Bronchoscopic management of endobronchial carcinoid presenting as asthma Mimic.

We report a 25-year-old woman with persistent dyspnea and wheezes that had been unsuccessfully treated with inhaled beta 2-agonists and steroids for about one year. Spirometry demonstrated a restrictive pattern. Chest CT demonstrated polypoidal lesion in left main bronchus. The lesion was excised via rigid bronchoscopy. Pathology showed a picture of typical bronchial carcinoid. In this patient, due to the lack of awareness, diagnosis of carcinoid was delayed for one year.

Analysis of the therapeutic role of platelet-rich plasma against cisplatin-induced hepatotoxicity in rats: controversy between oxidative and apoptotic markers

Cisplatin is a potent chemotherapeutic agent used to treat a variety of cancers such as ovarian, uterine, and bladder. The major limiting side effect of cisplatin is its hepatotoxicity. The possible mechanism of cisplatin hepatotoxicity was due to the affection of oxidant-antioxidant system. Platelet-rich plasma (PRP) has a powerful therapeutic option for its ability to deliver a great variety of biologically active GFs to the site of injury. PRP has grown as an attractive biologic instrument in regenerative medicine for its powerful healing properties. It is considered as a source of growth factors that may induce tissue repairing and improve fibrosis. This product has proven its efficacy in multiple studies, but its effect on cisplatin-induced hepatotoxicity has not yet been elucidated. The present study was designed to analyze the therapeutic role of PRP in cisplatin-induced hepatotoxicity. 30 adult male adult male albino rats were used in the present study divided into 3 groups (control group, cisplatin-treated group and PRP-treated group). By the end of the experimental period, blood samples were collected for measurement of serum AST, ALT and ALP enzymes; then the rats were sacrificed by cervical dislocation. Fresh liver parts were used to measure the oxidative markers in liver homogenates, while other parts were processed and subjected for histopathological and histomorphometric and immunohistochemical analyses for VEGF, Caspase 3 expression of the different experimental groups. The statistical study was done for the resultant data. Group II (Cisplatin-treated group) showed marked pathological hepatic changes; loss of architecture, congested dilated sinusoids lined by darkly stained pyknotic Kupffer cells; and hepatocytes nuclei were pyknotic and karyolitic. Dilated congested portal vein, interstitial acidophilic exudate, marked polymorphic cellular infiltration. There were increased collagen fibers deposition, a weak positive PAS reaction, strong positive caspase 3 reactions and strong positive VEGF reaction. Also, there were a marked increase in hepatic enzymes, MDA levels and a marked decrease in GSH level. Treatment with PRP in Group III revealed improvement of the hepatic parenchymal architecture with strong PAS reaction and minimal collagen fibers deposition. Weak positive caspase immunoreaction and strong positive VEGF reaction were noticed. Also, there was a marked improvement in the parameter of hepatic enzymes, MDA and GSH level comparable with the control group. It is concluded that PRP could ameliorate the liver against cisplatin-induced hepatotoxicity

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Can sildenafil citrate ameliorate cisplatin-induced nephrotoxicity? Crosstalk between the possible mechanisms

Nephrotoxicity is considered the most important side effect which limits cisplatin therapy in various diseases. It is might be due to oxidative stress, decreased renal blood flow and reduction in the glomerular filtration. Sildenafil citrate is used for treatment of erectile dysfunction, but its effect in ameliorating cisplatin nephrotoxicity was not yet clearly studied. So the present work aimed to evaluate the protective role of Sildenafil citrate against cisplatin-induced nephrotoxicity in adult male albino rats. 24 adult male albino rats were divided into 4 groups (6 rats each): Group I, control; Group II, sham control; Group III, Cisplatin-treated group, and Group IV, Sildenafil-and-Cisplatin-treated group. At the end of the experiment, the kidney of each animal was excised, trimmed and prepared for histological, histochemical and immunohistochemical study. Blood samples were obtained to evaluate the kidney functions. Kidney sections of Group III showed marked degenerative changes in the proximal convoluted tubules, vacuolations, exfoliation of the lining epithelium, cast formation and interstitial hemorrhagic exudate. There was marked elevation of serum creatinine and urea with significant increase in nitric oxide (NO) and decrease in glutathione reductase (GSH) concentrations in the kidney tissue and weak periodic acid Schiff (PAS) reaction. Treatment with Sildenafil citrate in Group IV offered marked improvement in the renal structure, kidney function tests and other parameters. The present study concluded that Sildenafil citrate could protect the kidney against Cisplatin-induced nephrotoxicity in adult male albino rat

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Preconditioning with atorvastatin against renal ischemia-reperfusion injury in nondiabetic versus diabetic rats.

Acute renal failure complicates renal ischemia-reperfusion (I/R) owing to reactive oxygen species production. Atorvastatin (ATO) has anti-inflammatory and antioxidant properties. The current study investigated whether ATO alleviated damage induced by renal I/R injury in nondiabetic versus diabetic rat models. Thirty-six rats were equally divided into 6 groups: group A1 (nondiabetic sham), group A2 (nondiabetic I/R), group A3 (nondiabetic ATO + I/R), group B1 (diabetic sham), group B2 (diabetic I/R), and group B3 (diabetic ATO + I/R). All groups experienced 45 min of bilateral renal ischemia followed by 24 h of reperfusion. Groups A3 and B3 were treated with single intraperitoneal doses of ATO (10 mg/kg) 30 min before ischemia. Histological analysis of kidney tissues, kidney function tests, and analyses of caspase-3 and CD44 expression and oxidative stress markers were performed to assess tubular injury. Histological analysis revealed marked tubular damage in groups A2 and B2 but improvement in groups A3 and B3. Improvements were also found in groups A3 and B3 for caspase-3 and CD44 expression, kidney function tests, and oxidative stress markers. Our results suggest ATO may ameliorate renal I/R injury differently between nondiabetic and diabetic rats.

