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INTRODUCTION: Acute symptomatic occlusion of the internal carotid artery (ICA) is associated with unfavorable prognosis. However, no clear definition of its optimal treatment exists. The aim of this study was to evaluate the efficacy and risks of urgent carotid endarterectomy (CEA) in patients with ischemic stroke due to acute extracranial ICA occlusion. METHODS: A retrospective analysis was performed of all consecutive patients undergoing urgent CEA for acute extracranial ICA occlusion during the period from July 2014 to June 2021. The primary outcome was functional independence at three months defined as modified Rankin Scale (mRS) score 2. Secondary outcomes included the severity of the neurological deficit at the time of discharge and its comparison with the preoperative condition as assessed using the National Institutes of Health Stroke Scale (NIHSS), the incidence of symptomatic intracerebral hemorrhage (ICH), and 30-day periprocedural mortality. RESULTS: During the study period, a total of 42 urgent CEAs were performed for acute extracranial ICA occlusions. The median preoperative NIHSS score was 7 (interquartile range [IQR] 5-13). The median time interval between the onset of symptoms and surgery was 290 minutes (IQR 235-340). Technical success rate of urgent CEA was 97.6% (41 patients). The median NIHSS at the time of hospital discharge was 2 (IQR 3-7; p.

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INTRODUCTION: Left paraduodenal hernia is an internal herniation that develops due to anomalous fetal development. If incarcerated, it becomes an unusual cause of acute abdomen. CASE REPORT: This case report presents an uncommon case of a 39-year-old man with acute abdominal pain with vomiting. The patients medical history included recurrent subileous events and Crohn´s disease in long-term remission. CT scan of abdominal cavity indicated a possible mechanical obstruction of small bowel loops in the upper left abdominal quadrant. Incarcerated left paraduodenal herniation was identified during surgery. Repositioned small bowel loops did not require resection and the entrance of Landzert´s fossa was sutured. CONCLUSION: Left paraduodenal hernia is the most common congenital internal herniation. Although rare, it should be considered in the differential diagnosis of acute abdomen.

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INTRODUCTION: Visceral artery aneurysms are rare vascular pathologies. They are usually incidental findings during the examination for other reasons. The most common clinical symptoms are nonspecific abdominal pain and bleeding caused by their rupture, with a severe clinical presentation. Aneurysms of pancreaticoduodenal arcade are more common in patients with well-developed collateral circulation due to the coeliac trunk stenosis or occlusion. CASE REPORT: In this case report the authors present a rare case of a patient with incidental finding of pancreaticoduodenal arcade aneurysm in the setting of severe stenosis of coeliac trunk origin caused by medial arcuate ligament compression. The diameter of the aneurysm was 40 mm and endovascular treatment was not possible because of unfavorable anatomical setting. The patient was successfully treated with resection of the aneurysm and the division of medial arcuate ligament during one surgery. CONCLUSION: There is no correlation between the diameter and the risk of rupture of the pancreaticoduodenal arcade aneurysm. Because of high morbidity and mortality of their rupture, most authors recommend active treatment of these aneurysms. The necessity to treat truncus coeliacus stenosis or occlusion remains a controversial issue.

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INTRODUCTION: Cerebrovascular events are among the most common causes of invalidity or death. The aim of treatment in acute cerebral ischemia is to restore the blood flow before irreversible necrosis of brain tissue and persistent neurologic deficit occur. Pharmacological, endovascular and surgical methods are employed in the treatment of these patients. CASE REPORT: The authors present a case report of a 56-year-old woman with acute cerebral ischemia caused by tandem occlusion of the left common carotid artery and the M1 segment of middle cerebral artery. In the initial phase the patient was treated by intravenous thrombolysis with minimal success. Common carotid artery was occluded and mechanical extraction of embolus was successfully performed through direct carotid bifurcation puncture. Almost complete regression of neurologic deficit occurred after the endovascular recanalization. Occluded common carotid stump and bifurcation was considered as a source of embolization and therefore, to prevent further cerebrovascular event, a subclavian-carotid bypass was performed on the 15th day after the stroke. CONCLUSION: In the reported patient with symptomatic tandem occlusion of common carotid artery and the M1 part of middle cerebral artery, recanalization of cerebral artery was attained by the combination of pharmacological and endovascular method. Consequent subclavian-to-carotid bypass was performed in tertiary prevention of further cerebrovascular event.

