Airsacculitis in fourteen juvenile southern Bornean orangutans (Pongo pygmaeus wurmbii)

BACKGROUND: Airsacculitis is a clinical condition which has been reported in a range of primates species, including orangutans. METHODS: This report describes the occurence and management of airsacculitis in fourteen juvenile Southern Bornean orangutans (Pongo pygmaeus wurmbii) that presented beween January 1st 1999 and January 31st 2001 at the Orangutan Care Center and Quarantine (OCC&Q), Kalimantan Tengah, Indonesia (S 2 degrees 43' 49.2"; E 111 degrees 38' 54.2"). Details of the signalment, clinical history, presenting clinical signs, clinicopathological findings and bacterial isolates in each case were reviewed. RESULTS: Cough, halitosis and nasal discharge were the most frequently observed clinical signs. A range of Gram-negative bacteria were isolated from infected air sacs, including Pseudomonas sp., Enterobacter sp. and Klebsiella pneumoniae. A simple drainage and lavage technique was used in cases where surgical intervention was indicated, in combination with local and systemic antibiotic therapy. CONCLUSIONS: The importance of early diagnosis, prompt management and antibiotic selection, based on bacterial culture and sensitivity profiles, is outlined.     

Foreign body perforation of the esophagus initiating traumatic pericarditis in an Australian fur seal.

Postmortem examination of a juvenile Australian fur seal, Arctocephalus pusillus doriferus, washed ashore on Philip Island, Victoria, revealed traumatic fibrinous pericarditis and hemothorax. A foreign body lodged in the right ventricle was identified as the barbed spine of the ray Urolophus paucimaculatus. A small puncture wound through the esophagus indicated the initial perforation site.     

Lung injury in the neonatal piglet caused by hyperoxia and mechanical ventilation

Neonatal lung injury from hyperoxia and mechanical hyperventilation was studied in newborn piglets hyperventilated (arterial PCO2 15-20 Torr) for 24-48 h with 100% O2 and compared with unventilated controls. Pulmonary function testing was performed, and biochemical indicators of lung injury were analyzed from tracheobronchial aspirates at 0, 24, and 48 h. Lung sections were obtained for light and electron microscopy, and bronchoalveolar lavage fluid was analyzed for surfactant composition and activity. At 24 h significant changes in tracheobronchial aspirate albumin concentrations (up 78%) and percent of polymorphonuclear cells (up 16%) were demonstrated. At 48 h a 35% decrease in dynamic lung compliance (P less than 0.05) and a 36% increase in pulmonary resistance (P less than 0.05) were noted. Further biochemical abnormalities occurred with total cell counts increased by 271% (P less than 0.02), albumin 163% (P less than 0.05), total protein 217% (P less than 0.01), and elastase 108% (P less than 0.02). Pathological analyses revealed mild lung injury at 24 h and marked inflammation, abnormal inflation patterns, flattening of Clara cells, fibrinous exudate and edema, early collagen formation, and cell necrosis observed at 48 h. Bronchoalveolar lavage surfactant had normal biophysical activity. Results demonstrate that exposure of neonatal piglets to O2 and mechanical hyperventilation for 48 h cause severe progressive lung injury.     

Acinetobacter infection associated with pneumonia in an orangutan

A 23-year old male orangutan (Pongo pygmaeus) had been treated for two years for respiratory disease believed to be tuberculosis. Terminally, the animal developed mucopurulent rhinitis and refused food. Necropsy examination revealed diffuse, severe, bilateral chronic pleuritis, fibrinous bronchopneumonia and air sacculitis. Large numbers of gram-negative bacteria seen in the lung histologically were cultured from both the lung and air sacs and identified asAcinetobacter calcoaceticus varietylwoffi. The resistance of the isolatein vitro to ampicillin may have accounted for the lack of clinical response of the ill orangutan.     

