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PubMed1991

Isolation and characterization of microvessels from normal brain and brain tumors.

We describe a new technique for isolating microvessels from both brain and brain tumors. This method is relatively quick and provides a microvessel preparation free of contamination by other brain tissue. Using this method, structurally intact microvessels from normal rat brain and from a malignant rat astrocytoma were isolated and characterized with light microscopy, scanning electron microscopy and transmission electron microscopy. In contrast to microvessels derived from normal rat brain, rat astrocytoma microvessels had endothelial cells with multilayered basement membranes, extensive microvilli on the cell surfaces, and a significant increase in the number of pinocytes in the cytoplasm. Furthermore, astrocytoma microvessel endothelial cells had pleomorphic electron dense nuclei with pale perichromatin, whereas the nuclei of endothelial cells of microvessels derived from normal brain tissue were finely granular and homogeneous with characteristically electron dense perichromatin. The morphologic characteristics of the astrocytoma microvessels are similar to the histologic changes seen in astrocytoma tissue in situ, and correlate well with the known altered functions of brain tumor neovasculature.

Animals↗
PubMed1994

Post-traumatic brain hypothermia reduces histopathological damage following concussive brain injury in the rat.

The purposes of this study were (1) to document the histopathological consequences of moderate traumatic brain injury (TBI) in anesthetized Sprague-Dawley rats, and (2) to determine whether post-traumatic brain hypothermia (30 degrees C) would protect histopathologically. Twenty-four hours prior to TBI, the fluid percussion interface was positioned over the right cerebral cortex. On the 2nd day, fasted rats were anesthetized with 70% nitrous oxide, 1% halothane, and 30% oxygen. Under controlled physiological conditions and normothermic brain temperature (37.5 degrees C), rats were injured with a fluid percussion pulse ranging from 1.7 to 2.2 atmospheres. In one group, brain temperature was maintained at normothermic levels for 3 h after injury. In a second group, brain temperature was reduced to 30 degrees C at 5 min post-trauma and maintained for 3 h. Three days after TBI, brains were perfusion-fixed for routine histopathological analysis. In the normothermic group, damage at the site of impact was seen in only one of nine rats. In contrast, all normothermic animals displayed necrotic neurons within ipsilateral cortical regions lateral and remote from the impact site. Intracerebral hemorrhagic contusions were present in all rats at the gray-white interface underlying the injured cortical areas. Selective neuronal necrosis was also present within the CA3 and CA4 hippocampal subsectors and thalamus. Post-traumatic brain hypothermia significantly reduced the overall sum of necrotic cortical neurons (519 +/- 122 vs 952 +/- 130, mean +/- SE, P = 0.03, Kruskal-Wallis test) as well as contusion volume (0.50 +/- 0.14 vs 2.14 +/- 0.71 mm3, P = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Noradrenergic neurotransmission in the brain of a convulsive mutant mouse, differences between the cerebral cortex and the brain stem.

The Quaking mouse is a genetically determined model of convulsive disorders. We investigated the modulation of noradrenergic neurotransmission through alpha 2-adrenoceptors in the occipital cortex and the brain stem of this mutant. The endogenous levels of noradrenaline were similar in the cerebral cortex of the Quaking mice and their corresponding controls, while a significant increase of endogenous noradrenaline was found in the brain stem of the mutants. The rate of disappearance of noradrenaline in the cerebral cortex and the brain stem after injection of FLA 63 was identical in control and Quaking mice. The calcium-dependent electrically evoked overflow of 3H-noradrenaline from slices of occipital cortex was inhibited by clonidine and enhanced by yohimbine in Quaking as well as in normal mice. The negative feed-back mechanism mediated by presynaptic alpha 2-adrenoceptors operates to a similar extent in both strains of mice. In contrast to the occipital cortex, in the brain stem, the amount of neurotransmitter released by electrical stimulation was significantly increased in Quaking mice when compared with controls. However, in the brain stem, the negative feed-back regulation of noradrenaline release operates to a similar extent in both strains of mice. When the endogenous levels of MOPEG were determined in the brain stem, they were found to be significantly higher in the Quaking mice when compared to the controls. The results suggest that an increase in noradrenergic neurotransmission in the brain stem, rather than in the cerebral cortex, could contribute to the behavioural abnormalities exhibited by the Quaking mice.

