The vertebrobasilar arterial system perfuses the medulla, cerebellum, pons, midbrain, thalamus, and occipital cortex. Occlusion of large vessels in this system usually leads to major disability or death. Vertebrobasilar stroke carries a mortality rate of more than 85%. Because of involvement of the brainstem and cerebellum, most survivors have multisystem dysfunction (eg, quadriplegia or hemiplegia, ataxia, dysphagia, dysarthria, gaze abnormalities, cranial neuropathies).
However, many vertebrobasilar lesions arise from small vessel disease and are correspondingly small and discrete. The clinical correlates of these smaller lesions consist of a variety of focal neurologic deficits, depending on their location within the brainstem. Patients with small lesions usually have a benign prognosis with reasonable functional recovery.
See the images below regarding vertebrobasilar stroke.
The vertebral arteries arise from the subclavian arteries, and as they course cephalad in the neck, they pass through the costotransverse foramina of C6 to C2. They enter the skull through the foramen magnum and merge at the pontomedullary junction to form the basilar artery. Each vertebral artery usually gives off the posterior inferior cerebellar artery (PICA). At the top of the pons, the basilar artery divides into 2 posterior cerebral arteries (PCAs).
Proximal to its bifurcation into the terminal branches (PCAs), the basilar artery gives off the superior cerebellar arteries that supply the lateral aspect of the pons and midbrain, as well as the superior surface of the cerebellum. The cerebellum is supplied by long circumferential arteries, the PICA, and the anterior inferior and superior cerebellar arteries from the basilar artery.
The medulla is perfused by the PICA and by direct, smaller branches from the vertebral arteries. The pons is perfused by small, penetrating branches from the basilar artery and its major branches. Penetrating arteries from the PCAs perfuse the midbrain and thalamus, and the occipital cortex is perfused by the PCAs.
The most common vascular condition affecting the vertebrobasilar system is atherosclerosis, in which plaques cause narrowing and occlusion of the large vessels.
The pathology of small vessel disease (affecting arteries 50-200 µm in diameter) is different from that of atherosclerosis, because the small vessels become occluded by a process called lipohyalinosis, which frequently occurs in association with hypertension. Occlusions of these small vessels lead to small, round infarctions called lacunes, which may appear as single lesions or may be distributed as multiple lesions scattered widely throughout the subcortex and brainstem.
Lipohyalinosis weakens the vessel wall, and in hypertensive individuals, rupture of the artery may occur, resulting in a focal hemorrhage. Almost all intracerebral hemorrhages originate from the rupture of these small, penetrating vessels.
Embolic occlusion of the vertebrobasilar system is not common and usually is artery-to-artery with occlusion of the basilar artery. Donor sites for the emboli typically are the aortic arch, the subclavian artery, and the origin of the vertebral arteries.
The frequency, incidence, and prevalence of the vertebrobasilar syndromes vary, depending on the specific area and syndrome involved. Approximately 80-85% of all strokes are ischemic, and 20% of the lesions producing ischemic strokes occur in the vertebrobasilar system.
Overall, hemorrhage causes 15-20% of strokes. Although most intracerebral hemorrhages occur in the region of the putamen and thalamus, about 7% of all hemorrhagic lesions involve the cerebellum in the area of the dentate nucleus, and approximately 6% of hemorrhagic lesions involve the pons.
In most of the reported series, mortality patients with basilar artery occlusion has been consistently greater than 75-80%.  Most survivors of basilar artery occlusion have severe, persisting disability.
The onset and duration of symptoms in vertebrobasilar stroke depends, in large part, upon the etiology. Patients with basilar artery thrombosis typically have a waxing and waning course of symptoms, with as many as 50% of patients experiencing transient ischemic attacks for several days to weeks prior to the occlusion.
Common clinical findings observed in more than 70% of patients with vertebrobasilar stroke include an abnormal level of consciousness, as well as hemiparesis or quadriparesis, which usually is asymmetric. Pupillary abnormalities and oculomotor signs are common, and bulbar manifestations, such as facial weakness, dysphonia, dysarthria, and dysphagia, occur in more than 40% of patients.
Oculomotor signs usually reflect the involvement of the abducens nucleus; the horizontal gaze center located in the pontine paramedian reticular formation (PPRF), contiguous to the abducens nucleus; and/or the medial longitudinal fasciculus (MLF). Lesions to these structures result in ipsilateral lateral gaze or conjugate gaze palsy.
Ocular bobbing is described as a brisk, downward movement of the eyeball with a subsequent return to the primary position. This deficit localizes the lesion to the pons. Other reported signs of pontine ischemia include ataxia and tremor associated with mild hemiparesis. The signs described can occur in different combinations, presenting a diagnostic challenge in lesion localization.
This syndrome is most often due to vertebral artery occlusion or, less commonly, to posterior inferior cerebellar artery (PICA) occlusion. Patients present with nausea, vomiting, and vertigo from involvement of the vestibular system.
Contralateral findings include the loss of pain and temperature sense in the body and extremities, indicating involvement of the lateral spinothalamic tract. Other findings include tachycardia and dyspnea (dorsal nucleus of CN X) and palatal myoclonus, a rhythmic involuntary jerking movement of the soft palate, pharyngeal muscles, and diaphragm. Palatal myoclonus sometimes follows infarction of the dentate nucleus of the cerebellum and inferior oliva.
The prognosis of patients with the lateral medullary syndrome usually is quite good for functional outcome; however, patients may die in the acute phase from aspiration pneumonia, and death has been reported from sleep apnea in a number of cases.
This syndrome is an uncommon lesion resulting from occlusion of a vertebral artery or its branch to the anterior spinal artery; it involves the pyramid, the medial lemniscus, and, sometimes, the hypoglossal nerve.
A stroke involving the cerebellum may result in a lack of coordination, clumsiness, intention tremor, ataxia, dysarthria, scanning speech, and even difficulties with memory and motor planning. Early diagnosis of cerebellar infarctions is important, because swelling may cause brainstem compression or hydrocephalus.
This dramatic clinical syndrome occurs when there is an infarction of the upper ventral pons. Locked-in syndrome can result from occlusion of the proximal and middle segments of the basilar artery or from hemorrhage involving that region. It can also be caused by trauma, central pontine myelinolysis, encephalitis, or a tumor.
Bilateral ventral pontine lesions involving corticospinal and corticobulbar tracts lead to quadriplegia. The patient is unable to speak, to produce facial movement (damage to the corticobulbar tracts), or to look to either side (horizontal eye movement is impaired due to a lesion of bilateral CN VI nuclei). Because the tegmentum of the pons is spared, the patient's consciousness is preserved, with the patient fully awake, sensate, and aware. The only movements preserved are vertical eye movements and blinking. The patient is paralyzed completely and communicates only by blinking. Some recovery of facial muscle movement and horizontal gaze may occur with time or in an incomplete form of this syndrome.
Coma may occur with bilateral involvement of the pontine tegmentum or with lesions of the midbrain reticular formation. Coma generally is associated with oculomotor abnormalities, and motor abnormalities may be present. A comatose patient is unresponsive, and the coma may be prolonged when it is due to basilar artery occlusion. Sleep-wake cycles are absent in patients with coma.
This syndrome is the manifestation of upper brainstem and diencephalic ischemia caused by occlusion of the rostral basilar artery; the occlusion usually results from an embolism.  Varying degrees of involvement of the midbrain, thalamus, and portions of the temporal and occipital lobes may occur and can produce severe disability.
Patients present with sudden changes in the level of consciousness, confusion, amnesia, and visual symptoms (eg, hemianopia, cortical blindness, abnormal color vision/color dysnomia). These patients can also demonstrate oculomotor abnormalities, most commonly of the vertical gaze, such as gaze palsy, skew deviation, convergence spasm resulting in pseudoabducens palsy, or convergence-retraction nystagmus.
CN III palsy and pupillary abnormalities, including small pupils with decreased light reactivity (diencephalic), large/mid-position and fixed pupils (midbrain), and ectopic or oval pupils, also are frequent.
Other abnormalities include varying degrees of weakness, sensory deficits, or posturing.
When a patient with a lesion in the right MLF attempts to look to his/her left (ie, away from the involved side), he/she shows no adduction of the right eye and full abduction of the left eye with the end-point abduction nystagmus.
By the same logic, in the case of bilateral INO, there is no adduction to either side with nystagmus of the abducting eye in both directions. Convergence is preserved, because the nuclei of CN III and peripheral innervation of the medial recti muscles are intact.
Because horizontal gaze requires coordinated activity of the ipsilateral CN III and contralateral CN VI (relative to the lesion), disruption of the communication pathway (ie, the MLF) between the nuclei of CN III (in the midbrain) and CN VI (in the pons) results in the inability of the eye ipsilateral to the lesion to adduct and the contralateral eye to exhibit abduction nystagmus when looking away from the involved side.
In elderly patients, INO is caused most often by occlusion of the basilar artery or its paramedian branches. In younger adults, it may occur due to multiple sclerosis (MS), commonly with bilateral involvement.
This syndrome is caused by a lesion affecting the PPRF and MLF simultaneously, resulting in ipsilateral conjugate gaze palsy and INO  A patient with this syndrome is completely unable to move the ipsilateral eye, and is able only to abduct the contralateral eye, with resulting nystagmus; the 'one' in the syndrome name refers to the former, and the 'half' to the latter.
The patient with a lesion in the ipsilateral PPRF or abducens nucleus and MLF connecting to the contralateral CN VI exhibits horizontal gaze palsy when looking toward the side of the lesion and exhibits INO when looking away from the side of the lesion. Associated features may include vertical nystagmus, exotropia of the contralateral eye, and skew deviation. Vertical gaze and convergence generally are preserved.
This syndrome occurs after paramedian infarction in the pons and results in ipsilateral lateral rectus palsy (CN VI) with diplopia, complete facial paresis (unilateral CN VII palsy), and contralateral hemiparesis/hemiplegia (corticospinal tract involvement) with sparing of the face.
This syndrome is due to obstruction of flow in the long circumferential branches of the basilar artery. This occlusion results in ipsilateral ataxia and coarse intention tremor (indicating involvement of the superior and middle cerebellar peduncles), weakness of mastication and sensory loss in the face (suggesting sensory and motor trigeminal nuclei and tracts), and contralateral loss of all sensory modalities (due to damage to medial lemniscus and spinothalamic tract) with or without facial weakness and hemiparesis (corticospinal tract).
Horizontal gaze palsy also may occur.
This syndrome may result from lesions to the dorsal tegmentum of the lower pons. The patient exhibits ipsilateral paresis of the whole face (nucleus and fibers of CN VII), horizontal gaze palsy on the ipsilateral side (ie, PPRF with or without CN VI nucleus), and contralateral hemiplegia (corticospinal tract) with sparing of the face.
Weber syndrome occurs with an occlusion of the median and/or paramedian perforating branches of the basilar artery. Typical clinical findings include ipsilateral CN III palsy, ptosis, and mydriasis (ie, damage to parasympathetic fibers of CN III) with contralateral hemiplegia. Weakness of the lower face (corticospinal and corticobulbar tracts) may be noted.
This syndrome is due to a lesion in the midbrain tegmentum resulting from occlusion of paramedian branches of the basilar artery, the PCA, or both.
The patient demonstrates ipsilateral oculomotor palsy, ptosis, and mydriasis (as in Weber syndrome), along with the contralateral involuntary movements, such as those of intention tremor, ataxia, or chorea (due to the involvement of the red nucleus).
The most common finding is occipital lobe infarction leading to contralateral hemianopia with macular sparing. Clinical symptoms associated with occlusion of the PCA vary depending on the location of the occlusion and may include the thalamic syndrome, thalamic perforate syndrome, Weber syndrome, cortical blindness, color blindness, failure to see to-and-fro movements, verbal dyslexia, and hallucinations.
The disadvantages of CT scanning include a low sensitivity for early ischemia and the presence of significant artifacts caused by the bony structures surrounding the brainstem and cerebellum.
