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Background : Being HIV positive, someone will face psychological pressure such as depression, anxiety and other negative ones. Pregnant women with HIV positive face two challenges, to keep her pregnancy and struggle to fight with HIV. Self-acceptance of those two dimensions gives high challenges for pregnant women who are HIV positive. The aim of the study is to understand deeper and describe about the self-acceptance of pregnant women with HIV positive Method : This study used qualitative research method with phenomenology approach. The participants are the pregnant women with HIV positive with inclusion criteria as: 1) woman in reproductive age 18-40 years old, 2) confirmed pregnant, 3) natural born of Indonesia, 4) can expressed her-selves verbally. The data analyzed with Collaizi’s analysis of qualitative research. Results : Data saturation was reached on the seventh participant. From the qualitative data analysis, there are three themes under the phenomenon of self-acceptance of pregnant-women with HIV positive, such as internal negativism, internal acceptance, and ready to enhanced health status. Conclusion : The process of self acceptance of being pregnant and infected with HIV gives contribution on the continuity of antenatal care and HIV therapy in order to the improvement of quality of life. Self-denial depicts as disappoint, anxiety, unbelief, blame herself, isolate her self, become as consequences of the situation. But, due to the support from family and people around, makes the pregnant mothers with HIV positive try to accept and disclose about her status. So, it will give better self-acceptance of to improve her health

Background Intravenous immunoglobulin (IVIG) is a biological product with adverse effects that appears to vary considerably among different IVIG preparations. Objectives To describe the adverse events of patients given intravenous immunoglobulin infusions. Method Data was collected on all patients receiving IVIG infusion at a tertiary hospital from January 2001 to December 2010. Descriptive statistics was used. Results 77 patients (45 males, 32 females) received IVIG infusions. Thirty two percent (n = 25) experienced adverse reactions. The most common indication was Kawasaki disease (85.7%) followed by immunodeficiency disorders (7.8%). Majority of the patients were children, with the highest frequency of infusions among those aged 2 to 8 years old (52%). 36 infusions were associated with occurrence of adverse effects. Fever was the most common adverse event (n = 11, 30.6%), followed by rash (n = 8, 22.2%) and chills (n = 7, 19.4%). Other adverse events were cyanosis (n = 3, 8.3%), hypotension (n = 2, 5.6%), hypothermia (n = 2, 5.6%), irritability (n = 1, 2.8%), vomiting (n = 1, 2.8%), and chest pain (n = 1, 2.8%). Adverse events were observed to occur most frequently within 1 to 6 h from onset of IVIG infusion. Among the various IVIG preparations available locally (Gammagard, Kiovig, Gamimune, Veno-S & IV Globulin S), Gammagard was the brand frequently used (50.7%). It also has the most number of adverse events, with 17 out of 41 (41.5%) infusions resulting in adverse reactions. Most of the reactions occurred with fast infusion rates, and clinical manifestations subsided when the rate of infusion was reduced. Conclusion In this study, thirty two percent of patients given IVIG infusions experienced adverse events. Fever was the most common manifestation. Symptoms occurred within 1 to 6 h from onset of infusion, were affected by fast infusion rates, and managed by reducing the rate of infusion.

Chronic myeloid leukemia patients call for quality and consistency when generics are introduced to treat their cancer

Although fibroblast growth factor-2 (FGF-2) plays an important role in cardioprotection and growth, little is known about the signals triggered by it in the adult heart. We therefore examined FGF-2-induced effects on phosphoinositide-specific phospholipase C (PI-PLC) isozymes, which produce second messengers linked to the inotropic and hypertrophic response of the myocardium. FGF-2, administered by retrograde perfusion to the isolated heart, induced an increase in inositol-1,4,5-trisphosphate levels in the cytosol, as well as an increase in total PI-PLC activity associated with sarcolemmal and cytosolic fractions. Furthermore FGF-2 induced a time-dependent elevation in cardiomyocyte membrane-associated PLC gamma1 and PLC β1 activities, assayed in immunoprecipitated fractions, and moreover, increased the membrane levels of PLC β1 and PLC β3. Activation of PLC β is suggestive of FGF-2-induced cross-talk between FGF-receptor tyrosine kinase and G-protein-coupled signaling in adult cardiomyocytes and underscores the importance of FGF-2 in cardiac physiology.Key words: FGF-2, signal transduction, PLC gamma, PLC β, cardiomyocytes.