Amiodarone-induced lung toxicity and the protective role of Vitamin E in adult male albino rat

Amiodarone is a highly effective anti-arrhythmic drug, used in the treatment of cardiac arrhythmias. However, it is of a limited use due its serious side effects especially lung toxicity. This study was designed to investigate the role of vitamin E in ameliorating amiodarone-induced lung toxicity in adult male albino rat. The study was carried out on 24 adult male albino rats, divided into 4 equal Groups: Group I (control), Group II (sham control), Group III (Amiodarone treated) and Group IV (Amiodarone and vitamin E treated). After the end of the experiment, the rats were sacrificed by cervical dislocation, then parts of the rat lungs of each Group were prepared for light microscopic, histochemical study, immune- histochemical and ultrastructural study. Fresh Lung sections were processed for electron microscopic study. The results revealed marked pathological alterations in the rat lungs of Group III: distortion in the pulmonary architecture, mononuclear cellular infiltration, presence of areas of consolidation with alveolar collapse, areas of emphysematous air spaces, marked degeneration of the pneumocytes and increased collagen fibers deposition and marked increase in iNOS immunoexpression. There were marked alterations in the level oxidative markers in the lung homogenates. The ultrastructural study confirmed these changes. Treatment with vitamin E in Group IV revealed noticeable improvement of the histological and ultrastructural architecture of the lung. There was marked improvement in the other parameters. The present study concluded that amiodarone has marked toxic effect on the lung of the adult male albino rat and vitamin E could partially protect the lung against such toxic effects

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Does silybin protect against toxicity induced by polymyxin E in rat kidney?

AIMS: Although once a common antibiotic, polymyxin E fell out of favor after reports of its nephrotoxicity. However, recent concerns with gram-negative bacteria, which are resistant to multiple antibiotics, have resulted in increased interest in polymyxin E. Silybin is a known antihepatotoxic drug and may have potential for protecting the kidney from polymyxin E. Therefore, the aim of the current study was to evaluate whether silybin affected the damages produced by polymyxin E on the rat kidney. METHODS: Four groups of rats with 10 rats per group were included in the study: control (no treatment, group I), vehicle (control vehicle treatment, group II), polymyxin E treatment (group III), and polymyxin E and silybin treatment (group IV). Groups II-IV received intravenous treatment twice a day for 7 days. All rats were euthanized after 7 days. Histological, ultrastructural, and morphometric analyses were performed on the rats' kidney tissues. RESULTS: Analysis of tissues from group III showed differences from groups I and II, such as glomerular and tubular affection and changes in morphometric measures. Results for group IV were more similar to those of groups I and II than those of group III. CONCLUSIONS: Our results suggested that administering silybin with polymyxin E alleviated polymyxin E-induced nephrotoxicity in the rat kidney. Future biochemical studies should investigate whether silybin could ameliorate the nephrotoxicity caused by polymyxin E in rats and whether concomitant administration of silybin could be an effective clinical pharmacological strategy to protect against polymyxin E-induced insult in human kidneys.

Age-related alterations in the lacrimal gland of adult albino rat: a light and electron microscopic study.

BACKGROUND: Age related changes in the lacrimal gland are associated with alterations in the structural organization and functional response in the gland of diverse mammalian species. Dry eye syndrome is one of the most common ocular problems in the world especially in old age. It results when the lacrimal gland fails to secrete proteins and fluid in sufficient quantity or appropriate composition. AIM OF THE WORK: The present study is designed to demonstrate the influence of aging on the structure of the lacrimal gland of albino rat and to provide a morphological basis to explain the pathogenesis of the dry eye syndrome with ageing. It also aims to carry out a comparative analysis of age-dependent changes in male and female rats and to address how the lacrimal gland ages in each sex. MATERIAL AND METHODS: Eighty albino rats were used in this study. The animals were divided into two age groups, young adult and senile. Tear secretion was measured using a modified Schirmer test. Corneal impression cytology of the anesthetized rats was done. The glands were subjected to gross morphologic examination, microscopic examination using H&E, PAS, Masson's trichrome and Giemsa stains. Electron microscopic examination was done in addition to quantitative histomorphometric estimations included acinar density, ductal count and mast cell count. RESULTS: Light microscopic examination of the lacimal glands of the senile rats revealed different pathological changes. These included acinar, ductal as well as stromal changes. Electron microscope examination of the lacrimal gland of the senile group showed a decrease in the electron dense secretory vesicles, mitochondrial swelling and lipofuscin-like inclusions were frequently seen in the cytoplasm of acinar cells in senile rats. CONCLUSION: The structural changes in the lacrimal glands of senile rats were associated with reduction in tear secretion as well as alterations in corneal epithelium. Gender difference in lacrimal gland structure was recorded.