MRI and magnetic resonance angiography (MRA) are very helpful in finding occult lesions, such as demyelinating plaques, tumors, vertebrobasilar dolichoectasia, or dissection. [23, 24, 25] MRA has a sensitivity of up to 97% and a specificity of up to 98% when used to identify vertebrobasilar occlusion.
A limitation of MRA is its tendency to overestimate the degree of stenosis. This overestimation occurs because the production of a vessel's image in MRA is a based on a flow-related phenomenon; hence, the presence of severe stenosis with significant flow compromise may result in poor visualization of a vessel and cause the MRA image to resemble vascular occlusion.
Angiography should be considered a first-line diagnostic test after a CT scan, once it has been decided that recanalization with thrombolysis should be completed. The most important goal of the workup is to establish the type of vascular lesion and the mechanism of the stroke.
Transcranial Doppler (TCD) is used in the evaluation of cerebrovascular disease, but it often is inaccurate. Absence of signal in an initial examination does not necessarily mean occlusion.
Findings that may affect management include valvular disorders, vegetations, intramural or extramural thrombi, ventricular aneurisms, cardiac tumors (myxoma), right-to-left shunts, and poor ejection fraction.
Hemodynamic management should be aimed at minimizing the ischemic injury. Cerebral ischemia impairs the brain's ability to autoregulate its circulation through vasoconstriction and vasodilatation. Therefore, under ischemic conditions, the cerebral blood flow becomes blood pressure–dependent.  An increase in the mean arterial pressure (MAP) results in vasoconstriction. This response limits the perfusion pressure and the blood volume. A decrease in the MAP results in vasodilatation.
In normotensive patients, the limits of autoregulation are within the range of 50-150 mm Hg of the MAP. In chronic hypertensive patients, the curve of autoregulation is shifted upward. In the patients with severe cerebral vascular occlusive disease, the MAP and the cerebral perfusion pressure (CPP) become critical in maintaining the cerebral blood flow. CPP is equal to MAP less intracranial pressure (ICP) (ie, CPP = MAP-ICP). Therefore, overzealous treatment of hypertension should be avoided, because it can decrease the cerebral perfusion pressure and exacerbate the ongoing ischemia.
No existing information from randomized trials indicates whether treating hypertension is better than not treating it. Based on evidence from experimental models and on data from clinical experience, hypertension should not be treated unless there is evidence of end-organ damage, such as hypertensive encephalopathy, unstable angina, acute myocardial infarction, heart failure, or acute renal failure.
Hypertension should be treated when the diastolic blood pressure is greater than 120 mm Hg or when the systolic blood pressure is over 200 mm Hg. Otherwise, when thrombolysis is a strong consideration, the treatment parameters become 110 mm Hg or more for diastolic blood pressure or greater than 180 mm Hg for systolic blood pressure.
Commonly used antihypertensives are labetalol and nitroprusside. When diastolic blood pressure is greater than 140 mm Hg, nitroprusside is the preferred drug, provided that no contraindications exist.
Patients with hypotension need to be treated to optimize the MAP and, consequently, the blood pressure–dependent cerebral blood flow. Maximal effort should be made to maintain a normal intravascular volume using isotonic solutions. If the MAP continues to be low despite fluid management, vasopressors, such as dopamine, dobutamine, and phenylephrine, should be used.
In patients with unknown intravascular volume status or those with complications, such as congestive heart failure and pulmonary edema, a pulmonary artery catheter should be placed to monitor the central venous pressure and the pulmonary capillary wedge pressure. This approach would improve monitoring of the intravascular volume to avoid overload.
Early assessment and management of the airway are critical due to the frequent involvement of lower cranial nerves and the impairment of consciousness in patients with brainstem ischemia. Assessment of the respiratory drive, gag reflex, and ability to handle secretions with a forceful cough also is of great importance.
Endotracheal intubation may be considered in patients with a decreased level of consciousness and a Glasgow coma score of less than 8. Of the mechanical ventilation modes, pressure support ventilation (PSV) and synchronized intermittent mandatory ventilation are used most often. For patients with good respiratory drive, the most comfortable mode is PSV. In this mode, the ventilator does not deliver a set of breaths but provides enough pressure support to maintain the desired tidal volume, usually in the range of 5-8 mL/kg. Most patients with no pulmonary comorbidities reach this goal with a PSV of 5-10.
For patients with poor respiratory drive, synchronized intermittent mandatory ventilation may be a better mode. This form of ventilation delivers a set number of breaths with a set tidal volume, which is synchronized with the patient's inspiratory effort while allowing the patient to take extra breaths. Adding PSV during the extra breaths can minimize the patient's respiratory effort when taking them.
Sedation and paralysis should be avoided, because they may obscure the neurologic assessment. Circumstances may exist that require the use of sedation and paralysis (eg, neurogenic hyperventilation) to avoid hypocarbia and worsening of the ischemic process.
In 1996, The US Food and Drug Administration (FDA) approved tissue plasminogen activator (tPA) for the treatment of acute ischemic stroke within the first 3 hours of onset.  Approval was based on data from the National Institute of Neurological Disorders and Stroke trial, which showed that a higher number of treated versus untreated patients had minimal deficit and minimal or no disability.
In 2009, the American Heart Association/American Stroke Association (AHA/ASA) published a science advisory recommending that the time window for tPA administration be increased to 4.5 hours after a stroke, although this change has not been approved by the FDA.  Research indicates that tPA is effective in patients even when administered within the 3- to 4.5-hour window, [33, 34, 35] but the AHA/ASA stated that, despite its recommendation, the effectiveness of tPA administration in comparison with other treatments for thrombosis, within that time period, is not yet known.
In the early 1980s, Nenci and colleagues reported the first 4 cases of local thrombolysis for vertebrobasilar occlusion, establishing a trend to treat patients with intra-arterial thrombolysis. [14, 37] To date, several case series have been published. The average time to treatment has ranged from 8-48 hours. Overall mortality has decreased from 46-75% to 26-60%. The patient's condition at presentation appears to be the major prognostic factor; patients with quadriplegia and/or coma have demonstrated the least favorable outcomes. Despite the above efforts, intra-arterial thrombolysis for vertebrobasilar occlusion has not been studied systematically in randomized, controlled trials.
Of the different agents currently used for thrombolysis (urokinase, prourokinase, streptokinase, tPA), prourokinase and tPA seem to have more selectivity for thrombi. Streptokinase has not been used for stroke since the multicenter European and Australian trials documented a greater mortality in the treated patients. Because of concerns with its production, urokinase is not currently available in the United States.
Prourokinase was tested in a prospective, randomized fashion, including only patients with middle cerebral artery stem occlusion. Results showed a better outcome in treated patients, but prourokinase has not been approved for use in acute stroke.
At this time, the only viable option for thrombolysis in the United States continues to be tPA. This drug has been studied prospectively in trials involving combined intravenous and intra-arterial therapy, in doses of 0.3 mg/kg, with a maximum of 10-20 mg. Limited experience with the use of GPIIb/IIIa inhibitors, such as abciximab, to block the platelet function and rethrombosis has shown an overall reocclusion rate of approximately 30%.
Anticoagulation therapy with heparin has been used, but there is no evidence that it has an impact on outcome. Results from a trial using low–molecular weight heparin intravenously in patients with acute stroke, although negative overall, did show a better outcome at 7 days for patients with large vessel disease.
Angioplasty has been performed to treat patients with atherosclerotic basilar artery stenosis. The use of angioplasty is based on the tendency of thrombosis to occur in stenosed arterial segments. Reports describe angioplasty performed in patients with acute vertebrobasilar occlusion, as well as electively. The published case series report a morbidity rate of 0-16% and a mortality rate of up to 33%; however, the role of angioplasty in the treatment of vertebrobasilar occlusion is not well defined.
Most patients with vertebrobasilar stroke have a significant degree of disability, due to involvement of the brainstem and cerebellum, with resultant multisystem dysfunction (eg, quadriplegia or hemiplegia, ataxia, dysphagia, dysarthria, gaze abnormalities, cranial neuropathies). They often require ongoing, acute rehabilitation, with attention paid to specific patient issues and the formulation of short-term and long-term care plans. The rehabilitation and planning are performed best in a multidisciplinary and interdisciplinary setting.
Rehabilitation services have been shown to play a critical role in recovery from acute stroke. Physicians and nurses play crucial roles on the rehabilitation team; nurses often are the first to suggest initiation of therapy services, because they have the most extensive involvement with the patient. Prior to a discussion of the specific therapy disciplines, address nursing issues in the care of patients with vertebrobasilar stroke.
A wide variation in symptoms may be seen with stroke, depending on the severity of the brain damage. Initial nursing intervention involves maintaining skin integrity, establishing a bowel and bladder program, maintaining nutrition, and ensuring the person's safety from injury.
Other important nursing issues include communication with the treating clinician in order to initiate therapy services for the assessment of ambulation, transfers, swallowing function, and the performance of activities of daily living (ADL). In some patients, the severity of the deficits makes ambulation impossible; however, patients should be mobilized out of bed and should be actively involved in physical and occupational therapy.
Positioning in bed and in a chair assures the patient's comfort and prevents complications from skin breakdown. If the upper extremity is flaccid or paretic, positioning is critical to the prevention of shoulder subluxation and pain from shoulder-hand syndrome.
Nursing staff always should involve family members in the care of a person who has sustained a stroke. The patient and family members may be unfamiliar with stroke and its effects. Education must be provided to make the patient and his/her family members aware of the importance of continuing with activities, of appropriate precautions, and of continuing therapy upon discharge to home.
Some patients have fluctuating symptoms and signs, which often are related to position. Because of this possibility, precautions are necessary with activities that can be undertaken until the symptoms have stabilized.
Physical therapy (PT) and occupational therapy (OT) should be initiated soon after admission, depending on the condition of the patient. Once the symptoms have stabilized, patients should be mobilized out of bed, which will allow them to participate in full PT and OT activities.
The physical therapist is responsible for retraining of gross motor skills, such as gait, balance, transfers, bed mobility, and wheelchair mobility. The physical or occupational therapist may be involved with assessing the patient for the proper wheelchair and seating system.
The physical therapist also develops a PT program and instructs the patient in general strengthening and range of motion. Training of the patient and family members in the use of lower extremity orthotics may be necessary to provide for functional mobility.
Vestibular evaluation and training are very important, due to a high prevalence of vestibular and cerebellar involvement in vertebrobasilar strokes. Patients often need extensive balance and gait training. Evaluation always should begin with a detailed and focused history. A premorbid vestibular status determination is of great importance, because dizziness is the third most frequent complaint during physician visits from patients aged 65 years and the most frequent complaint from patients aged 75 years and older.
An exercise-based approach has been successful in the treatment of vestibular disorders, due to several possible mechanisms. These include adaptation, substitution, habituation, and repositioning.
With adaptation by the central vestibular system, the brain modulates the gain of the vestibular response, attempting to correct for a retinal slip (error signal) caused by the decreased gain of the VOR. The VOR training strategy includes focusing on a stationary or moving target while rotating the head, resulting in a retinal slip that facilitates adaptation.
