Phytochemical-assisted green synthesis of CuFeOx nano-rose electrocatalysts for oxygen evolution reaction in alkaline media.

This study represents a green synthesis method for fabricating an oxygen evolution reaction (OER) electrode by depositing two-dimensional CuFeOx on nickel foam (NF). Two-dimensional CuFeOx was deposited on NF using in situ hydrothermal synthesis in the presence of Aloe vera extract. This phytochemical-assisted synthesis of CuFeOx resulted in a unique nano-rose-like morphology (petal diameter 30-70 nm), which significantly improved the electrochemical surface area of the electrode. The synthesized electrode was analyzed for its OER electrocatalytic activity and it was observed that using 75% Aloe vera extract in the phytochemical-assisted synthesis of CuFeOx resulted in improved OER electrocatalytic performance by attaining an overpotential of 310 mV for 50 mA cm-2 and 410 mV for 100 mA cm-2. The electrode also sustained robust stability throughout the 50 h of chronopotentiometry studies under alkaline electrolyte conditions, demonstrating its potential as an efficient OER electrode material. This study highlights the promising use of Aloe vera extract as a green and cost-effective way to synthesize efficient OER electrode materials.

Management of idiopathic granulomatous mastitis: a prospective study.

INTRODUCTION: Idiopathic granulomatous mastitis (IGM) is an evolving problem with varied presentation. No definite treatment guidelines are available at present that may reduce rate of recurrence. Current evidence suggests a ductal pathology behind IGM, which leads to periductal mastitis, leakage and sinus/fistula formation. Thus, excision of the sinus/fistulous tract with en-bloc wide local excision (WLE) of the lesion could be curative. The objective of this study was to look for the basic aetiology of IGM and evaluate the effectiveness of WLE with total or partial duct excision as a curative approach. METHODS: An institutional prospective comparative study was conducted over 4 years (2015-2019), in which 59 cases of IGM were randomly divided into three groups. After necessary investigations, patients in group A received steroid therapy, those in group B received WLE and patients in group C received WLE with total or partial duct excision as the mode of treatment. Postoperative follow-up was between 6 months and 3 years. RESULTS: Histopathological examination (HPE) was found to be the most suitable diagnostic procedure. Patients in group B showed the highest rate of recurrence (73.6%), followed by group A (35.0%) and group C (5.0%). Patients in group C had a significantly lower chance of recurrence compared with both group A and group B (p < 0.05). HPE reports of excised ducts from patients in group C showed ductal disruption and leakage along with periductal granuloma in 70% of cases. CONCLUSIONS: The presence of duct granuloma indicates the association of ductal pathology in IGM. IGM is therefore a disease of the mammary ducts and en-bloc duct excision is curative in non-responding cases.

Non-migratory tumorigenic intrinsic cancer stem cells ensure breast cancer metastasis by generation of CXCR4(+) migrating cancer stem cells.

Although the role of metastatic cancer stem cells (mCSCs) in tumor progression has been well documented, our study reveals a hitherto unidentified role of tumorigenic intrinsic CSCs (iCSCs) in breast cancer metastasis. We show that unlike highly migratory mCSCs residing in the breast tumor disseminating/peripheral regions, iCSCs populate the inner mass of the tumor and are non-migratory. However iCSCs, via paracrine signaling, induce conversion of non-stem cancer cells to CSCs that (i) are identical to the previously reported mCSCs, and (ii) in contrast to iCSCs, express chemokine receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), which is crucial for their metastatic potential. These mCSCs also demonstrate high in vivo tumorigenicity. Physical non-participation of iCSCs in metastasis is further validated in vivo, where only mCSCs are found to exist in the metastatic sites, lymph nodes and bone marrow, whereas the primary tumor retains both iCSCs and mCSCs. However, iCSCs ensure metastasis since their presence is crucial for deliverance of highly metastatic CXCR4(+) mCSCs to the migrating fraction of cells. Cumulatively, these results unveil a novel role of iCSCs in breast cancer metastasis as parental regulators of CXCR4(+) mCSCs, and highlight the therapeutic requisite of targeting iCSCs, but not CXCR4(+) mCSCs, to restrain breast cancer metastasis from the root by inhibiting the generation of mCSCs from iCSCs. Considering the pivotal role of iCSCs in tumor metastasis, the possibility of metastasis to be a 'stem cell phenomena' is suggested.

