Apigenin Provides Structural Protection to Human Fibrinogen against Nitrosative Stress: Biochemical and Molecular Insights.

BACKGROUND: Peroxynitrite (ONOO-) is an oxidant linked with several human pathologies. Apigenin, a natural flavonoid known for its health benefits, remains unexplored in relation to ONOO- effects. This study investigated the potential of apigenin to structurally protect fibrinogen, an essential blood clotting factor, from ONOO--induced damage. METHODS: Multi-approach analyses were carried out where fibrinogen was exposed to ONOO- generation while testing the efficacy of apigenin. The role of apigenin against ONOO--induced modifications in fibrinogen was investigated using UV spectroscopy, tryptophan or tyrosine fluorescence, protein hydrophobicity, carbonylation, and electrophoretic analyses. RESULTS: The findings demonstrate that apigenin significantly inhibits ONOO--induced oxidative damage in fibrinogen. ONOO- caused reduced UV absorption, which was reversed by apigenin treatment. Moreover, ONOO- diminished tryptophan and tyrosine fluorescence, which was effectively restored by apigenin treatment. Apigenin also reduced the hydrophobicity of ONOO--damaged fibrinogen. Moreover, apigenin exhibited protective effects against ONOO--induced protein carbonylation. SDS-PAGE analyses revealed that ONOO-treatment eliminated bands corresponding to fibrinogen polypeptide chains Aα and γ, while apigenin preserved these changes. CONCLUSIONS: This study highlights, for the first time, the role of apigenin in structural protection of human fibrinogen against peroxynitrite-induced nitrosative damage. Our data indicate that apigenin offers structural protection to all three polypeptide chains (Aα, Bß, and γ) of human fibrinogen. Specifically, apigenin prevents the dislocation or breakdown of the amino acids tryptophan, tyrosine, lysine, arginine, proline, and threonine and also prevents the exposure of hydrophobic sites in fibrinogen induced by ONOO-.

The energy-growth nexus in Canada: new empirical insights.

Over the past two decades, numerous developed and developing nations have witnessed a remarkable shift from manufacturing-based economies to those that center around the service sector. This development has led to a staggering growth in the consumption of energy-intensive goods, and Canada has not been immune to this trend. Despite being home to abundant energy reserves, the country's economic expansion has manifestly relied on prodigious energy consumption. Within this context of symbiotic energy-economic growth, this study investigates the empirical relationship between energy consumption and economic growth using Canadian time-series data from 1980 to 2020. In doing so, this paper offers a vital contribution to the development of theoretical frameworks within the sphere of endogenous growth. Besides, to arrive at empirical findings, a model known as the autoregressive distributed lag (ARDL) model, renowned for its ability to discern both short- and long-term coefficients, is employed. The results reveal that economic growth has a significant positive long-run effect on energy consumption and other explanatory variables. All variables other than trade openness demonstrate a positive relationship with economic growth in the short run. From Toda-Yamamoto causality test, it is evident that there exist bidirectional causal links between economic growth and energy consumption and between economic growth and financial development. Several unidirectional causalities were also observed for other variables. Based on these findings, it is recommended that Canada boosts its investment in energy infrastructure, especially in rural and backward regions, to deliver necessary energy services. An optimal trade-off between Canada's vast energy resources and economic growth can perhaps be achieved by minimizing the disparity in access to energy services across all parts of the country. Other policy implications are discussed.

Evaluation of oral health-related quality of life and its association with mental health status of patients with type 2 diabetes mellitus in the post-COVID-19 pandemic era: A study from Central Saudi Arabia.