Substitution for the loss of function by the remaining intact visual and somatosensory systems is used in treating patients with bilateral vestibular lesions (complete or partial loss of both labyrinths).
Habituation for postural vertigo results in decreased response to repeated provoking stimuli. Patients move into the provoking position 2-3 times during each session, and repeat these sessions 3-5 times per day.
Repositioning maneuvers (eg, Epley maneuver) are used for positional vertigo, based on the mechanical displacement of the debris from the affected canal(s) by a series of head movements. Alternating eye patches or prisms can help diplopia.
General conditioning also is incorporated into the overall rehabilitation plan, encouraging an increase in the performance of ADL as tolerated.
OT is used for retraining fine motor skills that are needed to perform ADL (eg, dressing, bathing, grooming), as well as for improving hand and arm function. OT also is involved in general strengthening, wheelchair mobility, upper extremity orthotics, and the evaluation of needs for adaptive equipment, as well as in family training and cognitive retraining for safety and ADL.
Speech therapy (ST) is used for cognitive retraining, speech and language skills, safety skills, swallowing assessment, and family training. In patients with dysphagia from brainstem lesions, the cricopharyngeus muscle may fail to open sufficiently, resulting in an impaired passage of the bolus from the pharynx to the esophagus. Increased pooling of a bolus in the vallecula and/or pyriform sinuses, which spills into the airway, poses a significant risk for aspiration and pneumonia.
Evaluation of these patients should be thorough and should include a videofluoroscopy with a modified barium swallow to assess for silent aspiration. The speech and language therapist often performs the initial swallowing evaluation and determines the risk for aspiration and the consistency of the patient's diet.
The patient's vocalization and possible reading, writing, and processing deficits also are addressed. Interventions for the prevention of aspiration include compensatory strategies, such as oromotor exercises and postural changes while swallowing, as well as facilitative strategies (eg, modification of bolus consistency, volume, delivery).
Surface electromyography biofeedback for dysphagia has shown promising results. Surface electromyography is used in training a patient to perform maneuvers that compensate for the weak swallow.
The Mendelsohn maneuver, for example, requires voluntary maintenance of the thyroid cartilage in an elevated position for a few seconds, resulting in further widening of the opening of the cricopharyngeus muscle and easier passage of the food bolus through to the esophagus. The patient observes the plateau (as opposed to the peak) of the generated waveform on the screen, reinforcing the concept of muscle activation in the desired position (thyroid cartilage elevation).
The patient should be on a nothing-by-mouth restriction until the swallowing mechanism has been assessed and cleared and the airway has been protected. If there is a high risk of aspiration, a nasogastric or nasoduodenal tube should be placed, although neither completely eliminates the aspiration risk. If the swallowing abnormalities are so severe that recovery is expected to take weeks or months, then a gastrostomy tube should be placed either surgically or percutaneously.
The recreational therapist should concentrate on finding alternative recreational activities for patients who are unable to perform at their premorbid level. Engaging in these activities provides a creative outlet and a positive emotional gain that potentially enhance the patient's psychological recovery.
In addition to consultations with physical, occupational, and speech therapists, consultation with a neuropsychologist and a social services worker may also be required in the management of patients with vertebrobasilar stroke.
Evaluation by a neuropsychologist is recommended to screen for depression, family dysfunction, coping skills, and subtle cognitive, memory, or processing deficits. All of these may affect future participation in and compliance with rehabilitation.
The social services department is responsible for coordinating intake and planning discharge. Depending on the setting, the social services representative may be a licensed social worker or may instead be someone with a more limited background. Home health agencies typically employ licensed social workers, but in nursing homes, the social worker usually is not licensed or certified.
Patients should follow up with the primary care provider, neurologist, and other specialists, including the physiatrist, and continue with the outpatient rehabilitation program. The patient requires continued reassessment of various factors (eg, functional gains, psychological status, mood, the need for further equipment, home and other modifications, skin care, bowel and bladder function, spasticity management, pain, vocational needs, and social issues).
Strict risk factor control is important to decrease the risk of stroke recurrence.  Prevention strategies depend on the primary cause of the stroke. Patients with a definite cardioembolic source, such as atrial fibrillation, should be treated with warfarin to maintain an international normalized ratio of 2-3.
Treatment of patients with basilar artery stenosis and, for that matter, vertebral artery stenosis is less clear. Retrospective evidence suggests that warfarin is better than aspirin for the prevention of stroke recurrence in patients with greater than 50% basilar artery stenosis. The ongoing warfarin-aspirin trial for symptomatic intracranial disease will provide valuable information in that regard.
Several oral anticoagulant medications are in various stages of clinical trials for the prophylaxis of ischemic thromboembolic stroke.  If approved for use, the potential of such drugs in the arena of stroke treatment is significant.
Patients with acute basilar artery occlusion have a mortality rate of more than 85%. Survivors usually are left with significant neurologic deficit. For symptomatic patients who survive, the risk of recurrent stroke is 10-15%.
For patient education information, see the Stroke Center, as well as Stroke.
How is vertebrobasilar stroke differentiated from hemispheric stroke?
What is the anatomy of vertebral and basilar arteries relative to vertebrobasilar stroke?
What is the pathophysiology of vertebrobasilar stroke?
What are the risk factors for vertebrobasilar stroke?
What is the prevalence of vertebrobasilar stroke?
Which clinical history findings are characteristic of vertebrobasilar stroke?
What are the signs and symptoms of vertebrobasilar stroke?
Which physical findings are characteristic of vertebrobasilar stroke?
Which physical findings help locate the lesions of vertebrobasilar stroke?
What are the possible complications of vertebrobasilar stroke?
Which neurologic syndromes are associated with vertebrobasilar artery stroke?
What are the signs and symptoms of lateral medullary (Wallenberg) syndrome in vertebrobasilar stroke?
What is the prognosis of lateral medullary (Wallenberg) syndrome?
What are the signs and symptoms of medial medullary syndrome in vertebrobasilar stroke?
What are the signs and symptoms of cerebellar infarction in vertebrobasilar stroke?
What are the signs and symptoms of locked-in syndrome in vertebrobasilar stroke?
What are the signs and symptoms of top-of-the-basilar syndrome in vertebrobasilar stroke?
What are the signs and symptoms of internuclear ophthalmoplegia (INO in vertebrobasilar stroke?
What are the signs and symptoms of one-and-a-half syndrome in vertebrobasilar stroke?
What are the signs and symptoms of ventral pontine (Millard-Gubler) syndrome in vertebrobasilar stroke?
What are the signs and symptoms of upper dorsal pontine (Raymond-Cestan) syndrome in vertebrobasilar stroke?
What are the signs and symptoms of lower dorsal pontine (Foville) syndrome in vertebrobasilar stroke?
What are the signs and symptoms of ventral midbrain (Weber) syndrome in vertebrobasilar stroke?
What are the signs and symptoms of dorsal midbrain syndrome in vertebrobasilar stroke?
What are the signs and symptoms of posterior cerebral artery occlusion in vertebrobasilar stroke?
Which conditions should be included in the differential diagnoses of vertebrobasilar stroke?
Which lab studies are performed in the workup of vertebrobasilar stroke?
Which patients should be evaluated for hypercoagulable states during the workup for vertebrobasilar stroke?
Who should undergo testing of creatine kinase, cardiac isoenzymes, and troponin levels in the workup of vertebrobasilar stroke?
What is the role of CT scanning in the diagnosis of vertebrobasilar stroke?
What is the role of MRI in the diagnosis of vertebrobasilar stroke?
What is the role of angiography in the diagnosis of vertebrobasilar stroke?
What is the role of ultrasonography in the diagnosis of vertebrobasilar stroke?
What is the role of electrocardiography in the diagnosis of vertebrobasilar stroke?
What is the role of echocardiography in the workup of vertebrobasilar stroke?
When is admission to the ICU indicated for the treatment of vertebrobasilar stroke?
What is included in hemodynamic management in patients with vertebrobasilar stroke?
What is included in respiratory management for the treatment of vertebrobasilar stroke?
What is the role of thrombolytic therapy in the treatment of vertebrobasilar stroke?
What are the eligibility criteria for thrombolytic therapy in vertebrobasilar stroke?
What is the efficacy of thrombolytic therapy for vertebrobasilar stroke?
What is the role of anticoagulation therapy in the treatment of vertebrobasilar stroke?
What is the role of angioplasty in the treatment of vertebrobasilar stroke?
How is vertebrobasilar stroke treated?
What is included in the long-term inpatient care for vertebrobasilar stroke?
What is the role of rehabilitation after a vertebrobasilar artery stroke?
What is included in nursing care of patients with vertebrobasilar stroke?
What is the role of physical therapy in the treatment of vertebrobasilar stroke?
Which clinical tests should be performed during rehabilitation of a vertebrobasilar stroke?
What is included in an exercise-based approach to rehabilitation of vertebrobasilar stroke?
What is the role of occupational therapy in the treatment of vertebrobasilar stroke?
What is the role of speech and swallowing therapy in the treatment of vertebrobasilar stroke?
What is the role of recreational therapy in the treatment of vertebrobasilar stroke?
Which consultations are beneficial to patients with vertebrobasilar stroke?
What is included in the follow-up care of patients with vertebrobasilar stroke?
How are recurrent vertebrobasilar strokes prevented?
What is the prognosis of vertebrobasilar stroke?
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Amin-Hanjani S, Turan TN, Du X, et al. Higher Stroke Risk with Lower Blood Pressure in Hemodynamic Vertebrobasilar Disease: Analysis from the VERiTAS Study. J Stroke Cerebrovasc Dis. 2017 Feb. 26 (2):403-410. [Medline].
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Adams RJ, Chimowitz MI, Alpert JS, et al. Coronary risk evaluation in patients with transient ischemic attack and ischemic stroke: a scientific statement for healthcare professionals from the Stroke Council and the Council on Clinical Cardiology of the AHA/ASA. Circulation. 2003 Sep 9. 108(10):1278-90. [Medline]. [Full Text].
Bahouth MN, LaMonte MP. Acute ischemic stroke: evaluation and management strategies. Top Adv Pract Nurs. 2005. 5(4):[Full Text].
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Pikija S, Magdic J, Hojs-Fabjan T. Calcifications of vertebrobasilar arteries on CT: detailed distribution and relation to risk factors in 245 ischemic stroke patients. Biomed Res Int. 2013. 2013:918970. [Medline]. [Full Text].
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Del Zoppo GJ, Saver JL, Jauch EC, et al. Expansion of the time window for treatment of acute ischemic stroke with intravenous tissue plasminogen activator. A science advisory from the American Heart Association/American Stroke Association. Stroke. 2009 May 28. [Medline]. [Full Text].
Hacke W, Kaste M, Bluhmki E, et al. Thrombolysis with alteplase 3 to 4.5 hours after acute ischemic stroke. N Engl J Med. 2008 Sep 25. 359(13):1317-29. [Medline]. [Full Text].
Wahlgren N, Ahmed N, Davalos A, et al. Thrombolysis with alteplase 3-4.5 h after acute ischaemic stroke (SITS-ISTR): an observational study. Lancet. 2008 Oct 11. 372(9646):1303-9. [Medline].
Adams HP Jr, del Zoppo G, Alberts MJ, et al. Guidelines for the early management of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the value of this guideline as an educational tool for neurologists. Stroke. 2007 May. 38(5):1655-711. [Medline]. [Full Text].
Hatano T, Tsukahara T. Endovascular treatment for intracranial vertebrobasilar artery stenosis. Acta Neurochir Suppl. 2014. 119:83-9. [Medline].
Alexander MD, Rebhun JM, Hetts SW, et al. Lesion location, stability, and pretreatment management: factors affecting outcomes of endovascular treatment for vertebrobasilar atherosclerosis. J Neurointerv Surg. 2015 Mar 20. [Medline].
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Bouslama M, Haussen DC, Aghaebrahim A, et al. Predictors of Good Outcome After Endovascular Therapy for Vertebrobasilar Occlusion Stroke. Stroke. 2017 Dec. 48 (12):3252-7. [Medline].