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OBJECTIVE: To test whether improved functional status correlates with more depressive symptoms after traumatic brain injury (TBI). This is based on the concept that increasing awareness of deficits may exacerbate depression, even while survivors are making functional improvements. PARTICIPANTS: A total of 471 individuals with TBI (72% white; 71% men; median Glasgow Coma Scale (GCS) score = 11) enrolled during acute care or inpatient rehabilitation and followed up at a median of 6 months. MAIN MEASURE: Beck Depression Inventory-II (BDI-II), Glasgow Outcome Scale-Extended, and Functional Status Examination (FSE). RESULTS: We found significant Spearman rank order correlations between BDI-II scores and the total FSE as well as all domains of the FSE. Lower functional levels correlated with more depressive symptoms. Modeling of predictive factors, including subject characteristics, injury-related characteristics, and outcome measures, resulted in 2 models, both containing age and GCS along with other factors. CONCLUSION: The relation between depressive symptoms and functional outcomes is complex and a fertile area for further research. The authors would encourage clinicians to monitor patients for depressive symptoms to help to prevent the detrimental impact on recovery.

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A continuous-flow reactor (CSTR) and a soil slurry-sequencing batch reactor (SS-SBR) were operated in 81 vessels for 200 days to treat a soil contaminated with polycyclic aromatic hydrocarbons (PAH). Filtered slurry samples were used to quantify bulk biosurfactant concentrations and PAH emulsification. Concentrations of Corynebacterium aquaticum, Flavobacterium mizutaii, Mycobacterium gastri, Pseudomonas aeruginosa, and Pseudomonas putida were determined using fatty acid methyl ester (FAME) analysis. The CSTR and SS-SBR selected microbial consortia with markedly different surfactant-producing and PAH-degrading abilities. Biosurfactant levels in the SS-SBR reached 4 times the critical micelle concentration (CMC) that resulted in considerable emulsification of PAH. In contrast, CSTR operation resulted in nomeasurable biosurfactant production. Total PAH removal efficiency was 93% in the SS-SBR, compared with only 66% in the CSTR, and stripping of PAH was 3 times less in the SS-SBR. Reversing the mode of operation on day 100 caused a complete reversal in microbial consortia and in reactor performance by day 140. These results show that bioslurry reactor operation can be manipulated to control overall reactor performance.

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Both cadmium and lead have pulmonary toxicity: cadmium can cause lung cancer, fibrosis and emphysema; lead can induce a moderate interstitial pulmonary fibrosis. Both metals give rise to depletion of glutathione and depletion of the protein-bound sulfhydryl groups, and lead to the production of reactive oxygen species. In the primary culture of type II pneumocytes, which is one of the most important cell groups from the aspect of glutathione metabolism and thus redox balance, the effect of cadmium chloride and lead nitrate upon the enzymes of the glutathione cycle, upon superoxide dismutase and upon the structure of type II pneumocytes was examined. Depending on the concentration, cadmium inhibited each of these parameters, whereas lead nitrate significantly increased the activity of glutathione reductase while inhibiting other parameters. Both metals induced damage of the membranes of type II cells, depending on the concentration, although cadmium caused significantly more damage than lead. The data obtained suggest that both substances cause an imbalance in the redox cycle and diversely affect the function and membrane structure of type II pneumocytes.

