Bee venom improves diabetic wound healing by protecting functional macrophages from apoptosis and enhancing Nrf2, Ang-1 and Tie-2 signaling.

Impaired wound healing is a serious complication of diabetes that negatively affects the patient's socioeconomic life. Multiple mechanisms contribute to impaired diabetic wound healing including deficient recruitment of wound macrophages/neutrophils and impaired neovascularization. Bee venom (BV) has been used as an anti-inflammatory agent for the treatment of several diseases. Nevertheless, the impacts of BV on the diabetic wound healing have been poorly studied. In the present study, we investigated the molecular mechanisms underlying BV treatment on diabetic wound healing in a type I diabetic mouse model. Three experimental groups were used: group 1, non-diabetic control mice; group 2, vehicle-diabetic mice; and group 3, BV-treated diabetic mice. We found that the diabetic mice exhibited impaired wound closure characterized by a significant decrease in collagen and ß-defensin-2 (BD-2) expression compared to control non-diabetic mice. The impairment of diabetic wound healing is attributed to increased ROS levels and abolished antioxidant enzymes activity in the wounded tissues. Additionally, wounded tissue in diabetic mice revealed aberrantly decreased levels of Ang-1 and Nrf2 (the agonist ligands of Tie-2) followed by a marked reduction in the phosphorylation of Tie2 and downstream signaling eNOS, AKT and ERK. Impaired diabetic wound healing was also characterized by a significant reduction in activities of total antioxidant enzymes followed by a marked reduction in the levels of CCL2, CCL3 and CXCL2; which led to impaired recruitment and functions of wound macrophages/neutrophils; and significant reduction in the expression of CD31, a marker for neovascularization and angiogenesis of the injured tissue. Interestingly, BV treatment significantly enhanced wound closure in diabetic mice by increasing collagen and BD-2 expression and restoring the levels of Ang-1 and Nrf2 and hence enhancing the Tie-2 downstream signaling. Most importantly, treatment of diabetic mice with BV significantly restored the activities of wounded tissue antioxidant enzymes and the levels of chemokines, and subsequently rescued wound macrophages from mitochondrial membrane potential-induced apoptosis. Our findings reveal the immune-enhancing effects of BV for improving healing process of diabetic wounds and provide the first insight concerning the underlying molecular mechanisms.

Antioxidant activity and protective effect of bee bread (honey and pollen) in aluminum-induced anemia, elevation of inflammatory makers and hepato-renal toxicity.

Aluminum toxicity might be related to oxidative stress, and the antioxidant activity and protective effect of bee bread, which contains pollen, honey and bees' enzymes, on aluminum induced blood and hepato-renal toxicity was investigated in rats. Chemical analysis and antioxidant capacity of bee bread were conducted. The animal experiment in rats included; group 1: received distilled water (10 ml/kg b.wt), group 2: received aluminum chloride (662.2 mg/kg b.wt), group 3: received aluminum chloride (662.2 mg/kg b.wt) and ethanolic extract of the bee bread (500 mg/kg b.wt), and group 4: received aluminum chloride (662.2 mg/kg b.wt) and ethanolic extract of the bee bread (750 mg/kg b.wt). Doses were given once daily via a gavage. C-reactive protein, transaminases, urea, creatinine, creatinine clearance, sodium and potassium and urine sodium and potassium were determined on day 28 of the experiment. Bee bread contained protein, fat, fiber, ash, carbohydrate, phenol and flavonoids and it exhibited antioxidant activity. Aluminum caused a significant elevation of blood urea, transaminase, C-reactive protein and monocyte count and significantly decreased hemoglobin. These changes were significantly ameliorated by the use of bee bread. Bee bread has an antioxidant property, and exhibited a protective effect on aluminum induced blood and hepato-renal toxicity and elevation of inflammatory markers C-reactive protein, leukocyte and monocyte counts.

Protective Effect of Morocco Carob Honey Against Lead-Induced Anemia and Hepato-Renal Toxicity.

