Focal Ifr 165-4
Jan Dominquez
I have previously used(and owned) both 165mm lenses. I don't really think that there are any optical tradeoffs, the F4 lens takes 77mm filters which is useful if you have the 55mm, it is also shorter and slightly lighter than the F2.8 which makes it easier to handle. On the old P67 the f2.8 makes for easier critical focusing though and has a built in hood which is useful for landscape work. Danny Gonzalez was quite critical of the F2.8 in his review and Hamish Reid was critical of the f4 version in his review.
The problem with both is that they don't focus close enough for a close head shot but IMO are too short a focal lenght for that anyway. I've just bought the new P67II and I am struggling with the portrait lens/short tele for landscapes decision. Nobody seems to have used both the 200mm and the 165mm and on this bboard and there seem to be conflicting reviews of the 200mm which I've never used. Nobody seems very convinced about the quality of the 300mm which would be my choice focal length for tight headshots with one of the 165mm (probably the 2.8) or 135mm for general portraits.
I have not done disciplined resolution tests but have been relieved and pleased with the results. Some postings I read before purchasing the lens (you might have read the same posts) would tend to make you feel uncomfortable with some P67 lenses as concerns sharpness and contrast. I have been extremely impressed with the lens' ability to produce both when used properly. It is a little long in focal length to effectively handhold if you plan to enlarge the image past 8X10.
Leaf shutter has worked flawlessly. It provides flash sync w/ 1/60, 125, 250 and 500 and requires the focal plane shutter to be set @ 1/8 sec. for use but the results have been what you need....predictable and accurate. If you need a leaf shutter and don't need the f/2.8 max aperture (which likely will not produce the image quality you'd want anyway) I can heartily recommend this lens but I understand the f/2.8 to be one fine piece of glass also.
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Neutrophil adhesion is fundamentally important during the onset of inflammatory responses. The adhesion signaling pathways control neutrophil arrest and extravasation and influence neutrophil shape and function at sites of inflammation. In the present study the intracellular signaling pathways for the adhesion of human neutrophils by pituitary growth hormone (GH) were examined. Pituitary GH triggered the tyrosine phosphorylation of Janus kinase 2 (Jak2) and STAT3 in neutrophils. In addition, pituitary GH treatment resulted in the morphological changes and the tyrosine phosphorylation of focal adhesion kinase (p125FAK) and paxillin. Preincubation with genistein, a tyrosine kinase inhibitor, blocked the GH-stimulated adhesion and Jak2, STAT3, p125FAK, and paxillin phosphorylation. Confocal microscopy revealed that pituitary GH stimulates the focal localization of p125FAK, paxillin, phosphotyrosine, and filamentous actin filament into the membrane rufflings and uropods of human neutrophils. Immunoprecipitation experiments revealed a physical association of Jak2 with p125FAK via STAT3 in vivo. Also an in vitro kinase assay showed an augmentation of p125FAK autophosphorylation as a result of pituitary GH treatment. These results suggest that pituitary GH modulates neutrophil adhesion through tyrosine phosphorylation of Jak2, p125FAK, and paxillin and actin polymerization.
A transtentorial herniation is the movement of brain tissue from one intracranial compartment to another. This includes uncal, central, and upward herniation. These are life-threatening and time-critical pathologies that may be reversible with emergent surgical intervention and medical management. This activity reviews the evaluation and treatment of transtentorial herniation syndromes and highlights the role of the interprofessional team in evaluating and treating patients with this condition.
Brain herniation is the movement of brain parenchyma from one cranial compartment to another.[1] The key cranial compartments include left and right supratentorial compartments and the posterior fossa, which is infratentorial. The tentorium cerebelli is a rigid fold of dura that divides the cranial contents into a supratentorial and infratentorial region. The infratentorial region contains the cerebellar and brainstem, while the supratentorial compartment contains the cerebral hemispheres. This is further divided into right and left by the falx cerebri, which is also a fold of dura running within the longitudinal fissure between the two hemispheres. The tentorium cerebelli contains an oval-shaped opening called the tentorial notch or incisor. The midbrain passes through this opening and is continuous with the diencephalon.[2][3] A transtentorial herniation is any parenchymal herniation through the tentorial notch; of which there are three kinds:
The incidence of transtentorial herniation is not documented, due to it being a physiological response to various underlying pathologies. The most common cause is traumatic brain injury (TBI).[7] A 2019 review estimates the worldwide incidence of TBI to be 69 million per year, with nearly 8% being classed as severe (Glasgow Coma Scale score - GCS - 8 or less).[8] In the United States, the annual incidence of TBI requiring medical attention is approximately 30 million.