Local and systemic impacts of pleural oxygen exposure in thoracotomy

The pleural cavity is normally in a state of negative pressure and low oxygen tension. It is exposed to the atmosphere during thoracic surgery. However, no reports of pathophysiological investigation of the effects of pleural oxygen exposure involved in thoracotomy are available. In this study, the effects of pleural oxygen exposure on systemic and pleural inflammation were investigated. Male Wistar rats (9 weeks old) were placed on mechanical ventilation and underwent thoracotomy with lipopolysaccharide (LPS) administration, which simulates latent inflammatory condition. The pleural cavity was exposed to nitrogen (N(2) thoracotomy group), air (20% oxygen, air thoracotomy group), or 100% oxygen (O(2) thoracotomy group) under mechanical ventilation for 2 h. Animals were sacrificed 2 h or 8 h after LPS administration, and inflammatory indices (plasma tumor necrosis factor-alpha and interleukin-6, histology) were examined. For examination of inflammatory mediators, pleural effusion was added to cultured RAW264 cells, a murine macrophage cell line, and tumor necrosis factor-alpha levels in supernatant were measured. The capacity of pleural superoxide generation was investigated without LPS administration. Results showed increases in plasma interleukin-6 concentration and lung injury in the air and O(2) thoracotomy groups. Pleural oxygen exposure stimulated pleural superoxide generation, and increased pleural 4-hydroxy-2-nonenal and lung lipid peroxide concentrations. Tumor necrosis factor-alpha levels in cell culture supernatants were increased by the addition of pleural effusion from the air and O(2) thoracotomy groups. In conclusion, pleural oxygen exposure induced pleural oxidative injury and aggravated latent systemic inflammatory response.     

Mycoplasma hyopneumoniae and Mycoplasma hyosynoviae Infection in Cases of Fibrinous Pericarditis in Slaughter Pigs

Pericarditis, acute or subacute, is found at post mortem meat inspection of baconers in about 0.02 to 0.04% of slaughtered pigs in Denmark. The pathological findings are usually restricted to the pericardial sac. The pericardial sac is filled with a fibrinous exudate, which may be blood stained. In some cases massive granulation tissue formation is seen underlying the fibrinous exudate. Other constantly occurring, but less aggravating lesions, are chronic catarrhal bronchopneumonia and increased volume of serosanguinous synovial fluid in the large joints of the limbs. Lesions usually seen as sequelae to septicaemia have not been observed. The lesions seem to be part of a pathological entity which may be involved in the pathogenesis of fibrinous pericarditis in baconers.     

Increased expression of Apaf-1 and procaspase-3 and the functionality of intrinsic apoptosis apparatus in non-small cell lung carcinoma

The intrinsic apoptosis apparatus plays a significant role in generating and amplifying cell death signals. In this study we examined whether there are differences in the expression of its components and in its functioning in non-small cell lung carcinoma (NSCLC) and the lung. We show that NSCLC cell lines express Apaf-1 and procaspase-9 and -3 proteins and that the expression of Apaf-1 and procaspase-3, but not of procaspase-9 and -7, is frequently up-regulated in NSCLC tissues as compared to the lung. NSCLC tissues and lungs and some NSCLC cell lines expressed also caspase-9S(b) and displayed a high caspase-9S(b)/procaspase-9 expression ratio. Procaspase-3 from NSCLCs and lungs was readily processed to caspase-3 by granzyme B or caspase-8, and the granzyme B-generated caspase-3-like activity was significantly higher in tumor tissues and cells than in lungs. By contrast, cytochrome c plus dATP could induce a significant increase of caspase-3-like activity in cytosol only in some NSCLC cell lines and in subsets of studied NSCLC tissues and lungs, while procaspase-3 and -7 were detectably processed only in NSCLC tissues which showed a high (cytochrome c+dATP)-induced caspase-3-like activity. Taken together, the present study provides evidence that the expression of Apaf-1 and procaspase-3 is up-regulated in NSCLCs and indicates that the tumors have a capability to suppress the apoptosome-driven caspase activation in their cytosol.     

Lung auscultation recordings from normal sheep and from sheep with well-defined respiratory tract pathology

Increased audibility of normal lung sounds is commonly caused by hyperventilation after exercise and during hot weather. Tachypnoea is common in toxaemic and septicaemic conditions, but there may be no adventitious sounds. Moderate to pronounced coarse crackles are readily identified in advanced cases of ovine pulmonary adenocarcinoma, but auscultation findings do not correspond well to the distribution of lesion(s) revealed at necropsy. Auscultation does not detect pleural abscesses (up to 10 cm diameter). Marked attenuation of normal lung sounds results from marked fibrinous pleurisy and extensive unilateral pyothorax. Pleural frictions rubs are not heard in cases of marked fibrinous pleurisy associated with pleural abscesses. Rumen contraction sounds are often superimposed upon lung sounds. Auscultation of the ovine chest alone does not allow the clinician to determine the presence of all superficial lung pathology nor accurately define its distribution. Ultrasonography provides more accurate information regarding the nature and extent of superficial lung pathology in sheep.     