BACKGROUND/AIMS: Natural honey has many biological activities including protective effect against toxic materials. The aim of this study was to evaluate the protective effect of carob honey against lead-induced hepato-renal toxicity and lead-induced anemia in rabbits. METHODS: Twenty four male rabbits were allocated into four groups six rabbits each; group 1: control group, received distilled water (0.1 ml / kg.b.wt /daily); group 2: received oral lead acetate (2 g/kg.b.wt/daily); group 3: treated with oral honey (1g /kg.b.wt/daily) and oral lead (2 g/kg.b.wt/daily), and group 4: received oral honey (1 g/kg.b.wt/daily). Honey and lead were given daily during 24 days of experimentation. Laboratory tests and histopathological evaluations of kidneys were done. RESULTS: Oral administration of lead induced hepatic and kidney injury and caused anemia during three weeks of the exposure. Treatment with honey prevented hepato-renal lead toxicity and ameliorated lead-induced anemia when honey was given to animals during lead exposure. CONCLUSION: It might be concluded that honey has a protective effect against lead-induced blood, hepatic and renal toxic effects.

Oral supplementation of diabetic mice with propolis restores the proliferation capacity and chemotaxis of B and T lymphocytes towards CCL21 and CXCL12 by modulating the lipid profile, the pro-inflammatory cytokine levels and oxidative stress.

BACKGROUND: Type 1 diabetes mellitus (T1D) is a chronic autoimmune disease caused by the selective destruction of pancreatic ß cells, followed by hyperglycemia, oxidative stress and the subsequent extensive impairment of immune cell functions, a phenomenon responsible for the development of chronic diabetic complications. Propolis, a natural bee product that is extensively used in foods and beverages, significantly benefits human health. Specifically, propolis exerts antioxidant, anti-inflammatory and analgesic effects that may improve diabetic complications. To further elucidate the potential benefits of propolis, the present study investigated the effect of dietary supplementation with propolis on the plasma cytokine profiles, free radical levels, lipid profile and lymphocyte proliferation and chemotaxis in a streptozotocin (STZ)-induced type I diabetic mouse model. METHODS: Thirty male mice were equally distributed into 3 experimental groups: group 1, non-diabetic control mice; group 2, diabetic mice; and group 3, diabetic mice supplemented daily with an ethanol-soluble derivative of propolis (100 mg/kg body weight) for 1 month. RESULTS: First, the induction of diabetes in mice was associated with hyperglycemia and significant decreases in the insulin level and the lymphocyte count. In this context, diabetic mice exhibited severe diabetic complications, as demonstrated by a significant decrease in the levels of IL-2, IL-4 and IL-7, prolonged elevation of the levels of pro-inflammatory cytokines (IL-1ß, IL-6 and TNF-α) and reactive oxygen species (ROS) and altered lipid profiles compared with control non-diabetic mice. Moreover, antigen stimulation of B and T lymphocytes markedly reduced the proliferative capacity and chemotaxis of these cells towards CCL21 and CXCL12 in diabetic mice compared with control mice. Interestingly, compared with diabetes induction alone, treatment of diabetic mice with propolis significantly restored the plasma cytokine and ROS levels and the lipid profile to nearly normal levels. Most importantly, compared with untreated diabetic mice, diabetic mice treated with propolis exhibited significantly enhanced lymphocyte proliferation and chemotaxis towards CCL21 and CXCL12. CONCLUSION: Our findings reveal the potential immuno-modulatory effects of propolis, which acts as a natural antioxidant to enhance the function of immune cells during diabetes.

Topical application of propolis enhances cutaneous wound healing by promoting TGF-beta/Smad-mediated collagen production in a streptozotocin-induced type I diabetic mouse model.

BACKGROUND/AIMS: Impaired wound healing is considered to be one of the most serious complications associated with diabetes as it significantly increases the susceptibility of patients to infection. Propolis is a natural bee product used extensively in foods and beverages that has significant benefits to human health. In particular, propolis has antioxidant, anti-inflammatory and analgesic effects that could be useful for improving wound healing. In this study, we investigated the effects of topical application of propolis on the healing and closure of diabetic wounds in a streptozotocin (STZ)-induced type I diabetic mouse model. METHODS: Sixty male mice were distributed equally into 3 experimental groups: group 1, non-diabetic control mice; group 2, diabetic mice; and group 3, diabetic mice treated daily with a topical application of propolis. RESULTS: We found that diabetic mice exhibited delayed wound closure characterized by a significant decrease in the levels of TGF-ß1 and a prolonged elevation of the levels of inflammatory cytokines (IL-1ß, IL-6 and TNF-α) and MMP9 in wound tissues compared with control non-diabetic mice. Moreover, the wound tissues of diabetic mice showed a marked reduction in the phosphorylation of Smad2 and Smad3 as well as a marked reduction in collagen production. Interestingly, compared with untreated diabetic mice, topical application of propolis significantly enhanced the closure of diabetic wounds and decreased the levels of IL-1ß, IL-6, TNF-α and MMP9 to near normal levels. Most importantly, compared with untreated diabetic mice, the treatment of diabetic mice with propolis significantly enhanced the production of collagen via the TGF-ß1/Smad2,3 signaling axis in wounded tissues. CONCLUSION: Our findings reveal the molecular mechanisms underlying the improved healing and closure of diabetic wounds following topical propolis application.

