Dietary Effects of Nanopowder Eggshells on Mineral Contents, Bone Turnover Biomarkers, and Regulators of Bone Resorption in Healthy Rats and Ovariectomy-Induced Osteoporosis Rat Model.

Postmenopausal osteoporosis is a critical issue for female health worldwide. This current study was designed to evaluate the role of nanopowder eggshell (NPES) in healthy and ovariectomy-induced osteoporosis rats. Fifty-six female rats were divided into healthy rats (35) and ovariectomized rats (21). The healthy rats were subdivided into five groups (G1-G5) and received one of the following treatments: saline, 20 or 40 mg/kg of calcium carbonate, and 20 or 40 mg/kg of NPES. The 21 ovariectomized rats were divided into three groups (G6-G8) and received either saline, 40 mg/kg of calcium carbonate, or 40 mg/kg of NPES. Biochemical and histopathological assessments of bone formation and resorption were performed. Biomarkers of bone formation (calcium and osteocalcin (OCN)) and calcium content in left femur ashes were significantly higher in healthy rats given 40-mg/kg NPES than in healthy control rats and healthy rats given 40-mg/kg calcium carbonate. The ovariectomized groups had significantly lower levels of vitamin D3, OCN, and osteoprotegerin (OPG) than the healthy control. Alanine transaminase (ALT), alkaline phosphatase (ALP), and receptor activator of nuclear factor-κB ligand (RANKL) were significantly increased in the ovariectomized group than in the healthy control group. Treatment with NPES and calcium carbonate reduced liver enzymes in ovariectomized rats. NPES treatment significantly increased Vit D3, OCN, OPG, and bone ash mineral content (calcium, magnesium, zinc, and phosphorus) in ovariectomized rats. NPES also increased femur cortical thickness, osteoblast number, and collagen fiber. The current study suggests that NPES can modulate bone turnover biomarkers and increase bone trace elements. Moreover, NPES alleviates bone resorption in ovariectomy-induced osteoporosis.

Evaluation of tripartite motif 59 and its diagnostic utility in benign bowel diseases and colorectal cancer.

Colorectal cancer (CRC) is the second leading cause of cancer-related mortality in developing countries. Tripartite motif-59 (TRIM59) a member of the TRIM ubiquitin ligase family, is a surface molecule that regulates biological processes such as cell proliferation, apoptosis, and tumorigenesis. Previous studies reported that TRIM59 expression was upregulated in human CRC, however, the expression pattern and role of TRIM59 in benign colorectal lesions remain unclear. Sixty patients diagnosed with CRC and 60 patients with benign lesions (Crohn's disease, ulcerative colitis, adenoma, and familial adenomatous polyposis) were recruited to the present study. TRIM59 gene expression was assessed by real-time quantitative polymerase chain reaction. Expression of TRIM59 protein and p-AKT were determined using, enzyme-linked immunoassay while p53 expression was detected by immunohistochemistry. Antioxidant/oxidant role of glutathione (GSH)/malondialdehyde (MDA) were evaluated by colorimetric methods in all of the studied groups. Our results showed upregulated expressions of TRIM59 gene and protein levels in CRC tissues and benign colonic lesions compared to nontumor tissues. Their levels were higher in inflammatory compared to noninflammatory bowel lesions. There were significant interrelations among TRIM59 gene expression, protein levels, tumor, node, metastasis staging, and the presence of metastasis (p < 0.0001). Receiver-operator characteristic curve analyses showed that at the cutoff point of 2.5 TRIM59 mRNA expression can discriminate between CRC cases and benign bowel group (area under the curve [AUC]: 0.639, sensitivity: 86.7%, specificity: 41.7%), and between CRC and controls (AUC: 0.962, sensitivity: 90%, specificity: 91.7%). TRIM59 could be a potential biomarker in the early detection, diagnosis, and treatment of benign colonic lesions and CRC.