text:
Proposed US data privacy bill aims to give you more control over information collected about you
It should make businesses change how they handle data
Anne Toomey McKenna, University of Richmond
The U.S. could soon catch up to the European Union in protecting
people's data privacy. Teera Konakan/Moment via Getty Images
Data privacy in the U.S. is, in many ways, a legal void. While there are limited protections for health and financial data, the cradle of the world's largest tech companies, like Apple, Amazon, Google, and Meta (Facebook), lacks any comprehensive federal data privacy law.
This leaves U.S. citizens with minimal data privacy protections compared with citizens of other nations. But that may be about to change.
With rare bipartisan support, the American Data and Privacy Protection Act moved out of the U.S. House of Representatives Committee on Energy and Commerce by a vote of 53-2 on July 20, 2022. The bill still needs to pass the full House and the Senate, and negotiations are ongoing. Given the Biden administration's responsible data practices strategy, White House support is likely if a version of the bill passes.
As a legal scholar and attorney who studies and practices technology and data privacy law, I've been closely following the act, known as ADPPA. If passed, it will fundamentally alter U.S. data privacy law.
ADPPA fills the data privacy void, builds in federal preemption over some state data privacy laws, allows individuals to file suit over violations and substantially changes data privacy law enforcement. Like all big changes, ADPPA is getting mixed reviews from media, scholars and businesses. But many see the bill as a triumph for U.S. data privacy that provides a needed national standard for data practices.
Who and what will ADPPA regulate?
ADPPA would apply to "covered" entities, meaning any entity collecting, processing or transferring covered data, including nonprofits and sole proprietors. It also regulates cellphone and internet providers and other common carriers, with potentially concerning changes to federal communications regulation. It does not apply to government entities.
ADPPA defines "covered" data as any information or device that identifies or can be reasonably linked to a person. It also protects biometric data, genetic data and geolocation information.
Protected data includes your location.
Christoph Hetzmannseder/Moment via Getty Images
The bill excludes three big data categories: deidentified data, employee data and publicly available information. That last category includes social media accounts with privacy settings open to public viewing.
While research has repeatedly shown deidentified data can be easily reidentified, the ADPPA attempts to address that by requiring covered entities to take "reasonable technical, administrative, and physical measures to ensure that the information cannot, at any point, be used to re-identify any individual or device."
How ADPPA protects your data
The act would require data collection to be as minimal as possible. The bill allows covered entities to collect, use or share an individual's data only when reasonably necessary and proportionate to a product or service the person requests or to respond to a communication the person initiates. It allows collection for authentication, security incidents, prevention of illegal activities or serious harm to persons, and compliance with legal obligations.
People would gain rights to access and have some control over their data. ADPPA gives users the right to correct inaccuracies and potentially delete their data held by covered entities.
The bill permits data collection as part of research for public good. It allows data collection for peer-reviewed research or research done in the public interest – for example, testing whether a website is unlawfully discriminating. This is important for researchers who might otherwise run afoul of site terms or hacking laws.
The ADPPA also has a provision that tackles the service-conditioned-on-consent problem – those annoying "I Agree" boxes that force people to accept a jumble of legal terms. When you click one of those boxes, you contractually waive your privacy rights as a condition to simply use a service, visit a website or buy a product. The bill will prevent covered entities from using contract law to get around the bill's protections.
Looking to federal electronic surveillance law for guidance
The U.S.'s Electronic Communications Privacy Act can provide federal law makers guidance in finalizing ADPPA. Like the ADPPA, the 1986 ECPA legislation involved a massive overhaul of U.S. electronic privacy law to address adverse effects to individual privacy and civil liberties posed by advancing surveillance and communication technologies. Once again, advances in surveillance and data technologies, such as artificial intelligence, are significantly affecting citizens' rights.
ECPA, still in effect today, provides a baseline national standard for electronic surveillance protections. ECPA protects communications from interception unless one party to the communication consents. But ECPA does not preempt states from passing more protective laws, so states can choose to provide greater privacy rights. The end result: Roughly a quarter of U.S. states require consent of all parties to intercept a communication, thus providing their citizens increased privacy rights.
ECPA's federal/state balance has worked for decades now, and ECPA has not overwhelmed the courts or destroyed commerce.
National preemption
As drafted, ADPPA preempts some state data privacy legislation. This affects California's Consumer Privacy Act, although it does not preempt the Illinois Biometric Information Privacy Act or state laws specifically regulating facial recognition technology. The preemption provisions, however, are in flux as members of the House continue to negotiate the bill.
The federal bill could end up preempting parts of California's tougher state data privacy law.
ADPPA's national standards provide uniform compliance requirements, serving economic efficiency; but its preemption of most state laws has some scholars concerned, and California opposes its passage.
If preemption stands, any final version of the ADPPA will be the law of the land, limiting states from more firmly protecting their citizens' data privacy.
Private right of action and enforcement
ADDPA provides for a private right of action, allowing people to sue covered entities who violate their rights under ADPPA. That gives the bill's enforcement mechanisms a big boost, although it has significant restrictions.
The U.S. Chamber of Commerce and the tech industry oppose a private right of action, preferring ADPPA enforcement be restricted to the Federal Trade Commission. But the FTC has far less staff and far fewer resources than U.S. trial attorneys do.
ECPA, for comparison, has a private right of action. It has not overwhelmed courts or businesses, and entities likely comply with ECPA to avoid civil litigation. Plus, courts have honed ECPA's terms, providing clear precedent and understandable compliance guidelines.
How big are the changes?
The changes to U.S. data privacy law are big, but ADPPA affords much-needed security and data protections to U.S. citizens, and I believe that it is workable with tweaks.
Given how the internet works, data routinely flows across international borders, so many U.S. companies have already built compliance with other nations' laws into their systems. This includes the E.U.'s General Data Protection Regulation – a law similar to the ADPPA. Facebook, for example, provides E.U. citizens with GDPR's protections, but it does not give U.S. citizens those protections, because it is not required to do so.
Congress has done little with data privacy, but ADPPA is poised to change that.
Anne Toomey McKenna, Visiting Professor of Law, University of Richmond
Topics: privacy, Technology
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redpajama_set_name: RedPajamaCommonCrawl