Background and objectives: The association between oral and mental health is reciprocal, in which poor oral health may lead to several mental health issues, especially among patients with diabetes. The present study evaluated oral health-related quality of life (OHRQOL) and its association with mental health conditions among patients with type 2 diabetes mellitus (T2DM) in central Saudi Arabia. Methods: The Arabic version of the Oral Health Impact Profile-14 (OHIP-14) questionnaire and the Depression, Anxiety, and Stress Scale-21 Items (DASS-21) were used to assess the OHRQOL and mental health status of patients with diabetes. We utilized logistic regression analysis to identify the predictors of poor OHRQOL, and Spearman's correlation test to identify any correlations between OHIP-14 and overall DASS-21 scores, as well as each subscale. Results: Of the 677 patients included in the present study, 52.7% had a poor OHRQOL, which was significantly higher (positive association) among patients with a longer duration of diabetes (adjusted odds ratio [AOR] = 3.31; 95% confidence interval [CI] = 1.96-4.17) and those who did not periodically monitor their oral health (AOR = 2.85; 95% CI = 1.76-3.89). Some forms (mild, moderate, severe, or extremely severe) of depression, anxiety, and stress were observed in 59.7, 71.1, and 67.1% of the participants, respectively. Furthermore, we found that the total OHRQOL scores had a significant positive association with depression (AOR = 2.32, 95% CI = 1.34-3.71, p = 0.001), anxiety (AOR = 1.81, 95% CI = 1.22-2.79, p = 0.003), and stress (AOR = 1.43, 95% CI = 1.14-2.19, p = 0.026). Conclusion: The results of the present study suggest the importance of appropriate and targeted health education programs for T2DM patients to ensure periodic dental examinations and oral health. Additionally, we recommend counseling sessions for all T2DM patients with trained healthcare providers to improve their mental health status during follow-up visits at outpatient diabetes care centers.

Renal Amyloid-Associated (AA) Amyloidosis in a Sickle Cell Patient: A Case Report and Literature Review.

Renal amyloid-associated (AA) amyloidosis is a rare occurrence in sickle cell disease (SCD). Very little literature is available on renal AA amyloidosis in sickle cell disease. Nephrotic range proteinuria is associated with higher mortality among patients with SCD. We present a case of a young reproductive-age African American woman who presented with massive nephrotic range proteinuria. Other more common causes of AA amyloidosis such as immunologic and infectious etiologies were ruled out by history, physical examination, radiologic investigation, and serology. Renal biopsy showed mesangial expansion with Congo red-positive material. Staining for immunoglobulins was negative. Electron microscopy showed nonbranching fibrils. These findings were consistent with AA amyloidosis. This case report adds to the rare findings of renal AA amyloidosis in sickle cell disease. The patient refused any intervention to decrease her Glomerular Filtration Rate (GFR) in the hopes of potentially reversing the disabling proteinuria. We report sickle cell disease presenting with nephrotic syndrome secondary to AA amyloid.

Effects of environmental quality on agricultural productivity in sub Saharan African countries: A second generation panel based empirical assessment.

Agriculture is the backbone of most sub-Saharan Africa economies, but environmental quality, so vital for agricultural production, is being challenged by climate change. However, most studies measure environmental quality using one variable, CO2 emissions. In this study, a more enhanced measure of environmental quality, which incorporates three indicators (per capita CO2 emissions, energy intensity and adjusted national savings), is used. A set of second-generation panel data techniques that address some potentially crucial panel data estimation issues such as cross sectional dependence and cross country heterogeneity, are employed. Data on 24 sub-Saharan Africa countries over the period 1984 to 2016 were analysed. The impact on agricultural productivity of two of the three indicators of environmental quality, namely CO2 emissions and adjusted national savings, has expected signs, negative and positive, respectively. Estimates using different methods suggest a detrimental effect of per capita CO2 emissions on agricultural productivity in sub-Saharan Africa. A 1% rise in per capita CO2 emissions induces a 0.04% to 0.06% decline in agricultural productivity. Deteriorating environment quality as a result of climate change is slowly but negatively impacting sub-Saharan Africa agricultural productivity.

Renewable energy and environmental quality: A second-generation panel evidence from the Sub Saharan Africa (SSA) countries.

This study employs dynamic panel data for 34 Sub Saharan Africa (SSA) countries for the period 1984-2016 to estimate the effects of renewable energy on environmental quality measured by three indicators, namely, per capita CO2 emissions, energy intensity (EI) and Aggregate National Savings (ANS). The study leveraged a battery of second-generation econometric tests and estimation and causality methods to obtain the coefficients between the regressed and the regressors. Results reveal that use of renewable energy reduces CO2 emissions and energy intensity while it enhances ANS. Economic growth still seems to be expensive for the region as it stimulates CO2 emissions. However, it has a positive effect on ANS. As expected, fossil fuels exacerbate CO2 emissions and energy intensity. FDI is found to be detrimental for the environment of SSA region with its positive significant coefficient on CO2 emissions. Financial development is reported to reduce CO2 emissions. Some causal links between variables are also noted.