Missense, silent, non-sense and frame-shift mutations in exon 3 of the filaggrin gene in patients with bronchial asthma, atopic dermatitis, allergic rhinitis and mixed atopy.

This study investigated the atopic march on the basis of genetics. This research detected 227 variants in the filaggrin gene (FLG gene). Missense, silent, non-sense, frame-shift and non-coding mutations were detected in exon 3 of the FLG gene in patients with bronchial asthma, atopic dermatitis, allergic rhinitis and mixed atopy. Missense mutation was detected at c.8343 G > C (p. Asp2781Glu) in all adult asthmatic and allergic rhinitis patients. Whereas, mutation at c.8360 C > T/A (p. Arg2787 His/Leu) was detected in all childhood asthmatic and mixed atopic patients. A non-coding mutation was detected at c.12365 in atopic dermatitis and bronchial asthma patients. Furthermore, DNA sequencing of asthmatic and mixed atopic patients showed missense mutations at c.6073 C > T (p. Gly2025Glu) and a silent mutation at c. 8341 G > A (p. Asp2781Asp).

Secondhand smoke as a risk factor for attention deficit hyperactivity disorder in children.

Background: Attention deficit hyperactivity disorder (ADHD) is recognized as a common childhood psychiatric disorder with a worldwide prevalence estimated at 5%. In Egypt, early exposure of children to smoke occurred due to many causes mainly tobacco use. This exposure is linked to a variety of developmental and behavioral consequences for children. This study aimed to investigate the potential association between secondhand smoke (SHS) exposure and ADHD in children and find the association between the level of exposure to SHS and the degree of ADHD symptoms.Method: Case-control study was done by a random selection of children from the outpatient Clinic of Assiut University Hospital of Children. Data were collected by a questionnaire to evaluate home exposure to SHS and blood sampling for serum cotinine measurement as an indicator of exposure to SHS.Results: Of 70 ADHD children, 62 (88.6%) of them reported home exposure to smoke while only 14 of 30 control children (46.7%) reported home exposure to smoke. The serum cotinine level was insignificantly higher in the ADHD group than the control group.Conclusion: In conclusion, there is a significant association between ADHD in the examined sample of children and exposure to SHS. Serum cotinine is a biomarker reflecting current exposure to SHS but it is not a reliable indicator of past and long-term exposure to SHS.

Therapeutic Role of Transcranial Direct Current Stimulation in Alzheimer Disease Patients: Double-Blind, Placebo-Controlled Clinical Trial.

OBJECTIVE: To explore the neuropsychological effects and levels of tau protein (TAU), amyloid ß 1-42 (Aß 1-42), and lipid peroxidase after 10 sessions of anodal transcranial direct current stimulation (tDCS) in patients with mild to moderate Alzheimer disease (AD). PATIENTS AND METHODS: A total of 46 consecutive patients with probable AD participated in this study. They were classified randomly into 2 equal groups: active versus sham. Each patient received 10 sessions of anodal tDCS over the left and right temporoparietal region for 20 minutes for each side with the cathode on the left arm. Patients were assessed using the Modified Mini Mental State Examination (MMMSE), clock drawing test, Montreal Cognitive Scale (MoCA), and the Cornell Scale for depression. Serum TAU, Aß 1-42, and lipid peroxidase were measured before and after the 10th session. RESULTS: There was a significant improvement in the total score of each cognitive rating scale (MMMSE, clock drawing test, and MoCA) in the real group, whereas no such change was observed in the sham group. The Cornell depression score improved significantly in both groups. There was a significant increase in serum Aß 1-42 ( P = .02) in the real but not in the sham group, with a significant Treatment condition × Time interaction ( P = .009). There was no significant effect on tau or lipid peroxidase in either group but a significant positive correlation between changes of Aß1-42 and MMMSE ( P = .005) and MoCA ( P = .02). CONCLUSION: The observed cognitive improvements were complemented by parallel changes in serum levels of Aß 1-42.

