Unlocking the secrets of soil microbes: How decades-long contamination and heavy metals accumulation from sewage water and industrial effluents shape soil biological health.

Heavy metals contamination is posing severe threat to the soil health and environmental sustainability. Application of industrial and sewage waste as irrigation and growing urbanization and agricultural industry is the main reason for heavy metals pollution. Therefore, the present study was planned to assess the influence of different irrigation sources such as industrial effluents, sewage wastewater, tube well water, and canal water on the soil physio-chemical, soil biological, and enzymatic characteristics. Results showed that sewage waste and industrial effluents affect the soil pH, organic matter, total organic carbon, and cation exchange capacity. The highest total nickel (383.71 mg kg-1), lead (312.46 mg kg-1), cadmium (147.75 mg kg-1), and chromium (163.64 mg kg-1) were recorded with industrial effluents application. Whereas, industrial effluent greatly reduced the soil microbial biomass carbon (SMB-C), soil microbial biomass nitrogen (SMB-N), soil microbial biomass phosphorus (SMB-P), and soil microbial biomass sulphur (SMB-S) in the winter season at sowing time. Industrial effluent and sewage waste inhibited the soil enzymes activities. For instance, the minimum activity of amidase, urease, alkaline-phosphatase, ß-glucosidase, arylsulphatase and dehydrogenase activity was noted with HMs contamination. The higher levels of metals accumulation was observed in vegetables grown in soil contaminated with untreated waste water and industrial effluent in comparison to soil irrigated with canal and tube well water. The mean increase in soil microbial parameters and enzyme activities was also observed in response to the change in season from winter to spring due to increase in soil mean temperature. The SMB-C, SMB-N, SMB-P and SMB-S showed significant positive correlation with soil enzymes (amidase, urease, alkaline-phosphatase, ß-glucosidase, arylsulphatase and dehydrogenase). The heavy metals accumulation in soil is toxic to microorganisms and inhibits enzyme functions critical for nutrient cycling and organic matter decomposition and can disrupt the delicate balance of soil ecosystem and may lead to long-term damage of soil biological health.

Frequency of Cerebral Venous Thrombosis in Dubai, UAE-A Multicenter, Retrospective Study.

Background and Purpose: Cerebral venous thrombosis (CVT), also known as cerebral dural venous thrombosis, is not a very common cause of stroke. It has a diverse clinical presentation, with multiple predisposing factors and imaging findings. The incidence of CVT varies in different studies. We hypothesized that the incidence of CVT in Dubai is more than that reported in the West owing to dehydration caused by the high atmospheric temperature. Methods: We retrospectively reviewed the medical records of all patients aged more than 13 years with appropriate International Classification of Diseases, 9th Revision, codes for the diagnosis of CVT from January 1, 2010 to December 31, 2018 from three major hospitals with an acute stroke service in Dubai, United Arab Emirates. Results: We identified 138 patients who presented with CVT. The average frequency of CVT was 6.6 per 100,000 population. Fifty percent of the patients presented between May and September, which are considered the hottest months in the UAE. Headache was the most common presentation, followed by seizures. The most important risk factors were the use of oral contraceptive pills, anemia, and polycythemia. Our study showed a higher incidence of anemia, polycythemia, thrombophilia, and abnormal CT brain findings. Conclusion: In our study, CVT was more common during the months of summer. Anemia and polycythemia were strongly associated with CVT. Public awareness about CVT, its higher incidence during summer months and strategies to avoid dehydration might be considered to reduce the incidence of CVT in summer months. However, larger studies are needed to confirm definite associations.

Rosuvastatin and retinoic acid may act as 'pleiotropic agents' against ß-adrenergic agonist-induced acute myocardial injury through modulation of multiple signalling pathways.

Cardiovascular disorders constitute the principal cause of deaths worldwide and will continue as the major disease-burden by the year 2060. A significant proportion of heart failures occur because of use and misuse of drugs and most of the investigational agents fail to achieve any clinical relevance. Here, we investigated rosuvastatin and retinoic acid for their "pharmacological pleiotropy" against high dose ß-adrenergic agonist (isoproterenol)-induced acute myocardial insult. Rats were pretreated with rosuvastatin and/or retinoic acid for seven days and the myocardial injury was induced by administering isoproterenol on the seventh and eighth day. After induction, rats were anaesthetized for electrocardiography, then sacrificed and different samples were collected/stored for various downstream assays. Myocardial injury with isoproterenol resulted in increased cardiac mass, decreased R-wave amplitude, increased QRS and QT durations; elevated levels of cardiac markers like cTnI, CK-MB, ALT and AST; increased lipid peroxidation, protein carbonylation and tissue nitric oxide levels; decreased endogenous antioxidants like SOD, CAT, GR, GST, GPx and total antioxidant activity; increased inflammatory markers like TNF-α and IL-6; decreased the mRNA expression of Nrf2 and Bcl-2; increased the mRNA expression of Bax, eNOS and iNOS genes. Pretreatment with rosuvastatin and/or retinoic acid mitigated many of the above biochemical and pathological alterations. Our results demonstrate that rosuvastatin and retinoic acid exert cardioprotective effects and may act as potential agents in the prevention of ß-adrenergic agonist-induced acute myocardial injury in rats. Cardioprotective potential of rosuvastatin and retinoic acid could be attributed to their influence on the redox pathways, immunomodulation, membrane stability, Nrf2 preservation, iNOS and Bax expression levels. Thus, they may act directly or indirectly at various steps, the breakpoints, in the pathophysiological cascade responsible for cardiac injury. Our study gives insights about the pharmacological pleiotropism of rosuvastatin and retinoic acid.