Urbanization-globalization-CO2 emissions nexus revisited: empirical evidence from South Africa.

The environmental effects of urbanization and globalization are still subject to debate among scholars. South Africa is the most globalized, most urbanized and the most carbon-intensive economy in Sub Saharan Africa (SSA) region. Taking this into cognizance, this study examines the effects of urbanization and globalization on CO2 emissions for South Africa using time series annual data for the period 1980-2017. Zivot and Andrews single and Bai and Perron multiple structural break unit root tests are employed to assess if all the series are stationary. This procedure follows ARDL cointegration test to check the presence of a long-run association among variables. Having been confirmed about such a cointegrating relation, ARDL short-run and long run coefficients indicate that urbanization induces CO2 emissions while only long-run significant emissions effect of globalization was noted. Toda-Yamamoto non-causality test reports a bi-directional causal link between urbanization and CO2 emissions. No causal link is observed between globalization and CO2 emissions. Variance decomposition results do not rule out these effects in future. Policy implications are discussed.

Effects of energy consumption and economic growth on environmental quality: evidence from Qatar.

This study examines the empirical effects of four variables: economic growth, energy consumption, foreign direct investment, and financial development on environmental quality in Qatar. Three environmental quality indicators, namely, per capita CO2 emissions, energy intensity (EI), and Adjusted National Savings (ANS) are used to examine the interactions between the variables using a time series dataset for the period 1980-2016. Following an appropriate multiple structural breaks unit root and cointegration tests, short- and long-run coefficients were estimated through the application of Autoregressive Distributive Lag (ARDL) model. The Toda-Yamamoto (TY) causality test was conducted to determine the causal link, if any, among the variables. Estimated results suggest a detrimental long-run effect of energy consumption on all three indicators of environmental quality. FDI has a negative long-run effect on environmental quality when it is measured by EI only. Financial development has no significant effect on any of the indicators. Bidirectional causality are noted between three variables: economic growth, energy consumption, and financial development and all three indicators of environmental quality. Policy implications are discussed.

The effects of urbanization and globalization on CO2 emissions: evidence from the Sub-Saharan Africa (SSA) countries.

Ecological modernization theories suggest that it is hard to determine a priori the environmental effects of urbanization, while neoliberal doctrine advocates a positive role of globalization in developing economies especially in terms of reducing poverty and inequality. Yet, the environmental effect of globalization is not unanimous. This study employs second-generation panel regression techniques that account for heterogeneous slope coefficients and cross-sectional dependence to estimate the impacts that urbanization and globalization have on CO2 emissions for a panel of 44 Sub-Saharan Africa (SSA) countries for the period 1984-2016. Also, a causality test that considers both these issues is performed. The estimated coefficient of urbanization is positive, statistically significant, and highly consistent across different estimation techniques. The magnitude of the coefficient and level of significance are different in different econometric estimations. In most specifications, the estimated coefficient on the globalization variable is statistically insignificant. Urbanization is found to cause emissions. The environmental implications of these results are discussed with a set of policy recommendations for an environmentally better SSA region.

Developmental lead (Pb)-induced deficits in hippocampal protein translation at the synapses are ameliorated by ascorbate supplementation.

BACKGROUND: Lead (Pb) is a persistent environmental neurotoxin and its exposure even in minute quantities has been known to induce neuronal defects. The immature brain is singularly sensitive to Pb neurotoxicity, and its exposure during development has permanent detrimental effects on the brain developmental trajectory and neuronal signaling and plasticity, culminating into compromises in the cognitive and behavioral attributes which persists even later in adulthood. Several molecular pathways have been implicated in the Pb-mediated disruption of neuronal signaling, including elevated oxidative stress, alterations in neurotransmitter biology, and mitochondrial dysfunction. Nevertheless, the neuronal targets and biochemical pathways underlying these Pb-mediated alterations in synaptic development and function have not been completely deduced. In this respect, recent studies have shown that synaptic signaling and its maintenance and plasticity are critically dependent on localized de novo protein translation at the synaptic terminals. MATERIALS AND METHODS: The present study hence aimed to assess the alterations in the synapse-specific translation induced by developmental Pb exposure. To this end, in vitro protein translation rate was analyzed in the hippocampal synaptoneurosomal fractions of rat pups pre- and postnatally exposed to Pb using a puromycin incorporation assay. Moreover, we evaluated the therapeutic effects of ascorbic acid supplementation against Pb-induced deficits in synapse-localized protein translation. RESULTS: We observed a significant loss in the rates of de novo protein translation in synaptoneurosomes of Pb-exposed pups compared to age-matched control pups. Interestingly, ascorbate supplementation lead to an appreciable recovery in Pb-induced translational deficits. Moreover, the deficit in activity-dependent synaptic protein translation was found to correlate significantly with the increase in the blood Pb levels. CONCLUSION: Dysregulation of synapse-localized de novo protein translation is a potentially critical determinant of Pb-induced synaptic dysfunction and the consequent deficits in behavioral, social, and psychological attributes of the organisms. In addition, our study establishes ascorbate supplementation as a key ameliorative agent against Pb-induced neurotoxicity.