Interrelations of Apoptotic and Cellular Senescence Genes Methylation in Inflammatory Bowel Disease Subtypes and Colorectal Carcinoma in Egyptians Patients.

Ras-related domain family member 1 transcript variant A (RASSF1A) controls apoptosis and cell proliferation while p14/ARF gene has a regulatory role in cellular senescence. Failure of apoptosis and cellular senescence occurs during inflammatory bowel disease (IBD) and colorectal cancer (CRC). To reveal the role of peripheral leukocyte promoter methylation of RASSF1A and p14/ARF in the pathogenesis of IBD subtypes and CRC we investigated the methylation state of the two genes by methylation-specific polymerase chain reaction (MSP-PCR) in 60 CRC patients, 60 patients with IBD; 27 with ulcerative colitis and 33 had Crohn's disease and also in 30 healthy subjects. Methylated RASSF1A and p14/ARF genes were detected in 55% and 60% of CRC, while the frequency of the methylated RASSF1A and p14/ARF genes was 23.3% and 43.3% in IBD patients and 3.3% and 13.3% in the control group (P = 0.000 each). Also, the frequency of methylated RASSF1A gene was significantly higher in ulcerative colitis than in Crohn's disease, while a non-significant frequency of methylated p14/ARF was detected between ulcerative colitis and Crohn's disease. Furthermore, methylated RASSF1A and p14/ARF were associated with the grade of CRC but not associated with the age of patients, family history, or tumor location. Results suggest that methylated RASSF1A and p14/ARF are related to CRC and IBD pathogenesis and may be used as molecular biomarkers for early detection of CRC and IBD.

Filaggrin, major basic protein and leukotriene B4: Biomarkers for adult patients of bronchial asthma, atopic dermatitis and allergic rhinitis.

Bronchial asthma (BA), atopic dermatitis (AD), and allergic rhinitis (AR) are well known atopic disorders with complex etiologies. This study was undertaken to investigate the role of filaggrin, eosinophil major basic protein (MBP) and leukotriene B4 (LTB4) in patients with BA, AD, and AR. Sera from 1,246 patients with different atopic disorders and 410 normal healthy controls were collected and were evaluated for filaggrin, MBP and LTB4 by specific sandwich ELISAs, whereas immunoglobulin E (IgE) was used as a positive control for atopic patients. Serum analysis showed that filaggrin levels were remarkably high in patients with AD and in patients with multiple (mixed) atopic disorders (p < 0.001), whereas its levels in BA and AR patients were low but much higher than in normal human sera (p < 0.01). MBP levels were also high in AR, BA and mixed atopic patients, whereas AD patients showed no increase of MBP (p > 0.05). In contrast, LTB4 level was found to be significantly low in all tested atopic patients groups as compared to the levels of LTB4 present in normal human sera (p < 0.001). In conclusion, these findings support an association between filaggrin, MBP or LTB4 and atopic disorders. Our data strongly suggest that filaggrin, MBP or LTB4 might be useful in elucidating the mechanisms involved in the pathogenesis of these atopic disorders.

Markers of atopic dermatitis, allergic rhinitis and bronchial asthma in pediatric patients: correlation with filaggrin, eosinophil major basic protein and immunoglobulin E.