Animals↗
PubMed1986

Brain swelling and brain oedema in acute head injury.

Chronological changes in diffuse brain swelling and brain oedema were studied in repeated CT studies following a closed head injury. These findings were compared with changes in intracranial pressure (ICP). The grades of diffuse brain swelling were classified into mild, moderate and marked according to the CT findings. Planimetry of low density areas of brain oedema was carried out on repeated CT images. Diffuse brain swelling was recognized in 71% of patients shortly after the head injury and subsided within days 3-5. Brain oedema first appeared 24 hours post injury and did not reach its maximum size and distribution before days 5-8. Thus, these two events can be clearly separated. The intracranial pressure reflected the course of the brain swelling and was not very high during the presence of maximum oedema.

Acute Disease↗
PubMed2003

[Brain abscesses in diffusion-weighted imaging (DWI)--comparison to cystic brain tumors].

PURPOSE: The clinical usefulness of diffusion-weighted imaging (DWI) was evaluated in patients with brain abscesses in comparison to patients with cystic brain tumors. MATERIAL AND METHODS: Five patients with surgically confirmed brain abscesses underwent beside a brain MRI examination with contrast media application diffusion weighted imaging. Apparent diffusion coefficients (rADC) in three orthogonal diffusion gradient were calculated. The same protocol was used to examine 5 patients with cystic brain tumors. RESULTS: Showing an rADC of 0.33 x 10(-3)/mm(2)/s abscesses have a highly restricted diffusion in comparison to cystic brain tumors with an rADC of 1,67 x 10(-3)/mm(2)/s. CONCLUSION: Diffusion weighted imaging is a usefull diagnostic tool in the work up of brain abscesses.

Adult↗
PubMed2004

R3-survey of traumatic brain injury management in European Brain IT centres year 2001.

OBJECTIVE: To obtain knowledge about the conditions and management of traumatic brain injury (TBI) in a collaborative network of Brain Information Technology centres. DESIGN: The Brain IT (Brain monitoring with Information Technology) survey comprised two parts: local conditions and policies (part A), and a case study part (part B). The information was gathered by written questionnaires followed by telephone interviews. PARTICIPANTS: Twenty-four Brain IT centres participated (two respondents from 18 sites). RESULTS: The average proportion of agreement between duplicate respondents was 0.79 (range 0.44-1.00). All Brain IT centres monitored ICP. The reported order of treatment for intracranial hypertension was: evacuation of mass-lesions and head elevation (1), increase of sedation and Mannitol scheme (2), hyperventilation (3), ventricular drainage (4), craniectomy and pentothal coma (5), and decompressive lobectomy (6). The respondents were less prone to evacuate expansive contusions in relation to extra cerebral hematomas. The most common suggested interventions (alone or in combination) for treatment of intracranial hypertension without mass lesions was the Mannitol scheme (included in 71% of the suggestions), CSF drainage (included in 56%), hyperventilation (included in 32%), and pentothal coma (included in 22%). CONCLUSIONS: The suggested management of TBI was mainly in accordance with published guidelines, although a minor proportion of the answers deviated to some extent. The suggested order and combinations of different treatment interventions varied. Variation of treatment within the range of prescribed standards provides optimal conditions for an interesting future analysis of treatment and monitoring data as collected prospectively in a Brain IT database.

Adult↗
PubMed1999

Role of diffusion-weighted echo-planar MRI in distinguishing between brain brain abscess and tumour: a preliminary report.

Our purpose was to evaluate diffusion-weighted (DW) echo-planar MRI in differentiating between brain abscess and tumour. We examined two patients with surgically confirmed pyogenic brain abscess and 18 with metastatic brain tumours or high-grade glioma, using a 1.5 T system. The apparent diffusion coefficient (ADC) of each necrotic or solid contrast-enhancing lesion was measured with two different b values (20 and 1200 s/mm2). All capsule-stage brain abscesses (4 lesions) and zones of cerebritis (2 lesions) were identified on high-b-value DWI as markedly high-signal areas of decreased ADC (range, 0.58-0.70 [(10-3 mm2/s; mean, 0.63)]). All cystic or necrotic portions of brain tumours (14 lesions) were identified on high-b-value DWI as low-signal areas of increased ADC (range, 2.20-3.20 [(10-3 mm2/s; mean, 2.70)]). Solid, contrast-enhancing portions of brain tumours (19 lesions) were identified on high-b-value DWI as high-signal areas of sightly decreased or increased ADC (range, 0.77-1.29 [(10-3 mm2/s; mean, 0.94)]). Our preliminary results indicate that DW echo-planar MRI be used for distinguishing between brain abscess and tumour.