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A continuous-flow reactor (CSTR) and a soil slurry-sequencing batch reactor (SS-SBR) were maintained in 8l vessels for 180 days to treat a soil contaminated with diesel fuel (DF). Concentrations of Candida tropicalis, Brevibacterium casei, Flavobacterium aquatile, Pseudomonas aeruginosa, and Pseudomonas fluorescens were determined using fatty acid methyl ester (FAME) analysis. DF removal (biological and volatile) and biosurfactant concentrations were measured. The SS-SBR encouraged the growth of biosurfactant-producing species relative to the CSTR. Counts of biosurfactant-producing species (C. tropicalis, P. aeruginosa, P. fluorescens) relative to total microbial counts were 88% in the SS-SBR and 23% in the CSTR. Biosurfactants were produced in the SS-SBR to levels of nearly 70 times the critical micelle concentration (CMC) early in the cycle, but were completely degraded by the end of each cycle. No biosurfactant production was observed in the CSTR. DF biodegradation rates were over 40% greater and DF stripping was over five times lower in the SS-SBR than the CSTR. However, considerable foaming occurred in the SS-SBR. Reversing the mode of operation in the reactors on day 80 caused a complete reversal in microbial consortia and reactor performance by day 120. These results show that bioslurry reactor operation can be manipulated to control overall reactor performance.

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The effects of cobalt sulfate administered to pregnant C57BI mice, OFA-SD rats, and New Zealand rabbits was studied on fetal and postnatal offspring. Cobalt concentration in the maternal blood was increased in proportion to the administered doses. Cobalt crossed the placenta and appeared in the fetal blood and amniotic fluid. Regardless of the administered dose of cobalt sulfate, cobalt concentration in the blood peaked 2 h after administration. Cobalt produced dose-dependent maternal toxicity and was found to be embryotoxic in all three species, as evidenced by elevated frequency of fetuses with body weight or skeletal retardation and embryolethality. Cobalt increased the frequency of major anomalies significantly in mice and rats, with anomalies of the eyes, kidneys, skull, spine, and sternum in mice, and anomalies of the urogenital system in rats. Cobalt sulfate was not teratogenic in rabbits. Intra-amnial administration of cobalt sulfate produced a dose-dependent increase of the frequency of dead fetuses, and weight retardation of the live fetuses. The direct cytotoxic effect probably plays a role in the embryotoxic and teratogenic effects of cobalt. The postnatal examinations revealed a decrease of the perinatal index in the treated group. The body weight of the pups in the treated group was lower during wk 1 of life, but no difference was found between the control and treated by the end of wk 2. Eye opening was completed in the usual time period in both groups, while time of appearance of the teeth, descending of the testes, shaping of ears, and development of hearing was delayed in the treated group. The development of muscle strength and of the locomotor system was delayed. All the functions studied (forward movement, swimming, righting reflex) normalized by postnatal d 21, with the exception of muscle strength. It was concluded that cobalt sulfate exposure decreases the perinatal viability of the fetuses, but the functions of the surviving fetuses with perinatal retardation become compensated by postnatal wk 2-3. The development of fetuses is undisturbed thereafter.

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Dithiocarbamates (DDTC) are chemicals widely used in the form of pesticides, therapeutic and chelating agents, and scavengers. Since DDTC interfere with SH, Cu, and Zn enzymes due to chelating properties, it was of interest to clarify, in primary culture of type II alveolar pneumocytes, the effect of this compound upon enzymes of glutathione cycle, Cu, Zn-superoxide dismutase, and the membrane structure of cells. DDTC significantly inhibited the activity of superoxide dismutase and the activity of gamma-glutamyl transpeptidase, glutathione reductase, and alkaline phosphatase, whereas an increase in the activity of glutathione peroxidase was found. The membranes of pneumocytes type II were injured. Data show that DDTC adversely affected type II pneumocyte function and structure.