Effects of natural honey on polymicrobial culture of various human pathogens.

INTRODUCTION: Honey has a wide range of antimicrobial activity. All previous studies have considered honey's effect on a single microbe. The present study investigated activity of honey towards a high dose of single or polymicrobial culture. MATERIAL AND METHODS: 10 µl specimens of Staphylococcus aureus (S. aureus), Streptococcus pyogenes (S. pyogenes), Escherichia coli (E. coli) and Candida albicans (C. albicans) were cultured in 10 ml of 10-100% (wt/v) honey diluted in broth. Six types of polymicrobial microbial cultures were prepared by culturing the isolates with each other onto broth (control) and broth containing various concentrations of honey (10-100% wt/v). Microbial growth was assessed on solid plate media after 24 h incubation. RESULTS: Honey (30-70%) prevents growth of 10 µl specimens of all the isolates. Greater reduction in growth of E. coli was observed when cultured with S. aureus. Culturing of S. aureus with S. pyogenes, C. albicans, or E. coli increased its sensitivity to honey. S. aureus and S. pyogenes increased sensitivity of C. albicans to honey while E. coli and C. albicans decreased sensitivity of S. pyogenes. CONCLUSIONS: It might be concluded that honey prevents and inhibits growth of single and polymicrobial pathogenic cultures. Polymicrobial culture affects growth of the isolates and increases their sensitivity to honey.

Effect of jujube honey on Candida albicans growth and biofilm formation.

BACKGROUND AND AIMS: Candida species, especially Candida albicans, are major fungal pathogens of humans that are capable of causing superficial mucosal infections and systemic infections in humans. The aim of this study was to evaluate the jujube (Zizyphus spina-christi) honey for its in vitro inhibitory activity against pre-formed biofilm and its interference with the biofilm formation of C. albicans. METHODS: The XTT reduction assay, scanning electron microscopy (SEM) and atomic force microscopy (AFM) were employed to determine the inhibitory effect of Jujube honey on C. albicans biofilm. Changes in the infrared spectrum after treatment with honey were also determined by Fourier transform infrared (FTIR) spectroscopy. RESULTS: Jujube honey affects biofilms by decreasing the size of mature biofilms and by disruption of their structure. At a concentration of 40% w/v, it interferes with formation of C. albicans biofilms and disrupts established biofilms. The SEM and AFM results indicated that this type of honey affected the cellular morphology of C. albicans and decreased biofilm thickness. CONCLUSIONS: The present findings show that jujube honey has antifungal properties against C. albicans and has the ability to inhibit the formation of C. albicans biofilms and disrupt established biofilms.

Honey and microbial infections: a review supporting the use of honey for microbial control.

Honey has been used as a medicine throughout the ages and has recently been reintroduced to modern medical practice. Much of the research to date has addressed honey's antibacterial properties and its effects on wound healing. Laboratory studies and clinical trials have shown that honey is an effective broad-spectrum antibacterial agent. Honey antimicrobial action explains the external and internal uses of honey. Honey has been used to treat adult and neonatal postoperative infection, burns, necrotizing fasciitis, infected and nonhealing wounds and ulcers, boils, pilonidal sinus, venous ulcers, and diabetic foot ulcers. These effects are ascribed to honey's antibacterial action, which is due to acidity, hydrogen peroxide content, osmotic effect, nutritional and antioxidants content, stimulation of immunity, and to unidentified compounds. When ingested, honey also promotes healing and shows antibacterial action by decreasing prostaglandin levels, elevating nitric oxide levels, and exerting prebiotic effects. These factors play a major role in controlling inflammation and promoting microbial control and healing processes. This article reviews data supporting the effectiveness of natural honey in eradicating human pathogens and discusses the mechanism of actions.