Lecithin-based deferoxamine nanoparticles accelerated cutaneous wound healing in diabetic rats.

Nanoparticles have higher frequency of being exposed to cells or tissue, and are thus more likely to gain access into cytoplasm or nuclei to modulate molecular events due to significantly larger surface area to volume ratio. As a result, they present amplified response or even different physiochemical and biomedical properties from bigger particles. Deferoxamine accelerates wound healing in diabetic rats by increased neovascularization, reduced inflammation and improved maturation of wound. We investigated the wound healing potential of deferoxamine-nanoparticles in diabetic rats. Lecithin based nanoparticles of deferoxamine were prepared and characterized. The diabetic rats were divided into five Groups, of which Group I was treated with pluronic-gel f-127 (25%), Group II with deferoxamine 0.1% and Group III, IV and V were treated with deferoxamine-nanoparticles incorporated in pluronic-gel f-127 25% at 0.03% (0.01% deferoxamine), 0.1% (0.03% deferoxamine) and 0.3% (0.1% deferoxamine) w/v respectively. The wound closure was significantly accelerated in group V as compared to control groups. HIF-1α, VEGF, SDF-1α, TGF-ß1, and IL-10 protein levels were significantly higher in group V. The collagen deposition and neovascularization was greater in deferoxamine-nanoparticle treated rats. In contrast, TNF-α level was lowest in group V. In summary, the deferoxamine-nanoparticle formulation we developed, when applied topically on diabetic wounds results in faster wound healing as compared to simple deferoxamine formulation. This formulation may prove to be an effective therapy for treatment of diabetic wounds.

Combination of TLR2 and TLR3 agonists derepress infectious bursal disease virus vaccine-induced immunosuppression in the chicken.

Live intermediate plus infectious bursal disease virus (IBDV) vaccines (hot vaccines) are used for protection against the virulent IBDV strains in young chickens. We evaluated the potential of Toll-like receptor (TLR) agonists to alleviate hot vaccine-induced immunosuppression. The combination of Pam3CSK4 and poly I:C synergistically upregulated IFN-ß, IFN-γ, IL-12, IL-4, and IL-13 transcripts and cross-inhibited IL-1ß, IL-10, and iNOS transcripts in the chicken peripheral blood mononuclear cells (PBMCs) as analyzed by quantitative real-time PCR. Further, four-week old specific pathogen free White Leghorn chickens (n = 60) were randomly divided into six groups and either immunized with hot IBDV vaccine with or without Pam3CSK4 and/or poly I:C or not vaccinated to serve as controls. The results indicated that poly I:C alone and in combination with Pam3CSK4 alleviated vaccine-induced immunosuppression, as evidenced by greater weight gain, increased overall antibody responses to both sheep erythrocytes and live infectious bronchitis virus vaccine, upregulated IFN-γ transcripts and nitric oxide production by PBMCs (P < 0.05), and lower bursal lesion score in the experimental birds. In conclusion, poly I:C alone and its combination with Pam3CSK4 reduced the destruction of B cells as well as bursal damage with restoration of function of T cells and macrophages when used with a hot IBDV vaccine.

Seizures with an atypical aetiology in an elderly patient: Eagle's syndrome--how does one treat it?

Onset of epilepsy can occur at any age, but it is relatively rare in the elderly. Late onset epilepsy is usually secondary to stroke, tumour, trauma or neurodegenerative disorders. A 62-year-old Indian woman presented with frequent drop attacks sometimes leading to unconsciousness and, rarely, associated with seizure. Her epilepsy work up was unremarkable. As the disease progressed, she was diagnosed as having idiopathic epilepsy, syncope or pseudo-seizure, on different occasions, and was treated at length with no response. Finally, detailed history-taking revealed her as having glossopharyngeal neuralgia leading to syncope and seizures. She subsequently improved. In clinical practice, such rare entities should also be considered for proper management of patients' ailments.

Acute peripheral polyneuropathy with multiorgan failure: a diagnostic dilemma.

We describe the case of a young man who presented with abdominal pain, vomiting and acute symmetric peripheral polyneuropathy. He was noted to have high anion gap metabolic acidosis with high lactate levels and persistently high arterial and venous pO2 values. The cerebrospinal fluid was acellular with a high protein and the nerve conduction study was consistent with axonal sensorimotor neuropathy. His clinical condition deteriorated rapidly despite full supportive care and he subsequently died of multiorgan failure. An extensive workup for various infectious, autoimmune and other possible aetiologies was carried out to identify the underlying cause for his fulminant illness. All diagnostic workup was non-conclusive except for a significantly elevated serum aluminium level. We have discussed the possibility of aluminium phosphide poisoning in view of the clinical presentation.