Articular hyaline cartilage has a fundamental role in mechanical load distribution on joints. Injuries of this tissue, which has limited potential to heal, often cause pain and have a serious impact on function. Managing these injuries is a real challenge for the orthopaedic surgeon, then many strategies were proposed to repair such type of lesions for restoring the joint surface and improving patients’ symptoms. The authors focused their attention on autologous chondrocyte transplantation and mosaicplasty. A careful literature analysis was performed on these strategies, trying to find the best evidence available on these topics. Our search strategies included: The Cochrane Library, Health Technology Assessment (HTA) Database, MEDLINE, TRIP, CINAHL, EMBASE, SPORTDiscus. Although the analysed techniques are so popular in orthopaedics, poor scientific evidences are reported in literature and many controversial data exist.

Bifid median nerve is an anatomic variation that occurs in about 18% of patients with symptoms suggestive of carpal tunnel syndrome and in about 15% of symptom-free subjects. Reversed palmaris longus is a rare anatomic muscular variation. The simultaneous presence of a bifid median nerve and a reversed palmaris longus has been very rarely described, usually during surgical exploration or in cadavers. We present two cases where ultrasound showed the presence of both abnormalities, allowing a correct diagnosis and influencing the treatment plan.

As a first step in addressing the question of function for basic fibroblast growth factor (bFGF) in the adult myocardium, expression of bFGF receptors by adult rat myocytes was investigated. Cross-linking of 125I-labeled bFGF to purified sarcolemmal vesicles from adult hearts indicated specific binding to 90- to 104-kDa proteins, whereas equilibrium binding studies revealed the presence of "low"-affinity (1 nM) and "high"-affinity (115 pM) sites. Adult myocytes were found to express short and long variants of bFGF receptor 1 (FGFR-1, tyrosine kinase) mRNA. Adult heart overall levels of FGFR-1 mRNA were decreased by about one-third of corresponding fetal values. Several lines of evidence indicated that bFGF receptors in adult cardiomyocytes in situ and/or in isolation are functional. Isolated adult myocytes were found to be capable of heparin-resistant internalization of 125I-labeled bFGF, to lose their viability after interaction with bFGF-saporin (a mitotoxin known to kill cells after entry via the bFGF receptor), and to respond to bFGF by activation of mitogen-activated protein kinase. In addition, introduction of exogenous bFGF into the myocardium by Langendorff perfusion resulted in stimulation of tyrosine phosphorylation in association with cardiomyocyte intercalated disks, as assessed by immunofluorescence. It is concluded that adult cardiomyocytes express functionally coupled high-affinity bFGF receptors and that they are capable of a biologic response to bFGF in vivo.

Basic FGF is a multifunctional protein which promotes regeneration in several tissues. To investigate involvement in cardiac injury-repair, bFGF accumulation and localization was examined in hearts of rats injected with a single high dose of isoproterenol. The bFGF content of cardiac extracts was analyzed at 6 and 24 hours as well as 1, 4, and 6 weeks by western blotting of heparin-sepharose-bound fractions. The 18 kilodalton bFGF species showed an approximately 2-fold increase in extracts from treated animals compared to non-treated controls. A transient rise in a 21-23 kilodalton bFGF species was seen at 24 hours after treatment. An induction of bFGF mRNA was also observed in treated animals. To localize bFGF in vivo, immunofluorescent labelling with specific antibodies was used at 4-24 hours and 1-4 weeks after treatment. Simultaneous labelling for the cytoskeletal proteins vinculin or vimentin was employed to identify viable myocytes or non-muscle interstitial cells, respectively. Necrotic myocytes, identified by loss of vinculin, displayed a pronounced increase in cytoplasmic anti-bFGF staining compared to adjacent normal myocytes. This increase occurred prior to and may play a role in promoting mobile cell migration and proliferation in areas of necrosis. Viable cardiomyocytes adjacent to fibrotic regions displayed strong pericellular anti-bFGF staining and, occasionally, were also stained by anti-vimentin antibodies, suggesting reexpression of an embryonic phenotype and thus an attempt for regeneration. These data showing increased accumulation and distinct patterns of localization of bFGF in the hearts of isoproterenol-treated animals suggest that this growth factor plays a role in short-term as well as long term response of the myocardium to injury.