BACKGROUND: Allergic reactions have been implicated as contributions in a number of atopic disorders, including atopic dermatitis (AD), allergic rhinitis (AR) and bronchial asthma (BA). However, the potential for filaggrin protein, eosinophil major basic protein (MBP) and immunoglobulin E (IgE) to elicit allergic response or to contribute to atopic disorders remains largely unexplored in pediatric patients. This study was undertaken to investigate the status and contribution of filaggrin protein, eosinophil MBP and total IgE in pediatric patients with AD, AR and BA. METHODS: Sera from 395 pediatric patients of AD, AR or BA with varying levels of disease activity according to the disease activity index and 410 age-matched non-atopic healthy controls were evaluated for serum levels of atopic markers, including filaggrin, eosinophil MBP and IgE. RESULTS: Serum analysis showed that filaggrin levels were remarkably high in pediatric patients with AD, followed by BA and AR, whereas its levels were low in non-atopic pediatric controls. Eosinophil MBP levels in sera of atopic patients were significantly high as compared with their respective controls, but its levels were highest in AR patients, followed by AD and BA. Total IgE in sera of AD patients was markedly high, followed by AR and BA patients, whereas its levels were low in non-atopic pediatric controls. Interestingly, not only was an increased number of subjects positive for filaggrin protein, eosinophil MBP or total IgE, but also their levels were statistically significantly higher among those atopic patients whose disease activity scores were higher as compared with atopic patients with lower disease activity scores. CONCLUSIONS: These findings strongly support a role of filaggrin protein, eosinophil MBP and IgE in the onset of allergic reactions in pediatric patients with AD, AR and BA. The data suggest that filaggrin, eosinophil MBP or IgE might be useful in evaluating the progression of AD, AR or BA and in elucidating the mechanisms involved in the pathogenesis of these pediatric disorders.

Urinary tumor markers could predict survival in bladder carcinoma.

The early diagnosis of bladder cancer is important for effective treatment of the disease. This study aimed to evaluate the nuclear matrix protein 22 (NMP 22), soluble epithelial cadherin (E-cadherin), cathepthin-D and total protein with clinico-pathological features of bladder cancer, and to determine the relation between each marker and tumor progression after treatment. The study includes 65 patients with bladder cancer, 14 benign urinary diseases and 11 healthy volunteers. Patients were categorized according to bilharzial infestation, T stage, tumor grade, size and the presence of lymph node metastasis. Forty patients were followed for disease progression after surgery. There was a significant increase of NMP22, E-cadherin, cathepthin-D and total protein detected in cancer group compared to healthy and benign groups. It was found that NMP 22 and E-cadherin had highest sensitivity (84.4, 76.9 %, respectively) while, total ddedprotein showed highest specificity (77.4 %). Tumor size correlated with urinary NMP22 (r = 0.3, p = 0.02), although, E-cadherin, cathepsin-D and total protein correlated with tumor size (r = 0.3, 0.28, 0.2; p = 0.01, p = 0.01, 0.04, respectively) and lymph node metastasis (r = 0.32, 0.34, 0.2; p = 0.003, 0.005, 0.04, respectively). Elevated pretreatment urinary NMP22, E-cadherin and total protein levels was associated significantly with bladder cancer recurrence (p = 0.02, 0.001, 0.005, respectively). In conclusion, determination of urinary NMP22, E-cadherin and total protein in bladder cancer patients or persons at risk of developing bladder cancer will help in early detection of the disease and prediction of recurrence. The use of a combination of tumor markers is markedly useful than the assessment of single one.

Clinical and biochemical effects of environmental tobacco smoking on pregnancy outcome.

The effects of environmental tobacco smoke (ETS) are less studied especially on neonates. This study evaluates the clinical and biochemical effects in neonates exposed to ETS during pregnancy. Two hundred pregnant women asked to complete the questioners about their ETS. Ninety from them were enrolled in biochemical assays as two groups according to ETS. The cotinine level determined in saliva and serum of mothers to confirm their tobacco exposure. The routine tracheal suction from the fetus was used to determine the level of neuron specific enolase (NSE), soluble E-cadherin, sApo-1/Fas, nitric oxide (NO) and cotinine. In clinical assessment, the percent of full term babies in non-exposed group (72 %) are higher compared to exposed group (67 %). Apgar score at the first min, admission to intensive care unit (ICU) and morbidity during the first month shows statistical significance increase in exposed compared to non-exposed group (p = 0.03, 0.05, 0.01, respectively). The new born weight in exposed group significantly decreased compared to non-exposed group (2,850 g ± 3.74 vs 2,967.67 g ± 3.34; p = 0.02). In biochemical assessment, NSE and sE-cadherin significantly increased, while NO significantly decreased (p = 0.000) in exposed compared to non-exposed group. There is a positive correlation between level of cotinine and both NSE, sE-cadherin (r = 0.7, 0.9; p = 0.000, 0.006, respectively). To our knowledge, this is the first study link between prenatal tobacco exposure (PTE) and biochemical parameters measured in tracheal suction. PTE will lead to decrease in birth weight most probably by decreasing NO, sFas, and increasing sE-cadherin. While, increased morbidity of neonates in the exposed group could be attributed to cessation of breast feeding and its complication and increased NSE in the studied markers.

