Human growth hormone may be detrimental when used to accelerate recovery from acute tendon-bone interface injuries.

Background: There have been few scientific studies that have examined usage of human growth hormone to accelerate recovery from injury. The hypothesis of this study was that human growth hormone would accelerate tendon-to-bone healing compared with control animals treated with placebo in a rat model of acute rotator cuff injury repair.

Methods: Seventy-two rats underwent repair of acute rotator cuff injuries and were randomized into the following postoperative dosing regimens: placebo, and human growth hormone at 0.

Optimization of intraperitoneal injection anesthesia in mice: drugs, dosages, adverse effects, and anesthesia depth.

Purpose: The goals of the study were to find a safe intraperitoneal injection anesthesia protocol for medium-duration surgery in mice (e.g., embryo transfer/vasectomy) coupled with a simple method to assess anesthesia depth under routine laboratory conditions.

Potential of two-cell mouse embryos to develop to term despite partial damage after cryopreservation.

Approximately 18% of cryopreserved 2-cell mouse embryos of 26 different batches showed various degrees of morphological damage after the freeze-thaw process. Normal and damaged morphology were assessed by light microscopy and the ability of an embryo to develop in vitro to a blastocyst, or to develop to term, after transfer to foster mothers. Using vital stains such as Fluorescein-diacetate (FDA) and 4', 6-Diamidino-2-Phenylindole (DAPI) it was found that in approximately 82% of the cases, both of the 2 blastomeres of the cryopreserved embryos survived the freeze-thaw process; in 10% only one cell survived the process; and in 8% none survived.

Mice devoid of PrP are resistant to scrapie.

S.B. Prusiner proposed that the infectious agent of scraple, the prion, is PrPSc, a modified form of the normal host protein PrPC.

Local T cell responses induce widespread MHC expression. Evidence that IFN-gamma induces its own expression in remote sites.

Local inflammation induces increased expression of MHC and other genes in the affected tissue because of the paracrine effects of cytokines such as IFN-gamma. We previously reported that one such process--local allograft rejection--was accompanied by increased expression of MHC in a remote tissue, namely kidney. To explore how local inflammation affects gene expression in remote tissues, we studied MHC, beta 2-microglobulin, and IFN-gamma expression in mice undergoing either of two T cell-dependent localized inflammatory processes: rejection of an ascites tumor allograft, and skin sensitization by oxazalone.

The elimination of mouse hepatitis virus by temporary transplantation of human tumors from infected athymic nude mice into athymic nude rats (rnuN/rnuN).

A nude mouse colony held in an isolation unit was found to harbor MHV despite the fact that all hygienic precautions were taken. The virus spread rapidly causing a high mortality rate predominantly in experimental animals. Moreover, we observed a high percentage of tumor regression in our tumor transplanted mice.

Regulation of MHC expression in vivo. II. IFN-alpha/beta inducers and recombinant IFN-alpha modulate MHC antigen expression in mouse tissues.

We examined the effect of type I IFN inducers and rIFN-alpha on MHC expression in mouse tissues in vivo. MHC expression was assessed in a radiolabeled mAb binding assay and by indirect immunoperoxidase staining of tissue sections. polyI:C, an inducer of IFN-alpha/beta, induced large increases in class I MHC in many tissues, with little effect on class II expression.

Increased class I and class II MHC products and mRNA in kidneys of MRL-lpr/lpr mice during autoimmune nephritis and inhibition by cyclosporine.

The expression of MHC products in the kidneys of MRL-1pr/1pr mice was investigated. As previously described, these mice develop lupus-like nephritis with intraglomerular and peritubular Ig deposition, vasculitis, and interstitial mononuclear cell infiltration at about 12 wk of age. As the nephritis appeared, the expression of MHC class I and II products rose, as demonstrated by absorption and by specific binding of radiolabeled antibodies.

Effects of cyclosporine on systemic MHC expression. Evidence that non-T cells produce interferon-gamma in vivo and are inhibitable by cyclosporine.

The ability of lipopolysaccharide to induce major histocompatibility complex hyperexpression in vivo in a variety of mouse tissues--particularly kidney--and the effect of cyclosporine on this process were studied. MHC expression was measured by a radiolabeled antibody-binding assay using tissue homogenates, as well as by assessment of tissue sections by indirect immunoperoxidase staining. LPS administered to mice in two doses, 4 days apart, induced an increase in class I expression in several tissues but also induced an increase in class II expression in kidney.

Cyclosporine blocks the induction of class I and class II MHC products in mouse kidney by graft-vs-host disease.

The ability of cyclosporine to prevent the increase in Ia and H-2K expression that occurs in mice with graft-vs-host disease (GVHD) was examined by means of absorption, indirect immunofluorescent staining (IIF), and indirect immunoperoxidase staining (IIP). Acute GVHD was induced in irradiated C3H/HeJ mice (H-2k) by injections of bone marrow and spleen cells from C57BL/6J mice (H-2b). Ten days after induction of acute GVHD, the spleens of mice not receiving cyclosporine expressed only donor Ia, reflecting their reconstitution by donor cells.