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J Surg Res. 2002 Jun 15;105(2):234-42.
Antiproteolytic action of insulin in burn-injured rats.

Solomon V, Madihally S, Mitchell RN, Yarmush M, Toner M.

Shriners Burns Hospital, Surgical Services and Center for Engineering in Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, 02114, USA.

BACKGROUND: Negative nitrogen balance is a typical metabolic response to burn injury resulting in decreased muscle mass and activity. Since insulin is an anabolic hormone, using insulin as a prophylactic agent in burned patients has received some attention. The present study was carried out to investigate the systemic effect of insulin on burn injury-induced muscle wasting. PATIENTS AND METHODS: A 15-20% total body surface area (TBSA) scald burn injury was inflicted on the shaved dorsum of rats. Rats were treated with a daily subcutaneous insulin injection for 3 days (0.25-1.0 U/day). After the treatment, a variety of insulin-dependent physiological parameters were monitored. Overall body protein degradation rates were determined by measuring the urinary tyrosine. Also, protein degradations were measured in diaphragm muscles, splenocytes, and peripheral blood mononuclear cells to directly confirm the antiproteolytic activity of insulin. RESULTS: Administration of insulin to burn-injured rats restored body weight primarily by reducing accelerated protein degradation and regaining the intracellular protein content in individual skeletal muscle. The measured physiological parameters showed no possible side effects. Protein degradation in immune cells was also suppressed after the therapy. CONCLUSION: Results indicate that lower dose insulin particularly suppresses protein degradation without causing secondary effects. It may be a useful approach to preventing burn injury-induced muscle wasting and also has a potential to improve immune response.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12121712&dopt=Abstract

J Clin Oncol. 2003 Jan 1;21(1):28-34.
Incidence of invasive breast cancer by hormone receptor status from 1992 to 1998.

Li CI, Daling JR, Malone KE.

Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA. cilhcrc.org

PURPOSE: Between 1987 and 1998, breast cancer incidence rates rose 0.5%/yr in the United States. A question of potential etiologic and clinical importance is whether the hormone receptor status of breast tumors is also changing over time. This is because hormone receptor status may reflect different etiologic pathways and is useful in predicting response to adjuvant therapy and prognosis. METHODS: Age-adjusted, age-specific breast cancer incidence rates by estrogen receptor (ER) and progesterone receptor (PR) status from 1992 to 1998 were obtained and compared from 11 population-based cancer registries in the United States that participate in the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program. RESULTS: From 1992 to 1998, the overall proportion of breast cancers that were ER-positive and PR-positive increased from 75.4% to 77.5% (P =.0002) and from 65.0% to 67.7% (P <.0001), respectively, continuing trends observed before 1992. These increases were limited to women 40 to 69 years of age. The proportions of ER-positive/PR-positive tumors increased from 56.7% to 62.3% (P =.0010) among 40- to 49-year-olds, from 58.0% to 63.2% (P =.0002) among 50- to 59-year-olds, and from 63.2% to 67.9% (P =.0020) among 60- to 69-year-olds. CONCLUSION: From 1992 to 1998, the proportion of tumors that are hormone receptor-positive rose as the proportion of hormone receptor-negative tumors declined. Because the incidence rates of hormone receptor-negative tumors remained fairly constant over these years, the overall rise in breast cancer incidence rates in the United States seems to be primarily a result of the increase in the incidence of hormone receptor-positive tumors. Hormonal factors may account for this trend.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12506166&dopt=Abstract

Brain Res Bull. 2002 May;58(1):67-75.
Glial fibrillary acidic protein immunodetection and immunoreactivity in the anterior and posterior medial amygdala of male and female rats.

Rasia-Filho AA, Xavier LL, dos Santos P, Gehlen G, Achaval M.

Laboratorio de Histofisiologia Comparada, Departamento de Ciencias Morfologicas, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil. aarfrgs.br