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Daily indium chloride doses of control (0), 50, 100, 200, or 400 mg/kg were administered orally to Sprague-Dawley rats by gavage, on d 6-15 of gestation, and daily metal doses of control (0), 50, 100, or 200 mg/kg were administered to New Zealand rabbits on d 6-20 of gestation. Further groups of pregnant rats were treated with control (0) or 400 mg/kg indium chloride orally on one of d 8, 9, 10, 11, 12, 13, 14, or 15 of gestation. The dams and fetuses were examined on d 21 (rats) and 30 (rabbits) of gestation, using standard teratological methods. Indium concentration was determined in the maternal and fetal blood, as well as in the amniotic fluid, by atomic absorption spectrometry. Indium was found to cross the placenta and appeared in fetal blood in proportion to the metal concentration of the maternal blood. In the amniotic fluid, indium concentrations remained below the detection limit. In rats, indium chloride produced dose-dependent maternal toxic effects, with a dose of 400 mg/kg inducing embryotoxicity (embryolethality) and teratogenicity. Doses of 200 and 100 mg/kg were embryotoxic (retarding) and teratogenic, causing skeletal and visceral anomalies in addition to external anomalies (rudimentary or missing tail, syndactylia, clubfoot, exencephalia) in rats. In rabbits, 200 mg/kg indium chloride was lethal for the dams and the embryos (some of the animals died, and the number of abortions and full resorptions increased). This dose was found to be teratogenic (caused gross renal anomalies) and increased the frequency of fetuses with skeletal retardation. In rats, the effects of indium chloride causing fetal retardation was found to be independent of exposure time. The teratogenic effects were the highest on d 11 and 12 of gestation, when indium chloride caused gross external malformations. Data suggest that the teratogenic effects of indium chloride can be attributed primarily to a direct cytotoxic action of indium resulting from placental transfer, but the effect is not a selective one, as it appears only in the presence of maternal toxic effects.

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The authors observed serious lead intoxication of a 18 year old female ceramic apprentice caused by tea with lemon stored in a glazed ceramic teapot made by the patient herself. The case history suggests: 1. the need of warning people to avoid the use of ceramic tablewares made by insufficient technology for alimentary purposes. 2. Patient with lead exposure can have also alimentary intoxication. 3. It seems advisable to perform screening tests of the ceramic apprentices who use lead glazes in order to detect the eventual increased absorption of lead in time.

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In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinetics, and UV-induced unscheduled DNA synthesis (UDS) were followed up three times during a 20-month period in peripheral blood lymphocytes (PBL) of 26 workers (13 maintainers and 13 fiber producers) occupationally exposed to ANC and/or DMF in a viscose rayon plant, 26 matched control subjects, and six industrial controls (all males). Six of the 26 exposed subjects were hospitalized because of liver dysfunction that had developed due to inhalative DMF exposure. The rate of smoking was estimated on the basis of serum thiocyanate (SCN) levels. Average peak air ACN and DMF concentrations were over the maximum concentration limits at the time of both investigations. Urine ACN and monomethyl-formamide (MMF) excretions of the exposed subjects were almost doubled after work shifts. An increase in lymphocyte count (in months 0 and 7), and severe alterations in the liver function were observed in the exposed subjects. In PBLs the proliferative rate index (PRI) was already increased in month 0 compared with the controls. In each study, significant increases in CA and SCE frequencies, as well as increases in UDS were found in PBLs of the exposed subjects. The frequencies of chromatid breaks and acentric fragments further increased in month 7 and remained constantly elevated in month 20. Increased yields of both chromatid and chromosome-type exchange aberrations first appeared in month 20, when HFCs were 2.72 times more frequent in fiber producers than in maintainers. The role of some important biological confounding factors (age, white blood cell count, and hematocrit) and lifestyle confounding factors (smoking and drinking habits) were subjected to an analysis of variance during the second study. Increased CA, SCE, and UDS were found both in control and exposed smokers when current smoking was established on the basis of the serum SCN levels. The cytogenetic data suggest that occupational exposures to ACN and DMF induce considerable genotoxic consequences and may increase the cancer risk in the exposed human populations.

