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Five guava seedlines of Hawaiian origin, namely GA9-37, GA12-1 6, GA10-48, GA11-56 and GA9-39 were yield tested in coastal sub-tropical south-eastern Queensland. The work demonstrated that seedling guavas produce attractive yields comparable with overseas countries. First crop mean yields were 30.72 kg/tree after 18 months in the field, demonstrating the precocious bearing of the guava. Yields for second and third cropping years were 45.6 and 77.9 kg/tree. These yields equate to 24.7, 37.2 and 61.5 tonnes ha-1 at a planting density of 805 trees ha-1. Third crop yields give the attractive gross returns of around $15,000 ha-1, at current prices paid by processors in Queensland. No differences were found between seedlines in annual yields, accumulated crop yields, fruit Number/tree, annual yield per unit cross sectional area of butt (an index of fruitfulness) and accumulated yield per unit cross sectional area of butt. Within seedline, variability masked differential response and these aspects are discussed. Fruit yields and relative increase in butt cross sectional area of butt varied with cropping year. Fruit. number per tree and yield per unit cross sectional area of butt varied with years, as did fruit number per kg (an index of fruit size). The latter also varied with seedlines. These effects were attributed to water rationing in spring of the second crop year. Preliminary selection based on fruit quality aspects of individuals identified four individuals which are undergoing detailed processing assessment, namely GA9-39R1T2, GA11-56T7, GA11-56R5T2 and GA1 1-56R5T1. Two further individuals were selected for fresh fruit market testing, namely GA11-56T3 and GA11 -56R1T1. We believe that market development rather than horticultural problems to be overcome will dictate the success of the guava as a crop for Australia, since the guava is comparatively easy to grow and manage.

Inhaled albuterol is most commonly self-administered by patients using a pressurized metered-dose inhaler (pMDI) but patients often have difficulty using the device. Dry powder devices such as the multi-dose, inspiratory flow driven inhaler (Turbuhaler) are often better handled by patients.

Five processing guava clones (GA6- 1, GA7- 12, GA8-30, GA9-35, GA11-56) were tested over 3 cropping years at Nambour, in coastal south-eastern Queensland. Mean marketable yield for the first crop at 2 years of age was 45 kg/tree or 36.23 t/ha at a density of 805 trees/ha. GA11-56, the most acceptable clone for processing, also gave the highest marketable yields of 627, 71.65 and 72.53 t/ha for the first 3 crops. Yield per unit cross sectional area of trunk was a more simple and useful index of yield efficiency than more complex parameters including a fruitfulness index and multiple regressions with yield of north-south canopy spread, number of primary branches and combinations of these and trunk girth. Similarly, trunk - - girth provided at least as good an estimate of tree size as the vigour index. Tree dimension measurements which included east-west canopy spread, north-south canopy spread, tree height, stem height, number of primary branches, crown height, crown radius, tree canopy volume, canopy surface area and an index of crown weight provided no consistent indication of tree size. They were not highly correlated with either accumulated or final yield of the guava. The GA11-56 clone because of its yield, fruit size and other desirable processing characteristics was the only clone that could be recommended for commercial plantings.

Four lychee (Litchi chinensis) cultivars (Bengal, Gee Kee, Tai So and Wai Chee) were grown in subtropical coastal southern Queensland. Yields after 8 years varied from 0.1 to 28.5 kg/tree (equivalent to a maximum of 6.6 t/ha at a density of 230 trees/ha). Wai Chee was superior to Gee Kee under all conditions and to Bengal and Tai So when flowering was reduced after warm wet winters or when fruiting was reduced during hot, dry springs.

A problem with young guava trees is that they carry light and variable crops, and both young and old trees flower and fruit over protracted periods. A 25 % urea spray plus wetting agent applied to 15-month-old guava seedlings of the variety GA9-EX39, produced a three-fold increase in yield over untreated trees at 22 months of age. In addition, the harvesting period was shortened from 15 weeks for control trees to four weeks for sprayed trees. Mean yields for sprayed trees were 34.69 kg, equal to 27.93 t ha-1 at a plant density of 805 trees ha-1; yields for unsprayed trees were 10.85 kg, or 8.73 t ha-1. Such yields exceed those attained in other countries at a similar age. Fruit size was not affected by the urea spray compared with controls, and the second crop 12 months later, also induced with urea sprays, was 40% more than the first. The use of urea as a defoliant spray permits early cropping of young, densely planted orchards and thus faster economic returns. In addition, shortening of the harvest period reduces labour costs and allows better economic control of fruit fly, a major pest of guava.

