nurse can describe the testing procedures such as laboratory values, ultrasounds, and biopsies, and explain the five stages of CKD. The occupational health nurse can assist employees in Stage 4 or 5 CKD in deciding on a treatment option modality that best suits their individual lifestyles, after they have seen a nephrologist and kidney patient educator. In addition, the occupational health nurse can guide employees with difficult lifestyle changes and provide support during the adjustment process. The occupational health nurse also can play a key role in facilitating and coordinating those changes with the renal social worker. Together they can explore available resources, such as the NKF, the American Association of Kidney Patients, and kidneydirections.com. See the Sidebar on pages 295 to 296 for other available resources. Kidney disease can be a devastating diagnosis. Support and education are key to a successful lifestyle transition. Employees who have CKD and work with an occupational health nurse who is informed about their disease and its stages of progression can benefit from educational processes that create informed choices to delay or retard the progression of their renal disease.     

Determination of rate-constants as a method to describe passive expiration

To describe the relaxed expiration by a two-compartment model, we introduced a gas/energy transfer between the lung compartment (V₁) and a second one (V₂). If V₂ were a real volume, the rate-constants (i.e. the flow/volume ratios) of the compartments would describe a real gas-exchange. Alternatively, if a viscoelastic behaviour of the lung or an energy-exchange between compartments was simulated, V₂ would become a "pseudo-volume". We studied nine mechanically ventilated subjects. Changes in volume were transduced by respiratory inductive plethysmography. The rate-constants were assumed (together with the initial volumes of the compartments) as parameters to fit the total volume [V₁(t)+V₂(t)]. Once the best fitting was performed using these "physiological" parameters, the system was directly identified and the compartments were independently analysed. The time profile of the second compartment showed a maximum that depended on the value of the rate-constants. Appropriate tests confirmed the reliability of our procedure. In conclusion, our analysis demonstrated that the energy/volume of the second compartment may increase at the beginning of expiration and then decrease, showing a maximum, even though the total curve can only be a decreasing one. In other words, the slowing down of the curve representing expiratory volume is due not only to the longer emptying of the second compartment, but also to the interaction between the two compartments. As presently proposed, this interaction can be represented by either a gas exchange between two actual volumes, or a mechanical energy transfer between the lung and the tissue compartment.     

Respiratory mechanics and pleural remodelling in pleurodesis induced by barium sulphate

The aim of this study was to determine whether an intrapleural injection of barium sulphate would produce pleurodesis in rats. Additionally, respiratory mechanics and pleural remodelling were analysed. Single intrapleural injection of barium sulphate (100%) or saline was given to Wistar rats. Respiratory system, lung, and chest wall elastic, resistive and viscoelastic/inhomogeneous pressures were measured by the end-inflation occlusion method at 2 and 30 days after injection. The pleura were examined for gross and histopathological evidence of pleural inflammation and fibrosis, and the underlying lungs were also studied by morphometry. All pulmonary mechanical parameters increased at day 2, but were not different from control at 30 days after injection. Chest wall mechanical parameters did not change. Macroscopic evaluation demonstrated pleural adherence without haemothorax. Histopathologic analysis showed pleural inflammation and fibrosis. There was no alveolar inflammation or fibrosis in both groups. In conclusion, barium sulphate induced pleurodesis with either no changes in respiratory mechanics or lung lesion at day 30.     

Combining lung-protective strategies in experimental acute lung injury: The impact of high-frequency partial liquid ventilation.

OBJECTIVE: To evaluate the independent and combined effects of high-frequency oscillatory ventilation (HFOV) and partial liquid ventilation (PLV) on gas exchange, pulmonary histopathology, inflammation, and oxidative tissue damage in an animal model of acute lung injury. DESIGN: Prospective, randomized animal study. SETTING: Research laboratory of a health sciences university. SUBJECTS: Fifty New Zealand White rabbits. INTERVENTIONS: Juvenile rabbits injured by lipopolysaccharide infusion and saline lung lavage were assigned to conventional ventilation (CMV), PLV, HFOV, or high-frequency partial liquid ventilation (HF-PLV) with a full or half dose (HF-PLV1/2) of perfluorochemical (PFC). Uninjured ventilated animals served as controls. Arterial blood gases were obtained every 30 mins during the 4-hr study. Histopathologic evaluation was performed using a lung injury scoring system. Oxidative lung injury was assessed by measuring malondialdehyde and 4-hydroxynonenal in lung homogenates. MEASUREMENTS AND MAIN RESULTS: HFOV, PLV, or a combination of both methods (HF-PLV) resulted in significantly improved oxygenation, more favorable lung histopathology, reduced neutrophil infiltration, and attenuated oxidative damage compared with CMV. HF-PLV with a full PFC dose did not provide any additional benefit compared with HFOV alone. HF-PLV1/2 was associated with decreased pulmonary leukostasis compared with HF-PLV. CONCLUSIONS: The combination of HFOV and PLV (HF-PLV) does not provide any additional benefit compared with HFOV or PLV alone in a combined model of lung injury when lung recruitment and volume optimization can be achieved. The use of a lower PFC dose (HF-PLV1/2) is associated with decreased pulmonary leukostasis compared with HF-PLV and deserves further study.     

Chromosomal inversions among insecticide-resistant strains of Anopheles stephensi Liston, a malaria mosquito

Polytene chromosomes were prepared from the ovarian nurse cells of semi-gravid females of ten insecticide-resistant strains of Anopheles stephensi. Altogether, 16 heterozygous paracentric inversions, namely b/+ (11D-16C) in alphamethrin; i/+ (14B-18A) and h/+ (27B-28A) in DDT; j/+ (14A-16B) in chlorpyrifos; k/+ (11D-16B) in cyfluthrin; l/+ (11A-16C) in deltamethrin; m/+ (14B-15C) and e/+ (32A-33B) in bifenthrin; n/+ (12D-14B), f/+ (33A-36A) and g/+ (33C-34A) in propoxur; o/+ (11A-12D), h/+ (37A-37C) and i/+ (31C-32C) in temephos; d/+ (33D-35C) in carbofuran and a/+ (41C-43B) in neem strains, were reported. No inversions were observed in X chromosome so far. The frequency of inversions in different insecticides was found to be highest in the 2R arm, followed by the 3R arm. Such inversions were not reported in the corresponding susceptible strains or in the parental stocks.     

Hepatocellular carcinoma: Where there is unmet need

Hepatocellular carcinoma (HCC) is a complex and heterogeneous tumor most commonly associated with underlying chronic liver disease, especially hepatitis. It is a growing problem in the United States and worldwide. There are two potential ways to prevent HCC. Primary prevention which is based on vaccination or secondary prevention involving agents that slow down carcinogenesis. Several pathways have been thought to play a role in the development of HCC; specifically, those involving vascular endothelial growth factor (VEGF)‐mediated angiogenesis, WNT, phosphatidylinositol 3‐kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR), AMP‐activated protein kinase (AMPK), and c‐MET. Currently, there are only a limited number of drugs which have been proven as effective treatment options for HCC and several clinical trials are testing drugs which target aberrations in the pathways mentioned above. In this review, we discuss currently approved therapies, monotherapies and combination therapy for the treatment of HCC.