Can atherosclerosis be one of the causes of anterior spinal artery thrombosis?

A middle aged diabetic, hypertensive, dyslipidemic, heavy alcohol consumer man came with sudden onset upper back pain and quadriparesis. Examination showed upper motor type quadriparesis with sensation of pain loss up to level of C7 and totally spared proprioception. MRI spine showed features suggestive of anterior spinal artery stroke. Can atherosclerosis be a causative factor for spinal stroke?

Systemic vasculitis with prolonged pyrexia, recurrent facial urticaria, skin nodules, pleural effusions and venous thrombosis: an unusual presentation of an uncommon disease.

Classically presenting with multiple or single peripheral cytopenias of variable severity, the myelodysplastic syndromes may occasionally present with bizarre manifestations that confuse the clinical picture and result in significant delays in making the correct diagnosis. We describe the case of an elderly male patient whose presentation with prolonged unexplained fever coupled with cutaneous, pulmonary and other systemic features of inflammation was finally diagnosed as having a primary myelodysplastic syndrome with associated vasculitis after a delay of 4 years.

Acute disseminated encephalomyelitis as the first presentation of CNS tuberculosis: report of a case with brief review.

Acute disseminated encephalomyelitis (ADEM) also known as post infectious encephalomyelitis is a demyelinating disease of the central nervous system (CNS) that typically presents as a monophasic disorder associated with multifocal neurological symptoms and disability. It may follow vaccination in children or infection. Viral infection like measles, rubella, influenza, Epstein bar, HIV, herpes, cytomegalusvirus (CMV) and West Nile virus have been implicated in the causation. Among bacteria, group A hemolytic streptococcus, mycoplasma pneumonia, Chlamydia, Rickettesia and leptospira have been shown to cause ADEM. There are few reports of ADEM due to tuberculosis (TB). We describe acute disseminated encephalomyelitis due to tuberculosis in a 35 year old female who initially started with neuropsychiatric manifestations and later developed florid neurological deficit and classical magnetic resonance imaging (MRI) lesions suggestive of the disease. The patient recovered completely after antitubercular therapy and is following our clinic for the last 12 months now.

Raised D-dimer levels in acute sickle cell crisis and their correlation with chest X-ray abnormalities.

OBJECTIVE: Quantitation of D-dimer level during a sickling crisis and its correlation with other clinical abnormalities. DESIGN: Prospective longitudinal study. SETTING: Armed Forces Hospital, Southern Region, Kingdom of Saudi Arabia. PATIENTS: Adult patients (12 years and older) admitted acutely with a sickle cell crisis who consent to taking part in the study. Candidates may re-participate if they are readmitted with a further acute painful crisis. RESULTS: 36 patients with homozygous sickle cell disease consented to take part in the study. D-dimer levels were raised in 31 (68.9%) of 45 episodes of painful crisis of whom 13 had an abnormal chest X-ray. Of those with a normal chest X-ray only one patient had a raised D-dimer level: sensitivity of 92.3%, specificity 40.6%, positive predictive value 38.7% and negative predictive value of 92.9% for an abnormal chest X-ray. CONCLUSION: D-dimer levels are frequently raised during an acute painful crisis. A normal level has a high negative predictive value for an abnormal chest X-ray.

Significant bronchospasm during sickle cell painful crises is associated with a lower peripheral eosinophil count.

BACKGROUND: Bronchial hyperresponsiveness and/or bronchospasm are recognized complications of sickle cell disease. OBJECTIVE: The aim of this study was to investigate the presence of bronchospasm during painful crises, using simple spirometry in patients with sickle cell disease. METHODS: A prospective, non-randomized study was undertaken in patients with homozygous sickle cell disease, who presented with increasing pain. A painful crisis was defined as any increase in bodily pains necessitating hospital admission. A 15% increase in FEV(1) following salbutamol nebulization was considered significant. RESULTS: Thirty-nine patients took part in the study. Significant bronchodilator responses were demonstrable in 48.7% of patients during painful crises. Patients with such a response had a significantly lower peripheral blood eosinophil count (mean count 0.17 x 10(9)/L vs. 0.445 x 10(9)/L, P = 0.02, confidence interval for difference between groups, 0.0, 0.39). Furthermore, the magnitudes of the bronchodilator responses were related to the degree of lowering of peripheral blood eosinophil counts (r(s) = -0.344, P = 0.037). CONCLUSION: Significant bronchospasm is demonstrable in a sizeable proportion of patients presenting with painful sickle cell crises. There seems to be a negative correlation between the magnitude of bronchospasm and the peripheral blood eosinophil count. We postulate a possible role for pulmonary sequestration of eosinophils in the pathophysiology of bronchospasm in sickle cell disease patients.