Psoriasin: a novel marker linked obesity with psoriasis.

To evaluate the role of psoriasin, koebnerisin, interleukn (IL)-12 and IL-23 in the pathogenesis of psoriasis and their relations to Psoriasis Area Severity Index (PASI) and obesity. Thirty patients had chronic plaque psoriasis and 30 healthy subjects matched in age and sex were enrolled in this study. Serum from all subjects were used for determination of psoriasin, koebnerisin, IL-12 and IL-23 by ELISA kits. IL-23 and psoriasin were significantly higher in skin psoriasis compared to controls and psoriatic arthritis (PsA). There was a correlation between psoriasin and both PASI and obesity. On the other hand, IL-12 was significantly increased in PsA compared to skin psoriasis (p=0.000) and controls. Its sensitivity and specificity were 87%, 93%; respectively. To our knowledge, psoriasin is the first biomarker confirm the link between obesity and psoriasis. The risk of developing psoriasis is directly related to higher BMI.

Matricaria chamomilla attenuates cisplatin nephrotoxicity.

Matricaria chamomilla is extensively consumed as a tea or tonic. Despite its widespread use as a home remedy, relatively few trials evaluated its benefits in nephro protection. Hence, this study evaluates the protective role of M. chamomilla in cisplatin nephrotoxicity rat model. The study was conducted on 32 rats divided into four groups. The first group (G1) was injected with saline intra-peritoneally (IP); G2 was injected with 5 mg/kg cisplatin on day 0 of the experiment and repeated four times, with five days free interval. G3 and G4 were injected daily with M. chamomilla (50 mg/kg) IP, starting five days before the experiment (-5 day); in addition, G4 was injected with cisplatin. On day 16, animals were scarified and serum and/or kidney tissue was used to determine: (a) kidney function tests (serum urea, creatinine, gamma glutamyl transferase (GGT), NAG, ß-gal), (b) oxidative stress indices (NO, LPO), (c) antioxidant activities (SOD, GSH, total thiols), (d) apoptotic indices (Cathepsin D, DNA fragmentation) and (e) mineral (calcium). M. chamomilla significantly increased the body weight, normalized the kidney functions, improved the apoptotic markers, reduced the oxidative stress markers and corrected the hypo-calcemia that resulted from cisplatin nephrotoxicity. M. chamomilla is a promising nephro-protective compound reducing cisplatin nephrotoxicity most probably by its antioxidant activities and inhibition of gamma glutamyl transferase activity.

Bone morphogenetic protein-2 will be a novel biochemical marker in urinary tract infections and stone formation.

OBJECTIVES: To investigate the role of bone morphogenetic protein-2 (BMP-2) in patients with urinary tract infection (UTI) and renal stone in relation to Tamm-Horsfall protein (THP) and osteopontin (OPN). DESIGN AND METHODS: ELISA kits were used to determine these markers in serum and urinary samples of 20 patients with UTI, 15 with renal stone and 10 controls. RESULTS: BMP-2 significantly increased in serum of patients who had UTI (P=0.05) and renal stone (P=0.01). In the case of UTI, serum BMP-2 at cutoff 44 pg/mL had sensitivity and specificity (92%, 80%), while cystatin C at cutoff 525 ng/mL showed sensitivity and specificity (85%, 91%). THP is a good predictor of renal diseases (P<0.001) by regression analysis. It is also the most sensitive urinary marker for UTI with sensitivity and specificity (94%, 75%) at cutoff 305 ng/mL. CONCLUSION: Combination of serum BMP-2 and cystatin C are more sensitive and accurate for early diagnosis of renal infection and damage.