Modulation of prostaglandin activity, part 1: prostaglandin inhibition in the management of nonrheumatologic diseases: immunologic and hematologic aspects.

Prostaglandins (PGs) are active biologic substances that are involved in a wide range of physiologic processes; when their production is out of balance, they are factors in the pathogenesis of illness. Modulation of PGs by inhibition or stimulation is promising for the management of various conditions. PG inhibitors are widely used to relieve pain and inflammation in patients with rheumatologic disease. Interest in the use of PG inhibitors to prevent cancer and cardiovascular events is growing. More than 27 y ago, investigators found that PG depresses antibody production in vivo; reduces serum iron, hemoglobin, and leukoid series in bone marrow during acute and chronic blood loss; reduces albumin during antigenic stimulation; suppresses hypercalcemia after bleeding; and reduces fasting blood sugar and hyperglycemia after ether anesthesia and bleeding. Chronic conditions that produce large quantities of PGs are associated with immunosuppression and secondary anemia. Investigators in the present study hypothesized (1) that the overproduction of PGs is responsible for immunosuppression and secondary anemia in conditions associated with increased PG synthesis, such as pathologic inflammation, malignancy, trauma, and injury, and (2) that PG inhibitors reverse immunosuppression and secondary anemia, thereby enhancing the immune response. This is supported by many reports that show the immunosuppressive effects of PGs and their role in the immunosuppression associated with pathologic inflammation, burns, trauma, and tumors. Inhibition of PGs can be achieved through the use of synthetic medicines and natural products. This article reviews the effects of PGs and inhibition of increased synthesis of PGs on the lymphoid system, hematologic indices, and bone marrow elements in trauma, injury, burns, and tumors. The Medline database (1966-2006) was used in this study. Investigators in the present study and others have provided evidence that shows the involvement of PGs in immunosuppression and secondary anemia, as well as the efficacy of inhibited overproduction of PGs in many pathologic conditions other than rheumatologic disease.

Effects of heating, storage, and ultraviolet exposure on antimicrobial activity of garlic juice.

This study was designed to investigate the effect of heating, storage, and ultraviolet exposure on antimicrobial activity of garlic juice and its bacteriocidal activity against common human pathogens. Antimicrobial activity of fresh garlic juice was tested against Escherichia coli, Staphylococcus aureus, Streptococcus hemolyticus B, S. hemolyticus A, Klebsiella sp., Shigella dysenteriae, and Candida albicans using the disc method. The dilution method was performed by addition of garlic juice to broth media to obtain 1-100% concentrations as vol/vol or wt/vol. Garlic juice was used after 24 hours of storage at 4 degrees C, heating to 100 degrees C for 5 minutes, 10 minutes, 30 minutes, and 60 minutes, heating to 80 degrees C for 60 minutes, and 4 hours of exposure to ultraviolet light. Re-culture of specimens taken from garlic-induced negative media was performed in fresh broth free of garlic juice. Results showed that all the isolates were sensitive to fresh garlic juice; the most sensitive was C. albicans, and the least sensitive was S. hemolyticus A. Heating to 100 degrees C for 30 and 60 minutes completely abolished the antimicrobial activity, while heating for 5 and 10 minutes, storage for 24 hours, and 4 hours of ultraviolet exposure decreased it. Garlic juice was bactericidal at concentrations of 5% and more. Thus garlic juice has marked antimicrobial activity that makes it a potential agent to be tested in clinical trials. The antimicrobial activity was compromised by storage and heating; therefore it is advisable to use fresh garlic and avoid boiling it for more than 5 minutes during cooking.

A potential concept in the management of tumors with modulation of prostaglandin, nitric oxide and antioxidants.

Prostaglandins (PGs), nitric oxide (NO), free radicals and chronic inflammation play a major role in tumorogenesis. We have found in vivo that PGs suppress antibody production; reduce serum iron, and modulate bone marrow function. Tumors are associated with immunosuppression and anemia. We have hypothesized that the over-production of PGs is responsible for immunosuppression and anemia in conditions associated with increased production of PG such as tumor, and that PG inhibitors might help reversing immunosuppression and anemia, and play a role in eradication and prevention of tumors. This is supported by reports that demonstrate the immunosuppressive effects of PGs in tumors. PG inhibitors have also been shown to be crucial in the prevention of tumors such as esophageal and colon cancers. Others and we have found that high NO production was encountered in patients with cancer while antioxidants are decreased. Evidence supports the efficacy of PG inhibition in malignancies, and the concept of PG inhibition, NO modulation, anti-oxidants, immunotherapy with antibody or immune cells, and anti-inflammatory agents when used in the prevention and management of malignancies are discussed.