In lumbar stenosis (LS) patients, clinical, neuroradiological and neurophysiological findings were not related to validated measurements of the outcomes that are more relevant to patients such as functional status and symptoms.We have retrospectively studied 30 patients surgically treated for LS. We have evaluated the patients by means of self-administered questionnaires (SF-36), clinical examination, and neuroradiological and neurophysiological measurements and we have registered preoperative and follow-up clinical and neurophysiological findings. Finally we evaluated the relations between patient-oriented data and validated conventional clinical and neurophysiological measurements.The comparison between pre- and post-operative clinical picture showed an improvement of most parameters tested. The comparison between pre- and post-operative neurophysiological picture revealed worsening of most tested parameters. The comparison between the current sample and the Italian normative data for the SF-36 showed a worsening of physical aspects of health related quality of life; conversely there was an improvement of some mental domains.In our sample of LS patients the most compromised SF-36 domain was Role-Physical that measures the difficulty in every-day activities due to physical problems. Conversely, the clinical findings showed a significant improvement after surgery: patients reported in particular lower sciatica after surgical treatment, but the neurophysiological evaluation did not show any improvement.

We examined the effect of fibroblast growth factor (FGF)-2 on myocardial resistance to injury when administered after the onset of ischemia , in vivo and ex vivo, and the role of FGF-2 receptors and protein kinase C (PKC). FGF-2 was injected into the left ventricle of rats undergoing permanent surgical coronary occlusion leading to myocardial infarction (MI). After 24 h, FGF-2-treated hearts displayed significantly reduced injury, determined by histological staining and troponin T release, and improved developed pressure compared with untreated controls. An FGF-2 mutant with diminished affinity for the tyrosine kinase FGF-2 receptor 1 (FGFR1) was not cardioprotective. FGF-2-treated hearts retained improved function and decreased damage at 6 wk after MI. In the ex vivo heart, FGF-2 administration during reperfusion after 30-min ischemia improved functional recovery and increased relative levels of PKC subtypes α, ε, and ζ in the particulate fraction, in a chelerythrine-preventable mode; it also decreased loss of energy metabolites. We conclude that intramyocardial FGF-2 administration shortly after the onset of ischemia confers protection from acute and chronic cardiac dysfunction and damage; FGF-2 delivered during reperfusion protects from ischemia-reperfusion injury; and protection by FGF-2 requires intact binding to FGFR1 and is likely mediated by PKC.

With the advances in diagnostic and surgical procedures, for degenerative disease of the lumbar spine an aggressive therapeutic approach is more frequently indicated. The available surgical procedures are numerous and in continuing evolution. Most common surgical procedures used in major degenerative disease of the lumbar spine as disk herniation and stenosis are described. Indications, results and complications associated to these procedures are also illustrated.

In September 1996, during a carpal tunnel syndrome (CTS) symposium, the Italian CTS Study Group was funded. The group designed a strict clinical and neurophysiological protocol for performing a wide multicentre study on idiopathic CTS in hands. In addition to the traditional evaluations, the group also adopted a validated patient-oriented measurement in order to obtain comprehensive and reliable data for the clinical picture. The study was designed to: (1) better assess the clinical picture of the CTS population, especially using new measurement tools (patient-oriented); (2) evaluate the sensitivity of an electrodiagnostic protocol; (3) re-evaluate the validity of a neurophysiological classification; and (4) evaluate the influence of social status and quantify some of the aspects regarding economic and social costs. The study design is described.

Although many studies on carpal tunnel syndrome (CTS) have been reported, few data on the natural history of CTS are available. Knowledge of the natural course of the disease has significant clinical and therapeutic value. We prospectively followed up 80 cases of untreated CTS. The evaluation was based on self-administered questionnaires and on neurophysiological investigation. According to the neurophysiological classification, cases of CTS were divided into six groups on the basis of impairment severity: negative, minimal, mild, moderate, severe, and extreme. Disease worsening was inversely related to severity of nerve entrapment. On the contrary, improvement was proportionally related to nerve function impairment (except for extreme cases that never improved), and about one-third of mild and moderate cases improved. Most minimally cases remained neurophysiologically unchanged. We hypothesize that in a good percentage of CTS cases, nerve impairment is self-limited. Our data suggest the utility of further studies on the natural course of this common disease.