text:
Septoria cornicola är en svampart som beskrevs av Desm. 1867. Septoria cornicola ingår i släktet Septoria och familjen Mycosphaerellaceae.   Inga underarter finns listade i Catalogue of Life.

Källor

Sporsäcksvampar
cornicola

redpajama_set_name: RedPajamaWikipedia


Marla Marhaban is a designer from estumes.com who designs belly dance costumes from thrift store finds.
You all will be pleased to learn that Marhaban Designs is giving belly dancing costumes away. Just go to http://www.facebook.com/estumes.costumes and subscribe to the estumes Bellydance group.
You'll be notified of the give-aways. Just today Carol Ward of Canada won a hand-made black and gold ghawazee dress. See how you can also win!


text:
Arranged Marriage: The Unloved Princess Solves Cases – Prologue
[TOC][Next Chapter]
translated by Grenn
Inside the grand Hall of Great Strength, there was a gigantic Buddha statue gilded in gold. Its left hand was horizontal, across its left foot, while its right hand pointed toward the ceiling with its index forming a circle with its thumb. The statue's eyes were but slits seeming to gaze at the worshippers coming to pray at its feet. A thick smoke of incense filled the hall while the believers and monks chanted Sanskrit in the background, giving the place a solemnity befitting a holy place.
In front of the altar, people of all age came to worship. Among the crowd, there were three eye-catching young girls, especially the one on the leftmost who was dressed in yellow sportswear. Her long hair swayed around her shoulders every time she prostrated and knocked her head on the kneeling cushion. Each time her forehead stuck on it for so long that it seemed as if they were lovers reunited after a long separation. She even seemed reluctant to part way with the kneeling cushion.
After they paid their respect, they went out together.
As soon as they left the hall, one of them, a girl with a ponytail and wearing red clothes, burst in anger. "Mu Wanqing, you were the one who invites us here, so don't give me that half dead expression. Are you asking for a beating?" She gritted her teeth while trying to repress displeasure.
"My dear mother, in her great kindness, told me I have a blind date today. She urged me to go to the temple and pray for… you know… romance and stuff. She hoped I will soon get married. Otherwise, she will break ties with me. I have no choice to come here to soothe her and reassure her that I will not become an old girl." The baby-face woman shrugged while yawning lazily. She could barely open her drowsy eyes. "So, I ask Miss Fang Jing for your understanding. Besides, I was up until 4 AM, working on that big case."
As a dedicated professional (a.k.a. a workaholic), she didn't mind doing overtime, but now she reaped what she sowed.
At that moment, despite how beautiful the daylight was, she only wanted to crash on her bed instead of wasting her time at the temple.
Mu Wanqing, that's her name; Her job, forensic investigator. The woman in red clothes with a fiery temper next to her is called Fang Jing, a comrade-in-arms within the police force. Finally, the girl in t-shirt and jeans with a cheeky face was Jiang Xiaofan, a famous web novelist. All three of them are childhood friends whose friendship is greater than the Great Wall.
Fang Jing fell into silence at once.
"Who could you blame? It's not my fault you had a baby face despite being a 26-year-old single dog since the day you were born. It's no wonder aunty cannot stand it anymore." Jiang Xiaofan stared at the deceivingly young face and sworn to the gods she was absolutely not jealous of Mu Wanqing's face.
However, she thinks her friend's name was the epitome of irony.
It was a very stark contrast for someone with such an elegant name to be a forensic investigator who dabbled with corpses and bloody cases. As a respectable author, she put great importance on beauty and wisdom, but her name couldn't be more common than the most common grass. Why is the world so unfair?!
"If you can look mature like Fang Jing and actively search for a boyfriend, aunty won't force you to go on a blind date!" Jiang Xiaofan flipped back her supple long hair while enjoying the breeze. Her gaze turned toward the sky and her posture exuded an arrogance mixed with elegance. She continued, "Of course, if you were like the great moi who had live amongst the forest and had seen and touch all kind of leaves, that's a different story, but that's impossible for you, so don't even try it."
Mu Wanqing rolled her eyes. Suddenly, she pointed somewhere and shouted, "Ah, a handsome guy!"
"Where? Where?" Jiang Xiaofan lost all her previous elegance and poured all her attention in the direction her friend pointed. Her eyes were like police searchlights, darting left to right, scrutinizing the surrounding, afraid of missing a single handsome male.
"Yeah, your speedy reaction doesn't lose to Miss Fang Jing's reflex. I am so jealous."
"As if, you are just jealous of my beauty and wisdom, not to mention my devastating luck in romance!" Jiang Xiaofan's right index lifted up Mu Wanqing's chin in an act of provocation. A smile streaks across her face as she said, "Lil' Wanqing, Big Sis will give you a piece of advice. You have to be brave at times and recognize your low EQ. When you understand your shortcomings, you can focus on it and change yourself. Only then, can you strive to nab yourself a handsome guy!"
Mu Wanqing could hardly repress a yawn. She was dozing off but willed herself to open her heavy lid eyes. "Jiang Xiaofan, your attitude is no different from a gangster."
"Don't insult me!" Jiang Xiaofan bellowed. In a tone full of righteousness, she continued, "So what if this great miss is a gangster? Have you never heard that a gangster can be cultivated? What's there to fear? A gangster can also be an expert in martial arts. Who would dare to resist? I have attained the realm of omnipotence in all arts. The road is mine to conquer! When you become well versed with the pen and sword, you will be like me – roaming the world unhindered, enjoying the glorious with beauties at hand!"
Mu Wanqing had no strength to roll eyes. She only felt contempt and disgust.
This woman, in front of people, she acts all smart, but inside, apart from being extremely narcissistic, her attitude could only be described as unbridled. Mu Wanqing felt sorry for those passionate fans who believed in Jiang Xiaofan's fake image.
"Jiang Xiaofan, if you want to be a gangster, I shall exterminate you!" Fang Jing was a policewoman with a fiery temper and condone unrestrained acts that don't put the laws in the eyes.
Fang Jing exuded great pressure which caused Jiang Xiaofan to tremble. She retorted fiercely, "It's Wanqing's fault. They said you have to pray with your heart and soul, but you have no sincerity. No wonder the Gods and Buddhas don't answer your prayers. You even dare to blame others!"
"Thank you for your care! But, as a believer of science, I am a true and true atheist." Mu Wanqing indifferently spat out. She even had the time to lazily survey her surroundings. "I can't stand it anymore. Instead of going to pray for love, can we find a place where I can rest first? I'm at my wits ends." Exhausted, she found an old tree, wide and broad, which was perfect for a quick nap.
An old grandma passed by them, but when she heard the three girls. She burst out in anger and croaked at them, "The Buddhas will punish disrespectful people!"
"Eh! If they want to punish, let it be." Mu Wanqing said thoughtlessly. Following that, she fell into a deep sleep.
"Sleep, sleep, sleep! You're really a pig!" Fang Jing scolded her angrily. However, she didn't leave her friend in deep sleep and defenseless. They approached the tree to accompany her.
At that moment, the sky suddenly turned dark. A violent gale blew dust up. Everyone raised their hands to cover their eyes and tried to find a place to shield themselves from the fury of the elements. The next moment, everything returned to normal – no more wind, and the sky was clear. People were shocked by the whimsical weather, but no one noticed that the three girls under the old trees had vanished without a trace.
Somewhere under another sky…
"Mu Wanqing, you're an unlucky star. I [beep] your [beep]! Why did you have to take a nap?!" Fang Jing let out her despair.
"Mu Wanqing, admit it, you're jealous of my popularity with the opposite sex!" Jiang Xiaofan shouted tearily.
As for Mu Wanqing, she was extremely grievous, but there were no tears. "Wasn't I sleeping at the temple just a moment ago? How did I end up in an ancient times movie? Aw, shit… there shouldn't be a law that forbid me from sleeping at the temple?"
One comment on "Arranged Marriage: The Unloved Princess Solves Cases – Prologue"
Kyogre says:


The coach holds the vision and calls the plays, while the quarterback goes out on the field and makes it happen.
Like a coach, elected officials have a vision for their communities. Professional city, town, or county managers, and the teams they lead, use their strengths in leadership, management, and ethics to make them a reality.
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The manager is bound by whatever action the council takes, and power always remains in the hands of the elected representatives of the people.
Receive a free copy of this ICMA book, Leading Your Community: A Guide for Local Elected Leaders.


1. Define SI base units for time, length, mass, and temperature.
2. Explain how adding a prefix changes a unit.
3. Compare the derived units for volume and density.
1. Express numbers in scientific notation.
2. Use dimensional analysis to convert different units of measure.
Section 2.3 How reliable are measurements?
1. Define and compare accuracy and precision.
2. Use significant figures and rounding to reflect the certainty of data.
3. Use percent error to describe the accuracy of experimental data.
9/27/2018 Use the Sig Fig number generator at the link shown. Test yourself on 15 problems. Write down the # the system generates, write down your response. If you miss or if your right, write down the rule that makes the correct answer correct.
10/8/2018 Complete both sides of handout. See link for 2-sided handout on significant figures.
If you were absent, you are not eligible for the extra credit assignment (#2 on small whiteboard for yesterday.
How to convert between Celsius and Kelvin temperature scales.
Demonstrate a knowledge of the Kelvin scale and compare it to the Celsius scale.
How to calculate the concentration of a solute in terms of grams per liter, molarity, parts per million and percent composition.
Prepare solutions to demonstrate their knowledge of the different units of concentration. I&E (12A): Select and use appropriate tools and technology (such as computer-linked probes, spreadsheets and graphing calculators) to perform tests, collect data, analyze relationships, and display data.
The relationship between the molarity of solute in a solution, and the solution's depressed freezing point or elevated boiling point.
Identify and communicate sources of unavoidable experimental error.
Density Problems - Calculations with Grids: The concept of using any equality as a conversion factor is used to introduce grid-style conversions and density density probs. Includes 20 pract. probs and 2 ex with solns.
SI Base Units Explained: SI Base Units of Measure are explained in this tutorial. Several examples are given to see what derived units are.


I am delighted to share that I have accepted an offer to join the Moltin advisory board.
Moltin provides APIs to make it easy to create highly branded eCommerce experiences that go beyond the bog-standard website. Their philosophy is that the way in which we browse and buy products and services is going to become increasingly diverse and innovative, in which people will want to purchase in different form factors, technologies, and places. They are building an API that serves this.
They are very focused on the developer experience and building an engaging community of developers who are not just using Moltin, but also helping to make Moltin itself better. They have assembled a great leadership team, have a solid technology, and I am excited to play a role here.
I first heard about Moltin via my friends at Underscore.vc. I will be helping to guide them in their developer strategy and execution. Speaking of which, they are looking to hire a talented developer lead to be based in Boston. See the role description here.


Within few hours of his comments the Rail Vikas Nigam Limited (RVNL) shot back denying his arguments in a statement.
Kolkata: State urban development minister Firhad Hakim has pointed finger at the ongoing Joka-BBD Bag Metro railway project and accumulation of mud as the possible reasons for the collapse of a portion of Majherhat Bridge in Taratola. Within few hours of his comments the Rail Vikas Nigam Limited (RVNL) shot back denying his arguments in a statement.
The bridge connecting Behala with New Alipore was built by the Kolkata Port Trust (KoPT) nearly 40 years ago, according to sources adding that the KoPT later handed over the maintenance of the bridge to the state public works department which has come under the scanner for alleged lack of supervision and inspection.


n SKY AUTORE, Viewers experience the disjointed world of pop culture through the eyes of the director, the action plays out scene by scene as animated typographic elements weave a common thread in the highly stylized branded SKY environment.
In SKY CLASSIC, classic film posters come to life through careful image manipulation, originally shot footage and seamlessly blended classical film footage.
For SKY DOCUMENTARY, we let strong visuals and arresting sounds take the lead as we evoked the frenzied excitement of the documentary world.


The Baltic sea anomaly is a crashed UFO (flying saucer) and has been there for a very, very long time according to scientists and archaeologists including geologists and me! It's practically turned to stone or should I say "the stuff that covers it that has grown on it over the Millennia has petrified" and that's what makes this datable and it is old!
Not as old as my ex but still VERY old. This thing is pre ice-age and pre humans as we know them today. It has stairs, it has streamlined shapes and a forward looking portal. The stairs are just killer and say's to me that when this thing went down, the occupants lowered the stairs and made an exit? Now that could be pure speculation but sounds about right to me?
I reckon this thing weighs at least 20 tons or more? With the growth it could be 30 tons or more? The scorched earth behind it screams thrusters burning out or on full thrust which is why we see a massive ditch bigger than the "scratched earth" behind it. It looks to me as if it was deliberately ditched and carefully manoeuvred in to place as best they could so it stayed upright? The lines and angles on the outside of the (BSA) craft bear a startling resemblance to the popular TV show's "Star Gate" Pyramid designs?
If you've seen the show, then you'll know what I mean? Even the Star Gate itself has the same design?
Similar design as to the Baltic sea anomaly, same angles and lines?
This video shows the Appolo Moon Mission 20 qactually going to the Moon to recover Alien technology from a crashed UFO BUT they got more than they ever could of imagined? They actually found two Aliens and one Alien that was destroyed probably upon impact when the UFO went down? The supposed captain of the UFO was a woman nicknamed "Mona Lisa" by the crew.
She was nicknamed this because of how she looked when they took away the tube like apparatus that was attached to her face? She is very, very pretty and of outstanding beauty. The video below is by far the best evidence so far and probably to date of the existence of Aliens? Because there's no atmosphere on the Moon, she was estimated to have been there for hundreds of thousands of years just by the state of preservation alone? Which needed to be thawed out.
Here is the source of the post.
Now explorers believe they are one step closer to discovering the truth behind the mysterious 140,000-year-old Baltic Sea Anomaly. Bearing a striking resemblance to the Star Wars Millennium Falcon, the Baltic Sea Anomaly appears to be formed of pieces of angular metal – prompting claims it is a crashed UFO. Swedish explorer Peter Lindberg and his Ocean X team of marine explorers discovered the strange object during a dive searching for an old shipwreck. Instead he discovered the so-called Anomaly.
Denis Asberg, who made the discovery alongside Mr Lindberg, told TV4 in Sweden: "There is a mountain, It could be 20-25 metres tall with a canyon in the middle, and below it there is a lot of loose rocks. "The trail starts from here. Actually there is two trails. There is the one that leads to this large circle. Then there is another trail that leads to the second object which is about 200 metres from the round circle. We found it at the same time as the circle.
Apollo manned Moon mission to recover Alien technology and Alien bodies, it was a SUCCESS!
Even more intriguingly a structure that looks like a staircase appears to lead to a dark hole with a second structure found nearby. Speculation is rife over what the object could be with some saying it could be an anti-submarine device left over from World War Two, a battleship gun turret or indeed a flying saucer. Despite looking like a huge rock, scientists say the structure appears to be made of metal. Electric and satellite diving equipment reportedly cuts out when near the object.
Stefan Hogerborn, a professional diver with Ocean X, said: "Anything electric out there, and the satellite phone as well, stopped working when we were above the object, then when we got away about 200 metres, it turned on again." Mr Lindberg's Ocean X team are continuing to investigate the object, five years after making the initial discovery while exploring the floor of the Bothnian Sea between Sweden and Finland. Sonar has found drag marks behind the object and geologist Steve Weiner says according to his tests, the structure is not a geological formation.
This is an amazing discovery and will go down in history! It need's to be recovered if you can? It's design is beautiful. It is pure Alien technology from the outside to the inside which we cannot see, YET!
An Ocean X interpretation of what the Baltic Sea Anomaly may look like based on their data.
It is thought the object could be at least 140,000 years old after a university professor linked the mysterious disc to the Ice Age. Volker Bruchert, an associate professor of geology at Stockholm University, said: "My hypothesis is that this object, this structure was formed during the Ice Age many thousands of years ago." Ocean X is expected to return to the wreck to continue investigating the discovery. Mr Lindberg said: "We will pretty much just be able to do the same things as we did in 2012. It is not for sure yet but since we're involved in a new TV project it might give us the opportunity."
Denis Asberg, who made the discovery alongside Mr Lindberg, told TV4 in Sweden: "There is a mountain, It could be 20-25 metres tall with a canyon in the middle, and below it there is a lot of loose rocks. "The trail starts from here. Actually there is two trails. There is the one that leads to this large circle. Then there is another trail that leads to the second object which is about 200 metres from the round circle. We found it at the same time as the circle. But we had such focus on the circle that we have not had enough time to look at the other object. It is not circular.