A combination of radiotherapy, nitric oxide and a hyperoxygenation sensitizing protocol for brain malignant tumor treatment.

Brain malignant tumor such as glioblastoma is a challenging medical and surgical problem. In spite of surgery, radiotherapy and chemotherapy, the prognosis is still very poor. The limitations of currently available treatment modalities to cure or significantly prolong and improve the quality of life should stimulate rigorous research and studies to combat brain malignant tumors. While precision radiotherapy to reduce tumor size and ameliorate symptoms is still the standard of care, tumor sensitivity to radiation is compromised by low oxygen tensions and a necrotic tumor center. We propose to take advantage of the fact that elevated oxygen increases sensitivity of tumor cells to radiation. A specific application of hyperbaric oxygen (HBO(2)), using nitric oxide (NO) donors and inducers (such as L-arginine, dinitrite or tocopheryl succinate) and ascorbic acid to dilate blood vessels, should permit oxygen tensions in the range of 1000 mmHg to diffuse into the cells and thus increase sensitivity to radiation. This should permit doses that are low enough to cause the death of tumors cells yet minimize injury to brain tissue near the tumor and induced neurological sequelae.

Hyperbaric oxygen and lymphoid system function: a review supporting possible intervention in tissue transplantation.

This review addresses the many ways that hyperbaric oxygen (HBO2) has been found to mitigate immune reactions, many of which are involved in rejection of allograft transplants, and thus offers a rationale for its possible use as an adjunct to help preserve and protect transplanted tissues. Rejection may involve both immunological reactions of the lymphoid system, or lymphoid-independent damage from trauma or other factors, including reperfusion injury. Lymphoid-induced damage involves cellular elements such as CD4 and macrophage cell types, as well as both proinflammatory and inhibitory cytokines. Cytokines such as TNFs and interleukins activate T-cells and macrophages, resulting in endothelial damage and its consequences. The immunosuppressive effects of HBO2 include suppression of autoimmune symptoms, decreased production of IL-1 and CD4 cells, and increased percentage and absolute number of CD8 cells. HBO2 normalizes cell-bound immunity and decreases the serum concentration of immune complexes. Studies have shown MHC class I expression to be altered when cultures were exposed to HBO2, so as to become undetectable by monoclonal antibodies or cytotoxic T lymphocytes. HBO2 has been used in support of replanted rabbit ear grafts, spinal cord tissue transplants, dislocated young permanent teeth in children, replanting of fingers, free fibula reconstruction of segmental mandibular resections, autogenous free bone grafts, transplantations of the cornea, and liver transplants. In addition to its specific effects on the immune system, HBO2 improves tissue oxygenation, reduces free radical damage during reperfusion, maintains marginally ischemic tissue, and accelerates wound healing. These properties make HBO2 a promising intervention to be tested in transplantation recipients.

Honey ameliorates influence of hemorrhage and food restriction on renal and hepatic functions, and hematological and biochemical variables.

The objectives were to assess the effects of various diets, including total food restriction with 50% honey feeding, total food restriction with 50% dextrose feeding or adlibitum (control group) commercial regular diet, on the hematology and biochemical variables, and to assess the effects of the various diets on the influence of acute blood loss on the same parameters. Thirty Sprague-Dawley albino rats were divided into three groups, 10 rats each: group A, fed a commercial regular diet; group B, total food restriction with 50% dextrose feeding; and group C, total food restriction with 50% honey feeding. After 8 days of feeding, rats were subjected to acute blood loss (6 ml/kg) and blood investigations were performed. After acute blood loss, the same feedings were continued for a further 8 days and the blood tests were repeated at day 8 post-bleeding. Total food restriction with 50% dextrose feeding compared with commercial regular diet reduces hematological and biochemical variables. Total food restriction with 50% honey feeding compared with total food restriction with 50% dextrose feeding causes a greater reduction in fasting blood glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and triacylglycerol. Acute blood loss causes elevation of white blood cells, lymphocyte percentage, fasting blood sugar, blood urea nitrogen, alkaline phosphatase and triacylglycerol, and a reduction in serum albumen, protein, cholesterol, AST, serum creatinine and hemoglobin; the results are significant (P<0.05) concerning fasting blood glucose, AST, alkaline phosphatase, serum albumin and protein. A significant reduction in fasting blood glucose, white blood cells, BUN, AST, ALT, alkaline phosphatase and triacylglycerol, and a significant elevation of hemoglobin and serum albumin are obtained after acute blood loss in rats on total food restriction with 50% honey feeding as compared with the other two groups. Total food restriction with 50% honey feeding increases serum albumin, serum protein, fasting blood glucose, and causes lower reduction in hemoglobin as compared with the other groups. Conclusively, honey feeding during total food restriction significantly modifies and ameliorates biochemical and hematological changes observed after acute blood loss. This will pave the way to use honey as part of bleeding management and during a food restriction regimen.