Venlafaxine protects against stress-induced oxidative DNA damage in hippocampus during antidepressant testing in mice.

UNLABELLED: Venlafaxine (VLF) is an approved antidepressant that is claimed to have superior clinical efficacy to comparable drugs. Recently, many studies showed the relationship between depression and increased oxidative stress. This study investigated the relationship between the antidepressant effect of VLF and its ability to protect animals against stress-induced oxidative lipid peroxidation and DNA damage induced during antidepressant testing. METHODS: The antidepressant effect of long-term treatment (21 days) of VLF in doses 5, 10 and 20mg/kg/day, i.p. was tested using forced swimming test (FST) and tail suspension test (TST). The effects of VLF on hippocampal lipid peroxidation (MDA), nitric oxide (NO), glutathione (GSH), total antioxidant (TAC) levels and glutathione-S-transferase (GST) activity were tested. Furthermore, the corresponding changes in serum and hippocampal 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured. RESULTS: Long-term VLF treatment showed a significant, antidepressant effect in both FST and TST. VLF could decrease the hippocampal MDA and NO and to increase hippocampal GSH and TAC levels and GST activity in the tested animals. Only GSH and TAC levels were increased by VLF in the non-tested animals. In addition, both serum and hippocampal 8-OHdG levels were significantly reduced by VLF in animals exposed to antidepressant tests. CONCLUSION: Long-term VLF treatment in the effective antidepressant doses can protect against stress-induced oxidative cellular and DNA damage. This action may be through antagonizing the oxidative stress and enhancing the antioxidant defense mechanisms. Consequently, pharmacological modulation of stress-induced oxidative DNA damage as a possible stress-management approach should be an important avenue of further research.

Implication of umbilical cord in preeclampsia.

OBJECTIVES: To investigate the role of biochemical changes in the umbilical cord and placenta in developing preeclampsia (PE). SUBJECTS AND METHODS: Thirty women with PE and 15 healthy pregnant women as controls were enrolled in this study. Vascular endothelial growth factor (VEGF), soluble vascular endothelial growth factor receptor 1 (sVEGFR-1), platelet-derived endothelial cell growth factor (PD-ECGF), neutrophil elastase and nitric oxide (NO) were measured. RESULTS: Both serum (maternal and fetal) and tissue (placenta and umbilical cord) levels of VEGF, sVEGFR-1, PD-ECGF and neutrophil elastase were significantly increased, whereas NO was significantly decreased (except placental tissue showed no changes) in preeclamptic patients. The cord serum level of PD-ECGF was significantly higher in severe PE compared to mild PE and normal pregnant women. The placental and cord tissue levels of PD-ECGF and neutrophil elastase were significantly higher in severe PE, while the cord tissue level of NO was significantly lower in severe PE. CONCLUSION: Our data showed that umbilical cord vessels and stroma can serve as an additional source of vasoactive and angiogenic substances that contribute to the biochemical changes occurring in PE.

N-TerminaL PRO-BNP in Acute Coronary Syndrome Patients with ST Elevation Versus Non ST Elevation in Qassim Region of Saudi Arabia.