The apoptosis-associated protein BNIPL interacts with two cell proliferation-related proteins,MIF and GFER

Bcl-2/adenovirus E1B 19 kDa interacting protein 2-like, BNIP-2-like (BNIPL) is a recently cloned and characterized apoptosis-associated protein that shares 72% homology with BNIP-2. It is highly expressed in human placenta and lung. A yeast two-hybrid system was used to obtain two BNIPL-interacting proteins, MIF (macrophage migration inhibitory factor) and GFER (growth factor erv1 (Saccharomyces cerevisiae)-like). The interactions were confirmed by glutathione S-transferase pull-down assay in vitro and co-immunoprecipitation assay in vivo. Colony formation assay and cell proliferation test suggest that overexpression of BNIPL could inhibit the growth of BEL-7402 cells. These findings suggest that BNIPL may physically bind to cell proliferation-related proteins, MIF and GFER.     

Genetic Adaptation to Elevated Carbon Dioxide Atmospheres by Pseudomonas-Like Bacteria Isolated from Rock Cod (Sebastes spp.)

The microorganisms on rock cod fillets stored in a modified atmosphere (MA; 80% CO₂-20% air) at 4°C for 21 days were isolated. Only Lactobacillus sp. (71 to 87%) and tan-colored Pseudomonas sp.-like isolates (TAN isolates) were found. The TAN isolates grew more slowly in MA than in air at 8°C. When TAN isolates were grown in air at 8°C and then transferred to MA at 8°C, there was an initial decline in viable counts for 10 to 30 h followed by exponential growth. During this exponential growth phase in MA, the growth rates of the TAN isolates from MA-stored fish were significantly greater than those of the TAN isolates from fresh fish. When a TAN isolate from fresh fish was grown under MA for 21 days, it then grew as rapidly under MA as isolates from MA-stored fish. These results suggest that the TAN isolates genetically adapt to high levels of CO₂.     

Concomitant cryptosporidia, coronavirus and parvovirus infection in a raccoon (Procyon lotor).

A juvenile raccoon (Procyon lotor) was found moribund near Fort Collins, Colorado (USA). Upon examination, the raccoon was dehydrated, had a mucopurulent oculonasal discharge and diarrhea, and was euthanized. Postmortem examination revealed emaciation, severe fibrinous gastroenteritis and a small, firm liver. Histopathological findings included blunting of villi, infiltration of lamina propria with neutrophils and plasma cells, and mild bronchopneumonia. Cryptosporidium sp. was demonstrated on intestinal villi and coronavirus and parvovirus were identified in feces. Fluorescent antibody test for rabies was negative and no evidence of canine distemper was found.     

Coccidia, X-cell pseudotumors and Ichthyophonus sp. infections in walleye pollock (Theregra chalcogramma) from Auke Bay, Alaska

One hundred twenty-five walleye pollock (Theragra chalcogramma) were collected from Auke Bay, Alaska (USA) in 1985 and examined for histologic evidence of disease-causing infectious agents in 1987. A Goussia sp.-like coccidium was found in the kidney tubules of 75% and an Eimeria sp.-like coccidium was found in the intestine of 18% of the fish examined. The kidney coccidium was associated with sloughing of the tubular epithelium, peritubular fibrosis and granuloma formation. The intestinal coccidium was associated with severe tissue displacement and inflammation. In addition, X-cell pseudotumors were observed in the pseudobranchs (4%), and the fungus Ichthyophonus sp. was observed in the kidney, intestine or brain of 2% of the pollock.     

Immunohystochemical expression of cancer/testis antigens (MAGE-A3/4, NY-ESO-1) in non-small cell lung cancer: the relationship with clinical-pathological features