Although fibroblast growth factor-2 (FGF-2) plays an important role in cardioprotection and growth, little is known about the signals triggered by it in the adult heart. We therefore examined FGF-2-induced effects on phosphoinositide-specific phospholipase C (PI-PLC) isozymes, which produce second messengers linked to the inotropic and hypertrophic response of the myocardium. FGF-2, administered by retrograde perfusion to the isolated heart, induced an increase in inositol-1,4,5-trisphosphate levels in the cytosol, as well as an increase in total PI-PLC activity associated with sarcolemmal and cytosolic fractions. Furthermore FGF-2 induced a time-dependent elevation in cardiomyocyte membrane-associated PLC gamma1 and PLC beta1 activities, assayed in immunoprecipitated fractions, and moreover, increased the membrane levels of PLC beta1 and PLC beta3. Activation of PLC beta is suggestive of FGF-2-induced cross-talk between FGF-receptor tyrosine kinase and G-protein-coupled signaling in adult cardiomyocytes and underscores the importance of FGF-2 in cardiac physiology.

To assess the clinical and neurophysiologic dissociation often observed in clinical practice, and to improve patient evaluation for diagnosis of carpal tunnel syndrome (CTS).The Italian CTS Study Group studied 1,123 idiopathic CTS hands with multiple measurements-clinical, neurophysiologic, and patient-oriented-of CTS.Clinical and neurophysiologic relationships were very strong when the clinical picture was evaluated by the hand functional measurements, with an exponential increase in functional impairment as the classification of neurophysiologic severity progressed. Conversely, symptoms and pain did not increase as the classification of neurophysiologic severity progressed: 1) A large part of the CTS population complained of severe symptoms, although minimal functional impairment and minimal or no electrophysiologic abnormalities were observed; and 2) symptoms improved in the patients with more severe neurophysiologic and clinical examination scenarios.Multiperspective and multimeasurement assessment, even when using a validated patient-oriented tool, provided interesting information that confirmed and clarified the clinical neurophysiologic dissociation often observed in carpal tunnel syndrome (CTS) patients. Furthermore, CTS appeared to be an ideal model for evaluating the importance of patient-oriented measurement.

Fibroblast growth factor-2 (FGF-2), administered to the isolated rat heart by perfusion and under constant pressure, is protective against ischemia-reperfusion (I-R). Here we have investigated whether FGF-2 cardioprotection: (a) is dependent on flow modulation; (b) is linked to effects on contractility; (c) is mediated by protein kinase C (PKC); and (d) is linked to PKC and/or mitogen activated protein kinase (MAPK) associated with the sarcolemma. The isolated rat heart was used as a model. Under conditions of constant flow FGF-2 induced significant improvement in recovery of contractile function during I-R. Under constant perfusion pressure, FGF-2 induced a negative inotropic effect (15% decrease in developed pressure). Chelerythrine, a specific PKC inhibitor, prevented both the FGF-2-induced negative inotropic effect before ischemia, and cardioprotection during I-R. FGF-2 induced a chelerythrine-preventable, five-fold increase in sarcolemmal calcium-independent PKC activity. It also increased the association of PKC subtypes -epsilon and -delta with sarcolemmal membranes, detected by Western blotting, as well as, for PKC delta, by immunolocalization. FGF-2 increased the association of PKC epsilon with the membrane fraction of adult cardiomyocyte in culture, confirming that it can affect PKC signaling in cardiomyocytes directly and in a manner similar to its effects in situ. Finally, FGF-2 induced increased active MAPK at sarcolemmal as well as cytosolic sites. Active sarcolemmal MAPK remained elevated when the FGF-2-induced protection was prevented by chelerythrine. In conclusion, we have provided evidence that cardioprotection by FGF-2 is independent of flow modulation. PKC activation mediates both the FGF-2-induced negative inotropic effect before ischemia and the cardioprotective effect assessed during reperfusion, suggesting a cause and effect relationship. Furthermore, FGF-2 cardioprotection is linked to targeting of sarcolemmal sites by calcium-independent PKC.