Simple, reliable, and time-efficient colorimetric method for the assessment of mitochondrial function and toxicity.

Mitochondria are organelles involved in the production of cellular energy, regulation of Ca2+ and redox signaling, and are critical for normal functioning of eukaryotic cells. The dysfunction of mitochondria has been implicated in a wide range of diseases, including metabolic and neurodegenerative disorders and different types of cancers. To better understand the role of mitochondria in healthy and disease states, the development of efficient and reliable tools for the assessment of mitochondrial function is particularly important. Janus green B (JG-B) is a supravital lipophilic cationic dye which, in its oxidized form, has a green-blue color. As JG-B is taken up and reduced by metabolically active mitochondria, the dye has been used for assessing the purity, integrity and metabolic activity of mitochondria with microscopy-based methods. Here we present a simple, time- and cost-efficient JG-B-based colorimetric assay for assessing mitochondrial function, activity and toxicity. The method is based upon reduction of JG-B by mitochondrial dehydrogenases to diethylsafranine, which is pink colored and has a maximum absorption at 550 nm. In this proof of principle study, using in vitro mitochondrial preparations isolated from rat brain, we provide evidence that monitoring JG-B conversion to diethylsafranine can be used as a reliable and robust indicator of mitochondrial activity and toxicity. Because of its simplicity and efficiency in terms of costs and time, this assay has a wide potential in analytical as well as therapeutic areas of biomedical research.

Dysfunction of cortical synapse-specific mitochondria in developing rats exposed to lead and its amelioration by ascorbate supplementation.

BACKGROUND: Lead (Pb) is a widespread environmental neurotoxin and its exposure even in minute quantities can lead to compromised neuronal functions. A developing brain is particularly vulnerable to Pb mediated toxicity and early-life exposure leads to permanent alterations in brain development and neuronal signaling and plasticity, culminating into cognitive and behavioral dysfunctions and elevated risk of neuropsychiatric disorders later in life. Nevertheless, the underlying biochemical mechanisms have not been completely discerned. METHODS: Because of their ability to fulfill high energy needs and to act as calcium buffers in events of high intensity neuronal activity as well as their adaptive regulatory capability to match the requirements of the dynamicity of synaptic signaling, synapse-specific or synaptic mitochondria (SM) are critical for synaptic development, function and plasticity. Our aim for the present study hence was to characterize the effects of early-life Pb exposure on the functions of SM of prepubertal rats. For this purpose, employing a chronic model of Pb neurotoxicity, we exposed rat pups perinatally and postnatally to Pb and used a plethora of colorimetric and fluorometric assays for assessing redox and bioenergetic properties of SM. In addition, taking advantage of its ability as an antioxidant and as a metal chelator, we employed ascorbic acid (vitamin C) supplementation as an ameliorative therapeutic strategy against Pb-induced neurotoxicity and dysfunction of SM. RESULTS: Our results suggest that early-life exposure to Pb leads to elevated oxidative stress in cortical SM with consequent compromises in its energy metabolism activity. Ascorbate supplementation resulted in significant recovery of Pb-induced oxidative stress and functional compromise of SM. CONCLUSION: Alterations in redox status and bioenergetic properties of SM could potentially contribute to the synaptic dysfunction observed in events of Pb neurotoxicity. Additionally, our study provides evidence for suitability of ascorbate as a significant ameliorative agent in tacking Pb neurotoxicity.