The aim of this study was to explore the expression of cancer/testis tumor associated antigens (C/T TAAs) MAGE-A 3/4 and NY-ESO-1 in lung squamous cell carcinoma and adenocarcinoma, and to evaluate their association with the standard clinical-pathological features of surgically treated lung cancer patients. The study included 80 patients with non-small cell lung cancer (40 adenocarcinomas, 40 squamous cell carcinomas) who had undergone surgery in the period between 2002 and 2005. The MAGE-A3/4 and NY-ESO-1 antigen expression was analyzed immunohistochemically (IHC). The results showed MAGE-A3/4 and NY-ESO-1 positive staining in 65.1% and 23.3% of squamous cell carcinomas and 18.9% and 10.8% of adenocarcinomas, respectively. A statistically higher MAGE-A3/4 expression was observed in planocellular bronchial carcinoma (p < 0.001), while no difference was found in the expression of NY-ESO-1 in adenocarcinoma and planocellular carcinoma (p = 0.144). A significant association was found between the MAGE-A3/4 expression and presence of tumor necrosis in squamous cell cancer specimens (p = 0.001), but not in adenocarcinoma (p = 0.033). A statistically significant association was noted between the NY-ESO-1 expression and positive hilar and mediastinal lymph nodes in adenocarcinoma (p = 0.025) whereas it was not the case in squamous cell carcinoma. Non-small cell lung cancer frequently expresses cancer/testis tumor associated antigens. Our results demonstrate that the MAGE-A3/4 and NY-ESO-1 expression was significant associated with prognostic factors of poor outcome of disease (presence of tumor necrosis and lymph node metastasis). As C/T antigens are important for inducing a specific immune reaction in lung cancer patients, there is an intention to form a subgroup of patients in the future, whose treatment would be enhanced by specific immunotherapy based on the observed scientific results.     

Disease not genetic but infectious: multiple tuberculomas and fibrinous pericarditis as symptoms pathognomonic for tuberculosis of Frederic Chopin

Chopin’s heart, generally enlarged, presented morphologic features pathognomonic for fibrinous pericarditis presumably of tubercular origin: multiple nodular hyalinization foci—tuberculomas and fibrillary coating covering the whole surface of pericardium (“frosted heart”). We show that these features differ significantly from post mortem-formed inorganic crystalline deposits, mold colonies, or fat deposits known from various preserved anatomical objects stored for a long period of time. In our opinion, these pathologies fully justify the claim that chronic cavernous pulmonary, laryngeal, and intestinal tuberculosis presents itself as the most plausible diagnosis of Frederic Chopin and that rapidly progressing tubercular pericarditis became the immediate cause of his death.     

Isolation of nifH and part of nifD by modified capture polymerase chain reaction from a natural population of the marine cyanobacterium Trichodesmium sp.

Abstract A modified capture polymerase chain reaction (CPCR) technique was used to isolate the entire sequence of the nifH gene and its flanking regions from a natural population of Trichodesmium sp. A set of specific CPCR primers derived from a known 72-bp DNA segment of the nifH sequence permitted isolation of both the upstream and the downstream region of Trichodesmium sp. nifH . The 882-bp nifH gene presented here is the first full-length gene isolated from Trichodesmium sp. A sequence similar to a nif -like promoter was found in front of nifH . The nifH open reading frame of Trichodesmium sp. encoded 294 amino acids. Comparative analysis of the Trichodesmium sp. NifH sequence revealed strong similarity with 23 known NifH proteins. Amino acids postulated to be involved in binding of the 4Fe:4S cluster and those subjected to ADP-ribosylation were present. An open reading frame for the nifD gene was identified 189 bp downstream of nifH . A sequence similar to the consensus of the nif -like promoter was also found in front of nifD .     