Nano-micro structured superhydrophobic zinc coating on steel for prevention of corrosion and ice adhesion.

Thin films of zinc have been deposited on steel substrates by electrodeposition process and further functionalized with ultra-thin films of commercial silicone rubber, in order to obtain superhydrophobic properties. Morphological feature, by scanning electron microscope (SEM), shows that the electrodeposited zinc films are composed of micro-nano rough patterns. Furthermore, chemical compositions of these films have been analyzed by X-ray diffraction (XRD) and infra-red (IRRAS). An optimum electrodeposition condition, based on electrical potential and deposition time, has been obtained which provides superhydrophobic properties with a water contact angle of 155±1°. The corrosion resistance properties, in artificial seawater, of the superhydrophobic zinc coated steel are found to be superior to bare steel. Similarly, the measured ice adhesion strength on superhydrophobic surfaces, using the centrifugal adhesion test (CAT), is found to be 6.3 times lower as compared to bare steel. This coating has promising applications in offshore environment, to mitigate corrosion and reduce ice adhesion.

Role of NF-κB as a Prognostic Marker in Breast Cancer : A Pilot Study in Indian Patients.

The nuclear factor κB (NF-κB) is a superfamily of transcription factors. It plays an important role in development & progression of cancer. This study was conducted in a tertiary care centre to investigate the significance of NF-κB as a prognostic marker in breast cancer and study its relation with established prognostic markers such as tumor grade, lymph node status, hormone receptor & HER-2/neu expression. We measured NF-κB expression of breast cancer tissue as a test sample & from fibroadenoma as a control. Measurement was done by Western Blot Technique using p65 protein of NF-κB super family of transcription factors. ER,PR and HER-2/neu were measured by immunohistochemistry methods. NF-κB/p65 is significantly associated with large tumor size (≥5 cm), high grade tumors, negative ER, negative PR, positive HER-2/neu and high NPI (≥5.4) scores. NF-κB/p65 expression implies aggressive biological behaviour of breast cancer & this study validates significant association of NF-κB /p65 overexpression with large tumor size, negative estrogen & progesterone receptor status and overexpression of c-erbB2 oncoprotein.

Estrogen inhibits D2S receptor-regulated Gi3 and Gs protein interactions to stimulate prolactin production and cell proliferation in lactotropic cells.

The neurotransmitter dopamine (DA) is known to inhibit prolactin (PRL) secretion and the proliferation of lactotropes in the pituitary gland. Dopamine-2 (D2) receptor short (D2S) isoform is expressed in a reduced level while the D2 receptor long (D2L) isoform is expressed in an elevated level during estradiol (E(2))-induced PRL production and cell proliferation in lactotropes. To evaluate the role of these D2 receptor isoforms in E(2)-regulated lactotropic cell function, we compared E(2) effects on the level of PRL, cell proliferation, and G proteins in enriched lactotropes and lactotrope-derived PR1 cells containing only D2S isoform (D2S cells), D2L isoform (D2L cells), or no D2 receptor (V cells). Additionally, we determined the effects of G protein blockade on the E(2)-induced PRL production and cell proliferation in these cells. We here show that E(2) actions on G proteins, PRL production, and cell proliferation were maximally achieved in D2S cells, oppositely or marginally achieved in D2L cells, and absent in V cells. We also show that the DA and pertussis toxin modulations of E(2) actions on PRL, G proteins, and cell proliferation were maximally achieved in D2S cells compared with in D2L or V cells. Furthermore, we provide evidence for the existence of an inhibitory action of Gi3 on Gs that is under the control of the D2S receptor and is inhibited by E(2). These results suggest that the suppression of D2S-regulated Gi3 inhibition of Gs protein may be one of the mechanisms controlling E(2)-activated PRL synthesis and cell proliferation in lactotropes.