The Italian CTS Study Group performed a wide multicentric and multiparametric study to quantify the increase of electrodiagnostic sensitivity using an extended neurophysiological protocol and particularly segmental and comparative tests. The study also evaluated the clinical features of carpal tunnel syndrome (CTS) diagnosed by these tests, using validated physician- and patient-oriented measurements. The study group was composed of 740 patients for a total of 1123 idiopathic CTS hands. Overall, the sensitivity of standard tests (median digit-wrist sensory conduction velocity and wrist-thenar distal motor latency) was 83.5%. Comparative/segmental tests disclosed abnormal findings in a further 11.4% of cases, providing CTS electrodiagnosis in about 7 of 10 "standard negative" cases. The overall sensitivity of the electrodiagnostic protocol was 94.9%. The CTS population diagnosed by segmental/comparative tests had a clinical picture characterized by a high percentage of pain, and severe discomfort but no limitation in functional daily activity. Our data confirm the usefulness of a complete neurophysiological assessment by using segmental/comparative tests when standard tests yield normal results.

We read with interest the recent report by Padua et al 1 on a body building champion with an isolated mononeuropathy of a distal branch of the femoral nerve, having recently seen a similar patient, with a different cause. A 39 year old sports physiologist underwent a resting muscle biopsy using the Bergstrom technique, for research purposes. He had previously undergone eight of these biopsies on the other leg without adverse effect, and this biopsy was performed by an experienced operator. Under lignocaine anaesthesia the biopsy needle was inserted. As manual suction was applied followed immediately by closing the biopsy needle, the subject had an intense feeling of cramp (that had not been noticed with previous biopsies). The …

The myelodysplastic syndromes comprise a heterogeneous group of neoplastic disorders characterized by ineffective hematopoiesis with an increased tendency to evolve to acute leukemia. Clinically, the common manifestations include peripheral blood cytopenias of one or more lineages and a normal to hyperplastic marrow. MDS has been defined on the basis of morphological criteria, namely the percentage of blast cells in the bone marrow, by the French-American-British study group. Scoring systems have been developed to include such factors as hemoglobin, leukocyte count and age in the evaluation of MDS prognosis. Although useful in the prediction of clinical course and design of therapy regimens, our understanding of the basis of MDS has come from recent advances in molecular analysis of these disorders. This review describes some of the established and recent contributions to our understanding of the molecular basis of the myelodysplastic syndromes.The authors of the present review have been working in the field of myelodysplastic syndromes for several years and have contributed original papers on the molecular pathogenesis of these disorders. In addition, in the present review they have critically examined articles and abstracts published in journals covered by the Science Citation Index and Medline.Cytogenetic anomalies and proto-oncogene abnormalities point to new understanding of the pathogenesis of MDS as a sequence of DNA lesions leading to the evolution of the pre-malignant clone. The prognostic significance of these factors in predicting leukemic transformation and survival remains controversial. Characterization of MDS cells in vitro in response to combinations of exogenous growth factors have not only provided valuable information regarding ineffective hematopoiesis in MDS but have provided a new insight into treatment of MDS. One major development in our understanding of MDS is the possible explanation for the apparent paradox of a cellular marrow in combination with peripheral cytopenias. Extensive premature programmed cell death or apoptosis has been reported to be at least partly responsible. It will remain to be seen whether this fundamental characteristic of myelodysplastic hematopoiesis will play a central role in the drug or genetic based therapy in the myelodysplastic syndromes.

Basic fibroblast growth factor (bFGF, or FGF-2) is a 18–25-kDa basic protein found in variable amounts in all tissues examined (see [1] for a recent review). It is highly conserved between species and belongs to a large family of FGF growth factors (FGF 1—9) with which it shares 40%–50% sequence homology; another widely studied member of this family is acidic FGF (FGF -1). As is the case with several other types of signaling polypeptides, bFGF is multifunctional. It is a mitogen for cells of mesodermal and neuroectodermal origin, affecting differentiation, motility, gene expression, and response to injury [1]. Although bFGF is found in the basement membrane and extracellular matrix, its mode of secretion is unknown, and it is considered primarily an intracellular molecule. There are few reports of bFGF detected in the serum, raising the possibility of an endocrine activity; however, this molecule is believed to act locally, in a paracrine or autocrine fashion, presumably by binding to tyrosine kinase cell surface receptors [2]. Heparan sulfate proteoglycans at the cell surface are considered to act as “low”-affinity bFGF receptors and have been shown to be important for the biololgical activity of bFGF in several systems [3].