Neonatal maternal deprivation impairs localized de novo activity-induced protein translation at the synapse in the rat hippocampus.

Neonatal neuropsychiatric stress induces alterations in neurodevelopment that can lead to irreversible damage to neuronal physiology, and social, behavioral, and cognitive skills. In addition, this culminates to an elevated vulnerability to stress and anxiety later in life. Developmental deficits in hippocampal synaptic function and plasticity are among the primary contributors of detrimental alterations in brain function induced by early-life stress. However, the underlying molecular mechanisms are not completely understood. Localized protein translation, occurring at the synapse and triggered by neuronal activity, is critical for synapse function, maintenance, and plasticity. We used a rodent model of chronic maternal deprivation to characterize the effects of early-life neuropsychiatric stress on localized de novo protein translation at synaptic connections between neurons. Synaptoneurosomal preparations isolated biochemically from the hippocampi of rat pups that were subjected to maternal deprivation were deficient in depolarization-induced activity-dependent protein translation when compared with littermate controls. Conversely, basal unstimulated protein translation was not affected. Moreover, deficits in activity-driven synaptic protein translation were significantly correlated with a reduction in phosphorylated cell survival protein kinase protein B or Akt (p473 Ser and p308 Thr), but not phosphorylated extracellular signal-regulated kinase.

Pulmonary embolism as a complication of an electrophysiological study: a case report.

BACKGROUND: Electrophysiological studies have become an established practice in the evaluation and treatment of arrhythmias. Symptomatic pulmonary embolism as a result of deep vein thrombosis arising from multiple venous sheath femoral vein catheterization is an uncommon complication associated with it. We report the case of a 33-year-old woman who developed pulmonary embolism after an electrophysiological study, which was successfully treated at a cardiac hospital in Bangladesh. CASE PRESENTATION: A 33-year-old Bangladeshi woman with hypertension and diabetes had initially presented with recurrent episodes of paroxysmal atrial fibrillation that manifested as palpitations for 2 years. Her atrial fibrillation was drug-refractory and could not be attributed to a treatable etiology. She had undergone an electrophysiological study at a different hospital, where right femoral venous catheterization was performed followed by the insertion of three venous sheaths. However, tachyarrhythmia could not be induced and a procedure to isolate the pulmonary vein was postponed because all the veins could not be isolated. Forty-eight hours later, she presented to our hospital with shortness of breath, chest heaviness, palpitations, and recurrent episodes of syncope. She had normal coronary arteries and no other risk factors for venous thromboembolism. She was hemodynamically stable on examination. There was echocardiographic evidence of pulmonary hypertension and right ventricular dilatation and dysfunction. A computed tomography pulmonary angiogram confirmed pulmonary embolus in the descending branch of her left pulmonary artery, extending up to the segmental arteries. Subsequently, a duplex ultrasound confirmed acute deep vein thrombosis affecting her right ilio-femoral segment. She was successfully managed with subcutaneous enoxaparin and oral warfarin (target international normalized ratio 2.5-3). CONCLUSIONS: Pulmonary embolism is a rare but serious complication that may occur in patients who undergo electrophysiological studies. Multiple venous sheaths inserted into the femoral vein and catheter-induced endothelial injury, further compounded by prolonged procedural time, may be responsible for the increased thrombogenicity leading to deep vein thrombosis and subsequent pulmonary embolism. An adequate observation time after the procedure and clinical alertness are necessary for rapid diagnosis and treatment.

The pacemaker-twiddler's syndrome: an infrequent cause of pacemaker failure.