Efficacy and safety of topical nadifloxacin and benzoyl peroxide versus clindamycin and benzoyl peroxide in acne vulgaris: A randomized controlled trial.

BACKGROUND: Topical therapy with comedolytics and antibiotics are often advocated for mild and moderate severity acne vulgaris. Nadifloxacin, a new fluoroquinolone with anti-Propionibacterium acnes activity and additional anti-inflammatory activity, is approved for use in acne. This randomized controlled assessor blind trial compared the clinical effectiveness and safety of eight weeks therapy of nadifloxacin 1% versus clindamycin 1% as add-on therapy to benzoyl peroxide (2.5%) in mild to moderate grade acne. MATERIALS AND METHODS: The efficacy parameters were changes in the total, inflammatory and non-inflammatory lesion counts, Investigator Global Assessment (IGA), and Cardiff Acne Disability Index (CADI) scales from baseline to study end (eight weeks). All treatment emergent dermatological adverse events were evaluated for safety assessment. RESULTS: Out of 84 randomized subjects (43-nadifloxacin arm) and (41-clindamycin) 42 in nadifloxacin group, 37 in clindamycin group completed the study. Reduction from baseline of total, inflammatory and non-inflammatory lesion counts were highly significant in both the groups (P<0.0001), but between group differences were not significant. Significant improvement in CADI and IGA scales were noted in both groups. Between-group comparison showed no significant differences. The safety and tolerability profile of both regimens were good and statistically comparable. CONCLUSIONS: Topical nadifloxacin, a new fluoroquinolone is effective, tolerable, and safe for mild o moderate facial acne. Its clinical effectiveness is comparable to clindamycin when used as add-on therapy to benzoyl peroxide.

Chemical nature of superhydrophobic aluminum alloy surfaces produced via a one-step process using fluoroalkyl-silane in a base medium.

Various surface characterization techniques were used to study the modified surface chemistry of superhydrophobic aluminum alloy surfaces prepared by immersing the substrates in an aqueous solution containing sodium hydroxide and fluoroalkyl-silane (FAS-17) molecules. The creation of a rough micronanostructure on the treated surfaces was revealed by scanning electron microscopy (SEM). X-ray photoelectron spectroscopy (XPS) and infrared reflection absorption spectroscopy (IRRAS) confirmed the presence of low surface energy functional groups of fluorinated carbon on the superhydrophobic surfaces. IRRAS also revealed the presence of a large number of OH groups on the hydrophilic surfaces. A possible bonding mechanism of the FAS-17 molecules with the aluminum alloy surfaces has been suggested based on the IRRAS and XPS studies. The resulting surfaces demonstrated water contact angles as high as ~166° and contact angle hystereses as low as ~4.5°. A correlation between the contact angle, rms roughnesses, and the chemical nature of the surface has been elucidated.

Synthesis of monodisperse fluorinated silica nanoparticles and their superhydrophobic thin films.

Monodispersive silica nanoparticles have been synthesized via the Stöber process and further functionalized by adding fluorinated groups using fluoroalkylsilane in an ethanolic solution. In this process, six different sizes of fluorinated silica nanoparticles of varying diameter from 40 to 300 nm are prepared and used to deposit thin films on aluminum alloy surfaces using spin coating processes. The functionalization of silica nanoparticles by fluorinated group has been confirmed by the presence C-F bonds along with Si-O-Si bonds in the thin films as analyzed by Fourier transform infrared spectroscopy (FTIR). The surface roughnesses as well as the water contact angles of the fluorinated silica nanoparticle containing thin films are found to be increased with the increase of the diameter of the synthesized fluorinated silica nanoparticles. The thin films prepared using the fluorinated silica nanoparticles having a critical size of 119 ± 12 nm provide a surface roughness of ∼0.697 µm rendering the surfaces superhydrophobic with a water contact angle of 151 ± 4°. The roughness as well as the water contact angle increases on the superhydrophobic thin films with further increase in the size of the fluorinated silica nanoparticles in the films.