AIM: To investigate the differences in the secretion of NT-proBNP and conventional cardiac markers in patients with STE-ACS vs. NSTE-ACS as a trial to solve the dilemma of the early detection of myocardial ischemia in NSTE-ACS. DESIGN: prospective case control hospital based study. SETTING: King Fahad Specialist Hospital, Buraidah, Kingdom of Saudi Arabia. PATIENTS AND METHODS: Sixty two patients with acute coronary syndrome (ACS) were divided into 2 groups according to ECG: group1 with elevated ST segment in ECG ( STE-ACS) and group 2 with non elevated ST segment (NSTE-ACS). Twenty healthy subjects with matched age and sex were enrolled as control group in this study. In the sera of all subjects, levels of NT -proBNP, CK-MB and troponin- T were measured by different kits. RESULTS: CK-MB and Tn-T were both significantly higher in STE-ACS patients as compared to NSTE-ACS patients. Conversely, NT-proBNP was significantly higher in NSTE-ACS patients than STE-ACS especially within 4 hours from onset of chest pain. This suggested a larger ischemic insult despite the smaller extent of myocardial necrosis compared with STE-ACS patients. Comparison between sensitivity and specificity of NT-proBNP, Tn-T and CK-MB levels by ROC curves revealed a marked difference of area under the curves with higher sensitivity and specificity of NT-proBNP in NSTE-ACS patients. CONCLUSIONS: NT-proBNP can serve as a sensitive marker in the early phase of NSTE-ACS patients as compared to conventional markers of myocardial damage.

Functional analysis of a novel I71N mutation in the GJB2 gene among Southern Egyptians causing autosomal recessive hearing loss.

Mutations in GJB2, a gene encoding the gap junction protein connexin 26 (Cx26), are a major cause for inherited and sporadic non-syndromic hearing loss, albeit with highly variable clinical effects. To determine new mutations and their frequencies in a Southern Egyptian population restriction fragment length polymorphism, gene sequencing, and single strand conformational polymorphism revealed only 2 mutations for GJB2: c.35delG and p.I71N. The allelic frequency of the c.35delG mutation was 8.7% (found in 27 out of 310 investigated alleles) resulting in a relatively low carrier frequency (1.6%) in Upper Egypt. The new mutation, a substitution of isoleucin (I) (a non-polar amino acid) by the polar amino acid asparagin (N), was localized within the conserved Cx26 structure. The functional significance of p.I71N was tested by injection of cRNA into Xenopus laevis oocytes. Cx26 hemi-channel activity was measured by depolarization activated conductance in non-coupled oocytes. As a result, the p.I71N mutated channel was non-functional. The study discloses a novel, functionally relevant GJB2 mutation and defines the contribution of Cx26 alterations to the hearing loss in the Southern Egyptian population.

A novel therapeutic drug (copper nicotinic acid complex) for non-alcoholic fatty liver.

BACKGROUND: Fatty liver is the accumulation of fat in liver cells, which leads to disruption of the normal liver structure and function. METHODS: A non-alcoholic fatty liver rat model received copper (Cu) (I)-nicotinate complex [CuCl(HNA)2] for 4 weeks. RESULTS: Clinical signs and histopathological examinations showed obvious improvements in rats that received Cu complex who were continuously on an (HCFF) diet than those returned to standard diet with Cu complex. The improvement was matched in total lipids in sera and hepatic tissue, with disappearance of fat droplets from liver sections. Furthermore, the gain in body weight and the corresponding decrease in liver weight, decreased liver transaminases and alkaline phosphatase were prominent. The oxidative stress markers such as nitric oxide, lipid peroxides, glutathione and superoxide dismutase were obviously changed to healthy normal levels. CONCLUSION: The Cu complex may serve as a novel chemical restoring agent in fatty degenerated liver cells and for renewal of their structure and functions. However, clinical trials are required for more evaluation of the Cu complex in humans.

Midkine, a heparin-binding growth factor, produced by the host enhances metastasis of Lewis lung carcinoma cells.

Midkine is a heparin-binding growth factor and is expressed by a number of tumor cells, contributing to their growth both in vitro and in vivo. Spontaneous lung metastasis of Lewis lung carcinoma cells, which did not significantly express MK, was significantly less extensive in mice deficient in the midkine gene than in wild-type mice, when the tumor was subcutaneously grown above the thigh. Midkine strongly enhanced migration of Lewis lung carcinoma cells in vitro. Therefore, midkine is also a host factor enhancing tumor metastasis. Anti-midkine therapy for malignancy may act on midkine produced by both the tumor and host.