EPO对肾脏缺血再灌注损伤大鼠肺内氧化应激状态的影响

目的:探讨促红细胞生成素(erythropoietin,EPO)对大鼠肾脏再灌注损伤模型肺内氧化应激状态的影响。方法:清洁级Sprague-Dawly(SD)大鼠36只适应性喂养1周后,随机分为3组,即假手术组(A组)、肾脏再灌注损伤组(B组)和EPO预处理组(C组),每组12只。A组大鼠只打开腹腔,游离双侧肾蒂但不夹闭;B组与C组都建立了大鼠肾脏再灌注损伤模型,且C组在夹闭肾蒂前2 h腹腔注射人重组EPO(5000 U/kg)。术后24 h,处死大鼠,检测肺内氧化应激水平。结果:A组大鼠精神状态良好,肾小管结构正常,未见明显上皮细胞肿胀、脱落,肺泡结构基本完整,肺泡间隔未增厚,有少量炎性细胞浸润;B组鼠毛耸立,无光泽,饮水量减少,肾小管结构破坏消失,肾小管扩张,可见大量蛋白管型,肺泡结构破坏,肺泡腔缩窄,肺泡间隔增厚,组织水肿,大量炎性细胞浸润;C组大鼠精神状态有所恢复,一般状况尚可,肾小管损伤较B组轻似,肾小管坏死区域有所减少,坏死偶见,肺泡壁轻度破坏,结构较为清晰,可见少量炎性细胞浸润。B组与C组大鼠的血尿素氮(blood urea nitrogen, BUN)与血肌酐(serum creatinine,Scr)水平、肺组织血红素氧合酶(heme oxygenase, HO)-1与丙二醛(malondialdehyde, MDA)水平都显著高于A组,C组以上指标均显著低于B组(P0.05)。B组超氧化物歧化酶(superoxide dismutase, SOD)和谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)的水平均显著高于A组(均P0.05),而C组SOD和GSH-Px的水平均显著高于B组(均P0.05),A组与C组间对比无显著差异。结论:EPO用于大鼠肾脏再灌注损伤模型能缓解肺内氧化应激状态,促进肾功能及肺组织恢复,发挥肾脏保护作用。     

Molecular mechanisms of An-Chuan Granule for the treatment of asthma based on a network pharmacology approach and experimental validation

An-Chuan Granule (ACG), a traditional Chinese medicine (TCM) formula, is an effective treatment for asthma but its pharmacological mechanism remains poorly understood. In the present study, network pharmacology was applied to explore the potential mechanism of ACG in the treatment of asthma. The tumor necrosis factor (TNF), Toll-like receptor (TLR), and Th17 cell differentiation-related, nucleotide-binding oligomerization domain (NOD)-like receptor, and NF-kappaB pathways were identified as the most significant signaling pathways involved in the therapeutic effect of ACG on asthma. A mouse asthma model was established using ovalbumin (OVA) to verify the effect of ACG and the underlying mechanism. The results showed that ACG treatment not only attenuated the clinical symptoms, but also reduced inflammatory cell infiltration, mucus secretion and MUC5AC production in lung tissue of asthmatic mice. In addition, ACG treatment notably decreased the inflammatory cell numbers in bronchoalveolar lavage fluid (BALF) and the levels of pro-inflammatory cytokines (including IL-6, IL-17, IL-23, TNF-alpha, IL-1beta and TGF-beta) in lung tissue of asthmatic mice. In addition, ACG treatment remarkably down-regulated the expression of TLR4, p-P65, NLRP3, Caspase-1 and adenosquamous carcinoma (ASC) in lung tissue. Further, ACG treatment decreased the expression of receptor-related orphan receptor (RORγt) in lung tissue but increased that of Forkhead box (Foxp3). In conclusion, the above results demonstrate that ACG alleviates the severity of asthma in a ´multi-compound and multi-target’ manner, which provides a basis for better understanding of the application of ACG in the treatment of asthma.     

Pathology of experimental mycoplasmosis in American alligators.

Mycoplasma alligatoris was the suspected etiology of an epidemic of acute multisystemic inflammatory disease which emerged in captive American alligators (Alligator mississippiensis) in Florida (USA) in 1995. In an experimental inoculation study conducted from April through October 1999, 18 alligators were inoculated with 10(2), 10(4), or 10(6) colony forming units (CFU) of M. alligatoris by instillation into the glottis. As early as 1 wk post-inoculation (PI), mycoplasma were cultured from blood of three of six alligators inoculated with 10(6) CFU. Two of those died and the third was euthanatized within 4 wk PI. Necropsy gross findings included fibrinous polyserositis and polyarthritis. Histopathologic changes in affected individuals included pulmonary edema, interstitial pneumonia, pericarditis, myocarditis, meningitis, and synovitis. Mycoplasma were cultured quantitatively in high numbers from trachea, lung, coelomic cavity, liver, spleen, interior of pericardial sac, heart, blood, brain, and limb joints. In alligators inoculated with 10(6) CFU, heterophilia and moderate hyperglycemia peaked about 4 wk PI, and seroconversion occurred by 6 to 8 wk PI. Necropsy gross and histologic findings were generally unremarkable for the surviving alligators inoculated with 10(6) CFU, alligators inoculated with 10(2) or 10(4) CFU, and four uninoculated control alligators. Mycoplasma were not cultured at any time point from those alligators. The findings confirm that M. alligatoris can cause fulminant inflammatory disease and rapid death of alligators.