For much of their existence, these entities have escaped the rigors of competition, sheltered in part by tariffs filed with the Federal Communications Commission (FCC). In 1968, however, the Commission exposed a significant portion of their business to competitive pressures. We are here called upon to apply the teachings ofBerkeyto the actions appellants took in response to this infusion of rivalry. To oversimplify somewhat, the question presented is whether appellants did no more than to engage in vigorous competition, or instead, attempted to subvert the competitive process by unfair or unreasonable means. Because we hold that Northeastern has, for the most part, failed to prove that appellants' conduct exceeded the bounds of competitive propriety outlined inBerkey,we reverse the judgment below in several major respects. As to the design of the "protective coupler arrangement" required by appellants for use with Northeastern's telephone equipment, we remand for a new trial on liability and damages.

additional

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Question1

Is the use of amlodipine or furosemide recommended to normalize blood

pressure in a case of hypertensive heart failure? If so, which is most

effective?

Question 2

How can diabetes cause endothelial dysfunction? What are the roles of

ACE inhibitors in the kinin-kallikrein system? What are the mechanisms

by which a decrease in the level of nitric oxide causes endothelial

dysfunction?

Question 3

Can sublingual nifedipine be given to a patient with malignant

hypertension/accelerated hypertension? It seems to be a controversial

issue with some favouring it and some against it.

Question 4

Is the diagnosis of malignant hypertension based only on the basis of the

retinopathy (even in the presence of a normotensive state)? Labetalol,

parenterally, is suggested as a treatment for malignant hypertension.

What other more readily available preparations (besides sodium

nitroprusside) are recommended in addition to this drug? Parental

labetalol is not available in Pakistan!

Question 5

Patients at medium risk of DVT and pulmonary embolism are usually

given specific prophylaxis with low-dose heparin at a dose of 5000 units

subcutaneously every 8-12 hours until the patient is ambulatory. Is the

Question 7

Can we use enoxaparin for deep vein thrombosis (DVT) prophylaxis

in the immediate postoperative period and in a case of cerebral

haemorrhage? Wouldn't it increase the risk of haemorrhage in

either case?

Question 8

Can external jugular vein thrombosis cause tingling numbness over

the earlobe and adjoining part of the lower face?

Question 9

For how long does a patient have to stay in bed to be labelled as

bedridden and to merit low-molecular-weight heparin (LMWH) as

prophylaxis for deep vein thrombosis?

Question 10

Is an inferior vena cava filter an alternative treatment for a patient with

a history of recurrent deep vein thrombosis on lifelong anticoagulation

with warfarin