Superhydrophobic aluminum alloy surfaces by a novel one-step process.

A simple one-step process has been developed to render aluminum alloy surfaces superhydrophobic by immersing the aluminum alloy substrates in a solution containing NaOH and fluoroalkyl-silane (FAS-17) molecules. Scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS) and water contact angle measurements have been performed to characterize the morphological features, chemical composition and superhydrophobicity of the surfaces. The resulting surfaces provided a water contact angle as high as ∼162° and a contact angle hysteresis as low as ∼4°. The study indicates that it is possible to fabricate superhydrophobic aluminum surfaces easily and effectively without involving the traditional two-step processes.

Dopamine, dopamine D2 receptor short isoform, transforming growth factor (TGF)-beta1, and TGF-beta type II receptor interact to inhibit the growth of pituitary lactotropes.

The neurotransmitter dopamine is known to inhibit prolactin secretion and the proliferation of lactotropes in the pituitary gland. In this study, we determined whether dopamine and TGFbeta1 interact to regulate lactotropic cell proliferation. We found that dopamine and the dopamine agonist bromocriptine stimulated TGFbeta1 secretion and TGFbeta1 mRNA expression but inhibited lactotropic cell proliferation both in vivo and in vitro. The dopamine's inhibitory action on lactotropic cell proliferation was blocked by a TGFbeta1-neutralizing antibody. We also found that PR1 cells, which express low amounts of the dopamine D2 receptor, demonstrated reduced expression of TGFbeta1 type II receptor and TGFbeta1 mRNA levels and had undetectable levels of TGFbeta1 protein. These cells showed a reduced TGFbeta1 growth-inhibitory response. Constitutive expression of the D2 receptor short isoform, but not the D2 receptor long isoform, induced TGFbeta1 and TGFbeta1 type II receptor gene expression and recovered dopamine- and TGFbeta1-induced growth inhibition in PR1 cells. The constitutive expression of D2 receptor short isoform also reduced the tumor cell growth rate. These data suggest that a TGFbeta1 system may mediate, in part, the growth-inhibitory action of dopamine on lactotropes.

Potential of gene therapy for the treatment of pituitary tumors.

Pituitary adenomas constitute the most frequent neuroendocrine pathology, comprising up to 15% of primary intracranial tumors. Current therapies for pituitary tumors include surgery and radiotherapy, as well as pharmacological approaches for some types. Although all of these approaches have shown a significant degree of success, they are not devoid of unwanted side effects, and in most cases do not offer a permanent cure. Gene therapy-the transfer of genetic material for therapeutic purposes-has undergone an explosive development in the last few years. Within this context, the development of gene therapy approaches for the treatment of pituitary tumors emerges as a promising area of research. We begin by presenting a brief account of the genesis of prolactinomas, with particular emphasis on how estradiol induces prolactinomas in animals. In so doing, we discuss the role of each of the recently discovered growth inhibitory and growth stimulatory substances and their interactions in estrogen action. We also evaluate the cell-cell communication that may govern these growth factor interactions and subsequently promote the growth and survival of prolactinomas. Current research efforts to implement gene therapy in pituitary tumors include the treatment of experimental prolactinomas or somatomammotropic tumors with adenoviral vector-mediated transfer of the suicide gene for the herpes simplex type 1 (HSV1) thymidine kinase, which converts the prodrug ganciclovir into a toxic metabolite. In some cases, the suicide transgene has been placed under the control of pituitary cell-type specific promoters, like the human prolactin or human growth hormone promoters. Also, regulatable adenoviral vector systems are being assessed in gene therapy approaches for experimental pituitary tumors. In a different type of approach, an adenoviral vector, encoding the human retinoblastoma suppressor oncogene, has been successfully used to rescue the phenotype of spontaneous pituitary tumors of the pars intermedia in mice. We close the article by discussing the future of molecular therapies. We point out that although, gene therapy represents a key step in the development of molecular medicine, it has inherent limitations. As a consequence, it is our view that at some point, genetic therapies will have to move from exogenous gene transfer (i.e. gene therapy) to endogenous gene repair. This approach will call for radically new technologies, such as nanotechnology, whose present state of development is outlined.

