Background Aluminum is one of the prevalent alloys on the earth. With the revolution industry, aluminum was very important in all aspects of life from cooking to war weapons. The aim of this work is to study the prevalence of respiratory hazards and changes in pulmonary function among aluminum industry workers. Materials and methods This is a case series study which was conducted in an aluminum factory in Nag Hammadi and included 320 workers, who were subdivided into 2 groups according to the duration of daily exposure to aluminum gases and exhausts. Group 1: it included 260 exposed workers, who were randomly selected from potrooms and cast house sectors, and exposed to hazardous effects of primary aluminum industry 8 h continuously per day. Group 2: it included 60 interrupted or partially exposed workers, who were randomly selected from the factory maintenance, potroom maintenance, cast house maintenance workers, as well as the general maintenance workers; and exposed to less than 8 h interrupted per day on average 2–3 h. Data were collected using modified British Medical Research Council (BMRC) questionnaire, and pulmonary function tests, chest X-ray, and laboratory studies were done. Results Group 1 workers had more chronic and acute work related respiratory symptoms. There was a significantly higher occurrence of asthma among exposed workers with p value 0.004 while no significant difference for the occurrence of COPD in both groups, also CRP significantly more frequently occurred in exposed workers with p value 0.001. There was a significant negative correlation between FVC%, FEV1% and PEF25–75% and duration of exposure in years among exposed workers. Interpretation of chest X-ray denoted that reticular, nodular and reticulo-nodular patterns significantly more frequently occurred in exposed group (p value 0.01) also diaphragmatic abnormalities were more in exposed ones (p value 0.04). Solitary pulmonary nodules could be detected in three cases. Conclusions Aluminum industry is hazardous to both the workers and the community. The pulmonary hazards are significantly higher in workers who are continuously exposed to gases and pollutants for more than 8 h/day. Moreover the free radicals of silica and polycyclic aromatic hydrocarbons may have a direct relationship with the recorded changes in diaphragmatic and pulmonary functions and may be precancerous.

The present investigation was conducted (during PM examination of the slaughtered carcasses) to evaluate the sensitivity and specificity of Enzyme-linked immunosorbent assay (ELISA) in identifying camels infected with hydatid cysts before slaughtering and to assess the prevalence of hydatidosis in camels sacrificed in Assuit Governorate. Hydatid cyst count and characterization were conducted based on routine meat inspection. Slaughterhouse samples of 200 camels were collected through weekly visits. Hydatid cysts in livers, lungs and kidneys were detected and counted, also the fertility rate of the cysts was examined. Out of these, 12 (6%) were found to harbor hydatid cyst, in livers 9(75%), lungs 2(17%) and kidney 1(8%).On the other side, fertile cysts 5(41.7%) were found more frequently in livers 4(33.3%) than in lungs 1(8.3%), while sterile cysts7(58.3%) found in livers , lungs and kidneys 5(41.7% ), 1(8.1) and 1(8.3%) respectively. In addition to PM examination, Enzyme-linked immunosorbent assay test (ELISA) was developed to the same camels for serological detection of hydatid cyst infection but in alive state. 16(8%) of the 200 camels were found harbouring hydatid cysts were serologically positive when screened for hydatidosis by ELISA test. Four animals (2%) out of the 188 non-infected camels gave serologically positive result. It is suggested that the ELISA as a serological assay, is a valuable method with high diagnostic efficiency for serodiagnosis of hydatid disease. The public health importance of hydatidosis as well as some recommended measures for controlling of the disease were discussed

Scorpion envenomation causes an autonomic storm resulting in changes in the vasoactive mediators’ levels which lead to myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary edema, multi-system-organ-failure and death. The study aimed to determine the circulating levels of adrenaline, noradrenaline, angiotensin converting enzyme (ACE), Angiotensin II (Ang II), kallikrein enzyme, nitric oxide (NO), aldosterone, and electrolytes Naþ, Kþ and Caþ2 in scorpion envenomed children and to evaluate the potential relation between these vasoactive mediators, the severity of scorpion envenoming and the clinical outcome of envenomed children. Forty envenomed children (22 mild and 18 severe cases) along with 10 healthy control children were enrolled in the study. The circulating levels of adrenaline, noradrenaline, Ang II, ACE, kallikrein enzyme, and NO were determined by ELISA, and spectrophotometric assays on admission and 24 h later. On admission, serum aldosterone, and electrolytes; Naþ, Kþ and Caþ2 were determined by RIA, Flame photometer and Flame atomic absorption respectively. All envenomed children showed significant surge of adrenaline, noradrenaline, ACE, Ang II, aldosterone, NO and Naþ, that concomitantly faced by significant reduction in kallikrein, Kþ and Caþ2 on admission. Twenty four hours later, all envenomed children continued to show significant elevation of ACE, Ang II and NO. The severely envenomed children showed considerable reduction in circulating levels of adrenaline, noradrenaline, ACE and Ang II, while dramatic increase in kallikrein activity was reported in comparison to mildly envenomed children after 24 h of medical care. Also, NO exhibited considerable accumulation in non survivors, on admission, that was persistent for the subsequent 24 h and was accompanied by high kallikrein, low catecholamines and Ang II levels compared to survivors. Finally, the hypertensive cases showed substantial higher levels of catecholamine, ACE and Ang II, 24 h after admission. These findings indicated that, disturbances of the studied vasoactive mediators were common in scorpion envenomed children and may account for several inflammatory manifestations and clinical outcome. ACE inhibitors could be considered as possible therapeutic agent in victims with prominent increase in ACE and Ang II while kallikrein inhibitor and antioxidants may be effective in the treatment of late hypotensive ones.