To examine whether basic fibroblast growth factor (bFGF) administered to the heart by perfusion can improve cardiac resistance to injury we employed an isolated rat heart model of ischemia-reperfusion injury and determined the extent of functional recovery in bFGF-treated and control hearts. Global ischemia was simulated by interruption of flow for 60 min. Recovery of developed force of contraction (DF), recorded after reestablishment of flow for 30 min, reached 63.8 +/- 1.5% and 96.5 +/- 3.5% of preischemic levels in control and bFGF-treated hearts (10 micrograms/heart), respectively, indicating that bFGF induced significantly improved recovery of mechanical function. Recoveries of the rates of contraction or relaxation were also significantly improved in bFGF-treated hearts. Extent of myocardial injury, assessed by determination of phosphocreatine kinase in the effluent, was reduced as a result of bFGF treatment. As a first step towards understanding the mechanism and direct cellular target(s) of bFGF-induced cardioprotection, we investigated its fate after perfusion. Perfusion of 10 micrograms bFGF/heart resulted in a 4-fold increase in bFGF associated with the heart compared to control levels, as estimated by biochemical fractionation and immunoblotting. Immunofluorescent staining of the bFGF-perfused hearts revealed intense anti-bFGF staining in association with blood vessels as well as the periphery of cardiomyocytes, suggesting that the latter may be a target for direct bFGF action. In conclusion, our findings of bFGF-induced increases in cardiac resistance to, and improved functional recovery from, ischemia-reperfusion injury indicate that bFGF may have clinical applications in the treatment of ischemic heart disease.

Ventricular myocytes of the adult mammalian myocardium are considered essentially incapable of regeneration. These cells cease dividing soon after birth and subsequent cardiac growth is brought about by increases in cellular size (hypertrophy) rather than cell number [1]. Following irreversible injury and death of cardiomyocytes, caused by a variety of factors such as ischemia, excess catecholamines or genetic defects, necrotic muscle becomes replaced by scar tissue. The remaining myocardium hypertrophies to meet the need for extra work but beyond a certain potential for adaptation, cardiac failure ensues. There is some evidence that ventricular myocytes may not have lost their proliferative potential irreversibly, since they can be stimulated to synthesize DNA in culture [2] and are apparently capable of a hyperplastic response in hypertrophie or ageing hearts [3].

Extracts from bovine pituitaries and other tissues contained basic fibroblast growth factor-like peptides of 22-26 kda, co-fractionating with smaller, 16-20 kda bFGFs. Heparin-bound, 22-26 kda bFGFs were converted to smaller, heparin-binding forms by tryptic proteolysis. In solution, 22-26 kda bFGFs were converted to smaller, heparin-binding forms by an activity present in pituitary extracts. Calcium protected higher molecular weight pituitary bFGFs from truncation by the endogenous activity, which was not acid-activated, co-purified with bFGF during heparin-sepharose chromatography, remained operant at high salt concentrations and was inhibited by phenylmethan-sulfonyl fluoride.

Immunoglobulins reactive against basic fibroblast growth factor (bFGF) were obtained from the serum of a single rabbit immunized against residues [1-24] of bFGF conjugated to keyhole limpet hemocyanin (KLH). Pure immunoglobulin preparations no. 1 and no. 2 were prepared using different affinity chromatography columns and preabsorption to KLH-coupled Sepharose for preparation no. 1. Both preparations no. 1 and no. 2 were specific for bFGF in in vitro assays. Competition with synthetic peptides suggests that preparations no. 1 and no. 2 recognize predominantly epitope(s) within residues [16-24]bFGF or residues [1-10]bFGF, respectively, in situ. Furthermore, no. 2 (but not no. 1) antibodies can react with tissue-(heparin-)-bound antigen. When used in indirect immunofluorescence for bFGF in frozen heart sections, preparation no. 1 stained predominantly muscle intercalated discs (IcDs); muscle nuclei were also stained, in an overall punctate fashion. Preparation no. 2 stained muscle nuclei strongly, in association with the nuclear envelope; it also stained basement-membrane associated bFGF. Differences in immunostaining were also observed in uterine smooth muscle and kidney sections but not in skeletal muscle. It is plausible that accessibility of various epitopes within the amino-terminal region depends strongly on the local interactions of bFGF. Our data illustrate the importance of using several different antibodies to localize bFGF in a tissue.

