Sun-climate connections. Earth's response to a variable Sun.
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Journal Article↗
Biomedical subjects
J Lean
Publications and source records attributed to J Lean.
Solar cycle variability, ozone, and climate
Results from a global climate model including an interactive parameterization of stratospheric chemistry show how upper stratospheric ozone changes may amplify observed, 11-year solar cycle irradiance changes to affect climate. In the model, circulation changes initially induced in the stratosphere subsequently penetrate into the troposphere, demonstrating the importance of the dynamical coupling between the stratosphere and troposphere. The model reproduces many observed 11-year oscillations, including the relatively long record of geopotential height variations; hence, it implies that these oscillations are likely driven, at least in part, by solar variability.
Journal Article↗
The prognostic utility of the Silicone Study Classification System. Silicone Study Report 9. Silicone Study Group.
OBJECTIVE: To evaluate the reproducibility and the prognostic utility of the Retina Society and Silicone Study Classification Systems in eyes after surgery for severe proliferative vitreoretinopathy (PVR). DESIGN: Subgroup analysis of the Silicone Study--a randomized, multicentered, surgical trial. SETTING: Community and university-based ophthalmology clinics. MATERIALS: Three hundred forty eyes with preoperative and intraoperative evaluations using both systems of grading PVR (reproducibility study), and 287 eyes with preoperative and intraoperative evaluations using both systems of grading PVR and with a 24-month follow-up examination (prognosis study). INTERVENTIONS: Vitrectomy for PVR with long-acting perfluoropropane gas or silicone oil as the intraocular tamponade. OUTCOME MEASURES: Retinal reattachment, visual acuity ( > or = 5/200), intraocular pressure, corneal clarity, and the need for reoperation. RESULTS: The reproducibility of the Silicone Study Classification System was 64% (type of contraction), 77% (number of clock hours), 67% (posterior PVR), 88% anterior and posterior PVR), and 94% (anterior, posterior, and subretinal PVR). The reproducibility of the Retina Society Classification System was 99%. Using the Silicone Study Classification System, location of PVR predicted visual acuity (P=.004, chi 2 test for trend) and hypotony (P=.03, chi 2 test for trend). Using the Retina Society Classification System, the grade of PVR predicted only visual acuity (P=.01, chi 2 test for trend). For eyes with anterior and posterior PVR, there was a decreasing trend in successful visual acuity outcome with increasing severity of PVR (from C-3 to D-3, P=.02, chi 2 test for trend). CONCLUSIONS: Although the classification of PVR using the Silicone Study classification System was not reproducible for the type of contraction or for posterior PVR, identification of the anteroposterior extent of the PVR was prognostic of visual acuity and hypotony at 24 months. The joint knowledge of the location of PVR (using the Silicone Study Classification System) and the tightness of the funnel for retinas with 9 to 12 clock hours involved by fixed folds (using the Retina Society Classification System) has prognostic utility for eyes with anterior and posterior PVR.
Adult↗
Relationships between resistance to cross-linking agents and glutathione metabolism, aldehyde dehydrogenase isozymes and adenovirus replication in human tumour cell lines.
In a panel of 10 human tumour cell lines with no prior exposure to drugs in vitro, resistance to cisplatin correlated with resistance to the nitrogen mustard derivatives Asta Z-7557 (mafosfamide, an activated form of cyclophosphamide), melphalan and chlorambucil. Simultaneous treatment with DL-buthionine-S,R-sulfoximine did not enhance the toxicity of cisplatin or Asta Z-7557, and no correlation was found between drug resistance and cellular levels of metallothioneins (as judged by sensitivity to cadmium chloride), glutathione (GSH), GSH reductase, GSH transferase, or gamma-glutamyltranspeptidase. The two cell lines most resistant to Asta Z-7557 expressed aldehyde dehydrogenase cytosolic isozyme 1, found also in normal ovary, but not isozyme 3. Treatment of resistant cells with cisplatin or Asta Z-7557 inhibited cellular DNA synthesis and replication of adenovirus 5 to a lesser extent than in sensitive cells. The virus could be directly inactivated by both drugs prior to infection, subsequent replication being inhibited to the same extent in sensitive and resistant cells. In contrast to Asta Z-7557 and other DNA damaging agents, cisplatin was much more toxic to adenovirus (D37 0.022-0.048 microM) than to cells (D37 0.25-2.5 microM). The adenovirus 5 mutant Ad5ts125 having a G----A substitution was even more sensitive to cisplatin (D37 7-8 nM) than wild type virus and another mutant. Cisplatin was detoxified less by sonicated resistant resistant cells than sensitive cells, as judged by inactivation of Ad5ts125 added to the reaction mixture. It can be inferred that (i) the major differences in cellular resistance to cisplatin and Asta Z-7557 in the present material did not involve enhanced DNA repair or protection by metallothioneins or GSH, but were associated with the ability to continue cellular and viral DNA synthesis during treatment, (ii) resistance was not associated with less template damage, and (iii) the adenovirus genome may be a suitable probe for predicting tumour resistance to cisplatin and for elucidating the DNA sequence dependence of cisplatin toxicity.
Adenoviruses, Human↗
Genotoxicity and cell cycle effects of platinum-based imaging agents in cisplatin-resistant human tumour cells.