BACKGROUND: The pacemaker-twiddler's syndrome is an uncommon cause of pacemaker malfunction. It occurs due to unintentional or deliberate manipulation of the pacemaker pulse generator within its skin pocket by the patient. This causes coiling of the lead and its dislodgement, resulting in failure of ventricular pacing. More commonly reported among elderly females with impaired cognition, the phenomenon usually occurs in the first year following pacemaker implantation. Treatment involves repositioning of the dislodged leads and suture fixation of the lead and pulse generator within its pocket. CASE PRESENTATION: An 87 year old Bangladeshi lady who underwent a single chamber ventricular pacemaker (VVI mode: i.e. ventricle paced, ventricle sensed, inhibitory mode) implantation with the indication of complete heart block, and presented to us again 7 weeks later, with syncopal attacks. She admitted to repeatedly manipulating the pacemaker generator in her left pectoral region. Physical examination revealed a heart rate of 42 beats/minute, blood pressure 140/80 mmHg and bilateral crackles on lung auscultation. She had no cognitive deficit. An immediate electrocardiogram showed complete heart block with pacemaker spikes and failure to capture. Chest X-ray showed coiled and retracted right ventricular lead and rotated pulse generator. An emergent temporary pace maker was set at a rate of 60 beats per minute. Subsequently, she underwent successful lead repositioning with strong counselling to avoid further twiddling. CONCLUSION: Twiddler's syndrome should be considered as a cause of pacemaker failure in elderly patients presenting with bradyarrythmias following pacemaker implantation. Chest X-ray and electrocardiograms are simple and easily-available first line investigations for its diagnosis. Lead repositioning is required, however proper patient education and counselling against further manipulation is paramount to long-term management.

Is rapid growth in Internet usage environmentally sustainable for Australia? An empirical investigation.

This study estimates the short- and long-run effects of Internet usage and economic growth on carbon dioxide (CO2) emissions using annual time series macro data for Australia for the period 1985-2012. Autoregressive distributive lag (ARDL) bounds and Gregory-Hansen structural break cointegration tests are applied. ARDL estimates indicate no significant long-run relationship between Internet usage and CO2 emissions, which implies that the rapid growth in Internet usage is still not an environmental threat for Australia. The study further indicates that higher level of economic growth is associated with lower level of CO2 emissions; however, Internet usage and economic growth have no significant short-run relationship with CO2 emissions. Financial development has both short-run and long-run significant positive association with CO2 emissions. The findings offer support in favor of energy efficiency gains and a reduction in energy intensity in Australia. However, impulse response and variance decomposition analysis suggest that Internet usage, economic growth and financial development will continue to impact CO2 emissions in the future, and as such, this study recommends that in addition to the existing measures to combat CO2 emissions, Australia needs to exploit the potential of the Internet not only to reduce its own carbon footprint but also to utilize information and communication technology (ICT)-enabled emissions abatement potential to reduce emissions in various other sectors across the economy, such as, power, renewable energy especially in solar and wind energy, agriculture, transport and service.

Prevalence of ultrasonography proved polycystic ovaries in North Indian women with type 2 diabetes mellitus.

BACKGROUND: Polycystic ovaries (PCO) and their clinical expression (the polycystic ovary syndrome [PCOS]) as well as type 2 diabetes mellitus (T2DM) are common medical conditions linked through insulin resistance. We studied the prevalence of PCO and PCOS in women with diet and/or oral hypoglycemic treated T2DM and non-diabetic control women. DESIGN: Prospective study. METHODS: One hundred and five reproductive age group women with diet and /or oral hypoglycemic treated T2DM were the subjects of the study. Sixty age-matched non-diabetic women served as controls. Transabdominal ultrasonographic assessment of the ovaries was used to diagnose PCO. Clinical, biochemical and hormonal parameters were also noted. RESULTS: Ultrasonographic prevalence of PCO was higher in women with diabetes than in non-diabetic subjects (61.0% vs. 36.7%, P < 0.003) whereas that of PCOS was 37.1% in diabetic subjects and 25% in non-diabetic controls (P > 0.1). Diabetic women with PCO had diabetes of significantly longer duration than those without PCO (4.19+/-2.0 versus 2.9+/-1.6 yrs; p < 0.05). Among both diabetic and non-diabetic women, those with PCO had significantly higher plasma LH, LH/FSH ratio, total testosterone and androstenedione levels. CONCLUSION: This study demonstrates a higher prevalence of PCO in women with T2DM as compared to non-diabetic subjects.

Polymorphonuclear leukocyte mediated oxidative inactivation of alpha-1-proteinase inhibitor: Modulation by nitric oxide.

