Post-polio syndrome. An emerging threat to polio survivors.

The manifestations of post-polio syndrome typically occur 20 to 40 years after an acute episode of poliomyelitis and are confined to previously affected muscles. Because of motor unit remodeling and direct mechanical damage, weakness increases in individual muscles until it exceeds their narrow margin of reserve and becomes clinically apparent. Although the exact cause is not clear, generalized weakness often occurs when several muscles are affected and various postural limb strategies used by the patient are no longer able to compensate for the loss of muscle strength. The mainstays of treatment are life-style changes to avoid overexertion and use of light-weight orthoses and assistive aids to unload the extremities. Exercise and surgery have a limited role in management.     

Selective enhancement of the tumour necrotic activity of TNF alpha with monoclonal antibody.

The binding and biological activity of human TNF alpha on endothelial and tumour cells has been studied in the presence of monoclonal antibodies (MAbs). In particular, one monoclonal antibody to TNF alpha (MAb 32) has been identified which failed to inhibit binding and cytotoxicity of TNF alpha on WEHI-164 tumour cells but which was a potent inhibitor of TNF alpha-induced endothelial cell procoagulant activity on bovine aortic endothelial cells. The ability of MAb 32 to inhibit selectively the actions of TNF alpha on endothelial cells but not on tumour cells suggests a mechanism for enhancement of the anti-tumour action of TNF alpha in vivo when in complex with this antibody. Treatment of tumour bearing mice (WEHI-164 and Meth A fibrosarcoma) with TNF alpha-MAb 32 complex resulted in a 5- to 10-fold enhancement in the potency of the cytokine in comparison to free TNF alpha. Complexes between this cytokine and other MAbs generally resulted in either no effect or inhibition of TNF alpha activity in vivo and in vitro. Neither intact MAb 32 nor FAb' fragments of MAb 32 showed any tumour regressive activity in the absence of TNF alpha. The FAb' fragments were equipotent to the bivalent form of the antibody in enhancing TNF alpha activity. These data provide evidence that it is possible to segregate the individual biological activities of TNF alpha with concomitant enhancement of the tumour regressive activity of the cytokine in vivo.     

The use of varicography to identify the sources of incompetence in recurrent varicose veins

We have studied patients with recurrent varicose veins which were incompletely controlled by a thigh tourniquet. We used varicography, (a phlebogram via the varices), to detect sites of incompetence. Thirty patients (mean age 46 years) were investigated, 38 limbs being subjected to varicography and surgery. A primary operation had been performed between 3 months and 30 years earlier. A non-thrombogenic contrast medium, sodium meglumine ioxaglate 320 (Hexabix 320) was used. Metal markers were placed alongside the limb to identify the site of perforating veins on the phlebograms. The principal value of the technique was in the identification of mid-thigh perforator incompetence (MTPI) as we cannot diagnose this accurately by clinical or Doppler-ultrasound examination. Varicography demonstrated MTPI in 15/38 limbs (39%) and in only one thigh was this not confirmed at exploration. Varicography can demonstrate short saphenous incompetence and this was mainly of value in 3 patients who had previously undergone attempted short saphenous ligation; in all 3 the short saphenous vein was present and had not been ligated. The technique was less useful in demonstrating recurrence in the groin. Overall varicography influenced the operation performed in 17/38 limbs (45%), its main value being in the diagnosis of MTPI.     

The graying of America: optometric considerations. Introduction

Normal and abnormal effects of aging impact greatly on individuals and their families. Health care providers must therefore be knowledgeable about how to care for elderly persons. In order to interact among elderly persons and within the aging network, optometrists need to have a broad understanding of gerontology.     

Plasma pyruvate kinase and creatine kinase activity in Becker muscular dystrophy

Plasma creatine kinase (CK) and pyruvate kinase (PK) were measured in 31 obligate carriers of Becker muscular dystrophy (BMD), 36 BMD patients and appropriate controls. Mean plasma CK was 108 U/l in obligate carriers and 62 U/l in 43 age- and sex-matched controls (P less than 0.001 carriers vs controls). Control CK reference range was 31-125 U/l (mean +/- 2 SD of log transformed values). Mean plasma PK was 40 U/l in obligate carriers and 34 U/l in 56 controls (P less than 0.02 carriers vs controls). Control PK reference range was 18-61 U/l. Values of CK above the reference range upper limit were found in 13 of 31 BMD obligate carriers but only 2 showed elevated PK values. The sensitivity of CK in determining BMD carrier status, although only 42%, was markedly better than PK at 6.5%. Mean plasma CK in BMD patients was 2366 U/l, a 19-fold increase over the control value of 127 U/l (P less than 0.001 patients vs controls). Control CK reference range was 40-316 U/l. In contrast, mean plasma PK in BMD patients was 353 U/l, only 7-fold higher than the mean control value of 57 U/l (P less than 0.001 patients vs controls). Control PK reference range was 22-126 U/l. Clearly, the estimation of plasma PK as a means of determining BMD carrier status is markedly inferior to CK. Previous reports of increased sensitivity of PK compared with CK may have been due to artefactually elevated PK levels produced during sample preparation.