Alpha-1 antitrypsin (A1AT) functions primarily to inhibit neutrophil elastase, and deficiency predisposes individuals to the development of chronic obstructive pulmonary disease (COPD). Severe A1AT deficiency occurs in one in 5000 to one in 5500 of the North American population. While the exact prevalence of A1AT deficiency in patients with diagnosed COPD is not known, results from small studies provide estimates of 1% to 5%. The present document updates a previous Canadian Thoracic Society position statement from 2001, and was initiated because of lack of consensus and understanding of appropriate patients suitable for targeted testing for A1AT deficiency, and for the use of A1AT augmentation therapy. Using revised guideline development methodology, the present clinical practice guideline document systematically reviews the published literature and provides an evidence-based update. The evidence supports the practice that targeted testing for A1AT deficiency be considered in individuals with COPD diagnosed before 65 years of age or with a smoking history of <20 pack years. The evidence also supports consideration of A1AT augmentation therapy in nonsmoking or exsmoking patients with COPD (forced expiratory volume in 1 s of 25% to 80% predicted) attributable to emphysema and documented A1AT deficiency (level ≤11 μmol/L) who are receiving optimal pharmacological and nonpharmacological therapies (including comprehensive case management and pulmonary rehabilitation) because of benefits in computed tomography scan lung density and mortality.

Primary or nonobstructive, endogenous lipoid pneumonia is a rare clinical entity usually associated with an underlying systemic disease. The present report describes a case involving a 21-year-old man with systemic-onset juvenile rheumatoid arthritis who developed primary endogenous lipoid pneumonia. Multiple treatment regimens were attempted; however, definitive management was only achieved through double-lung transplantation.

OBJECTIVE: To prepare new guidelines for the Canadian Thoracic Society (CTS) regarding severe alpha1-antitrypsin (AAT) deficiency and AAT replacement therapy.MATERIALS AND METHODS: Previously published guidelines and the medical literature about AAT deficiency and AAT replacement were reviewed. The prepared statement was reviewed and approved by the CTS Standards and Executive Committees.RESULTS: Three studies evaluated AAT replacement. The National Heart, Lung and Blood Institute’s AAT Registry was a nonrandomized comparison of patients receiving and not receiving AAT replacement, and evaluated the decline in forced expiratory volume in 1 s (FEV1) in 927 subjects. The rate of FEV1 decline was significantly less in those receiving AAT treatment (66 ± SE 5 mL/year versus 93 ± SE 11 mL/year; P=0.03) only in the subgroup with FEV1 35% to 49% predicted. In another study comparing 198 German patients receiving weekly AAT infusions and 97 untreated Danish patients, the mean annual decline in FEV1 was significantly less in treated patients only in the subgroup with FEV1 31% to 65% predicted (62 mL versus 83 mL, P=0.04). Neither of these studies was a randomized, controlled study and, thus, cannot be taken as proof of efficacy. A randomized, double-blind, placebo controlled trial of monthly replacement therapy over three years in 56 exsmokers with severe AAT deficiency and moderate emphysema showed a trend (P=0.07) favouring slower progression of emphysema by computed tomography scan in the group receiving AAT replacement.CONCLUSIONS: AAT replacement therapy has not been proven definitively to be clinically effective in reducing the progression of disease in AAT-deficient patients, but there is a possible benefit to selected patients. A placebo controlled, randomized clinical trial of AAT replacement therapy is required. The authors recommend reserving AAT replacement therapy for AAT-deficient patients with impaired FEV1 of 35% to 50% predicted who have quit smoking and are on optimal medical therapy but continue to show a rapid decline in FEV1, and participation of all AAT-deficient subjects in the Canadian AAT Registry.

BACKGROUND: Sudden, severe airway injury has been associated with an acute, and at times persisting, airway hyper-responsiveness with clinical features of asthma, termed reactive airways dysfunction syndrome (RADS). An attempt was made to develop a rat model of RADS by exposing inbred Fischer rats to inhaled 8 N acetic acid for 2 mins (13 N inhalation was lethal).METHODS: Lung resistance (RL) and lung elastance (EL) were measured in 14 eight- to 10-week old male rats. Baseline responsiveness to methacholine was quantified by calculating the dose required for doubling of RL. The next day, the study group (n=11) was exposed to aerosolized acetic acid. Control animals (n=3) were similarly exposed to buffered saline solution.RESULTS: Acetic acid exposure resulted in a significant (P <0.02) increase in RL (by 80%) and EL (by 67%), lasting less than 10 mins postexposure, but no significant change in methacholine responsiveness at one day and seven days postexposure.CONCLUSIONS: Failure to induce persistent airway hyper-responsiveness may relate to the choice of animal, choice of irritant, or insufficient level or duration of exposure, or may reflect a lack of individual predisposing cofactors such as smoking or underlying asthmatic predisposition.