Scorpion envenomation causes an autonomic storm resulting in changes in the vasoactive mediators’ levels which lead to myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary edema, multi-system-organ-failure and death. The study aimed to determine the circulating levels of adrenaline, noradrenaline, angiotensin converting enzyme (ACE), Angiotensin II (Ang II), kallikrein enzyme, nitric oxide (NO), aldosterone, and electrolytes Naþ, Kþ and Caþ2 in scorpion envenomed children and to evaluate the potential relation between these vasoactive mediators, the severity of scorpion envenoming and the clinical outcome of envenomed children. Forty envenomed children (22 mild and 18 severe cases) along with 10 healthy control children were enrolled in the study. The circulating levels of adrenaline, noradrenaline, Ang II, ACE, kallikrein enzyme, and NO were determined by ELISA, and spectrophotometric assays on admission and 24 h later. On admission, serum aldosterone, and electrolytes; Naþ, Kþ and Caþ2 were determined by RIA, Flame photometer and Flame atomic absorption respectively. All envenomed children showed significant surge of adrenaline, noradrenaline, ACE, Ang II, aldosterone, NO and Naþ, that concomitantly faced by significant reduction in kallikrein, Kþ and Caþ2 on admission. Twenty four hours later, all envenomed children continued to show significant elevation of ACE, Ang II and NO. The severely envenomed children showed considerable reduction in circulating levels of adrenaline, noradrenaline, ACE and Ang II, while dramatic increase in kallikrein activity was reported in comparison to mildly envenomed children after 24 h of medical care. Also, NO exhibited considerable accumulation in non survivors, on admission, that was persistent for the subsequent 24 h and was accompanied by high kallikrein, low catecholamines and Ang II levels compared to survivors. Finally, the hypertensive cases showed substantial higher levels of catecholamine, ACE and Ang II, 24 h after admission. These findings indicated that, disturbances of the studied vasoactive mediators were common in scorpion envenomed children and may account for several inflammatory manifestations and clinical outcome. ACE inhibitors could be considered as possible therapeutic agent in victims with prominent increase in ACE and Ang II while kallikrein inhibitor and antioxidants may be effective in the treatment of late hypotensive ones.

Scorpion envenomation causes an autonomic storm resulting in changes in the vasoactive mediators’ levels which lead to myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary edema, multi-system-organ-failure and death. The study aimed to determine the circulating levels of adrenaline, noradrenaline, angiotensin converting enzyme (ACE), Angiotensin II (Ang II), kallikrein enzyme, nitric oxide (NO), aldosterone, and electrolytes Naþ, Kþ and Caþ2 in scorpion envenomed children and to evaluate the potential relation between these vasoactive mediators, the severity of scorpion envenoming and the clinical outcome of envenomed children. Forty envenomed children (22 mild and 18 severe cases) along with 10 healthy control children were enrolled in the study. The circulating levels of adrenaline, noradrenaline, Ang II, ACE, kallikrein enzyme, and NO were determined by ELISA, and spectrophotometric assays on admission and 24 h later. On admission, serum aldosterone, and electrolytes; Naþ, Kþ and Caþ2 were determined by RIA, Flame photometer and Flame atomic absorption respectively. All envenomed children showed significant surge of adrenaline, noradrenaline, ACE, Ang II, aldosterone, NO and Naþ, that concomitantly faced by significant reduction in kallikrein, Kþ and Caþ2 on admission. Twenty four hours later, all envenomed children continued to show significant elevation of ACE, Ang II and NO. The severely envenomed children showed considerable reduction in circulating levels of adrenaline, noradrenaline, ACE and Ang II, while dramatic increase in kallikrein activity was reported in comparison to mildly envenomed children after 24 h of medical care. Also, NO exhibited considerable accumulation in non survivors, on admission, that was persistent for the subsequent 24 h and was accompanied by high kallikrein, low catecholamines and Ang II levels compared to survivors. Finally, the hypertensive cases showed substantial higher levels of catecholamine, ACE and Ang II, 24 h after admission. These findings indicated that, disturbances of the studied vasoactive mediators were common in scorpion envenomed children and may account for several inflammatory manifestations and clinical outcome. ACE inhibitors could be considered as possible therapeutic agent in victims with prominent increase in ACE and Ang II while kallikrein inhibitor and antioxidants may be effective in the treatment of late hypotensive ones.