Carvela have come up trumps this party season with a whole array of glitter shoes that quite frankly rival those seen on the designer catwalk at Miu Miu. We love the bright blue glitter court shoes for full-on glamour on New Year's Eve, but the multi-colour glitter courts will go with absolutely everything! It's shoe heaven ladies, we defy you not to love each and every single pair.


I have a pair of twins and am wondering how can I help them each have their own identity?
MOLLY: We received this question from a reader whose twins are in different classrooms at school and often don't get invited to the same birthday parties. She also wondered if she should ask the host parent if she can bring the other twin?
Dr. Susan Rutherford (MOM): No, no, no, and no.
MOM: Twins have a very special relationship but as they grow up they need to separate off and feel that each is a whole person unto himself. I am a twin myself and have had a lot of experience with this.
There's a special relationship between twins that often lasts a lifetime, but as you're growing up, it's very important to be in separate classes and to have separate friends. Generally twins should feel like they have each others' backs (unless there's something really bad going on between them), but they should each have their own sense of identity.
Adult angst often has a lot to do with the search for identity; think of a "mid-life crisis"! That's all about the search for your own identity, and you don't have to be a twin to experience this kind of angst. Twins need to establish their own sense of identity and not always be known as "one of the twins".
MOLLY: How do you help them each set their own identity?
MOM: You do it in a natural way. Twins often have different interests and you want to encourage each one's interests… maybe together when they are younger and more individually as they get older in elementary school. Twins can often have very different groups of friends because they have different personalities, and as a parent, you want to encourage that too.
MOLLY: Even if they are identical?
MOM: Yes, well, identical twins are probably a little different. I think it's a little easier with fraternal twins like myself because the twins don't look exactly alike. With identical twins, they are images of each other, but nevertheless, they still need to be viewed as separate individuals.
It's always better to feel like you're not just "one of the twins". It's okay from time to time, but you really want to make sure your twins each have a strong sense of being a separate self and and a unique, valued individual apart from their twin and from simply being a twin.
Comment below if you have success in helping your twins create their own identities. Or, Contact US if you have a parenting issue you would like to see addressed.


text:
Q: Form Validation with JavaScript, only one of the inputs works I am trying to implement a custom validation for the form, however only one of my inputs actually work. What's more, the function, for some reason, doesn't recognize if there is any text or not in the input field.
Here is the code of one of the inputs of the form:
<form class="formWrapper">

            <input
              class="formInput"
              required
              type="text"
              name="first-name"
              id="first-name"
              placeholder="First Name"
            />

              First name cannot be empty

            <input
              class="formInput"
              required
              type="text"
              name="last-name"
              id="last-name"
              placeholder="Last Name"
            />

              Last Name cannot be empty

            <input
              class="formInput"
              required
              type="text"
              name="Email"
              id="Email"
              placeholder="Email Address"
            />

              Email cannot be empty

            <input
              class="formInput"
              required
              type="text"
              name="Password"
              id="Password"
              placeholder="Password"
            />

              Password cannot be empty

          <button type="submit" class="claimButton">
            Claim Your Free Trial
          </button>

            By clicking the button, you are agreeing to our
            Terms and Services.

        </form>

And here is the JavaScript code, that I have written.
"use strict";

const formInput = document.querySelectorAll(`.formInput`);
const errorImg = document.querySelector(`.errorImg`);
const errorMessage = document.querySelector(`.errorMessage`);
const submitButton = document.querySelector(`.claimButton`);
const firstName = document.querySelector(`#first-name`);
const lastName = document.querySelector(`#last-name`);
const email = document.querySelector(`#Email`);
const password = document.querySelector(`#Password`);

const inputFields = [
  { inputName: firstName },
  {
    inputName: lastName,
  },
  {
    inputName: email,
  },
  {
    inputName: password,
  },
];

const errorOccured = function (i) {
  errorMessage.classList.remove(`hidden`);
  errorImg.classList.remove(`hidden`);
  formInput.classList.add(`errorState`);
};

for (let i = 0; i < inputFields.length; i++) {
  inputFields[i].inputName.addEventListener("invalid", function (e) {
    e.preventDefault();
  });
}

submitButton.addEventListener("click", function () {
  for (let i = 0; i < inputFields.length; i++) {
    if (inputFields[i].inputName.value === "") {
      errorOccured(i);
    }
  }
});

The form itself looks like this:

A: You are misusing both querySelectorAll and querySelector methods.
The querySelectorAll method returns a NodeList with all matched elements, one way to iterate through the result is using for (let item of result) { }, another way is using result.forEach(function (item) { }).
The querySelector method returns the first element matching the given selector/class. Then you can access result.classList on it, for example.
That said, I've made some changes to the submit handler, so it will validate the input fields by adding or removing the hidden class.

const wrappers = document.querySelectorAll('.inputWrapper');

for (let wrapper of wrappers) {
  const formInput = wrapper.querySelector('.formInput');
  formInput.addEventListener('invalid', function (e) {
    e.preventDefault();
  });
}

const submitButton = document.querySelector(`.claimButton`);
submitButton.addEventListener('click', function () {
  for (let wrapper of wrappers) {
    const formInput = wrapper.querySelector('.formInput');
    const errorImg = wrapper.querySelector('.errorImg');
    const errorMessage = wrapper.querySelector('.errorMessage');

    if (!formInput.value) {
      errorImg.classList.remove('hidden');
      errorMessage.classList.remove('hidden');
    } else {
      errorImg.classList.add('hidden');
      errorMessage.classList.add('hidden');
    }
  }
});
.hidden {
  display: none;
}

.inputWrapper {
  margin-bottom: 20px;
}

  <input class="formInput" required type="text" name="first-name" id="first-name" placeholder="First Name" />

    First name cannot be empty

  <input class="formInput" required type="text" name="last-name" id="last-name" placeholder="Last Name" />

    Last name cannot be empty

  <input class="formInput" required type="text" name="email" id="email" placeholder="Email" />

    Email cannot be empty

  <input class="formInput" required type="text" name="password" id="password" placeholder="Password" />

    Password cannot be empty

<button class="claimButton">CLAIM YOUR FREE TRIAL</button>

redpajama_set_name: RedPajamaStackExchange


text:
Q: How to capture login through JMeter into a Web application which has third party auth app integrated such as OKTA? My web application is using OKTA as a third-party authentication tool while login. I want to do load testing of this app through JMeter.
I captured a scenario which does following:

*

*Access URL

*Login into app

*Go to Required page.

*Update the data and Save it.

Script is capturing session token and I handled correlation. The script is showing all request pass while playing back but the data is not getting updated.
What am I missing here?

A: JMeter automatically considers HTTP response status codes below 400 as successful so "all request pass" may mean nothing if your server replies with positive HTTP Status code. Most likely you are hitting the login page with all your requests.
I would recommend running your test with View Results Tree listener enabled and inspect request and especially response details to ensure that your test is doing what it is supposed to be doing. Additionally you can add Debug Sampler(s) to inspect JMeter Variables and Properties names and values at different stages of your test. See How to Debug your Apache JMeter Script article to learn more about how to get to the bottom of your JMeter test script failure.
Once you figure out what was wrong you might want to add few Assertions implementing smarter pass/fail criteria for your test and avoid "false positive" results in the future.