Regulation of gonadotropin releasing hormone release by neuropeptide Y at the median eminence during the preovulatory period in ewes.

The median eminence (ME) of the hypothalamus is known to be an important brain site where hypophysiotropic release might be regulated by excitatory and inhibitory signals impinging on their neuronal terminals. Since a role for neuropeptide Y (NPY) on preovulatory luteinizing hormone (LH) release has been suggested, we hypothesized that NPY might act at the ME to control preovulatory gonadotropin-releasing hormone (GnRH) release and thus the onset of the preovulatory surge of LH. To examine this possibility, we used the ewe as an animal model to determine: (a) immunocytochemical distribution of GnRH and NPY in the ewe ME; (b) changes in in vivo release of NPY and GnRH using ME push-pull cannula (PPC) perfusate samples, as well as in plasma LH, during the luteal, follicular and preovulatory phases of a synchronized estrous cycle, and (c) effects of ME perfusion of NPY or a Y1-NPY antagonist, or an NPY antiserum on in vivo release of ME-GnRH and plasma LH during a synchronized follicular phase. Immunolocalization reveals a dense plexus of beaded GnRH-containing neurites in the arcuate nucleus and in its vicinity, the pituitary stalk and the palisade. In contrast, a dense plexus of NPY-containing neurites occurs in the internal layer, with occasional fibers found in the intermediate and lateral external zone of the ME. In the area between the lateral internal and lateral external layers, both NPY and GnRH-containing processes were found, thus providing opportunities for synaptic and/or paracrine interactions between NPY- and GnRH-containing neurons. Hormonal analysis indicated that a synchronized preovulatory surge of LH is elicited within a 2-hour window by the sequential implantation and removal of silastic-encased estradiol (E2) or progesterone (P4) implants. In this paradigm, there was a parallel increase in ME release of both NPY and GnRH preceding the synchronized LH surge. The onset of this synchronized LH surge was advanced by ME perfusion of exogenous NPY and was both delayed and blunted by ME perfusion with the NPY antagonist (both were perfused through the PPC probe for 2 h, starting 2-3 h before the expected onset of the LH surge). In addition, NPY perfusion in the ME increases, while perfusion of the Y1-NPY antagonist or of the NPY antiserum decreases ME-PPC GnRH content and plasma levels of LH in early follicular ewes. Finally, perfusion of NPY antiserum during an ongoing LH surge disrupted LH release. These results suggest that interactions between NPY and GnRH neurons are important in controlling the timing, magnitude and maintenance of the preovulatory LH surge.

Chronic ethanol inhibits NK cell cytolytic activity: role of opioid peptide beta-endorphin.

The role of beta-endorphin (beta-EP) in ethanol-altered NK cell cytolytic activity is studied using male Fischer-344 rats as an animal model. Ethanol was administered for 1, 2, 3, or 4 wk in a liquid diet containing 8.7% ethanol (v/v), which means that 37% of the total calories were derived from ethanol. Rats treated with ethanol for 1 wk showed an increase in hypothalamic and plasma levels of immunoreactive (IR)-beta-EP, but displayed no significant effect on NK cell activity determined by (51)Cr release assay, as compared with those in pair-fed and ad libitum-fed animals. However, animals treated with ethanol for 2, 3, or 4 wk showed decreased hypothalamic and plasma levels of IR-beta-EP and decreased splenic NK cell activity. No significant decrease in the number of splenocytes and NK cells or in the percentage of NK cells was seen until after 3 and 4 wk of ethanol treatment. Exposure in vitro of splenic lymphocytes obtained from control animals to various concentrations of beta-EP increased NK cell activity. The opiate antagonist naltrexone blocked the beta-EP-stimulated effect. The in vitro NK cell response to beta-EP was reduced in the splenocytes obtained from animals treated with ethanol for 2 wk, but not in those obtained from animals treated with ethanol for 1 wk as compared with those in control animals. Additionally, beta-EP administration into the paraventricular nucleus of the hypothalamus stimulated NK cell cytolytic activity, whereas the opiate blocker administration reduced NK cell activity. The NK cell responses to paraventricular nucleus beta-EP were reduced in the animals treated with ethanol for 2 wk. These data provide evidence for the first time that ethanol inhibits NK cell cytolytic activity, possibly by reducing beta-EP-regulated splenic NK cell function.