Scorpion envenomation causes an autonomic storm resulting in changes in the vasoactive mediators’ levels which lead to myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary edema, multi-system-organ-failure and death. The study aimed to determine the circulating levels of adrenaline, noradrenaline, angiotensin converting enzyme (ACE), Angiotensin II (Ang II), kallikrein enzyme, nitric oxide (NO), aldosterone, and electrolytes Naþ, Kþ and Caþ2 in scorpion envenomed children and to evaluate the potential relation between these vasoactive mediators, the severity of scorpion envenoming and the clinical outcome of envenomed children. Forty envenomed children (22 mild and 18 severe cases) along with 10 healthy control children were enrolled in the study. The circulating levels of adrenaline, noradrenaline, Ang II, ACE, kallikrein enzyme, and NO were determined by ELISA, and spectrophotometric assays on admission and 24 h later. On admission, serum aldosterone, and electrolytes; Naþ, Kþ and Caþ2 were determined by RIA, Flame photometer and Flame atomic absorption respectively. All envenomed children showed significant surge of adrenaline, noradrenaline, ACE, Ang II, aldosterone, NO and Naþ, that concomitantly faced by significant reduction in kallikrein, Kþ and Caþ2 on admission. Twenty four hours later, all envenomed children continued to show significant elevation of ACE, Ang II and NO. The severely envenomed children showed considerable reduction in circulating levels of adrenaline, noradrenaline, ACE and Ang II, while dramatic increase in kallikrein activity was reported in comparison to mildly envenomed children after 24 h of medical care. Also, NO exhibited considerable accumulation in non survivors, on admission, that was persistent for the subsequent 24 h and was accompanied by high kallikrein, low catecholamines and Ang II levels compared to survivors. Finally, the hypertensive cases showed substantial higher levels of catecholamine, ACE and Ang II, 24 h after admission. These findings indicated that, disturbances of the studied vasoactive mediators were common in scorpion envenomed children and may account for several inflammatory manifestations and clinical outcome. ACE inhibitors could be considered as possible therapeutic agent in victims with prominent increase in ACE and Ang II while kallikrein inhibitor and antioxidants may be effective in the treatment of late hypotensive ones.

Scorpion envenomation causes an autonomic storm resulting in changes in the vasoactive mediators’ levels which lead to myocardial damage, cardiovascular disturbances, peripheral circulatory failure, pulmonary edema, multi-system-organ-failure and death. The study aimed to determine the circulating levels of adrenaline, noradrenaline, angiotensin converting enzyme (ACE), Angiotensin II (Ang II), kallikrein enzyme, nitric oxide (NO), aldosterone, and electrolytes Naþ, Kþ and Caþ2 in scorpion envenomed children and to evaluate the potential relation between these vasoactive mediators, the severity of scorpion envenoming and the clinical outcome of envenomed children. Forty envenomed children (22 mild and 18 severe cases) along with 10 healthy control children were enrolled in the study. The circulating levels of adrenaline, noradrenaline, Ang II, ACE, kallikrein enzyme, and NO were determined by ELISA, and spectrophotometric assays on admission and 24 h later. On admission, serum aldosterone, and electrolytes; Naþ, Kþ and Caþ2 were determined by RIA, Flame photometer and Flame atomic absorption respectively. All envenomed children showed significant surge of adrenaline, noradrenaline, ACE, Ang II, aldosterone, NO and Naþ, that concomitantly faced by significant reduction in kallikrein, Kþ and Caþ2 on admission. Twenty four hours later, all envenomed children continued to show significant elevation of ACE, Ang II and NO. The severely envenomed children showed considerable reduction in circulating levels of adrenaline, noradrenaline, ACE and Ang II, while dramatic increase in kallikrein activity was reported in comparison to mildly envenomed children after 24 h of medical care. Also, NO exhibited considerable accumulation in non survivors, on admission, that was persistent for the subsequent 24 h and was accompanied by high kallikrein, low catecholamines and Ang II levels compared to survivors. Finally, the hypertensive cases showed substantial higher levels of catecholamine, ACE and Ang II, 24 h after admission. These findings indicated that, disturbances of the studied vasoactive mediators were common in scorpion envenomed children and may account for several inflammatory manifestations and clinical outcome. ACE inhibitors could be considered as possible therapeutic agent in victims with prominent increase in ACE and Ang II while kallikrein inhibitor and antioxidants may be effective in the treatment of late hypotensive ones.

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