Directional control-response relationships for mining equipment.

A variety of directional control-response relationships are currently found in mining equipment. Two experiments were conducted in a virtual environment to determine optimal direction control-response relationships in a wide variety of circumstances. Direction errors were measured as a function of control orientation (horizontal or vertical), location (left, front, right) and directional control-response relationships. The results confirm that the principles of consistent direction and visual field compatibility are applicable to the majority of situations. An exception is that fewer direction errors were observed when an upward movement of a horizontal lever or movement of a vertical lever away from the participants caused extension (lengthening) of the controlled device, regardless of whether the direction of movement of the control is consistent with the direction in which the extension occurs. Further, both the control of slew by horizontally oriented controls and the control of device movements in a frontal plane by the perpendicular movements of vertical levers were associated with relatively high rates of directional errors, regardless of the directional control-response relationship, and these situations should be avoided. STATEMENT OF RELEVANCE: The results are particularly applicable to the design of mining equipment such as drilling and bolting machines, and have been incorporated into MDG35.1 Guideline for bolting & drilling plant in mines (Industry & Investment NSW, 2010). The results are also relevant to the design of any equipment where vertical or horizontal levers are used to control the movement of equipment appendages, e.g. cranes mounted to mobile equipment and the like.

Fatal non-bacterial thrombotic endocarditis following viperine bite.

Non-bacterial thrombotic endocarditis (NBTE) commonly occurs in patients with wasting disease (e.g. malignancy) or with valves damaged following trauma due to intra-cardiac foreign body, scarring or marked turbulence. Although disseminated intravascular coagulation (DIC) is well documented following viperine bite and the underlying mechanism of NBTE is thought to be DIC, there is no report of NBTE in humans following snake bite. We report a young male who following viperine bite developed local swelling, superficial gangrene of tissues at the site of bite, and oliguria and died following multiple cerebral infarcts and acute renal failure. The post-mortem examination showed NBTE of the aortic valve, multiple embolic infarcts of brain, spleen and kidneys, acute tubular necrosis and features of DIC in the brain in the form of fibrin thrombi in the capillaries, perivascular hemorrhages and necrosis.

Use of lndomethacin as an antipyretic agent in malignant reticulosis.

No abstract available.

A double-blind comparison of flupenthixol decanoate and fluphenazine decanoate in the treatment of chronic schizophrenia.

Sixty-four chronic stabilised schizophrenics were studied for 18 months in order to assess the possible difference in therapeutic effects and side effects between flupenthixol decanoate and fluphenazine decanoate. Although certain differences in the BPRS sub-scores in favour of flupenthixol were present at various stages in the study, there was no significant difference between the two drugs in the overall antipsychotic scores at the end of the assessment period; however, more patients on fluphenating required additional therpay for depression or anxiety during the trial period.

Computed tomography of rectal lymphoma.

We present two human immunodeficiency virus positive patients with rectal lymphoma who on CT both demonstrated similar appearances of the rectal tumour, consisting of concentric thickening of the rectal wall and thickening of the levator ani muscles.

Polychemotherapy in squamous cell carcinoma of the buccal mucosa.

Thirty-nine patients with previously untreated squamous cell carcinoma of the buccal mucosa were treated by two polychemotherapeutic regimens. The first regimen consisted of bleomycin and methotrexate (BLM-MTX): bleomycin 30 mg was given intravenously twice weekly, and methotrexate 25 mg intravenously twice weekly for 2 1/2 and two weeks, respectively. The second program consisted of Cytoxan (cyclophosphamide), methotrexate and 5-FU (CMF): methotrexate 25 mg twice weekly for two weeks, Cytoxan 100 mg/day for two weeks, and 5-FU 500 mg twice weekly for 1 1/2 weeks. All of the patients were evaluated one week after completion of their chemotherapy regimen. Although the patients were not randomly allocated to either treatment, they matched in age and extent of disease. High response rates (88.9%) were noted with the BLM-MTX combination, which is comparable to the best responses reported previously using cis-platinum, Oncovin (vincristine), and methotrexate. This may suggest that buccal cancers are highly sensitive to an initial treatment by BLM-MTX, and therefore the authors highly recommend its use as preoperative adjuvant therapy in patients who present with Stage III and IV (Mo) disease.

Identification of a ubiquitin-like protein in the mammalian vitreous humor.