Aged↗
PubMed1997

The multidrug-resistance P-glycoprotein (Pgp, MDR1) is an early marker of blood-brain barrier development in the microvessels of the developing human brain.

The multidrug-resistance P-glycoprotein (Pgp) was initially identified as an energy-dependent proton pump, which transports a variety of non-related compounds out of chemotherapy-resistant cancer cells. Molecular biological investigations using knockout mice for the mouse homologue of the human Pgp showed that these mice partially lack a functioning blood-brain barrier, indicating that Pgp has an important role in the blood-brain barrier as its normal function. The presence of Pgp expression in formalin-fixed and wax-processed tissue sections can be assessed using the monoclonal antibody, JSB-1. Since no data on the developmental expression of Pgp are available, we stained a developmental series of human brain sections with JSB-1. Our results indicate that Pgp expression in endothelia of brain microvessels occurs regularly in embryos of about 30-mm crown-rump length (CRL). Strong reactivity is seen in blood vessels of fetuses from 123-mm CRL. There is also reactivity in pial blood vessels but not in choroid plexus blood vessels known to be without a blood-brain barrier. Pgp expression is therefore an early marker of the blood-brain barrier in the developing human brain.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2005

Breakdown of the blood-brain barrier to proteins in white matter of the developing brain following systemic inflammation.

Compromised blood-brain barrier permeability resulting from systemic inflammation has been implicated as a possible cause of brain damage in fetuses and newborns and may underlie white matter damage later in life. Rats at postnatal day (P) 0, P8 and P20 and opossums (Monodelphis domestica) at P15, P20, P35, P50 and P60 and adults of both species were injected intraperitoneally with 0.2-10 mg/kg body weight of 055:B5 lipopolysaccharide. An acute-phase response occurred in all animals. A change in the permeability of the blood-brain barrier to plasma proteins during a restricted period of postnatal development in both species was determined immunocytochemically by the presence of proteins surrounding cerebral blood vessels and in brain parenchyma. Blood vessels in white matter, but not grey matter, became transiently permeable to proteins between 10 and 24 h after lipopolysaccharide injection in P0 and P8 rats and P35-P60 opossums. Brains of Monodelphis younger than P35, rats older than P20 and adults of both species were not affected. Permeability of the blood-cerebrospinal fluid (CSF) barrier to proteins was not affected by systemic inflammation for at least 48 h after intraperitoneal injection of lipopolysaccharide. These results show that there is a restricted period in brain development when the blood-brain barrier, but not the blood-CSF barrier, to proteins is susceptible to systemic inflammation; this does not appear to be attributable to barrier "immaturity" but to its stage of development and only occurs in white matter.

Animals↗
PubMed1998

5-Aminolevulinic acid induced endogenous porphyrin fluorescence in 9L and C6 brain tumours and in the normal rat brain.

A new approach in photodynamic therapy is the use of endogenous porphyrins for sensitisation of tumours to light. The induction of endogenous porphyrins after intravenous injection of 5-aminolevulinic acid (ALA, 200 mg kg-1) was studied in 23 rats, bearing intracranial 9L or C6 tumours. After 0, 2, 4, 6, 8, and 22 hours the rats were sacrificed and the fluorescence distribution of endogenous porphyrins was studied in brain tissue sections with a standard fluorescence microscope and a confocal laser scanning microscope. The role of blood-brain barrier disruption on porphyrin production was studied in 2 rats with a cryo-lesion of the cortex. Additionally, 9L and C6 tumour cell cultures were incubated with ALA for 8 hours in vitro. Fluorescence was measured with a fluorescence spectrophotometer in cell cultures and in the brain sections. Porphyrins were detected in vitro in the tumour cells from 2 hours onwards and ex vivo in the tumour sections mainly from 2 to 8 hours, by 22 hours porphyrin fluorescence had almost disappeared. The contralateral brain showed low fluorescence levels between 2 and 6 hours after ALA administration. At the site of the cryo-lesions low fluorescence was measured 6 hours after ALA administration. The 9L tumours fluoresced homogeneously, with a sharp demarcation towards normal brain tissue. Fluorescence in the C6 tumours was patchy, with a poorly fluorescing edge. In both tumour models fluorescence was also detected in brain surrounding the tumour and sometimes in contralateral white matter and ventricle ependyma and pia mater. The slight increase of porphyrin fluorescence in the normal brain of tumour bearing rats, compared to the absence of this in rats without a tumour, was attributed to transport by bulk flow of porphyrins made in the tumours, and possibly also of circulating porphyrins or ALA leaking from the tumour vessels.