Alpha-1-proteinase inhibitor activity was studied in presence of resting and activated polymorphonuclear leucocytes. Four different agonists; phorbol myristic acetate, N-formyl-methionyl-leucyl-phenylalanine, opsonised zymosan and arachidonic acid decreased the inhibitor activity by 23.3%, 20%, 12% and 16.6^ respectively. The inhibitor activity was protected by using various free radical scavengers. Catalase and superoxide dismutase both restored activity by about 18%, mannitol by 13% and sodium azide by 17.3%. The inhibitor activity was also protected significantly by pretreatment of polymorphs with L-Arg, a precursor of nitric oxide, before activation. L-Arg was also observed to suppress the generation of superoxide and hydroxyl radical appreciably. The nitric oxide synthase inhibitor, aminoguanidine drastically inhibited the nitrite release and reversed the protection offered by L-Arg to the inhibitor activity. Our results indicate a multifactorial nature of the inactivation process, the culprit species being superoxide, hydrogen peroxide, hydroxyl radical and hypohalides. Nitric oxide seems to scavenge the superoxide radical directly after its formation rather than inhibiting its generation by NADPH oxidase as was believed earlier.

Clinical and endocrine aspects of pituitary tumors.

OBJECTIVE: To study the clinical spectrum and endocrine profile of pituitary tumors presenting to a tertiary care endocrine center. METHODS: Retrospective analysis of clinical and hormonal data of patients with pituitary tumors admitted in the Endocrinology Department of Sher-i-Kashmir Institute of Medical Sciences, Srinagar, Kashmir India between January 1989 and December 1998. RESULTS: Over a period of one decade, 75 subjects were diagnosed to have pituitary tumors. Somatotroph adenoma was the most common pituitary mass lesion seen (44/75) and followed in the decreasing order of frequency, by non-functioning pituitary tumor (12/75), prolactinoma (11/75) and corticotroph adenoma (8/75). Overall there was a male preponderance (male to female ratio was 41:34). Subjects with somatotroph adenoma presented with classical features of acromegaly: mean fasting and post glucose suppression growth hormone levels were 34.04+/-11.67 and 36.47+/-6.64 ng/ml. Eleven subjects (9 females and 2 males) had prolactinoma; females presented with the classical symptom complex of amenorrhea-galactorrhea while males presented with headache, visual disturbances and impotence. The 12 subjects with nonfunctioning pituitary tumors presented with features of mass lesion. Of the 8 subjects (6 females and 2 males) with corticotroph adenomas, 2 were confirmed to have periodic hormonogenesis. CONCLUSION: In an endocrine center, functioning pituitary tumors are more often seen than non-functioning tumors.

Epidemiologic and etiologic aspects of hirsutism in Kashmiri women in the Indian subcontinent.

OBJECTIVE: To assess the prevalence of hirsutism and study its etiology in the Kashmir Valley of the Indian subcontinent. DESIGN: Prospective random sample of the general population attending outpatient medical clinics and prospective evaluation of hirsute patients referred to our endocrinology clinic. SETTING: A tertiary care hospital and district-level primary care hospitals. PATIENT(S): Five thousand women attending various hospitals for reasons unrelated to hirsutism and 150 consecutive women referred for hirsutism. INTERVENTION(S): Assessment of body hair as per the Ferriman and Gallwey scoring system and an investigative protocol including detailed clinical assessment with endocrinologic workup including estimations of gonadotropins, PRL, T, and 17-hydroxyprogesterone and abdominopelvic ultrasound. MAIN OUTCOME MEASURE(S): Presence and cause of hirsutism. RESULT(S): Of 4,780 adult women for whom adequate data were available, 504 (10.5%) had hirsutism, among whom 484 (10.1%) had mild (score of 6-9) and 20 (0.4%) had moderate hirsutism (score of 10-14). The etiology of hirsutism revealed idiopathic hirsutism in 38.7%, polycystic ovary syndrome (PCOS) in 37.3%, postmenopausal state in 9.2%, adrenal tumors in 2.1%, congenital adrenal hyperplasia in 1.4%, and drug-induced hirsutism in 0.7%. The cause remained undetermined in 10.6% of patients for whom the available information was not adequate. CONCLUSION(S): Hirsutism is as common a problem in the Kashmir Valley (India) as elsewhere in the world. Idiopathic hirsutism (38.7%), PCOS (37.3%), and postmenopausal state (9.2%) are common causes of hirsutism. Late-onset congenital adrenal hyperplasia is a relatively uncommon cause of hirsutism in the Kashmir Valley.