An 8 kDa ubiquitin-like peptide (ULP) was isolated by high performance liquid chromatography from the rabbit vitreous humor, and the N-terminal amino acid sequence of this peptide showed complete homology with ubiquitin. Western blot revealed the presence of free ULP in both the iris-ciliary (IC) complex and the aqueous humor extracts. In the IC complex, fluorescence and immunoelectron microscopy detected high concentrations of ULP in the posterior epithelial cells, suggesting this tissue as a possible source of ULP in the ocular fluids. Significantly, this is the first time that the presence of free ULP has been reported in mammalian extracellular fluids. Furthermore, we recently demonstrated that the 8 kDa fraction of vitreous humor containing ULP is a potent inhibitor of protein synthesis [Banerjee et al. (1992): J Cell Biochem 49:66-73]. These findings taken together suggest a novel biological role for ULP in the control of lens cell growth.

Pericardiectomy for constrictive pericarditis: is prolonged inotropic support a bad omen?

Sixty-seven patients who underwent pericardiectomy for constrictive pericarditis at JIPMER, Pondicherry between 1987 and 1998 were the subjects of the study. Pre-operatively 70% of cases were in the New York Heart Association classes III and IV categories with clinical signs suggestive of constriction ie, raised jugular venous pressure in 99%, pleural effusion in 77%, pedal oedema in 61% and ascites in 55% of the cases. Seventy-five per cent of the cases underwent pericardiectomy through a median sternotomy and the rest via left anterolateral thoracotomy. Low cardiac output was evidenced in 70% of cases postoperatively which was managed by early institution and prolonged use of inotropes. There was 9% mortality especially in the early part of the experience. Tuberculous pathology was confirmed histologically in 57% cases. Sixty-three per cent of cases are presenting in follow-up in New York Heart Association class I. Prolonged use of inotropes instituted early in postoperative period is recommended to prevent postoperative ventricular dysfunction with adrenaline being the preferred inotrope. It is concluded that postoperative New York Heart Association class and long term survival were not significantly influenced by pre-operative New York Heart Association class, operative approach or peri-operative low cardiac output syndrome requiring prolonged inotropic support.

Alpha-adrenergic preservation of myocardial pH during ischemia is PKC isoform dependent.

alpha-adrenergic stimulation of patients with ischemic heart disease should intuitively impose a destructive stress. However, therapeutic alpha1-adrenergic receptor mediated cardioadaptation prior to myocardial ischemia protects ventricular mechanical function, promotes electrophysiologic stability, and preserves myocyte viability. Prior to an anticipated cardiac ischemic insult, alpha1-adrenergic preconditioning attenuates ischemic myocardial acidosis by a protein kinase C-(PKC) dependent mechanism. The alpha1-adrenoceptor can directly stimulate calcium-independent nPKC isoforms via diacylglycerol (DAG) or indirectly stimulate calcium-dependent cPKC isoforms through the release of intracellular calcium via inositol triphosphate, (IP3). We hypothesized that alpha1-adrenergic limitation of ischemic acidosis is mediated by the family of calcium-dependent PKC isoforms. [31P]NMR spectra were obtained in isolated, buffer perfused rat hearts treated with alpha1-adrenergic stimulation [phenylephrine (PE) 50 microM, 2 min]; PKC blockade [chelerythrine chloride, (Chel) 20 microM]; or stearoyl-arachidonoyl glycerol (SAG, a DAG analogue, 100 microM, 2 min) administered 10 min prior to ischemia. Control hearts were perfused under normoxic conditions for 20 min. All hearts were then subjected to global ischemia (20 min, 37.5 degrees C). Developed pressure (DP) and heart rate were recorded continuously. pHi was obtained from chemical shift of inorganic phosphate. Immunohistochemical staining was utilized to delineate the translocation and activation profiles of specific PKC profiles established with each stimulus. Pre-ischemic alpha1-adrenergic stimulation did attenuate the myocellular hydrogen ion accumulation during sustained normothermic ischemia (6.90 +/- 0.13 vs control 6.54 +/- 0.10; P < 0.05). General PKC inhibition abrogated this effect (end-ischemic pH 6.17 +/- 0.10; P < 0.05 vs control and PE). Ischemic acidosis was not attenuated following selective nPKC stimulation (SAG, 6.48 +/- 0.08; NS vs control). Myocellular immunohistochemical staining revealed translocation of the calcium-independent PKC-epsilon isoform in the calcium-dependent PKC (SAG) group, but not in response to alpha1-adrenergic stimulation. The results suggest that (1) alpha1-adrenoceptor stimulation limits ischemic acidosis, (2) alpha1-adrenergic stimulated attenuation of ischemic acidosis is PKC dependent, (3) direct nPKC stimulation with SAG does not limit ischemic acidosis, and (4) SAG stimulates nPKC-epsilon isoform activation where alpha1-adrenergic stimulation does not. We conclude that alpha1-adrenergic stimulation limits ischemic acidosis by a cPKC-dependent mechanism and that the mobilization of the IP3 arm by receptor stimuli suppresses PKC-epsilon thus permitting the limitation of ischemic acidosis.