Aminolevulinic Acid↗
PubMed1994

Antioxidant enzymes in the brain of zitter rats: abnormal metabolism of oxygen species and its relevance to pathogenic changes in the brain of zitter rats with genetic spongiform encephalopathy.

Zitter rats develop a genetic spongiform encephalopathy characterized by edematous changes in their brains. In order to elucidate the involvement of reactive oxygen species in this process we examined age-related alterations of the activities of the enzymes which metabolize reactive oxygen species. Activities of superoxide dismutase (SOD), D-amino acid oxidase (D-AAO), glutathione peroxidase (GSH-Px) and catalase in the brain and the liver of zitter rats are compared with those of control SD/J rats. In the brain of adult zitter rats which show degenerative changes, significantly enhanced activities of SOD and D-AAO were obtained, whereas activity of catalase was lower than that of the SD/J rats. Prominent abnormalities in catalase and D-AAO but not in SOD activity were demonstrated before or at the same time as the appearance of the morphological vacuolation in the brain of suckling zitter rats. There was no difference in GSH-Px activity between the brains from zitter and SD/J rats. These results suggest that the alteration of hydrogen peroxide (H2O2)-metabolism in microperoxisomes may play an important role in the initiation of degenerative changes in the brain of zitter rats. Enhanced SOD activity observed in the brain of adult zitter rats may be a compensatory response to the high superoxide anion produced in the course of cell damage caused by the H2O2 stagnation. Also, more SOD might produce more H2O2.

Animals↗
PubMed1983

Correlation between brain tissue and cerebrospinal fluid concentrations of selected compounds in rats with intact and injured blood-brain barrier.

We examined how the concentrations of exogenous compounds (and their metabolites) in rat brain tissue correlate with their concentrations in the cerebrospinal fluid (CSF) (i) when the blood-brain barrier (B-BB) is intact and increasing doses of compounds are administered, and (ii) when the function of the B-BB is impaired and small constant doses are given. The impairment of B-BB function was caused by chlorophenoxyacetic acid herbicides. An excellent linear correlation between brain tissue and CSF concentrations, calculated from 14C activities, was obtained with 14C-p-aminobenzoic acid, 14C-antipyrine, and 14C-sucrose administered in increasing doses (to 320 mg/kg, i.v.) to B-BB-intact animals (r = 0.92 to 0.99, P less than 0.001). After the administration of small, constant, i.v. doses of 14C-methyl-4-chlorophenoxyacetic acid, 14C-2,4-dichlorophenoxyacetic acid, or 14C-p-aminobenzoic acid into B-BB-damaged rats, both brain tissue and CSF radioactivities increased about linearly 10-fold or more when the lesions progressed. A close correlation between brain tissue and CSF radioactivities was calculated with each compound (r = 0.97 to 0.99, P less than 0.001). In tests with small constant amounts of 14C-antipyrine, 14C-sucrose, and 125I-labeled human albumin, however, no marked linear correlation could be drawn. This was due to the fact that these compounds always caused roughly the same 14C activities both in the brain tissue and in CSF, i.e., their cerebral penetration was only slightly or negligibly affected by the B-BB impairment. The results suggest that significant changes in compound penetration into rat brain tissue can be monitored in the CSF.

Animals↗
PubMed1985

Neuronotrophic factors for mammalian brain neurons: injury induction in neonatal, adult and aged rat brain.