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Authors describe the case-history of a 17 year old male who accidentally ingested a fishing weight that was retained in the stomach and caused a serious lead poisoning. It is worth mentioning that beside the wellknown symptoms and signs of lead intoxication also the liver was seriously affected. The histologically verified toxic lesion of the liver presumably can be attributed to the large quantities of lead absorbed within a short period. This also explains the appearance of symptoms and signs indicating to encephalopathy beside the young age of the patient. The foreign body could not be removed by means of gastroscopy, therefore a gastrotomy was carried out followed by chelating treatment with i.v. CaNa2EDTA that resulted in complete clinical and laboratory recovery. The case history draws the attention to the importance of the quick removal of the retained lead containing objects out of the gastrointestinal tract.

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Authors describe two cases of lead poisoning of unusual origin. A 43 year old male patient bought some waste metal in order to build a fence around his new house for saving money. He removed the old corroded coat of paint using a grinder without any protection. Consequently, he had got grave lead intoxication with colic and anemia. Another 34 year old unemployed male person moulded leaded chessmen in his own kitchen. This activity resulted in serious intoxication of the patient and highly increased lead absorption of the family members. In addition to the exploration of professional exposure the authors stress also the significance of the clearing up of occasional lead-related hobbies and home activities in case of lead intoxication of unknown origin.

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The authors have studied the effect of consumption of a humic acid based complex microelement preparation (potassium, magnesium, iron, zinc, manganese, copper, vanadium, cobalt, molibden, selenium bound to humic acids) for six weeks (10 ml daily) on the biological exposure indices (blood and urine cadmium levels) and clinical laboratory parameters (liver and kidney tests, blood picture) of men (n = 18; 39.7 +/- 10.4 years of age;) working in cadmium exposure for 8.3 +/- 5.0 years. The initial mean blood and urine cadmium levels of the non-smoking subjects was twice higher than that of the non-smoking male controls living in the same urban area (n = 35), and significantly correlated with the length of exposure. Their mean serum alanin-aminotransferase, gamma-glutamyl-transferase, creatinine, uric acid and urinary N-acetyl-beta-D-glucosaminidase levels were significantly higher than that of the controls. After the six-week treatment blood cadmium level, activity of serum alanin-aminotransferase, serum uric acid and urinary protein concentrations decreased significantly, the abnormal serum iron levels normalized. According to this results, the absorption of cadmium decreased on the effect of the complex microelement supplementation and the adverse laboratory changes attributable partly to cadmium exposure improved. Therefore humic acid based complex microelement supplementation is recommended as an effective tool for prevention and health protection in occupational cadmium exposure as well as for smokers known to be considerably burdened by cadmium.

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OBJECTIVE: Report of a lead intoxication epidemic caused by ingestion of contaminated ground paprika. DESIGN: Retrospective study of case histories. SETTING: Institutional, toxicological and medical referral center for ambulatory and hospitalized care. PATIENTS: One hundred forty-one adults consumed paprika contaminated with lead tetroxide (red lead). INTERVENTIONS: Intravenous calcium disodium versenate (edetic acid). MAIN OUTCOME MEASURES: Measurement of zinc protoporphyrin:heme ratio of whole blood and the blood lead level. EDTA mobilization test. RESULTS: Fifty-three patients had symptoms and signs of lead poisoning. The most common clinical signs were colic and/or anemia. Twenty-six persons showed increased lead absorption without clinical symptoms and signs. Chelation therapy with calcium disodium versenate resulted in complete clinical recovery. CONCLUSION: Lead-contaminated ground paprika, not previously described as a cause of alimentary lead intoxication, may cause symptomatic poisoning.

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We describe three men with disseminated, drug-sensitive tuberculosis and advanced human immunodeficiency virus disease (CD4+ lymphocyte count, < 50/mm3) who had flares of tuberculous lymphadenitis with suppuration during the initial weeks of successful chemotherapy. Bactericidal drugs may kindle these transient exacerbations, which involve neutrophils but apparently do not require normal helper T cell function. In patients with AIDS, as in immunocompetent individuals, treatment-related flares of lymphadenitis are usually not an adverse sign, provided that drug resistance and nonadherence have been excluded.

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