A series of cis-dichloroplatinum(II) 2,3-diaminopropionamide complexes synthesised as potential imaging agents was tested for activity against a human ovarian tumour cell line (CI-80-13S) with high natural resistance to cisplatin and carboplatin as compared with other human cells. The most potent compound, the dimethyl ester of dichloro-[4-(methyleneiminodiacetic acid)phenyl (2',3'-diamino-propionamide)]platinum(II) (complex III), exhibited toxicity towards CI-80-13S cells similar to that observed in other cell lines, an effect that was not shown by the ligand alone or by cis-dichloroplatinum(II) 2,3-diaminopropionamide. However, complex III ester reproduced the genotoxic effects of cisplatin as judged by differential inactivation of two strains of adenovirus and by inhibition of cellular DNA and RNA synthesis; no major differences in these properties were observed between CI-80-13S and cisplatin-sensitive cells. Substantial inhibition of DNA and RNA synthesis was found within 2 h of treatment, much earlier than the effect of cisplatin. Complex III ester, which was 30- to 100-fold less potent than cisplatin, inhibited cell cycle progression in a similar way to equitoxic cisplatin, with cells accumulating in G2 at a dose of low toxicity and being arrested in all stages at higher levels. The latter in combination with colcemid caused extensive fragmentation of CI-80-13S cells. These results suggest that the mechanism of toxicity of such complexes involves factors, in addition to DNA damage, which rapidly inhibit nucleic acid synthesis and overcome natural resistance to cisplatin in the CI-80-13S cell line.
Adenoviridae↗
Effects of adriamycin and etoposide on the replication of adenovirus 5 in sensitive and resistant human tumour cells.
Adenovirus is a potential probe for identifying and understanding drug sensitivity in primary, nonproliferating cultures of human normal and tumour cells but the scope and limitations of such an approach first need to be evaluated in established cell lines. For this purpose we have identified an ovarian tumour cell line (CI-80-13S) with natural resistance to adriamycin, etoposide and crosslinking agents compared with other human tumour lines. Resistance to adriamycin correlated poorly with resistance to etoposide in these cell lines (r = 0.05). Adenovirus replication in drug-treated cells (viral capacity) was found to be differentially inhibited in sensitive cells when the drug was administered to cells simultaneously with infection (adriamycin) or 20 hr after infection (etoposide). Viral capacity could not be inhibited by more than 90% in sensitive cells. In contrast, no such plateau was exhibited in the dose-responses of cell survival or inhibition of cellular DNA synthesis, both of which distinguished sensitive from resistant cells. Adenovirus was not inactivated by preincubation with high doses of adriamycin or etoposide, thus confirming that no functionally-relevant damage is directly induced by these agents in DNA. Uptake of adriamycin and etoposide was similar in sensitive and resistant cells and both agents blocked cells in the G2 phase of the cell cycle. Protein-linked DNA was induced in sensitive cells. The results indicate that (a) these drugs have two dose-dependent effects in cells, one of which does not inhibit replication of adenovirus; and (b) inhibition of adenovirus replication could in principle be used to predict sensitivity to adriamycin and etoposide.
Adenoviridae↗
Propionibacterium acnes lens abscess after traumatic implantation of intralenticular cilia.
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Abscess↗
Function of hormonally-induced corpora lutea in the domestic cat.
Hysterectomy (3 animals) or diversion of the uterine venous blood from the ovarian vasculature (3 animals) has no effect on the duration of hormonally-induced luteal activity in the pseudopregnant luteal-phase cat (control: 4 animals), suggesting that the uterus exerts no local or systemic influence on the duration of luteal function.
Journal Article↗
Peripheral progesterone concentrations in the luteal-phase ewe: effects of a beta-adrenergic receptor antagonist and two beta 2-adrenergic agonists.
Peripheral blood samples were collected at 10-min intervals from three conscious sheep in which ovulation had been induced 6-10 days previously using exogenous hormones. Saline was infused into a jugular vein for about 1 h, followed by the experimental drug for 1-2 h and followed by saline again for a further 2 h. The experiments were repeated following induced luteolysis and ovulation. The infusion of a beta-adrenergic antagonist (propranolol) into three conscious luteal-phase ewes decreased (P less than 0.05) the peripheral progesterone concentration in each animal. Infusions of beta 2-adrenergic agonists (ritodrine and salbutamol) increased (P less than 0.05) the progesterone concentration in four out of eight experiments. The beta-adrenergic antagonist decreased the heart rate and the beta 2-adrenergic agonist increased it; the arterial blood pressure and respiratory rate were unaffected. The decrease in the progesterone concentration in response to the beta-adrenergic antagonist suggests that the normal ovarian secretion of progesterone is partly the result of sympathetic stimulation, and that the sympathetic innervation of the ovary may have a physiological role in modulating progesterone secretion.
Albuterol↗
Influence of adrenergic receptors on ovarian progesterone secretion in the pseudopregnant cat and oestradiol secretion in the oestrous cat.
The infusion of isoprenaline or propranolol into the abdominal aorta of the pseudopregnant cat caused an increase or decrease respectively in the ovarian progesterone secretion rate. These observations suggest that the sympathetic innervation of the ovary has a physiological influence on normal progesterone secretion, and this mechanism may explain stress-related increases in progesterone concentrations. The infusion of isoprenaline or propranolol after the stimulation of follicular growth had no consistent or convincing effect on oestradiol secretion.
Animals↗