Tissue from neonatal, adult and aged Sprague-Dawley rat brain contained low levels of survival promoting activity for embryonic neurons from various rat brain regions. This basal neuronotrophic activity was 2-fold higher in adult and 4-fold higher in aged rat brain, with respect to that in neonatal brain. Tissue extracts also contained 4-fold higher levels of neuronotoxic activity in adult and aged than in neonatal brain. Ablation of the occipital/entorhinal cortex caused a 3-fold increase in neuronotrophic activity in the tissue surrounding the wound in neonates and 4-fold in adult and aged brain, with respect to the basal levels. Maximal activities occurred at 3 days, 6 days and 15 days postlesion in neonatal, adult and aged tissue respectively, and subsequently returned to basal levels. Neuronotoxic activity was not induced following injury. The slower neuronotrophic response to injury in older animals may be one of the determinant factors of the slower recovery from brain damage observed in aging.

Age Factors↗
PubMed1991

The severity of excitotoxic brain injury is dependent on brain temperature in immature rat.

The effect of brain temperature on the severity of excitotoxic brain injury was evaluated in perinatal rats. Postnatal day (PND) 7 rats received unilateral intrastriatal injections of 25 nmol N-methyl-D-aspartate (NMDA) and then were exposed for 2 h to one of six different ambient temperatures. Animals were sacrificed 5 days later and the severity of brain injury was assessed quantitatively by comparison of the weights of the injected and contralateral cerebral hemispheres. Injection of NMDA consistently produced extensive unilateral brain injury in rats maintained at normothermia (36 degrees C ambient temperature; 29 +/- 1.8% reduction in the weight of the injected hemisphere). In the range of ambient temperatures between 25 degrees C and 40 degrees C, there was a linear relationship between temperature and the severity of NMDA-induced injury (r2 = 0.95, P less than 0.001, linear regression). In a separate analysis, in PND 7 rats, a positive linear relationship between ambient temperature (28 degrees C and 40 degrees C) and brain temperature was observed (r2 = 0.96, P less than 0.001). These data suggest that the severity of excitotoxic brain injury is dependent upon brain temperature.

Animals↗
PubMed1992

Regionally specific and rapid increases in brain-derived neurotrophic factor messenger RNA in the adult rat brain following seizures induced by systemic administration of kainic acid.

In situ hybridization techniques were used to analyse the spatiotemporal pattern of brain-derived neurotrophic factor messenger RNA elevation associated with kainic acid-induced seizure activity in the rat. Pronounced increases in hippocampal brain-derived neurotrophic factor messenger RNA levels were observed as early as 30 min following the onset of behavioral seizures. The greatest increase (10-fold) occurred in the dentate granule cell layer, while pyramidal layers CA1, CA3, and CA4 exhibited increases of two- to six-fold. Peak elevation of brain-derived neurotrophic factor messenger RNA in CA1 hippocampal region was evident at 4 h in CA3, and in the dentate granule layer at 30 min postseizure. Elevations persisted in the dentate and hilar regions to four days, while the increases in CA1 and CA3 returned to control levels by 16 h following seizure. Significant increases in brain-derived neurotrophic factor messenger RNA were also observed in the superficial layers of cortex (II and III) and in the piriform cortex which reached peak elevations by 8 h. No detectable changes were observed in the dorsomedial thalamus. Although histologically defined pyramidal and granule cell layers displayed relatively uniform increases in brain-derived neurotrophic factor messenger RNA in response to kainate, a closer examination of the labeling patterns using emulsion autoradiography revealed discrete areas of high grain densities overlapping uniform, moderate hybridization densities in the dentate granule cell layer and CA3, suggesting that the capacity to upregulate brain-derived neurotrophic factor messenger RNA in these regions may differ among individual neurons. In conclusion, our studies revealed that brain-derived neurotrophic factor messenger RNA induction in response to systemic kainate administration differs in hippocampal and cortical areas, in magnitude, time of onset and duration. The observed temperospatial pattern does not correspond in a simple way to increases in metabolic or electrical activity associated with seizures or neuronal vulnerability coincident with the seizures.

Animals↗
PubMed1988

The effects of brain bilirubin deposition on auditory brain stem evoked responses in rats.