Transforming growth factor-beta regulation of estradiol-induced prolactinomas.

Prolactin-secreting adenomas (prolactinomas) are the most prevalent form of pituitary tumors in humans, and increased tumor growth under estrogenic influence in female patients is often of clinical concern. Extensive experimental work has uncovered the roles of estrogen receptors and various growth-regulatory peptides in estradiol action on lactotropes. However, it is only recently that we are beginning to gain insight into how these growth factors interact to regulate estradiol action on lactotrope cell proliferation. Recent studies have identified the regulatory role of TGF-beta-related peptides in estradiol action on lactotropes. Additionally, these studies determined that TGF-beta and FGF interact to facilitate the communication between lactotropes and folliculostellate cells that is necessary for the mitogenic action of estradiol. This review addresses the role of estradiol in prolactinoma formation and summarizes data that support a novel concept: Alterations in the expression and action of TGF-beta isoforms are crucial steps in estradiol-induced tumorigenesis.

Role of estrogen in alcohol promotion of breast cancer and prolactinomas.

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chair was Dipak K. Sarkar. The presentations were (1) Dual role of estrogen as hormone and carcinogen in mammary carcinogenesis, by Joachim G. Liehr; (2) Alcohol and breast cancer: Studies using animals, by Keith W. Singletary; and (3) Evaluation of the role of estrogen in mediation of ethanol effect on prolactinoma: Studies using animals, by Dipak K. Sarkar.

Effects of finasteride on size of the prostate gland and semen quality in dogs with benign prostatic hypertrophy.

OBJECTIVE: To determine the effect of the 5alpha-reductase inhibitor finasteride on prostatic diameter and volume, semen quality, and serum dihydrotestosterone (DHT) and testosterone concentrations in dogs with spontaneous benign prostatic hypertrophy (BPH). DESIGN: Double-blind placebo-controlled trial. ANIMALS: 9 dogs with BPH. PROCEDURE: Five dogs were treated with finasteride for 16 weeks (0.1 to 0.5 mg/kg [0.05 to 0.23 mg/lb] of body weight, PO, q 24 h); the other 4 received a placebo. Prostatic diameter, measured radiographically, prostatic volume, measured ultrasonographically, semen quality, and serum DHT and testosterone concentrations were evaluated before and during treatment. After receiving the placebo for 16 weeks, the 4 control dogs were treated with finasteride for 16 weeks, and evaluations were repeated. RESULTS: Finasteride significantly decreased prostatic diameter (mean percentage decrease, 20%), prostatic volume (mean percentage decrease, 43%), and serum DHT concentration (mean percentage decrease, 58%). Finasteride decreased semen volume but did not adversely effect semen quality or serum testosterone concentration. No adverse effects were reported by owners of dogs in the study. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that finasteride can be used to reduce prostatic size in dogs with BPH without adversely affecting semen quality or serum testosterone concentration.

Effect of antisense suppression of transforming growth factor-beta3 gene on lactotropic cell proliferation.

The mechanism by which oestrogen regulates lactotropic cell proliferation is not well understood. Recently it has been shown that a transforming growth factor beta (TGF-beta) gene-related peptide, TGF-beta3, is produced in the lactotropes and stimulates lactotropic cell proliferation in vitro. In this study, the role of this growth factor in oestrogen-induced lactotropic cell proliferation was determined in vitro using oligonucleotide designed to inhibit TGF-beta3 gene expression. We used the oligonucleotide in an antisense orientation, which is complementary to regions in the TGF-beta3 message. Oligonucleotides in sense and missense orientation were also used. We found that the antisense sequence that was effectively incorporated into pituitary cells produced a marked inhibition of the stimulatory action of oestrogen on lactotropic cell proliferation. Sense and missense oligonucleotides produced no significant effects on oestrogen-stimulated lactotropic cell proliferation. The growth-inhibitory effect of antisense oligonucleotide was blocked by TGF-beta3 peptide. These results suggest that TGF-beta3 may be involved in the processes that mediate oestrogen-regulated lactotropic cell proliferation.