Influence of various diet regimens on deterioration of hepatic function and hematological parameters following carbon tetrachloride: a potential protective role of natural honey.

The objective was to assess the effects of commercial regular diet as control, total food restriction with honey, commercial regular diet with dextrose, or total food restriction with dextrose, on blood variables after carbon tetrachloride (CCl4) administration. Sprague Dawley albino rats were divided into four groups, 10 rats each; Group 1 rats were on commercial regular diet, Group 2 rats were on commercial regular diet with 50% dextrose, Group 3 rats were on total food restriction with 50% dextrose, and Group 4 rats were on total food restriction with 50% honey. Rats in all the groups were i.m. administered CCL4 (2.4 mL kg b. wt.-1). Blood tests including ALT, AST, serum albumin, serum protein, BUN, blood glucose (BG), hemoglobin (Hb), and white blood cell (WBC) were performed before CCl4 administration and repeated after 48 and 96 h of post-injection. In Group 1, CCl4 caused significant elevation in AST and ALT, and decrease in BS, WBC, and BUN; lower elevation in AST and ALT at 48 h and decreased AST and ALT at 96 h were obtained when dextrose was added to commercial regular diet (Group 2). Using dextrose alone (Group 3), though there was significant elevation of AST and ALT and decrease in BUN and WBC as compared to baseline values, significant decrease in ALT, AST, and BUN as compared to control was obtained. During absolute honey feeding (Group 4), elevation in AST and ALT obtained, following CCl4 administration was significantly less than the values obtained in all other groups; with lower elevation in AST and ALT as compared to baseline values. Honey increased serum albumin, serum protein, BG, and caused lower reduction in Hb. Conclusively, exclusive honey feeding (50% concentration) significantly modifies and ameliorates biochemical and hematological changes obtained after CCl4 injection.

Influences of hyperbaric oxygen on blood pressure, heart rate and blood glucose levels in patients with diabetes mellitus and hypertension.

BACKGROUND: We investigated the influences of hyperbaric oxygen (HBO(2)) on systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) and blood glucose level (BGL). METHODS: Forty one patients with hypertension (HTN), diabetes mellitus (DM), HTN and DM and/or no HTN or DM underwent HBO(2) sessions (15-40 sessions for each patient). SBP, DBP, HR and BGL (for diabetics) were recorded before and after each session. RESULTS: HBO(2) caused significant elevation in SBP (11%) and DBP (12%) and a decrease in HR (18%) (p <0.001). Patients with DM and HTN showed higher elevation in SBP and DBP. HBO(2) lowered BGL by 23% (p <0.001). When basal BGL was in the range of 120-170 mg/dl, it dropped to <100 mg/dl in 31/60 treatment sessions (52%). When basal BGL was <120 mg/dl it dropped to <70 mg/dl in 8/34 sessions. There was a possibility of lowered BGL when basal BGL was <170 mg/dl and a marked reduction in BGL occurred when basal BGL was <120 mg/dl. HBO(2) caused a marked elevation in SBP and DBP when basal SBP was >140 mmHg. Critical elevation was obtained when SBP was >160 mmHg. The use of beta blockers caused significant elevation of blood pressure while reducing HR. CONCLUSIONS: HBO(2) causes elevation of blood pressure and lowering of HR and BGL, which were augmented in the presence of HTN, DM, or beta blocker. The use of beta blockers for the management of HTN should be avoided during HBO(2) therapy.

Improvement in human semen quality after oral supplementation of vitamin C.