Auditory brain stem evoked responses (ABR) in newborn infants are altered by elevated serum bilirubin levels and may be used as an indicator of bilirubin toxicity. The hypothesis of our study was that hyperbilirubinemia may affect ABR's because of bilirubin deposition in the brain stem. We examined this hypothesis by studying 21 male adult rats divided into three groups: group A, control (n = 8); group B, low bilirubin (n = 6); and group C, high bilirubin (n = 7). Each experimental group was studied over 150 min. The control group received a buffer solution. The low bilirubin group received a low dose bilirubin bolus of 50 mg/kg followed by continuous infusion of 20 mg/kg/h. The high bilirubin group received a bolus of 100 mg/kg bilirubin followed by continuous infusion of 40 mg/kg/h. All groups received sulfisoxazole (50 mg/kg X 3) during the second hour of the study. Auditory evoked potentials were recorded at 0 and 150 min. At the end of the study, the brains were analyzed for bilirubin content. Bilirubin deposition in the 3 groups was 0.6 +/- 0.28 micrograms/g, 0.93 +/- 0.07 micrograms/g and 3.2 +/- 2.2 micrograms/g for the control, low bilirubin and high bilirubin groups, respectively. Bilirubin deposition in the brain was associated with a significant amplitude reduction of Wave I and III, but had no effect on absolute latencies and interpeak latencies. Very high brain bilirubin concentrations were associated with absence of Waves I and IV. Wave I was also significantly reduced in the low bilirubin group where there was slightly increased bilirubin deposition in the brain. We conclude that ABR changes in the form of wave amplitude reduction were associated with brain stem and cerebellum bilirubin deposition. We speculate that previously reported observations of abnormal ABR changes in hyperbilirubinemic newborn infants are associated with bilirubin deposition.

Animals↗
PubMedDate not supplied

Seizures, brain damage and brain development.

Recent evidence suggests that hippocampal damage can be both the result of seizure activity and the cause of further chronic epilepsy. A review of current models of status epilepticus-induced brain damage reveals that excitotoxic mechanisms probably mediate the lesions in most brain regions. NMDA receptors appear to play a dominant role, although non-NMDA glutamate receptors are important in several specific neuronal populations. In the immature brain, a number of unique metabolic features determine a different set of vulnerabilities, resulting in a brain which is more resistant than the adult's to certain mechanisms of brain damage, but quite vulnerable to others. The inhibition of growth by severe seizure activity has implications for the developing brain that have not yet been fully explored. The mechanisms by which seizure-induced hippocampal lesions cause chronic epilepsy have been explored in several recent animal models. A rearrangement of hippocampal circuits may result from death of selected populations of inhibitory neurons, or from misdirected regeneration by excitatory neurons. It could lead to chronic epilepsy through loss of normal inhibition, through sprouting of new excitatory connections, through conservation of excitatory connections which in a healthy brain would be pruned during development, or through facilitation of kindling by one of these mechanisms. These recent results are beginning to reconcile the pathology seen in human hippocampi ablated for intractable epilepsy with that observed in experimental animals, and offer the promise of even greater advances in the future. They suggest a mechanism for Gower's dictum that "seizures beget seizures" and highlight the importance of the interneurons of the dentate gyrus in epileptogenesis.

Animals↗
PubMed2004

Modulation of the blood-brain barrier in oncology: therapeutic opportunities for the treatment of brain tumours?

Systemically administered chemotherapy is not very effective in the treatment of primary or metastatic brain tumours. An important reason for this low efficacy is insufficient drug delivery to the tumour site due to the presence of the blood-brain barrier (BBB). In this review, we give an overview of strategies that were tested to bypass the BBB or to increase its permeability for anticancer drugs. Local drug administration through intracerebral implants offers only little benefit to patients with brain tumours, probably due to the limited diffusion of the drugs in brain tissue. Temporary disruption of the BBB can be achieved with intracarotid infusions of hypertonic mannitol. This method has been used with some success; however, toxic side effects and the high complexity of the surgical procedure limit its usefulness. More recently, the use of the bradykinin agonist cereport was shown to be useful in preclinical studies, but unfortunately clinical studies did not show improved efficacy. Since P-glycoprotein in the BBB restricts the brain entry of many anticancer drugs, inhibition of this drug transporter may be an option for improved drug delivery to brain tumours. Pre-clinical studies have shown the feasibility to enhance the penetration of paclitaxel into the brain by co-administration with a potent P-glycoprotein inhibitor and further clinical research is warranted.

ATP Binding Cassette Transporter, Subfamily B, Mem↗