Transforming growth factor-beta1 induces transforming growth factor-beta1 and transforming growth factor-beta receptor messenger RNAs and reduces complement C1qB messenger RNA in rat brain microglia.

Transforming growth factor-beta1 is a multifunctional peptide with increased expression during Alzheimer's disease and other neurodegenerative conditions which involve inflammatory mechanisms. We examined the autoregulation of transforming growth factor-beta1 and transforming growth factor-beta receptors and the effects of transforming growth factor-beta1 on complement C1q in brains of adult Fischer 344 male rats and in primary glial cultures. Perforant path transection by entorhinal cortex lesioning was used as a model for the hippocampal deafferentation of Alzheimer's disease. In the hippocampus ipsilateral to the lesion, transforming growth factor-beta1 peptide was increased >100-fold; the messenger RNAs encoding transforming growth factor-beta1, transforming growth factor-beta type I and type II receptors were also increased, but to a smaller degree. In this acute lesion paradigm, microglia are the main cell type containing transforming growth factor-beta1, transforming growth factor-beta type I and II receptor messenger RNAs, shown by immunocytochemistry in combination with in situ hybridization. Autoregulation of the transforming growth factor-beta1 system was examined by intraventricular infusion of transforming growth factor-beta1 peptide, which increased hippocampal transforming growth factor-beta1 messenger RNA levels in a dose-dependent fashion. Similarly, transforming growth factor-beta1 increased levels of transforming growth factor-beta1 messenger RNA and transforming growth factor-beta type II receptor messenger RNA (IC(50), 5pM) and increased release of transforming growth factor-beta1 peptide from primary microglia cultures. Interactions of transforming growth factor-beta1 with complement system gene expression are also indicated, because transforming growth factor-beta1 decreased C1qB messenger RNA in the cortex and hippocampus, after intraventricular infusion, and in cultured glia. These indications of autocrine regulation of transforming growth factor-beta1 in the rodent brain support a major role of microglia in neural activities of transforming growth factor-beta1 and give a new link between transforming growth factor-beta1 and the complement system. The auto-induction of the transforming growth factor-beta1 system has implications for transgenic mice that overexpress transforming growth factor-beta1 in brain cells and for its potential role in amyloidogenesis.

Subjective and objective measurements of postoperative pain in cats.

OBJECTIVE: To evaluate the ability of various subjective and objective measurements to determine the presence and degree of postoperative pain in cats. DESIGN: Randomized controlled prospective clinical study. ANIMALS: 18 healthy client-owned cats. PROCEDURE: Cats were randomly assigned to 3 groups of 6: control, tenectomy, and onychectomy. Jugular catheters were placed the day prior to surgery. All surgeries were performed by the same surgeon, and all observations were made by the same blinded trained observer. One hour prior to surgery and at assigned intervals for 36 hours after surgery, heart rate, respiratory rate, and rectal temperature were measured. Scores were assigned for 3 interaction responses, including response to palpation, by use of simple descriptive scales, and to 2 pain assessments by use of visual analogue scales. Blood was collected to measure plasma beta-endorphin and cortisol concentrations. Butorphanol was administered to all cats before surgery and to any cat subjectively assessed to be experiencing pain after surgery. RESULTS: Only visual analogue scale scores and response to palpation scores differed significantly between control and surgical groups. CONCLUSIONS AND CLINICAL RELEVANCE: Determination of the presence of pain in cats can be made on the basis of observation and interaction by a trained observer. Physiologic measurements, including plasma cortisol and beta-endorphin concentrations, did not differentiate between control cats and cats that underwent surgery.