The tentorium cerebelli is very rigid due to its multiple tethering points. Anteriorly the petrous ridge and posterior clinoid processes secure the sheet-like tentorium. Laterally it forms the transverse sinus and attaches to the inner table of the occipital bone. The tentorium contains an oval-shaped opening through which the midbrain passes and is continuous with the diencephalon.[2]
Uncal herniation, as the name suggests, involves the uncal portion of the temporal lobe. The uncus is present in the medial aspect of the temporal lobe. MacEwen first described uncal herniation in the 1880s by freezing and dissecting heads of patients who had died of temporal lobe abscesses.[3] He noted that the medial surface of the temporal uncus was displaced medially and downwards, compressing the oculomotor nerve, which originates from the midbrain. This caused the dilatation of the ipsilateral pupil. The oculomotor nerve leaves the midbrain anteriorly and runs along the underneath surface of the tentorial notch. As the uncus herniates downwards over the notch, it compresses the nerve against the skull base.[3]
Due to the proximity of the uncus to the diencephalon and midbrain, loss of consciousness is a key component of uncal herniation. The distortion of the ascending arousal system that originates in the upper pons and midbrain and ascends through the diencephalon to stimulate the cerebral hemispheres causes changes in arousal. Loss of arousal is a key component of uncal herniation, and therefore pupillary dilatation with preserved consciousness should alert the examiner to search for a different cause.[3]
Hemiparesis is also encountered in these cases and can occur via a few mechanisms. Firstly, a hemispheric lesion can interrupt the corticospinal tracts within that hemisphere, causing contralateral hemiplegia. Secondly, direct compression onto the ipsilateral cerebral peduncle within the midbrain can cause contralateral hemiparesis, again due to the involvement of the corticospinal tract. Lastly, in 1928 Kernohan noted that a supratentorial tumor could cause a lateral shift of the midbrain resulting in compression of the contralateral cerebral peduncle on the edge of the tentorial notch. Due to the decussation of the corticospinal tracts below this level, this 'notching' resulted in ipsilateral hemiparesis. This is an example of a false lateralizing sign as a lesion in the right hemisphere can cause weakness on the right side of the body due to compression of the left cerebral peduncle on the tentorium. Therefore, it is important to acknowledge that hemiparesis cannot be reliable in the localization, and the whole clinical picture should be taken into perspective for an accurate diagnosis of the side of the lesion.[3]
With any supratentorial mass causing tentorial herniation, the posterior cerebral arteries (PCA) can be compressed against the tentorium. The basilar artery ends in two posterior cerebral arteries (PCAs) that travel around the midbrain and along the undersurface of the occipital lobes.[11] The downward pressure of the occipital lobes compresses the PCA against the tentorium. This can cause distal ischemia of the occipital lobes and lead to cortical blindness. This is usually not noted at the time of insult due to the associated loss of consciousness; however, later in the course of the patient's recovery as they awake from the coma, a visual disturbance may be noted.[12] Unilateral ischemia causes hemianopia, whereas bilateral compression results in a cortical blindness syndrome that may include anosognosia.[13]
Whereas in uncal herniation, the pressure shift causes medial and downward herniation of the uncus, which inevitably compresses the ascending arousal system of the midbrain and diencephalon, central herniation is due to direct pressure on the diencephalon and midbrain itself. Small perforating end arteries are easily stretched and compressed, leading to ischemia and, ultimately, loss of arousal supply the diencephalon. Pupils, due to bilateral compression of the diencephalon, become small but remain reactive. Central herniation can also compress the pituitary stalk, causing a lack of antidiuretic hormone (ADH) and diabetes insipidus.[3] Vascular compromise results in ischemia and necrosis of the midbrain. This can lead to distinctive slit-like hemorrhages seen on computed tomogram (CT) or magnetic resonance imaging (MRI), called Duret hemorrhages.[14]
Like supratentorial lesions cause descending herniation through the tentorial notch, though uncommon, posterior fossa lesions can cause upward herniation of the brainstem through the tentorial notch into the supratentorial compartment. Due to the compression of the ascending arousal system, there is a loss of consciousness. There can also be compression of the dorsal midbrain leading to up gaze palsy. If the cerebral aqueduct, which passes through the midbrain, is compressed, then obstructive hydrocephalus will develop.[15] The superior cerebellar artery can also be compressed upwards against the tentorium cerebelli by the cerebellar, causing cerebellar ischemia.[3]
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