The medial amygdala (MeA) has receptors for gonadal hormones and modulates reproductive behaviors in rats. Adult male and female rats were used for the immunodetection, a less accurate technique, and the immunohistochemistry for the astrocytic marker glial fibrillary acidic protein (GFAP) in the anterior and posterior MeA. Both procedures were done using polyclonal anti-GFAP and were quantified by densitometry. The first technique provided no evidence for a difference between sexes in the immunocontent of GFAP in any region of the MeA (p > 0.1). Nevertheless, the measure of the intensity of GFAP immunoreactivity (GFAP-IR) showed that females had a higher GFAP-IR in the posterodorsal (p < 0.01) and in the posteroventral subregions of the MeA (p < 0.01) than males. No sex difference was found in its anterodorsal part (p > 0.1). The present results point out the differences between these two above-mentioned techniques but add a new finding to the previously described sexual dimorphism in the MeA, i.e., the GFAP-IR. Data also suggest that probably astrocytes can be affected by sex steroids in this brain area. It is likely that this regionally specific difference in the GFAP-IR may contribute to the distinct functional roles that the MeA subregions have in male and female rats. 2002 Elsevier Science Inc.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12121815&dopt=Abstract

Endocr Relat Cancer. 2002 Jun;9(2):103-13.
A critical reappraisal of MIB-1 labelling index significance in a large series of pituitary tumours: secreting versus non-secreting adenomas.

Jaffrain-Rea ML, Di Stefano D, Minniti G, Esposito V, Bultrini A, Ferretti E, Santoro A, Faticanti Scucchi L, Gulino A, Cantore G.

Department of Experimental Medicine, Universita degli Studi di L'Aquila, Via Vetoio, Coppito 2, 67100 L'Aquila (AQ), Italy. jaffrain.ml.reatamail.com

Pituitary tumours are usually benign neoplasia, but may have a locally aggressive or malignant evolution. This study aimed to identify factors which mostly influence their proliferative activity, in order to clarify its value for clinical and research purposes. The proliferative index was determined in a prospective series of 132 pituitary tumours as the percentage of monoclonal antibody MIB-1-immunopositive cells and referred to as the MIB-1 labelling index (LI). Its distribution was analysed according to both univariate and multivariate models. A life-threatening pituitary tumour is presented separately. The mean LI was 1.24+/-1.59%, with significant differences between clinically secreting (CS) and clinically non-secreting (CNS) adenomas. In CS adenomas (n=65), LI was highly variable and markedly influenced by pre-operative pharmacological treatment (0.80+/-1.03 vs 2.06+/-2.39% in treated vs untreated cases, P=0.009); it decreased with patient's age (P=0.025, r=0.28) and increased with tumour volume and invasiveness. The influence of pre-operative treatment and macroscopic features on LI in this group was confirmed by multivariate analysis. In CNS adenomas (n=67), LI distribution was less variable than in CS adenomas (P<0.0001), it was age-independent and correlations with tumour volume, invasiveness or recurrence did not reach significance. In a rapidly growing parasellar tumour, the mean LI was 24% at first surgery and exceeded 50% at second surgery performed 4 months later. LI should be interpreted according to hormone secretion and pre-operative treatment. Unusually high LI values deserve particular attention.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12121834&dopt=Abstract

Am J Physiol Regul Integr Comp Physiol. 2002 Aug;283(2):R349-55.
Myogenic reactivity is reduced in small renal arteries isolated from relaxin-treated rats.

Novak J, Ramirez RJ, Gandley RE, Sherwood OD, Conrad KP.

Department of Obstetrics, University of Pittsburgh School of Medicine and Magee-Womens Research Institute, Pennsylvania 15213, USA.

Administration of the ovarian hormone relaxin to nonpregnant rats vasodilates the renal circulation comparable to pregnancy. This vasodilation is mediated by endothelin (ET), the ET(B) receptor, and nitric oxide. Furthermore, endogenous relaxin mediates the renal vasodilation and hyperfiltration that occur during gestation. The goal of this study was to investigate whether myogenic reactivity of small renal and mesenteric arteries is reduced in relaxin-treated rats comparable to the pregnant condition. Relaxin or vehicle was administered to virgin female Long-Evans rats for 5 days at 4 microg/h, thereby producing midgestational blood levels of the hormone. The myogenic responses of small renal arteries (200-300 microm in diameter) isolated from these animals were evaluated in an isobaric arteriograph system. Myogenic reactivity was significantly reduced in the small renal arteries from relaxin-treated compared with vehicle-treated rats. The reduced myogenic responses were mediated by the ET(B) receptor and nitric oxide since the selective ET(B) receptor antagonist RES-701-1 and the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester restored myogenic reactivity to virgin levels. The influence of relaxin was not limited to the renal circulation because myogenic reactivity was also reduced in small mesenteric arteries isolated from relaxin-treated rats. Thus relaxin administration to nonpregnant rats mimics pregnancy, insofar as myogenic reactivity of small renal and mesenteric arteries is reduced in both conditions.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12121847&dopt=Abstract

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