This study was carried out to monitor the effect of oral supplementation of vitamin C on various semen parameters in oligospermic, infertile, otherwise healthy individuals. Various semen parameters, including sperm motility, sperm count, and sperm morphology, were studied before and after the vitamin C treatment. A total of 13 infertile patients were included. Their ages ranged between 25 and 35 years. They had no genital infection or varicocele. Physical examination and other routine laboratory investigations were normal. General semen analysis revealed oligozoospermia (mean sperm count was 14.3 +/- 7.38 x 10(6) sperms/mL, mean sperm with normal morphology was 43 +/- 7.87%, and mean sperm motility was 31.2 +/- 9.61%). Testicular biopsy was not done. These patients received in an open trial of 1,000 mg of vitamin C twice daily for a maximum of 2 months. Results showed that the mean sperm count was increased to 32.8 +/- 10.3 x 10(6) sperms/mL (P < .001) after 2 months of vitamin C intake. The mean sperm motility was increased significantly to 60.1 +/- 8.47% (P < .001), and mean sperms with normal morphology increased significantly to 66.7 +/- 4.77% (P < .001). This study showed that vitamin C supplementation in infertile men might improve sperm count, sperm motility, and sperm morphology and might have a place as an additional supplement to improve the semen quality towards conception.

Phototherapy and malignancy: possible enhancement by iron administration and hyperbaric oxygen.

Photodynamic therapy (PDT) is a new therapeutic approach for the treatment of malignant tumors. Hyperbaric oxygen (HBO(2)) shows beneficial effects in various modalities of cancer interventions. Tumor cells tend to accumulate large amount of iron. There is interaction between tissue content of oxygen, iron, free radical production and tissue damage. Accumulation of intracellular iron is necessary for the production of oxygen radicals. HBO(2) increases tissue oxygen and hydrogen peroxide production in the cells. Malignant cells require iron, and exhibit more transferrin receptors. The photodynamic sensitization of human leukemic cells is achieved with accumulation of porphyrins stimulated by 5-aminolaevulanic acid (ALA) plus hemin. Further, a significant improvement in tumor response is obtained when PDT is delivered during hyperoxygenation. When PDT is combined with hyperoxygenation, the hypoxic condition is improved and the cell killing rate at various time points after PDT is significantly enhanced. Photosensitization with use of porphyrins is used with HBO(2) and PDT for treatment of certain tumors. PDT with ALA is used for treatment of actinic keratosis (AK). The combination of iron administration (by injection or oral rout), hemin, or transferrin, as a source for iron, HBO(2) as a source of oxygen under pressure and PDT as a source of generating free-radical tissue damage may be useful in the treatment of tumors. The possibility of combining HBO(2), iron, light and local photosensitizers to overcome skin tumors deserve extensive laboratory and clinical research work. Conclusively, iron, HBO(2), and PDT may have synergistic effect to hamper tumor cells.

Postsurgical psychosis: case report and review of literature.

A wide range of behavioral symptoms may occur following surgery, including depression, hallucinations, true psychosis, mania, and impulsivity. Psychoses, including those that occur postoperatively, are among the most frequent indications for hospitalization in the United States and are associated with a substantially increased rate of morbidity. The exact cause of postoperative psychosis has not been identified. A 59-year-old woman who developed acute psychosis after cholecystectomy is described here. The patient was brought to Mount Vernon Hospital in New York because she exhibited acute disruptive behavior following endoscopic retrograde cholangiopancreatography and laparoscopic cholecystectomy performed on 2 consecutive days. The patient was psychotic and was unable to be managed; she was disorganized, confused, and perplexed. Findings of computed tomography of the head, electroencephalography, and chemical and hematologic tests were normal. The patient was treated with lorazepam 1 mg every 6 h, olanzapine 5 mg at bedtime, and clonazepam 1 mg at bedtime. She experienced a mixture of auditory and visual hallucinations with a paranoid perspective and was then treated with haloperidol 5 mg, diphenhydramine chloride 25 mg, and divalproex sodium 500 mg. After 1 wk, the patient was described as acutely psychotic; antipsychotic medication dosages were readjusted and the patient's condition stabilized. The association between surgical procedures and psychosis is thoroughly reviewed here. Awareness, ability to diagnose, and an understanding of the cause of psychotic symptoms that emerge following surgery must be established if physicians are to provide better care and more effective treatment.