We randomised 31 patients with acute tears of the anterior cruciate ligament (ACL) to receive either early (within 2 weeks) or delayed (8 to 12 weeks) reconstruction using a quadruple hamstring graft in order to determine if there was any functional advantage to early reconstruction. Outcome measures included return of knee movement, muscle dynamometry, International Knee Documentation Committee (IKDC) scores and Tegner activity levels.Two cases of symptomatic deep-venous thrombosis occurred in the early group. The mean range of movement was significantly greater at two weeks in the delayed group. Quadriceps muscle power was significantly better in the delayed group at 12 weeks (p < 0.05). These trends were evident at later time points, but were not statistically significant. One patient in each group had clinically significant knee stiffness at 52 weeks. IKDC scores and Tegner activity levels were not significantly different at 52 weeks. We conclude that there is no functional advantage to be gained by e...

Testicular endocrine function and androgen-dependent secondary sexual characteristics were assessed in 283 men 18 to 96 years of age. Mean serum total testosterone levels remained unchanged up to age 70 and declined thereafter. In 29 per cent of the men over 70 years of age total testosterone levels were below the lower limit of normal for young adults, In contrast, mean free or unbound testosterone levels declined after age 50 and were below the lower limit of normal for young adults in 40 per cent of the men over 70 years of age. Serum-luteinizing hormone and follicle-stimulating hormone levels showed a slight but steady rise after age 40 which became more abrupt after age 70. Serum gonadotropin levels were elevated in approximately 60 per cent of the men over 70 years of age. Mean testis length and volume were decreased in 78 per cent and 37 per cent, respectively, of the men over 60 years of age. Facial, pubic and axillary hair were also reduced in amount whereas the prostate was enlarged in 73 per cent of the elderly men. There appeared to be an inverse relationship in older men between testicular size and gonadotropin levels, and a direct relationship between testicular and prostatic sizes. It would appear that some degree of Leydig cell hypofunction commonly begins at around 45 to 50 years of age, becoming more pronounced after age 70. The concomitant elevation in serum gonadotropin levels at this time indicates that this is due to a primary decline in testicular function and is not secondary to pituitary hypofunction.

Peanut flour (PF), whey protein concentrate (WPC), sodium caseinate (SC) and blends of WPC/PF or SC/PF at peanut protein concentrations of 25, 40 and 50% were dispersed in water at 7.0% protein. The dispersions were extensively dialyzed against 11.0% reconstituted nonfat dry milk followed by heating at 60 and 80°C for 1 h. K-Carrageenan was added to dialyzed dispersions at levels of 0.1, 0.15 and 0.2% followed by heating at 80°C for 1 h. Soluble protein was estimated in supernatants following mid-speed (MS) centrifugation (40,000 x g for 20 min) and ultra-speed (US) centrifugation (200,000 x g for 1 h) at 25° C. Viscosity of protein/carrageenan dispersions was evaluated from Brookfield viscometer data fitted to the power law function. Soluble protein in PF dispersions was lower than that of the milk proteins examined. Increased centrifugation force from MS to US did not affect soluble protein of PF while supernatant protein in the milk proteins decreased with increased centrifugation force. Increased levels of PF in the milk protein/PF blends generally resulted in lowered soluble protein. Heat treatment increased PF soluble protein, decreased WPC solubleprotein and had minimal effect on SC, SC/PF and WPC/PF soluble protein. Carrageenan addition generally increased PF and WPC/PF soluble protein, lowered WPC soluble protein and did not affect SC and SC/PF soluble protein. All heated protein/carrageenan systems exhibited pseudoplastic (shear-thinning) flow behavior. Highest viscosity and consistency index (κ) values were observed for WPC and for blends containing WPC. κ values for all proteidcarrageenan mixture increased with increased levels of carrageenan.