ALFRETON Town may have been involved in a goal-less draw on their first ever visit to Edgeley Park on Saturday, but there was plenty to enthuse over.
The Reds were denied by the woodwork three times as they picked up their first Blue Square Bet Premier Division away point since their 1-0 win at York City back on August Bank Holiday Monday, while the hosts themselves halted a run of five successive league defeats.
To be disappointed with a draw at Stockport County emphasises just how far Alfreton Town have come in the last decade, because ten years ago the third Saturday in December saw the Reds beating Glasshoughton Welfare 4-2 at home in the Northern Counties East League.
Josh Law's fourth minute cross won a corner with both Jake Moult and Nathan Jarman closing in on Hatters' keeper Matt Glennon, then in response Euan Holden played Sean McConville through but Joe Day raced out of goal to boot clear.
Joe Connor headed wide on his Stockport debut from a McConville cross in the ninth minute, then back at the other end Nathan Arnold fired over after good approach work by Anthony Wilson.
Carl Piergianni headed over in the 14th minute after Greg Young backtracked to halt McConville's by-line run, then Anton Brown's decisive tackle blocked Connor's shot at source.
Anthony Church fired a free-kick over the wall but without enough power to beat Glennon, then a strong run by Wilson in the 19th minute down the right petered out with a cross that was too deep.
Moult's volley from 22 yards was held by Glennon, then in the 22nd minute Wilson ran on to Jarman's clever pass but fired past the back post from a tight angle with only the keeper to beat.
Day needed two attempts to gather Joe Edwards' rebound after Tom Elliott's shot had been blocked, then in the 28th minute a cross from Danny Rowe landed on top of the Alfreton net after a penetrating run by Elliott.
Two minutes later Law's free-kick had to be turned behind by Glennon, and from the corner Law's shot was blocked by the keeper and Jarman lashed the loose ball against the upright from six yards.
McConville's angled drive was held by Day after 34 minutes, then three minutes later a Brown throw set up Moult for a thunderous volley that fairly smashed against the crossbar.
A promising run by Wilson eight minutes after the break ended when he was crowded out by covering defenders, then three minutes after that it was Stockport's turn to be thwarted by the upright when McConville let fly from the edge of the area.
Moult managed to intercept Cameron Darkwah's shot from an Edwards' cross in the 64th minute, then eight minutes later Adam Quinn's header from a Law corner was diverted against the post by a defender on the line.
Celebrations were cut short when Wilson found the net after 74 minutes, but an off-side flag ruled it out after Day's clearance had sent Arnold down the left and Church had helped on the cross to feed Wilson.
Another Law corner was delayed one minute later as Paul Clayton replaced Wilson, but the Reds' sub was only denied an immediate goal when Glennon punched the flag-kick clear as he rose to head in virtually on the goal-line.
As Alfreton stepped up the pressure with 11 minutes remaining Church forced the ball through to Arnold, whose shot rebounded off the keeper's legs with Andy Halls preventing it from entering the goal at the expense of a corner.
A clearance from Day struck Darkwah but rebounded for a harmless throw, then a Young through-ball found Arnold wide right but he fired over from a diminishing angle.
In the 90th minute Church fired across the face of goal from Clayton's nod through, then Arnold found the side-netting from another Clayton pass in added time.
Joe Day, Theo Streete, Adam Quinn, Greg Young (c), Anton Brown, Josh Law, Jake Moult, Anthony Church, Nathan Arnold, Anthony Wilson (Paul Clayton 75), Nathan Jarman.
Substitutes not used: Matt Wilson, Levi Mackin, Jamie Mullan, Rob Eagle.
Matt Glennon, Euan Holden (Cameron Darkwah 46), Danny O'Donnell, Sean McConville, Andy Halls, Carl Piergianni, Joe Edwards, Chris Blackburn (Sam Sheridan 76), Joe Connor, Rowe, Tom Elliott.
Substitutes not used: Ian Ormson, Kyle Brownhill, Aaron Cole.
Attendance breakdown: 2,802 including 169 from Alfreton.


"Ever has it been that love knows not its own depth until the hour of separation".
Its Monday evening and Henry is all cuddled up on my knee, having his final bottle of the day. His little eyes are fluttering and his little hands are closed together as if in his own little prayer. I love watching his gorgeous little face and kissing his cute little nose, while he drinks away his beloved milk.
I do this most nights, but tonight is different. As tomorrow my little guys life is about to change as he takes a big leap into nursery life. My mat leave has come to an abrupt end and come Monday I have to return to my full time job. So I'm enjoying this blissful moment and cuddling him closer to me as he feels safe in my arms.
Fast forward to Tuesday evening...My son hates me. He won't make eye contact, he won't laugh at my silly faces and won't even acknowledge my peek-a-boo antics. My 7 month old has become a difficult teen, withholding his smiles, kisses and usual teddy bear like hugs. To him I abandoned him. Instead of our usual fun filled days of "row row row your boat," playing with the hanger (remote, iPhone or nappy cream) & "this little piggy", have been rudely replaced with nursery. Instead of his Mummy's familiar face, he had new faces (some little, some big), new smells (some nice, mostly bad) and new toys (not made by Apple).
I know what you are thinking, how awful a time did Henry have at nursery? Well that's the thing, he had a great old time. On arrival we were greeted by so many smiles from staff and children and we took a spot on the floor amongst the babies and toys. Whilst I filled in some forms, Henry made friends with the other Henry's & Harry's (I told my husband it was a common name) and everything was rosy. I then kissed him goodbye (he was smiling) and went to my local coffee bar to cry in the corner. I called just under an hour later to see how he was doing & apparently he was rolling around happy.
2 hours later I arrived to pick him up and there nestled amongst the other babies, was my sleeping little boy. Enjoying his nap time under the dimmed lights and twinkle twinkle little star lullaby. Now I forgot to mention, Henry missed out on his morning nap, so must have been exhausted. & here I was waking him up when he'd only slept for 10 minutes.
So I'm hoping that his grumpy demeanour and "I hate you Mummy" snubs were in fact signs of sleep deprivation. & not (dare I utter it) separation anxiety. It didn't help that when my husband returned home, Henry returned to his usual self and was playful, super cute and full of smiles for his Daddy. Just proving that he did in fact hate me and it was all my fault.


Handsfree Player for YouTube is an Android app that lets you explore everything YouTube has to offer, hands free. The app brings YouTube content to you whenever you need it hands free.
The idea came about when founder Darren Bond got tired of listening to his CDs one day while on the road and wished that he could get YouTube to play his favorite music non-stop with a simple voice command. Darren wanted an app that could do this and more - it would need to instantly find the user's chosen track or video within YouTube's vast library and automatically start playing it - that's what Handsfree Player for YouTube is about!


CES 2010 Wrap Up Podcast!
We wanted to do something special for the end of CES 2010, so we've recorded a nice little wrap up of most of the mobile content we saw as well as some other good stuff like home entertainment, TV's, etc. Check out our wrap up podcast below!
Special shout out to Sprint for sponsoring our CES content.
We're slowly going to get back into doing them, yeah!
Hello New Year's Resolutions! Lol.
Was an RCA recorder used? There's an annoying buzz in the background.
Putting it on my Nook as I type.
Now let's see if I can get out of here and get to work on time.


text:
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Home World At Least 12 Dead in 2 Landslides in Indonesia
At Least 12 Dead in 2 Landslides in Indonesia
Jorge M.
JAKARTA, Indonesia — Two landslides set off by heavy rainfall and unstable soil killed a minimum of 12 individuals on Java, Indonesia's most populous island, and left rescue employees looking for survivors, catastrophe officers mentioned Sunday.
Among these killed in the landslides in West Java Province had been the top of a neighborhood catastrophe reduction company and an Indonesian Army captain who had gone to assist rescue survivors from the primary landslide on Saturday afternoon. They had been caught in a second landslide that night.
The landslides additionally destroyed a bridge and lower off a number of roads in the West Java village of Cihanjuang. Rescuers labored into the night time however confronted an pressing want for heavy equipment to assist transfer earth and attain any potential survivors.
"The first landslide was triggered by high rainfall and unstable soil conditions," mentioned Raditya Jati, spokesman for the National Disaster Mitigation Agency. "Subsequent landslides occurred while officers were still evacuating victims at the first landslide area."
A girl whose household lives in the village, Dameria Sihombing, mentioned that her father, mom, nephew and niece had been at residence in the village on the time of the landslide. All 4 stay lacking, she mentioned by telephone from Jakarta, the Indonesian capital about 90 miles to the northwest.
The first mudslide buried the household's residence, she mentioned, and the second slide, which was bigger than the primary, buried it even deeper. Many bystanders had been additionally in the trail of the second slide.
"Many people came to see the rescue team and suddenly the second landslide hit," she mentioned. "There were more victims from the second one because it was much bigger than the first landslide. My family is buried inside the house and so far they haven't been found."
Ms. Sihombing mentioned her mother and father, each 60, moved to the village after retirement two years in the past from town of Bandung, about an hour away.
Many individuals weren't in their properties on the time of the landslide as a result of it was afternoon, she mentioned. But amongst these at residence had been her mother and father' neighbors — a mom and three kids. She didn't know whether or not their our bodies had been discovered.
Deadly landslides are frequent in Indonesia, the place deforestation and unlawful small-scale gold mining operations typically contribute to unstable soil situations.
Indonesia's president, Joko Widodo, had warned in October that the nation might expertise extra flooding and landslides than common due to the periodic climate sample often called La Niña. The wet season is anticipated to final till March.
"I want all of us to prepare in anticipation of possible hydrometeorological disasters," the president said at the time.
An area catastrophe official mentioned that by noon Sunday, rescuers had been nonetheless trying to find out how many individuals had been lacking. Eighteen individuals had been reported injured.
A video of the scene confirmed a river of mud that had plowed via a densely packed neighborhood, apparently crushing and protecting quite a lot of buildings.
One video clip from the scene offered by the National Search and Rescue Agency confirmed rescuers working at night time, lifting a body onto a stretcher and carrying it away.
Another confirmed a backhoe lifting a muddy van in order that rescuers might attain the bottom beneath. The van mentioned "Fight Virus" on the again.
The first landslide struck the village hours after a Sriwijaya Air passenger jet crashed into the Java Sea upon takeoff from Jakarta, the Indonesian capital, in heavy rains, killing all 62 aboard.
Indonesia, an archipelago of 17,500 islands that straddles the Equator, was as soon as lined by huge rain forests. But during the last half-century, lots of the forests have been burned and logged to clear the way in which for palm plantations and different farmland.
With 270 million individuals, Indonesia is the world's fourth largest nation and Java, its most populous island, is residence to greater than 140 million.
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